Increased 20-HETE synthesis explains reduced cerebral blood flow but not impaired neurovascular coupling after cortical spreading depression in rat cerebral cortex

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Fordsmann, Jonas Christoffer; ko, Rebecca; Choi, Hyun B

2013-01-01

Cortical spreading depression (CSD) is associated with release of arachidonic acid (AA), impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstriction. We tested the hypothesis that the released AA is metabolized by the cytochrome P450 enzyme to produce...... neurovascular coupling after CSD. These findings suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD, and that the attenuation of stimulation-induced CBF responses after CSD has a different mechanism. We suggest that blockade of 20-HETE synthesis may be clinically relevant...

Computational model of cerebral blood flow redistribution during cortical spreading depression

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Verisokin, Andrey Y.; Verveyko, Darya V.; Postnov, Dmitry E.

2016-04-01

In recent decades modelling studies on cortical spreading depression (CSD) and migraine waves successfully contributed to formation of modern view on these fundamental phenomena of brain physiology. However, due to the extreme complexity of object under study (brain cortex) and the diversity of involved physiological pathways, the development of new mathematical models of CSD is still a very relevant and challenging research problem. In our study we follow the functional modelling approach aimed to map the action of known physiological pathways to the specific nonlinear mechanisms that govern formation and evolution of CSD wave patterns. Specifically, we address the role of cerebral blood flow (CBF) redistribution that is caused by excessive neuronal activity by means of neurovascular coupling and mediates a spatial pattern of oxygen and glucose delivery. This in turn changes the local metabolic status of neural tissue. To build the model we simplify the web of known cell-to-cell interactions within a neurovascular unit by selecting the most relevant ones, such as local neuron-induced elevation of extracellular potassium concentration and biphasic response of arteriole radius. We propose the lumped description of distance-dependent hemodynamic coupling that fits the most recent experimental findings.

Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex.

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Piilgaard, Henning; Lauritzen, Martin

2009-09-01

Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head trauma. Here we tested the hypothesis that single episodes of CSD induced acute hypoxia, and prolonged impairment of neurovascular and neurometabolic coupling. Cortical spreading depression was induced in rat frontal cortex, whereas cortical electrical activity and local field potentials (LFPs) were recorded by glass microelectrodes, cerebral blood flow (CBF) by laser-Doppler flowmetry, and tissue oxygen tension (tpO(2)) with polarographic microelectrodes. Cortical spreading depression increased cerebral metabolic rate of oxygen (CMRO(2)) by 71%+/-6.7% and CBF by 238%+/-48.1% for 1 to 2 mins. For the following 2 h, basal tpO(2) and CBF were reduced whereas basal CMRO(2) was persistently elevated by 8.1%+/-2.9%. In addition, within first hour after CSD we found impaired neurovascular coupling (LFP versus CBF), whereas neurometabolic coupling (LFP versus CMRO(2)) remained unaffected. Impaired neurovascular coupling was explained by both reduced vascular reactivity and suppressed function of cortical inhibitory interneurons. The protracted effects of CSD on basal CMRO(2) and neurovascular coupling may contribute to cellular dysfunction in patients with migraine and acutely injured cerebral cortex.

NR2A contributes to genesis and propagation of cortical spreading depression in rats.

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Bu, Fan; Du, Ruoxing; Li, Yi; Quinn, John P; Wang, Minyan

2016-03-22

Cortical spreading depression (CSD) is a transient propagating excitation of synaptic activity followed by depression, which is implicated in migraine. Increasing evidence points to an essential role of NR2A-containing NMDA receptors in CSD propagation in vitro; however, whether these receptors mediate CSD genesis in vivo requires clarification and the role of NR2A on CSD propagation is still under debate. Using in vivo CSD in rats with electrophysiology and in vitro CSD in chick retina with intrinsic optical imaging, we addressed the role of NR2A in CSD. We demonstrated that NVP-AAM077, a potent antagonist for NR2A-containing receptors, perfused through microdialysis probes, markedly reduced cortex susceptibility to CSD, but also reduced magnitude of CSD genesis in rats. Additionally, NVP-AAM077 at 0.3 nmol perfused into the contralateral ventricle, considerably suppressed the magnitude of CSD propagation wave and propagation rate in rats. This reduction in CSD propagation was also observed with TCN-201, a negative allosteric modulator selective for NR2A, at 3 μM, in the chick retina. Our data provides strong evidence that NR2A subunit contributes to CSD genesis and propagation, suggesting drugs selectively antagonizing NR2A-containing receptors might constitute a highly specific strategy treating CSD associated migraine with a likely better safety profile.

Nitroglycerin enhances the propagation of cortical spreading depression: comparative studies with sumatriptan and novel kynurenic acid analogues

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Knapp L

2016-12-01

Full Text Available Levente Knapp,1 Bence Szita,1 Kitti Kocsis,1,2 László Vécsei,2,3 József Toldi1,2 1Department of Physiology, Anatomy, and Neuroscience, University of Szeged, 2MTA-SZTE Neuroscience Research Group, 3Department of Neurology, Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary Background: The complex pathophysiology of migraine is not yet clearly understood; therefore, experimental models are essential for the investigation of the processes related to migraine headache, which include cortical spreading depression (CSD and NO donor-induced neurovascular changes. Data on the assessment of drug efficacy in these models are often limited, which prompted us to investigate a novel combined migraine model in which an effective pharmacon could be more easily identified. Materials and methods: In vivo electrophysiological experiments were performed to investigate the effect of nitroglycerin (NTG on CSD induced by KCl application. In addition, sumatriptan and newly synthesized neuroactive substances (analogues of the neuromodulator kynurenic acid [KYNA] were also tested. Results: The basic parameters of CSDs were unchanged following NTG administration; however, propagation failure was decreased compared to the controls. Sumatriptan decreased the number of CSDs, whereas propagation failure was as minimal as in the NTG group. On the other hand, both of the KYNA analogues restored the ratio of propagation to the control level. Discussion: The ratio of propagation appeared to be the indicator of the effect of NTG. This is the first study providing direct evidence that NTG influences CSD; furthermore, we observed different effects of sumatriptan and KYNA analogues. Sumatriptan changed the generation of CSDs, whereas the analogues acted on the propagation of the waves. Our experimental design overlaps with a large spectrum of processes present in migraine pathophysiology, and it can be a useful experimental model

Three-Dimensional Visualization with Large Data Sets: A Simulation of Spreading Cortical Depression in Human Brain

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Ertürk, Korhan Levent; Şengül, Gökhan

2012-01-01

We developed 3D simulation software of human organs/tissues; we developed a database to store the related data, a data management system to manage the created data, and a metadata system for the management of data. This approach provides two benefits: first of all the developed system does not require to keep the patient's/subject's medical images on the system, providing less memory usage. Besides the system also provides 3D simulation and modification options, which will help clinicians to use necessary tools for visualization and modification operations. The developed system is tested in a case study, in which a 3D human brain model is created and simulated from 2D MRI images of a human brain, and we extended the 3D model to include the spreading cortical depression (SCD) wave front, which is an electrical phoneme that is believed to cause the migraine. PMID:23258956

Three-Dimensional Visualization with Large Data Sets: A Simulation of Spreading Cortical Depression in Human Brain

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Korhan Levent Ertürk

2012-01-01

Full Text Available We developed 3D simulation software of human organs/tissues; we developed a database to store the related data, a data management system to manage the created data, and a metadata system for the management of data. This approach provides two benefits: first of all the developed system does not require to keep the patient's/subject's medical images on the system, providing less memory usage. Besides the system also provides 3D simulation and modification options, which will help clinicians to use necessary tools for visualization and modification operations. The developed system is tested in a case study, in which a 3D human brain model is created and simulated from 2D MRI images of a human brain, and we extended the 3D model to include the spreading cortical depression (SCD wave front, which is an electrical phoneme that is believed to cause the migraine.

Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury

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Lauritzen, Martin; Dreier, Jens Peter; Fabricius, Martin

2011-01-01

Cortical spreading depression (CSD) and depolarization waves are associated with dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells, increased energy metabolism and changes in cerebral blood flow (CBF). There is strong clinical and experimental evidence....... The consequences of these intrinsic mechanisms are intimately linked to the composition of the brain extracellular microenvironment and to the level of brain perfusion and in consequence brain energy supply. This paper summarizes the evidence provided by novel invasive techniques, which implicates CSD...... treatment strategies, which may be used to prevent or attenuate secondary neuronal damage in acutely injured human brain cortex caused by depolarization waves....

Randomized, double-blind, placebo-controlled, proof-of-concept study of the cortical spreading depression inhibiting agent tonabersat in migraine prophylaxis

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Goadsby, P J; Ferrari, M D; Csanyi, A

2009-01-01

Tonabersat is a novel putative migraine prophylactic agent with an unique stereospecific binding site in the brain. Tonabersat has been shown, in animal models, to inhibit experimentally induced cortical spreading depression, the likely underlying mechanism for migraine aura, and cerebrovascular...... the placebo (n = 65) and tonabersat (n = 58) groups. At the primary end-point there was a 1.0-day (95% confidence interval -0.33, 2.39; P = 0.14) difference in reduction in migraine days between tonabersat and placebo. There were 10 secondary efficacy end-points, of which two were statistically significant....... The good tolerability and promising efficacy results support further exploration of higher doses of tonabersat in larger controlled trials....

Influence of ovarian hormones on cortical spreading depression and its suppression by L-kynurenine in rat.

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Virginie Chauvel

Full Text Available Migraine is sexually dimorphic and associated in 20-30% of patients with an aura most likely caused by cortical spreading depression (CSD. We have previously shown that systemic L-kynurenine (L-KYN, the precursor of kynurenic acid, suppresses CSD and that this effect depends on the stage of the estrous cycle in female rats. The objectives here are to determine the influence of ovarian hormones on KCl-induced CSD and its suppression after L-KYN by directly modulating estradiol or progesterone levels in ovariectomized rats. Adult female rats were ovariectomized and subcutaneously implanted with silastic capsules filled with progesterone or 17β-estradiol mixed with cholesterol, with cholesterol only or left empty. Two weeks after the ovariectomy/capsule implantation, the animals received an i.p. injection of L-KYN (300 mg/kg or NaCl as control. Thirty minutes later CSDs were elicited by applying KCl over the occipital cortex and recorded by DC electrocorticogram for 1 hour. The results show that both estradiol and progesterone increase CSD frequency after ovariectomy. The suppressive effect of L-KYN on CSD frequency, previously reported in normal cycling females, is not found anymore after ovariectomy, but reappears after progesterone replacement therapy. Taken together, these results emphasize the complex role of sex hormones on cortical excitability. The CSD increase by estradiol and, more surprisingly, progesterone may explain why clinically migraine with aura appears or worsens during pregnancy or with combined hormonal treatments.

Unexpected effects of peripherally administered kynurenic acid on cortical spreading depression and related blood–brain barrier permeability

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Oláh G

2013-09-01

Full Text Available Gáspár Oláh,1 Judit Herédi,1 Ákos Menyhárt,1 Zsolt Czinege,2 Dávid Nagy,1 János Fuzik,1 Kitti Kocsis,1 Levente Knapp,1 Erika Krucsó,1 Levente Gellért,1 Zsolt Kis,1 Tamás Farkas,1 Ferenc Fülöp,3 Árpád Párdutz,4 János Tajti,4 László Vécsei,4 József Toldi1 1Department of Physiology, Anatomy and Neuroscience, 2Department of Software Engineering, 3Institute of Pharmaceutical Chemistry and MTA-SZTE Research Group for Stereochemistry, 4Department of Neurology and MTA-SZTE Neuroscience Research Group, University of Szeged, Szeged, Hungary Abstract: Cortical spreading depression (CSD involves a slowly-propagating depolarization wave in the cortex, which can appear in numerous pathophysiological conditions, such as migraine with aura, stroke, and traumatic brain injury. Neurons and glial cells are also depolarized transiently during the phenomena. CSD is followed by a massive increase in glutamate release and by changes in the brain microcirculation. The aim of this study was to investigate the effects of two N-methyl-D-aspartate receptor antagonists, endogenous kynurenic acid (KYNA and dizocilpine, on CSD and the related blood–brain barrier (BBB permeability in rats. In intact animals, KYNA hardly crosses the BBB but has some positive features as compared with its precursor L-Kynurenine, which is frequently used in animal studies (KYNA cannot be metabolized to excitotoxic agents such as 3-hydroxy-L-kynurenine and quinolinic acid. We therefore investigated the possible effects of peripherally administered KYNA. Repetitive CSD waves were elicited by the application of 1 M KCl solution to the cortex. Direct current-electrocorticograms were measured for 1 hour. Four parameters of the waves were compared. Evans blue dye and fluorescent microscopy were used to study the possible changes in the permeability of the BBB. The results demonstrated that N-methyl-D-aspartate receptor antagonists can reduce the number of CSD waves and decrease

Persistent increase in oxygen consumption and impaired neurovascular coupling after spreading depression in rat neocortex

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Hansen, Henning Piilgaard; Lauritzen, Martin

2009-01-01

Cortical spreading depression (CSD) is associated with a dramatic failure of brain ion homeostasis and increased energy metabolism. There is strong clinical and experimental evidence to suggest that CSD is the mechanism of migraine, and involved in progressive neuronal injury in stroke and head t...

Increased susceptibility to cortical spreading depression in the mouse model of familial hemiplegic migraine type 2.

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Loredana Leo

2011-06-01

Full Text Available Familial hemiplegic migraine type 2 (FHM2 is an autosomal dominant form of migraine with aura that is caused by mutations of the α2-subunit of the Na,K-ATPase, an isoform almost exclusively expressed in astrocytes in the adult brain. We generated the first FHM2 knock-in mouse model carrying the human W887R mutation in the Atp1a2 orthologous gene. Homozygous Atp1a2(R887/R887 mutants died just after birth, while heterozygous Atp1a2(+/R887 mice showed no apparent clinical phenotype. The mutant α2 Na,K-ATPase protein was barely detectable in the brain of homozygous mutants and strongly reduced in the brain of heterozygous mutants, likely as a consequence of endoplasmic reticulum retention and subsequent proteasomal degradation, as we demonstrate in transfected cells. In vivo analysis of cortical spreading depression (CSD, the phenomenon underlying migraine aura, revealed a decreased induction threshold and an increased velocity of propagation in the heterozygous FHM2 mouse. Since several lines of evidence involve a specific role of the glial α2 Na,K pump in active reuptake of glutamate from the synaptic cleft, we hypothesize that CSD facilitation in the FHM2 mouse model is sustained by inefficient glutamate clearance by astrocytes and consequent increased cortical excitatory neurotransmission. The demonstration that FHM2 and FHM1 mutations share the ability to facilitate induction and propagation of CSD in mouse models further support the role of CSD as a key migraine trigger.

Propagation of cortical spreading depression into the hippocampus: The role of the entorhinal cortex.

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Martens-Mantai, Tanja; Speckmann, Erwin-Josef; Gorji, Ali

2014-07-22

Propagation of cortical spreading depression (CSD) to the subcortical structures could be the underlying mechanism of some neurological deficits in migraine with aura. The entorhinal cortex (EC) as a gray matter bridge between the neocortex and subcortical regions plays an important role in this propagation. In vitro combined neocortex-hippocampus brain slices were used to study the propagation pattern of CSD between the neocortex and the hippocampus. The effects of different compounds as well as tetanic electrical stimulations in the EC on propagation of CSD to the hippocampus were investigated. Repetitive induction of CSD by KCl injection in the somatosensory cortex enhanced the probability of CSD entrance to the hippocampus via EC. Local application of AMPA receptor blocker CNQX and cannabinoid receptor agonist WIN 55212-2 in EC facilitated the propagation of CSD to the hippocampus, whereas application of NMDA receptor blocker APV and GABA A receptor blocker bicuculline in this region reduced the probability of CSD penetration to the hippocampus. Application of tetanic stimulation in EC also facilitated the propagation of CSD entrance to the hippocampus. Our data suggest the importance of synaptic plasticity of EC in filtering the propagation of CSD into subcortical structures and possibly the occurrence of concomitant neurological deficits. Synapse, 2014. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.

History of migraine with aura and cortical spreading depression from 1941 and onwards

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Tfelt-Hansen, P C

2010-01-01

Several personal descriptions of migraine with aura from 1870 onwards reported a slow, gradual progression of symptoms. Lashley in 1941 meticulously chartered his own auras and concluded that the symptomatology reflected a cortical process progressing with a speed of 3 mm/min across the primary...... for measurements of regional cerebral blood flow (rCBF) in 1974 made it possible to detect spreading oligaemia during migraine aura. Between 1981 and 1990 a series of studies of rCBF during migraine attacks showed reduced brain blood flow posteriorly spreading slowly and contiguously anteriorly and crossing...... and it was considerably strengthened by the demonstration of a long-lasting oligaemia in rats in the wake of CSD. In the primates CSD is not easily elicited, but it has in recent years been clearly demonstrated in patients with brain trauma and stroke. Finally, mutations for familial hemiplegic migraine have been...

'Spreading depression of Leão' and its emerging relevance to acute brain injury in humans

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Lauritzen, Martin; Strong, Anthony J

2016-01-01

experiencing the visual (or sensorimotor) aura of migraine. In this review, we trace from their first description in rabbits through to their detection and study in migraine and the injured human brain, and from our personal perspectives, the evolution of understanding of the importance of spread of mass......A new research field in translational neuroscience has opened as a result of the recognition since 2002 that "spreading depression of Leão" can be detected in many patients with acute brain injury, whether vascular and spontaneous, or traumatic in origin, as well as in those many individuals...... depolarisations in cerebral grey matter. Detection of spontaneous depolarisations occurring and spreading in the periphery or penumbra of experimental focal cortical ischemic lesions and of their adverse effects on the cerebral cortical microcirculation and on the tissue glucose and oxygen pools has led...

Cortical thickness differences between bipolar depression and major depressive disorder.

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Lan, Martin J; Chhetry, Binod Thapa; Oquendo, Maria A; Sublette, M Elizabeth; Sullivan, Gregory; Mann, J John; Parsey, Ramin V

2014-06-01

Bipolar disorder (BD) is a psychiatric disorder with high morbidity and mortality that cannot be distinguished from major depressive disorder (MDD) until the first manic episode. A biomarker able to differentiate BD and MDD could help clinicians avoid risks of treating BD with antidepressants without mood stabilizers. Cortical thickness differences were assessed using magnetic resonance imaging in BD depressed patients (n = 18), MDD depressed patients (n = 56), and healthy volunteers (HVs) (n = 54). A general linear model identified clusters of cortical thickness difference between diagnostic groups. Compared to the HV group, the BD group had decreased cortical thickness in six regions, after controlling for age and sex, located within the frontal and parietal lobes, and the posterior cingulate cortex. Mean cortical thickness changes in clusters ranged from 7.6 to 9.6% (cluster-wise p-values from 1.0 e-4 to 0.037). When compared to MDD, three clusters of lower cortical thickness in BD were identified that overlapped with clusters that differentiated the BD and HV groups. Mean cortical thickness changes in the clusters ranged from 7.5 to 8.2% (cluster-wise p-values from 1.0 e-4 to 0.023). The difference in cortical thickness was more pronounced when the subgroup of subjects with bipolar I disorder (BD-I) was compared to the MDD group. Cortical thickness patterns were distinct between BD and MDD. These results are a step toward developing an imaging test to differentiate the two disorders. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

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Ayata, Cenk; Lauritzen, Martin

2015-01-01

Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads...

Serotonin depletion can enhance the cerebrovascular responses induced by cortical spreading depression via the nitric oxide pathway.

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Saengjaroentham, Chonlawan; Supornsilpchai, Weera; Ji-Au, Wilawan; Srikiatkhachorn, Anan; Maneesri-le Grand, Supang

2015-02-01

Serotonin (5-HT) is an important neurotransmitter involved in the control of neural and vascular responses. 5-HT depletion can induce several neurological disorders, including migraines. Studies on a cortical spreading depression (CSD) migraine animal model showed that the cortical neurons sensitivity, vascular responses, and nitric oxide (NO) production were significantly increased in 5-HT depletion. However, the involvement of NO in the cerebrovascular responses in 5-HT depletion remains unclear. This study aimed to investigate the role of NO in the CSD-induced alterations of cerebral microvessels in 5-HT depletion. Rats were divided into four groups: control, control with L-NAME treatment, 5-HT depleted, and 5-HT depleted with L-NAME treatment. 5-HT depletion was induced by intraperitoneal injection with para-chlorophenylalanine (PCPA) 3 days before the experiment. The CSD was triggered by KCl application. After the second wave of CSD, N-nitro-l-arginine methyl ester (L-NAME) or saline was intravenously injected into the rats with or without L-NAME treatment groups, respectively. The intercellular adhesion molecules-1 (ICAM-1), cell adhesion molecules-1 (VCAM-1), and the ultrastructural changes of the cerebral microvessels were examined. The results showed that 5-HT depletion significantly increased ICAM-1 and VCAM-1 expressions in the cerebral cortex. The number of endothelial pinocytic vesicles and microvilli was higher in the 5-HT depleted group when compared to the control. Interestingly, L-NAME treatment significantly reduced the abnormalities observed in the 5-HT depleted group. The results of this study demonstrated that an increase of NO production is one of the mechanisms involved in the CSD-induced alterations of the cerebrovascular responses in 5-HT depletion.

Behavior in the open field predicts the number of KCl-induced cortical spreading depressions in rats.

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Bogdanov, Volodymyr Borysovych; Bogdanova, Olena Viktorivna; Koulchitsky, Stanislav Vladimirovich; Chauvel, Virginie; Multon, Sylvie; Makarchuk, Mykola Yukhymovych; Brennan, Kevin Christopher; Renshaw, Perry Franklin; Schoenen, Jean

2013-01-01

Anxiety disorders are known to be comorbid with migraine, and cortical spreading depression (CSD) is the most likely cause of the migraine aura. To search for possible correlations between susceptibility to CSD and anxiety we used the open field test in male Sprague-Dawley rats chronically treated with the preventive anti-migraine drugs valproate or riboflavin. Animals avoiding the central area of the open field chamber and those with less exploratory activity (i.e. rearing) were considered more anxious. After 4 weeks of treatment CSDs were elicited by application of 1M KCl over the occipital cortex and the number of CSDs occurring over a 2h period was compared to the previously assessed open field behavior. Higher anxiety-like behavior was significantly correlated with a higher frequency of KCl-induced CSDs. In saline-treated animals, fewer rearings were found in animals with more frequent CSDs (R=-1.00). The duration of ambulatory episodes in the open field center correlated negatively with number of CSDs in the valproate group (R=-0.83; popen field center in both groups (R=-0.75; p<0.05 and R=-0.58; p<0.1 respectively). These results suggest that anxiety symptoms are associated with susceptibility to CSD and might explain why it can be an aggravating factor in migraine with aura. Copyright © 2012 Elsevier B.V. All rights reserved.

Evidence for increased glutamatergic cortical facilitation in children and adolescents with major depressive disorder.

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Croarkin, Paul E; Nakonezny, Paul A; Husain, Mustafa M; Melton, Tabatha; Buyukdura, Jeylan S; Kennard, Betsy D; Emslie, Graham J; Kozel, F Andrew; Daskalakis, Zafiris J

2013-03-01

Converging lines of evidence implicate the glutamate and γ-aminobutyric acid neurotransmitter systems in the pathophysiology of major depressive disorder. Transcranial magnetic stimulation cortical excitability and inhibition paradigms have been used to assess cortical glutamatergic and γ-aminobutyric acid-mediated tone in adults with major depressive disorder, but not in children and adolescents. To compare measures of cortical excitability and inhibition with 4 different paradigms in a group of children and adolescents with major depressive disorder vs healthy controls. Cross-sectional study examining medication-free children and adolescents (aged 9-17 years) with major depressive disorder compared with healthy controls. Cortical excitability was assessed with motor threshold and intracortical facilitation measures. Cortical inhibition was measured with cortical silent period and intracortical inhibition paradigms. University-based child and adolescent psychiatry clinic and neurostimulation laboratory. Twenty-four participants with major depressive disorder and 22 healthy controls matched for age and sex. Patients with major depressive disorder were medication naive and had moderate to severe symptoms based on an evaluation with a child and adolescent psychiatrist and scores on the Children's Depression Rating Scale-Revised. Motor threshold, intracortical facilitation, cortical silent period, and intracortical inhibition. Compared with healthy controls, depressed patients had significantly increased intracortical facilitation at interstimulus intervals of 10 and 15 milliseconds bilaterally. There were no significant group differences in cortical inhibition measures. These findings suggest that major depressive disorder in children and adolescents is associated with increased intracortical facilitation and excessive glutamatergic activity.

Self-Referential Processing, Rumination, and Cortical Midline Structures in Major Depression

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Nejad, Ayna Baladi; Fossati, Philippe; Lemogne, Cédric

2013-01-01

Major depression is associated with a bias toward negative emotional processing and increased self-focus, i.e., the process by which one engages in self-referential processing. The increased self-focus in depression is suggested to be of a persistent, repetitive and self-critical nature, and is conceptualized as ruminative brooding. The role of the medial prefrontal cortex in self-referential processing has been previously emphasized in acute major depression. There is increasing evidence that self-referential processing as well as the cortical midline structures play a major role in the development, course, and treatment response of major depressive disorder. However, the links between self-referential processing, rumination, and the cortical midline structures in depression are still poorly understood. Here, we reviewed brain imaging studies in depressed patients and healthy subjects that have examined these links. Self-referential processing in major depression seems associated with abnormally increased activity of the anterior cortical midline structures. Abnormal interactions between the lateralized task-positive network, and the midline cortical structures of the default mode network, as well as the emotional response network, may underlie the pervasiveness of ruminative brooding. Furthermore, targeting this maladaptive form of rumination and its underlying neural correlates may be key for effective treatment. PMID:24124416

Self-referential processing, rumination, and cortical midline structures in major depression

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Ayna Baladi Nejad

2013-10-01

Full Text Available Major depression is associated with a bias towards negative emotional processing and increased self-focus, i.e. the process by which one engages in self-referential processing. The increased self-focus in depression is suggested to be of a persistent, repetitive and self-critical nature and is conceptualised as ruminative brooding. The role of the medial prefrontal cortex in self-referential processing has been previously emphasised in acute major depression. There is increasing evidence that self-referential processing as well as the cortical midline structures play a major role in the development, course and treatment response of major depressive disorder. However, the links between self-referential processing, rumination, and the cortical midline structures in depression are still poorly understood. Here, we reviewed brain imaging studies in depressed patients and healthy subjects that have examined these links. The literature suggests that self-referential processing in major depression is associated with increased activity of the anterior cortical midline structures. Abnormal interactions between the lateralised task-positive network, and the midline cortical structures of the default mode network, as well as the emotional response network, may underlie the pervasiveness of ruminative brooding. Furthermore, targeting this maladaptive form of rumination and its underlying neural correlates may be key for effective treatment.

l-Citrulline ameliorates cerebral blood flow during cortical spreading depression in rats: Involvement of nitric oxide- and prostanoids-mediated pathway

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Yuki Kurauchi

2017-03-01

Full Text Available l-Citrulline is a potent precursor of l-arginine, and exerts beneficial effect on cardiovascular system via nitric oxide (NO production. Migraine is one of the most popular neurovascular disorder, and imbalance of cerebral blood flow (CBF observed in cortical spreading depression (CSD contributes to the mechanism of migraine aura. Here, we investigated the effect of l-citrulline on cardiovascular changes to KCl-induced CSD. in rats. Intravenous injection of l-citrulline prevented the decrease in CBF, monitored by laser Doppler flowmetry, without affecting mean arterial pressure and heart rate during CSD. Moreover, l-citrulline attenuated propagation velocity of CSD induced by KCl. The effect of l-citrulline on CBF change was prevented by l-NAME, an inhibitor of NO synthase, but not by indomethacin, an inhibitor of cyclooxygenase. On the other hand, attenuation effect of l-citrulline on CSD propagation velocity was prevented not only by l-NAME but also by indomethacin. In addition, propagation velocity of CSD was attenuated by intravenous injection of NOR3, a NO donor, which was diminished by ODQ, an inhibitor of soluble guanylyl cyclase. These results suggest that NO/cyclic GMP- and prostanoids-mediated pathway differently contribute to the effect of l-citrulline on the maintenance of CBF.

The relationship of impulsivity and cortical thickness in depressed and non-depressed adolescents.

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Fradkin, Yuli; Khadka, Sabin; Bessette, Katie L; Stevens, Michael C

2017-10-01

Major Depressive Disorder (MDD) is recognized to be heterogeneous in terms of brain structure abnormality findings across studies, which might reflect previously unstudied traits that confer variability to neuroimaging measurements. The purpose of this study was to examine the relationships between different types of trait impulsivity and MDD diagnosis on adolescent brain structure. We predicted that adolescents with depression who were high on trait impulsivity would have more abnormal cortical structure than depressed patients or non-MDD who were low on impulsivity. We recruited 58 subjects, including 29 adolescents (ages 12-19) with a primary DSM-IV diagnosis of MDD and a history of suicide attempt and 29 demographically-matched healthy control participants. Our GLM-based analyses sought to describe differences in the linear relationships between cortical thickness and impulsivity trait levels. As hypothesized, we found significant moderation effects in rostral middle frontal gyrus and right paracentral lobule cortical thickness for different subscales of the Barratt Impulsiveness Scale. However, although these brain-behavior relationships differed between diagnostic study groups, they were not simple additive effects as we had predicted. For the middle frontal gyrus, non-MDD participants showed a strong positive association between cortical thickness and BIS-11 Motor scores, while MDD-diagnosed participants showed a negative association. For Non-Planning Impulsiveness, paracentral lobule cortical thickness was observed with greater impulsivity in MDD, but no association was found for controls. In conclusion, the findings confirm that dimensions of impulsivity have discrete neural correlates, and show that relationships between impulsivity and brain structure are expressed differently in adolescents with MDD compared to non-MDD.

Neonatal L-glutamine modulates anxiety-like behavior, cortical spreading depression, and microglial immunoreactivity: analysis in developing rats suckled on normal size- and large size litters.

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de Lima, Denise Sandrelly Cavalcanti; Francisco, Elian da Silva; Lima, Cássia Borges; Guedes, Rubem Carlos Araújo

2017-02-01

In mammals, L-glutamine (Gln) can alter the glutamate-Gln cycle and consequently brain excitability. Here, we investigated in developing rats the effect of treatment with different doses of Gln on anxiety-like behavior, cortical spreading depression (CSD), and microglial activation expressed as Iba1-immunoreactivity. Wistar rats were suckled in litters with 9 and 15 pups (groups L 9 and L 15 ; respectively, normal size- and large size litters). From postnatal days (P) 7-27, the animals received Gln per gavage (250, 500 or 750 mg/kg/day), or vehicle (water), or no treatment (naive). At P28 and P30, we tested the animals, respectively, in the elevated plus maze and open field. At P30-35, we measured CSD parameters (velocity of propagation, amplitude, and duration). Fixative-perfused brains were processed for microglial immunolabeling with anti-IBA-1 antibodies to analyze cortical microglia. Rats treated with Gln presented an anxiolytic behavior and accelerated CSD propagation when compared to the water- and naive control groups. Furthermore, CSD velocity was higher (p litter sizes, and for microglial activation in the L 15 groups. Besides confirming previous electrophysiological findings (CSD acceleration after Gln), our data demonstrate for the first time a behavioral and microglial activation that is associated with early Gln treatment in developing animals, and that is possibly operated via changes in brain excitability.

Cortical thickness predicts the first onset of major depression in adolescence.

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Foland-Ross, Lara C; Sacchet, Matthew D; Prasad, Gautam; Gilbert, Brooke; Thompson, Paul M; Gotlib, Ian H

2015-11-01

Given the increasing prevalence of Major Depressive Disorder and recent advances in preventative treatments for this disorder, an important challenge in pediatric neuroimaging is the early identification of individuals at risk for depression. We examined whether machine learning can be used to predict the onset of depression at the individual level. Thirty-three never-disordered adolescents (10-15 years old) underwent structural MRI. Participants were followed for 5 years to monitor the emergence of clinically significant depressive symptoms. We used support vector machines (SVMs) to test whether baseline cortical thickness could reliably distinguish adolescents who develop depression from adolescents who remained free of any Axis I disorder. Accuracies from subsampled cross-validated classification were used to assess classifier performance. Baseline cortical thickness correctly predicted the future onset of depression with an overall accuracy of 70% (69% sensitivity, 70% specificity; p=0.021). Examination of SVM feature weights indicated that the right medial orbitofrontal, right precentral, left anterior cingulate, and bilateral insular cortex contributed most strongly to this classification. These findings indicate that cortical gray matter structure can predict the subsequent onset of depression. An important direction for future research is to elucidate mechanisms by which these anomalies in gray matter structure increase risk for developing this disorder. Copyright © 2015 Elsevier Ltd. All rights reserved.

Neonatal taurine and alanine modulate anxiety-like behavior and decelerate cortical spreading depression in rats previously suckled under different litter sizes.

Science.gov (United States)

Francisco, Elian da Silva; Guedes, Rubem Carlos Araújo

2015-11-01

The amino acids taurine and alanine play a role in several physiological processes, including behavior and the electrical activity of the brain. In this study, we investigated the effect of treatment with taurine or alanine on anxiety-like behavior and the excitability-dependent phenomenon known as cortical spreading depression (CSD), using rats suckled in litters with 9 and 15 pups (groups L9 and L15). From postnatal days 7 to 27, the animals received per gavage 300 mg/kg/day of taurine or alanine or both. At 28 days, we tested the animals in the elevated plus maze, and at 33-35 days, we recorded CSD and analyzed its velocity of propagation, amplitude, and duration. Compared with water-treated controls, the L9 groups treated with taurine or alanine displayed anxiolytic behavior (higher number of entries in the open arms; p taurine, alanine, or both) treated at adulthood (90-110 days). The L15 condition resulted in smaller durations and higher CSD velocities compared with the L9 condition. Besides reinforcing previous evidence of behavioral modulation by taurine and alanine, our data are the first confirmation that treatment with these amino acids decelerates CSD regardless of lactation conditions (normal versus unfavorable lactation) or age at amino acid administration (young versus adult). The results suggest a modulating role for both amino acids on anxiety behavior and neuronal electrical activity.

Spreading depolarizations and late secondary insults after traumatic brain injury

DEFF Research Database (Denmark)

Hartings, Jed A; Strong, Anthony J; Fabricius, Martin

2009-01-01

Here we investigated the incidence of cortical spreading depolarizations (spreading depression and peri-infarct depolarization) after traumatic brain injury (TBI) and their relationship to systemic physiologic values during neurointensive care. Subdural electrode strips were placed on peri......-contusional cortex in 32 patients who underwent surgical treatment for TBI. Prospective electrocorticography was performed during neurointensive care with retrospective analysis of hourly nursing chart data. Recordings were 84 hr (median) per patient and 2,503 hr in total. In 17 patients (53%), 280 spreading...... depolarizations (spreading depressions and peri-infarct depolarizations) were observed. Depolarizations occurred in a bimodal pattern with peak incidence on days 1 and 7. The probability of a depolarization occurring increased significantly as a function of declining mean arterial pressure (MAP; R(2) = 0.78; p...

[Cortical Release Signs in Patients with Schizophrenia, Depressive Disorders, and Bipolar Affective Disorder].

Science.gov (United States)

de la Espriella, Ricardo Andrés; Hernández, José Fernando; Espejo, Lina María

2013-12-01

Determining the presence of cortical release signs associated with white matter damage, is a clinically easy method to perform. The objective of this study is to determine the presence of cortical release signs in patients with mental illnesses and cerebrovascular disease, as well as its clinical usefulness, given that it indicates cortical damage. A review was made of cortical release signs in patients hospitalized in clinical psychiatry and general hospitals with bipolar affective disorder (40), depression (37), schizophrenia (33), cardiovascular disease (33) and dementia (37). The signs of cortical release do not have the same importance as cortical damage. For example, the glabellar reflex was found in all the groups, that of paratonia, particularly in the group with schizophrenia, and others signs in the group of patients with dementia. It is suggested that these signs imply subcortical white matter damage. The appearance of these signs shows the need for a follow up of patients diagnosed with bipolar affective disorder, depression and schizophrenia. Copyright © 2013 Asociación Colombiana de Psiquiatría. Publicado por Elsevier España. All rights reserved.

Spreading depolarizations occur in human ischemic stroke with high incidence

DEFF Research Database (Denmark)

Dohmen, C.; Sakowitz, O.W.; Fabricius, M.

2008-01-01

Objective: Cortical spreading depression (CSD) and periinfarct depolarization (PID) have been shown in various experimental models of stroke to cause secondary neuronal damage and infarct expansion. For decades it has been questioned whether CSD or PID occur in human ischemic stroke. Here, we...... potential change spreading between adjacent channels was accompanied by transient depression of ECoG activity. In PID, a slow potential change spread between neighboring channels despite already established suppression of ECoG activity. Most CSDs and PIDs appeared repetitively in clusters. CSD or PID...... was observed in all but two patients. In these two patients, the electrode strip had been placed over infarcted tissue, and accordingly, no local ECoG or recurrent transient depolarization activity occurred throughout the observation period. Interpretation: CSD and PID occurred spontaneously with high...

An Exploratory Study of Spectroscopic Glutamatergic Correlates of Cortical Excitability in Depressed Adolescents

Directory of Open Access Journals (Sweden)

Charles P. Lewis

2016-11-01

Full Text Available Introduction: Transcranial magnetic stimulation (TMS research has suggested dysfunction in cortical glutamatergic systems in depression, while proton magnetic resonance spectroscopy (1H-MRS studies have demonstrated deficits in concentrations of glutamatergic metabolites in depressed individuals in several cortical regions, including the anterior cingulate cortex (ACC. However, few studies have combined TMS and MRS methods to examine relationships between glutamatergic neurochemistry and excitatory and inhibitory neural functions, and none have utilized TMS-MRS methodology in clinical populations or in youth. This exploratory study aimed to examine relationships between TMS measures of cortical excitability and inhibition and concentrations of glutamatergic metabolites as measured by 1H-MRS in depressed adolescents. Methods: Twenty-four children and adolescents (aged 11-18 years with depressive symptoms underwent TMS testing, which included measures of the resting motor threshold (RMT, cortical silent period (CSP, short-interval intracortical inhibition (SICI, and intracortical facilitation (ICF. Fourteen participants from the same sample also completed 1H-MRS in a 3 T MRI scanner after TMS testing. Glutamate + glutamine (Glx concentrations were measured in medial ACC and left primary motor cortex voxels with a TE-optimized PRESS sequence. Metabolite concentrations were corrected for cerebrospinal fluid after tissue segmentation. Pearson product-moment and Spearman rank-order correlations were calculated to assess relationships between TMS measures and Glx. Results: In the left primary motor cortex voxel, Glx had a significant positive correlation with the RMT. In the medial ACC voxel, Glx had significant positive correlations with ICF at the 10-ms and 20-ms ISIs.Conclusions: These preliminary data implicate glutamate in cortical excitatory processes measured by TMS. Limitations included small sample size, lack of healthy control comparators

Irritability Trajectories, Cortical Thickness, and Clinical Outcomes in a Sample Enriched for Preschool Depression.

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Pagliaccio, David; Pine, Daniel S; Barch, Deanna M; Luby, Joan L; Leibenluft, Ellen

2018-05-01

Cross-sectional, longitudinal, and genetic associations exist between irritability and depression. Prior studies have examined developmental trajectories of irritability, clinical outcomes, and associations with child and familial depression. However, studies have not integrated neurobiological measures. The present study examined developmental trajectories of irritability, clinical outcomes, and cortical structure among preschoolers oversampled for depressive symptoms. Beginning at 3 to 5 years old, a sample of 271 children enriched for early depressive symptoms were assessed longitudinally by clinical interview. Latent class mixture models identified trajectories of irritability severity. Risk factors, clinical outcomes, and cortical thickness were compared across trajectory classes. Cortical thickness measures were extracted from 3 waves of magnetic resonance imaging at 7 to 12 years of age. Three trajectory classes were identified among these youth: 53.50% of children exhibited elevated irritability during preschool that decreased longitudinally, 30.26% exhibited consistently low irritability, and 16.24% exhibited consistently elevated irritability. Compared with other classes, the elevated irritability class exhibited higher rates of maternal depression, early life adversity, later psychiatric diagnoses, and functional impairment. Further, elevated baseline irritability predicted later depression beyond adversity and personal and maternal depression history. The elevated irritability class exhibited a thicker cortex in the left superior frontal and temporal gyri and the right inferior parietal lobule. Irritability manifested with specific developmental trajectories in this sample enriched for early depression. Persistently elevated irritability predicted poor psychiatric outcomes, higher risk for later depression, and decreased overall function later in development. Greater frontal, temporal, and parietal cortical thickness also was found, providing neural

Stress preconditioning of spreading depression in the locust CNS.

Directory of Open Access Journals (Sweden)

Corinne I Rodgers

Full Text Available Cortical spreading depression (CSD is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG of locusts. Using K(+ -sensitive microelectrodes, we measured extracellular K(+ concentration ([K(+](o in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K(+ in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na(+/K(+ ATPase impairment, K(+ injection was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45 degrees C and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K(+ that was not linked to changes in ATP levels or total Na(+/K(+ ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin.

Increased cortical-limbic anatomical network connectivity in major depression revealed by diffusion tensor imaging.

Directory of Open Access Journals (Sweden)

Peng Fang

Full Text Available Magnetic resonance imaging studies have reported significant functional and structural differences between depressed patients and controls. Little attention has been given, however, to the abnormalities in anatomical connectivity in depressed patients. In the present study, we aim to investigate the alterations in connectivity of whole-brain anatomical networks in those suffering from major depression by using machine learning approaches. Brain anatomical networks were extracted from diffusion magnetic resonance images obtained from both 22 first-episode, treatment-naive adults with major depressive disorder and 26 matched healthy controls. Using machine learning approaches, we differentiated depressed patients from healthy controls based on their whole-brain anatomical connectivity patterns and identified the most discriminating features that represent between-group differences. Classification results showed that 91.7% (patients=86.4%, controls=96.2%; permutation test, p<0.0001 of subjects were correctly classified via leave-one-out cross-validation. Moreover, the strengths of all the most discriminating connections were increased in depressed patients relative to the controls, and these connections were primarily located within the cortical-limbic network, especially the frontal-limbic network. These results not only provide initial steps toward the development of neurobiological diagnostic markers for major depressive disorder, but also suggest that abnormal cortical-limbic anatomical networks may contribute to the anatomical basis of emotional dysregulation and cognitive impairments associated with this disease.

Temporal alteration of spreading depression by the glycine transporter type-1 inhibitors NFPS and Org-24461 in chicken retina.

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Kertesz, Szabolcs; Szabo, Geza; Udvari, Szabolcs; Levay, Gyorgy; Matyus, Peter; Harsing, Laszlo G

2013-01-25

We used isolated chicken retina to induce spreading depression by the glutamate receptor agonist N-methyl-d-aspartate. The N-methyl-d-aspartate-induced latency time of spreading depression was extended by the glycine(B) binding site competitive antagonist 7-chlorokynurenic acid. Addition of the glycine transporter type-1 inhibitors NFPS and Org-24461 reversed the inhibitory effect of 7-chlorokynurenic acid on N-methyl-d-aspartate-evoked spreading depression. The glycine uptake inhibitory activity of Org-24461, NFPS, and some newly synthesized analogs of NFPS was determined in CHO cells stably expressing human glycine transporter type-1b isoform. Compounds, which failed to inhibit glycine transporter type-1, also did not have effect on retinal spreading depression. These experiments indicate that the spreading depression model in chicken retina is a useful in vitro test to determine activity of glycine transporter type-1 inhibitors. In addition, our data serve further evidence for the role of glycine transporter type-1 in retinal neurotransmission and light processing. Copyright © 2012 Elsevier B.V. All rights reserved.

Brain-derived neurotrophic factor promoter methylation and cortical thickness in recurrent major depressive disorder

OpenAIRE

Na, Kyoung-Sae; Won, Eunsoo; Kang, June; Chang, Hun Soo; Yoon, Ho-Kyoung; Tae, Woo Suk; Kim, Yong-Ku; Lee, Min-Soo; Joe, Sook-Haeng; Kim, Hyun; Ham, Byung-Joo

2016-01-01

Recent studies have reported that methylation of the brain-derived neurotrophic factor (BDNF) gene promoter is associated with major depressive disorder (MDD). This study aimed to investigate the association between cortical thickness and methylation of BDNF promoters as well as serum BDNF levels in MDD. The participants consisted of 65 patients with recurrent MDD and 65 age- and gender-matched healthy controls. Methylation of BDNF promoters and cortical thickness were compared between the gr...

Longitudinal MRI study of cortical thickness, perfusion, and metabolite levels in major depressive disorder

DEFF Research Database (Denmark)

Järnum, Hanna; Eskildsen, Simon Fristed; Steffensen, Elena G

2011-01-01

OBJECTIVE: To determine whether patients with major depressive disorder (MDD) display morphologic, functional, and metabolic brain abnormalities in limbic-cortical regions at a baseline magnetic resonance (MR) scan and whether these changes are normalized in MDD patients in remission at a follow......-acetylaspartate, myo-inositol, and glutamate levels in MDD patients compared with healthy controls at baseline. CONCLUSION: Using novel MRI techniques, we have found abnormalities in cerebral regions related to cortical-limbic pathways in MDD patients....

Post-exercise cortical depression following repetitive passive finger movement.

Science.gov (United States)

Otsuka, Ryohei; Sasaki, Ryoki; Tsuiki, Shota; Kojima, Sho; Onishi, Hideaki

2017-08-24

This study aimed to clarify the influence of range of repetitive passive finger movement on corticospinal excitability. Thirteen healthy subjects participated in this study. Passive index finger adduction-abduction movements were performed from 15° abduction to 15° adduction, 15° abduction to 0°, 0° to 15° adduction, and 15° adduction to 30° adduction, each at 15°/s for 10min on separate days. Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation and M- and F-waves were measured before and after each repetitive passive index finger movement protocol to evaluate changes in corticospinal excitability. MEP amplitude significantly decreased after all passive movements, while F-wave amplitude, F-wave persistence, and M-wave amplitude remained stable. These results suggest that cortical excitability decreases after repetitive passive movement. However, the range of repetitive passive movement does not markedly influence the magnitude of cortical depression. Copyright © 2017 Elsevier B.V. All rights reserved.

Changes of cortical excitability as markers of antidepressant response in bipolar depression: preliminary data obtained by combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG).

Science.gov (United States)

Canali, Paola; Sferrazza Papa, Giovanna; Casali, Adenauer G; Schiena, Giandomenico; Fecchio, Matteo; Pigorini, Andrea; Smeraldi, Enrico; Colombo, Cristina; Benedetti, Francesco

2014-12-01

It is still unclear which biological changes are needed to recover from a major depressive episode. Current perspectives focus on cortical synaptic neuroplasticity. Measures of cortical responses evoked by transcranial magnetic stimulation (TMS) change with sleep homeostasic pressure in humans and approximate measures of synaptic strength in animal models. Using repeated total sleep deprivation as a model of antidepressant treatment, we aimed to correlate recovery from depression with these measures of cortical excitability. We recorded electroencephalographic responses to TMS in the prefrontal cortex of 21 depressed inpatients with bipolar disorder treated with repeated sleep deprivation combined with light therapy. We performed seven TMS/electroencephalography sessions during one week and calculated three measures of cortical excitability. Cortical excitability progressively increased during the antidepressant treatment and as a function of time awake. Higher values differentiated responders from non-responders at baseline and during and after treatment on all measures. Changes in measures of cortical excitability parallel and predict antidepressant response to combined sleep deprivation and light therapy. Data suggest that promoting cortical plasticity in bipolar depression could be a major effect of successful antidepressant treatments, and that patients not responding could suffer a persistent impairment in their neuroplasticity mechanisms. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Multi-dimensional modulations of alpha and gamma cortical dynamics following mindfulness-based cognitive therapy in Major Depressive Disorder

NARCIS (Netherlands)

Schoenberg, P.L.; Speckens, A.E.M.

2015-01-01

To illuminate candidate neural working mechanisms of Mindfulness-Based Cognitive Therapy (MBCT) in the treatment of recurrent depressive disorder, parallel to the potential interplays between modulations in electro-cortical dynamics and depressive symptom severity and self-compassionate experience.

Inadequate Brain Glycogen or Sleep Increases Spreading Depression Susceptibility

KAUST Repository

Kilic, Kivilcim; Karatas, Hulya; Donmez-Demir, Buket; Eren-Kocak, Emine; Gursoy-Ozdemir, Yasemin; Can, Alp; Petit, Jean-Marie; Magistretti, Pierre J.; Dalkara, Turgay

2017-01-01

Glycogen in astrocyte endfeet contributes to maintenance of low extracellular glutamate and K+ concentrations around synapses. Sleep deprivation (SD), a common migraine trigger induces transcriptional changes in astrocytes reducing glycogen breakdown. We hypothesize that when glycogen utilization cannot match synaptic energy demand, extracellular K+ can rise to levels that activate neuronal pannexin-1 channels and downstream inflammatory pathway, which might be one of the mechanisms initiating migraine headaches.We suppressed glycogen breakdown by inhibiting glycogen phosphorylation with 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) and by SD.DAB caused neuronal pannexin-1 large-pore opening and activation of the downstream inflammatory pathway as shown by procaspase-1 cleavage and HMGB1 release from neurons. Six-hour SD induced pannexin-1 mRNA. DAB and SD also lowered the cortical spreading depression (CSD) induction threshold, which was reversed by glucose or lactate supplement, suggesting that glycogen-derived energy substrates are needed to prevent CSD generation. Supporting this, knocking-down neuronal lactate transporter, MCT2 with an anti-sense oligonucleotide or inhibiting glucose transport from vessels to astrocytes with intracerebroventricularly given phloretin reduced the CSD threshold. In vivo recordings with a K+ -sensitive/selective fluoroprobe, APG-4 disclosed that DAB treatment or SD caused significant rise in extracellular K+ during whisker-stimulation, illustrating the critical role of glycogen in extracellular K+ clearance.Synaptic metabolic stress caused by insufficient glycogen-derived energy substrate supply can activate neuronal pannexin-1 channels as well as lowering the CSD threshold. Therefore, conditions that limit energy supply to synapse (e.g. SD) may predispose to migraine attacks as suggested by genetic studies associating glucose or lactate transporter deficiency with migraine. This article is protected by copyright. All rights reserved.

Inadequate Brain Glycogen or Sleep Increases Spreading Depression Susceptibility

KAUST Repository

Kilic, Kivilcim

2017-12-16

Glycogen in astrocyte endfeet contributes to maintenance of low extracellular glutamate and K+ concentrations around synapses. Sleep deprivation (SD), a common migraine trigger induces transcriptional changes in astrocytes reducing glycogen breakdown. We hypothesize that when glycogen utilization cannot match synaptic energy demand, extracellular K+ can rise to levels that activate neuronal pannexin-1 channels and downstream inflammatory pathway, which might be one of the mechanisms initiating migraine headaches.We suppressed glycogen breakdown by inhibiting glycogen phosphorylation with 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) and by SD.DAB caused neuronal pannexin-1 large-pore opening and activation of the downstream inflammatory pathway as shown by procaspase-1 cleavage and HMGB1 release from neurons. Six-hour SD induced pannexin-1 mRNA. DAB and SD also lowered the cortical spreading depression (CSD) induction threshold, which was reversed by glucose or lactate supplement, suggesting that glycogen-derived energy substrates are needed to prevent CSD generation. Supporting this, knocking-down neuronal lactate transporter, MCT2 with an anti-sense oligonucleotide or inhibiting glucose transport from vessels to astrocytes with intracerebroventricularly given phloretin reduced the CSD threshold. In vivo recordings with a K+ -sensitive/selective fluoroprobe, APG-4 disclosed that DAB treatment or SD caused significant rise in extracellular K+ during whisker-stimulation, illustrating the critical role of glycogen in extracellular K+ clearance.Synaptic metabolic stress caused by insufficient glycogen-derived energy substrate supply can activate neuronal pannexin-1 channels as well as lowering the CSD threshold. Therefore, conditions that limit energy supply to synapse (e.g. SD) may predispose to migraine attacks as suggested by genetic studies associating glucose or lactate transporter deficiency with migraine. This article is protected by copyright. All rights reserved.

Brain-derived neurotrophic factor promoter methylation and cortical thickness in recurrent major depressive disorder.

Science.gov (United States)

Na, Kyoung-Sae; Won, Eunsoo; Kang, June; Chang, Hun Soo; Yoon, Ho-Kyoung; Tae, Woo Suk; Kim, Yong-Ku; Lee, Min-Soo; Joe, Sook-Haeng; Kim, Hyun; Ham, Byung-Joo

2016-02-15

Recent studies have reported that methylation of the brain-derived neurotrophic factor (BDNF) gene promoter is associated with major depressive disorder (MDD). This study aimed to investigate the association between cortical thickness and methylation of BDNF promoters as well as serum BDNF levels in MDD. The participants consisted of 65 patients with recurrent MDD and 65 age- and gender-matched healthy controls. Methylation of BDNF promoters and cortical thickness were compared between the groups. The right medial orbitofrontal, right lingual, right lateral occipital, left lateral orbitofrontal, left pars triangularis, and left lingual cortices were thinner in patients with MDD than in healthy controls. Among the MDD group, right pericalcarine, right medical orbitofrontal, right rostral middle frontal, right postcentral, right inferior temporal, right cuneus, right precuneus, left frontal pole, left superior frontal, left superior temporal, left rostral middle frontal and left lingual cortices had inverse correlations with methylation of BDNF promoters. Higher levels of BDNF promoter methylation may be closely associated with the reduced cortical thickness among patients with MDD. Serum BDNF levels were significantly lower in MDD, and showed an inverse relationship with BDNF methylation only in healthy controls. Particularly the prefrontal and occipital cortices seem to indicate key regions in which BDNF methylation has a significant effect on structure.

Migraine generator network and spreading depression dynamics as neuromodulation targets in episodic migraine

Science.gov (United States)

Dahlem, Markus A.

2013-12-01

Migraine is a common disabling headache disorder characterized by recurrent episodes sometimes preceded or accompanied by focal neurological symptoms called aura. The relation between two subtypes, migraine without aura (MWoA) and migraine with aura (MWA), is explored with the aim to identify targets for neuromodulation techniques. To this end, a dynamically regulated control system is schematically reduced to a network of the trigeminal nerve, which innervates the cranial circulation, an associated descending modulatory network of brainstem nuclei, and parasympathetic vasomotor efferents. This extends the idea of a migraine generator region in the brainstem to a larger network and is still simple and explicit enough to open up possibilities for mathematical modeling in the future. In this study, it is suggested that the migraine generator network (MGN) is driven and may therefore respond differently to different spatio-temporal noxious input in the migraine subtypes MWA and MWoA. The noxious input is caused by a cortical perturbation of homeostasis, known as spreading depression (SD). The MGN might even trigger SD in the first place by a failure in vasomotor control. As a consequence, migraine is considered as an inherently dynamical disease to which a linear course from upstream to downstream events would not do justice. Minimally invasive and noninvasive neuromodulation techniques are briefly reviewed and their rational is discussed in the context of the proposed mechanism.

Recovery of slow potentials in AC-coupled electrocorticography: application to spreading depolarizations in rat and human cerebral cortex

DEFF Research Database (Denmark)

Hartings, Jed A; Watanabe, Tomas; Dreier, Jens P

2009-01-01

Cortical spreading depolarizations (spreading depressions and peri-infarct depolarizations) are a pathology intrinsic to acute brain injury, generating large negative extracellular slow potential changes (SPCs) that, lasting on the order of minutes, are studied with DC-coupled recordings in animals...... of the inverse filter was validated by its ability to recover both simulated and real low-frequency input test signals. The inverse filter was then applied to AC-coupled ECoG recordings from five patients who underwent invasive monitoring after aneurysmal subarachnoid hemorrhage. For 117 SPCs, the inverse filter...

Relationship between neurotoxic kynurenine metabolites and reductions in right medial prefrontal cortical thickness in major depressive disorder.

Science.gov (United States)

Meier, Timothy B; Drevets, Wayne C; Wurfel, Brent E; Ford, Bart N; Morris, Harvey M; Victor, Teresa A; Bodurka, Jerzy; Teague, T Kent; Dantzer, Robert; Savitz, Jonathan

2016-03-01

Reductions in gray matter volume of the medial prefrontal cortex (mPFC), especially the rostral and subgenual anterior cingulate cortex (rACC, sgACC) are a widely reported finding in major depressive disorder (MDD). Inflammatory mediators, which are elevated in a subgroup of patients with MDD, activate the kynurenine metabolic pathway and increase production of neuroactive metabolites such as kynurenic acid (KynA), 3-hydroxykynurenine (3HK) and quinolinic acid (QA) which influence neuroplasticity. It is not known whether the alterations in brain structure and function observed in major depressive disorders are due to the direct effect of inflammatory mediators or the effects of neurotoxic kynurenine metabolites. Here, using partial posterior predictive distribution mediation analysis, we tested whether the serum concentrations of kynurenine pathway metabolites mediated reductions in cortical thickness in mPFC regions in MDD. Further, we tested whether any association between C-reactive protein (CRP) and cortical thickness would be mediated by kynurenine pathway metabolites. Seventy-three unmedicated subjects who met DSM-IV-TR criteria for MDD and 91 healthy controls (HC) completed MRI scanning using a pulse sequence optimized for tissue contrast resolution. Automated cortical parcellation was performed using the PALS-B12 Brodmann area atlas as implemented in FreeSurfer in order to compare the cortical thickness and cortical area of six PFC regions: Brodmann areas (BA) 9, 10, 11, 24, 25, and 32. Serum concentrations of kynurenine pathway metabolites were determined by high performance liquid chromatography (HPLC) with tandem mass spectrometry (MS/MS) detection, while high-sensitivity CRP concentration was measured immunoturbidimetrically. Compared with HCs, the MDD group showed a reduction in cortical thickness of the right BA24 (pdepressive episodes displayed thinner cortex in BA32 (pmediated the relationship between diagnosis and cortical thickness of right BA32

Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-Nitro-L-arginine induces cortical spreading ischemia when K+0+ is increased in the subarachnoid space

DEFF Research Database (Denmark)

Dreier, J.P.; Körner, K.; Ebert, Nathalie

1998-01-01

Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)......Cerebral blood flow, nitric oxide, potassium, spreading depression, vasospasm, migraine, migrainous stroke, mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)...

Increase in cortical pyramidal cell excitability accompanies depression-like behavior in mice: a transcranial magnetic stimulation study.

Science.gov (United States)

Sun, Peng; Wang, Furong; Wang, Li; Zhang, Yu; Yamamoto, Ryo; Sugai, Tokio; Zhang, Qing; Wang, Zhengda; Kato, Nobuo

2011-11-09

Clinical evidence suggests that cortical excitability is increased in depressives. We investigated its cellular basis in a mouse model of depression. In a modified version of forced swimming (FS), mice were initially forced to swim for 5 consecutive days and then were treated daily with repetitive transcranial magnetic stimulation (rTMS) or sham treatment for the following 4 weeks without swimming. On day 2 through day 5, the mice manifested depression-like behaviors. The next and last FS was performed 4 weeks later, which revealed a 4 week maintenance of depression-like behavior in the sham mice. In slices from the sham controls, excitability in cingulate cortex pyramidal cells was elevated in terms of membrane potential and frequencies of spikes evoked by current injection. Depolarized resting potential was shown to depend on suppression of large conductance calcium-activated potassium (BK) channels. This BK channel suppression was confirmed by measuring spike width, which depends on BK channels. Chronic rTMS treatment during the 4 week period significantly reduced the depression-like behavior. In slices obtained from the rTMS mice, normal excitability and BK channel activity were recovered. Expression of a scaffold protein Homer1a was reduced by the FS and reversed by rTMS in the cingulate cortex. Similar recovery in the same behavioral, electrophysiological, and biochemical features was observed after chronic imipramine treatment. The present study demonstrated that manifestation and disappearance of depression-like behavior are in parallel with increase and decrease in cortical neuronal excitability in mice and suggested that regulation of BK channels by Homer1a is involved in this parallelism.

Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex

DEFF Research Database (Denmark)

Dreier, Jens P; Major, Sebastian; Pannek, Heinz-Wolfgang

2012-01-01

Spreading depolarization of cells in cerebral grey matter is characterized by massive ion translocation, neuronal swelling and large changes in direct current-coupled voltage recording. The near-complete sustained depolarization above the inactivation threshold for action potential generating...... stimulations. Eventually, epileptic field potentials were recorded during the period that had originally seen spreading depression of activity. Such spreading convulsions are characterized by epileptic field potentials on the final shoulder of the large slow potential change of spreading depolarization. We...

Cortical thickness and VBM in young women at risk for familial depression and their depressed mothers with positive family history.

Science.gov (United States)

Ozalay, Ozgun; Aksoy, Burcu; Tunay, Sebnem; Simsek, Fatma; Chandhoki, Swati; Kitis, Omer; Eker, Cagdas; Gonul, Ali Saffet

2016-06-30

It has been demonstrated that compared to low-risk subjects, high-risk subjects for depression have structural and functional alterations in their brain scans even before the disease onset. However, it is not known if these alterations are related to vulnerability to depression or epiphenomena. One way to resolve this ambiguity is to detect the structural alterations in the high-risk subjects and determine if the same alterations are present in the probands. In this study, we recruited 24 women with the diagnosis of Major Depressive Disorder (MDD) with recurrent episodes and their healthy daughters (the high-risk for familial depression group; HRFD). We compared structural brain scans of the patients and HRFG group with those of 24 age-matched healthy mothers and their healthy daughters at similar ages to the HRFD group; respectively. Both cortical gray matter (GM) volume and thickness analyses revealed that HRFD daughters and their MDD mothers had similar GM differences in two regions: the right temporoparietal region and the dorsomedial prefrontal cortex. These results suggested that the observed alterations may be related to trait clinical and neurophysiological characteristics of MDD and may present before the onset of illness. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage

DEFF Research Database (Denmark)

Dreier, Jens P; Major, Sebastian; Manning, Andrew

2009-01-01

flow and electrocorticography were simultaneously recorded in 417 CSDs. Isolated CSDs occurred in 12 patients and were associated with either physiological, absent or inverse haemodynamic responses. Whereas the physiological haemodynamic response caused tissue hyperoxia, the inverse response led......, causing either transient hyperperfusion (physiological haemodynamic response) in healthy tissue; or hypoperfusion [inverse haemodynamic response = cortical spreading ischaemia (CSI)] in tissue at risk for progressive damage, which has so far only been shown experimentally. Here, we performed a prospective......, multicentre study in 13 patients with aneurysmal subarachnoid haemorrhage, using novel subdural opto-electrode technology for simultaneous laser-Doppler flowmetry (LDF) and direct current-electrocorticography, combined with measurements of tissue partial pressure of oxygen (ptiO(2)). Regional cerebral blood...

Neonatal dexamethasone accelerates spreading depression in the rat, and antioxidant vitamins counteract this effect.

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Lopes-de-Morais, Andréia Albuquerque Cunha; Mendes-da-Silva, Rosângela Figueiredo; dos-Santos, Eryka Maria; Guedes, Rubem Carlos Araújo

2014-12-03

The use of dexamethasone (Dex) to treat chronic lung disease in preterm infants may produce adverse effects in the developing brain. Here, we evaluated the effects of neonatal Dex on the propagation of cortical spreading depression (CSD), and tested the action of vitamins C and E against the effect of Dex. Five groups of Wistar rats received, respectively: [1] no treatment (Naïve); [2] Vehicle (V); [3] tapering doses of Dex (Dex; 0.5mg/kg, 0.3mg/kg, and 0.1mg/kg) on postnatal day (PND) 1-3; [4] Dex plus 200mg/kg vitamin C and 100mg/kg vitamin E (DexCE); [5] only vitamins C and E (CE). Vehicle and vitamins were administered on PND 1-6. CSD was recorded after the pups reached maturity (PND 60-70). The Dex-treated group presented with higher CSD velocities (mean values ± SD, in mm/min: 4.14 ± 0.22, n=10) compared with the control groups (Naïve: 3.52 ± 0.13, n=8; V: 3.57 ± 0.18, n=10; CE: 3.51 ± 0.24, n=10; pVitamins C and E antagonized this effect (DexCE group; CSD velocity: 3.43 ± 0.12, n=9). No intergroup difference was observed concerning P-wave amplitude and duration. In all groups, after the cortex underwent CSD, the electrocorticogram (ECoG) amplitude increased approximately 50% compared with the baseline amplitude for the same animal (CSD-induced ECoG potentiation); however, no intergroup difference was observed. Data suggest that coadministration of antioxidant vitamins with Dex may be a helpful therapeutic strategy to reduce brain adverse effects of dexamethasone. Copyright © 2014 Elsevier B.V. All rights reserved.

Different associations of white matter lesions with depression and cognition

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Lee Jun-Young

2012-08-01

Full Text Available Abstract Background To test the hypothesis that white matter lesions (WML are primarily associated with regional frontal cortical volumes, and to determine the mediating effects of these regional frontal cortices on the associations of WML with depressive symptoms and cognitive dysfunction. Methods Structural brains MRIs were performed on 161 participants: cognitively normal, cognitive impaired but not demented, and demented participants. Lobar WML volumes, regional frontal cortical volumes, depressive symptom severity, and cognitive abilities were measured. Multiple linear regression analyses were used to identify WML volume effects on frontal cortical volume. Structural equation modeling was used to determine the MRI-depression and the MRI-cognition path relationships. Results WML predicted frontal cortical volume, particularly in medial orbirtofrontal cortex, irrespective of age, gender, education, and group status. WML directly predicted depressive score, and this relationship was not mediated by regional frontal cortices. In contrast, the association between WML and cognitive function was indirect and mediated by regional frontal cortices. Conclusions These findings suggest that the neurobiological mechanisms underpinning depressive symptoms and cognitive dysfunction in older adults may differ.

Cortico-cortical communication dynamics

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Per E Roland

2014-05-01

Full Text Available IIn principle, cortico-cortical communication dynamics is simple: neurons in one cortical area communicate by sending action potentials that release glutamate and excite their target neurons in other cortical areas. In practice, knowledge about cortico-cortical communication dynamics is minute. One reason is that no current technique can capture the fast spatio-temporal cortico-cortical evolution of action potential transmission and membrane conductances with sufficient spatial resolution. A combination of optogenetics and monosynaptic tracing with virus can reveal the spatio-temporal cortico-cortical dynamics of specific neurons and their targets, but does not reveal how the dynamics evolves under natural conditions. Spontaneous ongoing action potentials also spread across cortical areas and are difficult to separate from structured evoked and intrinsic brain activity such as thinking. At a certain state of evolution, the dynamics may engage larger populations of neurons to drive the brain to decisions, percepts and behaviors. For example, successfully evolving dynamics to sensory transients can appear at the mesoscopic scale revealing how the transient is perceived. As a consequence of these methodological and conceptual difficulties, studies in this field comprise a wide range of computational models, large-scale measurements (e.g., by MEG, EEG, and a combination of invasive measurements in animal experiments. Further obstacles and challenges of studying cortico-cortical communication dynamics are outlined in this critical review.

Spreading of healthy mood in adolescent social networks.

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Hill, E M; Griffiths, F E; House, T

2015-08-22

Depression is a major public health concern worldwide. There is evidence that social support and befriending influence mental health, and an improved understanding of the social processes that drive depression has the potential to bring significant public health benefits. We investigate transmission of mood on a social network of adolescents, allowing flexibility in our model by making no prior assumption as to whether it is low mood or healthy mood that spreads. Here, we show that while depression does not spread, healthy mood among friends is associated with significantly reduced risk of developing and increased chance of recovering from depression. We found that this spreading of healthy mood can be captured using a non-linear complex contagion model. Having sufficient friends with healthy mood can halve the probability of developing, or double the probability of recovering from, depression over a 6-12-month period on an adolescent social network. Our results suggest that promotion of friendship between adolescents can reduce both incidence and prevalence of depression. © 2015 The Authors.

Somatostatin-Positive Gamma-Aminobutyric Acid Interneuron Deficits in Depression: Cortical Microcircuit and Therapeutic Perspectives.

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Fee, Corey; Banasr, Mounira; Sibille, Etienne

2017-10-15

The functional integration of external and internal signals forms the basis of information processing and is essential for higher cognitive functions. This occurs in finely tuned cortical microcircuits whose functions are balanced at the cellular level by excitatory glutamatergic pyramidal neurons and inhibitory gamma-aminobutyric acidergic (GABAergic) interneurons. The balance of excitation and inhibition, from cellular processes to neural network activity, is characteristically disrupted in multiple neuropsychiatric disorders, including major depressive disorder (MDD), bipolar disorder, anxiety disorders, and schizophrenia. Specifically, nearly 3 decades of research demonstrate a role for reduced inhibitory GABA level and function across disorders. In MDD, recent evidence from human postmortem and animal studies suggests a selective vulnerability of GABAergic interneurons that coexpress the neuropeptide somatostatin (SST). Advances in cell type-specific molecular genetics have now helped to elucidate several important roles for SST interneurons in cortical processing (regulation of pyramidal cell excitatory input) and behavioral control (mood and cognition). Here, we review evidence for altered inhibitory function arising from GABAergic deficits across disorders and specifically in MDD. We then focus on properties of the cortical microcircuit, where SST-positive GABAergic interneuron deficits may disrupt functioning in several ways. Finally, we discuss the putative origins of SST cell deficits, as informed by recent research, and implications for therapeutic approaches. We conclude that deficits in SST interneurons represent a contributing cellular pathology and therefore a promising target for normalizing altered inhibitory function in MDD and other disorders with reduced SST cell and GABA functions. Copyright © 2017 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Synaptic release and extracellular actions of Zn2+ limit propagation of spreading depression and related events in vitro and in vivo.

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Aiba, Isamu; Carlson, Andrew P; Sheline, Christian T; Shuttleworth, C William

2012-02-01

Cortical spreading depression (CSD) is a consequence of a slowly propagating wave of neuronal and glial depolarization (spreading depolarization; SD). Massive release of glutamate contributes to SD propagation, and it was recently shown that Zn(2+) is also released from synaptic vesicles during SD. The present study examined consequences of extracellular Zn(2+) accumulation on the propagation of SD. SD mechanisms were studied first in murine brain slices, using focal KCl applications as stimuli and making electrical and optical recordings in hippocampal area CA1. Elevating extracellular Zn(2+) concentrations with exogenous ZnCl(2) reduced SD propagation rates. Selective chelation of endogenous Zn(2+) (using TPEN or CaEDTA) increased SD propagation rates, and these effects appeared due to chelation of Zn(2+) derived from synaptic vesicles. Thus, in tissues where synaptic Zn(2+) release was absent [knockout (KO) of vesicular Zn(2+) transporter ZnT-3], SD propagation rates were increased, and no additional increase was observed following chelation of endogenous Zn(2+) in these tissues. The role of synaptic Zn(2+) was then examined on CSD in vivo. ZnT-3 KO animals had higher susceptibility to CSD than wild-type controls as evidenced by significantly higher propagation rates and frequencies. Studies of candidate mechanisms excluded changes in neuronal excitability, presynaptic release, and GABA receptors but left open a possible contribution of N-methyl-d-aspartate (NMDA) receptor inhibition. These results suggest the extracellular accumulation of synaptically released Zn(2+) can serve as an intrinsic inhibitor to limit SD events. The inhibitory action of extracellular Zn(2+) on SD may counteract to some extent the neurotoxic effects of intracellular Zn(2+) accumulation in acute brain injury models.

Frontal and temporal cortical functional recovery after electroconvulsive therapy for depression: A longitudinal functional near-infrared spectroscopy study.

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Hirano, Jinichi; Takamiya, Akihiro; Yamagata, Bun; Hotta, Syogo; Miyasaka, Yukiko; Pu, Shenghong; Iwanami, Akira; Uchida, Hiroyuki; Mimura, Masaru

2017-08-01

While the efficacy and tolerability of electroconvulsive therapy (ECT) for depression has been well established, the acute effects of ECT on brain function remain unclear. Particularly, although cognitive dysfunction has been consistently observed after ECT, little is known about the extent and time course of ECT-induced brain functional changes, as observed during cognitive tasks. Considering the acute antidepressant effects of ECT on depression, aberrant brain functional responses during cognitive tasks in patients with depression may improve immediately after this treatment. To clarify changes in cortical functional responses to cognitive tasks following ECT, we used task-related functional near-infrared spectroscopy (NIRS) to assess 30 patients with major depressive disorder or bipolar depression before and after an ECT series, as well as 108 healthy controls. Prior to ECT, patients exhibited significantly smaller [oxy-Hb] values in the bilateral frontal cortex during a letter verbal fluency task (VFT) compared with healthy controls. We found a significant increase in [oxy-Hb] values in the bilateral frontal cortex during the VFT after ECT in the patient group. A decrease in depression severity was significantly correlated with an increase in [oxy-Hb] values in the right ventrolateral prefrontal cortex following ECT. This is the first NIRS study to evaluate brain functional changes before vs. after ECT. Impaired functional responses, observed during the cognitive task in depressed patients, were normalized after ECT. Thus, recovery from abnormal functional responses to cognitive tasks in the frontal brain regions may be associated with the acute therapeutic effects of ECT for depression. Copyright © 2017 Elsevier Ltd. All rights reserved.

A Preliminary Study of the Influence of Age of Onset and Childhood Trauma on Cortical Thickness in Major Depressive Disorder

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Natalia Jaworska

2014-01-01

Full Text Available Background. Major depressive disorder (MDD neural underpinnings may differ based on onset age and childhood trauma. We assessed cortical thickness in patients who differed in age of MDD onset and examined trauma history influence. Methods. Adults with MDD (N=36 and controls (HC; N=18 underwent magnetic resonance imaging. Twenty patients had MDD onset 25 years of age (adult onset. The MDD group was also subdivided into those with (N=12 and without (N=19 physical and/or sexual abuse as assessed by the Childhood Trauma Questionnaire (CTQ. Cortical thickness was analyzed with FreeSurfer software. Results. Thicker frontal pole and a tendency for thinner transverse temporal cortices existed in MDD. The former was driven by the pediatric onset group and abuse history (independently, particularly in the right frontal pole. Inverse correlations existed between CTQ scores and frontal pole cortex thickness. A similar inverse relation existed with left inferior and right superior parietal cortex thickness. The superior temporal cortex tended to be thinner in pediatric versus adult onset groups with childhood abuse. Conclusions. This preliminary work suggests neural differences between pediatric and adult MDD onset. Trauma history also contributes to cytoarchitectural modulation. Thickened frontal pole cortices as a compensatory mechanism in MDD warrant evaluation.

Gray matter trophism, cognitive impairment, and depression in patients with multiple sclerosis.

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Pravatà, Emanuele; Rocca, Maria A; Valsasina, Paola; Riccitelli, Gianna C; Gobbi, Claudio; Comi, Giancarlo; Falini, Andrea; Filippi, Massimo

2017-12-01

Cognitive impairment and depression frequently affects patients with multiple sclerosis (MS). However, the relationship between the occurrence of depression and cognitive impairment and the development of cortical atrophy has not been fully elucidated yet. To investigate the association of cortical and deep gray matter (GM) volume with depression and cognitive impairment in MS. Three-dimensional (3D) T1-weighted scans were obtained from 126 MS patients and 59 matched healthy controls. Cognitive impairment was assessed using the Brief Repeatable Battery of Neuropsychological Tests and depression with the Montgomery-Asberg Depression Rating Scale (MADRS). Using FreeSurfer and FIRST software, we assessed cortical thickness (CTh) and deep GM volumetry. Magnetic resonance imaging (MRI) variables explaining depression and cognitive impairment were investigated using factorial and classification analysis. Multivariate regression models correlated GM abnormalities with symptoms severity. Compared with controls, MS patients exhibited widespread bilateral cortical thinning involving all brain lobes. Depressed MS showed selective CTh decrease in fronto-temporal regions, whereas cognitive impairment MS exhibited widespread fronto-parietal cortical and subcortical GM atrophy. Frontal cortical thinning was the best predictor of depression ( C-statistic = 0.7), whereas thinning of the right precuneus and high T2 lesion volume best predicted cognitive impairment ( C-statistic = 0.8). MADRS severity correlated with right entorhinal cortex thinning, whereas cognitive impairment severity correlated with left entorhinal and thalamus atrophy. MS-related depression is linked to circumscribed CTh changes in areas deputed to emotional behavior, whereas cognitive impairment is correlated with cortical and subcortical GM atrophy of circuits involved in cognition.

Cortical-limbic regions modulate depression and anxiety factors in functional dyspepsia. A PET-CT study

International Nuclear Information System (INIS)

Liu Mailan; Liang Fanrong; Zeng Fang; Tang Yong; Lan Lei; Song Wenzhong

2012-01-01

The objective of this study was to observe some specific brain areas or cerebral functional network participating in the modulation of depression and anxiety factors in functional dyspepsia (FD) patients by detecting cerebral glucose metabolism (CGM) in fluorine-18 fluorodeoxyglucose ( 18 F-FDG) positron emission tomography-computed tomography (PET-CT) scans. Eight FD patients with depression and anxiety (DA-FD group) and eight FD patients without depression and anxiety (non-DA-FD group) were recruited and evaluated by the Nepean Dyspepsia Index (NDI) and Dyspepsia Symptom Scores (DSS). Cerebral 18 F-FDG PET-CT scans were performed on the DA-FD group and non-DA-FD group, respectively. The differences in CGM between the two groups were analyzed with Statistical Parametric Mapping 2.0 (SPM2). Extensive changes in the CGM signals were observed in the cerebral cortex and limbic system of FD patients with depression and anxiety. Compared to non-DA-FD patients, DA-FD patients showed a higher glucose metabolism in the right postcentral gyrus (BA 1 and 5), inferior frontal gyrus (BA 45), superior temporal gyrus (BA 22), middle temporal gyrus (BA 22), inferior parietal lobule (BA 40), lingual gyrus (BA 18) and the left middle occipital gyrus (BA 37), as well as the limbic system including the left thalamus, lateral globus pallidus, parahippocampal gyrus (BA 35), right insular cortex (BA 13) and parahippocampal gyrus (BA 18); a lower glucose metabolism was presented in the left middle cingulated gyrus (BA 24), the right superior frontal gyrus (BA 6), the medial frontal gyrus (BA 6) and middle temporal gyrus (BA 21). An extensive cortical-limbic brain network might modulate the procession of FD patients with depression and anxiety factors. (author)

 Cortical Atrophy is Associated with Accelerated Cognitive Decline in Mild Cognitive Impairment with Subsyndromal Depression.

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Gonzales, Mitzi M; Insel, Philip S; Nelson, Craig; Tosun, Duygu; Mattsson, Niklas; Mueller, Susanne G; Sacuiu, Simona; Bickford, David; Weiner, Michael W; Mackin, R Scott

2017-09-01

To investigate the association between cognitive decline and cortical atrophy in individuals with mild cognitive impairment (MCI) and chronic subsyndromal symptoms of depression (SSD) over a 4-year period. Prospective cohort study. Multicenter, clinic-based. Within the Alzheimer's Disease Neuroimaging Initiative repository, the Neuropsychiatric Inventory was used to identify individuals with MCI and stable endorsement (SSD group N = 32) or no endorsement (non-SSD group N = 69) of depressive symptoms across time points. Repeated measures of cognitive outcomes, cortical atrophy, and their associations were evaluated with mixed effects models adjusting for age, education, sex, and APOE genotype. The SSD group demonstrated accelerated decline on measures of global cognition (Alzheimer Disease Assessment Scale; df = 421, t = 2.242, p = 0.025), memory (Wechsler Memory Scale-Revised Logical Memory II; df = 244, t = -2.525, p = 0.011), information processing speed (Trail Making Test Parts A [df = 421, t = 2.376, p = 0.018] and B [df = 421, t = 2.533, p = 0.012]), and semantic fluency (Category Fluency; df = 424, t = -2.418, p = 0.016), as well as accelerated frontal lobe (df = 341, t = -2.648, p = 0.008) and anterior cingulate (df = 341, t = -3.786, p confrontation naming or for rate of atrophy in any other regions. Accelerated frontal lobe and anterior cingulate atrophy was associated with cognitive decline on measures of global cognition, information processing speed, and semantic fluency (all p < 0.05), but not memory. Individuals with chronic SSD may represent an MCI subgroup that is highly vulnerable to accelerated cognitive decline, an effect that may be governed by frontal lobe and anterior cingulate atrophy. Published by Elsevier Inc.

Cognitive impairment and medial temporal lobe structure in young adults with a depressive episode.

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Donix, Markus; Haussmann, Robert; Helling, Franziska; Zweiniger, Anne; Lange, Jan; Werner, Annett; Donix, Katharina L; Brandt, Moritz D; Linn, Jennifer; Bauer, Michael; Buthut, Maria

2018-09-01

Cognitive deficits are common in patients with a depressive episode although the predictors for their development and severity remain elusive. We investigated whether subjective and objective cognitive impairment in young depressed adults would be associated with cortical thinning in medial temporal subregions. High-resolution magnetic resonance imaging, cortical unfolding data analysis, and comprehensive assessments of subjective and objective cognitive abilities were performed on 27 young patients with a depressive episode (mean age: 29.0 ± 5.8 years) and 23 older participants without a history of a depressive disorder but amnestic mild cognitive impairment (68.5 ± 6.6 years) or normal cognition (65.2 ± 8.7 years). Thickness reductions in parahippocampal, perirhinal and fusiform cortices were associated with subjective memory deficits only among young patients with a depressive episode and a measurable cognitive impairment. Long-term longitudinal data would be desirable to determine the trajectories of cognitive impairment associated with depression in patients with or without cortical structure changes. The presence of clinically significant cognitive deficits in young people with a depressive episode may identify a patient population with extrahippocampal cortical thinning. Copyright © 2018 Elsevier B.V. All rights reserved.

Traumatic Brain Injury Increases Cortical Glutamate Network Activity by Compromising GABAergic Control.

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Cantu, David; Walker, Kendall; Andresen, Lauren; Taylor-Weiner, Amaro; Hampton, David; Tesco, Giuseppina; Dulla, Chris G

2015-08-01

Traumatic brain injury (TBI) is a major risk factor for developing pharmaco-resistant epilepsy. Although disruptions in brain circuitry are associated with TBI, the precise mechanisms by which brain injury leads to epileptiform network activity is unknown. Using controlled cortical impact (CCI) as a model of TBI, we examined how cortical excitability and glutamatergic signaling was altered following injury. We optically mapped cortical glutamate signaling using FRET-based glutamate biosensors, while simultaneously recording cortical field potentials in acute brain slices 2-4 weeks following CCI. Cortical electrical stimulation evoked polyphasic, epileptiform field potentials and disrupted the input-output relationship in deep layers of CCI-injured cortex. High-speed glutamate biosensor imaging showed that glutamate signaling was significantly increased in the injured cortex. Elevated glutamate responses correlated with epileptiform activity, were highest directly adjacent to the injury, and spread via deep cortical layers. Immunoreactivity for markers of GABAergic interneurons were significantly decreased throughout CCI cortex. Lastly, spontaneous inhibitory postsynaptic current frequency decreased and spontaneous excitatory postsynaptic current increased after CCI injury. Our results suggest that specific cortical neuronal microcircuits may initiate and facilitate the spread of epileptiform activity following TBI. Increased glutamatergic signaling due to loss of GABAergic control may provide a mechanism by which TBI can give rise to post-traumatic epilepsy. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Censoring distances based on labeled cortical distance maps in cortical morphometry.

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Ceyhan, Elvan; Nishino, Tomoyuki; Alexopolous, Dimitrios; Todd, Richard D; Botteron, Kelly N; Miller, Michael I; Ratnanather, J Tilak

2013-01-01

It has been demonstrated that shape differences in cortical structures may be manifested in neuropsychiatric disorders. Such morphometric differences can be measured by labeled cortical distance mapping (LCDM) which characterizes the morphometry of the laminar cortical mantle of cortical structures. LCDM data consist of signed/labeled distances of gray matter (GM) voxels with respect to GM/white matter (WM) surface. Volumes and other summary measures for each subject and the pooled distances can help determine the morphometric differences between diagnostic groups, however they do not reveal all the morphometric information contained in LCDM distances. To extract more information from LCDM data, censoring of the pooled distances is introduced for each diagnostic group where the range of LCDM distances is partitioned at a fixed increment size; and at each censoring step, the distances not exceeding the censoring distance are kept. Censored LCDM distances inherit the advantages of the pooled distances but also provide information about the location of morphometric differences which cannot be obtained from the pooled distances. However, at each step, the censored distances aggregate, which might confound the results. The influence of data aggregation is investigated with an extensive Monte Carlo simulation analysis and it is demonstrated that this influence is negligible. As an illustrative example, GM of ventral medial prefrontal cortices (VMPFCs) of subjects with major depressive disorder (MDD), subjects at high risk (HR) of MDD, and healthy control (Ctrl) subjects are used. A significant reduction in laminar thickness of the VMPFC in MDD and HR subjects is observed compared to Ctrl subjects. Moreover, the GM LCDM distances (i.e., locations with respect to the GM/WM surface) for which these differences start to occur are determined. The methodology is also applicable to LCDM-based morphometric measures of other cortical structures affected by disease.

Censoring Distances Based on Labeled Cortical Distance Maps in Cortical Morphometry

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Elvan eCeyhan

2013-10-01

Full Text Available It has been demonstrated that shape differences are manifested in cortical structures due to neuropsychiatric disorders. Such morphometric differences can be measured by labeled cortical distance mapping (LCDM which characterizes the morphometry of the laminar cortical mantle of cortical structures. LCDM data consist of signed/labeled distances of gray matter (GM voxels with respect to GM/white matter (WM surface. Volumes and other summary measures for each subject and the pooled distances can help determine the morphometric differences between diagnostic groups, however they do not reveal all the morphometric information con-tained in LCDM distances. To extract more information from LCDM data, censoring of the pooled distances is introduced for each diagnostic group where the range of LCDM distances is partitioned at a fixed increment size; and at each censoring step, the distances not exceeding the censoring distance are kept. Censored LCDM distances inherit the advantages of the pooled distances but also provide information about the location of morphometric differences which cannot be obtained from the pooled distances. However, at each step, the censored distances aggregate, which might confound the results. The influence of data aggregation is investigated with an extensive Monte Carlo simulation analysis and it is demonstrated that this influence is negligible. As an illustrative example, GM of ventral medial prefrontal cortices (VMPFCs of subjects with major depressive disorder (MDD, subjects at high risk (HR of MDD, and healthy control (Ctrl subjects are used. A significant reduction in laminar thickness of the VMPFC in MDD and HR subjects is observed compared to Ctrl subjects. Moreover, the GM LCDM distances (i.e., locations with respect to the GM/WM surface for which these differences start to occur are determined. The methodology is also applicable to LCDM-based morphometric measures of other cortical structures affected by disease.

Lateral Spread of Orientation Selectivity in V1 is Controlled by Intracortical Cooperativity

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Chavane, Frédéric; Sharon, Dahlia; Jancke, Dirk; Marre, Olivier; Frégnac, Yves; Grinvald, Amiram

2011-01-01

Neurons in the primary visual cortex receive subliminal information originating from the periphery of their receptive fields (RF) through a variety of cortical connections. In the cat primary visual cortex, long-range horizontal axons have been reported to preferentially bind to distant columns of similar orientation preferences, whereas feedback connections from higher visual areas provide a more diverse functional input. To understand the role of these lateral interactions, it is crucial to characterize their effective functional connectivity and tuning properties. However, the overall functional impact of cortical lateral connections, whatever their anatomical origin, is unknown since it has never been directly characterized. Using direct measurements of postsynaptic integration in cat areas 17 and 18, we performed multi-scale assessments of the functional impact of visually driven lateral networks. Voltage-sensitive dye imaging showed that local oriented stimuli evoke an orientation-selective activity that remains confined to the cortical feedforward imprint of the stimulus. Beyond a distance of one hypercolumn, the lateral spread of cortical activity gradually lost its orientation preference approximated as an exponential with a space constant of about 1 mm. Intracellular recordings showed that this loss of orientation selectivity arises from the diversity of converging synaptic input patterns originating from outside the classical RF. In contrast, when the stimulus size was increased, we observed orientation-selective spread of activation beyond the feedforward imprint. We conclude that stimulus-induced cooperativity enhances the long-range orientation-selective spread. PMID:21629708

Concordant Patterns of Brain Structure in Mothers with Recurrent Depression and Their Never-Depressed Daughters.

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Foland-Ross, Lara C; Behzadian, Negin; LeMoult, Joelle; Gotlib, Ian H

2016-01-01

A growing body of research has demonstrated that having a mother with a history of major depressive disorder (MDD) is one of the strongest predictors of depression in adolescent offspring. Few studies, however, have assessed neural markers of this increased risk for depression, or examined whether risk-related anomalies in adolescents at maternal risk for depression are related to neural abnormalities in their depressed mothers. We addressed these questions by examining concordance in brain structure in two groups of participants: mothers with a history of depression and their never-depressed daughters, and never-depressed mothers and their never-depressed daughters. We scanned mothers with (remitted; RMD) and without (control; CTL) a history of recurrent episodes of depression and their never-depressed daughters, computed cortical gray matter thickness, and tested whether mothers' thickness predicted daughters' thickness. Both RMD mothers and their high-risk daughters exhibited focal areas of thinner cortical gray matter compared with their CTL/low-risk counterparts. Importantly, the extent of thickness anomalies in RMD mothers predicted analogous abnormalities in their daughters; this pattern was not present in CTL/low-risk dyads. We identified neuroanatomical risk factors that may underlie the intergenerational transmission of risk for MDD. Our findings suggest that there is concordance in brain structure in dyads that is affected by maternal depression, and that the location, direction, and extent of neural anomalies in high-risk offspring mirror those of their recurrent depressed mothers. © 2016 S. Karger AG, Basel.

Mitochondrial dysfunction precedes depression of AMPK/AKT signaling in insulin resistance induced by high glucose in primary cortical neurons.

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Peng, Yunhua; Liu, Jing; Shi, Le; Tang, Ying; Gao, Dan; Long, Jiangang; Liu, Jiankang

2016-06-01

Recent studies have demonstrated brain insulin signaling impairment and mitochondrial dysfunction in diabetes. Hyperinsulinemia and hyperlipidemia arising from diabetes have been linked to neuronal insulin resistance, and hyperglycemia induces peripheral sensory neuronal impairment and mitochondrial dysfunction. However, how brain glucose at diabetic conditions elicits cortical neuronal insulin signaling impairment and mitochondrial dysfunction remains unknown. In the present study, we cultured primary cortical neurons with high glucose levels and investigated the neuronal mitochondrial function and insulin response. We found that mitochondrial function was declined in presence of 10 mmol/L glucose, prior to the depression of AKT signaling in primary cortical neurons. We further demonstrated that the cerebral cortex of db/db mice exhibited both insulin resistance and loss of mitochondrial complex components. Moreover, we found that adenosine monophosphate-activated protein kinase (AMPK) inactivation is involved in high glucose-induced mitochondrial dysfunction and insulin resistance in primary cortical neurons and neuroblastoma cells, as well as in cerebral cortex of db/db mice, and all these impairments can be rescued by mitochondrial activator, resveratrol. Taken together, our results extend the finding that high glucose (≥10 mmol/L) comparable to diabetic brain extracellular glucose level leads to neuronal mitochondrial dysfunction and resultant insulin resistance, and targeting mitochondria-AMPK signaling might be a promising strategy to protect against diabetes-related neuronal impairment in central nerves system. We found that high glucose (≥10 mmol/L), comparable to diabetic brain extracellular glucose level, leads to neuronal mitochondrial dysfunction and resultant insulin resistance in an AMPK-dependent manner, and targeting mitochondria-AMPK signaling might be a promising strategy to protect against diabetes-related neuronal impairment in central

Modulatory Effects of Dopamine D2 Receptors on Spreading Depression in Rat Somatosensory Neocortex

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Anna Maria Haarmann

2014-11-01

Full Text Available Introduction: Spreading depression (SD is a propagating wave of depolarization followed by depression of the neuroglial activities and can modulate extracellular dopamine concentrations in the neocortex. It has been shown that the dopaminergic system plays a role in migraine. SD has been suggested as a critical phenomenon in the pathophysiology of migraine. The aim of this study was to investigate the effect of dopamine D2 receptors on the characteristic features of SD in rat neocortical tissues. Methods: The effect of dopamine D2 receptor agonist quinpirole and D2 receptor antagonist sulpiride was tested on different characteristic features (amplitude, duration and velocity of KCl-induced SD in somatosensory neocortical slices of adult rats. The effect of above-mentioned substances on production of long-term potentiation (LTP in the neocortex was also evaluated. Results: The present data revealed a dose-dependent suppression of the amplitude and duration of SD in the presence of the dopamine D2 receptor antagonist sulpiride in the neocortex. D2 dopamine receptor agonist quinpirole dose-dependently enhanced the amplitude and duration of the neocortical SD. Furthermore, application of D2 receptor antagonist significantly suppressed induction of LTP. Discussion: These results indicate that D2 receptors modulate the initiation of SD in the neocortex. This finding refers to the potential role of D2 receptor antagonist in treatment of migraine pain.

Perceived stress is associated with increased rostral middle frontal gyrus cortical thickness: a family-based and discordant-sibling investigation.

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Michalski, L J; Demers, C H; Baranger, D A A; Barch, D M; Harms, M P; Burgess, G C; Bogdan, R

2017-11-01

Elevated stress perception and depression commonly co-occur, suggesting that they share a common neurobiology. Cortical thickness of the rostral middle frontal gyrus (RMFG), a region critical for executive function, has been associated with depression- and stress-related phenotypes. Here, we examined whether RMFG cortical thickness is associated with these phenotypes in a large family-based community sample. RMFG cortical thickness was estimated using FreeSurfer among participants (n = 879) who completed the ongoing Human Connectome Project. Depression-related phenotypes (i.e. sadness, positive affect) and perceived stress were assessed via self-report. After accounting for sex, age, ethnicity, average whole-brain cortical thickness, twin status and familial structure, RMFG thickness was positively associated with perceived stress and sadness and negatively associated with positive affect at small effect sizes (accounting for 0.2-2.4% of variance; p-fdr: 0.0051-0.1900). Perceived stress was uniquely associated with RMFG thickness after accounting for depression-related phenotypes. Further, among siblings discordant for perceived stress, those reporting higher perceived stress had increased RMFG thickness (P = 4 × 10 -7 ). Lastly, RMFG thickness, perceived stress, depressive symptoms, and positive affect were all significantly heritable, with evidence of shared genetic and environmental contributions between self-report measures. Stress perception and depression share common genetic, environmental, and neural correlates. Variability in RMFG cortical thickness may play a role in stress-related depression, although effects may be small in magnitude. Prospective studies are required to examine whether variability in RMFG thickness may function as a risk factor for stress exposure and/or perception, and/or arises as a consequence of these phenotypes. © 2017 John Wiley & Sons Ltd and International Behavioural and Neural Genetics Society.

Increased frontal sleep slow wave activity in adolescents with major depression

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Noemi Tesler

2016-01-01

Full Text Available Sleep slow wave activity (SWA, the major electrophysiological characteristic of deep sleep, mirrors both cortical restructuring and functioning. The incidence of Major Depressive Disorder (MDD substantially rises during the vulnerable developmental phase of adolescence, where essential cortical restructuring is taking place. The goal of this study was to assess characteristics of SWA topography in adolescents with MDD, in order to assess abnormalities in both cortical restructuring and functioning on a local level. All night high-density EEG was recorded in 15 patients meeting DSM-5 criteria for MDD and 15 sex- and age-matched healthy controls. The actual symptom severity was assessed using the Children's Depression Rating Scale—Revised (CDRS-R. Topographical power maps were calculated based on the average SWA of the first non-rapid eye movement (NREM sleep episode. Depressed adolescents exhibited significantly more SWA in a cluster of frontal electrodes compared to controls. SWA over frontal brain regions correlated positively with the CDRS-R subscore “morbid thoughts”. Self-reported sleep latency was significantly higher in depressed adolescents compared to controls whereas sleep architecture did not differ between the groups. Higher frontal SWA in depressed adolescents may represent a promising biomarker tracing cortical regions of intense use and/or restructuring.

Left dorso-lateral repetitive transcranial magnetic stimulation affects cortical excitability and functional connectivity, but does not impair cognition in major depression.

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Shajahan, Polash M; Glabus, Mike F; Steele, J Douglas; Doris, Alan B; Anderson, Kay; Jenkins, Jenny A; Gooding, Patricia A; Ebmeier, Klaus P

2002-06-01

Transcranial magnetic stimulation (TMS) has been used for over a decade to investigate cortical function. More recently, it has been employed to treat conditions such as major depression. This study was designed to explore the effects of differential treatment parameters, such as stimulation frequency. In addition, the data were examined to determine whether a change in connectivity occurred following TMS. Fifteen patients with major depression were entered into a combined imaging and treatment experiment with single photon emission computed tomography (SPECT) and repetitive transcranial magnetic stimulation (rTMS) over left dorso-lateral prefrontal cortex (DLPFC). Brain perfusion during a verbal fluency task was compared between pre- and poststimulation conditions. Patients were then treated with 80% of motor threshold for a total of 10 days, using 5000 stimuli at 5, 10 or 20 Hz. Tests of cortical excitability and neuropsychological tests were done throughout the trial. Patients generally improved with treatment. There was no perceptible difference between stimulation frequencies, which may have reflected low study power. An increase in rostral anterior cingulate activation after the treatment day was associated with increased functional connectivity in the dorso-lateral frontal loop on the left and the limbic loop on both sides. No noticeable deterioration in neuropsychological function was observed. TMS at the stimulation frequencies used seems to be safe over a course of 5000 stimuli. It appears to have an activating effect in anterior limbic structures and increase functional connectivity in the neuroanatomical networks under the stimulation coil within an hour of stimulation.

Incoordination among Subcellular Compartments Is Associated with Depression-Like Behavior Induced by Chronic Mild Stress

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Xu, Aiping; Cui, Shan

2016-01-01

Background: Major depressive disorder is characterized as persistent low mood. A chronically stressful life in genetically susceptible individuals is presumably the major etiology that leads to dysfunctions of monoamine and hypothalamus-pituitary-adrenal axis. These pathogenic factors cause neuron atrophy in the limbic system for major depressive disorder. Cell-specific pathophysiology is unclear, so we investigated prelimbic cortical GABAergic neurons and their interaction with glutamatergic neurons in depression-like mice. Methods: Mice were treated with chronic unpredictable mild stress for 3 weeks until they expressed depression-like behaviors confirmed by sucrose preference, Y-maze, and forced swimming tests. The structures and functions of GABAergic and glutamatergic units in prelimbic cortices were studied by cell imaging and electrophysiology in chronic unpredictable mild stress-induced depression mice vs controls. Results: In depression-like mice, prelimbic cortical GABAergic neurons show incoordination among the subcellular compartments, such as decreased excitability and synaptic outputs as well as increased reception from excitatory inputs. GABAergic synapses on glutamatergic cells demonstrate decreased presynaptic innervation and increased postsynaptic responsiveness. Conclusions: Chronic unpredictable mild stress-induced incoordination in prelimbic cortical GABAergic and glutamatergic neurons dysregulates their target neurons, which may be the pathological basis for depressive mood. The rebalance of compatibility among subcellular compartments would be an ideal strategy to treat neural disorders. PMID:26506857

Cortical correlates of affective syndrome in dementia due to Alzheimer’s disease

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Thaís T. Hayata

2015-07-01

Full Text Available Neuropsychiatric symptoms in Alzheimer’s disease (AD are prevalent, however their relationship with patterns of cortical atrophy is not fully known. Objectives To compare cortical atrophy’s patterns between AD patients and healthy controls; to verify correlations between neuropsychiatric syndromes and cortical atrophy. Method 33 AD patients were examined by Neuropsychiatric Inventory (NPI. Patients and 29 controls underwent a 3T MRI scanning. We considered four NPI syndromes: affective, apathy, hyperactivity and psychosis. Correlations between structural imaging and neuropsychiatric scores were performed by Freesurfer. Results were significant with a p-value < 0.05, corrected for multiple comparisons. Results Patients exhibited atrophy in entorhinal cortices, left inferior and middle temporal gyri, and precuneus bilaterally. There was correlation between affective syndrome and cortical thickness in right frontal structures, insula and temporal pole. Conclusion Cortical thickness measures revealed atrophy in mild AD. Depression and anxiety symptoms were associated with atrophy of right frontal, temporal and insular cortices.

Spatiotemporal Propagation of the Cortical Atrophy: Population and Individual Patterns

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Igor Koval

2018-05-01

Full Text Available Repeated failures in clinical trials for Alzheimer’s disease (AD have raised a strong interest for the prodromal phase of the disease. A better understanding of the brain alterations during this early phase is crucial to diagnose patients sooner, to estimate an accurate disease stage, and to give a reliable prognosis. According to recent evidence, structural alterations in the brain are likely to be sensitive markers of the disease progression. Neuronal loss translates in specific spatiotemporal patterns of cortical atrophy, starting in the enthorinal cortex and spreading over other cortical regions according to specific propagation pathways. We developed a digital model of the cortical atrophy in the left hemisphere from prodromal to diseased phases, which is built on the temporal alignment and combination of several short-term observation data to reconstruct the long-term history of the disease. The model not only provides a description of the spatiotemporal patterns of cortical atrophy at the group level but also shows the variability of these patterns at the individual level in terms of difference in propagation pathways, speed of propagation, and age at propagation onset. Longitudinal MRI datasets of patients with mild cognitive impairments who converted to AD are used to reconstruct the cortical atrophy propagation across all disease stages. Each observation is considered as a signal spatially distributed on a network, such as the cortical mesh, each cortex location being associated to a node. We consider how the temporal profile of the signal varies across the network nodes. We introduce a statistical mixed-effect model to describe the evolution of the cortex alterations. To ensure a spatiotemporal smooth propagation of the alterations, we introduce a constrain on the propagation signal in the model such that neighboring nodes have similar profiles of the signal changes. Our generative model enables the reconstruction of personalized

Unimodal primary sensory cortices are directly connected by long-range horizontal projections in the rat sensory cortex

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Jimmy eStehberg

2014-09-01

Full Text Available Research based on functional imaging and neuronal recordings in the barrel cortex subdivision of primary somatosensory cortex (SI of the adult rat has revealed novel aspects of structure-function relationships in this cortex. Specifically, it has demonstrated that single whisker stimulation evokes subthreshold neuronal activity that spreads symmetrically within gray matter from the appropriate barrel area, crosses cytoarchitectural borders of SI and reaches deeply into other unimodal primary cortices such as primary auditory (AI and primary visual (VI. It was further demonstrated that this spread is supported by a spatially matching underlying diffuse network of border-crossing, long-range projections that could also reach deeply into AI and VI. Here we seek to determine whether such a network of border-crossing, long-range projections is unique to barrel cortex or characterizes also other primary, unimodal sensory cortices and therefore could directly connect them. Using anterograde (BDA and retrograde (CTb tract-tracing techniques, we demonstrate that such diffuse horizontal networks directly and mutually connect VI, AI and SI. These findings suggest that diffuse, border-crossing axonal projections connecting directly primary cortices are an important organizational motif common to all major primary sensory cortices in the rat. Potential implications of these findings for topics including cortical structure-function relationships, multisensory integration, functional imaging and cortical parcellation are discussed.

Suppression of motor cortical excitability in anesthetized rats by low frequency repetitive transcranial magnetic stimulation.

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Paul A Muller

Full Text Available Repetitive transcranial magnetic stimulation (rTMS is a widely-used method for modulating cortical excitability in humans, by mechanisms thought to involve use-dependent synaptic plasticity. For example, when low frequency rTMS (LF rTMS is applied over the motor cortex, in humans, it predictably leads to a suppression of the motor evoked potential (MEP, presumably reflecting long-term depression (LTD -like mechanisms. Yet how closely such rTMS effects actually match LTD is unknown. We therefore sought to (1 reproduce cortico-spinal depression by LF rTMS in rats, (2 establish a reliable animal model for rTMS effects that may enable mechanistic studies, and (3 test whether LTD-like properties are evident in the rat LF rTMS setup. Lateralized MEPs were obtained from anesthetized Long-Evans rats. To test frequency-dependence of LF rTMS, rats underwent rTMS at one of three frequencies, 0.25, 0.5, or 1 Hz. We next tested the dependence of rTMS effects on N-methyl-D-aspartate glutamate receptor (NMDAR, by application of two NMDAR antagonists. We find that 1 Hz rTMS preferentially depresses unilateral MEP in rats, and that this LTD-like effect is blocked by NMDAR antagonists. These are the first electrophysiological data showing depression of cortical excitability following LF rTMS in rats, and the first to demonstrate dependence of this form of cortical plasticity on the NMDAR. We also note that our report is the first to show that the capacity for LTD-type cortical suppression by rTMS is present under barbiturate anesthesia, suggesting that future neuromodulatory rTMS applications under anesthesia may be considered.

Up-regulation of β-adrenoreceptors by drugs which cause depression

International Nuclear Information System (INIS)

Brand, L.; Van Rooyen, J.M.; Offermeier, J.

1988-01-01

A number of drugs associated with depressive episodes in man were investigated for their effects on rat cortical β-adrenoceptors, in view of the down-regulation of β-adrenoceptors caused by chronic administration of anti-depressant drugs. Scatchard analyses of [ 3 H]dihydro-alprenolol binding data provided B max and K D values for the cortical β-adrenoceptors. Up-regulation of the receptors occurred after daily injections of phenobarbitone for seven days (by 55%), pentobarbitone (by 143%), reserpine (by 82%) and propranolol (by 64%). β-adrenoceptors were not affected by daily injections of clonidine, chlorpromazine and flupenthixol for seven days. This work confirms the up-regulatory effect on β-adrenoceptors of certain drugs which produce depressions in man

Mapping cortical mesoscopic networks of single spiking cortical or sub-cortical neurons.

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Xiao, Dongsheng; Vanni, Matthieu P; Mitelut, Catalin C; Chan, Allen W; LeDue, Jeffrey M; Xie, Yicheng; Chen, Andrew Cn; Swindale, Nicholas V; Murphy, Timothy H

2017-02-04

Understanding the basis of brain function requires knowledge of cortical operations over wide-spatial scales, but also within the context of single neurons. In vivo, wide-field GCaMP imaging and sub-cortical/cortical cellular electrophysiology were used in mice to investigate relationships between spontaneous single neuron spiking and mesoscopic cortical activity. We make use of a rich set of cortical activity motifs that are present in spontaneous activity in anesthetized and awake animals. A mesoscale spike-triggered averaging procedure allowed the identification of motifs that are preferentially linked to individual spiking neurons by employing genetically targeted indicators of neuronal activity. Thalamic neurons predicted and reported specific cycles of wide-scale cortical inhibition/excitation. In contrast, spike-triggered maps derived from single cortical neurons yielded spatio-temporal maps expected for regional cortical consensus function. This approach can define network relationships between any point source of neuronal spiking and mesoscale cortical maps.

A stepped-wedge evaluation of an initiative to spread the collaborative care model for depression in primary care.

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Solberg, Leif I; Crain, A Lauren; Maciosek, Michael V; Unützer, Jürgen; Ohnsorg, Kris A; Beck, Arne; Rubenstein, Lisa; Whitebird, Robin R; Rossom, Rebecca C; Pietruszewski, Pamela B; Crabtree, Benjamin F; Joslyn, Kenneth; Van de Ven, Andrew; Glasgow, Russell E

2015-09-01

Scale-up and spread of evidence-based practices is one of the most important challenges facing health care. We tested whether a statewide initiative, Depression Improvement Across Minnesota-Offering a New Direction (DIAMOND), to implement the collaborative care model for depression in 75 primary care clinics resulted in patient outcome improvements corresponding to those reported in randomized controlled trials. Health plans provided a new monthly payment to participating clinics after a 6-month intensive training program with ongoing data submission, networking, and consultation. Implementation was staggered, with 5 sequences of 10 to 40 clinics every 6 months. Payers provided weekly contact information for members from participating clinics who were filling antidepressant prescriptions, and we conducted baseline and 6-month surveys of 1,578 patients about their care and outcomes. There were 466 patients in DIAMOND clinics who received usual care before implementation (UCB), 559 who received usual care in DIAMOND clinics after implementation (UCA), 245 who received DIAMOND care after implementation (DCA), and 308 who received usual care in comparison clinics (UC). Patients who received DIAMOND care after implementation reported more collaborative care depression services than the 3 comparison groups (10.9 vs 6.4-6.7, on a scale of 0 of 14, where higher numbers indicate more services; P <.001) and more satisfaction with their care (4.0 vs 3.4 on a scale 1 to 5, in which higher scores indicate higher satisfaction; P ≤.001). Depression remission rates, however, were not significantly different among the 4 groups (36.4% DCA vs 35.8% UCB, 35.0% UCA, 33.9% UC; P = .94). Despite the incentive of a supporting payment change and intensive training and support for clinics volunteering to participate, no difference in depression outcomes was documented. Specific unmeasured actions present in trials but not present in these clinics may be critical for successful outcome

Spreading of healthy mood in adolescent social networks

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Hill, E. M.; Griffiths, F. E.; House, T.

2015-01-01

Depression is a major public health concern worldwide. There is evidence that social support and befriending influence mental health, and an improved understanding of the social processes that drive depression has the potential to bring significant public health benefits. We investigate transmission of mood on a social network of adolescents, allowing flexibility in our model by making no prior assumption as to whether it is low mood or healthy mood that spreads. Here, we show that while depr...

Imaging Cajal's neuronal avalanche: how wide-field optical imaging of the point-spread advanced the understanding of neocortical structure-function relationship.

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Frostig, Ron D; Chen-Bee, Cynthia H; Johnson, Brett A; Jacobs, Nathan S

2017-07-01

This review brings together a collection of studies that specifically use wide-field high-resolution mesoscopic level imaging techniques (intrinsic signal optical imaging; voltage-sensitive dye optical imaging) to image the cortical point spread (PS): the total spread of cortical activation comprising a large neuronal ensemble evoked by spatially restricted (point) stimulation of the sensory periphery (e.g., whisker, pure tone, point visual stimulation). The collective imaging findings, combined with supporting anatomical and electrophysiological findings, revealed some key aspects about the PS including its very large (radius of several mm) and relatively symmetrical spatial extent capable of crossing cytoarchitectural borders and trespassing into other cortical areas; its relationship with underlying evoked subthreshold activity and underlying anatomical system of long-range horizontal projections within gray matter, both also crossing borders; its contextual modulation and plasticity; the ability of its relative spatiotemporal profile to remain invariant to major changes in stimulation parameters; its potential role as a building block for integrative cortical activity; and its ubiquitous presence across various cortical areas and across mammalian species. Together, these findings advance our understanding about the neocortex at the mesoscopic level by underscoring that the cortical PS constitutes a fundamental motif of neocortical structure-function relationship.

Alterations in visual cortical activation and connectivity with prefrontal cortex during working memory updating in major depressive disorder.

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Le, Thang M; Borghi, John A; Kujawa, Autumn J; Klein, Daniel N; Leung, Hoi-Chung

2017-01-01

The present study examined the impacts of major depressive disorder (MDD) on visual and prefrontal cortical activity as well as their connectivity during visual working memory updating and related them to the core clinical features of the disorder. Impairment in working memory updating is typically associated with the retention of irrelevant negative information which can lead to persistent depressive mood and abnormal affect. However, performance deficits have been observed in MDD on tasks involving little or no demand on emotion processing, suggesting dysfunctions may also occur at the more basic level of information processing. Yet, it is unclear how various regions in the visual working memory circuit contribute to behavioral changes in MDD. We acquired functional magnetic resonance imaging data from 18 unmedicated participants with MDD and 21 age-matched healthy controls (CTL) while they performed a visual delayed recognition task with neutral faces and scenes as task stimuli. Selective working memory updating was manipulated by inserting a cue in the delay period to indicate which one or both of the two memorized stimuli (a face and a scene) would remain relevant for the recognition test. Our results revealed several key findings. Relative to the CTL group, the MDD group showed weaker postcue activations in visual association areas during selective maintenance of face and scene working memory. Across the MDD subjects, greater rumination and depressive symptoms were associated with more persistent activation and connectivity related to no-longer-relevant task information. Classification of postcue spatial activation patterns of the scene-related areas was also less consistent in the MDD subjects compared to the healthy controls. Such abnormalities appeared to result from a lack of updating effects in postcue functional connectivity between prefrontal and scene-related areas in the MDD group. In sum, disrupted working memory updating in MDD was revealed by

Abnormal left and right amygdala-orbitofrontal cortical functional connectivity to emotional faces: state versus trait vulnerability markers of depression in bipolar disorder.

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Versace, Amelia; Thompson, Wesley K; Zhou, Donli; Almeida, Jorge R C; Hassel, Stefanie; Klein, Crystal R; Kupfer, David J; Phillips, Mary L

2010-03-01

Amygdala-orbitofrontal cortical (OFC) functional connectivity (FC) to emotional stimuli and relationships with white matter remain little examined in bipolar disorder individuals (BD). Thirty-one BD (type I; n = 17 remitted; n = 14 depressed) and 24 age- and gender-ratio-matched healthy individuals (HC) viewed neutral, mild, and intense happy or sad emotional faces in two experiments. The FC was computed as linear and nonlinear dependence measures between amygdala and OFC time series. Effects of group, laterality, and emotion intensity upon amygdala-OFC FC and amygdala-OFC FC white matter fractional anisotropy (FA) relationships were examined. The BD versus HC showed significantly greater right amygdala-OFC FC (p relationship (p = .001) between left amygdala-OFC FC to sad faces and FA in HC. In BD, antidepressants were associated with significantly reduced left amygdala-OFC FC to mild sad faces (p = .001). In BD, abnormally elevated right amygdala-OFC FC to sad stimuli might represent a trait vulnerability for depression, whereas abnormally elevated left amygdala-OFC FC to sad stimuli and abnormally reduced amygdala-OFC FC to intense happy stimuli might represent a depression state marker. Abnormal FC measures might normalize with antidepressant medications in BD. Nonlinear amygdala-OFC FC-FA relationships in BD and HC require further study. Copyright 2010 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Amygdala functional disconnection with the prefrontal-cingulate-temporal circuit in chronic tinnitus patients with depressive mood.

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Chen, Yu-Chen; Bo, Fan; Xia, Wenqing; Liu, Shenghua; Wang, Peng; Su, Wen; Xu, Jin-Jing; Xiong, Zhenyu; Yin, Xindao

2017-10-03

Chronic tinnitus is often accompanied with depressive symptom, which may arise from aberrant functional coupling between the amygdala and cerebral cortex. To explore this hypothesis, resting-state functional magnetic resonance imaging (fMRI) was used to investigate the disrupted amygdala-cortical functional connectivity (FC) in chronic tinnitus patients with depressive mood. Chronic tinnitus patients with depressive mood (n=20), without depressive mood (n=20), and well-matched healthy controls (n=23) underwent resting-state fMRI scanning. Amygdala-cortical FC was characterized using a seed-based whole-brain correlation method. The bilateral amygdala FC was compared among the three groups. Compared to non-depressed patients, depressive tinnitus patients showed decreased amygdala FC with the prefrontal cortex and anterior cingulate cortex as well as increased amygdala FC with the postcentral gyrus and lingual gyrus. Relative to healthy controls, depressive tinnitus patients revealed decreased amygdala FC with the superior and middle temporal gyrus, anterior and posterior cingulate cortex, and prefrontal cortex, as well as increased amygdala FC with the postcentral gyrus and lingual gyrus. The current study identified for the first time abnormal resting-state amygdala-cortical FC with the prefrontal-cingulate-temporal circuit in chronic tinnitus patients with depressive mood, which will provide novel insight into the underlying neuropathological mechanisms of tinnitus-induced depressive disorder. Copyright © 2017 Elsevier Inc. All rights reserved.

Perspectives on How Human Simultaneous Multi-Modal Imaging Adds Directionality to Spread Models of Alzheimer’s Disease

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Julia Neitzel

2018-01-01

Full Text Available Previous animal research suggests that the spread of pathological agents in Alzheimer’s disease (AD follows the direction of signaling pathways. Specifically, tau pathology has been suggested to propagate in an infection-like mode along axons, from transentorhinal cortices to medial temporal lobe cortices and consequently to other cortical regions, while amyloid-beta (Aβ pathology seems to spread in an activity-dependent manner among and from isocortical regions into limbic and then subcortical regions. These directed connectivity-based spread models, however, have not been tested directly in AD patients due to the lack of an in vivo method to identify directed connectivity in humans. Recently, a new method—metabolic connectivity mapping (MCM—has been developed and validated in healthy participants that uses simultaneous FDG-PET and resting-state fMRI data acquisition to identify directed intrinsic effective connectivity (EC. To this end, postsynaptic energy consumption (FDG-PET is used to identify regions with afferent input from other functionally connected brain regions (resting-state fMRI. Here, we discuss how this multi-modal imaging approach allows quantitative, whole-brain mapping of signaling direction in AD patients, thereby pointing out some of the advantages it offers compared to other EC methods (i.e., Granger causality, dynamic causal modeling, Bayesian networks. Most importantly, MCM provides the basis on which models of pathology spread, derived from animal studies, can be tested in AD patients. In particular, future work should investigate whether tau and Aβ in humans propagate along the trajectories of directed connectivity in order to advance our understanding of the neuropathological mechanisms causing disease progression.

Prediction of pediatric unipolar depression using multiple neuromorphometric measurements: a pattern classification approach.

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Wu, Mon-Ju; Wu, Hanjing Emily; Mwangi, Benson; Sanches, Marsal; Selvaraj, Sudhakar; Zunta-Soares, Giovana B; Soares, Jair C

2015-03-01

Diagnosis of pediatric neuropsychiatric disorders such as unipolar depression is largely based on clinical judgment - without objective biomarkers to guide diagnostic process and subsequent therapeutic interventions. Neuroimaging studies have previously reported average group-level neuroanatomical differences between patients with pediatric unipolar depression and healthy controls. In the present study, we investigated the utility of multiple neuromorphometric indices in distinguishing pediatric unipolar depression patients from healthy controls at an individual subject level. We acquired structural T1-weighted scans from 25 pediatric unipolar depression patients and 26 demographically matched healthy controls. Multiple neuromorphometric indices such as cortical thickness, volume, and cortical folding patterns were obtained. A support vector machine pattern classification model was 'trained' to distinguish individual subjects with pediatric unipolar depression from healthy controls based on multiple neuromorphometric indices and model predictive validity (sensitivity and specificity) calculated. The model correctly identified 40 out of 51 subjects translating to 78.4% accuracy, 76.0% sensitivity and 80.8% specificity, chi-square p-value = 0.000049. Volumetric and cortical folding abnormalities in the right thalamus and right temporal pole respectively were most central in distinguishing individual patients with pediatric unipolar depression from healthy controls. These findings provide evidence that a support vector machine pattern classification model using multiple neuromorphometric indices may qualify as diagnostic marker for pediatric unipolar depression. In addition, our results identified the most relevant neuromorphometric features in distinguishing PUD patients from healthy controls. Copyright © 2015 Elsevier Ltd. All rights reserved.

Effect of aerobic training on EEG alpha asymmetry and depressive symptoms in the elderly: a 1-year follow-up study

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A.C. Deslandes

2010-06-01

Full Text Available The effect of physical exercise on the treatment of depressive elderly adults has not been investigated thus far in terms of changes in cortical hemispheric activity. The objective of the present study was to identify changes in depressive symptoms, quality of life, and cortical asymmetry produced by aerobic activity. Elderly subjects with a diagnosis of major depressive disorder (DSM-IV were included. Twenty patients (70% females, 71 ± 3 years were divided into an exercise group (pharmacological treatment plus aerobic training and a control group (undergoing pharmacological treatment in a quasi-experimental design. Pharmacological treatment was maintained stable throughout the study (antidepressants and anxiolytics. Subjects were evaluated by depression scales (Beck Depression Inventory, Hamilton Depression Rating Scale, Montgomery-Asberg Depression Rating Scale and the Short Form Health Survey-36, and electroencephalographic measurements (frontal and parietal alpha asymmetry before and after 1 year of treatment. After 1 year, the control group showed a decrease in cortical activity on the right hemisphere (increase of alpha power, which was not observed in the exercise group. The exercise group showed a significant decrease of depressive symptoms, which was not observed in the control group. This result was also accompanied by improved treatment response and remission rate after 1 year of aerobic exercise associated with treatment. This study provides support for the effect of aerobic training on alpha activity and on depressive symptoms in elderly patients. Exercise facilitates the treatment of depressive elderly adults, leading to clinical and physical improvement and protecting against a decrease in cortical activity.

Emittance growth in displaced, space-charge-dominated beams with energy spread

International Nuclear Information System (INIS)

Barnard, J.J.; Miller, J.; Haber, I.

1993-01-01

Conversion of transverse energy associated with the coherent motion of displaced beams into thermal energy, and thus emittance growth, has been predicted theoretically by a number of authors. Here, they authors show, using 2-D particle-in-cell simulations, that emittance growth is inhibited for tune depressed beams, if the energy spread of the beam is not too large. Further, using a uniform density model to calculate the space charge field of the beam, they numerically determine the criteria for emittance growth as a function of tune depression, energy spread, and beam displacement over a wide range of parameters. A theoretical interpretation of the results is presented. This study is applicable to an inertial fusion reactor driven by a heavy ion accelerator

Early Childhood Depression and Alterations in the Trajectory of Gray Matter Maturation in Middle Childhood and Early Adolescence.

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Luby, Joan L; Belden, Andy C; Jackson, Joshua J; Lessov-Schlaggar, Christina N; Harms, Michael P; Tillman, Rebecca; Botteron, Kelly; Whalen, Diana; Barch, Deanna M

2016-01-01

The trajectory of cortical gray matter development in childhood has been characterized by early neurogenesis and volume increase, peaking at puberty followed by selective elimination and myelination, resulting in volume loss and thinning. This inverted U-shaped trajectory, as well as cortical thickness, has been associated with cognitive and emotional function. Synaptic pruning-based volume decline has been related to experience-dependent plasticity in animals. To date, there have been no data to inform whether and how childhood depression might be associated with this trajectory. To examine the effects of early childhood depression, from the preschool age to the school age period, on cortical gray matter development measured across 3 waves of neuroimaging from late school age to early adolescence. Data were collected in an academic research setting from September 22, 2003, to December 13, 2014, on 193 children aged 3 to 6 years from the St Louis, Missouri, metropolitan area who were observed for up to 11 years in a longitudinal behavioral and neuroimaging study of childhood depression. Multilevel modeling was applied to explore the association between the number of childhood depression symptoms and prior diagnosis of major depressive disorder and the trajectory of gray matter change across 3 scan waves. Data analysis was conducted from October 29, 2014, to September 28, 2015. Volume, thickness, and surface area of cortical gray matter measured using structural magnetic resonance imaging at 3 scan waves. Of the 193 children, 90 had a diagnosis of major depressive disorder; 116 children had 3 full waves of neuroimaging scans. Findings demonstrated marked alterations in cortical gray matter volume loss (slope estimate, -0.93 cm³; 95% CI, -1.75 to -0.10 cm³ per scan wave) and thinning (slope estimate, -0.0044 mm; 95% CI, -0.0077 to -0.0012 mm per scan wave) associated with experiencing an episode of major depressive disorder before the first magnetic resonance

Lower cortical serotonin 2A receptors in major depressive disorder, suicide and in rats after administration of imipramine.

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Dean, Brian; Tawadros, Nahed; Seo, Myoung Suk; Jeon, Won Je; Everall, Ian; Scarr, Elizabeth; Gibbons, Andrew

2014-06-01

We have attempted to replicate studies showing higher levels of serotonin 2A receptors (HTR2A) in the cortex of people with mood disorders and to determine the effects of treating rats with antidepressant drugs on levels of that receptor. In situ [3H]ketanserin binding and autoradiography was used to measure levels of HTR2A in Brodmann's area (BA) 46 and 24 from people with major depressive disorders (MDD, n = 16), bipolar disorders (BD, n = 14) and healthy controls (n = 14) as well as the central nervous system (CNS) of rats (20 per treatment arm) treated for 10 or 28 d with fluoxetine (10 mg/kg/d) or imipramine (20 mg/kg/d). Compared with controls, HTR2A were lower in BA 24, but not BA 46, from people with MDD (p = 0.005); HTR2A were not changed in BD. Levels of HTR2A were lower in BA 24 (p = 0.007), but not BA 46, from people who had died by suicide. Finally, levels of HTR2A were lower in the CNS of rats treated with imipramine, but not fluoxetine, for 28 d, but not 10 d. From our current and previous data we conclude cortical HTR2A are lower in schizophrenia, MDD, people with mood disorders who died by suicide, rats treated with some antipsychotic or some antidepressant drugs. As levels of cortical HTR2A can be affected by the aetiologies of different disorders and mechanisms of action of different drugs, a better understanding of how such changes can occur needs to be elucidated.

Neural correlates of self-perceptions in adolescents with major depressive disorder.

Science.gov (United States)

Bradley, Kailyn A L; Colcombe, Stan; Henderson, Sarah E; Alonso, Carmen M; Milham, Michael P; Gabbay, Vilma

2016-06-01

Alteration in self-perception is a salient feature in major depression. Hyperactivity of anterior cortical midline regions has been implicated in this phenomenon in depressed adults. Here, we extend this work to depressed adolescents during a developmental time when neuronal circuitry underlying the sense of self matures by using task-based functional magnetic resonance imaging (fMRI) and connectivity analyses. Twenty-three depressed adolescents and 18 healthy controls (HC) viewed positive and negative trait words in a scanner and judged whether each word described them ('self' condition) or was a good trait to have ('general' condition). Self-perception scores were based on participants' endorsements of positive and negative traits during the fMRI task. Depressed adolescents exhibited more negative self-perceptions than HC. Both groups activated cortical midline regions in response to self-judgments compared to general-judgments. However, depressed adolescents recruited the posterior cingulate cortex/precuneus more for positive self-judgments. Additionally, local connectivity of the dorsal medial prefrontal cortex was reduced during self-reflection in depressed adolescents. Our findings highlight differences in self-referential processing network function between depressed and healthy adolescents and support the need for further investigation of brain mechanisms associated with the self, as they may be paramount to understanding the etiology and development of major depressive disorder. Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.

Neural correlates of self-perceptions in adolescents with major depressive disorder

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Kailyn A.L. Bradley

2016-06-01

Full Text Available Alteration in self-perception is a salient feature in major depression. Hyperactivity of anterior cortical midline regions has been implicated in this phenomenon in depressed adults. Here, we extend this work to depressed adolescents during a developmental time when neuronal circuitry underlying the sense of self matures by using task-based functional magnetic resonance imaging (fMRI and connectivity analyses. Twenty-three depressed adolescents and 18 healthy controls (HC viewed positive and negative trait words in a scanner and judged whether each word described them (‘self’ condition or was a good trait to have (‘general’ condition. Self-perception scores were based on participants’ endorsements of positive and negative traits during the fMRI task. Depressed adolescents exhibited more negative self-perceptions than HC. Both groups activated cortical midline regions in response to self-judgments compared to general-judgments. However, depressed adolescents recruited the posterior cingulate cortex/precuneus more for positive self-judgments. Additionally, local connectivity of the dorsal medial prefrontal cortex was reduced during self-reflection in depressed adolescents. Our findings highlight differences in self-referential processing network function between depressed and healthy adolescents and support the need for further investigation of brain mechanisms associated with the self, as they may be paramount to understanding the etiology and development of major depressive disorder.

Spreading Depressions as Secondary Insults after Traumatic Injury to the Human Brain

Science.gov (United States)

2012-09-01

excitotoxicity.10 Since the 1990s, spontaneous waves of peri-infarct spreading depolar- isations have been appreciated as a central mechanism of the...for webappendix Articles 1060 www.thelancet.com/neurology Vol 10 December 2011 We analysed recordings offline for spreading depolar- isations ...further tissue is terminally depolarised,24,25 whereas necrosis is not observed in remote tissue, where shorter depolar- isations cause transient

Cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans.

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Dania eVecchia

2015-02-01

Full Text Available Familial hemiplegic migraine type 1 (FHM1 is caused by gain-of-function mutations in CaV2.1 (P/Q-type Ca2+ channels. Knockin (KI mice carrying the FHM1 R192Q missense mutation show enhanced cortical excitatory synaptic transmission at pyramidal cell synapses but unaltered cortical inhibitory neurotransmission at fast-spiking interneuron synapses. Enhanced cortical glutamate release was shown to cause the facilitation of cortical spreading depression (CSD in R192Q KI mice. It, however, remains unknown how other FHM1 mutations affect cortical synaptic transmission. Here, we studied neurotransmission in cortical neurons in microculture from KI mice carrying the S218L mutation, which causes a severe FHM syndrome in humans and an allele-dosage dependent facilitation of experimental CSD in KI mice, which is larger than that caused by the R192Q mutation. We show gain-of-function of excitatory neurotransmission, due to increased action-potential evoked Ca2+ influx and increased probability of glutamate release at pyramidal cell synapses, but unaltered inhibitory neurotransmission at multipolar interneuron synapses in S218L KI mice. In contrast with the larger gain-of-function of neuronal CaV2.1 current in homozygous than heterozygous S218L KI mice, the gain-of-function of evoked glutamate release, the paired-pulse ratio and the Ca2+ dependence of the EPSC were all similar in homozygous and heterozygous S218L KI mice, suggesting compensatory changes in the homozygous mice. Furthermore, we reveal a unique feature of S218L KI cortical synapses which is the presence of a fraction of mutant CaV2.1 channels being open at resting potential. Our data suggest that, while the gain-of-function of evoked glutamate release may explain the facilitation of CSD in heterozygous S218L KI mice, the further facilitation of CSD in homozygous S218L KI mice is due to other CaV2.1-dependent mechanisms, that likely include Ca2+ influx at voltages sub-threshold for action

The Bat as a New Model of Cortical Development.

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Martínez-Cerdeño, Verónica; Camacho, Jasmin; Ariza, Jeanelle; Rogers, Hailee; Horton-Sparks, Kayla; Kreutz, Anna; Behringer, Richard; Rasweiler, John J; Noctor, Stephen C

2017-11-09

The organization of the mammalian cerebral cortex shares fundamental features across species. However, while the radial thickness of grey matter varies within one order of magnitude, the tangential spread of the cortical sheet varies by orders of magnitude across species. A broader sample of model species may provide additional clues for understanding mechanisms that drive cortical expansion. Here, we introduce the bat Carollia perspicillata as a new model species. The brain of C. perspicillata is similar in size to that of mouse but has a cortical neurogenic period at least 5 times longer than mouse, and nearly as long as that of the rhesus macaque, whose brain is 100 times larger. We describe the development of laminar and regional structures, neural precursor cell identity and distribution, immune cell distribution, and a novel population of Tbr2+ cells in the caudal ganglionic eminence of the developing neocortex of C. perspicillata. Our data indicate that unique mechanisms guide bat cortical development, particularly concerning cell cycle length. The bat model provides new perspective on the evolution of developmental programs that regulate neurogenesis in mammalian cerebral cortex, and offers insight into mechanisms that contribute to tangential expansion and gyri formation in the cerebral cortex. © The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Integrated mechanisms of anticipation and rate-of-change computations in cortical circuits.

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Gabriel D Puccini

2007-05-01

Full Text Available Local neocortical circuits are characterized by stereotypical physiological and structural features that subserve generic computational operations. These basic computations of the cortical microcircuit emerge through the interplay of neuronal connectivity, cellular intrinsic properties, and synaptic plasticity dynamics. How these interacting mechanisms generate specific computational operations in the cortical circuit remains largely unknown. Here, we identify the neurophysiological basis of both the rate of change and anticipation computations on synaptic inputs in a cortical circuit. Through biophysically realistic computer simulations and neuronal recordings, we show that the rate-of-change computation is operated robustly in cortical networks through the combination of two ubiquitous brain mechanisms: short-term synaptic depression and spike-frequency adaptation. We then show how this rate-of-change circuit can be embedded in a convergently connected network to anticipate temporally incoming synaptic inputs, in quantitative agreement with experimental findings on anticipatory responses to moving stimuli in the primary visual cortex. Given the robustness of the mechanism and the widespread nature of the physiological machinery involved, we suggest that rate-of-change computation and temporal anticipation are principal, hard-wired functions of neural information processing in the cortical microcircuit.

Accuracy limits for the determination of cortical width and density: the influence of object size and CT imaging parameters

International Nuclear Information System (INIS)

Prevrhal, S.; Engelke, K.; Kalender, W.A.

1999-01-01

In this study we analysed the accuracy of computed tomography (CT) measurements in assessing cortical bone. We determined the dependency of thickness and density measurements on the true width and density of the cortex and on the spatial resolution in the CT images using two optimized segmentation methods. As a secondary goal, we assessed the ability of CT to reflect small changes in cortical thickness. Two different bone-mimicking phantoms with varying cortical thickness were scanned with single-slice CT on a Somatom Plus 4 scanner. Images were reconstructed with both a standard and a high-resolution convolution kernel. Two special operator-independent segmentation methods were used to automatically detect the edges of the cortical shell. We measured cortical thickness and density and compared the phantom measurements with theoretical computations by simulating a cross-sectional shape of the cortical shell. Based on the simulations, we calculated CT's power to detect small changes in cortical thickness. Simulations and phantom measurements were in very good agreement. Cortical thickness could be measured with an error of less than 10% if the true thickness was larger than 0.9 (0.7) mm for the standard (high-resolution) kernel which is close to the full width at half maximum (FWHM) of the point spread functions for these kernels and our scanner. Density measurements yielded errors of less than 10% for true cortical thickness values above two to three times the FWHM corresponding to 2.5 (2) mm in our case. The simulations showed that a 10% change in cortical width would not be detected with satisfying probability in bones with a cortical shell thinner than 1.2 mm. An accurate determination of the cortical thickness is limited to bones with a thickness higher than the FWHM of the scanner's point spread function. Therefore, the use of a high-resolution reconstruction kernel is crucial. Cortical bone mineral density can only be measured accurately in bones two to three

Abnormal cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans

Science.gov (United States)

Vecchia, Dania; Tottene, Angelita; van den Maagdenberg, Arn M.J.M.; Pietrobon, Daniela

2015-01-01

Familial hemiplegic migraine type 1 (FHM1) is caused by gain-of-function mutations in CaV2.1 (P/Q-type) Ca2+ channels. Knockin (KI) mice carrying the FHM1 R192Q missense mutation show enhanced cortical excitatory synaptic transmission at pyramidal cell synapses but unaltered cortical inhibitory neurotransmission at fast-spiking interneuron synapses. Enhanced cortical glutamate release was shown to cause the facilitation of cortical spreading depression (CSD) in R192Q KI mice. It, however, remains unknown how other FHM1 mutations affect cortical synaptic transmission. Here, we studied neurotransmission in cortical neurons in microculture from KI mice carrying the S218L mutation, which causes a severe FHM syndrome in humans and an allele-dosage dependent facilitation of experimental CSD in KI mice, which is larger than that caused by the R192Q mutation. We show gain-of-function of excitatory neurotransmission, due to increased action-potential evoked Ca2+ influx and increased probability of glutamate release at pyramidal cell synapses, but unaltered inhibitory neurotransmission at multipolar interneuron synapses in S218L KI mice. In contrast with the larger gain-of-function of neuronal CaV2.1 current in homozygous than heterozygous S218L KI mice, the gain-of-function of evoked glutamate release, the paired-pulse ratio and the Ca2+ dependence of the excitatory postsynaptic current were similar in homozygous and heterozygous S218L KI mice, suggesting compensatory changes in the homozygous mice. Furthermore, we reveal a unique feature of S218L KI cortical synapses which is the presence of a fraction of mutant CaV2.1 channels being open at resting potential. Our data suggest that, while the gain-of-function of evoked glutamate release may explain the facilitation of CSD in heterozygous S218L KI mice, the further facilitation of CSD in homozygous S218L KI mice is due to other CaV2.1-dependent mechanisms, that likely include Ca2+ influx at voltages sub-threshold for action

[Psychotherapy of Depression as Neurobiological Process - Evidence from Neuroimaging].

Science.gov (United States)

Rubart, Antonie; Hohagen, Fritz; Zurowski, Bartosz

2018-06-01

Research on neurobiological effects of psychotherapy in depression facilitates the improvement of treatment strategies. The cortico-limbic dysregulation model serves as a framework for numerous studies on neurobiological changes in depression. In this model, depression is described as hypoactivation of dorsal cortical brain regions in conjunction with hyperactivation of ventral paralimbic regions. This assumption has been supported by various studies of structural and functional brain abnormalities in depression. However, also regions not included in the original cortico-limbic dysregulation model, such as the dorsomedial prefrontal cortex, seem to play an important role in depression. Functional connectivity studies of depression have revealed an enhanced connectivity within the so-called default mode network which is involved in self-referential thinking. Studies also point to a normalization of limbic and cortical brain activity, especially in the anterior cingulate cortex, during psychotherapy. Some neurobiological markers like the activity of the anterior cingulate cortex, striatum and insula as well as hippocampal volume have been proposed to predict treatment response on a group-level. The activity of the anterior insula appears to be a candidate bio-marker for differential indication for psychotherapy or pharmacotherapy. The cortico-limbic dysregulation model and following research have inspired new forms of treatment for depression like deep brain stimulation of the subgenual anterior cingulate cortex, repetitive transcranial magnetic stimulation of the dorsolateral prefrontal cortex, neurofeedback and attention training. © Georg Thieme Verlag KG Stuttgart · New York.

Cortical and subcortical hyperfusion during migraine and cluster headache measured by Xe CT-CBF

International Nuclear Information System (INIS)

Kobari, M.; Meyer, J.S.; Ichijo, M.; Kawamura, J.; Baylor Univ., Houston, TX

1990-01-01

High-resolution, color-coded images of local cerebral blood flow (LCBF) were made utilizing stable xenon-enhanced computed tomography among patients with common migraine (n=18), classic migraine (n=12) and cluster headache (n=5). During spontaneously occurring headache in common and classic migraine patients, LCBF values for cerebral cortex and subcortical gray and white matter were diffusely increased by 20-40% with the exception of the occipital lobes. LCBF increases involved both hemispheres whether the head pain was unilateral or bilateral. No significant differences were noted in the degree or pattern of LCBF increases during headaches of common and classic migraineurs. Similar cerebral hyperperfusion of greater magnitude was observed during cluster headaches but was more prominent on the side of the head pain. Present observations do not support the hypothesis of spreading cortical depression as a cause of classic migraine. From a hemodynamic viewpoint, LCBF increases during headaches of common or classic migraine or cluster appear similar. Evidence is adduced that sympathetic hypofunction with denervation hypersensitivity of cerebral vessels plays a role in the cerebral hyperperfusion of migraine headaches. More pronounced unilateral autonomic derangements appear to account for the symptoms and cerebral hyperperfusion associated with cluster headaches. (orig.)

Competing spreading processes and immunization in multiplex networks

International Nuclear Information System (INIS)

Gao, Bo; Deng, Zhenghong; Zhao, Dawei

2016-01-01

Epidemic spreading on physical contact network will naturally introduce the human awareness information diffusion on virtual contact network, and the awareness diffusion will in turn depress the epidemic spreading, thus forming the competing spreading processes of epidemic and awareness in a multiplex networks. In this paper, we study the competing dynamics of epidemic and awareness, both of which follow the SIR process, in a two-layer networks based on microscopic Markov chain approach and numerical simulations. We find that strong capacities of awareness diffusion and self-protection of individuals could lead to a much higher epidemic threshold and a smaller outbreak size. However, the self-awareness of individuals has no obvious effect on the epidemic threshold and outbreak size. In addition, the immunization of the physical contact network under the interplay between of epidemic and awareness spreading is also investigated. The targeted immunization is found performs much better than random immunization, and the awareness diffusion could reduce the immunization threshold for both type of random and targeted immunization significantly.

Suckling in litters with different sizes, and early and late swimming exercise differentially modulates anxiety-like behavior, memory and electrocorticogram potentiation after spreading depression in rats.

Science.gov (United States)

E Silva-Gondim, Mariana Barros; de Souza, Thays Kallyne Marinho; Rodrigues, Marcelo Cairrão Araújo; Guedes, Rubem Carlos Araújo

2017-11-28

Analyze the hypothesis that swimming exercise, in rats suckled under distinct litter sizes, alters behavioral parameters suggestive of anxiety and recognition memory, and the electrocorticogram potentiation that occurs after the excitability-related phenomenon that is known as cortical spreading depression (CSD). Male Wistar rats were suckled in litters with six or 12 pups (L 6 and L 12 groups). Animals swam at postnatal days (P) 8-23, or P60-P75 (early-exercised or late-exercised groups, respectively), or remained no-exercised. Behavioral tests (open field - OF and object recognition - OR) were conducted between P77 and P80. Between P90 and P120, ECoG was recorded for 2 hours. After this 'baseline' recording, CSD was elicited every 30 minutes over the course of 2 hours. Early swimming enhanced the number of entries and the percentage of time in the OF-center (P < 0.05). In animals that swam later, this effect occurred in the L6 group only. Compared to the corresponding sedentary groups, OR-test showed a better memory in the L6 early exercised rats, and a worse memory in all other groups (P < 0.05). In comparison to baseline values, ECoG amplitudes after CSD increased 14-43% for all groups (P < 0.05). In the L 6 condition, early swimming and late swimming, respectively, reduced and enhanced the magnitude of the post-CSD ECoG potentiation in comparison with the corresponding L 6 no-exercised groups (P < 0.05). Our data suggest a differential effect of early- and late-exercise on the behavioral and electrophysiological parameters, suggesting an interaction between the age of exercise and the nutritional status during lactation.

Stage IVN neuroblastoma: MRI diagnosis of left supraclavicular ''Virchow's'' nodal spread

International Nuclear Information System (INIS)

Abramson, S.J.; Berdon, W.E.; Stolar, C.; Ruzal-Shapiro, C.; Garvin, J.

1996-01-01

Stage IV neuroblastoma is associated with high mortality; an exception are patients whose stage IV status includes distant positive nodes, but no skeletal metastases - stage IVN neuroblastoma. We describe our experience with preoperative MRI in three patients with extensive abdominal neuroblastoma without cortical bony involvement but with unsuspected metastatic involvement to the left supraclavicular (Virchow's) node. We review findings of left supraclavicular nodal spread in five earlier cases of IVN neuroblastoma. (orig.). With 3 figs., 1 tab

Plasticity of cerebrovascular smooth muscle cells after subarachnoid hemorrhage

DEFF Research Database (Denmark)

Edvinsson, Lars; Larsen, Stine Schmidt; Maddahi, Aida

2014-01-01

Subarachnoid hemorrhage (SAH) is most often followed by a delayed phase of cerebral ischemia which is associated with high morbidity and mortality rates. The causes underlying this delayed phase are still unsettled, but are believed to include cerebral vasospasm, cortical spreading depression...

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

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Brendel, Matthias; Xiong, Guoming; Delker, Andreas [University of Munich, Department of Nuclear Medicine, Munich (Germany); Pogarell, Oliver [University of Munich, Department of Psychiatry, Munich (Germany); Bartenstein, Peter; Rominger, Axel [University of Munich, Department of Nuclear Medicine, Munich (Germany); Munich Cluster for Systems Neurology (SyNergy), Munich (Germany); Collaboration: for the Alzheimer' s Disease Neuroimaging Initiative

2015-04-01

Late-life depression even in subsyndromal stages is strongly associated with Alzheimer's disease (AD). Furthermore, brain amyloidosis is an early biomarker in subjects who subsequently suffer from AD and can be sensitively detected by amyloid PET. Therefore, we aimed to compare amyloid load and glucose metabolism in subsyndromally depressed subjects with mild cognitive impairment (MCI). [{sup 18}F]AV45 PET, [{sup 18}F]FDG PET and MRI were performed in 371 MCI subjects from the Alzheimer's Disease Neuroimaging Initiative Subjects were judged β-amyloid-positive (Aβ+; 206 patients) or β-amyloid-negative (Aβ-; 165 patients) according to [{sup 18}F]AV45 PET. Depressive symptoms were assessed by the Neuropsychiatric Inventory Questionnaire depression item 4. Subjects with depressive symptoms (65 Aβ+, 41 Aβ-) were compared with their nondepressed counterparts. Conversion rates to AD were analysed (mean follow-up time 21.5 ± 9.1 months) with regard to coexisting depressive symptoms and brain amyloid load. Aβ+ depressed subjects showed large clusters with a higher amyloid load in the frontotemporal and insular cortices (p < 0.001) with coincident hypermetabolism (p < 0.001) in the frontal cortices than nondepressed subjects. Faster progression to AD was observed in subjects with depressive symptoms (p < 0.005) and in Aβ+ subjects (p < 0.001). Coincident depressive symptoms additionally shortened the conversion time in all Aβ+ subjects (p < 0.005) and to a greater extent in those with a high amyloid load (p < 0.001). Our results clearly indicate that Aβ+ MCI subjects with depressive symptoms have an elevated amyloid load together with relative hypermetabolism of connected brain areas compared with cognitively matched nondepressed individuals. MCI subjects with high amyloid load and coexistent depressive symptoms are at high risk of faster conversion to AD. (orig.)

Depressive symptoms accelerate cognitive decline in amyloid-positive MCI patients

International Nuclear Information System (INIS)

Brendel, Matthias; Xiong, Guoming; Delker, Andreas; Pogarell, Oliver; Bartenstein, Peter; Rominger, Axel

2015-01-01

Late-life depression even in subsyndromal stages is strongly associated with Alzheimer's disease (AD). Furthermore, brain amyloidosis is an early biomarker in subjects who subsequently suffer from AD and can be sensitively detected by amyloid PET. Therefore, we aimed to compare amyloid load and glucose metabolism in subsyndromally depressed subjects with mild cognitive impairment (MCI). [ 18 F]AV45 PET, [ 18 F]FDG PET and MRI were performed in 371 MCI subjects from the Alzheimer's Disease Neuroimaging Initiative Subjects were judged β-amyloid-positive (Aβ+; 206 patients) or β-amyloid-negative (Aβ-; 165 patients) according to [ 18 F]AV45 PET. Depressive symptoms were assessed by the Neuropsychiatric Inventory Questionnaire depression item 4. Subjects with depressive symptoms (65 Aβ+, 41 Aβ-) were compared with their nondepressed counterparts. Conversion rates to AD were analysed (mean follow-up time 21.5 ± 9.1 months) with regard to coexisting depressive symptoms and brain amyloid load. Aβ+ depressed subjects showed large clusters with a higher amyloid load in the frontotemporal and insular cortices (p < 0.001) with coincident hypermetabolism (p < 0.001) in the frontal cortices than nondepressed subjects. Faster progression to AD was observed in subjects with depressive symptoms (p < 0.005) and in Aβ+ subjects (p < 0.001). Coincident depressive symptoms additionally shortened the conversion time in all Aβ+ subjects (p < 0.005) and to a greater extent in those with a high amyloid load (p < 0.001). Our results clearly indicate that Aβ+ MCI subjects with depressive symptoms have an elevated amyloid load together with relative hypermetabolism of connected brain areas compared with cognitively matched nondepressed individuals. MCI subjects with high amyloid load and coexistent depressive symptoms are at high risk of faster conversion to AD. (orig.)

Statistical mechanics of attractor neural network models with synaptic depression

International Nuclear Information System (INIS)

Igarashi, Yasuhiko; Oizumi, Masafumi; Otsubo, Yosuke; Nagata, Kenji; Okada, Masato

2009-01-01

Synaptic depression is known to control gain for presynaptic inputs. Since cortical neurons receive thousands of presynaptic inputs, and their outputs are fed into thousands of other neurons, the synaptic depression should influence macroscopic properties of neural networks. We employ simple neural network models to explore the macroscopic effects of synaptic depression. Systems with the synaptic depression cannot be analyzed due to asymmetry of connections with the conventional equilibrium statistical-mechanical approach. Thus, we first propose a microscopic dynamical mean field theory. Next, we derive macroscopic steady state equations and discuss the stabilities of steady states for various types of neural network models.

Functional and structural brain correlates of risk for major depression in children with familial depression

Directory of Open Access Journals (Sweden)

Xiaoqian J. Chai

2015-01-01

Full Text Available Despite growing evidence for atypical amygdala function and structure in major depression, it remains uncertain as to whether these brain differences reflect the clinical state of depression or neurobiological traits that predispose individuals to major depression. We examined function and structure of the amygdala and associated areas in a group of unaffected children of depressed parents (at-risk group and a group of children of parents without a history of major depression (control group. Compared to the control group, the at-risk group showed increased activation to fearful relative to neutral facial expressions in the amygdala and multiple cortical regions, and decreased activation to happy relative to neutral facial expressions in the anterior cingulate cortex and supramarginal gyrus. At-risk children also exhibited reduced amygdala volume. The extensive hyperactivation to negative facial expressions and hypoactivation to positive facial expressions in at-risk children are consistent with behavioral evidence that risk for major depression involves a bias to attend to negative information. These functional and structural brain differences between at-risk children and controls suggest that there are trait neurobiological underpinnings of risk for major depression.

Self-Referential Thinking, Suicide, and Function of the Cortical Midline Structures and Striatum in Mood Disorders: Possible Implications for Treatment Studies of Mindfulness-Based Interventions for Bipolar Depression

Directory of Open Access Journals (Sweden)

William R. Marchand

2012-01-01

Full Text Available Bipolar depression is often refractory to treatment and is frequently associated with anxiety symptoms and elevated suicide risk. There is a great need for adjunctive psychotherapeutic interventions. Treatments with effectiveness for depressive and anxiety symptoms as well as suicide-related thoughts and behaviors would be particularly beneficial. Mindfulness-based interventions hold promise, and studies of these approaches for bipolar disorder are warranted. The aim of this paper is to provide a conceptual background for such studies by reviewing key findings from diverse lines of investigation. Results of that review indicate that cortical midline structures (CMS appear to link abnormal self-referential thinking to emotional dysregulation in mood disorders. Furthermore, CMS and striatal dysfunction may play a role in the neuropathology underlying suicide-related thoughts and behaviors. Thus, combining studies of mindfulness interventions targeting abnormal self-referential thinking with functional imaging of CMS and striatal function may help delineate the neurobiological mechanisms of action of these treatments.

Effect of growth hormone on glycogenesis in rat cerebral cortical slices

International Nuclear Information System (INIS)

Visweswaran, P.; Binod Kumar; Azad, V.S.S.; Brahamchari, A.K.; Singh, S.P.

1994-01-01

Incubation of cerebral cortical slices of growth hormone treated diabetic and normal rats with U- 14 C glucose showed a two-fold increase in glycogenesis in diabetic rats. Glucose-6-phosphatase activity was lowered while the activities of phosphoglucomutase and phosphorylase were elevated in the cerebral cortex of diabetic rats treated with growth hormone. However, glycogen synthetase activity was slightly depressed. (author). 13 refs., 2 tabs

Lack of association between prior depressive episodes and cerebral [(11)C]PiB binding

DEFF Research Database (Denmark)

Madsen, K; Hasselbalch, Bo Jacob; Frederiksen, K S

2012-01-01

Depressive symptoms are frequent in Alzheimer's disease (AD), but it is controversial whether depression is a risk factor for AD. This study measured for the first time cortical amyloid-ß (Aß) levels using [(11)C] Pittsburgh Compound B (PiB) positron emission tomography (PET) in a group of nondem...

Frontal Brain Asymmetry in Depression with Comorbid Anxiety: A Neuropsychological Investigation

OpenAIRE

Nelson, Brady D.; Sarapas, Casey; Robison-Andrew, E. Jenna; Altman, Sarah E.; Campbell, Miranda L.; Shankman, Stewart A.

2012-01-01

The approach-withdrawal model posits that depression and anxiety are associated with a relative right asymmetry in frontal brain activity. Most studies have tested this model using measures of cortical brain activity such as electroencephalography. However, neuropsychological tasks that differentially employ left vs. right frontal cortical regions can also be used to test hypotheses from the model. In two independent samples (Study 1 and 2), the present study investigated the performance of c...

Regional cerebral blood flow in mood disorders. I. Comparison of major depressives and normal controls at rest

International Nuclear Information System (INIS)

Sackeim, H.A.; Prohovnik, I.; Moeller, J.R.; Brown, R.P.; Apter, S.; Prudic, J.; Devanand, D.P.; Mukherjee, S.

1990-01-01

We measured regional cerebral blood flow with the xenon 133 inhalation technique in 41 patients with major depressive disorder and 40 matched, normal controls during an eyes-closed, resting condition. The depressed group had a marked reduction in global cortical blood flow. To examine topographic abnormalities, traditional multivariate analyses were applied, as well as a new scaled subprofile model developed to identify abnormal functional neural networks in clinical samples. Both approaches indicated that the depressed sample had an abnormality in topographic distribution of blood flow, in addition to the global deficit. The scaled subprofile model identified the topographic abnormality as being due to flow reduction in the depressed patients in selective frontal, central, superior temporal, and anterior parietal regions. This pattern may reflect dysfunction in the parallel distributed cortical network involving frontal and temporoparietal polymodal association areas. The extent of this topographic abnormality, as revealed by the scaled subprofile model, was associated with both patient age and severity of depressive symptoms

A review of selected candidate endophenotypes for depression.

Science.gov (United States)

Goldstein, Brandon L; Klein, Daniel N

2014-07-01

Endophenotypes are proposed to occupy an intermediate position in the pathway between genotype and phenotype in genetically complex disorders such as depression. To be considered an endophenotype, a construct must meet a set of criteria proposed by Gottesman and Gould (2003). In this qualitative review, we summarize evidence for each criterion for several putative endophenotypes for depression: neuroticism, morning cortisol, frontal asymmetry of cortical electrical activity, reward learning, and biases of attention and memory. Our review indicates that while there is strong support for some depression endophenotypes, other putative endophenotypes lack data or have inconsistent findings for core criteria. Copyright © 2014 Elsevier Ltd. All rights reserved.

Chronic Depressive Symptomatology in Mild Cognitive Impairment Is Associated with Frontal Atrophy Rate which Hastens Conversion to Alzheimer Dementia.

Science.gov (United States)

Sacuiu, Simona; Insel, Philip S; Mueller, Susanne; Tosun, Duygu; Mattsson, Niklas; Jack, Clifford R; DeCarli, Charles; Petersen, Ronald; Aisen, Paul S; Weiner, Michael W; Mackin, R Scott

2016-02-01

Investigate the association of chronic depressive symptomatology (chrDS) with cortical atrophy rates and conversion to Alzheimer dementia (AD) over 3 years in mild cognitive impairment (MCI). In a multicenter, clinic-based study, MCI elderly participants were selected from the Alzheimer's Disease Neuroimaging Initiative repository, based on availability of both serial structural magnetic resonance imaging and chrDS endorsed on three depression-related items from the Neuropsychiatric Inventory Questionnaire (chrDS N = 32 or no depressive symptoms N = 62) throughout follow-up. Clinical and laboratory investigations were performed every 6 months during the first 2 years and yearly thereafter (median follow-up: 3 years; interquartile range: 1.5-4.0 years). Cortical atrophy rates in 16 predefined frontotemporoparietal regions affected in major depression and AD and the rate of incident AD at follow-up. ChrDS in a single domain amnestic MCI sample were associated with accelerated cortical atrophy in the frontal lobe and anterior cingulate but not with atrophy rates in temporomedial or other AD-affected regions. During follow-up, 38 participants (42.7%) developed AD. Participants with chrDS had 60% shorter conversion time to AD than those without depressive symptoms. This association remained significant in survival models adjusted for temporomedial atrophy rates and showed the same trend in models adjusted for frontal cortical atrophy rate, which all increased the risk of AD. Our results suggest that chrDS associated with progressive atrophy of frontal regions may represent an additional risk factor for conversion to dementia in MCI as opposite to representing typical prodromal AD symptomatology. Published by Elsevier Inc.

Cortical visual impairment

OpenAIRE

Koželj, Urša

2013-01-01

In this thesis we discuss cortical visual impairment, diagnosis that is in the developed world in first place, since 20 percent of children with blindness or low vision are diagnosed with it. The objectives of the thesis are to define cortical visual impairment and the definition of characters suggestive of the cortical visual impairment as well as to search for causes that affect the growing diagnosis of cortical visual impairment. There are a lot of signs of cortical visual impairment. ...

Habituation of evoked responses is greater in patients with familial hemiplegic migraine than in controls

DEFF Research Database (Denmark)

Hansen, Jakob Møller; Bolla, M; Magis, D

2011-01-01

have associated with disturbed ion homeostasis, altered cellular excitability, neurotransmitter release, and decreased threshold for cortical spreading depression. The common forms of migraine are characterized interictally by a habituation deficit of cortical and subcortical evoked responses that has...... been attributed to neuronal dysexcitability. FHM and the common forms of migraine are thought to belong to a spectrum of migraine phenotypes with similar pathophysiology, and we therefore examined whether an abnormal habituation pattern would also be found in FHM patients....

Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala.

Science.gov (United States)

Mirante, Osvaldo; Brandalise, Federico; Bohacek, Johannes; Mansuy, Isabelle M

2014-01-01

N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced post-synaptically at the thalamic input but presynaptically at the cortical input, since post-synaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD).

Permeability of dura mater

DEFF Research Database (Denmark)

Tfelt-Hansen, Peer Carsten

2011-01-01

In the wake of cortical spreading depression (CSD) it has been suggested that noxious substances diffuse through the dura with resulting firing of epidural nerves. In my view this is unlikely because there are good reasons to suggest that there must be a dura-brain barrier. Alternatively collateral...

Restriction of the spread of epileptic discharges in cats by means of Bragg peak, intracranial irradiation

International Nuclear Information System (INIS)

Gaffey, C.T.; Montoya, V.J.; Lyman, J.T.; Howard, J.

1981-01-01

Adult male cats with a single epileptic focus receive neon ion Bragg peak radiation at the Bevalac at Lawrence Berkeley Laboratory. Bragg peak radiation is deposited in a thin disc of brain tissue beneath an epileptogenic focus produced with alumina cream. Paroxysmal electroencephalograms (EEGs) from the occipital cortex of cats confirm the biolectric changes in the pathogenesis of epilepsy. Distant spread of seizure activity occurs when the cells in the cortical focus fire a series of relatively simultaneous spikes at high frequency with sufficient intensity to develop self-sustained discharges in remote brain areas. The development of a 'mirror focus' in the EEG records in the contralateral cortex gives a measure of the distances paroxysmal discharges spread. Interhemispheric responses (IHR) that travel from the alumina-treated cortex via the corpus callosum to the contralateral cortex are a second measure of pathways over which paroxysmal discharges spread. In cat studies Bragg peak radiation is positioned beneath the epileptic cortical focus. Various heavy ion doses are employed to test whether an absorbed dose per cat is sufficient to block the transmission of epileptic activity as a function of the post-irradiation time. The relationship between neon ion dose and the post-irradiation time for the loss of IHR is a measure of the physiological dissociation of the epileptic brain tissue from the remainder of the brain. The loss of the 'mirror focus' in EEG records agrees with the IHR findings. (author)

SLEEP AND OLFACTORY CORTICAL PLASTICITY

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Dylan eBarnes

2014-04-01

Full Text Available In many systems, sleep plays a vital role in memory consolidation and synaptic homeostasis. These processes together help store information of biological significance and reset synaptic circuits to facilitate acquisition of information in the future. In this review, we describe recent evidence of sleep-dependent changes in olfactory system structure and function which contribute to odor memory and perception. During slow-wave sleep, the piriform cortex becomes hypo-responsive to odor stimulation and instead displays sharp-wave activity similar to that observed within the hippocampal formation. Furthermore, the functional connectivity between the piriform cortex and other cortical and limbic regions is enhanced during slow-wave sleep compared to waking. This combination of conditions may allow odor memory consolidation to occur during a state of reduced external interference and facilitate association of odor memories with stored hedonic and contextual cues. Evidence consistent with sleep-dependent odor replay within olfactory cortical circuits is presented. These data suggest that both the strength and precision of odor memories is sleep-dependent. The work further emphasizes the critical role of synaptic plasticity and memory in not only odor memory but also basic odor perception. The work also suggests a possible link between sleep disturbances that are frequently co-morbid with a wide range of pathologies including Alzheimer’s disease, schizophrenia and depression and the known olfactory impairments associated with those disorders.

Diurnal trend in EEG interhemispheric asymmetry in endogenous depressions

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T S Melnikova

2011-01-01

Full Text Available A trend in EEG interhemispheric asymmetry was studied in patients with endogenous depressions in morning and evening hours. In the morning, the spectral power of alpha rhythm particularly in the occipital cortical regions, proved to be higher than that in the evening. In the morning, the interhemispheric differences in the power of occipital alpha rhythm were leveled off while in the evening there was normalization of interhemispheric balance with the higher power of alpha rhythm in the right occipital region. Analysis of the mean coherence (mean Coh of alpha rhythm in individual cortical regions revealed that the patients with endogenous depression had higher readings mainly in the parietal and central regions of both hemispheres and in the right temporal regions in the morning than in the evening. The occipital and posttemporal regions showed an inverse trend in the mean Coh - it was lower in the morning than in the evening

Clinical study of correlation of pre-senile and senile depressive stage with silent cerebral infarction

International Nuclear Information System (INIS)

Fujikawa, Tokumi; Yamawaki, Shigeto; Fujita, Yasunobu; Shibata, Youko; Touhouda, Yoshikuni.

1992-01-01

The relationship between the pre-senile/senile depressive state and silent cerebral infarction was examined by MRI. Consecutive 56 depressive patients aged 50 years or older underwnt MRI. MRI revealed silent cerebral infarction in 60.3% of patients in whom depression occurred at the age of less than 65 years. The complication rate was significantly higher in these patients than the younger patients (60.9% vs 20%). Complications of silent cerebral infarction were found in 53.6% for patients in whom depression occurred at the age of less than 65 years and symptoms were deteriorated at the age of 65 years or older and in 100% for patients in whom it occurred at the age of 65 years or older and hospitalization was simultaneously required. These figures were remarkably higher than the age-related complication rate of silent cerebral infarction in non-depressive normal persons. This suggested that approximately half of depressive patients of pre-senile onset and majority of depressive patients of senile onset might have parenchymal involvement due to silent cerebral infarction. Both perforating-type and cortical-type infarcts were found. This has a implication for the involvement of multiple infarct-related foci in depressive state. For cortical-type infarcts, partial lesions were predominant, followed by frontal and temporal lesions. The incidence of left frontal infarcts was significanly higher than that of right frontal infarcts. Infarcts in both the parietal and left frontal lobes may be responsible for depressive state. (N.K.)

Depression and anxious apprehension distinguish frontocingulate cortical activity during top-down attentional control.

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Silton, Rebecca Levin; Heller, Wendy; Engels, Anna S; Towers, David N; Spielberg, Jeffrey M; Edgar, J Christopher; Sass, Sarah M; Stewart, Jennifer L; Sutton, Bradley P; Banich, Marie T; Miller, Gregory A

2011-05-01

A network consisting of left dorsolateral prefrontal cortex (LDLPFC) and dorsal anterior cingulate cortex (dACC) has been implicated in top-down attentional control. Few studies have systematically investigated how this network is altered in psychopathology, despite evidence that depression and anxiety are associated with attentional control impairments. Functional MRI and dense-array event-related brain potential (ERP) data were collected in separate sessions from 100 participants during a color-word Stroop task. Functional MRI results guided ERP source modeling to characterize the time course of activity in LDLPFC (300-440 ms) and dACC (520-680 ms). At low levels of depression, LDLPFC activity was indirectly related to Stroop interference and only via dACC activity. In contrast, at high levels of depression, dACC did not play an intervening role, and increased LDLPFC activity was directly related to decreased Stroop interference. Specific to high levels of anxious apprehension, higher dACC activity was related to more Stroop interference. Results indicate that depression and anxious apprehension modulate temporally and functionally distinct aspects of the frontocingulate network involved in top-down attention control.

Spreading depolarizations have prolonged direct current shifts and are associated with poor outcome in brain trauma

DEFF Research Database (Denmark)

Hartings, Jed A; Watanabe, Tomas; Bullock, M Ross

2011-01-01

, although prolonged events have not been observed in animal models. To determine whether detrimental penumbral-type depolarizations occur in human brain trauma, we analysed electrocorticographic recordings obtained by subdural electrode-strip monitoring during intensive care. Of 53 patients studied, 10......Cortical spreading depolarizations occur spontaneously after ischaemic, haemorrhagic and traumatic brain injury. Their effects vary spatially and temporally as graded phenomena, from infarction to complete recovery, and are reflected in the duration of depolarization measured by the negative direct...... current shift of electrocorticographic recordings. In the focal ischaemic penumbra, peri-infarct depolarizations have prolonged direct current shifts and cause progressive recruitment of the penumbra into the core infarct. In traumatic brain injury, the effects of spreading depolarizations are unknown...

Variability and Reliability of Paired-Pulse Depression and Cortical Oscillation Induced by Median Nerve Stimulation.

Science.gov (United States)

Onishi, Hideaki; Otsuru, Naofumi; Kojima, Sho; Miyaguchi, Shota; Saito, Kei; Inukai, Yasuto; Yamashiro, Koya; Sato, Daisuke; Tamaki, Hiroyuki; Shirozu, Hiroshi; Kameyama, Shigeki

2018-05-08

Paired-pulse depression (PPD) has been widely used to investigate the functional profiles of somatosensory cortical inhibition. However, PPD induced by somatosensory stimulation is variable, and the reasons for between- and within-subject PPD variability remains unclear. Therefore, the purpose of this study was to clarify the factors influencing PPD variability induced by somatosensory stimulation. The study participants were 19 healthy volunteers. First, we investigated the relationship between the PPD ratio of each component (N20m, P35m, and P60m) of the somatosensory magnetic field, and the alpha, beta, and gamma band changes in power [event-related desynchronization (ERD) and event-related synchronization (ERS)] induced by median nerve stimulation. Second, because brain-derived neurotrophic factor (BDNF) gene polymorphisms reportedly influence the PPD ratio, we assessed whether BDNF genotype influences PPD ratio variability. Finally, we evaluated the test-retest reliability of PPD and the alpha, beta, and gamma ERD/ERS induced by somatosensory stimulation. Significant positive correlations were observed between the P60m_PPD ratio and beta power change, and the P60m_PPD ratio was significantly smaller for the beta ERD group than for the beta ERS group. P35m_PPD was found to be robust and highly reproducible; however, P60m_PPD reproducibility was poor. In addition, the ICC values for alpha, beta, and gamma ERD/ERS were 0.680, 0.760, and 0.552 respectively. These results suggest that the variability of PPD for the P60m deflection may be influenced by the ERD/ERS magnitude, which is induced by median nerve stimulation.

Aristides Leão: a birth centennial homage with comments on his spreading depression

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Eliasz Engelhardt

2015-06-01

Full Text Available The year of 2014 is the birth centenary of Aristides Azevedo Pacheco Leão (1914-1993, and also marks seventy years of the publication of his discovery of the novel electrophysiological phenomenon, named by him “spreading depression” (SD, soon designated “Leão’s wave” or “Leão’s spreading depression”. This was a remarkable scientific milestone, and the author must be celebrated for this achievement, as the studies he triggered proceeded worldwide, with new concepts, as spreading depolarization, until the present days. Robust experimental and clinical evidence emerged to suggest that these and related electrophysiological phenomena are involved in the mechanisms of migraine aura, acute cerebrovascular diseases, traumatic brain injury, transient global amnesia, epileptic seizures, and their pathophysiological characteristics come to offer new therapeutic perspectives. He was a remarkable and complex personality, and the authors remit the readers to a paper where his personal life is contemplated.

Functional networks in parallel with cortical development associate with executive functions in children.

Science.gov (United States)

Zhong, Jidan; Rifkin-Graboi, Anne; Ta, Anh Tuan; Yap, Kar Lai; Chuang, Kai-Hsiang; Meaney, Michael J; Qiu, Anqi

2014-07-01

Children begin performing similarly to adults on tasks requiring executive functions in late childhood, a transition that is probably due to neuroanatomical fine-tuning processes, including myelination and synaptic pruning. In parallel to such structural changes in neuroanatomical organization, development of functional organization may also be associated with cognitive behaviors in children. We examined 6- to 10-year-old children's cortical thickness, functional organization, and cognitive performance. We used structural magnetic resonance imaging (MRI) to identify areas with cortical thinning, resting-state fMRI to identify functional organization in parallel to cortical development, and working memory/response inhibition tasks to assess executive functioning. We found that neuroanatomical changes in the form of cortical thinning spread over bilateral frontal, parietal, and occipital regions. These regions were engaged in 3 functional networks: sensorimotor and auditory, executive control, and default mode network. Furthermore, we found that working memory and response inhibition only associated with regional functional connectivity, but not topological organization (i.e., local and global efficiency of information transfer) of these functional networks. Interestingly, functional connections associated with "bottom-up" as opposed to "top-down" processing were more clearly related to children's performance on working memory and response inhibition, implying an important role for brain systems involved in late childhood. © The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala

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Osvaldo eMirante

2014-07-01

Full Text Available N-methyl-D-aspartate receptor (NMDAR-dependent long-term depression (LTD in the lateral nucleus of the amygdala (LA is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that a paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced postsynaptically at the thalamic input but presynaptically at the cortical input, since postsynaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD.

Cortical tremor: a variant of cortical reflex myoclonus.

Science.gov (United States)

Ikeda, A; Kakigi, R; Funai, N; Neshige, R; Kuroda, Y; Shibasaki, H

1990-10-01

Two patients with action tremor that was thought to originate in the cerebral cortex showed fine shivering-like finger twitching provoked mainly by action and posture. Surface EMG showed relatively rhythmic discharge at a rate of about 9 Hz, which resembled essential tremor. However, electrophysiologic studies revealed giant somatosensory evoked potentials (SEPs) with enhanced long-loop reflex and premovement cortical spike by the jerk-locked averaging method. Treatment with beta-blocker showed no effect, but anticonvulsants such as clonazepam, valproate, and primidone were effective to suppress the tremor and the amplitude of SEPs. We call this involuntary movement "cortical tremor," which is in fact a variant of cortical reflex myoclonus.

Cortical hypometabolism and its recovery following nucleus basalis lesions in baboons: a PET study

International Nuclear Information System (INIS)

Kiyosawa, M.; Pappata, S.; Duverger, D.

1987-01-01

The cerebral metabolic rate for glucose was measured serially with positron emission tomography and [ 18 F]fluorodeoxyglucose in five baboons with stereotactic electrocoagulation of the left nucleus basalis of Meynert (NbM). Four days after lesion, a significant metabolic depression was present in the ipsilateral cerebral cortex, most marked in the frontotemporal region, and which recovered progressively within 6-13 weeks. These data demonstrate that adaptive mechanisms efficiently compensate for the cortical metabolic effects of NbM-lesion-induced cholinergic deafferentation. Moreover, unilateral NbM lesions also induced a transient reduction in contralateral cortical metabolic rate, the mechanisms of which are discussed. Explanation of these effects of cholinergic deafferentation in the primate could further our understanding of the metabolic deficits observed in dementia of the Alzheimer's type

A cortical attractor network with Martinotti cells driven by facilitating synapses.

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Pradeep Krishnamurthy

Full Text Available The population of pyramidal cells significantly outnumbers the inhibitory interneurons in the neocortex, while at the same time the diversity of interneuron types is much more pronounced. One acknowledged key role of inhibition is to control the rate and patterning of pyramidal cell firing via negative feedback, but most likely the diversity of inhibitory pathways is matched by a corresponding diversity of functional roles. An important distinguishing feature of cortical interneurons is the variability of the short-term plasticity properties of synapses received from pyramidal cells. The Martinotti cell type has recently come under scrutiny due to the distinctly facilitating nature of the synapses they receive from pyramidal cells. This distinguishes these neurons from basket cells and other inhibitory interneurons typically targeted by depressing synapses. A key aspect of the work reported here has been to pinpoint the role of this variability. We first set out to reproduce quantitatively based on in vitro data the di-synaptic inhibitory microcircuit connecting two pyramidal cells via one or a few Martinotti cells. In a second step, we embedded this microcircuit in a previously developed attractor memory network model of neocortical layers 2/3. This model network demonstrated that basket cells with their characteristic depressing synapses are the first to discharge when the network enters an attractor state and that Martinotti cells respond with a delay, thereby shifting the excitation-inhibition balance and acting to terminate the attractor state. A parameter sensitivity analysis suggested that Martinotti cells might, in fact, play a dominant role in setting the attractor dwell time and thus cortical speed of processing, with cellular adaptation and synaptic depression having a less prominent role than previously thought.

Spreading Depressions as Secondary Insults After Traumatic Injury to the Human Brain

Science.gov (United States)

2010-09-01

meeting of the COSBID consortium took place on 6-8 May 2010 in Barcelona , Spain. Drs. Hartings and Wilson attended and made presentations on the topics...questions. 11 VI. REFERENCES aHartings JA, Strong AJ, Fabricius M, Manning A, Bhatia R, Dreier JP, Mazzeo AT, Tortella FC , Bullock MR. Spreading

Changes in community structure of resting state functional connectivity in unipolar depression.

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Anton Lord

Full Text Available Major depression is a prevalent disorder that imposes a significant burden on society, yet objective laboratory-style tests to assist in diagnosis are lacking. We employed network-based analyses of "resting state" functional neuroimaging data to ascertain group differences in the endogenous cortical activity between healthy and depressed subjects.We additionally sought to use machine learning techniques to explore the ability of these network-based measures of resting state activity to provide diagnostic information for depression. Resting state fMRI data were acquired from twenty two depressed outpatients and twenty two healthy subjects matched for age and gender. These data were anatomically parcellated and functional connectivity matrices were then derived using the linear correlations between the BOLD signal fluctuations of all pairs of cortical and subcortical regions.We characterised the hierarchical organization of these matrices using network-based matrics, with an emphasis on their mid-scale "modularity" arrangement. Whilst whole brain measures of organization did not differ between groups, a significant rearrangement of their community structure was observed. Furthermore we were able to classify individuals with a high level of accuracy using a support vector machine, primarily through the use of a modularity-based metric known as the participation index.In conclusion, the application of machine learning techniques to features of resting state fMRI network activity shows promising potential to assist in the diagnosis of major depression, now suggesting the need for validation in independent data sets.

[The hypothalamic-pituitary-adrenal axis and depressive disorder: recent progress].

Science.gov (United States)

Kunugi, Hiroshi; Hori, Hiroaki; Numakawa, Tadahiro; Ota, Miho

2012-08-01

Depression is a stress-induced disorder and there is compelling evidence for the involvement of hypothalamic-pituitary-adrenal (HPA) axis abnormalities in the disease. Chronic hyperactivity of the HPA axis and resultant excessive glucocorticoid (hypercortisolism) may be causal to depression. We demonstrated that the dexamethasone (DEX)/CRH test is a sensitive state-dependent marker to monitor HPA axis abnormalities. Restoration from HPA axis abnormalities occurs with clinical responses to treatment. Brain-derived neurotrophic factor (BDNF) has also been implicated in depression. We found that glucocorticoid (DEX) suppresses BDNF-induced dendrite outgrowth and synaptic formation via blocking the MAPK pathway in early-developing cultured hippocampal neurons. Furthermore, we demonstrated that glucocorticoid receptor (GR) and TrkB (a specific receptor of BDNF) interact and that DEX acutely suppresses BDNF-induced glutamate release by affecting the PLC-gamma pathway in cultured cortical neurons, indicating a mechanism underlying the effect of excessive glucocorticoid on BDNF function and resultant damage in cortical neurons. In a macroscopic view using magnetic resonance imaging (MRI), we found that individuals with hypercortisolism detected by the DEX/CRH test demonstrated volume loss in gray matter and reduced neural network assessed with diffusion tensor imaging in several brain regions. Finally, we observed that individuals with hypocortisolism detected by the DEX/CRH test tend to present more distress symptoms, maladaptive coping styles, and schizotypal personality traits than their counterparts, which points to the important role of hypocortisolism as well as hypercortisolism in depression spectrum disorders.

Extent of cortical involvement in amyotrophic lateral sclerosis--an analysis based on cortical thickness.

Science.gov (United States)

Thorns, Johannes; Jansma, Henk; Peschel, Thomas; Grosskreutz, Julian; Mohammadi, Bahram; Dengler, Reinhard; Münte, Thomas F

2013-10-18

Besides the defining involvement of upper and lower motor neurons, the involvement of extramotor structures has been increasingly acknowledged in amyotrophic lateral sclerosis (ALS). Here we investigated a group of 14 mildly to moderately affected ALS patients and 14 age-matched healthy control participants using cortical thickness analysis. Cortical thickness was determined from high resolution 3D T1 magnetic resonance images and involved semiautomatic segmentation in grey and white matter, cortical alignment and determination of thickness using the Laplace method. In addition to a whole-cortex analysis a region of interest approach was applied. ALS patients showed regions of significant cortical thinning in the pre- and postcentral gyri bilaterally. Further regions of cortical thinning included superior and inferior parietal lobule, angular and supramarginal gyrus, insula, superior frontal, temporal and occipital regions, thus further substantiating extramotor involvement in ALS. A relationship between cortical thickness of the right superior frontal cortex and clinical severity (assessed by the ALS functional rating scale) was also demonstrated. Cortical thickness is reduced in ALS not only in motor areas but in widespread non-motor cortical areas. Cortical thickness is related to clinical severity.

Subthalamic stimulation modulates cortical motor network activity and synchronization in Parkinson’s disease

Science.gov (United States)

Klotz, Rosa; Govindan, Rathinaswamy B.; Scholten, Marlieke; Naros, Georgios; Ramos-Murguialday, Ander; Bunjes, Friedemann; Meisner, Christoph; Plewnia, Christian; Krüger, Rejko

2015-01-01

coherence in the beta band was significantly attenuated over the bilateral sensorimotor areas. Similarly, the global cortico-cortical phase synchronization was attenuated, and the topographic differentiation revealed stronger desynchronization over the (ipsilateral) right-hemispheric prefrontal, premotor and sensorimotor areas compared to ‘stimulation off’. We further demonstrated that the cortico-cortical phase synchronization was largely dominated by genuine neuronal coupling. The clinical improvement with ‘stimulation on’ compared to ‘stimulation off’ could be predicted from this cortical decoupling with multiple regressions, and the reduction of synchronization over the right prefrontal area showed a linear univariate correlation with clinical improvement. Our study demonstrates wide-spread activity and synchronization modulations of the cortical motor network, and highlights subthalamic stimulation as a network-modulating therapy. Accordingly, subthalamic stimulation may release bilateral cortical computational resources by facilitating movement-related desynchronization. Moreover, the subthalamic nucleus is critical to balance inhibitory and facilitatory cortical players within the motor program. PMID:25558877

Regional cerebral blood flow (rCBF) changes in major depression

International Nuclear Information System (INIS)

Ohtaki, Junichi

1992-01-01

Regional cerebral blood flow (rCBF) in patients with major depression and in normal controls was measured by single photon emission computed tomography (SPECT) using N-isopropyl-p [ 123 I]-iodoamphetamine (IMP). The subjects were 22 patients with major depression and 14 normal controls. The rCBF was calculated by the ratio of activity per pixel in the cortical regions to activity per pixel in the cerebellum. IMP-SPECT was conducted in patients with major depression under the depressive and remitted states. rCBF values in the frontal, parietal, temporal, basal ganglia and the occipital regions, and the mean rCBF values were significantly lower in depressive patients than in the controls. Increased rCBF values were observed, and the mean rCBF became normal in the state of remittence. There was no significant difference in mean rCBF between depressive patients and the controls. Therefore, because the lower rCBF was normalized following improvement in expressive symptoms, the rCBF values could be useful as 'state dependent markers' in patients with major depression. (author)

Detection and quantification of regional cortical gray matter damage in multiple sclerosis utilizing gradient echo MRI

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Jie Wen

2015-01-01

Full Text Available Cortical gray matter (GM damage is now widely recognized in multiple sclerosis (MS. The standard MRI does not reliably detect cortical GM lesions, although cortical volume loss can be measured. In this study, we demonstrate that the gradient echo MRI can reliably and quantitatively assess cortical GM damage in MS patients using standard clinical scanners. High resolution multi-gradient echo MRI was used for regional mapping of tissue-specific MRI signal transverse relaxation rate values (R2* in 10 each relapsing–remitting, primary-progressive and secondary-progressive MS subjects. A voxel spread function method was used to correct artifacts induced by background field gradients. R2* values from healthy controls (HCs of varying ages were obtained to establish baseline data and calculate ΔR2* values – age-adjusted differences between MS patients and HC. Thickness of cortical regions was also measured in all subjects. In cortical regions, ΔR2* values of MS patients were also adjusted for changes in cortical thickness. Symbol digit modalities (SDMT and paced auditory serial addition (PASAT neurocognitive tests, as well as Expanded Disability Status Score, 25-foot timed walk and nine-hole peg test results were also obtained on all MS subjects. We found that ΔR2* values were lower in multiple cortical GM and normal appearing white matter (NAWM regions in MS compared with HC. ΔR2* values of global cortical GM and several specific cortical regions showed significant (p < 0.05 correlations with SDMT and PASAT scores, and showed better correlations than volumetric measures of the same regions. Neurological tests not focused on cognition (Expanded Disability Status Score, 25-foot timed walk and nine-hole peg tests showed no correlation with cortical GM ΔR2* values. The technique presented here is robust and reproducible. It requires less than 10 min and can be implemented on any MRI scanner. Our results show that quantitative tissue-specific R2

Changes in brain connectivity related to the treatment of depression measured through fMRI: a systematic review

Science.gov (United States)

Gudayol-Ferré, Esteve; Peró-Cebollero, Maribel; González-Garrido, Andrés A.; Guàrdia-Olmos, Joan

2015-01-01

Depression is a mental illness that presents alterations in brain connectivity in the Default Mode Network (DMN), the Affective Network (AN) and other cortical-limbic networks, and the Cognitive Control Network (CCN), among others. In recent years the interest in the possible effect of the different antidepressant treatments on functional connectivity has increased substantially. The goal of this paper is to conduct a systematic review of the studies on the relationship between the treatment of depression and brain connectivity. Nineteen studies were found in a systematic review on this topic. In all of them, there was improvement of the clinical symptoms after antidepressant treatment. In 18 out of the 19 studies, clinical improvement was associated to changes in brain connectivity. It seems that both DMN and the connectivity between cortical and limbic structures consistently changes after antidepressant treatment. However, the current evidence does not allow us to assure that the treatment of depression leads to changes in the CCN. In this regard, some papers report a positive correlation between changes in brain connectivity and improvement of depressive symptomatology, particularly when they measure cortical-limbic connectivity, whereas the changes in DMN do not significantly correlate with clinical improvement. Finally, some papers suggest that changes in connectivity after antidepressant treatment might be partly related to the mechanisms of action of the treatment administered. This effect has been observed in two studies with stimulation treatment (one with rTMS and one with ECT), and in two papers that administered three different pharmacological treatments. Our review allows us to make a series of recommendations that might guide future researchers exploring the effect of anti-depression treatments on brain connectivity. PMID:26578927

Cortico-cortical white matter motor pathway microstructure is related to psychomotor retardation in major depressive disorder.

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Tobias Bracht

Full Text Available Alterations of brain structure and function have been associated with psychomotor retardation in major depressive disorder (MDD. However, the association of motor behaviour and white matter integrity of motor pathways in MDD is unclear. The aim of the present study was to first investigate structural connectivity of white matter motor pathways in MDD. Second, we explore the relation of objectively measured motor activity and white matter integrity of motor pathways in MDD. Therefore, 21 patients with MDD and 21 healthy controls matched for age, gender, education and body mass index underwent diffusion tensor imaging and 24 hour actigraphy (measure of the activity level the same day. Applying a probabilistic fibre tracking approach we extracted connection pathways between the dorsolateral prefrontal cortex (dlPFC, the rostral anterior cingulate cortex (rACC, the pre-supplementary motor area (pre-SMA, the SMA-proper, the primary motor cortex (M1, the caudate nucleus, the putamen, the pallidum and the thalamus. Patients had lower activity levels and demonstrated increased mean diffusivity (MD in pathways linking left pre-SMA and SMA-proper, and right SMA-proper and M1. Exploratory analyses point to a positive association of activity level and mean-fractional anisotropy in the right rACC-pre-SMA connection in MDD. Only MDD patients with low activity levels had a negative linear association of activity level and mean-MD in the left dlPFC-pre-SMA connection. Our results point to structural alterations of cortico-cortical white matter motor pathways in MDD. Altered white matter organisation of rACC-pre-SMA and dlPFC-pre-SMA pathways may contribute to movement initiation in MDD.

[Dysfunctional resting-state connectivity of default mode network in adolescent patients with first-episode drug-naive major depressive disorder].

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Li, S Y; Zhu, Y; Wang, Y L; Lü, P P; Zuo, W B; Li, F Y

2017-12-05

Objective: To study resting-state functional connectivity (FC) of default mode network (DMN) in adolescent patients with first-episode drug-naive major depressive disorder (MDD). Methods: We enrolled thirty first-episode and drug-naive adolescent MDD patients and twenty-nine adolescent healthy control (HC) participants in the First Affiliated Hospital of Zhengzhou University. There were no differences in age, sex, and education between the MDD and HC group. Resting-state functional magnetic resonance images (fMRI) was performed. We selected posterior cingulate cortex (PCC) and medial prefrontal cortex (MPFC) of DMN as regions of interests (ROI). The differences of these regions from the whole brain functional connectivity were analyzed. The relations between abnormalities in FCs of DMN and clinical variables were further investigated. Results: Compared to the HCs, the MDD patients had congruently reduced FCs between the PCC and cerebellum, temporal cortices, occipital cortices, fusiform, dorsolateral prefrontal cortex. MPFC not only had reduced FCs with fusiform, temporal cortices, anterior cingulate cortex, but also had enhanced FCs with occipital cortices, parietal cortices, and precentral gyrus. In addition, the increased FC between the right MPFC and right precentral gyrus was positive correlated with Hamilton Rating Scale for Depression (HAMD) scores ( r =0.38, P =0.04). The reduced FC between the left middle temporal gyrus and left PCC as well as the enhanced FC between the right middle cingulum and right MPFC were positive correlated with the duration of depression since onset ( r =0.39, P =0.03; r =0.38, P =0.04). Conclusions: These findings show dysfunctional DMN connectivity of adolescent MDD patients. Neurodevelopmental abnormalities in DMN may present in adolescent MDD.

Ataxic Hemiparesis Associated with Cortical Infarct Localized in the Postcentral Gyrus.

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Kinjo, Yoshino; Suda, Satoshi; Sakamoto, Yuki; Okubo, Seiji; Kimura, Kazumi

2017-09-15

Ataxic hemiparesis (AH) is a classic lacunar syndrome associated with localized damage to the pons, internal capsule, thalamus, or corona radiata. A depression of metabolic activity known as crossed cerebellar diaschisis (CCD) is frequently observed in the cerebellar hemisphere contralateral to the site of the lesion in patients with AH. Though small cortical or subcortical lesions may result in AH, such occurrences are rare. The current report details the case of a patient with AH resulting from acute infarction associated with localized lesions of the postcentral gyrus who presented without CCD.

Comparing the influence of crestal cortical bone and sinus floor cortical bone in posterior maxilla bi-cortical dental implantation: a three-dimensional finite element analysis.

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Yan, Xu; Zhang, Xinwen; Chi, Weichao; Ai, Hongjun; Wu, Lin

2015-05-01

This study aimed to compare the influence of alveolar ridge cortical bone and sinus floor cortical bone in sinus areabi-cortical dental implantation by means of 3D finite element analysis. Three-dimensional finite element (FE) models in a posterior maxillary region with sinus membrane and the same height of alveolar ridge of 10 mm were generated according to the anatomical data of the sinus area. They were either with fixed thickness of crestal cortical bone and variable thickness of sinus floor cortical bone or vice versa. Ten models were assumed to be under immediate loading or conventional loading. The standard implant model based on the Nobel Biocare implant system was created via computer-aided design software. All materials were assumed to be isotropic and linearly elastic. An inclined force of 129 N was applied. Von Mises stress mainly concentrated on the surface of crestal cortical bone around the implant neck. For all the models, both the axial and buccolingual resonance frequencies of conventional loading were higher than those of immediate loading; however, the difference is less than 5%. The results showed that bi-cortical implant in sinus area increased the stability of the implant, especially for immediately loading implantation. The thickness of both crestal cortical bone and sinus floor cortical bone influenced implant micromotion and stress distribution; however, crestal cortical bone may be more important than sinus floor cortical bone.

Pharmacological Mechanisms of Cortical Enhancement Induced by the Repetitive Pairing of Visual/Cholinergic Stimulation.

Directory of Open Access Journals (Sweden)

Jun-Il Kang

Full Text Available Repetitive visual training paired with electrical activation of cholinergic projections to the primary visual cortex (V1 induces long-term enhancement of cortical processing in response to the visual training stimulus. To better determine the receptor subtypes mediating this effect the selective pharmacological blockade of V1 nicotinic (nAChR, M1 and M2 muscarinic (mAChR or GABAergic A (GABAAR receptors was performed during the training session and visual evoked potentials (VEPs were recorded before and after training. The training session consisted of the exposure of awake, adult rats to an orientation-specific 0.12 CPD grating paired with an electrical stimulation of the basal forebrain for a duration of 1 week for 10 minutes per day. Pharmacological agents were infused intracortically during this period. The post-training VEP amplitude was significantly increased compared to the pre-training values for the trained spatial frequency and to adjacent spatial frequencies up to 0.3 CPD, suggesting a long-term increase of V1 sensitivity. This increase was totally blocked by the nAChR antagonist as well as by an M2 mAChR subtype and GABAAR antagonist. Moreover, administration of the M2 mAChR antagonist also significantly decreased the amplitude of the control VEPs, suggesting a suppressive effect on cortical responsiveness. However, the M1 mAChR antagonist blocked the increase of the VEP amplitude only for the high spatial frequency (0.3 CPD, suggesting that M1 role was limited to the spread of the enhancement effect to a higher spatial frequency. More generally, all the drugs used did block the VEP increase at 0.3 CPD. Further, use of each of the aforementioned receptor antagonists blocked training-induced changes in gamma and beta band oscillations. These findings demonstrate that visual training coupled with cholinergic stimulation improved perceptual sensitivity by enhancing cortical responsiveness in V1. This enhancement is mainly mediated by n

High social desirability and prefrontal cortical activity in cancer patients: a preliminary study.

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Tashiro, Manabu; Juengling, Freimut D; Moser, Ernst; Reinhardt, Michael J; Kubota, Kazuo; Yanai, Kazuhiko; Sasaki, Hidetada; Nitzsche, Egbert U; Kumano, Hiroaki; Itoh, Masatoshi

2003-04-01

Social desirability is sometimes associated with poor prognosis in cancer patients. Psycho-neuro-immune interaction has been hypothesized as an underlying mechanism of the negative clinical outcome. Purpose of this study was to examine possible effects of high social desirability on the regional brain activity in patients with malignant diseases. Brain metabolism of 16 patients with various malignant diseases was measured by PET with 18F-fluorodeoxyglucose (FDG). Patients were divided into 2 groups using median split on Marlowe & Crown's Social Desirability Scale (MC), controlling for age, gender, and for severity of depression and anxiety, the possible two major influential factors. A group comparison of the regional cerebral activity was calculated on a voxel-by-voxel basis using statistical parametric mapping (SPM). The subgroup comparison showed that the high social desirability was associated with relatively increased metabolism in the cortical regions in the prefrontal, temporal and occipital lobes as well as in the anterior cingulate gyrus. High social desirability seems to be associated with increased activity in the prefrontal and other cortical areas. The finding is in an accordance with previous studies that demonstrated an association between prefrontal damage and anti-social behavior. Functional neuroimaging seems to be useful not only for psychiatric evaluation of major factors such as depression and anxiety but also for further psychosocial factors in cancer patients.

Rab3A, a possible marker of cortical granules, participates in cortical granule exocytosis in mouse eggs

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Bello, Oscar Daniel; Cappa, Andrea Isabel; Paola, Matilde de; Zanetti, María Natalia [Instituto de Histología y Embriología, CONICET – Universidad Nacional de Cuyo, Av. Libertador 80, 5500 Mendoza (Argentina); Fukuda, Mitsunori [Department of Developmental Biology and Neurosciences, Graduate School of Life Sciences, Tohoku University, Sendai, Miyagi 980-8578 (Japan); Fissore, Rafael A. [Department of Veterinary and Animal Sciences, University of Massachusetts Amherst, 661 North Pleasant Street, Amherst, MA 01003 (United States); Mayorga, Luis S. [Instituto de Histología y Embriología, CONICET – Universidad Nacional de Cuyo, Av. Libertador 80, 5500 Mendoza (Argentina); Michaut, Marcela A., E-mail: mmichaut@gmail.com [Instituto de Histología y Embriología, CONICET – Universidad Nacional de Cuyo, Av. Libertador 80, 5500 Mendoza (Argentina); Facultad de Ciencias Exactas y Naturales, Universidad Nacional de Cuyo (Argentina)

2016-09-10

Fusion of cortical granules with the oocyte plasma membrane is the most significant event to prevent polyspermy. This particular exocytosis, also known as cortical reaction, is regulated by calcium and its molecular mechanism is still not known. Rab3A, a member of the small GTP-binding protein superfamily, has been implicated in calcium-dependent exocytosis and is not yet clear whether Rab3A participates in cortical granules exocytosis. Here, we examine the involvement of Rab3A in the physiology of cortical granules, particularly, in their distribution during oocyte maturation and activation, and their participation in membrane fusion during cortical granule exocytosis. Immunofluorescence and Western blot analysis showed that Rab3A and cortical granules have a similar migration pattern during oocyte maturation, and that Rab3A is no longer detected after cortical granule exocytosis. These results suggested that Rab3A might be a marker of cortical granules. Overexpression of EGFP-Rab3A colocalized with cortical granules with a Pearson correlation coefficient of +0.967, indicating that Rab3A and cortical granules have almost a perfect colocalization in the egg cortical region. Using a functional assay, we demonstrated that microinjection of recombinant, prenylated and active GST-Rab3A triggered cortical granule exocytosis, indicating that Rab3A has an active role in this secretory pathway. To confirm this active role, we inhibited the function of endogenous Rab3A by microinjecting a polyclonal antibody raised against Rab3A prior to parthenogenetic activation. Our results showed that Rab3A antibody microinjection abolished cortical granule exocytosis in parthenogenetically activated oocytes. Altogether, our findings confirm that Rab3A might function as a marker of cortical granules and participates in cortical granule exocytosis in mouse eggs. - Highlights: • Rab3A has a similar migration pattern to cortical granules in mouse oocytes. • Rab3A can be a marker of

Cortical Visual Impairment

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... resolves by one year of life. Is “cortical blindness” the same thing as CVI? Cortical blindness is ... What visual characteristics are associated with CVI? • Distinct color preferences • Variable level of vision loss, often demonstrating ...

Optimization of power output and study of electron beam energy spread in a Free Electron Laser oscillator

International Nuclear Information System (INIS)

Abramovich, A.; Pinhasi, Y.; Yahalom, A.; Bar-Lev, D.; Efimov, S.; Gover, A.

2001-01-01

Design of a multi-stage depressed collector for efficient operation of a Free Electron Laser (FEL) oscillator requires knowledge of the electron beam energy distribution. This knowledge is necessary to determine the voltages of the depressed collector electrodes that optimize the collection efficiency and overall energy conversion efficiency of the FEL. The energy spread in the electron beam is due to interaction in the wiggler region, as electrons enter the interaction region at different phases relative to the EM wave. This interaction can be simulated well by a three-dimensional simulation code such as FEL3D. The main adjustable parameters that determine the electron beam energy spread after interaction are the e-beam current, the initial beam energy, and the quality factor of the resonator out-coupling coefficient. Using FEL3D, we study the influence of these parameters on the available radiation power and on the electron beam energy distribution at the undulator exit. Simulations performed for I=1.5 A, E=1.4 MeV, L=20% (Internal loss factor) showed that the highest radiated output power and smallest energy spread are attained for an output coupler transmission coefficient T m congruent with 30%

[Spinal cord stimulation (SCS) as a treatment for the spread phenomenon related to complex regional pain syndrome type- I (CRPS-I )].

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Goto, Shinichi; Taira, Takaomi; Hori, Tomokatsu

2009-09-01

The authors describe an experience of spinal cord stimulation (SCS) in a 30-year-old woman who developed complex regional pain syndrome type-I (CRPS-I) with spread phenomenon. She had received lumbar SCS under a diagnosis of CRPS-I in her left leg for 8 years. She had refractory pain in her right arm for the recent two years. There was no new lesion explaining her refractory pain on physical or radiological examination. Thus, the pain in her right upper arm was considered as spread phenomenon of CRPS-I. Test stimulation with cervical epidural spinal electrode showed good results and the pulse generator was implanted. It is suggested that the symptom of CRPS-I involving spread phenomenon was possibly due to a cortical reorganization. But a certain effect of SCS may be contributing to the favorable results of test stimulation for the treatment of CRPS-I with spread phenomenon in this case.

Fenómenos de despolarización cortical propagada en los pacientes con lesiones cerebrales traumáticas e isquémicas. Resultados de un estudio piloto

DEFF Research Database (Denmark)

Sueiras, M; Sahuquillo, J; García-López, B

2014-01-01

OBJECTIVES: To determine the frequency and duration of cortical spreading depolarization (CSD) and CSD-like episodes in patients with traumatic brain injury (TBI) and malignant middle cerebral artery infarction (MMCAI) requiring craniotomy. DESIGN: A descriptive observational study was carried ou...

Nanofibrillar scaffolds induce preferential activation of Rho GTPases in cerebral cortical astrocytes

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Tiryaki, Volkan Mujdat; Ayres, Virginia M; Khan, Adeel A; Ahmed, Ijaz; Shreiber, David I; Meiners, Sally

2012-01-01

Cerebral cortical astrocyte responses to polyamide nanofibrillar scaffolds versus poly-L-lysine (PLL)-functionalized planar glass, unfunctionalized planar Aclar coverslips, and PLL-functionalized planar Aclar surfaces were investigated by atomic force microscopy and immunocytochemistry. The physical properties of the cell culture environments were evaluated using contact angle and surface roughness measurements and compared. Astrocyte morphological responses, including filopodia, lamellipodia, and stress fiber formation, and stellation were imaged using atomic force microscopy and phalloidin staining for F-actin. Activation of the corresponding Rho GTPase regulators was investigated using immunolabeling with Cdc42, Rac1, and RhoA. Astrocytes cultured on the nanofibrillar scaffolds showed a unique response that included stellation, cell–cell interactions by stellate processes, and evidence of depression of RhoA. The results support the hypothesis that the extracellular environment can trigger preferential activation of members of the Rho GTPase family, with demonstrable morphological consequences for cerebral cortical astrocytes. PMID:22915841

Cortical influences drive amyotrophic lateral sclerosis.

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Eisen, Andrew; Braak, Heiko; Del Tredici, Kelly; Lemon, Roger; Ludolph, Albert C; Kiernan, Matthew C

2017-11-01

The early motor manifestations of sporadic amyotrophic lateral sclerosis (ALS), while rarely documented, reflect failure of adaptive complex motor skills. The development of these skills correlates with progressive evolution of a direct corticomotoneuronal system that is unique to primates and markedly enhanced in humans. The failure of this system in ALS may translate into the split hand presentation, gait disturbance, split leg syndrome and bulbar symptomatology related to vocalisation and breathing, and possibly diffuse fasciculation, characteristic of ALS. Clinical neurophysiology of the brain employing transcranial magnetic stimulation has convincingly demonstrated a presymptomatic reduction or absence of short interval intracortical inhibition, accompanied by increased intracortical facilitation, indicating cortical hyperexcitability. The hallmark of the TDP-43 pathological signature of sporadic ALS is restricted to cortical areas as well as to subcortical nuclei that are under the direct control of corticofugal projections. This provides anatomical support that the origins of the TDP-43 pathology reside in the cerebral cortex itself, secondarily in corticofugal fibres and the subcortical targets with which they make monosynaptic connections. The latter feature explains the multisystem degeneration that characterises ALS. Consideration of ALS as a primary neurodegenerative disorder of the human brain may incorporate concepts of prion-like spread at synaptic terminals of corticofugal axons. Further, such a concept could explain the recognised widespread imaging abnormalities of the ALS neocortex and the accepted relationship between ALS and frontotemporal dementia. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Association of Higher Cortical Amyloid Burden With Loneliness in Cognitively Normal Older Adults.

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Donovan, Nancy J; Okereke, Olivia I; Vannini, Patrizia; Amariglio, Rebecca E; Rentz, Dorene M; Marshall, Gad A; Johnson, Keith A; Sperling, Reisa A

2016-12-01

Emotional and behavioral symptoms in cognitively normal older people may be direct manifestations of Alzheimer disease (AD) pathophysiology at the preclinical stage, prior to the onset of mild cognitive impairment. Loneliness is a perceived state of social and emotional isolation that has been associated with cognitive and functional decline and an increased risk of incident AD dementia. We hypothesized that loneliness might occur in association with elevated cortical amyloid burden, an in vivo research biomarker of AD. To determine whether cortical amyloid burden is associated with greater loneliness in cognitively normal older adults. Cross-sectional analyses using data from the Harvard Aging Brain Study of 79 cognitively normal, community-dwelling participants. A continuous, aggregate measure of cortical amyloid burden, determined by Pittsburgh Compound B-positron emission tomography (PiB-PET), was examined in association with loneliness in linear regression models adjusting for age, sex, apolipoprotein E ε4 (APOEε4), socioeconomic status, depression, anxiety, and social network (without and with the interaction of amyloid and APOEε4). We also quantified the association of high amyloid burden (amyloid-positive group) to loneliness (lonely group) using logistic regression, controlling for the same covariates, with the amyloid-positive group and the lonely group, each composing 32% of the sample (n = 25). Loneliness, as determined by the 3-item UCLA Loneliness Scale (possible range, 3-12, with higher score indicating greater loneliness). The 79 participants included 43 women and 36 men with a mean (SD) age of 76.4 (6.2) years. Mean (SD) cortical amyloid burden via PiB-PET was 1.230 (0.209), and the mean (SD) UCLA-3 loneliness score was 5.3 (1.8). Twenty-two (28%) had positive APOEε4 carrier status, and 25 (32%) were in the amyloid-positive group with cortical PiB distribution volume ratio greater than 1.2. Controlling for age, sex, APOEε4, socioeconomic

PRENATAL EXPOSURE TO MATERNAL AND PATERNAL DEPRESSIVE SYMPTOMS AND BRAIN MORPHOLOGY: A POPULATION-BASED PROSPECTIVE NEUROIMAGING STUDY IN YOUNG CHILDREN.

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El Marroun, Hanan; Tiemeier, Henning; Muetzel, Ryan L; Thijssen, Sandra; van der Knaap, Noortje J F; Jaddoe, Vincent W V; Fernández, Guillén; Verhulst, Frank C; White, Tonya J H

2016-07-01

Prenatal depressive symptoms have been associated with multiple adverse outcomes. Previously, we demonstrated that prenatal depressive symptoms were associated with impaired growth of the fetus and increased behavioral problems in children aged between 1.5 and 6 years. In this prospective study, we aimed to assess whether prenatal maternal depressive symptoms at 3 years have long-term consequences on brain development in a cohort of children aged 6-10 years. As a contrast, the association of paternal depressive symptoms during pregnancy and brain morphology was assessed to serve as a marker of background confounding due to shared genetic and environmental family factors. We assessed parental depressive symptoms during pregnancy with the Brief Symptom Inventory. At approximately 8 years of age, we collected structural neuroimaging data, using cortical thickness, surface area, and gyrification as outcomes (n = 654). We found that exposure to prenatal maternal depressive symptoms during pregnancy was associated with a thinner superior frontal cortex in the left hemisphere. Additionally, prenatal maternal depressive symptoms were related to larger caudal middle frontal area in the left hemisphere. Maternal depressive symptoms at 3 years were not associated with cortical thickness, surface area, or gyrification in the left and right hemispheres. No effects of paternal depressive symptoms on brain morphology were observed. Prenatal maternal depressive symptoms were associated with differences in brain morphology in children. It is important to prevent, identify, and treat depressive symptoms during pregnancy as it may have long-term consequences on child brain development. © 2016 Wiley Periodicals, Inc.

Detection of spreading depolarization with intraparenchymal electrodes in the injured human brain

DEFF Research Database (Denmark)

Jeffcote, Toby; Hinzman, Jason M; Jewell, Sharon L

2014-01-01

be detected using intra-cortical electrodes, opening the way for electrode insertion via burr hole. METHODS: Animal work was carried out on adult Sprague-Dawley rats in a laboratory setting to investigate the feasibility of recording depolarization events. Subsequently, 8 human patients requiring craniotomy...... for craniotomy. The method provides a new investigative tool for the evaluation of the contribution of these events to secondary brain injury in human patients.......BACKGROUND: Spreading depolarization events following ischemic and traumatic brain injury are associated with poor patient outcome. Currently, monitoring these events is limited to patients in whom subdural electrodes can be placed at open craniotomy. This study examined whether these events can...

Recent progress in migraine pathophysiology: role of cortical spreading depression and magnetic resonance imaging

NARCIS (Netherlands)

Bhaskar, S.; Saeidi, K.; Borhani, P.; Amiri, H.

2013-01-01

Migraine is characterised by debilitating pain, which affects the quality of life in affected patients in both the western and the eastern worlds. The purpose of this article is to give a detailed outline of the pathophysiology of migraine pain, which is one of the most confounding pathologies among

Network Supervision of Adult Experience and Learning Dependent Sensory Cortical Plasticity.

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Blake, David T

2017-06-18

The brain is capable of remodeling throughout life. The sensory cortices provide a useful preparation for studying neuroplasticity both during development and thereafter. In adulthood, sensory cortices change in the cortical area activated by behaviorally relevant stimuli, by the strength of response within that activated area, and by the temporal profiles of those responses. Evidence supports forms of unsupervised, reinforcement, and fully supervised network learning rules. Studies on experience-dependent plasticity have mostly not controlled for learning, and they find support for unsupervised learning mechanisms. Changes occur with greatest ease in neurons containing α-CamKII, which are pyramidal neurons in layers II/III and layers V/VI. These changes use synaptic mechanisms including long term depression. Synaptic strengthening at NMDA-containing synapses does occur, but its weak association with activity suggests other factors also initiate changes. Studies that control learning find support of reinforcement learning rules and limited evidence of other forms of supervised learning. Behaviorally associating a stimulus with reinforcement leads to a strengthening of cortical response strength and enlarging of response area with poor selectivity. Associating a stimulus with omission of reinforcement leads to a selective weakening of responses. In some preparations in which these associations are not as clearly made, neurons with the most informative discharges are relatively stronger after training. Studies analyzing the temporal profile of responses associated with omission of reward, or of plasticity in studies with different discriminanda but statistically matched stimuli, support the existence of limited supervised network learning. © 2017 American Physiological Society. Compr Physiol 7:977-1008, 2017. Copyright © 2017 John Wiley & Sons, Inc.

Restoration of Thickness, Density, and Volume for Highly Blurred Thin Cortical Bones in Clinical CT Images.

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Pakdel, Amirreza; Hardisty, Michael; Fialkov, Jeffrey; Whyne, Cari

2016-11-01

In clinical CT images containing thin osseous structures, accurate definition of the geometry and density is limited by the scanner's resolution and radiation dose. This study presents and validates a practical methodology for restoring information about thin bone structure by volumetric deblurring of images. The methodology involves 2 steps: a phantom-free, post-reconstruction estimation of the 3D point spread function (PSF) from CT data sets, followed by iterative deconvolution using the PSF estimate. Performance of 5 iterative deconvolution algorithms, blind, Richardson-Lucy (standard, plus Total Variation versions), modified residual norm steepest descent (MRNSD), and Conjugate Gradient Least-Squares were evaluated using CT scans of synthetic cortical bone phantoms. The MRNSD algorithm resulted in the highest relative deblurring performance as assessed by a cortical bone thickness error (0.18 mm) and intensity error (150 HU), and was subsequently applied on a CT image of a cadaveric skull. Performance was compared against micro-CT images of the excised thin cortical bone samples from the skull (average thickness 1.08 ± 0.77 mm). Error in quantitative measurements made from the deblurred images was reduced 82% (p < 0.01) for cortical thickness and 55% (p < 0.01) for bone mineral mass. These results demonstrate a significant restoration of geometrical and radiological density information derived for thin osseous features.

Real-time optical diagnosis of the rat brain exposed to a laser-induced shock wave: observation of spreading depolarization, vasoconstriction and hypoxemia-oligemia.

Directory of Open Access Journals (Sweden)

Shunichi Sato

Full Text Available Despite many efforts, the pathophysiology and mechanism of blast-induced traumatic brain injury (bTBI have not yet been elucidated, partially due to the difficulty of real-time diagnosis and extremely complex factors determining the outcome. In this study, we topically applied a laser-induced shock wave (LISW to the rat brain through the skull, for which real-time measurements of optical diffuse reflectance and electroencephalogram (EEG were performed. Even under conditions showing no clear changes in systemic physiological parameters, the brain showed a drastic light scattering change accompanied by EEG suppression, which indicated the occurrence of spreading depression, long-lasting hypoxemia and signal change indicating mitochondrial energy impairment. Under the standard LISW conditions examined, hemorrhage and contusion were not apparent in the cortex. To investigate events associated with spreading depression, measurement of direct current (DC potential, light scattering imaging and stereomicroscopic observation of blood vessels were also conducted for the brain. After LISW application, we observed a distinct negative shift in the DC potential, which temporally coincided with the transit of a light scattering wave, showing the occurrence of spreading depolarization and concomitant change in light scattering. Blood vessels in the brain surface initially showed vasodilatation for 3-4 min, which was followed by long-lasting vasoconstriction, corresponding to hypoxemia. Computer simulation based on the inverse Monte Carlo method showed that hemoglobin oxygen saturation declined to as low as ∼35% in the long-term hypoxemic phase. Overall, we found that topical application of a shock wave to the brain caused spreading depolarization/depression and prolonged severe hypoxemia-oligemia, which might lead to pathological conditions in the brain. Although further study is needed, our findings suggest that spreading depolarization/depression is one of

Assessment of cortical maturation with prenatal MRI. Part I: normal cortical maturation

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Fogliarini, Celine [Faculte Timone, Centre de Resonance Magnetique Biologique et Medicale, Marseille (France); Chaumoitre, Katia [Hopital Nord, Department of Radiology, Marseille (France); Chapon, Frederique; Levrier, Olivier; Girard, Nadine [Hopital Timone, Department of Neuroradiology, Marseille Cedex 5 (France); Fernandez, Carla; Figarella-Branger, Dominique [Hopital Timone, Department of Pathology, Marseille (France)

2005-08-01

Cortical maturation, especially gyral formation, follows a temporospatial schedule and is a good marker of fetal maturation. Although ultrasonography is still the imaging method of choice to evaluate fetal anatomy, MRI has an increasingly important role in the detection of brain abnormalities, especially of cortical development. Knowledge of MRI techniques in utero with the advantages and disadvantages of some sequences is necessary, in order to try to optimize the different magnetic resonance sequences to be able to make an early diagnosis. The different steps of cortical maturation known from histology represent the background necessary for the understanding of maturation in order to be then able to evaluate brain maturation through neuroimaging. Illustrations of the normal cortical maturation are given for each step accessible to MRI for both the cerebral hemispheres and the posterior fossa. (orig.)

Assessment of cortical maturation with prenatal MRI. Part I: normal cortical maturation

International Nuclear Information System (INIS)

Fogliarini, Celine; Chaumoitre, Katia; Chapon, Frederique; Levrier, Olivier; Girard, Nadine; Fernandez, Carla; Figarella-Branger, Dominique

2005-01-01

Cortical maturation, especially gyral formation, follows a temporospatial schedule and is a good marker of fetal maturation. Although ultrasonography is still the imaging method of choice to evaluate fetal anatomy, MRI has an increasingly important role in the detection of brain abnormalities, especially of cortical development. Knowledge of MRI techniques in utero with the advantages and disadvantages of some sequences is necessary, in order to try to optimize the different magnetic resonance sequences to be able to make an early diagnosis. The different steps of cortical maturation known from histology represent the background necessary for the understanding of maturation in order to be then able to evaluate brain maturation through neuroimaging. Illustrations of the normal cortical maturation are given for each step accessible to MRI for both the cerebral hemispheres and the posterior fossa. (orig.)

The cortical signature of amyotrophic lateral sclerosis.

Directory of Open Access Journals (Sweden)

Federica Agosta

Full Text Available The aim of this study was to explore the pattern of regional cortical thickness in patients with non-familial amyotrophic lateral sclerosis (ALS and to investigate whether cortical thinning is associated with disease progression rate. Cortical thickness analysis was performed in 44 ALS patients and 26 healthy controls. Group differences in cortical thickness and the age-by-group effects were assessed using vertex-by-vertex and multivariate linear models. The discriminatory ability of MRI variables in distinguishing patients from controls was estimated using the Concordance Statistics (C-statistic within logistic regression analyses. Correlations between cortical thickness measures and disease progression rate were tested using the Pearson coefficient. Relative to controls, ALS patients showed a bilateral cortical thinning of the primary motor, prefrontal and ventral frontal cortices, cingulate gyrus, insula, superior and inferior temporal and parietal regions, and medial and lateral occipital areas. There was a significant age-by-group effect in the sensorimotor cortices bilaterally, suggesting a stronger association between age and cortical thinning in ALS patients compared to controls. The mean cortical thickness of the sensorimotor cortices distinguished patients with ALS from controls (C-statistic ≥ 0.74. Cortical thinning of the left sensorimotor cortices was related to a faster clinical progression (r = -0.33, p = 0.03. Cortical thickness measurements allowed the detection and quantification of motor and extramotor involvement in patients with ALS. Cortical thinning of the precentral gyrus might offer a marker of upper motor neuron involvement and disease progression.

The cortical signature of amyotrophic lateral sclerosis.

Science.gov (United States)

Agosta, Federica; Valsasina, Paola; Riva, Nilo; Copetti, Massimiliano; Messina, Maria Josè; Prelle, Alessandro; Comi, Giancarlo; Filippi, Massimo

2012-01-01

The aim of this study was to explore the pattern of regional cortical thickness in patients with non-familial amyotrophic lateral sclerosis (ALS) and to investigate whether cortical thinning is associated with disease progression rate. Cortical thickness analysis was performed in 44 ALS patients and 26 healthy controls. Group differences in cortical thickness and the age-by-group effects were assessed using vertex-by-vertex and multivariate linear models. The discriminatory ability of MRI variables in distinguishing patients from controls was estimated using the Concordance Statistics (C-statistic) within logistic regression analyses. Correlations between cortical thickness measures and disease progression rate were tested using the Pearson coefficient. Relative to controls, ALS patients showed a bilateral cortical thinning of the primary motor, prefrontal and ventral frontal cortices, cingulate gyrus, insula, superior and inferior temporal and parietal regions, and medial and lateral occipital areas. There was a significant age-by-group effect in the sensorimotor cortices bilaterally, suggesting a stronger association between age and cortical thinning in ALS patients compared to controls. The mean cortical thickness of the sensorimotor cortices distinguished patients with ALS from controls (C-statistic ≥ 0.74). Cortical thinning of the left sensorimotor cortices was related to a faster clinical progression (r = -0.33, p = 0.03). Cortical thickness measurements allowed the detection and quantification of motor and extramotor involvement in patients with ALS. Cortical thinning of the precentral gyrus might offer a marker of upper motor neuron involvement and disease progression.

A passerine spreads its tail to facilitate a rapid recovery of its body posture during hovering.

Science.gov (United States)

Su, Jian-Yuan; Ting, Shang-Chieh; Chang, Yu-Hung; Yang, Jing-Tang

2012-07-07

We demonstrate experimentally that a passerine exploits tail spreading to intercept the downward flow induced by its wings to facilitate the recovery of its posture. The periodic spreading of its tail by the White-eye bird exhibits a phase correlation with both wingstroke motion and body oscillation during hovering flight. During a downstroke, a White-eye's body undergoes a remarkable pitch-down motion, with the tail undergoing an upward swing. This pitch-down motion becomes appropriately suppressed at the end of the downstroke; the bird's body posture then recovers gradually to its original status. Employing digital particle-image velocimetry, we show that the strong downward flow induced by downstroking the wings serves as an external jet flow impinging upon the tail, providing a depressing force on the tail to counteract the pitch-down motion of the bird's body. Spreading of the tail enhances a rapid recovery of the body posture because increased forces are experienced. The maximum force experienced by a spread tail is approximately 2.6 times that of a non-spread tail.

Cortical bone metastases

International Nuclear Information System (INIS)

Davis, T.M. Jr.; Rogers, L.F.; Hendrix, R.W.

1986-01-01

Twenty-five cases of bone metastases involving the cortex alone are reviewed. Seven patients had primary lung carcinoma, while 18 had primary tumors not previously reported to produce cortical bone metastases (tumors of the breast, kidney, pancreas, adenocarcinoma of unknown origin, multiple myeloma). Radiographically, these cortical lesions were well circumscribed, osteolytic, and produced soft-tissue swelling and occasional periosteal reaction. A recurrent pattern of metadiaphyseal involvement of the long bones of the lower extremity (particularly the femur) was noted, and is discussed. Findings reported in the literature, review, pathophysiology, and the role of skeletal radiographs, bone scans, and CT scans in evaluating cortical bone metastases are addressed

Optimization of power output and study of electron beam energy spread in a Free Electron Laser oscillator

CERN Document Server

Abramovich, A; Efimov, S; Gover, A; Pinhasi, Y; Yahalom, A

2001-01-01

Design of a multi-stage depressed collector for efficient operation of a Free Electron Laser (FEL) oscillator requires knowledge of the electron beam energy distribution. This knowledge is necessary to determine the voltages of the depressed collector electrodes that optimize the collection efficiency and overall energy conversion efficiency of the FEL. The energy spread in the electron beam is due to interaction in the wiggler region, as electrons enter the interaction region at different phases relative to the EM wave. This interaction can be simulated well by a three-dimensional simulation code such as FEL3D. The main adjustable parameters that determine the electron beam energy spread after interaction are the e-beam current, the initial beam energy, and the quality factor of the resonator out-coupling coefficient. Using FEL3D, we study the influence of these parameters on the available radiation power and on the electron beam energy distribution at the undulator exit. Simulations performed for I=1.5 A, E...

Migraine aura pathophysiology: the role of blood vessels and microembolisation

OpenAIRE

Dalkara, Turgay; Nozari, Ala; Moskowitz, Michael A

2010-01-01

Migraine attacks with auras are sometimes associated with underlying hereditary or acquired cerebrovascular disorders. A unifying pathophysiological explanation linking migraine to these conditions has been diffcult to identify. On the basis of genetic and epidemiological evidence, we suggest that changes in blood vessels, hypoperfusion disorders, and microembolisation can cause neurovascular dysfunction and evoke cortical spreading depression, an event that is widely thought to underlie aura...

Do studies on cortical plasticity provide a rationale for using non invasive brain stimulation as a treatment for Parkinson’s disease patients?

Directory of Open Access Journals (Sweden)

Giacomo eKoch

2013-11-01

Full Text Available Animal models of Parkinson’s disease (PD have shown that key mechanisms of cortical plasticity such as long-term potentiation (LTP and long-term depression (LTD can be impaired by the PD pathology. In humans protocols of non-invasive brain stimulation, such as paired associative stimulation (PAS and theta burst stimulation (TBS, can be used to investigate cortical plasticity of the primary motor cortex. Through the amplitude of the motor evoked potential (MEP these transcranial magnetic stimulation methods allow to measure both LTP-like and LTD-like mechanisms of cortical plasticity. So far these protocols have reported some controversial findings when tested in PD patients. While various studies described evidence for reduced LTP- and LTD-like plasticity, others showed different results, demonstrating increased LTP-like and normal LTD-like plasticity. Recent evidence provided support to the hypothesis that these different patterns of cortical plasticity likely depend on the stage of the disease and on the concomitant administration of levo-dopa. However, it still unclear how and if these altered mechanisms of cortical plasticity can be taken as a reliable model to build appropriate protocols aimed at treating PD symptoms b

Altered Cortical Activation in Adolescents With Acute Migraine: A Magnetoencephalography Study

Science.gov (United States)

Xiang, Jing; deGrauw, Xinyao; Korostenskaja, Milena; Korman, Abraham M.; O’Brien, Hope L.; Kabbouche, Marielle A.; Powers, Scott W.; Hershey, Andrew D.

2013-01-01

To quantitatively assess cortical dysfunction in pediatric migraine, 31 adolescents with acute migraine and age- and gender-matched controls were studied using a magnetoencephalography (MEG) system at a sampling rate of 6,000 Hz. Neuromagnetic brain activation was elicited by a finger-tapping task. The spectral and spatial signatures of magnetoencephalography data in 5 to 2,884 Hz were analyzed using Morlet wavelet and beamformers. Compared with controls, 31 migraine subjects during their headache attack phases (ictal) showed significantly prolonged latencies of neuromagnetic activation in 5 to 30 Hz, increased spectral power in 100 to 200 Hz, and a higher likelihood of neuromagnetic activation in the supplementary motor area, the occipital and ipsilateral sensorimotor cortices, in 2,200 to 2,800 Hz. Of the 31 migraine subjects, 16 migraine subjects during their headache-free phases (interictal) showed that there were no significant differences between interictal and control MEG data except that interictal spectral power in 100 to 200 Hz was significantly decreased. The results demonstrated that migraine subjects had significantly aberrant ictal brain activation, which can normalize interictally. The spread of abnormal ictal brain activation in both low- and high-frequency ranges triggered by movements may play a key role in the cascade of migraine attacks. Perspective This is the first study focusing on the spectral and spatial signatures of cortical dysfunction in adolescents with migraine using MEG signals in a frequency range of 5 to 2,884 Hz. This analyzing aberrant brain activation may be important for developing new therapeutic interventions for migraine in the future. PMID:23792072

Neural Correlates of Indicators of Sound Change in Cantonese: Evidence from Cortical and Subcortical Processes.

Science.gov (United States)

Maggu, Akshay R; Liu, Fang; Antoniou, Mark; Wong, Patrick C M

2016-01-01

Across time, languages undergo changes in phonetic, syntactic, and semantic dimensions. Social, cognitive, and cultural factors contribute to sound change, a phenomenon in which the phonetics of a language undergo changes over time. Individuals who misperceive and produce speech in a slightly divergent manner (called innovators ) contribute to variability in the society, eventually leading to sound change. However, the cause of variability in these individuals is still unknown. In this study, we examined whether such misperceptions are represented in neural processes of the auditory system. We investigated behavioral, subcortical (via FFR), and cortical (via P300) manifestations of sound change processing in Cantonese, a Chinese language in which several lexical tones are merging. Across the merging categories, we observed a similar gradation of speech perception abilities in both behavior and the brain (subcortical and cortical processes). Further, we also found that behavioral evidence of tone merging correlated with subjects' encoding at the subcortical and cortical levels. These findings indicate that tone-merger categories, that are indicators of sound change in Cantonese, are represented neurophysiologically with high fidelity. Using our results, we speculate that innovators encode speech in a slightly deviant neurophysiological manner, and thus produce speech divergently that eventually spreads across the community and contributes to sound change.

Learning in AN Oscillatory Cortical Model

Science.gov (United States)

Scarpetta, Silvia; Li, Zhaoping; Hertz, John

We study a model of generalized-Hebbian learning in asymmetric oscillatory neural networks modeling cortical areas such as hippocampus and olfactory cortex. The learning rule is based on the synaptic plasticity observed experimentally, in particular long-term potentiation and long-term depression of the synaptic efficacies depending on the relative timing of the pre- and postsynaptic activities during learning. The learned memory or representational states can be encoded by both the amplitude and the phase patterns of the oscillating neural populations, enabling more efficient and robust information coding than in conventional models of associative memory or input representation. Depending on the class of nonlinearity of the activation function, the model can function as an associative memory for oscillatory patterns (nonlinearity of class II) or can generalize from or interpolate between the learned states, appropriate for the function of input representation (nonlinearity of class I). In the former case, simulations of the model exhibits a first order transition between the "disordered state" and the "ordered" memory state.

The circadian oscillator of the cerebral cortex: molecular, biochemical and behavioral effects of deleting the Arntl clock gene in cortical neurons

DEFF Research Database (Denmark)

Bering, Tenna; Carstensen, Mikkel Bloss; Wörtwein, Gitta

2018-01-01

for normal function of the cortical circadian oscillator. Daily rhythms in running activity and temperature were not influenced, whereas the resynchronization response to experimental jet-lag exhibited minor though significant differences between genotypes. The tail-suspension test revealed significantly...... prolonged immobility periods in the knockout mouse indicative of a depressive-like behavioral state. This phenotype was accompanied by reduced norepinephrine levels in the cerebral cortex. Our data show that Arntl is required for normal cortical clock function and further give reason to suspect...... that the circadian oscillator of the cerebral cortex is involved in regulating both circadian biology and mood-related behavior and biochemistry....

LTS and FS inhibitory interneurons, short-term synaptic plasticity, and cortical circuit dynamics.

Directory of Open Access Journals (Sweden)

Itai Hayut

2011-10-01

Full Text Available Somatostatin-expressing, low threshold-spiking (LTS cells and fast-spiking (FS cells are two common subtypes of inhibitory neocortical interneuron. Excitatory synapses from regular-spiking (RS pyramidal neurons to LTS cells strongly facilitate when activated repetitively, whereas RS-to-FS synapses depress. This suggests that LTS neurons may be especially relevant at high rate regimes and protect cortical circuits against over-excitation and seizures. However, the inhibitory synapses from LTS cells usually depress, which may reduce their effectiveness at high rates. We ask: by which mechanisms and at what firing rates do LTS neurons control the activity of cortical circuits responding to thalamic input, and how is control by LTS neurons different from that of FS neurons? We study rate models of circuits that include RS cells and LTS and FS inhibitory cells with short-term synaptic plasticity. LTS neurons shift the RS firing-rate vs. current curve to the right at high rates and reduce its slope at low rates; the LTS effect is delayed and prolonged. FS neurons always shift the curve to the right and affect RS firing transiently. In an RS-LTS-FS network, FS neurons reach a quiescent state if they receive weak input, LTS neurons are quiescent if RS neurons receive weak input, and both FS and RS populations are active if they both receive large inputs. In general, FS neurons tend to follow the spiking of RS neurons much more closely than LTS neurons. A novel type of facilitation-induced slow oscillations is observed above the LTS firing threshold with a frequency determined by the time scale of recovery from facilitation. To conclude, contrary to earlier proposals, LTS neurons affect the transient and steady state responses of cortical circuits over a range of firing rates, not only during the high rate regime; LTS neurons protect against over-activation about as well as FS neurons.

Assessment of cortical and sub-cortical function in neonates by electrophysiological monitoring

NARCIS (Netherlands)

Jennekens, W.

2012-01-01

The aim of this thesis was the assessment of cortical and sub-cortical function in neonates by electrophysiological monitoring, i.e. to evaluate the function of the neonatal cortex and brainstem through quantitative analysis of signals readily available in the NICU. These signals include

Commentary on "A non-reward attractor theory of depression" : A proposal to include the habenula connection

NARCIS (Netherlands)

Loonen, Anton J M; Ivanova, Svetlana A

2017-01-01

The non-reward attractor theory of depression describes this mood disorder as originating from a neuronal dysfunction that arises from increased vulnerability of a cortical network that detects failure to receive an expected reward. From an evolutionary standpoint, the concept that the cerebral

Reconfiguration of Cortical Networks in MDD Uncovered by Multiscale Community Detection with fMRI.

Science.gov (United States)

He, Ye; Lim, Sol; Fortunato, Santo; Sporns, Olaf; Zhang, Lei; Qiu, Jiang; Xie, Peng; Zuo, Xi-Nian

2018-04-01

Major depressive disorder (MDD) is known to be associated with altered interactions between distributed brain regions. How these regional changes relate to the reorganization of cortical functional systems, and their modulation by antidepressant medication, is relatively unexplored. To identify changes in the community structure of cortical functional networks in MDD, we performed a multiscale community detection algorithm on resting-state functional connectivity networks of unmedicated MDD (uMDD) patients (n = 46), medicated MDD (mMDD) patients (n = 38), and healthy controls (n = 50), which yielded a spectrum of multiscale community partitions. we selected an optimal resolution level by identifying the most stable community partition for each group. uMDD and mMDD groups exhibited a similar reconfiguration of the community structure of the visual association and the default mode systems but showed different reconfiguration profiles in the frontoparietal control (FPC) subsystems. Furthermore, the central system (somatomotor/salience) and 3 frontoparietal subsystems showed strengthened connectivity with other communities in uMDD but, with the exception of 1 frontoparietal subsystem, returned to control levels in mMDD. These findings provide evidence for reconfiguration of specific cortical functional systems associated with MDD, as well as potential effects of medication in restoring disease-related network alterations, especially those of the FPC system.

Frontal cortical control of posterior sensory and association cortices through the claustrum.

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White, Michael G; Mathur, Brian N

2018-04-06

The claustrum is a telencephalic gray matter nucleus that is richly interconnected with the neocortex. This structure subserves top-down executive functions that require frontal cortical control of posterior cortical regions. However, functional anatomical support for the claustrum allowing for long-range intercortical communication is lacking. To test this, we performed a channelrhodopsin-assisted long-circuit mapping strategy in mouse brain slices. We find that anterior cingulate cortex input to the claustrum is transiently amplified by claustrum neurons that, in turn, project to parietal association cortex or to primary and secondary visual cortices. Additionally, we observe that claustrum drive of cortical neurons in parietal association cortex is layer-specific, eliciting action potential generation briefly in layers II/III, IV, and VI but not V. These data are the first to provide a functional anatomical substrate through claustrum that may underlie top-down functions, such as executive attention or working memory, providing critical insight to this most interconnected and enigmatic nucleus.

Sex Differences in the Relationship Between Conduct Disorder and Cortical Structure in Adolescents.

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Smaragdi, Areti; Cornwell, Harriet; Toschi, Nicola; Riccelli, Roberta; Gonzalez-Madruga, Karen; Wells, Amy; Clanton, Roberta; Baker, Rosalind; Rogers, Jack; Martin-Key, Nayra; Puzzo, Ignazio; Batchelor, Molly; Sidlauskaite, Justina; Bernhard, Anka; Martinelli, Anne; Kohls, Gregor; Konrad, Kerstin; Baumann, Sarah; Raschle, Nora; Stadler, Christina; Freitag, Christine; Sonuga-Barke, Edmund J S; De Brito, Stephane; Fairchild, Graeme

2017-08-01

Previous studies have reported reduced cortical thickness and surface area and altered gyrification in frontal and temporal regions in adolescents with conduct disorder (CD). Although there is evidence that the clinical phenotype of CD differs between males and females, no studies have examined whether such sex differences extend to cortical and subcortical structure. As part of a European multisite study (FemNAT-CD), structural magnetic resonance imaging (MRI) data were collected from 48 female and 48 male participants with CD and from 104 sex-, age-, and pubertal-status-matched controls (14-18 years of age). Data were analyzed using surface-based morphometry, testing for effects of sex, diagnosis, and sex-by-diagnosis interactions, while controlling for age, IQ, scan site, and total gray matter volume. CD was associated with cortical thinning and higher gyrification in ventromedial prefrontal cortex in both sexes. Males with CD showed lower, and females with CD showed higher, supramarginal gyrus cortical thickness compared with controls. Relative to controls, males with CD showed higher gyrification and surface area in superior frontal gyrus, whereas the opposite pattern was seen in females. There were no effects of diagnosis or sex-by-diagnosis interactions on subcortical volumes. Results are discussed with regard to attention-deficit/hyperactivity disorder, depression, and substance abuse comorbidity, medication use, handedness, and CD age of onset. We found both similarities and differences between males and females in CD-cortical structure associations. This initial evidence that the pathophysiological basis of CD may be partly sex-specific highlights the need to consider sex in future neuroimaging studies and suggests that males and females may require different treatments. Copyright © 2017 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.

Trade-off of cerebello-cortical and cortico-cortical functional networks for planning in 6-year-old children.

Science.gov (United States)

Kipping, Judy A; Margulies, Daniel S; Eickhoff, Simon B; Lee, Annie; Qiu, Anqi

2018-05-03

Childhood is a critical period for the development of cognitive planning. There is a lack of knowledge on its neural mechanisms in children. This study aimed to examine cerebello-cortical and cortico-cortical functional connectivity in association with planning skills in 6-year-olds (n = 76). We identified the cerebello-cortical and cortico-cortical functional networks related to cognitive planning using activation likelihood estimation (ALE) meta-analysis on existing functional imaging studies on spatial planning, and data-driven independent component analysis (ICA) of children's resting-state functional MRI (rs-fMRI). We investigated associations of cerebello-cortical and cortico-cortical functional connectivity with planning ability in 6-year-olds, as assessed using the Stockings of Cambridge task. Long-range functional connectivity of two cerebellar networks (lobules VI and lateral VIIa) with the prefrontal and premotor cortex were greater in children with poorer planning ability. In contrast, cortico-cortical association networks were not associated with the performance of planning in children. These results highlighted the key contribution of the lateral cerebello-frontal functional connectivity, but not cortico-cortical association functional connectivity, for planning ability in 6-year-olds. Our results suggested that brain adaptation to the acquisition of planning ability during childhood is partially achieved through the engagement of the cerebello-cortical functional connectivity. Copyright © 2018 Elsevier Inc. All rights reserved.

EEG asymmetry in borderline personality disorder and depression following rejection.

Science.gov (United States)

Beeney, Joseph E; Levy, Kenneth N; Gatzke-Kopp, Lisa M; Hallquist, Michael N

2014-04-01

Borderline personality disorder (BPD) and major depressive disorder (MDD) share numerous features, including dysphoric affect, irritability, suicidality, and a heightened sensitivity to perceived interpersonal rejection. However, these disorders are associated with divergent profiles of reactivity to rejection: Individuals with MDD are more likely to respond with withdrawal and isolation, and those with BPD appear to respond with increased approach behaviors and greater hostility. Potential mechanisms underlying these divergent patterns of response have not been elaborated. The goal of the present study was to assess whether prefrontal cortical asymmetry is associated with these behavioral profiles. EEG alpha activity was recorded at baseline and after individuals with BPD, MDD and healthy controls (HCs) participated in a rejection task. Although no differences were found at baseline, results demonstrated that following rejection, individuals with BPD showed greater left cortical activation, consistent with approach motivation, whereas those with MDD showed greater right cortical activation, consistent with withdrawal motivation. HCs evidenced a more balanced cortical profile, as hypothesized. Although BPD and MDD are highly comorbid, are easily confused, and are phenomenologically similar in a number of ways, individuals with these two disorders respond in very different ways to perceived rejection. PsycINFO Database Record (c) 2014 APA, all rights reserved

Circuits Regulating Pleasure and Happiness-Mechanisms of Depression.

Science.gov (United States)

Loonen, Anton J M; Ivanova, Svetlana A

2016-01-01

According to our model of the regulation of appetitive-searching vs. distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (pre)frontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure). Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness). These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above) of the regulation of reward-seeking vs. misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood) may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating depression with

Spatial integration and cortical dynamics.

Science.gov (United States)

Gilbert, C D; Das, A; Ito, M; Kapadia, M; Westheimer, G

1996-01-23

Cells in adult primary visual cortex are capable of integrating information over much larger portions of the visual field than was originally thought. Moreover, their receptive field properties can be altered by the context within which local features are presented and by changes in visual experience. The substrate for both spatial integration and cortical plasticity is likely to be found in a plexus of long-range horizontal connections, formed by cortical pyramidal cells, which link cells within each cortical area over distances of 6-8 mm. The relationship between horizontal connections and cortical functional architecture suggests a role in visual segmentation and spatial integration. The distribution of lateral interactions within striate cortex was visualized with optical recording, and their functional consequences were explored by using comparable stimuli in human psychophysical experiments and in recordings from alert monkeys. They may represent the substrate for perceptual phenomena such as illusory contours, surface fill-in, and contour saliency. The dynamic nature of receptive field properties and cortical architecture has been seen over time scales ranging from seconds to months. One can induce a remapping of the topography of visual cortex by making focal binocular retinal lesions. Shorter-term plasticity of cortical receptive fields was observed following brief periods of visual stimulation. The mechanisms involved entailed, for the short-term changes, altering the effectiveness of existing cortical connections, and for the long-term changes, sprouting of axon collaterals and synaptogenesis. The mutability of cortical function implies a continual process of calibration and normalization of the perception of visual attributes that is dependent on sensory experience throughout adulthood and might further represent the mechanism of perceptual learning.

SKA2 Methylation is associated with Decreased Prefrontal Cortical Thickness and Greater PTSD Severity among Trauma-Exposed Veterans

Science.gov (United States)

Sadeh, Naomi; Spielberg, Jeffrey M.; Logue, Mark W.; Wolf, Erika J.; Smith, Alicia K.; Lusk, Joanna; Hayes, Jasmeet P.; Sperbeck, Emily; Milberg, William P.; McGlinchey, Regina E.; Salat, David H.; Carter, Weleetka C.; Stone, Annjanette; Schichman, Steven A.; Humphries, Donald E.; Miller, Mark W.

2015-01-01

Methylation of the SKA2 gene has recently been identified as a promising biomarker of suicide risk. Based on this finding, we examined associations between SKA2 methylation, cortical thickness, and psychiatric phenotypes linked to suicide in trauma-exposed veterans. 200 trauma-exposed white non-Hispanic veterans of the recent conflicts in Iraq and Afghanistan (91% male) underwent clinical assessment and had blood drawn for genotyping and methylation analysis. 145 participants also had neuroimaging data available. Based on previous research, we examined DNA methylation at the CpG locus cg13989295 as well as DNA methylation adjusted for genotype at the methylation-associated SNP (rs7208505) in relationship to whole-brain cortical thickness, posttraumatic stress disorder symptoms (PTSD), and depression symptoms. Whole-brain vertex-wise analyses identified three clusters in prefrontal cortex that were associated with genotype-adjusted SKA2 DNA methylation (methylationadj). Specifically, DNA methylationadj was associated with bilateral reductions of cortical thickness in frontal pole and superior frontal gyrus, and similar effects were found in the right orbitofrontal cortex and right inferior frontal gyrus. PTSD symptom severity was positively correlated with SKA2 DNA methylationadj and negatively correlated with cortical thickness in these regions. Mediation analyses showed a significant indirect effect of PTSD on cortical thickness via SKA2 methylation status. Results suggest that DNA methylationadj of SKA2 in blood indexes stress-related psychiatric phenotypes and neurobiology, pointing to its potential value as a biomarker of stress exposure and susceptibility. PMID:26324104

Discrimination of cortical laminae using MEG.

Science.gov (United States)

Troebinger, Luzia; López, José David; Lutti, Antoine; Bestmann, Sven; Barnes, Gareth

2014-11-15

Typically MEG source reconstruction is used to estimate the distribution of current flow on a single anatomically derived cortical surface model. In this study we use two such models representing superficial and deep cortical laminae. We establish how well we can discriminate between these two different cortical layer models based on the same MEG data in the presence of different levels of co-registration noise, Signal-to-Noise Ratio (SNR) and cortical patch size. We demonstrate that it is possible to make a distinction between superficial and deep cortical laminae for levels of co-registration noise of less than 2mm translation and 2° rotation at SNR > 11 dB. We also show that an incorrect estimate of cortical patch size will tend to bias layer estimates. We then use a 3D printed head-cast (Troebinger et al., 2014) to achieve comparable levels of co-registration noise, in an auditory evoked response paradigm, and show that it is possible to discriminate between these cortical layer models in real data. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

Is cortical bone hip? What determines cortical bone properties?

Science.gov (United States)

Epstein, Sol

2007-07-01

Increased bone turnover may produce a disturbance in bone structure which may result in fracture. In cortical bone, both reduction in turnover and increase in hip bone mineral density (BMD) may be necessary to decrease hip fracture risk and may require relatively greater proportionate changes than for trabecular bone. It should also be noted that increased porosity produces disproportionate reduction in bone strength, and studies have shown that increased cortical porosity and decreased cortical thickness are associated with hip fracture. Continued studies for determining the causes of bone strength and deterioration show distinct promise. Osteocyte viability has been observed to be an indicator of bone strength, with viability as the result of maintaining physiological levels of loading and osteocyte apoptosis as the result of a decrease in loading. Osteocyte apoptosis and decrease are major factors in the bone loss and fracture associated with aging. Both the osteocyte and periosteal cell layer are assuming greater importance in the process of maintaining skeletal integrity as our knowledge of these cells expand, as well being a target for pharmacological agents to reduce fracture especially in cortical bone. The bisphosphonate alendronate has been seen to have a positive effect on cortical bone by allowing customary periosteal growth, while reducing the rate of endocortical bone remodeling and slowing bone loss from the endocortical surface. Risedronate treatment effects were attributed to decrease in bone resorption and thus a decrease in fracture risk. Ibandronate has been seen to increase BMD as the spine and femur as well as a reduced incidence of new vertebral fractures and non vertebral on subset post hoc analysis. And treatment with the anabolic agent PTH(1-34) documented modeling and remodelling of quiescent and active bone surfaces. Receptor activator of nuclear factor kappa B ligand (RANKL) plays a key role in bone destruction, and the human monoclonal

[Gap junctions: A new therapeutic target in major depressive disorder?].

Science.gov (United States)

Sarrouilhe, D; Dejean, C

2015-11-01

Major depressive disorder is a multifactorial chronic and debilitating mood disease with high lifetime prevalence and is associated with excess mortality, especially from cardiovascular diseases and through suicide. The treatments of this disease with tricyclic antidepressants and monoamine oxidase inhibitors are poorly tolerated and those that selectively target serotonin and norepinephrine re-uptake are not effective in all patients, showing the need to find new therapeutic targets. Post-mortem studies of brains from patients with major depressive disorders described a reduced expression of the gap junction-forming membrane proteins connexin 30 and connexin 43 in the prefrontal cortex and the locus coeruleus. The use of chronic unpredictable stress, a rodent model of depression, suggests that astrocytic gap junction dysfunction contributes to the pathophysiology of major depressive disorder. Chronic treatments of rats with fluoxetine and of rat cultured cortical astrocytes with amitriptyline support the hypothesis that the upregulation of gap junctional intercellular communication between brain astrocytes could be a novel mechanism for the therapeutic effect of antidepressants. In conclusion, astrocytic gap junctions are emerging as a new potential therapeutic target for the treatment of patients with major depressive disorder. Copyright © 2015 Elsevier Masson SAS. All rights reserved.

Transcranial Direct Current Stimulation: Considerations for Research in Adolescent Depression

Directory of Open Access Journals (Sweden)

Jonathan C. Lee

2017-06-01

Full Text Available Adolescent depression is a prevalent disorder with substantial morbidity and mortality. Current treatment interventions do not target relevant pathophysiology and are frequently ineffective, thereby leading to a substantial burden for individuals, families, and society. During adolescence, the prefrontal cortex undergoes extensive structural and functional changes. Recent work suggests that frontolimbic development in depressed adolescents is delayed or aberrant. The judicious application of non-invasive brain stimulation techniques to the prefrontal cortex may present a promising opportunity for durable interventions in adolescent depression. Transcranial direct current stimulation (tDCS applies a low-intensity, continuous current that alters cortical excitability. While this modality does not elicit action potentials, it is thought to manipulate neuronal activity and neuroplasticity. Specifically, tDCS may modulate N-methyl-d-aspartate receptors and L-type voltage-gated calcium channels and effect changes through long-term potentiation or long-term depression-like mechanisms. This mini-review considers the neurobiological rationale for developing tDCS protocols in adolescent depression, reviews existing work in adult mood disorders, surveys the existing tDCS literature in adolescent populations, reviews safety studies, and discusses distinct ethical considerations in work with adolescents.

Effect of age at onset on cortical thickness and cognition in posterior cortical atrophy

Science.gov (United States)

Suárez-González, Aida; Lehmann, Manja; Shakespeare, Timothy J.; Yong, Keir X.X.; Paterson, Ross W.; Slattery, Catherine F.; Foulkes, Alexander J.M.; Rabinovici, Gil D.; Gil-Néciga, Eulogio; Roldán-Lora, Florinda; Schott, Jonathan M.; Fox, Nick C.; Crutch, Sebastian J.

2016-01-01

Age at onset (AAO) has been shown to influence the phenotype of Alzheimer’s disease (AD), but how it affects atypical presentations of AD remains unknown. Posterior cortical atrophy (PCA) is the most common form of atypical AD. In this study, we aimed to investigate the effect of AAO on cortical thickness and cognitive function in 98 PCA patients. We used Freesurfer (v5.3.0) to compare cortical thickness with AAO both as a continuous variable, and by dichotomizing the groups based on median age (58 years). In both the continuous and dichotomized analyses, we found a pattern suggestive of thinner cortex in precuneus and parietal areas in earlier-onset PCA, and lower cortical thickness in anterior cingulate and prefrontal cortex in later-onset PCA. These cortical thickness differences between PCA subgroups were consistent with earlier-onset PCA patients performing worse on cognitive tests involving parietal functions. Our results provide a suggestion that AAO may not only affect the clinico-anatomical characteristics in AD but may also affect atrophy patterns and cognition within atypical AD phenotypes. PMID:27318138

Abnormal cortical synaptic plasticity in primary motor area in progressive supranuclear palsy.

Science.gov (United States)

Conte, Antonella; Belvisi, Daniele; Bologna, Matteo; Ottaviani, Donatella; Fabbrini, Giovanni; Colosimo, Carlo; Williams, David R; Berardelli, Alfredo

2012-03-01

No study has yet investigated whether cortical plasticity in primary motor area (M1) is abnormal in patients with progressive supranuclear palsy (PSP). We studied M1 plasticity in 15 PSP patients and 15 age-matched healthy subjects. We used intermittent theta-burst stimulation (iTBS) to investigate long-term potentiation (LTP) and continuous TBS (cTBS) to investigate long-term depression (LTD)-like cortical plasticity in M1. Ten patients underwent iTBS again 1 year later. We also investigated short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) in M1 with paired-pulse transcranial magnetic stimulation, tested H reflex from upper limb flexor muscles before and after iTBS, and measured motor evoked potential (MEP) input-output (I/O) curves before and after iTBS. iTBS elicited a significantly larger MEP facilitation after iTBS in patients than in healthy subjects. Whereas in healthy subjects, cTBS inhibited MEP, in patients it significantly facilitated MEPs. In patients, SICI was reduced, whereas ICF was normal. H reflex size remained unchanged after iTBS. Patients had steeper MEP I/O slopes than healthy subjects at baseline and became even more steeper after iTBS only in patients. The iTBS-induced abnormal MEP facilitation in PSP persisted at 1-year follow-up. In conclusion, patients with PSP have abnormal M1 LTP/LTD-like plasticity. The enhanced LTP-like cortical synaptic plasticity parallels disease progression.

Trajectories of cortical surface area and cortical volume maturation in normal brain development

Directory of Open Access Journals (Sweden)

Simon Ducharme

2015-12-01

Full Text Available This is a report of developmental trajectories of cortical surface area and cortical volume in the NIH MRI Study of Normal Brain Development. The quality-controlled sample included 384 individual typically-developing subjects with repeated scanning (1–3 per subject, total scans n=753 from 4.9 to 22.3 years of age. The best-fit model (cubic, quadratic, or first-order linear was identified at each vertex using mixed-effects models, with statistical correction for multiple comparisons using random field theory. Analyses were performed with and without controlling for total brain volume. These data are provided for reference and comparison with other databases. Further discussion and interpretation on cortical developmental trajectories can be found in the associated Ducharme et al.׳s article “Trajectories of cortical thickness maturation in normal brain development – the importance of quality control procedures” (Ducharme et al., 2015 [1].

Focal cortical dysplasia – review

International Nuclear Information System (INIS)

Kabat, Joanna; Król, Przemysław

2012-01-01

Focal cortical dysplasia is a malformation of cortical development, which is the most common cause of medically refractory epilepsy in the pediatric population and the second/third most common etiology of medically intractable seizures in adults. Both genetic and acquired factors are involved in the pathogenesis of cortical dysplasia. Numerous classifications of the complex structural abnormalities of focal cortical dysplasia have been proposed – from Taylor et al. in 1971 to the last modification of Palmini classification made by Blumcke in 2011. In general, three types of cortical dysplasia are recognized. Type I focal cortical dysplasia with mild symptomatic expression and late onset, is more often seen in adults, with changes present in the temporal lobe. Clinical symptoms are more severe in type II of cortical dysplasia usually seen in children. In this type, more extensive changes occur outside the temporal lobe with predilection for the frontal lobes. New type III is one of the above dysplasias with associated another principal lesion as hippocampal sclerosis, tumor, vascular malformation or acquired pathology during early life. Brain MRI imaging shows abnormalities in the majority of type II dysplasias and in only some of type I cortical dysplasias. The most common findings on MRI imaging include: focal cortical thickening or thinning, areas of focal brain atrophy, blurring of the gray-white junction, increased signal on T2- and FLAIR-weighted images in the gray and subcortical white matter often tapering toward the ventricle. On the basis of the MRI findings, it is possible to differentiate between type I and type II cortical dysplasia. A complete resection of the epileptogenic zone is required for seizure-free life. MRI imaging is very helpful to identify those patients who are likely to benefit from surgical treatment in a group of patients with drug-resistant epilepsy. However, in type I cortical dysplasia, MR imaging is often normal, and also in both

BDNF-Val66Met-Polymorphism Impact on Cortical Plasticity in Schizophrenia Patients: A Proof-of-Concept Study

Science.gov (United States)

Nitsche, Michael A.; Wobrock, Thomas; Bunse, Tilmann; Rein, Bettina; Herrmann, Maximiliane; Schmitt, Andrea; Nieratschker, Vanessa; Witt, Stephanie H.; Rietschel, Marcella; Falkai, Peter; Hasan, Alkomiet

2015-01-01

Background: Brain-derived neurotrophic factor (BDNF) has been shown to be a moderator of neuroplasticity. A frequent BDNF-polymorphism (Val66Met) is associated with impairments of cortical plasticity. In patients with schizophrenia, reduced neuroplastic responses following non-invasive brain stimulation have been reported consistently. Various studies have indicated a relationship between the BDNF-Val66Met-polymorphism and motor-cortical plasticity in healthy individuals, but schizophrenia patients have yet to be investigated. The aim of this proof-of-concept study was, therefore, to test the impact of the BDNF-Val66Met-polymorphism on inhibitory and facilitatory cortical plasticity in schizophrenia patients. Methods: Cortical plasticity was investigated in 22 schizophrenia patients and 35 healthy controls using anodal and cathodal transcranial direct-current stimulation (tDCS) applied to the left primary motor cortex. Animal and human research indicates that excitability shifts following anodal and cathodal tDCS are related to molecular long-term potentiation and long-term depression. To test motor-cortical excitability before and after tDCS, well-established single- and paired-pulse transcranial magnetic stimulation protocols were applied. Results: Our analysis revealed increased glutamate-mediated intracortical facilitation in met-heterozygotes compared to val-homozygotes at baseline. Following cathodal tDCS, schizophrenia met-heterozygotes had reduced gamma-amino-butyric-acid-mediated short-interval intracortical inhibition, whereas healthy met-heterozygotes displayed the opposite effect. The BDNF-Val66Met-polymorphism did not influence single-pulse motor-evoked potential amplitudes after tDCS. Conclusions: These preliminary findings support the notion of an association of the BDNF-Val66Met-polymorphism with observable alterations in plasticity following cathodal tDCS in schizophrenia patients. This indicates a complex interaction between inhibitory

Communication and Wiring in the Cortical Connectome

Directory of Open Access Journals (Sweden)

Julian eBudd

2012-10-01

Full Text Available In cerebral cortex, the huge mass of axonal wiring that carries information between near and distant neurons is thought to provide the neural substrate for cognitive and perceptual function. The goal of mapping the connectivity of cortical axons at different spatial scales, the cortical connectome, is to trace the paths of information flow in cerebral cortex. To appreciate the relationship between the connectome and cortical function, we need to discover the nature and purpose of the wiring principles underlying cortical connectivity. A popular explanation has been that axonal length is strictly minimized both within and between cortical regions. In contrast, we have hypothesized the existence of a multi-scale principle of cortical wiring where to optimise communication there is a trade-off between spatial (construction and temporal (routing costs. Here, using recent evidence concerning cortical spatial networks we critically evaluate this hypothesis at neuron, local circuit, and pathway scales. We report three main conclusions. First, the axonal and dendritic arbor morphology of single neocortical neurons may be governed by a similar wiring principle, one that balances the conservation of cellular material and conduction delay. Second, the same principle may be observed for fibre tracts connecting cortical regions. Third, the absence of sufficient local circuit data currently prohibits any meaningful assessment of the hypothesis at this scale of cortical organization. To avoid neglecting neuron and microcircuit levels of cortical organization, the connectome framework should incorporate more morphological description. In addition, structural analyses of temporal cost for cortical circuits should take account of both axonal conduction and neuronal integration delays, which appear mostly of the same order of magnitude. We conclude the hypothesized trade-off between spatial and temporal costs may potentially offer a powerful explanation for

Perceptual learning and adult cortical plasticity.

Science.gov (United States)

Gilbert, Charles D; Li, Wu; Piech, Valentin

2009-06-15

The visual cortex retains the capacity for experience-dependent changes, or plasticity, of cortical function and cortical circuitry, throughout life. These changes constitute the mechanism of perceptual learning in normal visual experience and in recovery of function after CNS damage. Such plasticity can be seen at multiple stages in the visual pathway, including primary visual cortex. The manifestation of the functional changes associated with perceptual learning involve both long term modification of cortical circuits during the course of learning, and short term dynamics in the functional properties of cortical neurons. These dynamics are subject to top-down influences of attention, expectation and perceptual task. As a consequence, each cortical area is an adaptive processor, altering its function in accordance to immediate perceptual demands.

Basic visual function and cortical thickness patterns in posterior cortical atrophy.

Science.gov (United States)

Lehmann, Manja; Barnes, Josephine; Ridgway, Gerard R; Wattam-Bell, John; Warrington, Elizabeth K; Fox, Nick C; Crutch, Sebastian J

2011-09-01

Posterior cortical atrophy (PCA) is characterized by a progressive decline in higher-visual object and space processing, but the extent to which these deficits are underpinned by basic visual impairments is unknown. This study aimed to assess basic and higher-order visual deficits in 21 PCA patients. Basic visual skills including form detection and discrimination, color discrimination, motion coherence, and point localization were measured, and associations and dissociations between specific basic visual functions and measures of higher-order object and space perception were identified. All participants showed impairment in at least one aspect of basic visual processing. However, a number of dissociations between basic visual skills indicated a heterogeneous pattern of visual impairment among the PCA patients. Furthermore, basic visual impairments were associated with particular higher-order object and space perception deficits, but not with nonvisual parietal tasks, suggesting the specific involvement of visual networks in PCA. Cortical thickness analysis revealed trends toward lower cortical thickness in occipitotemporal (ventral) and occipitoparietal (dorsal) regions in patients with visuoperceptual and visuospatial deficits, respectively. However, there was also a lot of overlap in their patterns of cortical thinning. These findings suggest that different presentations of PCA represent points in a continuum of phenotypical variation.

Optimizing hybrid spreading in metapopulations.

Science.gov (United States)

Zhang, Changwang; Zhou, Shi; Miller, Joel C; Cox, Ingemar J; Chain, Benjamin M

2015-04-29

Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by local spreading, where infected nodes can only infect a limited set of direct target nodes and global spreading, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemics, and examine the optimum balance between spreading mechanisms in terms of achieving the maximum outbreak size. We show the existence of critically hybrid epidemics where neither spreading mechanism alone can cause a noticeable spread but a combination of the two spreading mechanisms would produce an enormous outbreak. Our results provide new strategies for maximising beneficial epidemics and estimating the worst outcome of damaging hybrid epidemics.

Effect of age at onset on cortical thickness and cognition in posterior cortical atrophy.

Science.gov (United States)

Suárez-González, Aida; Lehmann, Manja; Shakespeare, Timothy J; Yong, Keir X X; Paterson, Ross W; Slattery, Catherine F; Foulkes, Alexander J M; Rabinovici, Gil D; Gil-Néciga, Eulogio; Roldán-Lora, Florinda; Schott, Jonathan M; Fox, Nick C; Crutch, Sebastian J

2016-08-01

Age at onset (AAO) has been shown to influence the phenotype of Alzheimer's disease (AD), but how it affects atypical presentations of AD remains unknown. Posterior cortical atrophy (PCA) is the most common form of atypical AD. In this study, we aimed to investigate the effect of AAO on cortical thickness and cognitive function in 98 PCA patients. We used Freesurfer (v5.3.0) to compare cortical thickness with AAO both as a continuous variable, and by dichotomizing the groups based on median age (58 years). In both the continuous and dichotomized analyses, we found a pattern suggestive of thinner cortex in precuneus and parietal areas in earlier-onset PCA, and lower cortical thickness in anterior cingulate and prefrontal cortex in later-onset PCA. These cortical thickness differences between PCA subgroups were consistent with earlier-onset PCA patients performing worse on cognitive tests involving parietal functions. Our results provide a suggestion that AAO may not only affect the clinico-anatomical characteristics in AD but may also affect atrophy patterns and cognition within atypical AD phenotypes. Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.

Methylomic profiling of cortex samples from completed suicide cases implicates a role for PSORS1C3 in major depression and suicide.

Science.gov (United States)

Murphy, T M; Crawford, B; Dempster, E L; Hannon, E; Burrage, J; Turecki, G; Kaminsky, Z; Mill, J

2017-01-03

Major depressive disorder (MDD) represents a major social and economic health issue and constitutes a major risk factor for suicide. The molecular pathology of suicidal depression remains poorly understood, although it has been hypothesised that regulatory genomic processes are involved in the pathology of both MDD and suicidality. In this study, genome-wide patterns of DNA methylation were assessed in depressed suicide completers (n=20) and compared with non-psychiatric, sudden-death controls (n=20) using tissue from two cortical brain regions (Brodmann Area 11 (BA11) and Brodmann Area 25 (BA25)). Analyses focused on identifying differentially methylated regions (DMRs) associated with suicidal depression and epigenetic variation were explored in the context of polygenic risk scores for major depression and suicide. Weighted gene co-methylation network analysis was used to identify modules of co-methylated loci associated with depressed suicide completers and polygenic burden for MDD and suicide attempt. We identified a DMR upstream of the PSORS1C3 gene, subsequently validated using bisulfite pyrosequencing and replicated in a second set of suicide samples, which is characterised by significant hypomethylation in both cortical brain regions in MDD suicide cases. We also identified discrete modules of co-methylated loci associated with polygenic risk burden for suicide attempt, but not major depression. Suicide-associated co-methylation modules were enriched among gene networks implicating biological processes relevant to depression and suicidality, including nervous system development and mitochondria function. Our data suggest that there are coordinated changes in DNA methylation associated with suicide that may offer novel insights into the molecular pathology associated with depressed suicide completers.

Methylomic profiling of cortex samples from completed suicide cases implicates a role for PSORS1C3 in major depression and suicide

Science.gov (United States)

Murphy, T M; Crawford, B; Dempster, E L; Hannon, E; Burrage, J; Turecki, G; Kaminsky, Z; Mill, J

2017-01-01

Major depressive disorder (MDD) represents a major social and economic health issue and constitutes a major risk factor for suicide. The molecular pathology of suicidal depression remains poorly understood, although it has been hypothesised that regulatory genomic processes are involved in the pathology of both MDD and suicidality. In this study, genome-wide patterns of DNA methylation were assessed in depressed suicide completers (n=20) and compared with non-psychiatric, sudden-death controls (n=20) using tissue from two cortical brain regions (Brodmann Area 11 (BA11) and Brodmann Area 25 (BA25)). Analyses focused on identifying differentially methylated regions (DMRs) associated with suicidal depression and epigenetic variation were explored in the context of polygenic risk scores for major depression and suicide. Weighted gene co-methylation network analysis was used to identify modules of co-methylated loci associated with depressed suicide completers and polygenic burden for MDD and suicide attempt. We identified a DMR upstream of the PSORS1C3 gene, subsequently validated using bisulfite pyrosequencing and replicated in a second set of suicide samples, which is characterised by significant hypomethylation in both cortical brain regions in MDD suicide cases. We also identified discrete modules of co-methylated loci associated with polygenic risk burden for suicide attempt, but not major depression. Suicide-associated co-methylation modules were enriched among gene networks implicating biological processes relevant to depression and suicidality, including nervous system development and mitochondria function. Our data suggest that there are coordinated changes in DNA methylation associated with suicide that may offer novel insights into the molecular pathology associated with depressed suicide completers. PMID:28045465

Localization of dysfunction in major depressive disorder: Prefrontal cortex and amygdala

OpenAIRE

Murray, Elisabeth A.; Wise, Steven P.; Drevets, Wayne C.

2010-01-01

Despite considerable effort, the localization of dysfunction in major depressive disorder (MDD) remains poorly understood. We present a hypothesis about its localization that builds on recent findings from primate neuropsychology. The hypothesis has four key components: a deficit in the valuation of ‘self’ underlies the core disorder in MDD; the medial frontal cortex represents ‘self’; interactions between the amygdala and cortical representations update their valuation; and inefficiency in u...

Circuits regulating pleasure and happiness – mechanisms of depression

Directory of Open Access Journals (Sweden)

Anton J.M. Loonen

2016-11-01

Full Text Available According to our model of the regulation of appetitive-searching versus distress-avoiding behaviors, the motivation to display these essential conducts is regulated by two parallel cortico-striato-thalamo-cortical, re-entry circuits, including the core and the shell parts of the nucleus accumbens, respectively. An entire series of basal ganglia, running from the caudate nucleus on one side, to the centromedial amygdala on the other side, controls the intensity of these reward-seeking and misery-fleeing behaviors by stimulating the activity of the (prefrontal and limbic cortices. Hyperactive motivation to display behavior that potentially results in reward induces feelings of hankering (relief leads to pleasure. Hyperactive motivation to exhibit behavior related to avoidance of misery results in dysphoria (relief leads to happiness. These two systems collaborate in a reciprocal fashion. In clinical depression, a mismatch exists between the activities of these two circuits: the balance is shifted to the misery-avoiding side. Five theories have been developed to explain the mechanism of depressive mood disorders, including the monoamine, biorhythm, neuro-endocrine, neuro-immune, and kindling/neuroplasticity theories. This paper describes these theories in relationship to the model (described above of the regulation of reward-seeking versus misery-avoiding behaviors. Chronic stress that leads to structural changes may induce the mismatch between the two systems. This mismatch leads to lack of pleasure, low energy, and indecisiveness, on one hand, and dysphoria, continuous worrying, and negative expectations on the other hand. The neuroplastic effects of monoamines, cortisol, and cytokines may mediate the induction of these structural alterations. Long-term exposure to stressful situations (particularly experienced during childhood may lead to increased susceptibility for developing this condition. This hypothesis opens up the possibility of treating

The role of BDNF in depression on the basis of its location in the neural circuitry

Institute of Scientific and Technical Information of China (English)

Hui YU; Zhe-yu CHEN

2011-01-01

Depression is one of the most prevalent and life-threatening forms of mental illnesses and the neural circuitry underlying depression remains incompletely understood. Most attention in the field has focused on hippocampal and frontal cortical regions for their roles in depression and antidepressant action. While these regions no doubt play important roles in the mental illness, there is compelling evi-dence that other brain regions are also involved. Brain-derived neurotrophic factor (BDNF) is broadly expressed in the developing and adult mammalian brain and has been implicated in development, neural regeneration, synaptic transmission, synaptic plasticity and neurogenesis. Recently BDNF has been shown to play an important role in the pathophysiology of depression, however there are con-troversial reports about the effects of BDNF on depression. Here, we present an overview of the current knowledge concerning BDNF actions and associated intracellular signaling in hippocampus, prefrontal cortex, nucleus accumbens (NAc) and amygdala as their rela-tion to depression.

Depression in Parkinson's disease: A case-control study.

Directory of Open Access Journals (Sweden)

Yu-Hsuan Wu

Full Text Available To evaluate the association between Parkinson's disease (PD prognosis and the patient's onset of depression.A total of 353 patients with newly-diagnosed PD and a history of depression were enrolled. On the basis of the onset of depression before or after PD diagnosis, we divided participants into PD patients with pre- or post-diagnostic depression. Cox's regression analysis was used to detect risks between the onset of depression and outcomes (including death, accidental injury, dementia, and aspiration pneumonia. The association between the onset of depression and levodopa equivalent dosage (LED and cumulative equivalent dosage of antidepressants were assessed.PD patients with post-diagnostic depression were associated with significantly higher risks of dementia (adjusted HR = 2·01, p = 0·015, and were older (58·5 ± 17·7 vs. 53·7 ± 18·6, p = 0·020 at the time of PD diagnosis than PD patients with pre-diagnostic depression. The higher incident rate of accidental injury was also noted in PD patients with post-diagnostic depression (48·1 vs. 31·3/1000 person-years, HR = 1·60, p = 0·041, but no statistical significance was observed in the adjusted hazard ratio (HR (HR = 1·52, p = 0·069. Otherwise, mortality, motor condition and severity of depression revealed no significant difference between PD patients with pre-diagnostic and post-diagnostic depression.PD patients with post-diagnostic depression had higher incidence of dementia, implying different onset time of depression could be associated with different subtypes and spreading routes which should be examined in follow-up studies.

Roles of the spreading scope and effectiveness in spreading dynamics on multiplex networks

Science.gov (United States)

Li, Ming; Liu, Run-Ran; Peng, Dan; Jia, Chun-Xiao; Wang, Bing-Hong

2018-02-01

Comparing with single networks, the multiplex networks bring two main effects on the spreading process among individuals. First, the pathogen or information can be transmitted to more individuals through different layers at one time, which enlarges the spreading scope. Second, through different layers, an individual can also transmit the pathogen or information to the same individuals more than once at one time, which makes the spreading more effective. To understand the different roles of the spreading scope and effectiveness, we propose an epidemic model on multiplex networks with link overlapping, where the spreading effectiveness of each interaction as well as the variety of channels (spreading scope) can be controlled by the number of overlapping links. We find that for Poisson degree distribution, increasing the epidemic scope (the first effect) is more efficient than enhancing epidemic probability (the second effect) to facilitate the spreading process. However, for power-law degree distribution, the effects of the two factors on the spreading dynamics become complicated. Enhancing epidemic probability makes pathogen or rumor easier to outbreak in a finite system. But after that increasing epidemic scopes is still more effective for a wide spreading. Theoretical results along with reasonable explanation for these phenomena are all given in this paper, which indicates that the epidemic scope could play an important role in the spreading dynamics.

Optimizing Hybrid Spreading in Metapopulations.

OpenAIRE

Zhang, C.; Zhou, S.; Miller, J. C.; Cox, I. J.; Chain, B. M.

2015-01-01

Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by local spreading, where infected nodes can only infect a limited set of direct target nodes and global spreading, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemic...

Optimizing Hybrid Spreading in Metapopulations

OpenAIRE

Zhang, Changwang; Zhou, Shi; Miller, Joel C.; Cox, Ingemar J.; Chain, Benjamin M.

2014-01-01

Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by local spreading, where infected nodes can only infect a limited set of direct target nodes and global spreading, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemic...

White matter lesions and temporal lobe atrophy related to incidence of both dementia and major depression in 70-year-olds followed over 10 years.

Science.gov (United States)

Gudmundsson, P; Olesen, P J; Simoni, M; Pantoni, L; Östling, S; Kern, S; Guo, X; Skoog, I

2015-05-01

A number of studies have suggested associations between dementia and depression in older adults. One reason could be that these disorders share structural correlates, such as white matter lesions (WMLs) and cortical atrophy. No study has examined whether these lesions precede both dementia and depression independently of each other in the general population. Whether WMLs and cortical atrophy on computed tomography predict dementia and depression was investigated in a population-based sample of 70-year-olds (n = 380) followed over 10 years. Exclusion criteria were dementia, major depression, history of stroke and a Mini-Mental State Examination score below 26 at baseline in 2000-2001. Dementia was diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, third edition, revised, and depression according to the Diagnostic and Statistical Manual of Mental Disorders, fifth edition. Primary outcomes included dementia and major depression at 10-year follow-up. Adjusted logistic regression models, including both WMLs and temporal lobe atrophy, showed that moderate to severe WMLs [odds ratio (OR) 3.96, 95% confidence interval (CI) 1.23-12.76] and temporal lobe atrophy (OR 2.93, 95% CI 1.13-7.60) predicted dementia during a 10-year follow-up independently of major depression. Similarly, both moderate to severe WMLs (OR 3.84, 95% CI 1.25-11.76) and temporal lobe atrophy (OR 2.52, 95% CI 1.06-5.96) predicted depression even after controlling for incident dementia. White matter lesions and temporal lobe atrophy preceded 10-year incidence of both dementia and depression in 70-year-olds. Shared structural correlates could explain the reported associations between dementia and depression. These brain changes may represent independent and complementary pathways to dementia and depression. Strategies to slow progression of vascular pathology and neurodegeneration could indirectly prevent both dementia and depression in older adults. © 2015 EAN.

Spread effects - methodology

International Nuclear Information System (INIS)

2004-01-01

Diffusion of technology, environmental effects and rebound effects are the principal effects from the funding of renewable energy and energy economising. It is difficult to estimate the impact of the spread effects both prior to the measures are implemented and after the measures are carried out. Statistical methods can be used to estimate the spread effects, but they are insecure and always need to be complemented with qualitative and subjective evaluations. It is more adequate to evaluate potential spread effects from market and market data surveillance for a selection of technologies and parties. Based on this information qualitative indicators for spread effects can be constructed and used both ex ante and ex post (ml)

Cortical feedback control of olfactory bulb circuits.

Science.gov (United States)

Boyd, Alison M; Sturgill, James F; Poo, Cindy; Isaacson, Jeffry S

2012-12-20

Olfactory cortex pyramidal cells integrate sensory input from olfactory bulb mitral and tufted (M/T) cells and project axons back to the bulb. However, the impact of cortical feedback projections on olfactory bulb circuits is unclear. Here, we selectively express channelrhodopsin-2 in olfactory cortex pyramidal cells and show that cortical feedback projections excite diverse populations of bulb interneurons. Activation of cortical fibers directly excites GABAergic granule cells, which in turn inhibit M/T cells. However, we show that cortical inputs preferentially target short axon cells that drive feedforward inhibition of granule cells. In vivo, activation of olfactory cortex that only weakly affects spontaneous M/T cell firing strongly gates odor-evoked M/T cell responses: cortical activity suppresses odor-evoked excitation and enhances odor-evoked inhibition. Together, these results indicate that although cortical projections have diverse actions on olfactory bulb microcircuits, the net effect of cortical feedback on M/T cells is an amplification of odor-evoked inhibition. Copyright © 2012 Elsevier Inc. All rights reserved.

Cortical myoclonus and cerebellar pathology

NARCIS (Netherlands)

Tijssen, MAJ; Thom, M; Ellison, DW; Wilkins, P; Barnes, D; Thompson, PD; Brown, P

2000-01-01

Objective To study the electrophysiologic and pathologic findings in three patients with cortical myoclonus. In two patients the myoclonic ataxic syndrome was associated with proven celiac disease. Background: The pathologic findings in conditions associated with cortical myoclonus commonly involve

Cortical myoclonus and cerebellar pathology

NARCIS (Netherlands)

Tijssen, M. A.; Thom, M.; Ellison, D. W.; Wilkins, P.; Barnes, D.; Thompson, P. D.; Brown, P.

2000-01-01

OBJECTIVE: To study the electrophysiologic and pathologic findings in three patients with cortical myoclonus. In two patients the myoclonic ataxic syndrome was associated with proven celiac disease. BACKGROUND: The pathologic findings in conditions associated with cortical myoclonus commonly involve

Cortical Gamma-Aminobutyric Acid and Glutamate in Posttraumatic Stress Disorder and Their Relationships to Self-Reported Sleep Quality

Science.gov (United States)

Meyerhoff, Dieter J.; Mon, Anderson; Metzler, Thomas; Neylan, Thomas C.

2014-01-01

Study Objectives: To test if posttraumatic stress disorder (PTSD) is associated with low brain gamma-aminobutyric acid (GABA) levels and if reduced GABA is mediated by poor sleep quality. Design: Laboratory study using in vivo proton magnetic resonance spectroscopy (1H MRS) and behavioral testing. Setting: VA Medical Center Research Service, Psychiatry and Radiology. Patients or Participants: Twenty-seven patients with PTSD (PTSD+) and 18 trauma-exposed controls without PTSD (PTSD−), recruited from United States Army reservists, Army National Guard, and mental health clinics. Interventions: None. Measurements and Results: 1H MRS at 4 Tesla yielded spectra from three cortical brain regions. In parieto-occipital and temporal cortices, PTSD+ had lower GABA concentrations than PTSD−. As expected, PTSD+ had higher depressive and anxiety symptom scores and a higher Insomnia Severity Index (ISI) score. Higher ISI correlated with lower GABA and higher glutamate levels in parieto-occipital cortex and tended to correlate with lower GABA in the anterior cingulate. The relationship between parieto-occipital GABA and PTSD diagnosis was fully mediated through insomnia severity. Lower N-acetylaspartate and glutamate concentrations in the anterior cingulate cortex correlated with higher arousal scores, whereas depressive and anxiety symptoms did generally not influence metabolite concentrations. Conclusions: Low brain gamma-aminobutyric acid (GABA) concentration in posttraumatic stress disorder (PTSD) is consistent with most findings in panic and social anxiety disorders. Low GABA associated with poor sleep quality is consistent with the hyperarousal theory of both primary insomnia and PTSD. Our data demonstrate that poor sleep quality mediates low parieto-occipital GABA in PTSD. The findings have implications for PTSD treatment approaches. Citation: Meyerhoff DJ, Mon A, Metzler T, Neylan TC. Cortical gamma-aminobutyric acid and glutamate in posttraumatic stress disorder and

[Laughter and depression: hypothesis of pathogenic and therapeutic correlation].

Science.gov (United States)

Fonzi, Laura; Matteucci, Gabriella; Bersani, Giuseppe

2010-01-01

Laughter is a very common behaviour in everyday life, nevertheless scientific literature is lacking in studies which examine closely its nature. The study aims are: to summarise the present knowledge about laughter and its relation with depression and to make hypotheses on its possible therapeutic function. In the first part of the review the main data existing about encephalic structures involved in laughter genesis, which show participation of cortical and subcortical regions, are reported and the effects of laughter on the organism physiologic equilibrium, particularly on the neuroendocrine and immune systems, are described. In the second part, scientific evidence about the influence of depression on the ability to laugh are referred, which suggests that reduction of laughter frequency is a symptom of the disease and that its increase may be used as a marker of clinical improvement. Finally, the main assumptions supporting the hypothesis of the therapeutic action of laughter on depression are examined: first of all, it has been demonstrated that laughter is able to improve mood directly and to moderate negative consequences of stressful events on psychological well-being; in addition, it is possible that the stimulation of particular cerebral regions, involved in depression pathogenesis, and the normalisation of the hypothalamic pituitary adrenocortical system dysfunctions, both mediated by laughter, can counteract efficiently depressive symptoms; finally, the favourable effects of laughter on social relationships and physical health may have a role in influencing the ability of depressed patients to face the disease.

Effect of chondroitin sulfate proteoglycans on neuronal cell adhesion, spreading and neurite growth in culture

Directory of Open Access Journals (Sweden)

Jingyu Jin

2018-01-01

Full Text Available As one major component of extracellular matrix (ECM in the central nervous system, chondroitin sulfate proteoglycans (CSPGs have long been known as inhibitors enriched in the glial scar that prevent axon regeneration after injury. Although many studies have shown that CSPGs inhibited neurite outgrowth in vitro using different types of neurons, the mechanism by which CSPGs inhibit axonal growth remains poorly understood. Using cerebellar granule neuron (CGN culture, in this study, we evaluated the effects of different concentrations of both immobilized and soluble CSPGs on neuronal growth, including cell adhesion, spreading and neurite growth. Neurite length decreased while CSPGs concentration arised, meanwhile, a decrease in cell density accompanied by an increase in cell aggregates formation was observed. Soluble CSPGs also showed an inhibition on neurite outgrowth, but it required a higher concentration to induce cell aggregates formation than coated CSPGs. We also found that growth cone size was significantly reduced on CSPGs and neuronal cell spreading was restrained by CSPGs, attributing to an inhibition on lamellipodial extension. The effect of CSPGs on neuron adhesion was further evidenced by interference reflection microscopy (IRM which directly demonstrated that both CGNs and cerebral cortical neurons were more loosely adherent to a CSPG substrate. These data demonstrate that CSPGs have an effect on cell adhesion and spreading in addition to neurite outgrowth.

Transcranial magnetic stimulation potentiates glutamatergic neurotransmission in depressed adolescents.

Science.gov (United States)

Croarkin, Paul E; Nakonezny, Paul A; Wall, Christopher A; Murphy, Lauren L; Sampson, Shirlene M; Frye, Mark A; Port, John D

2016-01-30

Abnormalities in glutamate neurotransmission may have a role in the pathophysiology of adolescent depression. The present pilot study examined changes in cortical glutamine/glutamate ratios in depressed adolescents receiving high-frequency repetitive transcranial magnetic stimulation. Ten adolescents with treatment-refractory major depressive disorder received up to 30 sessions of 10-Hz repetitive transcranial magnetic stimulation at 120% motor threshold with 3000 pulses per session applied to the left dorsolateral prefrontal cortex. Baseline, posttreatment, and 6-month follow-up proton magnetic resonance spectroscopy scans of the anterior cingulate cortex and left dorsolateral prefrontal cortex were collected at 3T with 8-cm(3) voxels. Glutamate metabolites were quantified with 2 distinct proton magnetic resonance spectroscopy sequences in each brain region. After repetitive transcranial magnetic stimulation and at 6 months of follow-up, glutamine/glutamate ratios increased in the anterior cingulate cortex and left dorsolateral prefrontal cortex with both measurements. The increase in the glutamine/glutamate ratio reached statistical significance with the TE-optimized PRESS sequence in the anterior cingulate cortex. Glutamine/glutamate ratios increased in conjunction with depressive symptom improvement. This reached statistical significance with the TE-optimized PRESS sequence in the left dorsolateral prefrontal cortex. High-frequency repetitive transcranial magnetic stimulation applied to the left dorsolateral prefrontal cortex may modulate glutamate neurochemistry in depressed adolescents. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Reduced Inhibitory Control Mediates the Relationship Between Cortical Thickness in the Right Superior Frontal Gyrus and Body Mass Index.

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Lavagnino, Luca; Mwangi, Benson; Bauer, Isabelle E; Cao, Bo; Selvaraj, Sudhakar; Prossin, Alan; Soares, Jair C

2016-08-01

Unhealthy eating behaviors often develop in the setting of inadequate inhibitory control, a function broadly ascribed to the prefrontal cortex (PFC). Regulation of inhibitory control by the PFC and its anatomical components and their contribution to increasing body mass index (BMI) are poorly understood. To study the role of PFC in the regulation of inhibitory control and body weight, we examined measures of cortical thickness in PFC sub-regions, inhibitory control (color-word interference task (CWIT)), and BMI in 91 healthy volunteers. We tested the predictive effect of PFC sub-regional cortical thickness on BMI and mediation by inhibitory control measured with CWIT. Measures of depression (BDI-II), anxiety (STAI-T) and trauma-related symptoms (TSC-40) were collected; the disinhibition scale of the three-factor eating questionnaire (TFEQ) was used to assess disinhibited eating. We then tested the relationship between BD-II, STAI-T, TSC-40, TFEQ, CWIT, and BMI with correlation analyses. Right superior frontal gyrus cortical thickness significantly predicted BMI (β=-0.91; t=-3.2; p=0.002). Mediation analysis showed a significant indirect effect of cortical thickness on BMI mediated by inhibitory control (95% CI=-6.1, -0.67). BMI was unrelated to BDI-II, STAI-T, TSC-40, or TFEQ scores. We found an inverse relationship between cortical thickness in the right-superior frontal gyrus and BMI, which was fully mediated by inhibitory control neurocognitive performance. Our results suggest possible targets for neuromodulation in obesity (ie superior frontal gyrus) and a quantifiable mediator of their effects (ie inhibitory control).

Long-term lithium treatment increases intracellular and extracellular brain-derived neurotrophic factor (BDNF) in cortical and hippocampal neurons at subtherapeutic concentrations.

Science.gov (United States)

De-Paula, Vanessa J; Gattaz, Wagner F; Forlenza, Orestes V

2016-12-01

The putative neuroprotective effects of lithium treatment rely on the fact that it modulates several homeostatic mechanisms involved in the neurotrophic response, autophagy, oxidative stress, inflammation, and mitochondrial function. Lithium is a well-established therapeutic option for the acute and long-term management of bipolar disorder and major depression. The aim of this study was to evaluate the effects of subtherapeutic and therapeutic concentrations of chronic lithium treatment on brain-derived neurotrophic factor (BDNF) synthesis and secretion. Primary cultures of cortical and hippocampal neurons were treated with different subtherapeutic (0.02 and 0.2 mM) and therapeutic (2 mM) concentrations of chronic lithium treatment in cortical and hippocampal cell culture. Lithium treatment increased the intracellular protein expression of cortical neurons (10% at 0.02 mM) and hippocampal neurons (28% and 14% at 0.02 mM and 0.2 mM, respectively). Extracellular BDNF of cortical neurons increased 30% and 428% at 0.02 and 0.2 mM, respectively and in hippocampal neurons increased 44% at 0.02 mM. The present study indicates that chronic, low-dose lithium treatment up-regulates BDNF production in primary neuronal cell culture. © 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Migraine aura: retracting particle-like waves in weakly susceptible cortex.

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Markus A Dahlem

Full Text Available Cortical spreading depression (SD has been suggested to underlie migraine aura. Despite a precise match in speed, the spatio-temporal patterns of SD observed in animal cortex and aura symptoms mapped to the cortical surface ordinarily differ in aspects of size and shape. We show that this mismatch is reconciled by utilizing that both pattern types bifurcate from an instability point of generic reaction-diffusion models. To classify these spatio-temporal pattern we suggest a susceptibility scale having the value sigma = 1 at the instability point. We predict that human cortex is only weakly susceptible to SD (sigma1, and potentially silent aura occurring below a second bifurcation point at sigma = 0 on the susceptible scale.

Combinatorics of spreads and parallelisms

CERN Document Server

Johnson, Norman

2010-01-01

Partitions of Vector Spaces Quasi-Subgeometry Partitions Finite Focal-SpreadsGeneralizing André SpreadsThe Going Up Construction for Focal-SpreadsSubgeometry Partitions Subgeometry and Quasi-Subgeometry Partitions Subgeometries from Focal-SpreadsExtended André SubgeometriesKantor's Flag-Transitive DesignsMaximal Additive Partial SpreadsSubplane Covered Nets and Baer Groups Partial Desarguesian t-Parallelisms Direct Products of Affine PlanesJha-Johnson SL(2,

Computed tomographic anatomy of the mandibular first and second molars and their surrounding structures in the spread of odontogenic infection

International Nuclear Information System (INIS)

Ohshima, Aya; Ariji, Yoshiko; Gotoh, Masakazu; Izumi, Masahiro; Naitoh, Munetaka; Kurita, Kenichi; Shimozato, Kazuo; Ariji, Eiichiro

2009-01-01

The purposes of this study were to analyze the CT anatomy of the mandibular first and second molars in uninfected subjects and to clarify the pathway of odontogenic infection originating from the mandibular first and second molars. CT anatomies, especially for bucco-lingual aspects and the surrounding soft tissues, were investigated in 100 uninfected subjects and 17 infected patients. At the level of bifurcation, disappearance of the cortical plates was frequently observed on the buccal and lingual sides of the first molars, and it was reduced on the buccal side in the second molar. In the first molar, the bony width was thinner on the buccal than the lingual side. The lingual cortices were thinner in the second molar. All medial pterygoid and 88% of masseter muscles were situated posteriorly, without horizontally overlapping the second molar, whereas the mylohyoid muscle (MhM) overlapped horizontally with the first and second molars. The MhM was positioned superior to the root apices in 10 and 39% of first and second molars, respectively. All patients with first molar infection showed involvement of buccal structures, and one showed lingual side involvement. In contrast, six of nine patients with second molar infection showed involvement on the lingual side. Infection originating from the second molar was more likely to spread to the lingual side than infection originating from the first molar. CT anatomy surrounding the causal teeth supported the spread pathways of mandibular first and second molar infection. (author)

The human dorsal premotor cortex facilitates the excitability of ipsilateral primary motor cortex via a short latency cortico-cortical route

DEFF Research Database (Denmark)

Groppa, Sergiu; Schlaak, Boris H; Münchau, Alexander

2012-01-01

In non-human primates, invasive tracing and electrostimulation studies have identified strong ipsilateral cortico-cortical connections between dorsal premotor- (PMd) and the primary motor cortex (M1(HAND) ). Here, we applied dual-site transcranial magnetic stimulation (dsTMS) to left PMd and M1......(HAND) through specifically designed minicoils to selectively probe ipsilateral PMd-to-M1(HAND) connectivity in humans. A suprathreshold test stimulus (TS) was applied to M1(HAND) producing a motor evoked potential (MEP) of about 0.5 mV in the relaxed right first dorsal interosseus muscle (FDI......) facilitation did not change as a function of CS intensity. Even at higher intensities, the CS alone failed to elicit a MEP or a cortical silent period in the pre-activated FDI, excluding a direct spread of excitation from PMd to M1(HAND). No MEP facilitation was present while CS was applied rostrally over...

Age, spreading rates, and spreading asymmetry of the world's ocean crust

Data.gov (United States)

National Oceanic and Atmospheric Administration, Department of Commerce — The authors present four companion digital models of the age, age uncertainty, spreading rates and spreading asymmetries of the world's ocean basins as geographic...

State-dependent intrinsic predictability of cortical network dynamics.

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Leila Fakhraei

Full Text Available The information encoded in cortical circuit dynamics is fleeting, changing from moment to moment as new input arrives and ongoing intracortical interactions progress. A combination of deterministic and stochastic biophysical mechanisms governs how cortical dynamics at one moment evolve from cortical dynamics in recently preceding moments. Such temporal continuity of cortical dynamics is fundamental to many aspects of cortex function but is not well understood. Here we study temporal continuity by attempting to predict cortical population dynamics (multisite local field potential based on its own recent history in somatosensory cortex of anesthetized rats and in a computational network-level model. We found that the intrinsic predictability of cortical dynamics was dependent on multiple factors including cortical state, synaptic inhibition, and how far into the future the prediction extends. By pharmacologically tuning synaptic inhibition, we obtained a continuum of cortical states with asynchronous population activity at one extreme and stronger, spatially extended synchrony at the other extreme. Intermediate between these extremes we observed evidence for a special regime of population dynamics called criticality. Predictability of the near future (10-100 ms increased as the cortical state was tuned from asynchronous to synchronous. Predictability of the more distant future (>1 s was generally poor, but, surprisingly, was higher for asynchronous states compared to synchronous states. These experimental results were confirmed in a computational network model of spiking excitatory and inhibitory neurons. Our findings demonstrate that determinism and predictability of network dynamics depend on cortical state and the time-scale of the dynamics.

A social marketing approach to implementing evidence-based practice in VHA QUERI: the TIDES depression collaborative care model.

Science.gov (United States)

Luck, Jeff; Hagigi, Fred; Parker, Louise E; Yano, Elizabeth M; Rubenstein, Lisa V; Kirchner, JoAnn E

2009-09-28

Collaborative care models for depression in primary care are effective and cost-effective, but difficult to spread to new sites. Translating Initiatives for Depression into Effective Solutions (TIDES) is an initiative to promote evidence-based collaborative care in the U.S. Veterans Health Administration (VHA). Social marketing applies marketing techniques to promote positive behavior change. Described in this paper, TIDES used a social marketing approach to foster national spread of collaborative care models. The approach relied on a sequential model of behavior change and explicit attention to audience segmentation. Segments included VHA national leadership, Veterans Integrated Service Network (VISN) regional leadership, facility managers, frontline providers, and veterans. TIDES communications, materials and messages targeted each segment, guided by an overall marketing plan. Depression collaborative care based on the TIDES model was adopted by VHA as part of the new Primary Care Mental Health Initiative and associated policies. It is currently in use in more than 50 primary care practices across the United States, and continues to spread, suggesting success for its social marketing-based dissemination strategy. Development, execution and evaluation of the TIDES marketing effort shows that social marketing is a promising approach for promoting implementation of evidence-based interventions in integrated healthcare systems.

A social marketing approach to implementing evidence-based practice in VHA QUERI: the TIDES depression collaborative care model

Science.gov (United States)

2009-01-01

Abstract Collaborative care models for depression in primary care are effective and cost-effective, but difficult to spread to new sites. Translating Initiatives for Depression into Effective Solutions (TIDES) is an initiative to promote evidence-based collaborative care in the U.S. Veterans Health Administration (VHA). Social marketing applies marketing techniques to promote positive behavior change. Described in this paper, TIDES used a social marketing approach to foster national spread of collaborative care models. TIDES social marketing approach The approach relied on a sequential model of behavior change and explicit attention to audience segmentation. Segments included VHA national leadership, Veterans Integrated Service Network (VISN) regional leadership, facility managers, frontline providers, and veterans. TIDES communications, materials and messages targeted each segment, guided by an overall marketing plan. Results Depression collaborative care based on the TIDES model was adopted by VHA as part of the new Primary Care Mental Health Initiative and associated policies. It is currently in use in more than 50 primary care practices across the United States, and continues to spread, suggesting success for its social marketing-based dissemination strategy. Discussion and conclusion Development, execution and evaluation of the TIDES marketing effort shows that social marketing is a promising approach for promoting implementation of evidence-based interventions in integrated healthcare systems. PMID:19785754

The Roles of Cortical Slow Waves in Synaptic Plasticity and Memory Consolidation.

Science.gov (United States)

Miyamoto, Daisuke; Hirai, Daichi; Murayama, Masanori

2017-01-01

Sleep plays important roles in sensory and motor memory consolidation. Sleep oscillations, reflecting neural population activity, involve the reactivation of learning-related neurons and regulate synaptic strength and, thereby affect memory consolidation. Among sleep oscillations, slow waves (0.5-4 Hz) are closely associated with memory consolidation. For example, slow-wave power is regulated in an experience-dependent manner and correlates with acquired memory. Furthermore, manipulating slow waves can enhance or impair memory consolidation. During slow wave sleep, inter-areal interactions between the cortex and hippocampus (HC) have been proposed to consolidate declarative memory; however, interactions for non-declarative (HC-independent) memory remain largely uninvestigated. We recently showed that the directional influence in a slow-wave range through a top-down cortical long-range circuit is involved in the consolidation of non-declarative memory. At the synaptic level, the average cortical synaptic strength is known to be potentiated during wakefulness and depressed during sleep. Moreover, learning causes plasticity in a subset of synapses, allocating memory to them. Sleep may help to differentiate synaptic strength between allocated and non-allocated synapses (i.e., improving the signal-to-noise ratio, which may facilitate memory consolidation). Herein, we offer perspectives on inter-areal interactions and synaptic plasticity for memory consolidation during sleep.

The Roles of Cortical Slow Waves in Synaptic Plasticity and Memory Consolidation

Directory of Open Access Journals (Sweden)

Daisuke Miyamoto

2017-11-01

Full Text Available Sleep plays important roles in sensory and motor memory consolidation. Sleep oscillations, reflecting neural population activity, involve the reactivation of learning-related neurons and regulate synaptic strength and, thereby affect memory consolidation. Among sleep oscillations, slow waves (0.5–4 Hz are closely associated with memory consolidation. For example, slow-wave power is regulated in an experience-dependent manner and correlates with acquired memory. Furthermore, manipulating slow waves can enhance or impair memory consolidation. During slow wave sleep, inter-areal interactions between the cortex and hippocampus (HC have been proposed to consolidate declarative memory; however, interactions for non-declarative (HC-independent memory remain largely uninvestigated. We recently showed that the directional influence in a slow-wave range through a top-down cortical long-range circuit is involved in the consolidation of non-declarative memory. At the synaptic level, the average cortical synaptic strength is known to be potentiated during wakefulness and depressed during sleep. Moreover, learning causes plasticity in a subset of synapses, allocating memory to them. Sleep may help to differentiate synaptic strength between allocated and non-allocated synapses (i.e., improving the signal-to-noise ratio, which may facilitate memory consolidation. Herein, we offer perspectives on inter-areal interactions and synaptic plasticity for memory consolidation during sleep.

Influence of the topography of brain damage on depression and fatigue in patients with multiple sclerosis.

Science.gov (United States)

Gobbi, C; Rocca, M A; Riccitelli, G; Pagani, E; Messina, R; Preziosa, P; Colombo, B; Rodegher, M; Falini, A; Comi, G; Filippi, M

2014-02-01

Involvement of selected central nervous system (CNS) regions has been associated with depression and fatigue in MS. We assessed whether specific regional patterns of lesion distribution and atrophy of the gray (GM) and white matter (WM) are associated with these symptoms in MS. Brain dual-echo and 3D T1-weighted images were acquired from 123 MS patients (69 depressed (D), 54 non-depressed (nD), 64 fatigued, 59 non-fatigued) and 90 controls. Lesion distribution, GM and WM atrophy were estimated using VBM and SPM8. Gender, age, disease duration and conventional MRI characteristics did not differ between D-MS and nD-MS patients. Fatigued patients experienced higher EDSS and depression than non-fatigued ones. Lesion distribution and WM atrophy were not related to depression and fatigue. Atrophy of regions in the frontal, parietal and occipital lobes had a combined effect on depression and fatigue. Atrophy of the left middle frontal gyrus and right inferior frontal gyrus were selectively related to depression. No specific pattern of GM atrophy was found to be related to fatigue. Depression in MS is linked to atrophy of cortical regions located in the bilateral frontal lobes. A distributed pattern of GM atrophy contributes to the concomitant presence of depression and fatigue in these patients.

The VULCANO spreading programme

Energy Technology Data Exchange (ETDEWEB)

Cognet, G.; Laffont, G.; Jegou, C.; Journeau, C.; Sudreau, F.; Pierre, J.; Ramacciotti, M. [CEA (Atomic Energy Commission), DRN/DER - Bat. 212, CEA Cadarache, 13108 St. Paul Lez Durance (France)

1999-07-01

Among the currently studied core-catcher projects, some of them suppose corium spreading before cooling, in particular the EPR (European Pressurized Reactor) core-catcher concept is based on mixing the corium with a special concrete, spreading the molten mixture on a large multi-layer surface cooled from the bottom and subsequently cooling by flooding with water. Therefore, melt spreading deserves intensive investigation in order to determine and quantify key phenomena which govern the stopping of spreading. In France, for some years, the Nuclear Reactor Division of the Atomic Energy Commission (CEA/DRN) has undertaken a large program to improve knowledge on corium behaviour and coolability. This program is based on experimental and theoretical investigations which are finally gathered in scenario and mechanistic computer codes. In this framework, the real material experimental programme, VULCANO, conducted within an European frame, is currently devoted to the study of corium spreading. In 1997 and 1998, several tests have been performed on dry corium spreading with various composition of melts. Although all the observed phenomena, in particular the differences between simulant and real material melts have not been yet totally explained, these tests have already provided a lot of information about: The behaviour of complex mixtures including refractory oxides, silica, iron oxides and in one case iron metal; Spreading progression, which was never stopped in any of these tests by a crust formation at the front; The structure of spread melts (porosity, crusts,...); Physico-chemical interaction between melt and the refractory substratum which was composed of zirconia bricks. (authors)

The VULCANO spreading programme

International Nuclear Information System (INIS)

Cognet, G.; Laffont, G.; Jegou, C.; Journeau, C.; Sudreau, F.; Pierre, J.; Ramacciotti, M.

1999-01-01

Among the currently studied core-catcher projects, some of them suppose corium spreading before cooling, in particular the EPR (European Pressurized Reactor) core-catcher concept is based on mixing the corium with a special concrete, spreading the molten mixture on a large multi-layer surface cooled from the bottom and subsequently cooling by flooding with water. Therefore, melt spreading deserves intensive investigation in order to determine and quantify key phenomena which govern the stopping of spreading. In France, for some years, the Nuclear Reactor Division of the Atomic Energy Commission (CEA/DRN) has undertaken a large program to improve knowledge on corium behaviour and coolability. This program is based on experimental and theoretical investigations which are finally gathered in scenario and mechanistic computer codes. In this framework, the real material experimental programme, VULCANO, conducted within an European frame, is currently devoted to the study of corium spreading. In 1997 and 1998, several tests have been performed on dry corium spreading with various composition of melts. Although all the observed phenomena, in particular the differences between simulant and real material melts have not been yet totally explained, these tests have already provided a lot of information about: The behaviour of complex mixtures including refractory oxides, silica, iron oxides and in one case iron metal; Spreading progression, which was never stopped in any of these tests by a crust formation at the front; The structure of spread melts (porosity, crusts,...); Physico-chemical interaction between melt and the refractory substratum which was composed of zirconia bricks. (authors)

Cortical Thinning and Altered Cortico-Cortical Structural Covariance of the Default Mode Network in Patients with Persistent Insomnia Symptoms.

Science.gov (United States)

Suh, Sooyeon; Kim, Hosung; Dang-Vu, Thien Thanh; Joo, Eunyeon; Shin, Chol

2016-01-01

Recent studies have suggested that structural abnormalities in insomnia may be linked with alterations in the default-mode network (DMN). This study compared cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia (PI) and good sleepers (GS). The current study used a clinical subsample from the longitudinal community-based Korean Genome and Epidemiology Study (KoGES). Cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia symptoms (PIS; n = 57) were compared to good sleepers (GS; n = 40). All participants underwent MRI acquisition. Based on literature review, we selected cortical regions corresponding to the DMN. A seed-based structural covariance analysis measured cortical thickness correlation between each seed region of the DMN and other cortical areas. Association of cortical thickness and covariance with sleep quality and neuropsychological assessments were further assessed. Compared to GS, cortical thinning was found in PIS in the anterior cingulate cortex, precentral cortex, and lateral prefrontal cortex. Decreased structural connectivity between anterior and posterior regions of the DMN was observed in the PIS group. Decreased structural covariance within the DMN was associated with higher PSQI scores. Cortical thinning in the lateral frontal lobe was related to poor performance in executive function in PIS. Disrupted structural covariance network in PIS might reflect malfunctioning of antero-posterior disconnection of the DMN during the wake to sleep transition that is commonly found during normal sleep. The observed structural network alteration may further implicate commonly observed sustained sleep difficulties and cognitive impairment in insomnia. © 2016 Associated Professional Sleep Societies, LLC.

The biology and dynamics of mammalian cortical granules

Directory of Open Access Journals (Sweden)

Liu Min

2011-11-01

Full Text Available Abstract Cortical granules are membrane bound organelles located in the cortex of unfertilized oocytes. Following fertilization, cortical granules undergo exocytosis to release their contents into the perivitelline space. This secretory process, which is calcium dependent and SNARE protein-mediated pathway, is known as the cortical reaction. After exocytosis, the released cortical granule proteins are responsible for blocking polyspermy by modifying the oocytes' extracellular matrices, such as the zona pellucida in mammals. Mammalian cortical granules range in size from 0.2 um to 0.6 um in diameter and different from most other regulatory secretory organelles in that they are not renewed once released. These granules are only synthesized in female germ cells and transform an egg upon sperm entry; therefore, this unique cellular structure has inherent interest for our understanding of the biology of fertilization. Cortical granules are long thought to be static and awaiting in the cortex of unfertilized oocytes to be stimulated undergoing exocytosis upon gamete fusion. Not till recently, the dynamic nature of cortical granules is appreciated and understood. The latest studies of mammalian cortical granules document that this organelle is not only biochemically heterogeneous, but also displays complex distribution during oocyte development. Interestingly, some cortical granules undergo exocytosis prior to fertilization; and a number of granule components function beyond the time of fertilization in regulating embryonic cleavage and preimplantation development, demonstrating their functional significance in fertilization as well as early embryonic development. The following review will present studies that investigate the biology of cortical granules and will also discuss new findings that uncover the dynamic aspect of this organelle in mammals.

Increased Cortical Thickness in Professional On-Line Gamers

Science.gov (United States)

Hyun, Gi Jung; Shin, Yong Wook; Kim, Bung-Nyun; Cheong, Jae Hoon; Jin, Seong Nam

2013-01-01

Objective The bulk of recent studies have tested whether video games change the brain in terms of activity and cortical volume. However, such studies are limited by several factors including cross-sectional comparisons, co-morbidity, and short-term follow-up periods. In the present study, we hypothesized that cognitive flexibility and the volume of brain cortex would be correlated with the career length of on-line pro-gamers. Methods High-resolution magnetic resonance scans were acquired in twenty-three pro-gamers recruited from StarCraft pro-game teams. We measured cortical thickness in each individual using FreeSurfer and the cortical thickness was correlated with the career length and the performance of the pro-gamers. Results Career length was positively correlated with cortical thickness in three brain regions: right superior frontal gyrus, right superior parietal gyrus, and right precentral gyrus. Additionally, increased cortical thickness in the prefrontal cortex was correlated with winning rates of the pro-game league. Increased cortical thickness in the prefrontal and parietal cortices was also associated with higher performance of Wisconsin Card Sorting Test. Conclusion Our results suggest that in individuals without pathologic conditions, regular, long-term playing of on-line games is associated with volume changes in the prefrontal and parietal cortices, which are associated with cognitive flexibility. PMID:24474988

Transcranial magnetic simulation in the treatment of migraine.

Science.gov (United States)

Lipton, Richard B; Pearlman, Starr H

2010-04-01

Transcranial magnetic stimulation (TMS) is a diagnostic and therapeutic modality that is being developed as both an acute and preventive treatment for migraine. TMS delivers a fluctuating magnetic field from the scalp surface to induce current in the subjacent cortex. Magnetic pulses are delivered one at a time in single-pulse TMS (sTMS) or as a train of pulses in repetitive TMS (rTMS). For most of its 30-year history, TMS has been delivered in clinical and research settings using large tabletop devices. Based on the theory that sTMS may disrupt cortical spreading depression, sTMS has been studied and shown to be effective as an acute treatment for migraine with aura. Subsequent work in animal models confirms that sTMS disrupts cortical spreading depression. To make outpatient self-treatment possible, a portable device has been developed for acute treatment of migraine with aura. Based on the theory that rTMS alters brain excitability and neurotransmitter activity, rTMS has been studied as a preventive migraine treatment. A small body of evidence suggests that rTMS may have a role, but further studies are needed. In this review, we summarize the data on TMS as a treatment of migraine, and we suggest directions for future research. Copyright 2010 The American Society for Experimental NeuroTherapeutics, Inc. Published by Elsevier Inc. All rights reserved.

Localization of dysfunction in major depressive disorder: prefrontal cortex and amygdala.

Science.gov (United States)

Murray, Elisabeth A; Wise, Steven P; Drevets, Wayne C

2011-06-15

Despite considerable effort, the localization of dysfunction in major depressive disorder (MDD) remains poorly understood. We present a hypothesis about its localization that builds on recent findings from primate neuropsychology. The hypothesis has four key components: a deficit in the valuation of "self" underlies the core disorder in MDD; the medial frontal cortex represents "self"; interactions between the amygdala and cortical representations update their valuation; and inefficiency in using positive feedback by orbital prefrontal cortex contributes to MDD. Published by Elsevier Inc.

Functional specialisation within the cortical language network: effects of cortical dysfunction.

Science.gov (United States)

Vandenberghe, R

2007-01-01

In the 1990's neuroanatomical models of language and semantic memory have been mainly based on functional neuroimaging studies of brain activity in healthy volunteers and correlational studies between structural lesions in patients and behavioral deficits. In this paper we present a novel approach where we test models that have been developed in healthy volunteers by means of functional imaging in patients in combination with behavioral studies. Study populations consist of patients with focal cortical stroke (n = 2), amnestic mild cognitive impairment (n = 14) and primary progressive aphasia (n = 18). The experiments provide converging evidence that 1. the integrity of the right mid- and anterior fusiform gyrus is required for full and detailed retrieval of knowledge of visual attributes of concrete entities 2. the left posterior superior temporal sulcus is critically involved in lexical-semantic retrieval 3. the anterior temporal pole to the left functions as an associative structure that links the representations of meaning that are distribured over the cortical brain surface. Our experiments also provide us with new insight into the degradation and re-organisation of the language system in cortical neurodegenerative disease.

Direct cortical hemodynamic mapping of somatotopy of pig nostril sensation by functional near-infrared cortical imaging (fNCI).

Science.gov (United States)

Uga, Minako; Saito, Toshiyuki; Sano, Toshifumi; Yokota, Hidenori; Oguro, Keiji; Rizki, Edmi Edison; Mizutani, Tsutomu; Katura, Takusige; Dan, Ippeita; Watanabe, Eiju

2014-05-01

Functional near-infrared spectroscopy (fNIRS) is a neuroimaging technique for the noninvasive monitoring of human brain activation states utilizing the coupling between neural activity and regional cerebral hemodynamics. Illuminators and detectors, together constituting optodes, are placed on the scalp, but due to the presence of head tissues, an inter-optode distance of more than 2.5cm is necessary to detect cortical signals. Although direct cortical monitoring with fNIRS has been pursued, a high-resolution visualization of hemodynamic changes associated with sensory, motor and cognitive neural responses directly from the cortical surface has yet to be realized. To acquire robust information on the hemodynamics of the cortex, devoid of signal complications in transcranial measurement, we devised a functional near-infrared cortical imaging (fNCI) technique. Here we demonstrate the first direct functional measurement of temporal and spatial patterns of cortical hemodynamics using the fNCI technique. For fNCI, inter-optode distance was set at 5mm, and light leakage from illuminators was prevented by a special optode holder made of a light-shielding rubber sheet. fNCI successfully detected the somatotopy of pig nostril sensation, as assessed in comparison with concurrent and sequential somatosensory-evoked potential (SEP) measurements on the same stimulation sites. Accordingly, the fNCI system realized a direct cortical hemodynamic measurement with a spatial resolution comparable to that of SEP mapping on the rostral region of the pig brain. This study provides an important initial step toward realizing functional cortical hemodynamic monitoring during neurosurgery of human brains. Copyright © 2014. Published by Elsevier Inc.

Cerebellar cortical infarct cavities and vertebral artery disease

Energy Technology Data Exchange (ETDEWEB)

Cocker, Laurens J.L. de [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); Kliniek Sint-Jan Radiologie, Brussels (Belgium); Compter, A.; Kappelle, L.J.; Worp, H.B. van der [University Medical Center Utrecht, Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, Utrecht (Netherlands); Luijten, P.R.; Hendrikse, J. [University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands)

2016-09-15

Cerebellar cortical infarct cavities are a newly recognised entity associated with atherothromboembolic cerebrovascular disease and worse physical functioning. We aimed to investigate the relationship of cerebellar cortical infarct cavities with symptomatic vertebrobasilar ischaemia and with vascular risk factors. We evaluated the MR images of 46 patients with a recent vertebrobasilar TIA or stroke and a symptomatic vertebral artery stenosis ≥50 % from the Vertebral Artery Stenting Trial (VAST) for the presence of cerebellar cortical infarct cavities ≤1.5 cm. At inclusion in VAST, data were obtained on age, sex, history of vertebrobasilar TIA or stroke, and vascular risk factors. Adjusted risk ratios were calculated with Poisson regression analyses for the relation between cerebellar cortical infarct cavities and vascular risk factors. Sixteen out of 46 (35 %) patients showed cerebellar cortical infarct cavities on the initial MRI, and only one of these 16 patients was known with a previous vertebrobasilar TIA or stroke. In patients with symptomatic vertebrobasilar ischaemia, risk factor profiles of patients with cerebellar cortical infarct cavities were not different from patients without these cavities. Cerebellar cortical infarct cavities are seen on MRI in as much as one third of patients with recently symptomatic vertebral artery stenosis. Since patients usually have no prior history of vertebrobasilar TIA or stroke, cerebellar cortical infarct cavities should be added to the spectrum of common incidental brain infarcts visible on routine MRI. (orig.)

Short term depression unmasks the ghost frequency.

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Tjeerd V Olde Scheper

Full Text Available Short Term Plasticity (STP has been shown to exist extensively in synapses throughout the brain. Its function is more or less clear in the sense that it alters the probability of synaptic transmission at short time scales. However, it is still unclear what effect STP has on the dynamics of neural networks. We show, using a novel dynamic STP model, that Short Term Depression (STD can affect the phase of frequency coded input such that small networks can perform temporal signal summation and determination with high accuracy. We show that this property of STD can readily solve the problem of the ghost frequency, the perceived pitch of a harmonic complex in absence of the base frequency. Additionally, we demonstrate that this property can explain dynamics in larger networks. By means of two models, one of chopper neurons in the Ventral Cochlear Nucleus and one of a cortical microcircuit with inhibitory Martinotti neurons, it is shown that the dynamics in these microcircuits can reliably be reproduced using STP. Our model of STP gives important insights into the potential roles of STP in self-regulation of cortical activity and long-range afferent input in neuronal microcircuits.

Anatomical alterations of the visual motion processing network in migraine with and without aura.

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Cristina Granziera

2006-10-01

Full Text Available Patients suffering from migraine with aura (MWA and migraine without aura (MWoA show abnormalities in visual motion perception during and between attacks. Whether this represents the consequences of structural changes in motion-processing networks in migraineurs is unknown. Moreover, the diagnosis of migraine relies on patient's history, and finding differences in the brain of migraineurs might help to contribute to basic research aimed at better understanding the pathophysiology of migraine.To investigate a common potential anatomical basis for these disturbances, we used high-resolution cortical thickness measurement and diffusion tensor imaging (DTI to examine the motion-processing network in 24 migraine patients (12 with MWA and 12 MWoA and 15 age-matched healthy controls (HCs. We found increased cortical thickness of motion-processing visual areas MT+ and V3A in migraineurs compared to HCs. Cortical thickness increases were accompanied by abnormalities of the subjacent white matter. In addition, DTI revealed that migraineurs have alterations in superior colliculus and the lateral geniculate nucleus, which are also involved in visual processing.A structural abnormality in the network of motion-processing areas could account for, or be the result of, the cortical hyperexcitability observed in migraineurs. The finding in patients with both MWA and MWoA of thickness abnormalities in area V3A, previously described as a source in spreading changes involved in visual aura, raises the question as to whether a "silent" cortical spreading depression develops as well in MWoA. In addition, these experimental data may provide clinicians and researchers with a noninvasively acquirable migraine biomarker.

Information spreading dynamics in hypernetworks

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Suo, Qi; Guo, Jin-Li; Shen, Ai-Zhong

2018-04-01

Contact pattern and spreading strategy fundamentally influence the spread of information. Current mathematical methods largely assume that contacts between individuals are fixed by networks. In fact, individuals are affected by all his/her neighbors in different social relationships. Here, we develop a mathematical approach to depict the information spreading process in hypernetworks. Each individual is viewed as a node, and each social relationship containing the individual is viewed as a hyperedge. Based on SIS epidemic model, we construct two spreading models. One model is based on global transmission, corresponding to RP strategy. The other is based on local transmission, corresponding to CP strategy. These models can degenerate into complex network models with a special parameter. Thus hypernetwork models extend the traditional models and are more realistic. Further, we discuss the impact of parameters including structure parameters of hypernetwork, spreading rate, recovering rate as well as information seed on the models. Propagation time and density of informed nodes can reveal the overall trend of information dissemination. Comparing these two models, we find out that there is no spreading threshold in RP, while there exists a spreading threshold in CP. The RP strategy induces a broader and faster information spreading process under the same parameters.

Cortical thickness patterns as state biomarker of anorexia nervosa.

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Lavagnino, Luca; Mwangi, Benson; Cao, Bo; Shott, Megan E; Soares, Jair C; Frank, Guido K W

2018-03-01

Only few studies have investigated cortical thickness in anorexia nervosa (AN), and it is unclear whether patterns of altered cortical thickness can be identified as biomarkers for AN. Cortical thickness was measured in 19 adult women with restricting-type AN, 24 individuals recovered from restricting-type AN (REC-AN) and 24 healthy controls. Those individuals with current or recovered from AN had previously shown altered regional cortical volumes across orbitofrontal cortex and insula. A linear relevance vector machine-learning algorithm estimated patterns of regional thickness across 24 subdivisions of those regions. Region-based analysis showed higher cortical thickness in AN and REC-AN, compared to controls, in the right medial orbital (olfactory) sulcus, and greater cortical thickness for short insular gyri in REC-AN versus controls bilaterally. The machine-learning algorithm identified a pattern of relatively higher right orbital, right insular and left middle frontal cortical thickness, but lower left orbital, right middle and inferior frontal, and bilateral superior frontal cortical thickness specific to AN versus controls (74% specificity and 74% sensitivity, χ 2 p < .004); predicted probabilities differed significantly between AN and controls (p < .023). No pattern significantly distinguished the REC-AN group from controls. Higher cortical thickness in medial orbitofrontal cortex and insula probably contributes to higher gray matter volume in AN in those regions. The machine-learning algorithm identified a mixed pattern of mostly higher orbital and insular, but relatively lower superior frontal cortical thickness in individuals with current AN. These novel results suggest that regional cortical thickness patterns could be state markers for AN. © 2018 Wiley Periodicals, Inc.

Volumetric MRI analysis of the amygdala and the hippocampus in patients with major depression

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Xia Jun; Zhou Yicheng; Zhang Jingfeng; Yang Bo; Xia Liming; Wang Chengyuan; Chen Jun

2005-01-01

Objective: To study the MRI volume of the amygdala and hippocampus in patients with major depression. Methods: Quantitative MRI of the amygdala and hippocampus was studied in 22 patients with major depression and compared with 13 age-matched controls. Results: Both groups exhibited similar significant hippocampal asymmetry (left smaller than right). The volume of the bilateral hippocampus was significantly smaller in the patient group than that in the controls (left: t=9.96, P<0.01; right: t=11.88, P<0.01). The right amygdala was smaller in the patient group than that in the control group (t=5.50, P<0.01), No correlation was found between the hippocampal volume abnormalities and the course of disease. Conclusion: These findings support the hypothesis that the hippocampus and amygdala within limbic-cortical networks may play a crucial role in the pathogenesis of major depression. (authors)

Evidence for Neuroplastic Compensation in the Cerebral Cortex of Persons with Depressive Illness

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Bansal, Ravi; Hellerstein, David J.; Peterson, Bradley S.

2017-01-01

We yoked anatomical brain Magnetic Resonance Imaging to a randomized, double-blind, placebo-controlled trial (RCT) of antidepressant medication for 10-week’s duration in patients with dysthymia. The RCT study design mitigated ascertainment bias by randomizing patients to receive either duloxetine or placebo, and it supported true causal inferences about treatment effects on the brain by controlling treatment assignment experimentally. We acquired 121 anatomical scans: at baseline and endpoint in 41 patients, and once in 39 healthy controls. At baseline, patients had diffusely thicker cortices than did healthy participants, and patients who had thicker cortices had proportionately less severe symptoms. During the trial, symptoms improved significantly more in medication- compared with placebo-treated patients; concurrently, thicknesses in medication-treated patients declined toward values in healthy controls, but they increased slightly, away from control values, in placebo-treated patients. Changes in symptom severity during the trial mediated the association of treatment assignment with the change in thickness, suggesting that the beneficial effects of medication on symptom severity were at least partially responsible for normalizing cortical thickness. Together our findings suggest that baseline cortical hypertrophy in medication-free patients likely represented a compensatory, neuroplastic response that attenuated symptom severity. Medication then reduced symptoms and lessened the need for compensation, thereby normalizing thickness. This is to the best of our knowledge the first study to report within an RCT a differential change in cortical morphology during medication treatment for depressive illness and the first to provide within an RCT in vivo evidence for the presence of neuroanatomical plasticity in humans. PMID:28265119

Widespread cortical thinning in patients with neuromyelitis optica spectrum disorder.

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Kim, S-H; Kwak, K; Hyun, J-W; Jeong, I H; Jo, H-J; Joung, A; Kim, J-H; Lee, S H; Yun, S; Joo, J; Lee, J-M; Kim, H J

2016-07-01

Studies on cortical involvement and its relationship with cognitive function in patients with neuromyelitis optica spectrum disorder (NMOSD) remain scarce. The objective of this study was to compare cortical thickness on magnetic resonance imaging (MRI) between patients with NMOSD and multiple sclerosis (MS) and to investigate its relationship with clinical features and cognitive function. This observational clinical imaging study of 91 patients with NMOSD, 52 patients with MS and 44 healthy controls was conducted from 1 December 2013 to 30 April 2015 at the institutional referral center. Three tesla MRI of the brain and neuropsychological tests were performed. Cortical thickness was measured using three-dimensional surface-based analysis. Both sets of patients exhibited cortical thinning throughout the entire brain cortex. Patients with MS showed a significantly greater reduction in cortical thickness over broad regions of the bilateral frontal and parieto-temporal cortices and the left precuneus compared to those with NMOSD. Memory functions in patients with MS were correlated with broad regional cortical thinning, whereas no significant associations were observed between cortical thickness and cognitive function in patients with NMOSD. Widespread cortical thinning was observed in patients with NMOSD and MS, but the extent of cortical thinning was greater in patients with MS. The more severe cortical atrophy may contribute to memory impairment in patients with MS but not in those with NMOSD. These results provide in vivo evidence that the severity and clinical relevance of cortical thinning differ between NMOSD and MS. © 2016 EAN.

The Diversity of Cortical Inhibitory Synapses

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Yoshiyuki eKubota

2016-04-01

Full Text Available The most typical and well known inhibitory action in the cortical microcircuit is a strong inhibition on the target neuron by axo-somatic synapses. However, it has become clear that synaptic inhibition in the cortex is much more diverse and complicated. Firstly, at least ten or more inhibitory non-pyramidal cell subtypes engage in diverse inhibitory functions to produce the elaborate activity characteristic of the different cortical states. Each distinct non-pyramidal cell subtype has its own independent inhibitory function. Secondly, the inhibitory synapses innervate different neuronal domains, such as axons, spines, dendrites and soma, and their IPSP size is not uniform. Thus cortical inhibition is highly complex, with a wide variety of anatomical and physiological modes. Moreover, the functional significance of the various inhibitory synapse innervation styles and their unique structural dynamic behaviors differ from those of excitatory synapses. In this review, we summarize our current understanding of the inhibitory mechanisms of the cortical microcircuit.

Cortical Plasticity Induction by Pairing Subthalamic Nucleus Deep-Brain Stimulation and Primary Motor Cortical Transcranial Magnetic Stimulation in Parkinson's Disease.

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Udupa, Kaviraja; Bahl, Nina; Ni, Zhen; Gunraj, Carolyn; Mazzella, Filomena; Moro, Elena; Hodaie, Mojgan; Lozano, Andres M; Lang, Anthony E; Chen, Robert

2016-01-13

Noninvasive brain stimulation studies have shown abnormal motor cortical plasticity in Parkinson's disease (PD). These studies used peripheral nerve stimulation paired with transcranial magnetic stimulation (TMS) to primary motor cortex (M1) at specific intervals to induce plasticity. Induction of cortical plasticity through stimulation of the basal ganglia (BG)-M1 connections has not been studied. In the present study, we used a novel technique of plasticity induction by repeated pairing of deep-brain stimulation (DBS) of the BG with M1 stimulation using TMS. We hypothesize that repeated pairing of subthalamic nucleus (STN)-DBS and M1-TMS at specific time intervals will lead to plasticity in the M1. Ten PD human patients with STN-DBS were studied in the on-medication state with DBS set to 3 Hz. The interstimulus intervals (ISIs) between STN-DBS and TMS that produced cortical facilitation were determined individually for each patient. Three plasticity induction conditions with repeated pairings (180 times) at specific ISIs (∼ 3 and ∼ 23 ms) that produced cortical facilitation and a control ISI of 167 ms were tested in random order. Repeated pairing of STN-DBS and M1-TMS at short (∼ 3 ms) and medium (∼ 23 ms) latencies increased M1 excitability that lasted for at least 45 min, whereas the control condition (fixed ISI of 167 ms) had no effect. There were no specific changes in motor thresholds, intracortical circuits, or recruitment curves. Our results indicate that paired-associative cortical plasticity can be induced by repeated STN and M1 stimulation at specific intervals. These results show that STN-DBS can modulate cortical plasticity. We introduced a new experimental paradigm to test the hypothesis that pairing subthalamic nucleus deep-brain stimulation (STN-DBS) with motor cortical transcranial magnetic stimulation (M1-TMS) at specific times can induce cortical plasticity in patients with Parkinson's disease (PD). We found that repeated pairing of STN

Mild traumatic brain injury is associated with reduced cortical thickness in those at risk for Alzheimer's disease.

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Hayes, Jasmeet P; Logue, Mark W; Sadeh, Naomi; Spielberg, Jeffrey M; Verfaellie, Mieke; Hayes, Scott M; Reagan, Andrew; Salat, David H; Wolf, Erika J; McGlinchey, Regina E; Milberg, William P; Stone, Annjanette; Schichman, Steven A; Miller, Mark W

2017-03-01

Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. Whole-genome polygenic risk scores for the development of Alzheimer's disease were calculated using summary statistics from the largest Alzheimer's disease genome-wide association study to date. Results showed that mild traumatic brain injury moderated the relationship between genetic risk for Alzheimer's disease and cortical thickness, such that individuals with mild traumatic brain injury and high genetic risk showed reduced cortical thickness in Alzheimer's disease-vulnerable regions. Among males with mild traumatic brain injury, high genetic risk for Alzheimer's disease was associated with cortical thinning as a function of time since injury. A moderated mediation analysis showed that mild traumatic brain injury and high genetic risk indirectly influenced episodic memory performance through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brain regions is a mechanism for reduced memory performance. Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance

Reboxetine Enhances the Olanzapine-Induced Antipsychotic-Like Effect, Cortical Dopamine Outflow and NMDA Receptor-Mediated Transmission

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Marcus, Monica M; Jardemark, Kent; Malmerfelt, Anna; Björkholm, Carl; Svensson, Torgny H

2010-01-01

Preclinical data have shown that addition of the selective norepinephrine transporter (NET) inhibitor reboxetine increases the antipsychotic-like effect of the D2/3 antagonist raclopride and, in parallel, enhances cortical dopamine output. Subsequent clinical results suggested that adding reboxetine to stable treatments with various antipsychotic drugs (APDs) may improve positive, negative and depressive symptoms in schizophrenia. In this study, we investigated in rats the effects of adding reboxetine to the second-generation APD olanzapine on: (i) antipsychotic efficacy, using the conditioned avoidance response (CAR) test, (ii) extrapyramidal side effect (EPS) liability, using a catalepsy test, (iii) dopamine efflux in the medial prefrontal cortex and the nucleus accumbens, using in vivo microdialysis in freely moving animals and (iv) cortical N-methyl--aspartate (NMDA) receptor-mediated transmission, using intracellular electrophysiological recording in vitro. Reboxetine (6 mg/kg) enhanced the suppression of CAR induced by a suboptimal dose (1.25 mg/kg), but not an optimal (2.5 mg/kg) dose of olanzapine without any concomitant catalepsy. Addition of reboxetine to the low dose of olanzapine also markedly increased cortical dopamine outflow and facilitated prefrontal NMDA receptor-mediated transmission. Our data suggest that adjunctive treatment with a NET inhibitor may enhance the therapeutic effect of low-dose olanzapine in schizophrenia without increasing EPS liability and add an antidepressant action, thus in principle allowing for a dose reduction of olanzapine with a concomitant reduction of dose-related side effects, such as EPS and weight gain. PMID:20463659

Emergence of depression following job loss prospectively predicts lower rates of reemployment.

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Stolove, Catherine A; Galatzer-Levy, Isaac R; Bonanno, George A

2017-07-01

Job loss has been associated with the emergence of depression and subsequent long-term diminished labor market participation. In a sample of 500 adults who lost their jobs, trajectories of depression severity from four years before to four years after job loss were identified using Latent Growth Mixture Modeling. Rates of unemployment by trajectory were compared at two and four years following job loss. Four trajectories demonstrated optimal model fit including resilience (72%), chronic pre-to-post job loss depression (9%), emergent depression (10%), and remitting depression (9%). Logistic regression comparing reemployment status by class while controlling for age, gender, and education at two-years post job loss revealed no significant differences by class. An identical logistic regression on four-year reemployment revealed significant differences by class with post-hoc analyses revealing emergent depression resulting in a 33.3% reemployment rate compared to resilient individuals (60.4%) together indicating that depression affects reemployment rather than lack of reemployment causing the emergence of depression. The emergence of depression following job loss significantly increases the risk of continued unemployment. However, observed high rates of resilience with resulting downstream benefits in reemployment mitigates significant concern about the effects of wide spread unemployment on ongoing global economic recovery following the Great Recession. Copyright © 2017 Elsevier Ireland Ltd. All rights reserved.

Cerebrospinal fluid space alterations in melancholic depression.

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Esther Via

Full Text Available Melancholic depression is a biologically homogeneous clinical entity in which structural brain alterations have been described. Interestingly, reports of structural alterations in melancholia include volume increases in Cerebro-Spinal Fluid (CSF spaces. However, there are no previous reports of CSF volume alterations using automated whole-brain voxel-wise approaches, as tissue classification algorithms have been traditionally regarded as less reliable for CSF segmentation. Here we aimed to assess CSF volumetric alterations in melancholic depression and their clinical correlates by means of a novel segmentation algorithm ('new segment', as implemented in the software Statistical Parametric Mapping-SPM8, incorporating specific features that may improve CSF segmentation. A three-dimensional Magnetic Resonance Image (MRI was obtained from seventy patients with melancholic depression and forty healthy control subjects. Although imaging data were pre-processed with the 'new segment' algorithm, in order to obtain a comparison with previous segmentation approaches, tissue segmentation was also performed with the 'unified segmentation' approach. Melancholic patients showed a CSF volume increase in the region of the left Sylvian fissure, and a CSF volume decrease in the subarachnoid spaces surrounding medial and lateral parietal cortices. Furthermore, CSF increases in the left Sylvian fissure were negatively correlated with the reduction percentage of depressive symptoms at discharge. None of these results were replicated with the 'unified segmentation' approach. By contrast, between-group differences in the left Sylvian fissure were replicated with a non-automated quantification of the CSF content of this region. Left Sylvian fissure alterations reported here are in agreement with previous findings from non-automated CSF assessments, and also with other reports of gray and white matter insular alterations in depressive samples using automated approaches

OBscure but not OBsolete: Perturbations of the frontal cortex in common between rodent olfactory bulbectomy model and major depression.

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Rajkumar, Ramamoorthy; Dawe, Gavin S

2018-04-07

Olfactory bulbectomy (OBX) has been used as a model of depression over several decades. This model presupposes a mechanism that is still not proven in clinical depression. A wealth of clinical literature has focused on the derangements in frontal cortex (prefrontal, orbitofrontal and anterior cingulate cortices) associated with depression. In this comprehensive review, anatomical, electrophysiological and molecular sequelae of bulbectomy in the rodent frontal cortex are explored and compared with findings on brains of humans with major depression. Certain commonalities in neurobiological features of the perturbed frontal cortex in the bulbectomised rodent and the depressed human brain are evident. Also, meta-analysis reports on clinical studies on depressed patients provide prima facie evidence that perturbations in the frontal cortex are associated with major depression. Analysing the pattern of perturbations in the chemical neuroanatomy of the frontal cortex will contribute to understanding of the neurobiology of depression. Revisiting the OBX model of depression to examine these neurobiological changes in frontal cortex with contemporary imaging, proteomics, lipidomics, metabolomics and epigenomics technologies is proposed as an approach to enhance the translational value of this animal model to facilitate identification of targets and biomarkers for clinical depression. Copyright © 2018 Elsevier B.V. All rights reserved.

Reverse preferential spread in complex networks

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Toyoizumi, Hiroshi; Tani, Seiichi; Miyoshi, Naoto; Okamoto, Yoshio

2012-08-01

Large-degree nodes may have a larger influence on the network, but they can be bottlenecks for spreading information since spreading attempts tend to concentrate on these nodes and become redundant. We discuss that the reverse preferential spread (distributing information inversely proportional to the degree of the receiving node) has an advantage over other spread mechanisms. In large uncorrelated networks, we show that the mean number of nodes that receive information under the reverse preferential spread is an upper bound among any other weight-based spread mechanisms, and this upper bound is indeed a logistic growth independent of the degree distribution.

Age Effects on Cortical Thickness in Cognitively Normal Elderly Individuals

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Sona Hurtz

2014-07-01

Full Text Available Background/Aims: Atrophy in both grey and white matter is found in normal aging. The prefrontal cortex and the frontal lobe white matter are thought to be the most affected regions. Our aim was to examine the effects of normal aging on cortical grey matter using a 3D quantitative cortical mapping method. Methods: We analyzed 1.5-tesla brain magnetic resonance imaging data from 44 cognitively normal elderly subjects using cortical pattern matching and cortical thickness analyses. Linear regression analysis was used to study the effect of age on cortical thickness. 3D map-wide correction for multiple comparisons was conducted with permutation analyses using a threshold of p Results: We found a significant negative association between age and cortical thickness in the right hemisphere (pcorrected = 0.009 and a trend level association in the left hemisphere (pcorrected = 0.081. Age-related changes were greatest in the sensorimotor, bilateral dorsal anterior cingulate and supplementary motor cortices, and the right posterior middle and inferior frontal gyri. Age effects greater in the medial than lateral visual association cortices were also seen bilaterally. Conclusion: Our novel method further validates that normal aging results in diffuse cortical thinning that is most pronounced in the frontal and visual association cortices.

Major depressive disorder is associated with abnormal interoceptive activity and functional connectivity in the insula.

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Avery, Jason A; Drevets, Wayne C; Moseman, Scott E; Bodurka, Jerzy; Barcalow, Joel C; Simmons, W Kyle

2014-08-01

Somatic complaints and altered interoceptive awareness are common features in the clinical presentation of major depressive disorder (MDD). Recently, neurobiological evidence has accumulated demonstrating that the insula is one of the primary cortical structures underlying interoceptive awareness. Abnormal interoceptive representation within the insula may thus contribute to the pathophysiology and symptomatology of MDD. We compared functional magnetic resonance imaging blood oxygenation level-dependent responses between 20 unmedicated adults with MDD and 20 healthy control participants during a task requiring attention to visceral interoceptive sensations and also assessed the relationship of this blood oxygenation level-dependent response to depression severity, as rated using the Hamilton Depression Rating Scale. Additionally, we examined between-group differences in insula resting-state functional connectivity and its relationship to Hamilton Depression Rating Scale ratings of depression severity. Relative to the healthy control subjects, unmedicated MDD subjects exhibited decreased activity bilaterally in the dorsal mid-insula cortex (dmIC) during interoception. Activity within the insula during the interoceptive attention task was negatively correlated with both depression severity and somatic symptom severity in depressed subjects. Major depressive disorder also was associated with greater resting-state functional connectivity between the dmIC and limbic brain regions implicated previously in MDD, including the amygdala, subgenual prefrontal cortex, and orbitofrontal cortex. Moreover, functional connectivity between these regions and the dmIC was positively correlated with depression severity. Major depressive disorder and the somatic symptoms of depression are associated with abnormal interoceptive representation within the insula. © 2013 Society of Biological Psychiatry Published by Society of Biological Psychiatry All rights reserved.

How Is Mono Spread?

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... How Is Mono Spread? Print My sister has mononucleosis. I drank out of her drink before we ... that I have mono now? – Kyle* Mono, or mononucleosis, is spread through direct contact with saliva. This ...

Cortical changes in cerebral small vessel diseases: a 3D MRI study of cortical morphology in CADASIL

International Nuclear Information System (INIS)

Jouvent, E.; Bousser, M.G.; Chabriat, H.; Jouvent, E.; Bousser, M.G.; Chabriat, H.; Porcher, R.; Viswanathan, A.; Viswanathan, A.; Viswanathan, A.; O'Sullivan, M.; Dichgans, M.; Guichard, J.P.

2008-01-01

Brain atrophy represents a key marker of disease progression in cerebrovascular disorders. The 3D changes of cortex morphology occurring during the course of small vessel diseases of the brain (SVDB) remain poorly understood. The objective of this study was to assess the changes affecting depth and surface area of cortical sulci and their clinical and radiological correlates in a cohort of patients with cerebral autosomal dominant arteriolopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a genetic SVDB. Data were obtained from a series of 69 CADASIL patients. Validated methods were used to determine depth and surface area of four cortical sulci. The ratio of brain to intracranial cavity volumes (brain parenchymal fraction-BPF), volume of lacunar lesions (LL) and of white matter hyper-intensities, number of cerebral micro-haemorrhages, and mean apparent diffusion coefficient were also measured. Association between depth and surface area of the cortical sulci and BPF, clinical status and subcortical MRI lesions were tested. Depth and surface area of cortical sulci obtained in 54 patients were strongly correlated with both cognitive score and disability scales. Depth was related to the extent of subcortical lesions, surface area was related only to age. In additional analyses, the depth of the cingular sulcus was independently associated with the volume of LL (P 0.001), and that of the superior frontal sulcus with the mean apparent diffusion coefficient (P 0.003). In CADASIL, important morphological changes of cortical sulci occur in association with clinical worsening,extension of subcortical tissue damage and progression of global cerebral atrophy. These results suggest that the examination of cortical morphology may be of high clinical relevance in SVDB. (authors)

Prominent microglial activation in cortical white matter is selectively associated with cortical atrophy in primary progressive aphasia.

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Ohm, Daniel T; Kim, Garam; Gefen, Tamar; Rademaker, Alfred; Weintraub, Sandra; Bigio, Eileen; Mesulam, M-Marsel; Rogalski, Emily; Geula, Changiz

2018-04-21

Primary progressive aphasia (PPA) is a clinical syndrome characterized by selective language impairments associated with focal cortical atrophy favouring the language dominant hemisphere. PPA is associated with Alzheimer's disease (AD), frontotemporal lobar degeneration (FTLD), and significant accumulation of activated microglia. Activated microglia can initiate an inflammatory cascade that may contribute to neurodegeneration, but their quantitative distribution in cortical white matter and their relationship with cortical atrophy are unknown. We investigated white matter activated microglia and their association with grey matter atrophy in 10 PPA cases with either AD or FTLD-TDP pathology. Activated microglia were quantified with optical density measures of HLA-DR immunoreactivity in two regions with peak cortical atrophy, and one non-atrophied region within the language dominant hemisphere of each PPA case. Non-atrophied contralateral homologues of the language dominant regions were examined for hemispheric asymmetry. Qualitatively, greater densities of activated microglia were observed in cortical white matter when compared to grey matter. Quantitative analyses revealed significantly greater densities of activated microglia in the white matter of atrophied regions compared to non-atrophied regions in the language dominant hemisphere (p<0.05). Atrophied regions of the language dominant hemisphere also showed significantly more activated microglia compared to contralateral homologues (p<0.05). White matter activated microglia accumulate more in atrophied regions in the language dominant hemisphere of PPA. While microglial activation may constitute a response to neurodegenerative processes in white matter, the resultant inflammatory processes may also exacerbate disease progression and contribute to cortical atrophy. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.

Acute hepatic encephalopathy with diffuse cortical lesions

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Arnold, S.M.; Spreer, J.; Schumacher, M. [Section of Neuroradiology, Univ. of Freiburg (Germany); Els, T. [Dept. of Neurology, University of Freiburg (Germany)

2001-07-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Acute hepatic encephalopathy with diffuse cortical lesions

International Nuclear Information System (INIS)

Arnold, S.M.; Spreer, J.; Schumacher, M.; Els, T.

2001-01-01

Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. (orig.)

Post-adolescent developmental changes in cortical complexity.

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Sandu, Anca-Larisa; Izard, Edouard; Specht, Karsten; Beneventi, Harald; Lundervold, Arvid; Ystad, Martin

2014-11-27

Post-adolescence is known to be a period of general maturation and development in the human brain. In brain imaging, volumetric and morphologic cortical grey-matter changes can easily be assessed, but the analysis of cortical complexity seems to have been broadly neglected for this age interval. Magnetic resonance imaging (MRI) was used to acquire structural brain images. The study involved 17 adolescents (mean age 14.1 ± 0.27, 11 girls) who were compared with 14 young adults (mean age 24.24 ± 2.76, 7 women) for measures of brain complexity (fractal dimension--FD), grey matter (GM) volume and surface-area of cortical ribbon. FD was calculated using box-counting and Minkowski-Bouligand methods; FD and GM volume were measured for the whole brain, each hemisphere and lobes: frontal, occipital, parietal and temporal. The results show that the adults have a lower cortical complexity than the adolescents, which was significant for whole brain, left and right hemisphere, frontal and parietal lobes for both genders; and only for males in left temporal lobe. The GM volume was smaller in men than in boys for almost all measurements, and smaller in women than in girls just for right parietal lobe. A significant Pearson correlation was found between FD and GM volume for whole brain and each hemisphere in both genders. The decrease of the GM surface-area was significant in post-adolescence for males, not for females. During post-adolescence there are common changes in cortical complexity in the same regions for both genders, but there are also gender specific changes in some cortical areas. The sex differences from different cortical measurements (FD, GM volume and surface-area of cortical ribbon) could suggest a maturation delay in specific brain regions for each gender in relation to the other and might be explained through the functional role of the corresponding regions reflected in gender difference of developed abilities.

Cortical areas involved in Arabic number reading.

Science.gov (United States)

Roux, F-E; Lubrano, V; Lauwers-Cances, V; Giussani, C; Démonet, J-F

2008-01-15

Distinct functional pathways for processing words and numbers have been hypothesized from the observation of dissociated impairments of these categories in brain-damaged patients. We aimed to identify the cortical areas involved in Arabic number reading process in patients operated on for various brain lesions. Direct cortical electrostimulation was prospectively used in 60 brain mappings. We used object naming and two reading tasks: alphabetic script (sentences and number words) and Arabic number reading. Cortical areas involved in Arabic number reading were identified according to location, type of interference, and distinctness from areas associated with other language tasks. Arabic number reading was sustained by small cortical areas, often extremely well localized (area (Brodmann area 45), the anterior part of the dominant supramarginal gyrus (Brodmann area 40; p area (Brodmann area 37; p areas.

"Loser" or "Popular"?: Neural response to social status words in adolescents with major depressive disorder.

Science.gov (United States)

Silk, Jennifer S; Lee, Kyung Hwa; Kerestes, Rebecca; Griffith, Julianne M; Dahl, Ronald E; Ladouceur, Cecile D

2017-12-01

Concerns about social status are ubiquitous during adolescence, with information about social status often conveyed in text formats. Depressed adolescents may show alterations in the functioning of neural systems supporting processing of social status information. We examined whether depressed youth exhibited altered neural activation to social status words in temporal and prefrontal cortical regions thought to be involved in social cognitive processing, and whether this response was associated with development. Forty-nine adolescents (ages 10-18; 35 female), including 20 with major depressive disorder and 29 controls, were scanned while identifying the valence of words that connoted positive and negative social status. Results indicated that depressed youth showed reduced late activation to social status (vs neutral) words in the superior temporal cortex (STC) and medial prefrontal cortex (MPFC); whereas healthy youth did not show any significant differences between word types. Depressed youth also showed reduced late activation in the dorsolateral prefrontal cortex and fusiform gyrus to negative (vs positive) social status words; whereas healthy youth showed the opposite pattern. Finally, age was positively associated with MPFC activation to social status words. Findings suggest that hypoactivation in the "social cognitive brain network" might be implicated in altered interpersonal functioning in adolescent depression. Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.

Cortical gamma-aminobutyric acid and glutamate in posttraumatic stress disorder and their relationships to self-reported sleep quality.

Science.gov (United States)

Meyerhoff, Dieter J; Mon, Anderson; Metzler, Thomas; Neylan, Thomas C

2014-05-01

To test if posttraumatic stress disorder (PTSD) is associated with low brain gamma-aminobutyric acid (GABA) levels and if reduced GABA is mediated by poor sleep quality. Laboratory study using in vivo proton magnetic resonance spectroscopy (1H MRS) and behavioral testing. VA Medical Center Research Service, Psychiatry and Radiology. Twenty-seven patients with PTSD (PTSD+) and 18 trauma-exposed controls without PTSD (PTSD-), recruited from United States Army reservists, Army National Guard, and mental health clinics. None. 1H MRS at 4 Tesla yielded spectra from three cortical brain regions. In parieto-occipital and temporal cortices, PTSD+ had lower GABA concentrations than PTSD-. As expected, PTSD+ had higher depressive and anxiety symptom scores and a higher Insomnia Severity Index (ISI) score. Higher ISI correlated with lower GABA and higher glutamate levels in parieto-occipital cortex and tended to correlate with lower GABA in the anterior cingulate. The relationship between parieto-occipital GABA and PTSD diagnosis was fully mediated through insomnia severity. Lower N-acetylaspartate and glutamate concentrations in the anterior cingulate cortex correlated with higher arousal scores, whereas depressive and anxiety symptoms did generally not influence metabolite concentrations. Low brain gamma-aminobutyric acid (GABA) concentration in posttraumatic stress disorder (PTSD) is consistent with most findings in panic and social anxiety disorders. Low GABA associated with poor sleep quality is consistent with the hyperarousal theory of both primary insomnia and PTSD. Our data demonstrate that poor sleep quality mediates low parieto-occipital GABA in PTSD. The findings have implications for PTSD treatment approaches.

Cortical enhancement in chronic subdural hematoma

International Nuclear Information System (INIS)

Taguchi, Yoshio; Sato, Jun; Makita, Tadatoshi; Hayashi, Shigetoshi; Nakamura, Norio.

1981-01-01

In the CT findings of chronic subdural hematoma, brain enhancement adjacent to a subdural hematoma was seen occasionally after the injection of a contrast material. The authors called this finding ''cortical enhancement'', and 35 cases of chronic subdural hematoma were studied concerning cortical enhancement in relation to age, clinical signs and symptoms, hematoma density, and volume of the hematoma. Eight cases out of the 35 were subjected to measurements of the regional cerebral blood flow preoperatively by the method of the carotid injection of Xe-133. Cortical enhancement was apt to be seen in the cases which revealed intracranial hypertension or disturbance of consciousness, in isodensity or mixed-density hematomas, and in huge subdural hematomas. There was no specific correlation with age distribution. The pathogenesis of cortical enhancement seemed to be the result of cerebral compression with an increase in the contrast material per unit of volume and a prolonged venous outflow from the hemisphere, but no characteristic feature was detected in the average regional cerebral blood flow in our cases. (author)

rCBF change in the brain of patients with major depressive disorder

International Nuclear Information System (INIS)

Sun Da; Xu Wei; Zhan Hongwei; Liu Hongbiao

2010-01-01

Purpose Major depressive disorder is a frequent emotional mood disorder. To evaluate the changes of brain blood flow in patients with depressive disorder and the correlation between rCBF and clinical feature is very important to diagnosis and treatment of this decease. Methods: Regional cerebral perfusion was investigated using SPECT in 75 patients with depressive disorders. The mean ages of the patients were 41.9 (17-74) Years old. The course of disease was different from several days to over 20 years. Results: 97.3 per cent of patients (73/75) had relative hypoperfusions in some cerebral regions. The patients had a significant decrease of rCBF in the frontal lobesbilaterally, and temporal lobes, basal ganglia, thalamus and parietal lobe. The course of disease and age of the patients had a negative correlation with the changes of rCBF. Conclusion: According to the results of our study, patients with depressive disorders had profound dysfunction of the frontal lobes bilaterally. The temporal cortices and basal ganglia were involved in most patients too. It is coincident with the results of other studies. The function of frontal lobes and temporal lobes is close relation close with affective action, attention, memory, thinking, abstraction, and other brain cognitive function. The clinical symptom of depressive disorder may be relevant with hypoperfusions of frontal lobes and temporal lobes. (authors)

Hybrid spread spectrum radio system

Science.gov (United States)

Smith, Stephen F [London, TN; Dress, William B [Camas, WA

2010-02-09

Systems and methods are described for hybrid spread spectrum radio systems. A method, includes receiving a hybrid spread spectrum signal including: fast frequency hopping demodulating and direct sequence demodulating a direct sequence spread spectrum signal, wherein multiple frequency hops occur within a single data-bit time and each bit is represented by chip transmissions at multiple frequencies.

Spatial integration and cortical dynamics.

OpenAIRE

Gilbert, C D; Das, A; Ito, M; Kapadia, M; Westheimer, G

1996-01-01

Cells in adult primary visual cortex are capable of integrating information over much larger portions of the visual field than was originally thought. Moreover, their receptive field properties can be altered by the context within which local features are presented and by changes in visual experience. The substrate for both spatial integration and cortical plasticity is likely to be found in a plexus of long-range horizontal connections, formed by cortical pyramidal cells, which link cells wi...

Somatostatin-expressing inhibitory interneurons in cortical circuits

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Iryna Yavorska

2016-09-01

Full Text Available Cortical inhibitory neurons exhibit remarkable diversity in their morphology, connectivity, and synaptic properties. Here, we review the function of somatostatin-expressing (SOM inhibitory interneurons, focusing largely on sensory cortex. SOM neurons also comprise a number of subpopulations that can be distinguished by their morphology, input and output connectivity, laminar location, firing properties, and expression of molecular markers. Several of these classes of SOM neurons show unique dynamics and characteristics, such as facilitating synapses, specific axonal projections, intralaminar input, and top-down modulation, which suggest possible computational roles. SOM cells can be differentially modulated by behavioral state depending on their class, sensory system, and behavioral paradigm. The functional effects of such modulation have been studied with optogenetic manipulation of SOM cells, which produces effects on learning and memory, task performance, and the integration of cortical activity. Different classes of SOM cells participate in distinct disinhibitory circuits with different inhibitory partners and in different cortical layers. Through these disinhibitory circuits, SOM cells help encode the behavioral relevance of sensory stimuli by regulating the activity of cortical neurons based on subcortical and intracortical modulatory input. Associative learning leads to long-term changes in the strength of connectivity of SOM cells with other neurons, often influencing the strength of inhibitory input they receive. Thus despite their heterogeneity and variability across cortical areas, current evidence shows that SOM neurons perform unique neural computations, forming not only distinct molecular but also functional subclasses of cortical inhibitory interneurons.

Reye's syndrome with cortical laminar necrosis: MRI

International Nuclear Information System (INIS)

Kinoshita, T.; Takahashi, S.; Ishii, K.; Higano, S.; Matsumoto, K.; Sakamoto, K.; Haginoya, K.; Iinuma, K.

1996-01-01

Serial MRI findings are described in two patients with Reye's syndrome, demonstrating diffuse cortical and white matter changes. In the acute stage, T2-weighted images showed subtle but definite laminar high signal and contrast-enhanced T1-weighted images laminar enhancement, along the entire cerebral cortex bilaterally. In the chronic stage, unenhanced T1-weighted images showed diffuse cortical laminar high signal. These characteristic MRI features seemed very similar to those of laminar cortical necrosis in hypoxic brain damage. MRI also displayed delayed white matter changes with cerebral atrophy. (orig.)

Autosomal dominant arteriopathy with sub cortical infarcts and leucoencephalopathy (CADASIL)

International Nuclear Information System (INIS)

Ojeda, Adriana; Tiezzi, Gerardo; Uriarte, Ana M.; Eguren, Leonor

2002-01-01

Cerebral autosomal dominant arteriopathy with sub cortical infarcts and leucoencephalopathy (CASADIL) is a systemic hereditary, vascular disease that involves small arteries. Recurrent ischemia, pseudo bulbar paralysis and dementia are characteristic. Other manifestations include migraine and depression. We report an Argentine family with VI generations with evidence of disease in IV. MR examinations were performed on 21 family members (both symptomatic and asymptomatic). The main findings on MR on symptomatic and asymptomatic patients were small lesions with high signal on T2 localised in periventricular white matter, brain stem, basal ganglia and thalamus, and confluent patches on white matter although with high signal on T2 images, usually symmetric. In conclusion we can assess that diffuse myelin loss and small infarcts occurring in cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy well demonstrated with MR. In addition, some of the abnormalities in pre symptomatic patients can be identified on MR images. (author)

Cortical thickness abnormalities in late adolescence with online gaming addiction.

Science.gov (United States)

Yuan, Kai; Cheng, Ping; Dong, Tao; Bi, Yanzhi; Xing, Lihong; Yu, Dahua; Zhao, Limei; Dong, Minghao; von Deneen, Karen M; Liu, Yijun; Qin, Wei; Tian, Jie

2013-01-01

Online gaming addiction, as the most popular subtype of Internet addiction, had gained more and more attention from the whole world. However, the structural differences in cortical thickness of the brain between adolescents with online gaming addiction and healthy controls are not well unknown; neither was its association with the impaired cognitive control ability. High-resolution magnetic resonance imaging scans from late adolescence with online gaming addiction (n = 18) and age-, education- and gender-matched controls (n = 18) were acquired. The cortical thickness measurement method was employed to investigate alterations of cortical thickness in individuals with online gaming addiction. The color-word Stroop task was employed to investigate the functional implications of the cortical thickness abnormalities. Imaging data revealed increased cortical thickness in the left precentral cortex, precuneus, middle frontal cortex, inferior temporal and middle temporal cortices in late adolescence with online gaming addiction; meanwhile, the cortical thicknesses of the left lateral orbitofrontal cortex (OFC), insula, lingual gyrus, the right postcentral gyrus, entorhinal cortex and inferior parietal cortex were decreased. Correlation analysis demonstrated that the cortical thicknesses of the left precentral cortex, precuneus and lingual gyrus correlated with duration of online gaming addiction and the cortical thickness of the OFC correlated with the impaired task performance during the color-word Stroop task in adolescents with online gaming addiction. The findings in the current study suggested that the cortical thickness abnormalities of these regions may be implicated in the underlying pathophysiology of online gaming addiction.

Dynamic Causal Modeling of the Cortical Responses to Wrist Perturbations

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Yuan Yang

2017-09-01

Full Text Available Mechanical perturbations applied to the wrist joint typically evoke a stereotypical sequence of cortical and muscle responses. The early cortical responses (<100 ms are thought be involved in the “rapid” transcortical reaction to the perturbation while the late cortical responses (>100 ms are related to the “slow” transcortical reaction. Although previous studies indicated that both responses involve the primary motor cortex, it remains unclear if both responses are engaged by the same effective connectivity in the cortical network. To answer this question, we investigated the effective connectivity cortical network after a “ramp-and-hold” mechanical perturbation, in both the early (<100 ms and late (>100 ms periods, using dynamic causal modeling. Ramp-and-hold perturbations were applied to the wrist joint while the subject maintained an isometric wrist flexion. Cortical activity was recorded using a 128-channel electroencephalogram (EEG. We investigated how the perturbation modulated the effective connectivity for the early and late periods. Bayesian model comparisons suggested that different effective connectivity networks are engaged in these two periods. For the early period, we found that only a few cortico-cortical connections were modulated, while more complicated connectivity was identified in the cortical network during the late period with multiple modulated cortico-cortical connections. The limited early cortical network likely allows for a rapid muscle response without involving high-level cognitive processes, while the complexity of the late network may facilitate coordinated responses.

Human cerebral cortices: signal variation on diffusion-weighted MR imaging

Energy Technology Data Exchange (ETDEWEB)

Asao, Chiaki [Kumamoto Regional Medical Center, Department of Radiology, Kumamoto (Japan); National Hospital Organization Kumamoto Medical Center, Department of Radiology, Kumamoto (Japan); Hirai, Toshinori; Yamashita, Yasuyuki [Kumamoto University Graduate School of Medical Sciences, Department of Diagnostic Radiology, Kumamoto (Japan); Yoshimatsu, Shunji [National Hospital Organization Kumamoto Medical Center, Department of Radiology, Kumamoto (Japan); Matsukawa, Tetsuya; Imuta, Masanori [Kumamoto Regional Medical Center, Department of Radiology, Kumamoto (Japan); Sagara, Katsuro [Kumamoto Regional Medical Center, Department of Internal Medicine, Kumamoto (Japan)

2008-03-15

We have often encountered high signal intensity (SI) of the cingulate gyrus and insula during diffusion-weighted magnetic resonance imaging (DW-MRI) on neurologically healthy adults. To date, cortical signal heterogeneity on DW images has not been investigated systematically. The purpose of our study was to determine whether there is regional signal variation in the brain cortices of neurologically healthy adults on DW-MR images. The SI of the cerebral cortices on DW-MR images at 1.5 T was evaluated in 50 neurologically healthy subjects (34 men, 16 women; age range 33-84 years; mean age 57.6 years). The cortical SI in the cingulate gyrus, insula, and temporal, occipital, and parietal lobes was graded relative to the SI of the frontal lobe. Contrast-to-noise ratios (CNRs) on DW-MR images were compared for each cortical area. Diffusion changes were analyzed by visually assessment of the differences in appearance among the cortices on apparent diffusion coefficient (ADC) maps. Increased SI was frequently seen in the cingulate gyrus and insula regardless of patient age. There were no significant gender- or laterality-related differences. The CNR was significantly higher in the cingulate gyrus and insula than in the other cortices (p <.01), and significant differences existed among the cortical regions (p <.001). There were no apparent ADC differences among the cortices on ADC maps. Regional signal variation of the brain cortices was observed on DW-MR images of healthy subjects, and the cingulate gyrus and insula frequently manifested high SI. These findings may help in the recognition of cortical signal abnormalities as visualized on DW-MR images. (orig.)

Human cerebral cortices: signal variation on diffusion-weighted MR imaging

International Nuclear Information System (INIS)

Asao, Chiaki; Hirai, Toshinori; Yamashita, Yasuyuki; Yoshimatsu, Shunji; Matsukawa, Tetsuya; Imuta, Masanori; Sagara, Katsuro

2008-01-01

We have often encountered high signal intensity (SI) of the cingulate gyrus and insula during diffusion-weighted magnetic resonance imaging (DW-MRI) on neurologically healthy adults. To date, cortical signal heterogeneity on DW images has not been investigated systematically. The purpose of our study was to determine whether there is regional signal variation in the brain cortices of neurologically healthy adults on DW-MR images. The SI of the cerebral cortices on DW-MR images at 1.5 T was evaluated in 50 neurologically healthy subjects (34 men, 16 women; age range 33-84 years; mean age 57.6 years). The cortical SI in the cingulate gyrus, insula, and temporal, occipital, and parietal lobes was graded relative to the SI of the frontal lobe. Contrast-to-noise ratios (CNRs) on DW-MR images were compared for each cortical area. Diffusion changes were analyzed by visually assessment of the differences in appearance among the cortices on apparent diffusion coefficient (ADC) maps. Increased SI was frequently seen in the cingulate gyrus and insula regardless of patient age. There were no significant gender- or laterality-related differences. The CNR was significantly higher in the cingulate gyrus and insula than in the other cortices (p <.01), and significant differences existed among the cortical regions (p <.001). There were no apparent ADC differences among the cortices on ADC maps. Regional signal variation of the brain cortices was observed on DW-MR images of healthy subjects, and the cingulate gyrus and insula frequently manifested high SI. These findings may help in the recognition of cortical signal abnormalities as visualized on DW-MR images. (orig.)

Are the Symptoms of Parkinsonism Cortical in Origin?

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Gordon W. Arbuthnott

Full Text Available We present three reasons to suspect that the major deleterious consequence of dopamine loss from the striatum is a cortical malfunction. We suggest that it is cortex, rather than striatum, that should be considered as the source of the debilitating symptoms of Parkinson's disease (PD since: 1. Cortical synapses onto striatal dendritic spines are lost in PD. 2. All known treatments of the symptoms of PD disrupt beta oscillations. Oscillations that are also disrupted following antidromic activation of cortical neurons. 3. The final output of basal ganglia directly modulates thalamic connections to layer I of frontal cortical areas, regions intimately associated with motor behaviour.These three reasons combined with evidence that the current summary diagram of the basal ganglia involvement in PD is imprecise at best, suggest that a re-orientation of the treatment strategies towards cortical, rather than striatal malfunction, is overdue. Keywords: Parkinson's disease, Deep brain stimulation, Layer I, Motor cortex

Relating Cortical Wave Dynamics to Learning and Remembering

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Eduardo Mercado III

2014-12-01

Full Text Available Electrical waves propagate across sensory and motor cortices in stereotypical patterns. These waves have been described as potentially facilitating sensory processing when they travel through sensory cortex, as guiding movement preparation and performance when they travel across motor cortex, and as possibly promoting synaptic plasticity and the consolidation of memory traces, especially during sleep. Here, an alternative theoretical framework is suggested that integrates Pavlovian hypotheses about learning and cortical function with concepts from contemporary proceduralist theories of memory. The proposed framework postulates that sensory-evoked cortical waves are gradually modified across repeated experiences such that the waves more effectively differentiate sensory events, and so that the waves are more likely to reverberate. It is argued that the qualities of cortical waves—their origins, form, intensity, speed, periodicity, extent, and trajectories —are a function of both the structural organization of neural circuits and ongoing reverberations resulting from previously experienced events. It is hypothesized that experience-dependent cortical plasticity, both in the short- and long-term, modulates the qualities of cortical waves, thereby enabling individuals to make progressively more precise distinctions between complex sensory events, and to reconstruct components of previously experienced events. Unlike most current neurobiological theories of learning and memory mechanisms, this hypothesis does not assume that synaptic plasticity, or any other form of neural plasticity, serves to store physical records of previously experienced events for later reactivation. Rather, the reorganization of cortical circuits may alter the potential for certain wave patterns to arise and persist. Understanding what factors determine the spatiotemporal dynamics of cortical waves, how structural changes affect their qualities, and how wave dynamics

The stability of mandibular prognathism corrected by bilateral sagittal split osteotomies: a comparison of bi-cortical osteosynthesis and mono-cortical osteosynthesis.

Science.gov (United States)

Hsu, S S-P; Huang, C-S; Chen, P K-T; Ko, E W-C; Chen, Y-R

2012-02-01

This study evaluated the differences in surgical changes and post-surgical changes between bi-cortical and mono-cortical osteosynthesis (MCO) in the correction of skeletal Class III malocclusion with bilateral sagittal split osteotomies (BSSOs). Twenty-five patients had bi-cortical osteosynthesis (BCO), 32 patients had mono-cortical fixation. Lateral and postero-anterior cephalometric radiographs, taken at the time of surgery, before surgery, 1 month after surgery, and on completion of orthodontic treatment (mean 9.9 months after surgery), were obtained for evaluation. Cephalometric analysis and superimposition were used to investigate the surgical and post-surgical changes. Independent t-test was performed to compare the difference between the two groups. Pearson's correlations were tested to evaluate the factors related to the relapse of the mandible. The sagittal relapse rate was 20% in the bi-cortical and 25% in the mono-cortical group. The forward-upward rotation of the mandible in the post-surgical period contributed most of the sagittal relapse. There were no statistically significant differences in sagittal and vertical changes between the two groups during surgery and in the post-surgical period. No factors were found to correlate with post-surgical relapse, but the intergonial width increased more in the bi-cortical group. The study suggested that both methods of skeletal fixation had similar postoperative stability. Copyright © 2011 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.

Deficits in Beam-Walking After Neonatal Motor Cortical Lesions are not Spared by Fetal Cortical Transplants in Rats

OpenAIRE

Swenson, R. S.; Danielsen, E. H.; Klausen, B. S.; Erlich, E.; Zimmer, J.; Castro, A. J.

1989-01-01

Adult rats that sustained unilateral motor cortical lesions at birth demonstrated deficits in traversing an elevated narrow beam. These deficits, manifested by hindlimb slips off the edge of the beam, were not spared in animals that received fetal cortical transplants into the lesion cavity immediately after lesion placement.

A technetium-99m hexamethylpropylene amine oxime brain single-photon emission tomography study in adolescent patients with major depressive disorder

Energy Technology Data Exchange (ETDEWEB)

Tutus, A. [Department of Nuclear Medicine, Erciyes University School of Medicine, Kayseri (Turkey); Kibar, M. [Department of Nuclear Medicine, Cukurova University School of Medicine, Kayseri (Turkey); Sofuoglu, S.; Basturk, M.; Goenuel, A.S. [Department of Psychiatry, Erciyes University School of Medicine, Kayseri (Turkey)

1998-06-01

We have not encountered any brain single-photon emission tomography (SPET) study performed in adolescent depressed patients in the literature. Therefore, we used technetium-99m hexamethylpropylene amine oxime ({sup 99m}Tc-HMPAO) brain SPET in adolescent patients with major depressive disorder (MDD) to examine the possible changes in cerebral perfusion and the possible association between perfusion indices and clinical variables. Fourteen adolescent out-patients (nine females, five males; mean{+-}SD age: 13.11{+-}1.43 years; range: 11-15 years) fulfilling the DSM-IV criteria for MDD and 11 age-matched healthy control subjects (six females, five males; mean{+-}SD age: 13.80{+-}1.60 years; range: 12-15 years) were included in the study. {sup 99}Tc-HMPAO brain SPET was performed twice in the patient group and once in the control group. The first SPET investigation was performed under non-medicated conditions and the second was performed after depressive symptoms had subsided. A relative perfusion index (PI) was calculated as the ratio of regional cortical activity to the whole brain activity. We found significant differences between the PI values of the untreated depressed patients and those of the controls, indicating relatively reduced perfusion in the left anterofrontal and left temporal cortical areas. No significant differences in regional PI values were found between the remitted depressed patients and the controls. Our study suggests that adolescent patients with MDD may have regional cerebral blood flow deficits in frontal regions and a greater anterofrontal right-left perfusion asymmetry compared with normal subjects. The fact that these abnormalities in perfusion indices have a trend toward normal values with symptomatic improvement suggests that they may be state-dependent markers for adolescent MDD. (orig.) With 3 figs., 2 tabs., 37 refs.

A technetium-99m hexamethylpropylene amine oxime brain single-photon emission tomography study in adolescent patients with major depressive disorder

International Nuclear Information System (INIS)

Tutus, A.; Kibar, M.; Sofuoglu, S.; Basturk, M.; Goenuel, A.S.

1998-01-01

We have not encountered any brain single-photon emission tomography (SPET) study performed in adolescent depressed patients in the literature. Therefore, we used technetium-99m hexamethylpropylene amine oxime ( 99m Tc-HMPAO) brain SPET in adolescent patients with major depressive disorder (MDD) to examine the possible changes in cerebral perfusion and the possible association between perfusion indices and clinical variables. Fourteen adolescent out-patients (nine females, five males; mean±SD age: 13.11±1.43 years; range: 11-15 years) fulfilling the DSM-IV criteria for MDD and 11 age-matched healthy control subjects (six females, five males; mean±SD age: 13.80±1.60 years; range: 12-15 years) were included in the study. 99 Tc-HMPAO brain SPET was performed twice in the patient group and once in the control group. The first SPET investigation was performed under non-medicated conditions and the second was performed after depressive symptoms had subsided. A relative perfusion index (PI) was calculated as the ratio of regional cortical activity to the whole brain activity. We found significant differences between the PI values of the untreated depressed patients and those of the controls, indicating relatively reduced perfusion in the left anterofrontal and left temporal cortical areas. No significant differences in regional PI values were found between the remitted depressed patients and the controls. Our study suggests that adolescent patients with MDD may have regional cerebral blood flow deficits in frontal regions and a greater anterofrontal right-left perfusion asymmetry compared with normal subjects. The fact that these abnormalities in perfusion indices have a trend toward normal values with symptomatic improvement suggests that they may be state-dependent markers for adolescent MDD. (orig.)

Effects of vitamin K2 on cortical and cancellous bone mass, cortical osteocyte and lacunar system, and porosity in sciatic neurectomized rats.

Science.gov (United States)

Iwamoto, Jun; Matsumoto, Hideo; Takeda, Tsuyoshi; Sato, Yoshihiro; Yeh, James K

2010-09-01

The purpose of the present study was to examine the effects of vitamin K2 on cortical and cancellous bone mass, cortical osteocyte and lacunar system, and porosity in sciatic neurectomized rats. Thirty-four female Sprague-Dawley retired breeder rats were randomized into three groups: age-matched control, sciatic neurectomy (NX), and NX + vitamin K2 administration (menatetrenone, 30 mg/kg/day p.o., three times a week). At the end of the 8-week experiment, bone histomorphometric analysis was performed on cortical and cancellous bone of the tibial diaphysis and proximal metaphysis, respectively, and osteocyte lacunar system and porosity were evaluated on cortical bone of the tibial diaphysis. NX decreased cortical and cancellous bone mass compared with age-matched controls as a result of increased endocortical and trabecular bone erosion and decreased trabecular mineral apposition rate (MAR). Vitamin K2 ameliorated the NX-induced increase in bone erosion, prevented the NX-induced decrease in MAR, and increased bone formation rate (BFR/bone surface) in cancellous bone, resulting in an attenuation of NX-induced cancellous bone loss. However, vitamin K2 did not significantly influence cortical bone mass. NX also decreased osteocyte density and lacunar occupancy and increased porosity in cortical bone compared with age-matched controls. Vitamin K2 ameliorated the NX-induced decrease in lacunar occupancy by viable osteocytes and the NX-induced increase in porosity. The present study showed the efficacy of vitamin K2 for cancellous bone mass and cortical lacunar occupancy by viable osteocytes and porosity in sciatic NX rats.

Control of Somatosensory Cortical Processing by Thalamic Posterior Medial Nucleus: A New Role of Thalamus in Cortical Function.

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Carlos Castejon

Full Text Available Current knowledge of thalamocortical interaction comes mainly from studying lemniscal thalamic systems. Less is known about paralemniscal thalamic nuclei function. In the vibrissae system, the posterior medial nucleus (POm is the corresponding paralemniscal nucleus. POm neurons project to L1 and L5A of the primary somatosensory cortex (S1 in the rat brain. It is known that L1 modifies sensory-evoked responses through control of intracortical excitability suggesting that L1 exerts an influence on whisker responses. Therefore, thalamocortical pathways targeting L1 could modulate cortical firing. Here, using a combination of electrophysiology and pharmacology in vivo, we have sought to determine how POm influences cortical processing. In our experiments, single unit recordings performed in urethane-anesthetized rats showed that POm imposes precise control on the magnitude and duration of supra- and infragranular barrel cortex whisker responses. Our findings demonstrated that L1 inputs from POm imposed a time and intensity dependent regulation on cortical sensory processing. Moreover, we found that blocking L1 GABAergic inhibition or blocking P/Q-type Ca2+ channels in L1 prevents POm adjustment of whisker responses in the barrel cortex. Additionally, we found that POm was also controlling the sensory processing in S2 and this regulation was modulated by corticofugal activity from L5 in S1. Taken together, our data demonstrate the determinant role exerted by the POm in the adjustment of somatosensory cortical processing and in the regulation of cortical processing between S1 and S2. We propose that this adjustment could be a thalamocortical gain regulation mechanism also present in the processing of information between cortical areas.

Reduced cortical thickness in gambling disorder

DEFF Research Database (Denmark)

Grant, Jon E; Odlaug, Brian Lawrence; Chamberlain, Samuel R

2015-01-01

with significant reductions (average 15.8-19.9 %) in cortical thickness, versus controls, predominantly in right frontal cortical regions. Pronounced right frontal morphometric brain abnormalities occur in gambling disorder, supporting neurobiological overlap with substance disorders and its recent......Gambling disorder has recently been recognized as a prototype 'behavioral addiction' by virtue of its inclusion in the DSM-5 category of 'Substance-Related and Addictive Disorders.' Despite its newly acquired status and prevalence rate of 1-3 % globally, relatively little is known regarding...... the neurobiology of this disorder. The aim of this study was to explore cortical morphometry in untreated gambling disorder, for the first time. Subjects with gambling disorder (N = 16) free from current psychotropic medication or psychiatric comorbidities, and healthy controls (N = 17), were entered...

Autosomal dominant cortical tremor, myoclonus and epilepsy.

Science.gov (United States)

Striano, Pasquale; Zara, Federico

2016-09-01

The term 'cortical tremor' was first introduced by Ikeda and colleagues to indicate a postural and action-induced shivering movement of the hands which mimics essential tremor, but presents with the electrophysiological findings of cortical reflex myoclonus. The association between autosomal dominant cortical tremor, myoclonus and epilepsy (ADCME) was first recognized in Japanese families and is now increasingly reported worldwide, although it is described using different acronyms (BAFME, FAME, FEME, FCTE and others). The disease usually takes a benign course, although drug-resistant focal seizures or slight intellectual disability occur in some cases. Moreover, a worsening of cortical tremor and myoclonus is common in advanced age. Although not yet recognized by the International League Against Epilepsy (ILAE), this is a well-delineated epilepsy syndrome with remarkable features that clearly distinguishes it from other myoclonus epilepsies. Moreover, genetic studies of these families show heterogeneity and different susceptible chromosomal loci have been identified.

Chronic diseases, lack of medications, and depression among Syrian refugees in Jordan, 2013-2014.

Science.gov (United States)

Gammouh, Omar Salem; Al-Smadi, Ahmed Mohammad; Tawalbeh, Loai Issa; Khoury, Laurice Sami

2015-01-29

Studying mental and physical health problems in refugees facilitates providing suitable health care, thus improving their quality of life. We studied depression tendency in Syrian refugees in Jordan in the light of chronic diseases and medication availability. Also, depression prevalence and depression comorbidity with chronic diseases were identified. In this multicenter cross-sectional survey, data from Syrian refugees attending Caritas centers in 6 Jordanian cities from November 2013 through June 2014 were analyzed. Participants' demographics, depression, previously diagnosed chronic diseases, and newly diagnosed chronic diseases and the availability of medications were studied. Logistic regression was used to examine predictors for depression. Of 765 refugees who participated, about one-third demonstrated significant depression as measured by the Beck Depression Inventory. Descriptive analyses showed that depression was comorbid in 35% of participants with previously diagnosed chronic diseases and in 40% of participants with newly diagnosed chronic diseases. Newly diagnosed chronic diseases and lack of medications significantly contributed to depression, but the regression model as a whole explained less than 5% of the variance. Because the regression model showed low effect size, we concluded that newly diagnosed chronic diseases and medication shortages could not predict depression in Syrian refugees residing in Jordan. Therefore, further studies of additional factors are recommended. Prompt measures have to be taken to prevent the spread of chronic diseases and improve mental health in this fragile population.

Default Spread dan Term Spread sebagai Variabel Proxy Siklus Bisnis pada Model Fama-French

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Edwin Hendra

2015-08-01

Full Text Available This research aims to apply the Fama-French models and test the effect of alternative variable of bond yield spread, default spread (RBBB – RAAA and RAAA – RF, and the term spread (RSUN10-RSUN1, as proxy variables of the business cycle, in IDX stock data during 2005-2010. Four types of asset pricing models tested are Sharpe-Lintner CAPM, Fama-French models, Hwang et al.model, and hybrid model. The results showed that the size effect and value effect has an impact on excess stock returns. Slopes of market beta, SMB, and HML are more sensitive to stock big size and high B / M. Default spreads and term spreads in Hwang et al. model can explain the value effect, and weakly explain the size effect, meanwhile the power of explanation disappeared on Hybrid models. Based on the assessment adjusted R2 and the frequency of rejection of non-zero alpha, is found that the hybrid model is the most suitable model.  

Person identification based on multiscale matching of cortical images

NARCIS (Netherlands)

Kruizinga, P; Petkov, N; Hertzberger, B; Serazzi, G

1995-01-01

A set of so-called cortical images, motivated by the function of simple cells in the primary visual cortex of mammals, is computed from each of two input images and an image pyramid is constructed for each cortical image. The two sets of cortical image pyramids are matched synchronously and an

Canonical cortical circuits: current evidence and theoretical implications

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Capone F

2016-04-01

Full Text Available Fioravante Capone,1,2 Matteo Paolucci,1,2 Federica Assenza,1,2 Nicoletta Brunelli,1,2 Lorenzo Ricci,1,2 Lucia Florio,1,2 Vincenzo Di Lazzaro1,2 1Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, Università Campus Bio-Medico di Roma, Rome, Italy; 2Fondazione Alberto Sordi – Research Institute for Aging, Rome, ItalyAbstract: Neurophysiological and neuroanatomical studies have found that the same basic structural and functional organization of neuronal circuits exists throughout the cortex. This kind of cortical organization, termed canonical circuit, has been functionally demonstrated primarily by studies involving visual striate cortex, and then, the concept has been extended to different cortical areas. In brief, the canonical circuit is composed of superficial pyramidal neurons of layers II/III receiving different inputs and deep pyramidal neurons of layer V that are responsible for cortex output. Superficial and deep pyramidal neurons are reciprocally connected, and inhibitory interneurons participate in modulating the activity of the circuit. The main intuition of this model is that the entire cortical network could be modeled as the repetition of relatively simple modules composed of relatively few types of excitatory and inhibitory, highly interconnected neurons. We will review the origin and the application of the canonical cortical circuit model in the six sections of this paper. The first section (The origins of the concept of canonical circuit: the cat visual cortex reviews the experiments performed in the cat visual cortex, from the origin of the concept of canonical circuit to the most recent developments in the modelization of cortex. The second (The canonical circuit in neocortex and third (Toward a canonical circuit in agranular cortex sections try to extend the concept of canonical circuit to other cortical areas, providing some significant examples of circuit functioning in different cytoarchitectonic

Overweight is not associated with cortical thickness alterations in children

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Rachel Jane Sharkey

2015-02-01

Full Text Available IntroductionSeveral studies report an association between body mass index (BMI and cortical thickness in adults. Some studies demonstrate diffuse cortical thinning in obesity, while others report effects in areas that are associated with self-regulation, such as lateral prefrontal cortex. MethodsThis study used multilevel modelling of data from the NIH Pediatric MRI Data Repository, a mixed longitudinal and cross-sectional database, to examine the relationship between cortical thickness and body weight in children. Cortical thickness was computed at 81,942 vertices of 716 MRI scans from 378 children aged between 4 and 18 years. Body mass index Z score for age was computed for each participant. We preformed vertex-wise statistical analysis of the relationship between cortical thickness and BMI, accounting for age and gender. In addition, cortical thickness was extracted from regions of interest in prefrontal cortex and insula.ResultsNo significant association between cortical thickness and BMI was found, either by statistical parametric mapping or by region of interest analysis. Results remained negative when the analysis was restricted to children aged 12-18.ConclusionsThe correlation between BMI and cortical thickness was not found in this large pediatric sample. The association between BMI and cortical thinning develops after adolescence. This has implications for the nature of the relationship between brain anatomy and weight gain.

Transcranial magnetic stimulation in the treatment of depression.

Science.gov (United States)

Gershon, Ari A; Dannon, Pinhas N; Grunhaus, Leon

2003-05-01

Transcranial magnetic stimulation (TMS) is a noninvasive and easily tolerated method of altering cortical physiology. The authors evaluate evidence from the last decade supporting a possible role for TMS in the treatment of depression and explore clinical and technical considerations that might bear on treatment success. The authors review English-language controlled studies of nonconvulsive TMS therapy for depression that appeared in the MEDLINE database through early 2002, as well as one study that was in press in 2002 and was published in 2003. In addition, the authors discuss studies that have examined technical, methodological, and clinical treatment parameters of TMS. Most data support an antidepressant effect of high-frequency repetitive TMS administered to the left prefrontal cortex. The absence of psychosis, younger age, and certain brain physiologic markers might predict treatment success. Technical parameters possibly affecting treatment success include intensity and duration of treatment, but these suggestions require systematic testing. TMS shows promise as a novel antidepressant treatment. Systematic and large-scale studies are needed to identify patient populations most likely to benefit and treatment parameters most likely to produce success. In addition to its potential clinical role, TMS promises to provide insights into the pathophysiology of depression through research designs in which the ability of TMS to alter brain activity is coupled with functional neuroimaging.

Significance of frontal cortical atrophy in Parkinson's disease: computed tomographic study

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Lee, Kyung Sang; Suh, Jung Ho; Chung, Tae Sub; Kim, Dong Ik [College of Medicine, Yonsei University, Seoul (Korea, Republic of)

1987-10-15

Fifty-five patients with Parkinson's disease were evaluated clinically and with brain computed tomography (CT) in order to determine the incidence of frontal cortical and subcortical atrophy. Twenty cases of age-related healthy control group were also scanned. The CT criteria of frontal cortical atrophy that was used in this study were the maximum width of frontal hemispheric cortical sulci and width of anterior interhemispheric fissure between frontal lobes comparing with maximum width of hemispheric cortical sulci except frontal lobes. And the criteria of frontal subcortical atrophy were bifrontal index bicaudate index, and Evans index. The results are as follows: 1. Cortical atrophic changes in Parkinson's disease were more prominent in frontal lobe rather than other causes of cortical atrophy. 2. Frontal cortical and subcortical atrophic changes were also more prominent in Parkinson's disease rather than age-related control group. 3. Subcortical atrophic changes in frontal lobe were always associated with cortical atrophic changes. 4. Changes of basal ganglia were hardly seen in Parkinson's disease. 5. Cortical atrophic changes in frontal lobe must be the one of significant findings in Parkinson's disease.

Significance of frontal cortical atrophy in Parkinson's disease: computed tomographic study

International Nuclear Information System (INIS)

Lee, Kyung Sang; Suh, Jung Ho; Chung, Tae Sub; Kim, Dong Ik

1987-01-01

Fifty-five patients with Parkinson's disease were evaluated clinically and with brain computed tomography (CT) in order to determine the incidence of frontal cortical and subcortical atrophy. Twenty cases of age-related healthy control group were also scanned. The CT criteria of frontal cortical atrophy that was used in this study were the maximum width of frontal hemispheric cortical sulci and width of anterior interhemispheric fissure between frontal lobes comparing with maximum width of hemispheric cortical sulci except frontal lobes. And the criteria of frontal subcortical atrophy were bifrontal index bicaudate index, and Evans index. The results are as follows: 1. Cortical atrophic changes in Parkinson's disease were more prominent in frontal lobe rather than other causes of cortical atrophy. 2. Frontal cortical and subcortical atrophic changes were also more prominent in Parkinson's disease rather than age-related control group. 3. Subcortical atrophic changes in frontal lobe were always associated with cortical atrophic changes. 4. Changes of basal ganglia were hardly seen in Parkinson's disease. 5. Cortical atrophic changes in frontal lobe must be the one of significant findings in Parkinson's disease

Spatiotemporal Dynamics of Cortical Representations during and after Stimulus Presentation

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Marieke Esther van de Nieuwenhuijzen

2016-05-01

Full Text Available Visual perception is a spatiotemporally complex process. In this study, we investigated cortical dynamics during and after stimulus presentation. We observed that visual category information related to the difference between faces and objects became apparent in the occipital lobe after 63 ms. Within the next 110 ms, activation spread out to include the temporal lobe before returning to residing mainly in the occipital lobe again. After stimulus offset, a peak in information was observed, comparable to the peak after stimulus onset. Moreover, similar processes, albeit not identical, seemed to underlie both peaks. Information about the categorical identity of the stimulus remained present until 677 ms after stimulus offset, during which period the stimulus had to be retained in working memory. Activation patterns initially resembled those observed during stimulus presentation. After about 200 ms, however, this representation changed and class-specific activity became more equally distributed over the four lobes. These results show that, although there are common processes underlying stimulus representation both during and after stimulus presentation, these representations change depending on the specific stage of perception and maintenance.

Cortical thickness abnormalities in late adolescence with online gaming addiction.

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Kai Yuan

Full Text Available Online gaming addiction, as the most popular subtype of Internet addiction, had gained more and more attention from the whole world. However, the structural differences in cortical thickness of the brain between adolescents with online gaming addiction and healthy controls are not well unknown; neither was its association with the impaired cognitive control ability. High-resolution magnetic resonance imaging scans from late adolescence with online gaming addiction (n = 18 and age-, education- and gender-matched controls (n = 18 were acquired. The cortical thickness measurement method was employed to investigate alterations of cortical thickness in individuals with online gaming addiction. The color-word Stroop task was employed to investigate the functional implications of the cortical thickness abnormalities. Imaging data revealed increased cortical thickness in the left precentral cortex, precuneus, middle frontal cortex, inferior temporal and middle temporal cortices in late adolescence with online gaming addiction; meanwhile, the cortical thicknesses of the left lateral orbitofrontal cortex (OFC, insula, lingual gyrus, the right postcentral gyrus, entorhinal cortex and inferior parietal cortex were decreased. Correlation analysis demonstrated that the cortical thicknesses of the left precentral cortex, precuneus and lingual gyrus correlated with duration of online gaming addiction and the cortical thickness of the OFC correlated with the impaired task performance during the color-word Stroop task in adolescents with online gaming addiction. The findings in the current study suggested that the cortical thickness abnormalities of these regions may be implicated in the underlying pathophysiology of online gaming addiction.

Outline of a novel architecture for cortical computation

OpenAIRE

Majumdar, Kaushik

2007-01-01

In this paper a novel architecture for cortical computation has been proposed. This architecture is composed of computing paths consisting of neurons and synapses only. These paths have been decomposed into lateral, longitudinal and vertical components. Cortical computation has then been decomposed into lateral computation (LaC), longitudinal computation (LoC) and vertical computation (VeC). It has been shown that various loop structures in the cortical circuit play important roles in cortica...

Early and phasic cortical metabolic changes in vestibular neuritis onset.

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Marco Alessandrini

Full Text Available Functional brain activation studies described the presence of separate cortical areas responsible for central processing of peripheral vestibular information and reported their activation and interactions with other sensory modalities and the changes of this network associated to strategic peripheral or central vestibular lesions. It is already known that cortical changes induced by acute unilateral vestibular failure (UVF are various and undergo variations over time, revealing different cortical involved areas at the onset and recovery from symptoms. The present study aimed at reporting the earliest change in cortical metabolic activity during a paradigmatic form of UVF such as vestibular neuritis (VN, that is, a purely peripheral lesion of the vestibular system, that offers the opportunity to study the cortical response to altered vestibular processing. This research reports [(18F]fluorodeoxyglucose positron emission tomography brain scan data concerning the early cortical metabolic activity associated to symptoms onset in a group of eight patients suffering from VN. VN patients' cortical metabolic activity during the first two days from symptoms onset was compared to that recorded one month later and to a control healthy group. Beside the known cortical response in the sensorimotor network associated to vestibular deafferentation, we show for the first time the involvement of Entorhinal (BAs 28, 34 and Temporal (BA 38 cortices in early phases of symptomatology onset. We interpret these findings as the cortical counterparts of the attempt to reorient oneself in space counteracting the vertigo symptom (Bas 28, 34 and of the emotional response to the new pathologic condition (BA 38 respectively. These interpretations were further supported by changes in patients' subjective ratings in balance, anxiety, and depersonalization/derealization scores when tested at illness onset and one month later. The present findings contribute in expanding

Aberrant cortical associative plasticity associated with severe adult Tourette syndrome.

Science.gov (United States)

Martín-Rodríguez, Juan Francisco; Ruiz-Rodríguez, María Adilia; Palomar, Francisco J; Cáceres-Redondo, María Teresa; Vargas, Laura; Porcacchia, Paolo; Gómez-Crespo, Mercedes; Huertas-Fernández, Ismael; Carrillo, Fátima; Madruga-Garrido, Marcos; Mir, Pablo

2015-03-01

Recent studies have shown altered cortical plasticity in adult patients with Tourette syndrome. However, the clinical significance of this finding remains elusive. Motor cortical plasticity was evaluated in 15 adult patients with severe Tourette syndrome and 16 healthy controls using the paired associative stimulation protocol by transcranial magnetic stimulation. Associations between paired associative stimulation-induced plasticity and relevant clinical variables, including cortical excitability, psychiatric comorbidities, drug treatment and tic severity, were assessed. Motor cortical plasticity was abnormally increased in patients with Tourette syndrome compared with healthy subjects. This abnormal plasticity was independently associated with tic severity. Patients with severe Tourette syndrome display abnormally increased cortical associative plasticity. This aberrant cortical plasticity was associated with tic severity, suggesting an underlying mechanism for tic pathophysiology. © 2015 International Parkinson and Movement Disorder Society.

Cooperative spreading processes in multiplex networks.

Science.gov (United States)

Wei, Xiang; Chen, Shihua; Wu, Xiaoqun; Ning, Di; Lu, Jun-An

2016-06-01

This study is concerned with the dynamic behaviors of epidemic spreading in multiplex networks. A model composed of two interacting complex networks is proposed to describe cooperative spreading processes, wherein the virus spreading in one layer can penetrate into the other to promote the spreading process. The global epidemic threshold of the model is smaller than the epidemic thresholds of the corresponding isolated networks. Thus, global epidemic onset arises in the interacting networks even though an epidemic onset does not arise in each isolated network. Simulations verify the analysis results and indicate that cooperative spreading processes in multiplex networks enhance the final infection fraction.

Effect of Elevated KP+, Hypotonic Stress, and Cortical Spreading Depression on Astrocyte Swelling in GFAP-Deficient Mice..

Czech Academy of Sciences Publication Activity Database

Anděrová, Miroslava; Kubinová, Šárka; Mazel, Tomáš; Chvátal, Alexandr; Eliasson, C.; Pekny, M.; Syková, Eva

2001-01-01

Roč. 35, - (2001), s. 189-203 ISSN 0894-1491 R&D Projects: GA ČR GA305/99/0655; GA ČR GA309/99/0657; GA MŠk LN00A065 Institutional research plan: CEZ:AV0Z5039906 Keywords : glia l fibrillar acidic protein spinal cord Subject RIV: FH - Neurology Impact factor: 4.193, year: 2001

Spread effects - methodology; Spredningseffekter - metodegrunnlag

Energy Technology Data Exchange (ETDEWEB)

NONE

2004-07-01

Diffusion of technology, environmental effects and rebound effects are the principal effects from the funding of renewable energy and energy economising. It is difficult to estimate the impact of the spread effects both prior to the measures are implemented and after the measures are carried out. Statistical methods can be used to estimate the spread effects, but they are insecure and always need to be complemented with qualitative and subjective evaluations. It is more adequate to evaluate potential spread effects from market and market data surveillance for a selection of technologies and parties. Based on this information qualitative indicators for spread effects can be constructed and used both ex ante and ex post (ml)

The changing roles of neurons in the cortical subplate

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Michael J Friedlander

2009-08-01

Full Text Available Neurons may serve different functions over the course of an organism’s life. Recent evidence suggests that cortical subplate neurons including those that reside in the white matter may perform longitudinal multi-tasking at different stages of development. These cells play a key role in early cortical development in coordinating thalamocortical reciprocal innervation. At later stages of development, they become integrated within the cortical microcircuitry. This type of longitudinal multi-tasking can enhance the capacity for information processing by populations of cells serving different functions over the lifespan. Subplate cells are initially derived when cells from the ventricular zone underlying the cortex migrate to the cortical preplate that is subsequently split by the differentiating neurons of the cortical plate with some neurons locating in the marginal zone and others settling below in the subplate (SP. While the cortical plate neurons form most of the cortical layers (layers 2-6, the marginal zone neurons form layer 1 and the SP neurons become interstitial cells of the white matter as well as forming a compact sublayer along the bottom of layer 6. After serving as transient innervation targets for thalamocortical axons, most of these cells die and layer 4 neurons become innervated by thalamic axons. However, 10-20% survives, remaining into adulthood along the bottom of layer 6 and as a scattered population of interstitial neurons in the white matter. Surviving subplate cells’ axons project throughout the overlying laminae, reaching layer 1 and issuing axon collaterals within white matter and in lower layer 6. This suggests that they participate in local synaptic networks, as well. Moreover, they receive excitatory and inhibitory synaptic inputs, potentially monitoring outputs from axon collaterals of cortical efferents, from cortical afferents and/or from each other. We explore our understanding of the functional connectivity of

Development of cortical thickness and surface area in autism spectrum disorder

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Vincent T. Mensen

2017-01-01

Full Text Available Autism spectrum disorder (ASD is a neurodevelopmental disorder often associated with changes in cortical volume. The constituents of cortical volume – cortical thickness and surface area – have separable developmental trajectories and are related to different neurobiological processes. However, little is known about the developmental trajectories of cortical thickness and surface area in ASD. In this magnetic resonance imaging (MRI study, we used an accelerated longitudinal design to investigate the cortical development in 90 individuals with ASD and 90 typically developing controls, aged 9 to 20 years. We quantified cortical measures using the FreeSurfer software package, and then used linear mixed model analyses to estimate the developmental trajectories for each cortical measure. Our primary finding was that the development of surface area follows a linear trajectory in ASD that differs from typically developing controls. In typical development, we found a decline in cortical surface area between the ages of 9 and 20 that was absent in ASD. We found this pattern in all regions where developmental trajectories for surface area differed between groups. When we applied a more stringent correction that takes the interdependency of measures into account, this effect on cortical surface area retained significance for left banks of superior temporal sulcus, postcentral area, and right supramarginal area. These areas have previously been implicated in ASD and are involved in the interpretation and processing of audiovisual social stimuli and distinction between self and others. Although some differences in cortical volume and thickness were found, none survived the more stringent correction for multiple testing. This study underscores the importance of distinguishing between cortical surface area and thickness in investigating cortical development, and suggests the development of cortical surface area is of importance to ASD.

Recurrent Wernicke's aphasia: migraine and not stroke!

Science.gov (United States)

Mishra, Nishant Kumar; Rossetti, Andrea O; Ménétrey, André; Carota, Antonio

2009-05-01

We report the clinical findings of a 40-year-old woman with recurrent migraine presenting with Wernicke's aphasia in accordance with the results of a standardized battery for language assessment (Boston Aphasia Diagnostic Examination). The patient had no evidence of parenchymal or vascular lesions on MRI and showed delta and theta slowing over the left posterior temporal leads on the EEG. Although the acute onset of a fluent aphasia suggested stroke as a likely etiology, the recurrence of aphasia as the initial symptom of migraine was related to cortical spreading depression and not to stroke.

Cortical basis of communication: local computation, coordination, attention.

Science.gov (United States)

Alexandre, Frederic

2009-03-01

Human communication emerges from cortical processing, known to be implemented on a regular repetitive neuronal substratum. The supposed genericity of cortical processing has elicited a series of modeling works in computational neuroscience that underline the information flows driven by the cortical circuitry. In the minimalist framework underlying the current theories for the embodiment of cognition, such a generic cortical processing is exploited for the coordination of poles of representation, as is reported in this paper for the case of visual attention. Interestingly, this case emphasizes how abstract internal referents are built to conform to memory requirements. This paper proposes that these referents are the basis for communication in humans, which is firstly a coordination and an attentional procedure with regard to their congeners.

Predictive value of brain perfusion SPECT for rTMS response in pharmacoresistant depression

International Nuclear Information System (INIS)

Richieri, Raphaelle; Lancon, Christophe; Boyer, Laurent; Farisse, Jean; Colavolpe, Cecile; Mundler, Olivier; Guedj, Eric

2011-01-01

The aim of this study was to determine the predictive value of whole-brain voxel-based regional cerebral blood flow (rCBF) for repetitive transcranial magnetic stimulation (rTMS) response in patients with pharmacoresistant depression. Thirty-three right-handed patients who met DSM-IV criteria for major depressive disorder (unipolar or bipolar depression) were included before rTMS. rTMS response was defined as at least 50% reduction in the baseline Beck Depression Inventory scores. The predictive value of 99m Tc-ethyl cysteinate dimer (ECD) single photon emission computed tomography (SPECT) for rTMS response was studied before treatment by comparing rTMS responders to non-responders at voxel level using Statistical Parametric Mapping (SPM) (p 0.10). In comparison to responders, non-responders showed significant hypoperfusions (p < 0.001, uncorrected) in the left medial and bilateral superior frontal cortices (BA10), the left uncus/parahippocampal cortex (BA20/BA35) and the right thalamus. The area under the curve for the combination of SPECT clusters to predict rTMS response was 0.89 (p < 0.001). Sensitivity, specificity, positive predictive value and negative predictive value for the combination of clusters were: 94, 73, 81 and 92%, respectively. This study shows that, in pharmacoresistant depression, pretreatment rCBF of specific brain regions is a strong predictor for response to rTMS in patients with homogeneous demographic/clinical features. (orig.)

Developmental Trajectories of the Orbitofrontal Cortex and Anhedonia in Middle Childhood and Risk for Substance Use in Adolescence in a Longitudinal Sample of Depressed and Healthy Preschoolers.

Science.gov (United States)

Luby, Joan L; Agrawal, Arpana; Belden, Andy; Whalen, Diana; Tillman, Rebecca; Barch, Deanna M

2018-03-21

Deficits in reward processing are established in mood and substance use disorders and are known risk factors for these disorders. Volume reductions of the orbitofrontal cortex and the striatum, regions that subserve neural response to reward, have been shown to be related to anhedonia in depressive and substance use disorders. The authors sought to investigate how structural maturation of these regions in childhood varies with level of anhedonia and predicts later substance use. The study employed data from a sample of depressed and healthy preschoolers studied longitudinally that included three waves of neuroimaging from school age to adolescence. Three years after scan 3, at ages 13-18, participants underwent a comprehensive behavioral and substance use assessment. Multilevel modeling was used to investigate the relationship between anhedonia and the growth trajectories of the striatum and orbitofrontal cortex. Zero-inflated Poisson regression models were then used to determine whether the intercepts and slopes of these trajectories predicted later alcohol and marijuana use frequency in adolescence. The anhedonia-by-age interaction was significant in the multilevel modeling of orbitofrontal cortical but not striatal volume. Higher anhedonia ratings were significantly associated with steeper decline in orbitofrontal cortical volume with age. Orbitofrontal cortical volume and thickness at age 12 and trajectory over time significantly and negatively predicted subsequent alcohol and marijuana use frequency but not depression during adolescence. The findings suggest that the development of the orbitofrontal cortex during childhood is strongly linked to experiences of anhedonia and that these growth trajectories predict substance use during a developmentally critical period.

A Mechanistic Link from GABA to Cortical Architecture and Perception.

Science.gov (United States)

Kolasinski, James; Logan, John P; Hinson, Emily L; Manners, Daniel; Divanbeighi Zand, Amir P; Makin, Tamar R; Emir, Uzay E; Stagg, Charlotte J

2017-06-05

Understanding both the organization of the human cortex and its relation to the performance of distinct functions is fundamental in neuroscience. The primary sensory cortices display topographic organization, whereby receptive fields follow a characteristic pattern, from tonotopy to retinotopy to somatotopy [1]. GABAergic signaling is vital to the maintenance of cortical receptive fields [2]; however, it is unclear how this fine-grain inhibition relates to measurable patterns of perception [3, 4]. Based on perceptual changes following perturbation of the GABAergic system, it is conceivable that the resting level of cortical GABAergic tone directly relates to the spatial specificity of activation in response to a given input [5-7]. The specificity of cortical activation can be considered in terms of cortical tuning: greater cortical tuning yields more localized recruitment of cortical territory in response to a given input. We applied a combination of fMRI, MR spectroscopy, and psychophysics to substantiate the link between the cortical neurochemical milieu, the tuning of cortical activity, and variability in perceptual acuity, using human somatosensory cortex as a model. We provide data that explain human perceptual acuity in terms of both the underlying cellular and metabolic processes. Specifically, higher concentrations of sensorimotor GABA are associated with more selective cortical tuning, which in turn is associated with enhanced perception. These results show anatomical and neurochemical specificity and are replicated in an independent cohort. The mechanistic link from neurochemistry to perception provides a vital step in understanding population variability in sensory behavior, informing metabolic therapeutic interventions to restore perceptual abilities clinically. Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Contextual control of audiovisual integration in low-level sensory cortices

NARCIS (Netherlands)

Van Atteveldt, N.; Peterson, Bradley S; Schroeder, Charles E

Potential sources of multisensory influences on low-level sensory cortices include direct projections from sensory cortices of different modalities, as well as more indirect feedback inputs from higher order multisensory cortical regions. These multiple architectures may be functionally

Fluorescent visualization of a spreading surfactant

Energy Technology Data Exchange (ETDEWEB)

Fallest, David W; Lichtenberger, Adele M; Fox, Christopher J; Daniels, Karen E, E-mail: kdaniel@ncsu.ed [Department of Physics, North Carolina State University, Raleigh, NC 27695 (United States)

2010-07-15

The spreading of surfactants on thin films is an industrially and medically important phenomenon, but the dynamics are highly nonlinear and visualization of the surfactant dynamics has been a long-standing experimental challenge. We perform the first quantitative, spatiotemporally resolved measurements of the spreading of an insoluble surfactant on a thin fluid layer. During the spreading process, we directly observe both the radial height profile of the spreading droplet and the spatial distribution of the fluorescently tagged surfactant. We find that the leading edge of a spreading circular layer of surfactant forms a Marangoni ridge in the underlying fluid, with a trough trailing the ridge as expected. However, several novel features are observed using the fluorescence technique, including a peak in the surfactant concentration that trails the leading edge, and a flat, monolayer-scale spreading film that differs from concentration profiles predicted by current models. Both the Marangoni ridge and the surfactant leading edge can be described to spread as R{approx}t{sup {delta}}. We find spreading exponents {delta}{sub H}{approx}0.30 and {delta}{sub {Gamma}}{approx}0.22 for the ridge peak and surfactant leading edge, respectively, which are in good agreement with theoretical predictions of {delta}=1/4. In addition, we observe that the surfactant leading edge initially leads the peak of the Marangoni ridge, with the peak later catching up to the leading edge.

Cortical heterotopia in Aicardi's syndrome - CT findings

International Nuclear Information System (INIS)

Besenski, N.; Bosnjak, V.; Ligutic, I.; Marusic-Della Marina, B.

1988-01-01

The case of 5-month-old female infant with Aicardi's syndrome is presented. The main clinical features were severe developmental retardation and intractable epileptic seizures. Ophthalmoscopic examination revealed pathognomonic choriorethinopathy. Ultrasonic examination of the brain detected agenesis of the corpus callosum, whereas CT showed a coexisting malformation of the brain, i.e. cortical heterotopia of the gray matter. Agenesis of the corpus callosum is an entity well-recognized by sonography. However, ultrasonography is an insufficient modality for the visualization of cortical heterotopia which is common to all cases of Aicardi's syndrome. Therefore, in cases of suspected Aicardi's syndrome CT is recommended, as it enables the diagnosis of cortical heterotopia. (orig.)

The cortical signature of impaired gesturing: Findings from schizophrenia

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Petra Verena Viher

2018-01-01

Full Text Available Schizophrenia is characterized by deficits in gesturing that is important for nonverbal communication. Research in healthy participants and brain-damaged patients revealed a left-lateralized fronto-parieto-temporal network underlying gesture performance. First evidence from structural imaging studies in schizophrenia corroborates these results. However, as of yet, it is unclear if cortical thickness abnormalities contribute to impairments in gesture performance. We hypothesized that patients with deficits in gesture production show cortical thinning in 12 regions of interest (ROIs of a gesture network relevant for gesture performance and recognition. Forty patients with schizophrenia and 41 healthy controls performed hand and finger gestures as either imitation or pantomime. Group differences in cortical thickness between patients with deficits, patients without deficits, and controls were explored using a multivariate analysis of covariance. In addition, the relationship between gesture recognition and cortical thickness was investigated. Patients with deficits in gesture production had reduced cortical thickness in eight ROIs, including the pars opercularis of the inferior frontal gyrus, the superior and inferior parietal lobes, and the superior and middle temporal gyri. Gesture recognition correlated with cortical thickness in fewer, but mainly the same, ROIs within the patient sample. In conclusion, our results show that impaired gesture production and recognition in schizophrenia is associated with cortical thinning in distinct areas of the gesture network.

Phenomena Conflict, Anxiety, and Depression for Cancer Survivor One Year and After Have Therapy in General Hospital

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Maria Turnip

2016-03-01

Full Text Available Introduction. Psychosocial distress emerges in cancer disease. This research explores experience of conflict, anxiety, and depression in one year cancer survivor. Methods. Data were collected through in-depth semi structured interviews with fifteen participants when seeking treatment at a public hospital in Bandung. Result. There nine themes emerge: anxiety about cancer’s spread and recurrence, changing relationships with a partner, 'labeling' from oneself and others, physical discomfort along treatment, psychological discomfort along treatment, self-concept, religious/spiritual, hiding diagnose and complain, and deficit information about cancer. But, four themes among were not characterized with conflict, anxiety, and depression. Conflict, anxiety, and depression impact condition of the client cancer. Discussion. Experience of conflict, anxiety, and depression became the basis for the development of management system service and provision of facilities for integrated mental health nursing therapy. Key word: cancer, conflict, anxiety, depression

The cortical focus in childhood absence epilepsy; evidence from nonlinear analysis of scalp EEG recordings.

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Sarrigiannis, Ptolemaios G; Zhao, Yifan; He, Fei; Billings, Stephen A; Baster, Kathleen; Rittey, Chris; Yianni, John; Zis, Panagiotis; Wei, Hualiang; Hadjivassiliou, Marios; Grünewald, Richard

2018-03-01

To determine the origin and dynamic characteristics of the generalised hyper-synchronous spike and wave (SW) discharges in childhood absence epilepsy (CAE). We applied nonlinear methods, the error reduction ratio (ERR) causality test and cross-frequency analysis, with a nonlinear autoregressive exogenous (NARX) model, to electroencephalograms (EEGs) from CAE, selected with stringent electro-clinical criteria (17 cases, 42 absences). We analysed the pre-ictal and ictal strength of association between homologous and heterologous EEG derivations and estimated the direction of synchronisation and corresponding time lags. A frontal/fronto-central onset of the absences is detected in 13 of the 17 cases with the highest ictal strength of association between homologous frontal followed by centro-temporal and fronto-central areas. Delays consistently in excess of 4 ms occur at the very onset between these regions, swiftly followed by the emergence of "isochronous" (0-2 ms) synchronisation but dynamic time lag changes occur during SW discharges. In absences an initial cortico-cortical spread leads to dynamic lag changes to include periods of isochronous interhemispheric synchronisation, which we hypothesize is mediated by the thalamus. Absences from CAE show ictal epileptic network dynamics remarkably similar to those observed in WAG/Rij rats which guided the formulation of the cortical focus theory. Copyright © 2017 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

Interest of targeting either cortical area Brodmann 9 or 46 in rTMS treatment for depression: a preliminary randomized study.

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Trojak, Benoit; Meille, Vincent; Jonval, Lysiane; Schuffenecker, Nicolas; Haffen, Emmanuel; Schwan, Raymund; Bonin, Bernard; Chauvet-Gelinier, Jean-Christophe

2014-12-01

To assess the interest of specifically targeting Brodmann Areas (BA) 9 or 46 for rTMS treatment of depression. Patients with Treatment-Resistant Depression were randomly assigned to two treatment groups to receive either rTMS on BA 9 or on BA 46. Each patient underwent 10 sessions of 1Hz-rTMS for 2weeks. The Hamilton and Montgomery-Asberg Depression Rating Scales (HDRS, MADRS) were used under blind conditions to assess the therapeutic response (50% improvement). A Wilcoxon signed-rank test was used to compare the depression rating scales scores obtained before and after the 10 rTMS sessions for each of the two groups. The therapeutic results in the two groups were compared using the Mann-Whitney-Wilcoxon test. We also reported the effect sizes using Hedges's g. Fifteen patients were included. Stimulation of both BA 9 (n=7) and BA 46 (n=8) led to similar therapeutic responses in the two groups (with moderate effect size), such as the mean decrease in HDRS (BA 9: p=0.015; BA 46: p=0.010) and MADRS (BA 9: p=0.042; BA 46: p=0.038) scores. Our results do not come out in favor of one or the other BA. Stimulation of BA 9 and BA 46 appears to be equally effective in the treatment of depression. Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Outline of a novel architecture for cortical computation.

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Majumdar, Kaushik

2008-03-01

In this paper a novel architecture for cortical computation has been proposed. This architecture is composed of computing paths consisting of neurons and synapses. These paths have been decomposed into lateral, longitudinal and vertical components. Cortical computation has then been decomposed into lateral computation (LaC), longitudinal computation (LoC) and vertical computation (VeC). It has been shown that various loop structures in the cortical circuit play important roles in cortical computation as well as in memory storage and retrieval, keeping in conformity with the molecular basis of short and long term memory. A new learning scheme for the brain has also been proposed and how it is implemented within the proposed architecture has been explained. A few mathematical results about the architecture have been proposed, some of which are without proof.

Terrestrial spreading centers under Venus conditions - Evaluation of a crustal spreading model for Western Aphrodite Terra

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Sotin, C.; Senske, D. A.; Head, J. W.; Parmentier, E. M.

1989-01-01

The model of Reid and Jackson (1981) for terrestrial spreading centers is applied to Venus conditions. On the basis of spreading rate, mantle temperature, and surface temperature, the model predicts both isostatic topography and crustal thickness. The model and Pioneer Venus altimetry and gravity data are used to test the hypothesis of Head and Crumpler (1987) that Western Aphrodite Terra is the location of crustal spreading on Venus. It is concluded that a spreading center model for Ovda Regio in Western Aphrodite Terra could account for the observed topography and line-of-sight gravity anomalies found in the Pioneer data.

The antidepressant effect of melatonin and fluoxetine in diabetic rats is associated with a reduction of the oxidative stress in the prefrontal and hippocampal cortices.

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Rebai, Redouane; Jasmin, Luc; Boudah, Abdennacer

2017-09-01

In the past few years possible mechanisms that link diabetes and depression have been found. One of these mechanisms is the increase in lipid peroxidation and decrease in antioxidant activity in the hippocampal and prefrontal cortices, which are brain areas involved in mood. The goal of the present study was to evaluate the effect of an antidepressant and of an antioxidant on behavior and oxidative activity in brains of diabetic rats. Rats rendered diabetic after a treatment with streptozotocin (STZ) (60mg/kg) were treated with fluoxetine (15mg/kg), melatonin (10mg/kg), or vehicle for 4 weeks. All animals were tested for signs of depression and anxiety using the elevated plus maze (EPM), open field test (OFT) and the forced swim test (FST). Four groups were compared: (1) normoglycemic, (2) hyperglycemic vehicle treated, and hyperglycemic (3) fluoxetine or (4) melatonin treated rats. On the last day of the study, blood samples were obtained to determine the levels of hemoglobin A1c (HbA1c). Also, brain samples were collected to measure the oxidative stress in the hippocampal and prefrontal cortices using the thiobarbituric acid reactive substances (TBARS) assay. The activity of the antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST) were also measured on the brain samples. The results show that both fluoxetine and melatonin decrease the signs of depression and anxiety in all tests. Concomitantly, the levels of HbA1c were reduced in drug treated rats, and to a greater degree in the fluoxetine group. In the cerebral cortex of diabetic rats, TBARS was increased, while the activity of CAT, GPx and GST were decreased. Fluoxetine and melatonin treatments decreased TBARS in both cortices. In the prefrontal cortex, fluoxetine and melatonin restored the activity of CAT, while only melatonin improved the activity of GPx and GST. In the hippocampus, the activity of GPx alone was restored by melatonin, while fluoxetine had no

Investigation of cortical thickness abnormalities in lithium-free adults with bipolar type I disorder using cortical pattern matching

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Foland-Ross, Lara C.; Thompson, Paul M.; Sugar, Catherine A.; Madsen, Sarah K.; Shen, Jim K.; Penfold, Conor; Ahlf, Kyle; Rasser, Paul E.; Fischer, Jeffrey; Yang, Yilan; Townsend, Jennifer; Bookheimer, Susan Y.; Altshuler, Lori L.

2013-01-01

Objective Several lines of evidence implicate gray matter abnormalities in the prefrontal cortex and anterior cingulate cortex in patients with bipolar disorder. Findings however, have been largely inconsistent across studies. Differences in patients’ medication status or mood state, or the application of traditional volumetric methods that are insensitive to subtle neuroanatomic differences may have contributed to these inconsistent findings. Given this, we used magnetic resonance imaging (MRI) in conjunction with cortical pattern matching methods to assess cortical thickness abnormalities in euthymic bipolar subjects who were not treated with lithium. Method Sixty-five subjects, including 34 lithium-free euthymic subjects with bipolar (type I) disorder and 31 healthy subjects were scanned using magnetic resonance imaging (MRI). Data were processed to measure cortical gray matter thickness. Cortical pattern matching methods associated homologous brain regions across subjects. Spatially normalized thickness maps were analyzed to assess illness effects and associations with clinical variables. Results Relative to healthy subjects, euthymic bipolar I subjects had significantly thinner gray matter in bilateral prefrontal cortex (Brodmann Areas 11, 10, 8 and 44) and left anterior cingulate cortex (Brodmann Areas 24/32). Additionally, thinning in these regions was more pronounced in patients with a history of psychosis. No areas of thicker cortex were detected in bipolar subjects versus healthy subjects. Conclusions Using a technique that is highly sensitive to subtle neuroanatomic differences, significant regional cortical thinning was found in euthymic subjects with bipolar disorder. Clinical implications are discussed. PMID:21285139

Differences in prefrontal, limbic, and white matter lesion volumes according to cognitive status in elderly patients with first-onset subsyndromal depression.

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Jun-Young Lee

Full Text Available The purpose of this preliminary study was to test the hypothesis that subsyndromal depression is associated with the volume of medial prefrontal regional gray matter and that of white matter lesions (WMLs in the brains of cognitively normal older people. We also explored the relationships between subsyndromal depression and medial prefrontal regional gray matter volume, limbic regional gray matter volume, and lobar WMLs in the brains of patients with mild cognitive impairment (MCI and Alzheimer's disease (AD. We performed a cross-sectional study comparing patients with subsyndromal depression and nondepressed controls with normal cognition (n = 59, MCI (n = 27, and AD (n = 27, adjusting for sex, age, years of education, and results of the Mini-Mental State Examination. Frontal WML volume was greater, and right medial orbitofrontal cortical volume was smaller in cognitively normal participants with subsyndromal depression than in those without subsyndromal depression. No volume differences were observed in medial prefrontal, limbic, or WML volumes according to the presence of subsyndromal depression in cognitively impaired patients. The absence of these changes in patients with MCI and AD suggests that brain changes associated with AD pathology may override the changes associated with subsyndromal depression.

Transcranial magnetic stimulation: a new tool in the fight against depression.

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Grunhaus, Leon; Dannon, Pinhas N; Gershon, Ari A

2002-03-01

Since its introduction to the clinical realm in 1985, transcranial magnetic stimulation (TMS) has rapidly developed into a tool for exploring central nervous system function in both health and disease. The antidepressant effects of TMS were initially observed in 1993. Since then, a solid body of evidence has accumulated suggesting antidepressant effects for both slow TMS (sTMS) and repetitive TMS (rTMS). This review is divided into four parts. First, it addresses the basic concepts governing TMS, and then, second, it discusses the technical parameters involved in administering TMS. Knowledge of these parameters is necessary for understanding how TMS is administered, and how manipulation of the technique impacts on the results obtained. Third, we review the most relevant studies on the antidepressant effects of sTMS and rTMS published to date. Finally, we discuss cortical excitability and how the understanding of this basic neurophysiological function of cortical neurons can be used for monitoring the effects of TMS. In our discussion, we conclude that the time has arrived for TMS to be offered to depressed patients as a treatment.

Altered Regional Brain Cortical Thickness in Pediatric Obstructive Sleep Apnea

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Paul M. Macey

2018-01-01

Full Text Available RationaleObstructive sleep apnea (OSA affects 2–5% of all children and is associated with cognitive and behavioral deficits, resulting in poor school performance. These psychological deficits may arise from brain injury, as seen in preliminary findings of lower gray matter volume among pediatric OSA patients. However, the psychological deficits in OSA are closely related to functions in the cortex, and such brain areas have not been specifically assessed. The objective was to determine whether cortical thickness, a marker of possible brain injury, is altered in children with OSA.MethodsWe examined regional brain cortical thicknesses using high-resolution T1-weighted magnetic resonance images in 16 pediatric OSA patients (8 males; mean age ± SD = 8.4 ± 1.2 years; mean apnea/hypopnea index ± SD = 11 ± 6 events/h and 138 controls (8.3 ± 1.1 years; 62 male; 138 subjects from the NIH Pediatric MRI database to identify cortical thickness differences in pediatric OSA subjects.ResultsCortical thinning occurred in multiple regions including the superior frontal, ventral medial prefrontal, and superior parietal cortices. The left side showed greater thinning in the superior frontal cortex. Cortical thickening was observed in bilateral precentral gyrus, mid-to-posterior insular cortices, and left central gyrus, as well as right anterior insula cortex.ConclusionChanges in cortical thickness are present in children with OSA and likely indicate disruption to neural developmental processes, including maturational patterns of cortical volume increases and synaptic pruning. Regions with thicker cortices may reflect inflammation or astrocyte activation. Both the thinning and thickening associated with OSA in children may contribute to the cognitive and behavioral dysfunction frequently found in the condition.

Regional quantitative analysis of cortical surface maps of FDG PET images

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Protas, H D; Hayashi, K M; Chin Lung, Yu; Bergsneider, M; Sung Cheng, Huang

2006-01-01

Cortical surface maps are advantageous for visualizing the 3D profile of cortical gray matter development and atrophy, and for integrating structural and functional images. In addition, cortical surface maps for PET data, when analyzed in conjunction with structural MRI data allow us to investigate, and correct for, partial volume effects. Here we compared quantitative regional PET values based on a 3D cortical surface modeling approach with values obtained directly from the 3D FDG PET images in various atlas-defined regions of interest (ROIs; temporal, parietal, frontal, and occipital lobes). FDG PET and 3D MR (SPGR) images were obtained and aligned to ICBM space for 15 normal subjects. Each image was further elastically warped in 2D parameter space of the cortical surface, to align major cortical sulci. For each point within a 15 mm distance of the cortex, the value of the PET intensity was averaged to give a cortical surface map of FDG uptake. The average PET values on the cortical surface map were calcula...

TOMM40 rs2075650 May Represent a New Candidate Gene for Vulnerability to Major Depressive Disorder

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McFarquhar, Martyn; Elliott, Rebecca; McKie, Shane; Thomas, Emma; Downey, Darragh; Mekli, Krisztina; Toth, Zoltan G; Anderson, Ian M; Deakin, JF William; Juhasz, Gabriella

2014-01-01

Evidence suggests that depression is a risk factor for dementia; however, the relationship between the two conditions is not fully understood. A novel gene (TOMM40) has been consistently associated with Alzheimer's disease (AD), but has received no attention in depression. We conducted a three-level cross-sectional study to investigate the association of the TOMM40 rs2075650 SNP with depression. We recruited a community sample of 1220 participants (571 controls, 649 lifetime depression) to complete a psychiatric background questionnaire, the Brief Symptom Inventory, and Big Five Inventory at Level-1, 243 (102 controls, 97 remitted, 44 currently depressed) to complete a face-to-face clinical interview and neuropsychological testing at Level-2 and 58 (33 controls, 25 remitted) to complete an emotional face-processing task during fMRI at Level-3. Our results indicated that the TOMM40 rs2075650 G allele was a significant risk factor for lifetime depression (p=0.00006) and, in depressed subjects, was a significant predictor of low extraversion (p=0.009). Currently depressed risk allele carriers showed subtle executive dysfunction (p=0.004) and decreased positive memory bias (p=0.021) together with reduced activity in the posterior (p(FWE)=0.045) and anterior (p(FWE)=0.041) cingulate during sad face emotion processing. Our results suggest that TOMM40 rs2075650 may be a risk factor for the development of depression characterized by reduced extraversion, impaired executive function, and decreased positive emotional recall, and reduced top-down cortical control during sad emotion processing. PMID:24549102

Jealousy increased by induced relative left frontal cortical activity.

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Kelley, Nicholas J; Eastwick, Paul W; Harmon-Jones, Eddie; Schmeichel, Brandon J

2015-10-01

Asymmetric frontal cortical activity may be one key to the process linking social exclusion to jealous feelings. The current research examined the causal role of asymmetric frontal brain activity in modulating jealousy in response to social exclusion. Transcranial direct-current stimulation (tDCS) over the frontal cortex to manipulate asymmetric frontal cortical activity was combined with a modified version of the Cyberball paradigm designed to induce jealousy. After receiving 15 min of tDCS, participants were excluded by a desired partner and reported how jealous they felt. Among individuals who were excluded, tDCS to increase relative left frontal cortical activity caused greater levels of self-reported jealousy compared to tDCS to increase relative right frontal cortical activity or sham stimulation. Limitations concerning the specificity of this effect and implications for the role of the asymmetric prefrontal cortical activity in motivated behaviors are discussed. (c) 2015 APA, all rights reserved).

Cortical gyrification is abnormal in children with prenatal alcohol exposure

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Timothy J. Hendrickson

2017-01-01

Conclusions: Abnormalities in cortical development were seen across the brain in children with PAE compared to controls. Cortical gyrification and IQ were strongly correlated, suggesting that examining mechanisms by which alcohol disrupts cortical formation may yield clinically relevant insights and potential directions for early intervention.

Impairment of GABA transporter GAT-1 terminates cortical recurrent network activity via enhanced phasic inhibition

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Daniel Simon Razik

2013-09-01

Full Text Available In the central nervous system, GABA transporters (GATs very efficiently clear synaptically released GABA from the extracellular space, and thus exert a tight control on GABAergic inhibition. In neocortex, GABAergic inhibition is heavily recruited during recurrent phases of spontaneous action potential activity which alternate with neuronally quiet periods. Therefore, such activity should be quite sensitive to minute alterations of GAT function. Here, we explored the effects of a gradual impairment of GAT-1 and GAT-2/3 on spontaneous recurrent network activity – termed network bursts and silent periods – in organotypic slice cultures of rat neocortex. The GAT-1 specific antagonist NO-711 depressed activity already at nanomolar concentrations (IC50 for depression of spontaneous multiunit firing rate of 42 nM, reaching a level of 80% at 500-1000 nM. By contrast, the GAT-2/3 preferring antagonist SNAP-5114 had weaker and less consistent effects. Several lines of evidence pointed towards an enhancement of phasic GABAergic inhibition as the dominant activity-depressing mechanism: network bursts were drastically shortened, phasic GABAergic currents decayed slower, and neuronal excitability during ongoing activity was diminished. In silent periods, NO-711 had little effect on neuronal excitability or membrane resistance, quite in contrast to the effects of muscimol, a GABA mimetic which activates GABAA receptors tonically. Our results suggest that an enhancement of phasic GABAergic inhibition efficiently curtails cortical recurrent activity and may mediate antiepileptic effects of therapeutically relevant concentrations of GAT-1 antagonists.

Frontal white matter anisotropy and antidepressant remission in late-life depression.

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Warren D Taylor

2008-09-01

Full Text Available Neuroanatomic features associated with antidepressant treatment outcomes in older depressed individuals are not well established. This study used diffusion tensor imaging to examine frontal white matter structure in depressed subjects undergoing a 12-week trial of sertraline. We hypothesized that remission would be associated with higher frontal anisotropy measures, and failure to remit with lower anisotropy.74 subjects with Major Depressive Disorder and age 60 years or older were enrolled in a twelve-week open-label trial of sertraline and completed clinical assessments and 1.5T magnetic resonance brain imaging. The apparent diffusion coefficient (ADC and fractional anisotropy (FA were measured in regions of interest placed in the white matter of the dorsolateral prefrontal cortex, anterior cingulate cortex, and corpus callosum. Differences in ADC and FA values between subjects who did and did not remit to treatment over the study period were assessed using generalized estimating equations, controlling for age, sex, medical comorbidity and baseline depression severity.Subjects who did not remit to sertraline exhibited higher FA values in the superior frontal gyri and anterior cingulate cortices bilaterally. There were no statistically significant associations between ADC measures and remission.Failure to remit to sertraline is associated with higher frontal FA values. Functional imaging studies demonstrate that depression is characterized by functional disconnection between frontal and limbic regions. Those individuals where this disconnection is related to structural changes as detected by DTI may be more likely to respond to antidepressants.ClinicalTrials.gov NCT00339066.

Response of cortical bone to antiresorptive treatment

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Hyldstrup, Lars; Jørgensen, J T; Sørensen, T K

2001-01-01

of the spine, hip, and forearm. Longitudinal changes in bone densitometry were compared with changes captured by DXR: BMD evaluated by DXR (BMDDXR), cortical thickness of the second metacarpal (CTMC2), and porosity of cortical bone. The expected annual postmenopausal reduction in BMD in the control group...... treatment regimens used in the prevention of osteoporosis....

The cortical structure of consolidated memory: a hypothesis on the role of the cingulate-entorhinal cortical connection.

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Insel, Nathan; Takehara-Nishiuchi, Kaori

2013-11-01

Daily experiences are represented by networks of neurons distributed across the neocortex, bound together for rapid storage and later retrieval by the hippocampus. While the hippocampus is necessary for retrieving recent episode-based memory associations, over time, consolidation processes take place that enable many of these associations to be expressed independent of the hippocampus. It is generally thought that mechanisms of consolidation involve synaptic weight changes between cortical regions; or, in other words, the formation of "horizontal" cortico-cortical connections. Here, we review anatomical, behavioral, and physiological data which suggest that the connections in and between the entorhinal and cingulate cortices may be uniquely important for the long-term storage of memories that initially depend on the hippocampus. We propose that current theories of consolidation that divide memory into dual systems of hippocampus and neocortex might be improved by introducing a third, middle layer of entorhinal and cingulate allocortex, the synaptic weights within which are necessary and potentially sufficient for maintaining initially hippocampus-dependent associations over long time periods. This hypothesis makes a number of still untested predictions, and future experiments designed to address these will help to fill gaps in the current understanding of the cortical structure of consolidated memory. Copyright © 2013 Elsevier Inc. All rights reserved.

Spontaneously emerging cortical representations of visual attributes

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Kenet, Tal; Bibitchkov, Dmitri; Tsodyks, Misha; Grinvald, Amiram; Arieli, Amos

2003-10-01

Spontaneous cortical activity-ongoing activity in the absence of intentional sensory input-has been studied extensively, using methods ranging from EEG (electroencephalography), through voltage sensitive dye imaging, down to recordings from single neurons. Ongoing cortical activity has been shown to play a critical role in development, and must also be essential for processing sensory perception, because it modulates stimulus-evoked activity, and is correlated with behaviour. Yet its role in the processing of external information and its relationship to internal representations of sensory attributes remains unknown. Using voltage sensitive dye imaging, we previously established a close link between ongoing activity in the visual cortex of anaesthetized cats and the spontaneous firing of a single neuron. Here we report that such activity encompasses a set of dynamically switching cortical states, many of which correspond closely to orientation maps. When such an orientation state emerged spontaneously, it spanned several hypercolumns and was often followed by a state corresponding to a proximal orientation. We suggest that dynamically switching cortical states could represent the brain's internal context, and therefore reflect or influence memory, perception and behaviour.

Spreading to localized targets in complex networks

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Sun, Ye; Ma, Long; Zeng, An; Wang, Wen-Xu

2016-12-01

As an important type of dynamics on complex networks, spreading is widely used to model many real processes such as the epidemic contagion and information propagation. One of the most significant research questions in spreading is to rank the spreading ability of nodes in the network. To this end, substantial effort has been made and a variety of effective methods have been proposed. These methods usually define the spreading ability of a node as the number of finally infected nodes given that the spreading is initialized from the node. However, in many real cases such as advertising and news propagation, the spreading only aims to cover a specific group of nodes. Therefore, it is necessary to study the spreading ability of nodes towards localized targets in complex networks. In this paper, we propose a reversed local path algorithm for this problem. Simulation results show that our method outperforms the existing methods in identifying the influential nodes with respect to these localized targets. Moreover, the influential spreaders identified by our method can effectively avoid infecting the non-target nodes in the spreading process.

Agmatine for combined treatment of epilepsy, depression and cognitive impairment in chronic epileptic animals.

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Singh, Tanveer; Bagga, Neetu; Kaur, Anureet; Kaur, Navjot; Gawande, Dinesh Yugraj; Goel, Rajesh Kumar

2017-08-01

Epilepsy is fourth most common neurological disorders associated with depression and cognitive deficits. As per present scenario, none of the antiseizure drugs have been reported successful to have ameliorative effect on epilepsy associated depression and cognitive deficits. Thus, the study was envisioned to assess an ameliorative potential of agmatine on epilepsy and its efficacy and safety for management of associated depression and cognitive deficits. The animals were made epileptic employing pentylenetetrazole (35mg/kg i.p. every 48±2h) kindling model of epilepsy and subsequently were treated with vehicle, valproic acid (300mg/kg/day i.p.) and agmatine (2.5, 5, and 10mg/kg)/day/i.p. for 15days. Except naïve, all the groups were challenged with same pentylenetetrazole dose as employed during kindling on days 5, 10, and 15 to evaluate seizure severity. Two hours after seizure severity test, tail suspension test and passive shock avoidance paradigm was employed to evaluate depression and cognitive behavior respectively. Results suggested that epileptic animals were significantly associated with depression and cognitive impairment. Chronic valproate treatment significantly reduced seizure severity, but was found unable to mitigate depression and cognitive deficits. However, agmatine treatment dose dependently ameliorated seizure severity as well as associated depression and cognitive deficits. On 15th day, animals were euthanized and pertinent neurochemical estimations were carried out in cortical and hippocampal areas of the mice brain. Thus, study concluded that agmatine ameliorated seizure severity, depression and cognitive impairment in epileptic animals, possibly via restoring glutamate-GABA neurotransmission and serotonin synthesis with decreased nitrosative stress. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Estimation of wave directional spreading

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Deo, M.C.; Gondane, D.S.; SanilKumar, V.

One of the useful measures of waves directional spreading at a given location is the directional spreading parameter. This paper presents a new approach to arrive at its characteristic value using the computational technique of Artificial Neural...

Abnormalities of fixation, saccade and pursuit in posterior cortical atrophy.

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Shakespeare, Timothy J; Kaski, Diego; Yong, Keir X X; Paterson, Ross W; Slattery, Catherine F; Ryan, Natalie S; Schott, Jonathan M; Crutch, Sebastian J

2015-07-01

The clinico-neuroradiological syndrome posterior cortical atrophy is the cardinal 'visual dementia' and most common atypical Alzheimer's disease phenotype, offering insights into mechanisms underlying clinical heterogeneity, pathological propagation and basic visual phenomena (e.g. visual crowding). Given the extensive attention paid to patients' (higher order) perceptual function, it is surprising that there have been no systematic analyses of basic oculomotor function in this population. Here 20 patients with posterior cortical atrophy, 17 patients with typical Alzheimer's disease and 22 healthy controls completed tests of fixation, saccade (including fixation/target gap and overlap conditions) and smooth pursuit eye movements using an infrared pupil-tracking system. Participants underwent detailed neuropsychological and neurological examinations, with a proportion also undertaking brain imaging and analysis of molecular pathology. In contrast to informal clinical evaluations of oculomotor dysfunction frequency (previous studies: 38%, current clinical examination: 33%), detailed eyetracking investigations revealed eye movement abnormalities in 80% of patients with posterior cortical atrophy (compared to 17% typical Alzheimer's disease, 5% controls). The greatest differences between posterior cortical atrophy and typical Alzheimer's disease were seen in saccadic performance. Patients with posterior cortical atrophy made significantly shorter saccades especially for distant targets. They also exhibited a significant exacerbation of the normal gap/overlap effect, consistent with 'sticky fixation'. Time to reach saccadic targets was significantly associated with parietal and occipital cortical thickness measures. On fixation stability tasks, patients with typical Alzheimer's disease showed more square wave jerks whose frequency was associated with lower cerebellar grey matter volume, while patients with posterior cortical atrophy showed large saccadic intrusions

Cortical thinning and clinical heterogeneity in amyotrophic lateral sclerosis.

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Mezzapesa, Domenico Maria; D'Errico, Eustachio; Tortelli, Rosanna; Distaso, Eugenio; Cortese, Rosa; Tursi, Marianna; Federico, Francesco; Zoccolella, Stefano; Logroscino, Giancarlo; Dicuonzo, Franca; Simone, Isabella Laura

2013-01-01

Amyotrophic lateral sclerosis (ALS) has heterogeneous clinical features that could be translated into specific patterns of brain atrophy. In the current study we have evaluated the relationship between different clinical expressions of classical ALS and measurements of brain cortical thickness. Cortical thickness analysis was conducted from 3D-MRI using FreeSurfer software in 29 ALS patients and 20 healthy controls. We explored three clinical traits of the disease, subdividing the patients into two groups for each of them: the bulbar or spinal onset, the higher or lower upper motor neuron burden, the faster or slower disease progression. We used both a whole brain vertex-wise analysis and a ROI analysis on primary motor areas. ALS patients showed cortical thinning in bilateral precentral gyrus, bilateral middle frontal gyrus, right superior temporal gyrus and right occipital cortex. ALS patients with higher upper motor neuron burden showed a significant cortical thinning in the right precentral gyrus and in other frontal extra-motor areas, compared to healthy controls. ALS patients with spinal onset showed a significant cortical thinning in the right precentral gyrus and paracentral lobule, compared to healthy controls. ALS patients with faster progressive disease showed a significant cortical thinning in widespread bilateral frontal and temporal areas, including the bilateral precentral gyrus, compared to healthy controls. Focusing on the primary motor areas, the ROI analysis revealed that the mean cortical thickness values were significantly reduced in ALS patients with higher upper motor neuron burden, spinal onset and faster disease progression related to healthy controls. In conclusion, the thickness of primary motor cortex could be a useful surrogate marker of upper motor neuron involvement in ALS; also our results suggest that cortical thinning in motor and non motor areas seem to reflect the clinical heterogeneity of the disease.

Cortical thinning and clinical heterogeneity in amyotrophic lateral sclerosis.

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Domenico Maria Mezzapesa

Full Text Available Amyotrophic lateral sclerosis (ALS has heterogeneous clinical features that could be translated into specific patterns of brain atrophy. In the current study we have evaluated the relationship between different clinical expressions of classical ALS and measurements of brain cortical thickness. Cortical thickness analysis was conducted from 3D-MRI using FreeSurfer software in 29 ALS patients and 20 healthy controls. We explored three clinical traits of the disease, subdividing the patients into two groups for each of them: the bulbar or spinal onset, the higher or lower upper motor neuron burden, the faster or slower disease progression. We used both a whole brain vertex-wise analysis and a ROI analysis on primary motor areas. ALS patients showed cortical thinning in bilateral precentral gyrus, bilateral middle frontal gyrus, right superior temporal gyrus and right occipital cortex. ALS patients with higher upper motor neuron burden showed a significant cortical thinning in the right precentral gyrus and in other frontal extra-motor areas, compared to healthy controls. ALS patients with spinal onset showed a significant cortical thinning in the right precentral gyrus and paracentral lobule, compared to healthy controls. ALS patients with faster progressive disease showed a significant cortical thinning in widespread bilateral frontal and temporal areas, including the bilateral precentral gyrus, compared to healthy controls. Focusing on the primary motor areas, the ROI analysis revealed that the mean cortical thickness values were significantly reduced in ALS patients with higher upper motor neuron burden, spinal onset and faster disease progression related to healthy controls. In conclusion, the thickness of primary motor cortex could be a useful surrogate marker of upper motor neuron involvement in ALS; also our results suggest that cortical thinning in motor and non motor areas seem to reflect the clinical heterogeneity of the disease.

Spreading gossip in social networks

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Lind, Pedro G.; da Silva, Luciano R.; Andrade, José S., Jr.; Herrmann, Hans J.

2007-09-01

We study a simple model of information propagation in social networks, where two quantities are introduced: the spread factor, which measures the average maximal reachability of the neighbors of a given node that interchange information among each other, and the spreading time needed for the information to reach such a fraction of nodes. When the information refers to a particular node at which both quantities are measured, the model can be taken as a model for gossip propagation. In this context, we apply the model to real empirical networks of social acquaintances and compare the underlying spreading dynamics with different types of scale-free and small-world networks. We find that the number of friendship connections strongly influences the probability of being gossiped. Finally, we discuss how the spread factor is able to be applied to other situations.

Spreading gossip in social networks.

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Lind, Pedro G; da Silva, Luciano R; Andrade, José S; Herrmann, Hans J

2007-09-01

We study a simple model of information propagation in social networks, where two quantities are introduced: the spread factor, which measures the average maximal reachability of the neighbors of a given node that interchange information among each other, and the spreading time needed for the information to reach such a fraction of nodes. When the information refers to a particular node at which both quantities are measured, the model can be taken as a model for gossip propagation. In this context, we apply the model to real empirical networks of social acquaintances and compare the underlying spreading dynamics with different types of scale-free and small-world networks. We find that the number of friendship connections strongly influences the probability of being gossiped. Finally, we discuss how the spread factor is able to be applied to other situations.

Default mode network connectivity in children with a history of preschool onset depression.

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Gaffrey, Michael S; Luby, Joan L; Botteron, Kelly; Repovš, Grega; Barch, Deanna M

2012-09-01

Atypical Default Mode Network (DMN) functional connectivity has been previously reported in depressed adults. However, there is relatively little data informing the developmental nature of this phenomenon. The current case-control study examined the DMN in a unique prospective sample of school-age children with a previous history of preschool depression. DMN functional connectivity was assessed using resting state functional connectivity magnetic resonance imaging data and the posterior cingulate (PCC) as a seed region of interest. Thirty-nine medication naïve school age children (21 with a history of preschool depression and 18 healthy peers) and their families who were ascertained as preschoolers and prospectively assessed over at least 4 annual waves as part of a federally funded study of preschool depression were included.   Decreased connectivity between the PCC and regions within the middle temporal gyrus (MTG), inferior parietal lobule, and cerebellum was found in children with known depression during the preschool period. Increased connectivity between the PCC and regions within the subgenual and anterior cingulate cortices and anterior MTG bilaterally was also found in these children. Additionally, a clinically relevant 'brain-behavior' relationship between atypical functional connectivity of the PCC and disruptions in emotion regulation was identified. To our knowledge, this is the first study to examine the DMN in children known to have experienced the onset of a clinically significant depressive syndrome during preschool. Results suggest that a history of preschool depression is associated with atypical DMN connectivity. However, longitudinal studies are needed to clarify whether the current findings of atypical DMN connectivity are a precursor or a consequence of preschool depression. © 2012 The Authors. Journal of Child Psychology and Psychiatry © 2012 Association for Child and Adolescent Mental Health.

Decreased prefrontal cortical dopamine transmission in alcoholism.

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Narendran, Rajesh; Mason, Neale Scott; Paris, Jennifer; Himes, Michael L; Douaihy, Antoine B; Frankle, W Gordon

2014-08-01

Basic studies have demonstrated that optimal levels of prefrontal cortical dopamine are critical to various executive functions such as working memory, attention, inhibitory control, and risk/reward decisions, all of which are impaired in addictive disorders such as alcoholism. Based on this and imaging studies of alcoholism that have demonstrated less dopamine in the striatum, the authors hypothesized decreased dopamine transmission in the prefrontal cortex in persons with alcohol dependence. To test this hypothesis, amphetamine and [11C]FLB 457 positron emission tomography were used to measure cortical dopamine transmission in 21 recently abstinent persons with alcohol dependence and 21 matched healthy comparison subjects. [11C]FLB 457 binding potential, specific compared to nondisplaceable uptake (BPND), was measured in subjects with kinetic analysis using the arterial input function both before and after 0.5 mg kg-1 of d-amphetamine. Amphetamine-induced displacement of [11C]FLB 457 binding potential (ΔBPND) was significantly smaller in the cortical regions in the alcohol-dependent group compared with the healthy comparison group. Cortical regions that demonstrated lower dopamine transmission in the alcohol-dependent group included the dorsolateral prefrontal cortex, medial prefrontal cortex, orbital frontal cortex, temporal cortex, and medial temporal lobe. The results of this study, for the first time, unambiguously demonstrate decreased dopamine transmission in the cortex in alcoholism. Further research is necessary to understand the clinical relevance of decreased cortical dopamine as to whether it is related to impaired executive function, relapse, and outcome in alcoholism.

Cortical desmoid of the humerus: radiographic and MRI correlation

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Kay, Matthew; Counsel, Peter [Princess Margaret Hospital for Children, Department of Diagnostic Imaging, Perth (Australia); Perth Radiological Clinic, Perth (Australia); Wood, David [Princess Margaret Hospital for Children, Department of Orthopedic Surgery, Perth (Australia); Breidahl, William [Perth Radiological Clinic, Perth (Australia)

2017-07-15

Cortical desmoids are self-limiting fibro-osseous lesions commonly occurring at the medial supracondylar femur in active adolescents, at either the origin of the medial head of the gastrocnemius or at the insertion of the adductor magnus aponeurosis. Less commonly, in a similar demographic, cortical desmoids may occur in the proximal humerus medially at the insertion of the pectoralis major muscle or laterally at the insertion of the deltoid. The radiographic appearance of the proximal humerus cortical desmoid has been described previously, but not the MRI appearance. We present the radiographic and MRI appearances of a proximal humerus cortical desmoid in a young adolescent who presented for investigation of right shoulder pain. (orig.)

Cortical desmoid of the humerus: radiographic and MRI correlation

International Nuclear Information System (INIS)

Kay, Matthew; Counsel, Peter; Wood, David; Breidahl, William

2017-01-01

Cortical desmoids are self-limiting fibro-osseous lesions commonly occurring at the medial supracondylar femur in active adolescents, at either the origin of the medial head of the gastrocnemius or at the insertion of the adductor magnus aponeurosis. Less commonly, in a similar demographic, cortical desmoids may occur in the proximal humerus medially at the insertion of the pectoralis major muscle or laterally at the insertion of the deltoid. The radiographic appearance of the proximal humerus cortical desmoid has been described previously, but not the MRI appearance. We present the radiographic and MRI appearances of a proximal humerus cortical desmoid in a young adolescent who presented for investigation of right shoulder pain. (orig.)

On the homogeneity and heterogeneity of cortical thickness profiles in Homo sapiens sapiens.

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Koten, Jan Willem; Schüppen, André; Morozova, Maria; Lehofer, Agnes; Koschutnig, Karl; Wood, Guilherme

2017-12-20

Cortical thickness has been investigated since the beginning of the 20th century, but we do not know how similar the cortical thickness profiles among humans are. In this study, the local similarity of cortical thickness profiles was investigated using sliding window methods. Here, we show that approximately 5% of the cortical thickness profiles are similarly expressed among humans while 45% of the cortical thickness profiles show a high level of heterogeneity. Therefore, heterogeneity is the rule, not the exception. Cortical thickness profiles of somatosensory homunculi and the anterior insula are consistent among humans, while the cortical thickness profiles of the motor homunculus are more variable. Cortical thickness profiles of homunculi that code for muscle position and skin stimulation are highly similar among humans despite large differences in sex, education, and age. This finding suggests that the structure of these cortices remains well preserved over a lifetime. Our observations possibly relativize opinions on cortical plasticity.

The Unique Brain Anatomy of Meditation Practitioners: Alterations in Cortical Gyrification

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Eileen eLuders

2012-02-01

Full Text Available Several cortical regions are reported to vary in meditation practitioners. However, since prior analyses were focused on examining gray matter or cortical thickness, additional effects with respect to other cortical features might have remained undetected. Gyrification (the pattern and degree of cortical folding is an important cerebral characteristic related to the geometry of the brain’s surface. Cortical folding occurs early in development and might be linked to behavioral traits. Thus, exploring cortical gyrification in long-term meditators may provide additional clues with respect to the underlying anatomical correlates of meditation. This study examined cortical gyrification in a large sample (n=100 of meditators and controls, carefully matched for sex and age. Cortical gyrification was established via calculating mean curvature across thousands of vertices on individual cortical surface models. Pronounced group differences indicating larger gyrification in meditators were evident within the left precentral gyrus, right fusiform gyrus, right cuneus, as well as left and right anterior dorsal insula (the latter representing the global significance maximum. Although the exact functional implications of larger cortical gyrification remain to be established, these findings suggest the insula to be a key structure involved in aspects of meditation. For example, variations in insular complexity could affect the regulation of well-known distractions in the process of meditation, such as daydreaming, mind-wandering, and projections into past or future. Moreover, given that meditators are masters in introspection, awareness, and emotional control, increased insular gyrification may reflect an ideal integration of autonomic, affective, and cognitive processes. Due to the cross-sectional nature of this study, further research is necessary determine the relative contribution of nature and nurture to links between cortical gyrification and meditation.

COMBINED SURGERY OF SPREAD THYROID CANCER

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V. Zh. Brzhezovsky

2014-01-01

Full Text Available Results of treating of 99 patients with differentiated thyroid cancer spreading beyond the capsule of the organ were analysed. In most cases with spreading the tumor to the tracheal rings performing of organ-preserving operations (from “window-like” tracheal resections to circular tracheal resection with intertracheal anastomosis is possible. Choosing of type of operation to be performed depends on localisation and spread of tumor invasion of trachea, pharynx and esophagus. Using of combined operations in patients with locally-spread thyroid cancer allows to achieve long and stable remission in most of the cases.

Reward signals, attempted suicide, and impulsivity in late-life depression.

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Dombrovski, Alexandre Y; Szanto, Katalin; Clark, Luke; Reynolds, Charles F; Siegle, Greg J

2013-10-01

IMPORTANCE—Suicide can be viewed as an escape from unendurable punishment at the cost of any future rewards. Could faulty estimation of these outcomes predispose to suicidal behavior? In behavioral studies, many of those who have attempted suicide misestimate expected rewards on gambling and probabilistic learning tasks.OBJECTIVES—To describe the neural circuit abnormalities that underlie disadvantageous choices in people at risk for suicide and to relate these abnormalities to impulsivity, which is one of the components of vulnerability to suicide.DESIGN—Case-control functional magnetic resonance imaging study of reward learning using are inforcement learning model.SETTING—University hospital and outpatient clinic.PATIENTS—Fifty-three participants 60 years or older, including 15 depressed patients who had attempted suicide, 18 depressed patients who had never attempted suicide (depressed control subjects), and 20 psychiatrically healthy controls.MAIN OUTCOMES AND MEASURES—Components of the cortical blood oxygenation level–dependent response tracking expected and unpredicted rewards.RESULTS—Depressed elderly participants displayed 2 distinct disruptions of control over reward-guided behavior. First, impulsivity and a history of suicide attempts (particularly poorly planned ones) were associated with a weakened expected reward signal in the paralimbic cortex,which in turn predicted the behavioral insensitivity to contingency change. Second, depression was associated with disrupted corticostriatothalamic encoding of unpredicted rewards, which in turn predicted the behavioral over sensitivity to punishment. These results were robust to the effects of possible brain damage from suicide attempts, depressive severity, co-occurring substance use and anxiety disorders, antidepressant and anticholinergic exposure, lifetime exposure to electroconvulsive therapy, vascular illness, and incipient dementia.CONCLUSIONS AND RELEVANCE—Altered paralimbic reward

Effects of Parecoxib and Fentanyl on nociception-induced cortical activity

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Wang Ying-Wei

2010-01-01

Full Text Available Abstract Background Analgesics, including opioids and non-steroid anti-inflammatory drugs reduce postoperative pain. However, little is known about the quantitative effects of these drugs on cortical activity induced by nociceptive stimulation. The aim of the present study was to determine the neural activity in response to a nociceptive stimulus and to investigate the effects of fentanyl (an opioid agonist and parecoxib (a selective cyclooxygenase-2 inhibitor on this nociception-induced cortical activity evoked by tail pinch. Extracellular recordings (electroencephalogram and multi-unit signals were performed in the area of the anterior cingulate cortex while intracellular recordings were made in the primary somatosensory cortex. The effects of parecoxib and fentanyl on induced cortical activity were compared. Results Peripheral nociceptive stimulation in anesthetized rats produced an immediate electroencephalogram (EEG desynchronization resembling the cortical arousal (low-amplitude, fast-wave activity, while the membrane potential switched into a persistent depolarization state. The induced cortical activity was abolished by fentanyl, and the fentanyl's effect was reversed by the opioid receptor antagonist, naloxone. Parecoxib, on the other hand, did not significantly affect the neural activity. Conclusion Cortical activity was modulated by nociceptive stimulation in anesthetized rats. Fentanyl showed a strong inhibitory effect on the nociceptive-stimulus induced cortical activity while parecoxib had no significant effect.

Neuroimaging of malformation of cortical development

International Nuclear Information System (INIS)

Zlatareva, D.; Hadjidekov, V.; Tournev, I.; Rossi, A.

2012-01-01

Malformations of cortical development (MCD) are heterogeneous group of disease which result from disruption of 3 main stages of cortical development.The common clinical presentation is refractory epilepsy and or developmental delay. The aim of this paper is to describe and analyze magnetic resonance (MR) findings and to present protocol for examination. We analyze MR findings in 17 patients with MCD. The average age was 12,1 year (from 2 months - 57 years). The main indications from reference physician are epilepsy and developmental delay. In 12 patients 1.5T MR was performed, and in 5 - 0.5T. Subependymal heterotopias was found in 6 patients, focal cortical dysplasia - 3. polymicrogyria - 3, schizencephaly - 2, hemimegalencephaly -1, lizencephaly -1, tuberous sclerosis -1. The most common MCD are heterotopias, focal cortical dysplasia, polymicrogyria. schizencephaiy, pachygyria and lizencephaly. In our study the number of patients is not big enough to make a conclusion about frequency of the forms of MCD and our goal is to analyze MR findings which are not well studied in our country. MRI is the method of choice for diagnosis of MCD. The protocol should be different from routine brain protocol to interpret the images with good quality and not miss the pathology. Knowledge of MR findings in MCD would help for genetic counselling in some cases or can predict prognosis in some patients. (authors)

Epidemic spreading through direct and indirect interactions.

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Ganguly, Niloy; Krueger, Tyll; Mukherjee, Animesh; Saha, Sudipta

2014-09-01

In this paper we study the susceptible-infected-susceptible epidemic dynamics, considering a specialized setting where popular places (termed passive entities) are visited by agents (termed active entities). We consider two types of spreading dynamics: direct spreading, where the active entities infect each other while visiting the passive entities, and indirect spreading, where the passive entities act as carriers and the infection is spread via them. We investigate in particular the effect of selection strategy, i.e., the way passive entities are chosen, in the spread of epidemics. We introduce a mathematical framework to study the effect of an arbitrary selection strategy and derive formulas for prevalence, extinction probabilities, and epidemic thresholds for both indirect and direct spreading. We also obtain a very simple relationship between the extinction probability and the prevalence. We pay special attention to preferential selection and derive exact formulas. The analysis reveals that an increase in the diversity in the selection process lowers the epidemic thresholds. Comparing the direct and indirect spreading, we identify regions in the parameter space where the prevalence of the indirect spreading is higher than the direct one.

Zic deficiency in the cortical marginal zone and meninges results in cortical lamination defects resembling those in type II lissencephaly.

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Inoue, Takashi; Ogawa, Masaharu; Mikoshiba, Katsuhiko; Aruga, Jun

2008-04-30

The formation of the highly organized cortical structure depends on the production and correct placement of the appropriate number and types of neurons. The Zic family of zinc-finger transcription factors plays essential roles in regulating the proliferation and differentiation of neuronal progenitors in the medial forebrain and the cerebellum. Examination of the expression of Zic genes demonstrated that Zic1, Zic2, and Zic3 were expressed by the progenitor cells in the septum and cortical hem, the sites of generation of the Cajal-Retzius (CR) cells. Immunohistochemical studies have revealed that Zic proteins were abundantly expressed in the meningeal cells and that the majority of the CR cells distributed in the medial and dorsal cortex also expressed Zic proteins in the mid-late embryonic and postnatal cortical marginal zones. During embryonic cortical development, Zic1/Zic3 double-mutant and hypomorphic Zic2 mutant mice showed a reduction in the number of CR cells in the rostral cortex, whereas the cell number remained unaffected in the caudal cortex. These mutants also showed mislocalization of the CR cells and cortical lamination defects, resembling the changes noted in type II (cobblestone) lissencephaly, throughout the brain. In the Zic1/3 mutant, reduced proliferation of the meningeal cells was observed before the thinner and disrupted organization of the pial basement membrane (BM) with reduced expression of the BM components and the meningeal cell-derived secretory factor. These defects correlated with the changes in the end feet morphology of the radial glial cells. These findings indicate that the Zic genes play critical roles in cortical development through regulating the proliferation of meningeal cells and the pial BM assembly.

Shortened cortical silent period in adductor spasmodic dysphonia: evidence for widespread cortical excitability.

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Samargia, Sharyl; Schmidt, Rebekah; Kimberley, Teresa Jacobson

2014-02-07

The purpose of this study was to compare cortical inhibition in the hand region of the primary motor cortex between subjects with focal hand dystonia (FHD), adductor spasmodic dysphonia (AdSD), and healthy controls. Data from 28 subjects were analyzed (FHD n=11, 53.25 ± 8.74 y; AdSD: n=8, 56.38 ± 7.5 y; and healthy controls: n=941.67 ± 10.85 y). All subjects received single pulse TMS to the left motor cortex to measure cortical silent period (CSP) in the right first dorsal interosseus (FDI) muscle. Duration of the CSP was measured and compared across groups. A one-way ANCOVA with age as a covariate revealed a significant group effect (p<0.001). Post hoc analysis revealed significantly longer CSP duration in the healthy group vs. AdSD group (p<0.001) and FHD group (p<0.001). These results suggest impaired intracortical inhibition is a neurophysiologic characteristic of FHD and AdSD. In addition, the shortened CSP in AdSD provides evidence to support a widespread decrease in cortical inhibition in areas of the motor cortex that represent an asymptomatic region of the body. These findings may inform future investigations of differential diagnosis as well as alternative treatments for focal dystonias. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Abnormalities of cortical structures in adolescent-onset conduct disorder.

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Jiang, Y; Guo, X; Zhang, J; Gao, J; Wang, X; Situ, W; Yi, J; Zhang, X; Zhu, X; Yao, S; Huang, B

2015-12-01

Converging evidence has revealed both functional and structural abnormalities in adolescents with early-onset conduct disorder (EO-CD). The neurological abnormalities underlying EO-CD may be different from that of adolescent-onset conduct disorder (AO-CD) patients. However, the cortical structure in AO-CD patients remains largely unknown. The aim of the present study was to investigate the cortical alterations in AO-CD patients. We investigated T1-weighted brain images from AO-CD patients and age-, gender- and intelligence quotient-matched controls. Cortical structures including thickness, folding and surface area were measured using the surface-based morphometric method. Furthermore, we assessed impulsivity and antisocial symptoms using the Barratt Impulsiveness Scale (BIS) and the Antisocial Process Screening Device (APSD). Compared with the controls, we found significant cortical thinning in the paralimbic system in AO-CD patients. For the first time, we observed cortical thinning in the precuneus/posterior cingulate cortex (PCC) in AO-CD patients which has not been reported in EO-CD patients. Prominent folding abnormalities were found in the paralimbic structures and frontal cortex while diminished surface areas were shown in the precentral and inferior temporal cortex. Furthermore, cortical thickness of the paralimbic structures was found to be negatively correlated with impulsivity and antisocial behaviors measured by the BIS and APSD, respectively. The present study indicates that AO-CD is characterized by cortical structural abnormalities in the paralimbic system, and, in particular, we highlight the potential role of deficient structures including the precuneus and PCC in the etiology of AO-CD.

Cortical functional connectivity decodes subconscious, task-irrelevant threat-related emotion processing

OpenAIRE

Pantazatos, Spiro P.; Talati, Ardesheer; Pavlidis, Paul; Hirsch, Joy

2012-01-01

It is currently unclear to what extent cortical structures are required for and engaged during subconscious processing of biologically salient affective stimuli (i.e. the ‘low-road’ vs. ‘many-roads’ hypotheses). Here we show that cortical-cortical and cortical-subcortical functional connectivity (FC) contain substantially more information, relative to subcortical-subcortical FC (i.e. ‘subcortical alarm’ and other limbic regions), that predicts subliminal fearful face processing within individ...

Cortical activity in tinnitus patients and its modification by phonostimulation

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Katarzyna Pawlak-Osińska

2013-04-01

Full Text Available OBJECTIVE: The goal of this study was to observe spontaneous cortical activity and cortical activity modulated by tinnitus-matched sound in tinnitus patients and healthy subjects with no otoneurologic symptoms. METHOD: Data were prospectively collected from 50 tinnitus patients and 25 healthy subjects. Cortical activity was recorded in all subjects with eyes closed and open and during photostimulation, hyperventilation and acoustic stimulation using 19-channel quantitative electroencephalography. The sound applied in the tinnitus patients was individually matched with the ability to mask or equal the tinnitus. The maximal and mean amplitude of the delta, theta, alpha and beta waves and the type and amount of the pathologic EEG patterns were noted during each recording. Differences in cortical localization and the influence of sound stimuli on spontaneous cortical activity were evaluated between the groups. RESULTS: The tinnitus group exhibited decreased delta activity and increased alpha and beta activity. Hyperventilation increased the intensity of the differences. The tinnitus patients had more sharp-slow waves and increased slow wave amplitude. Sound stimuli modified the EEG recordings; the delta and beta wave amplitudes were increased, whereas the alpha-1 wave amplitude was decreased. Acoustic stimulation only slightly affected the temporal region. CONCLUSION: Cortical activity in the tinnitus patients clearly differed from that in healthy subjects, i.e., tinnitus is not a “phantom” sign. The changes in cortical activity included decreased delta wave amplitudes, increased alpha-1, beta-1 and beta-h wave amplitudes and pathologic patterns. Cortical activity modifications occurred predominantly in the temporal region. Acoustic stimulation affected spontaneous cortical activity only in tinnitus patients, and although the applied sound was individually matched, the pathologic changes were only slightly improved.

Cortical Networks for Visual Self-Recognition

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Sugiura, Motoaki

This paper briefly reviews recent developments regarding the brain mechanisms of visual self-recognition. A special cognitive mechanism for visual self-recognition has been postulated based on behavioral and neuropsychological evidence, but its neural substrate remains controversial. Recent functional imaging studies suggest that multiple cortical mechanisms play self-specific roles during visual self-recognition, reconciling the existing controversy. Respective roles for the left occipitotemporal, right parietal, and frontal cortices in symbolic, visuospatial, and conceptual aspects of self-representation have been proposed.

Cortical networks for visual self-recognition

International Nuclear Information System (INIS)

Sugiura, Motoaki

2007-01-01

This paper briefly reviews recent developments regarding the brain mechanisms of visual self-recognition. A special cognitive mechanism for visual self-recognition has been postulated based on behavioral and neuropsychological evidence, but its neural substrate remains controversial. Recent functional imaging studies suggest that multiple cortical mechanisms play self-specific roles during visual self-recognition, reconciling the existing controversy. Respective roles for the left occipitotemporal, right parietal, and frontal cortices in symbolic, visuospatial, and conceptual aspects of self-representation have been proposed. (author)

Cortical-Cortical Interactions And Sensory Information Processing in Autism

Science.gov (United States)

2008-04-30

significant development for disseminating the results of biomedical research in our lifetime." Sir Paul Nurse , Cancer Research UK Your research papers...of the evidence for local cortical over-connectivity is anecdotal. Belmonte and colleagues suggested the co-morbidity with epilepsy that is highly...Tomma-Halme J, Lahti-Nuuttila P, Service E, Virsu V: Rate of information segregation in developmentally dyslexic children . Brain Lang 2000, 75:66-81

Multimodal surface-based morphometry reveals diffuse cortical atrophy in traumatic brain injury.

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Sorenson Donna J

2009-12-01

Full Text Available Abstract Background Patients with traumatic brain injury (TBI often present with significant cognitive deficits without corresponding evidence of cortical damage on neuroradiological examinations. One explanation for this puzzling observation is that the diffuse cortical abnormalities that characterize TBI are difficult to detect with standard imaging procedures. Here we investigated a patient with severe TBI-related cognitive impairments whose scan was interpreted as normal by a board-certified radiologist in order to determine if quantitative neuroimaging could detect cortical abnormalities not evident with standard neuroimaging procedures. Methods Cortical abnormalities were quantified using multimodal surfaced-based morphometry (MSBM that statistically combined information from high-resolution structural MRI and diffusion tensor imaging (DTI. Normal values of cortical anatomy and cortical and pericortical DTI properties were quantified in a population of 43 healthy control subjects. Corresponding measures from the patient were obtained in two independent imaging sessions. These data were quantified using both the average values for each lobe and the measurements from each point on the cortical surface. The results were statistically analyzed as z-scores from the mean with a p Results The TBI patient showed significant regional abnormalities in cortical thickness, gray matter diffusivity and pericortical white matter integrity that replicated across imaging sessions. Consistent with the patient's impaired performance on neuropsychological tests of executive function, cortical abnormalities were most pronounced in the frontal lobes. Conclusions MSBM is a promising tool for detecting subtle cortical abnormalities with high sensitivity and selectivity. MSBM may be particularly useful in evaluating cortical structure in TBI and other neurological conditions that produce diffuse abnormalities in both cortical structure and tissue properties.

Sensorimotor modulation of mood and depression: In search of an optimal mode of stimulation

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RESIT eCANBEYLI

2013-07-01

Full Text Available Depression involves a dysfunction in an affective fronto-limbic circuitry including the prefrontal cortices, several limbic structures including the cingulate cortex, the amygdala and the hippocampus as well as the basal ganglia. A major emphasis of research on the etiology and treatment of mood disorders has been to assess the impact of centrally generated (top-down processes impacting the affective fronto-limbic circuitry. The present review shows that peripheral (bottom-up unipolar stimulation via the visual and the auditory modalities as well as by physical exercise modulates mood and depressive symptoms in humans and animals and activates the same central affective neurocircuitry involved in depression. It is proposed that the amygdala serves as a gateway by articulating the mood regulatory sensorimotor stimulation with the central affective circuitry by emotionally labeling and mediating the storage of such emotional events in long-term memory. Since both amelioration and aggravation of mood is shown to be possible by unipolar stimulation, the review suggests that a psychophysical assessment of mood modulation by multi-modal stimulation may uncover mood ameliorative synergisms and serve as adjunctive treatment for depression. Thus, the integrative review not only emphasizes the relevance of investigating the optimal levels of mood regulatory sensorimotor stimulation, but also provides a conceptual springboard for related future research.

A randomized placebo-controlled study of noninvasive cortical electrostimulation in the treatment of fibromyalgia patients.

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Hargrove, Jeffrey B; Bennett, Robert M; Simons, David G; Smith, Susan J; Nagpal, Sunil; Deering, Donald E

2012-01-01

The aim of this multicenter study was to evaluate the efficacy, safety, and tolerability of noninvasive cortical electrostimulation in the management of fibromyalgia (FM). A prospective, randomized, double-blind, placebo-controlled design was used. Setting.  Subjects received therapy at two different outpatient clinical locations. There were 77 subjects meeting the American College of Rheumatology 1990 classification criteria for FM. Intervention.  Thirty-nine (39) active treatment (AT) FM patients and 38 placebo controls received 22 applications of either noninvasive cortical electrostimulation or a sham therapy over an 11-week period. The primary outcome measures were the number of tender points (TePs) and pressure pain threshold (PPT). Secondary outcome measures were responses to the Fibromyalgia Impact Questionnaire (FIQ), Symptom Checklist-90 (SCL-90), Beck Depression Inventory-II, and a novel sleep questionnaire, all evaluated at baseline and at the end of treatment. Intervention provided significant improvements in TeP measures: compared with placebo, the AT patients improved in the number of positive TePs (-7.4 vs -0.2, PFIQ score (-15.5 vs -5.6, P=0.03), FIQ pain (-2.0 vs -0.6, P=0.03), FIQ fatigue (-2.0 vs -0.4, P=0.02), and FIQ refreshing sleep (-2.1 vs -0.7, P=0.02); and while FIQ function improved (-1.0 vs -0.2), the between-group change had a 14% likelihood of occurring due to chance (P=0.14). There were no significant side effects observed. Noninvasive cortical electrostimulation in FM patients provided modest improvements in pain, TeP measures, fatigue, and sleep; and the treatment was well tolerated. This form of therapy could potentially provide worthwhile adjunctive symptom relief for FM patients. Wiley Periodicals, Inc.

Beta-amyloid deposition and cognitive function in patients with major depressive disorder with different subtypes of mild cognitive impairment: 18F-florbetapir (AV-45/Amyvid) PET study

International Nuclear Information System (INIS)

Wu, Kuan-Yi; Liu, Chia-Yih; Chen, Chia-Hsiang; Lee, Chin-Pang; Chen, Cheng-Sheng; Hsiao, Ing-Tsung; Hsieh, Chia-Ju; Yen, Tzu-Chen; Lin, Kun-Ju

2016-01-01

The objective of this study was to evaluate the amyloid burden, as assessed by 18 F-florbetapir (AV-45/Amyvid) positron emission tomography PET, in patients with major depressive disorder (MDD) with different subtypes of mild cognitive impairment (MCI) and the relationship between amyloid burden and cognition in MDD patients. The study included 55 MDD patients without dementia and 21 healthy control subjects (HCs) who were assessed using a comprehensive cognitive test battery and 18 F-florbetapir PET imaging. The standardized uptake value ratios (SUVR) in eight cortical regions using the whole cerebellum as reference region were determined and voxel-wise comparisons between the HC and MDD groups were performed. Vascular risk factors, serum homocysteine level and the apolipoprotein E (ApoE) genotype were also determined. Among the 55 MDD patients, 22 (40.0 %) had MCI, 12 (21.8 %) non-amnestic MCI (naMCI) and 10 (18.2 %) amnestic MCI (aMCI). The MDD patients with aMCI had the highest relative 18 F-florbetapir uptake in all cortical regions, and a significant difference in relative 18 F-florbetapir uptake was found in the parietal region as compared with that in naMCI subjects (P < 0.05) and HCs (P < 0.01). Voxel-wise analyses revealed significantly increased relative 18 F-florbetapir uptake in the MDD patients with aMCI and naMCI in the frontal, parietal, temporal and occipital areas (P < 0.005). The global cortical SUVR was significantly negatively correlated with MMSE score (r = -0.342, P = 0.010) and memory function (r = -0.328, P = 0.015). The negative correlation between the global SUVR and memory in the MDD patients remained significant in multiple regression analyses that included age, educational level, ApoE genotype, and depression severity (β = -3.607, t = -2.874, P = 0.006). We found preliminary evidence of brain beta-amyloid deposition in MDD patients with different subtypes of MCI. Our findings in MDD patients support the hypothesis that a higher

Growth and Age-Related Abnormalities in Cortical Structure and Fracture Risk

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Ego Seeman

2015-12-01

Full Text Available Vertebral fractures and trabecular bone loss have dominated thinking and research into the pathogenesis and the structural basis of bone fragility during the last 70 years. However, 80% of all fractures are non-vertebral and occur at regions assembled using large amounts of cortical bone; only 20% of fractures are vertebral. Moreover, ~80% of the skeleton is cortical and ~70% of all bone loss is cortical even though trabecular bone is lost more rapidly than cortical bone. Bone is lost because remodelling becomes unbalanced after midlife. Most cortical bone loss occurs by intracortical, not endocortical remodelling. Each remodelling event removes more bone than deposited enlarging existing canals which eventually coalesce eroding and thinning the cortex from 'within.' Thus, there is a need to study the decay of cortical as well as trabecular bone, and to develop drugs that restore the strength of both types of bone. It is now possible to accurately quantify cortical porosity and trabecular decay in vivo. The challenges still to be met are to determine whether measurement of porosity identifies persons at risk for fracture, whether this approach is compliments information obtained using bone densitometry, and whether changes in cortical porosity and other microstructural traits have the sensitivity to serve as surrogates of treatment success or failure.

Wireless Cortical Brain-Machine Interface for Whole-Body Navigation in Primates

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Rajangam, Sankaranarayani; Tseng, Po-He; Yin, Allen; Lehew, Gary; Schwarz, David; Lebedev, Mikhail A.; Nicolelis, Miguel A. L.

2016-03-01

Several groups have developed brain-machine-interfaces (BMIs) that allow primates to use cortical activity to control artificial limbs. Yet, it remains unknown whether cortical ensembles could represent the kinematics of whole-body navigation and be used to operate a BMI that moves a wheelchair continuously in space. Here we show that rhesus monkeys can learn to navigate a robotic wheelchair, using their cortical activity as the main control signal. Two monkeys were chronically implanted with multichannel microelectrode arrays that allowed wireless recordings from ensembles of premotor and sensorimotor cortical neurons. Initially, while monkeys remained seated in the robotic wheelchair, passive navigation was employed to train a linear decoder to extract 2D wheelchair kinematics from cortical activity. Next, monkeys employed the wireless BMI to translate their cortical activity into the robotic wheelchair’s translational and rotational velocities. Over time, monkeys improved their ability to navigate the wheelchair toward the location of a grape reward. The navigation was enacted by populations of cortical neurons tuned to whole-body displacement. During practice with the apparatus, we also noticed the presence of a cortical representation of the distance to reward location. These results demonstrate that intracranial BMIs could restore whole-body mobility to severely paralyzed patients in the future.

Horizontal integration and cortical dynamics.

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Gilbert, C D

1992-07-01

We have discussed several results that lead to a view that cells in the visual system are endowed with dynamic properties, influenced by context, expectation, and long-term modifications of the cortical network. These observations will be important for understanding how neuronal ensembles produce a system that perceives, remembers, and adapts to injury. The advantage to being able to observe changes at early stages in a sensory pathway is that one may be able to understand the way in which neuronal ensembles encode and represent images at the level of their receptive field properties, of cortical topographies, and of the patterns of connections between cells participating in a network.

PET in malformations of cortical development

International Nuclear Information System (INIS)

Bouilleret, V.; O'Brien, T.J.; Bouilleret, V.; Bouilleret, V.; Chiron, C.; Chiron, C.

2009-01-01

Within the group of malformations of cortical development, focal cortical dysplasia (FCD) are an increasingly recognized cause of intractable epilepsy that can be cured by surgery. The success of cortical resection for intractable epilepsy is highly dependent on the accurate pre-surgical delineation of the regions responsible for generating seizures. [ 18 F]-FDG PET, which images cerebral metabolism studying brain glucose uptake, is the most established functional imaging modality in the evaluation of patients with epilepsy. The aim of this article is to review [ 18 F]-FDG PET usefulness as a pre-surgical tool in the evaluation of medically refractory partial epilepsy. It has an established place in assisting in the localisation and definition of FCD in patients with no lesion, or only a subtle abnormality, on MRI. The role of FDG-PET in defining the extent of the surgical resection is still uncertain and needs to be the focus of future research. (authors)

Chronic Diseases, Lack of Medications, and Depression Among Syrian Refugees in Jordan, 2013–2014

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Al-Smadi, Ahmed Mohammad; Tawalbeh, Loai Issa; Khoury, Laurice Sami

2015-01-01

Introduction Studying mental and physical health problems in refugees facilitates providing suitable health care, thus improving their quality of life. We studied depression tendency in Syrian refugees in Jordan in the light of chronic diseases and medication availability. Also, depression prevalence and depression comorbidity with chronic diseases were identified. Methods In this multicenter cross-sectional survey, data from Syrian refugees attending Caritas centers in 6 Jordanian cities from November 2013 through June 2014 were analyzed. Participants’ demographics, depression, previously diagnosed chronic diseases, and newly diagnosed chronic diseases and the availability of medications were studied. Logistic regression was used to examine predictors for depression. Results Of 765 refugees who participated, about one-third demonstrated significant depression as measured by the Beck Depression Inventory. Descriptive analyses showed that depression was comorbid in 35% of participants with previously diagnosed chronic diseases and in 40% of participants with newly diagnosed chronic diseases. Newly diagnosed chronic diseases and lack of medications significantly contributed to depression, but the regression model as a whole explained less than 5% of the variance. Conclusion Because the regression model showed low effect size, we concluded that newly diagnosed chronic diseases and medication shortages could not predict depression in Syrian refugees residing in Jordan. Therefore, further studies of additional factors are recommended. Prompt measures have to be taken to prevent the spread of chronic diseases and improve mental health in this fragile population. PMID:25633485

Transcranial magnetic stimulation reveals cortical hyperexcitability in episodic cluster headache.

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Cosentino, Guiseppe; Brighina, Filippo; Brancato, Sara; Valentino, Francesca; Indovino, Serena; Fierro, Brigida

2015-01-01

Evidence shows involvement of the cerebral cortex in the pathophysiology of cluster headache (CH). Here we investigated cortical excitability in episodic CH patients by using transcranial magnetic stimulation. In 25 patients with episodic CH and 13 healthy subjects we evaluated the motor cortical response to single-pulse (ie, motor threshold, input-output curves, cortical silent period) and paired-pulse (ie, intracortical facilitation, short intracortical inhibition) transcranial magnetic stimulation in both hemispheres. Thirteen patients were evaluated outside bout and the remaining 12 patients inside bout. Our results showed increased slope of the input-output curves after stimulation of both hemispheres in patients outside bout and in the hemisphere contralateral to the headache side in patients inside bout. Increased intracortical facilitation was observed in the hemisphere ipsilateral to the headache side in patients evaluated both outside and inside bout; reduced short intracortical inhibition was observed in patients inside bout ipsilateral to the side of pain. In conclusion, we provide evidence of increased cortical excitability in episodic CH both outside and inside bout, especially in the hemisphere ipsilateral to the side of headache attacks. Our results suggest that an abnormal regulation of cortical excitability could be involved in the pathophysiology of CH. We investigated cortical excitability in episodic cluster headache by using transcranial magnetic stimulation, providing evidence of cortical hyperexcitability in patients both inside and outside bout. We suggest that an abnormal state of cortical excitability could be involved in the pathophysiology of the disease. Copyright © 2015 American Pain Society. Published by Elsevier Inc. All rights reserved.

Stroke rehabilitation using noninvasive cortical stimulation: aphasia.

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Mylius, Veit; Zouari, Hela G; Ayache, Samar S; Farhat, Wassim H; Lefaucheur, Jean-Pascal

2012-08-01

Poststroke aphasia results from the lesion of cortical areas involved in the motor production of speech (Broca's aphasia) or in the semantic aspects of language comprehension (Wernicke's aphasia). Such lesions produce an important reorganization of speech/language-specific brain networks due to an imbalance between cortical facilitation and inhibition. In fact, functional recovery is associated with changes in the excitability of the damaged neural structures and their connections. Two main mechanisms are involved in poststroke aphasia recovery: the recruitment of perilesional regions of the left hemisphere in case of small lesion and the acquisition of language processing ability in homotopic areas of the nondominant right hemisphere when left hemispheric language abilities are permanently lost. There is some evidence that noninvasive cortical stimulation, especially when combined with language therapy or other therapeutic approaches, can promote aphasia recovery. Cortical stimulation was mainly used to either increase perilesional excitability or reduce contralesional activity based on the concept of reciprocal inhibition and maladaptive plasticity. However, recent studies also showed some positive effects of the reinforcement of neural activities in the contralateral right hemisphere, based on the potential compensatory role of the nondominant hemisphere in stroke recovery.

Brain cortical characteristics of lifetime cognitive ageing.

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Cox, Simon R; Bastin, Mark E; Ritchie, Stuart J; Dickie, David Alexander; Liewald, Dave C; Muñoz Maniega, Susana; Redmond, Paul; Royle, Natalie A; Pattie, Alison; Valdés Hernández, Maria; Corley, Janie; Aribisala, Benjamin S; McIntosh, Andrew M; Wardlaw, Joanna M; Deary, Ian J

2018-01-01

Regional cortical brain volume is the product of surface area and thickness. These measures exhibit partially distinct trajectories of change across the brain's cortex in older age, but it is unclear which cortical characteristics at which loci are sensitive to cognitive ageing differences. We examine associations between change in intelligence from age 11 to 73 years and regional cortical volume, surface area, and thickness measured at age 73 years in 568 community-dwelling older adults, all born in 1936. A relative positive change in intelligence from 11 to 73 was associated with larger volume and surface area in selective frontal, temporal, parietal, and occipital regions (r cognitive ageing and a thinner cortex for any region. Interestingly, thickness and surface area were phenotypically independent across bilateral lateral temporal loci, whose surface area was significantly related to change in intelligence. These findings suggest that associations between regional cortical volume and cognitive ageing differences are predominantly driven by surface area rather than thickness among healthy older adults. Regional brain surface area has been relatively underexplored, and is a potentially informative biomarker for identifying determinants of cognitive ageing differences.

Free energy analysis of cell spreading.

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McEvoy, Eóin; Deshpande, Vikram S; McGarry, Patrick

2017-10-01

In this study we present a steady-state adaptation of the thermodynamically motivated stress fiber (SF) model of Vigliotti et al. (2015). We implement this steady-state formulation in a non-local finite element setting where we also consider global conservation of the total number of cytoskeletal proteins within the cell, global conservation of the number of binding integrins on the cell membrane, and adhesion limiting ligand density on the substrate surface. We present a number of simulations of cell spreading in which we consider a limited subset of the possible deformed spread-states assumed by the cell in order to examine the hypothesis that free energy minimization drives the process of cell spreading. Simulations suggest that cell spreading can be viewed as a competition between (i) decreasing cytoskeletal free energy due to strain induced assembly of cytoskeletal proteins into contractile SFs, and (ii) increasing elastic free energy due to stretching of the mechanically passive components of the cell. The computed minimum free energy spread area is shown to be lower for a cell on a compliant substrate than on a rigid substrate. Furthermore, a low substrate ligand density is found to limit cell spreading. The predicted dependence of cell spread area on substrate stiffness and ligand density is in agreement with the experiments of Engler et al. (2003). We also simulate the experiments of Théry et al. (2006), whereby initially circular cells deform and adhere to "V-shaped" and "Y-shaped" ligand patches. Analysis of a number of different spread states reveals that deformed configurations with the lowest free energy exhibit a SF distribution that corresponds to experimental observations, i.e. a high concentration of highly aligned SFs occurs along free edges, with lower SF concentrations in the interior of the cell. In summary, the results of this study suggest that cell spreading is driven by free energy minimization based on a competition between decreasing

Forecasting oil price movements with crack spread futures

International Nuclear Information System (INIS)

Murat, Atilim; Tokat, Ekin

2009-01-01

In oil markets, the crack spread refers to the crude-product price relationship. Refiners are major participants in oil markets and they are primarily exposed to the crack spread. In other words, refiner activity is substantially driven by the objective of protecting the crack spread. Moreover, oil consumers are active participants in the oil hedging market and they are frequently exposed to the crack spread. From another perspective, hedge funds are heavily using crack spread to speculate in oil markets. Based on the high volume of crack spread futures trading in oil markets, the question we want to raise is whether the crack spread futures can be a good predictor of oil price movements. We investigated first whether there is a causal relationship between the crack spread futures and the spot oil markets in a vector error correction framework. We found the causal impact of crack spread futures on spot oil market both in the long- and the short-run after April 2003 where we detected a structural break in the model. To examine the forecasting performance, we use the random walk model (RWM) as a benchmark, and we also evaluate the forecasting power of crack spread futures against the crude oil futures. The results showed that (a) both the crack spread futures and the crude oil futures outperformed the RWM; and (b) the crack spread futures are almost as good as the crude oil futures in predicting the movements in spot oil markets. (author)

Comparison of depression symptoms between primary depression and secondary-to-schizophrenia depression.

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Rahim, Twana; Rashid, Roshe

2017-11-01

This study exclusively aimed to clinically assess which symptom pattern discriminates primary depression from depression-secondary to-schizophrenia. A total of 98 patients with primary depression and 71 patients with secondary-to-schizophrenia depression were assessed for identifying the clinical phenomena of depression. Diagnosis of schizophrenia was confirmed by Mini International Neuropsychiatric Interview. Each participant was, however, assessed by Patient Health Questionnaire-9 as well as Calgary Depression Scale for Schizophrenia (CDSS) for possible concurrent depressive symptoms. Depressed mood, loss of interest, reduced energy and pathological guilt were more common in primary depression, whereas sleep disturbance and guilty ideas of reference were more amounting towards the diagnosis of depression secondary-to-schizophrenia. It is clinically hard to differentiate primary from secondary-to-schizophrenia depression, especially in the absence of obvious psychotic symptoms. However, the classical symptoms of depression like subjective depressed mood, anhedonia, reduced energy and pathological guilt are more prominent in the primary depression.

Juxtacortical Lesions and Cortical Thinning in Multiple Sclerosis.

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Pareto, D; Sastre-Garriga, J; Auger, C; Vives-Gilabert, Y; Delgado, J; Tintoré, M; Montalban, X; Rovira, A

2015-12-01

The role of juxtacortical lesions in brain volume loss in multiple sclerosis has not been fully clarified. The aim of this study was to explore the role of juxtacortical lesions on cortical atrophy and to investigate whether the presence of juxtacortical lesions is related to local cortical thinning in the early stages of MS. A total of 131 patients with clinically isolated syndrome or with relapsing-remitting MS were scanned on a 3T system. Patients with clinically isolated syndrome were classified into 3 groups based on the presence and topography of brain lesions: no lesions (n = 24), only non-juxtacortical lesions (n = 33), and juxtacortical lesions and non-juxtacortical lesions (n = 34). Patients with relapsing-remitting MS were classified into 2 groups: only non-juxtacortical lesions (n = 10) and with non-juxtacortical lesions and juxtacortical lesions (n = 30). A juxtacortical lesion probability map was generated, and cortical thickness was measured by using FreeSurfer. Juxtacortical lesion volume in relapsing-remitting MS was double that of patients with clinically isolated syndrome. The insula showed the highest density of juxtacortical lesions, followed by the temporal, parietal, frontal, and occipital lobes. Patients with relapsing-remitting MS with juxtacortical lesions showed significantly thinner cortices overall and in the parietal and temporal lobes compared with those with clinically isolated syndrome with normal brain MR imaging. The volume of subcortical structures (thalamus, pallidum, putamen, and accumbens) was significantly decreased in relapsing-remitting MS with juxtacortical lesions compared with clinically isolated syndrome with normal brain MR imaging. The spatial distribution of juxtacortical lesions was not found to overlap with areas of cortical thinning. Cortical thinning and subcortical gray matter volume loss in patients with a clinically isolated syndrome or relapsing-remitting MS was related to the presence of juxtacortical

Cortical entrainment to music and its modulation by expertise.

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Doelling, Keith B; Poeppel, David

2015-11-10

Recent studies establish that cortical oscillations track naturalistic speech in a remarkably faithful way. Here, we test whether such neural activity, particularly low-frequency (music and whether experience modifies such a cortical phenomenon. Music of varying tempi was used to test entrainment at different rates. In three magnetoencephalography experiments, we recorded from nonmusicians, as well as musicians with varying years of experience. Recordings from nonmusicians demonstrate cortical entrainment that tracks musical stimuli over a typical range of tempi, but not at tempi below 1 note per second. Importantly, the observed entrainment correlates with performance on a concurrent pitch-related behavioral task. In contrast, the data from musicians show that entrainment is enhanced by years of musical training, at all presented tempi. This suggests a bidirectional relationship between behavior and cortical entrainment, a phenomenon that has not previously been reported. Additional analyses focus on responses in the beta range (∼15-30 Hz)-often linked to delta activity in the context of temporal predictions. Our findings provide evidence that the role of beta in temporal predictions scales to the complex hierarchical rhythms in natural music and enhances processing of musical content. This study builds on important findings on brainstem plasticity and represents a compelling demonstration that cortical neural entrainment is tightly coupled to both musical training and task performance, further supporting a role for cortical oscillatory activity in music perception and cognition.

Basal Forebrain Gating by Somatostatin Neurons Drives Prefrontal Cortical Activity.

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Espinosa, Nelson; Alonso, Alejandra; Morales, Cristian; Espinosa, Pedro; Chávez, Andrés E; Fuentealba, Pablo

2017-11-17

The basal forebrain provides modulatory input to the cortex regulating brain states and cognitive processing. Somatostatin-expressing neurons constitute a heterogeneous GABAergic population known to functionally inhibit basal forebrain cortically projecting cells thus favoring sleep and cortical synchronization. However, it remains unclear if somatostatin cells can regulate population activity patterns in the basal forebrain and modulate cortical dynamics. Here, we demonstrate that somatostatin neurons regulate the corticopetal synaptic output of the basal forebrain impinging on cortical activity and behavior. Optogenetic inactivation of somatostatin neurons in vivo rapidly modified neural activity in the basal forebrain, with the consequent enhancement and desynchronization of activity in the prefrontal cortex, reflected in both neuronal spiking and network oscillations. Cortical activation was partially dependent on cholinergic transmission, suppressing slow waves and potentiating gamma oscillations. In addition, recruitment dynamics was cell type-specific, with interneurons showing similar temporal profiles, but stronger responses than pyramidal cells. Finally, optogenetic stimulation of quiescent animals during resting periods prompted locomotor activity, suggesting generalized cortical activation and increased arousal. Altogether, we provide physiological and behavioral evidence indicating that somatostatin neurons are pivotal in gating the synaptic output of the basal forebrain, thus indirectly controlling cortical operations via both cholinergic and non-cholinergic mechanisms. © The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Influences of brain development and ageing on cortical interactive networks.

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Zhu, Chengyu; Guo, Xiaoli; Jin, Zheng; Sun, Junfeng; Qiu, Yihong; Zhu, Yisheng; Tong, Shanbao

2011-02-01

To study the effect of brain development and ageing on the pattern of cortical interactive networks. By causality analysis of multichannel electroencephalograph (EEG) with partial directed coherence (PDC), we investigated the different neural networks involved in the whole cortex as well as the anterior and posterior areas in three age groups, i.e., children (0-10 years), mid-aged adults (26-38 years) and the elderly (56-80 years). By comparing the cortical interactive networks in different age groups, the following findings were concluded: (1) the cortical interactive network in the right hemisphere develops earlier than its left counterpart in the development stage; (2) the cortical interactive network of anterior cortex, especially at C3 and F3, is demonstrated to undergo far more extensive changes, compared with the posterior area during brain development and ageing; (3) the asymmetry of the cortical interactive networks declines during ageing with more loss of connectivity in the left frontal and central areas. The age-related variation of cortical interactive networks from resting EEG provides new insights into brain development and ageing. Our findings demonstrated that the PDC analysis of EEG is a powerful approach for characterizing the cortical functional connectivity during brain development and ageing. Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Meditative Movement for Depression and Anxiety

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Peter ePayne

2013-07-01

Full Text Available This review focuses on Meditative Movement (MM and its effects on anxiety, depression and other affective states. MM is a term identifying forms of exercise that use movement in conjunction with meditative attention to body sensations, including proprioception, interoception and kinesthesis. MM includes the traditional Chinese methods of Qigong (Chi Kung and Taijiquan (Tai Chi, some forms of Yoga and other Asian practices, as well as Western Somatic practices; however this review focuses primarily on Qigong and Taijiquan. We clarify the differences between MM and conventional exercise, present descriptions of several of the key methodologies of MM, and suggest how research into these practices may be approached in a systematic way. We also present evidence for possible mechanisms of the effects of MM on affective states, including the roles of posture, rhythm, coherent breathing, and the involvement of specific cortical and subcortical structures. We survey research outcomes summarized in reviews published since 2007. Results suggest that MM may be at least as effective as conventional exercise or other interventions in ameliorating anxiety and depression; however, study quality is generally poor and there are many confounding factors. This makes it difficult to draw definitive conclusions at this time. We suggest, however, that more research is warranted, and we offer specific suggestions for ensuring high-quality and productive future studies.

rab3 mediates cortical granule exocytosis in the sea urchin egg.

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Conner, S; Wessel, G M

1998-11-15

Egg activation at fertilization in the sea urchin results in the exocytosis of approximately 15,000 cortical granules that are docked at the plasma membrane. Previously, we reported that several integral membrane proteins modeled in the SNARE hypothesis, synaptotagmin, VAMP, and syntaxin, in addition to a small GTPase of the ras superfamily, rab3, were present on cortical granules (Conner, S., Leaf, D., and Wessel, G., Mol. Reprod. Dev. 48, 1-13, 1997). Here we report that rab3 is associated with cortical granules throughout oogenesis, during cortical granule translocation, and while docked at the egg plasma membrane. Following cortical granule exocytosis, however, rab3 reassociates with a different population of vesicles, at least some of which are of endocytic origin. Because of its selective association with cortical granules in eggs and oocytes, we hypothesize that rab3 functions in cortical granule exocytosis. To test this hypothesis, we used a strategy of interfering with rab3 function by peptide competition with its effector domain, a conserved region within specific rab types. We first identified the effector domain sequence in Lytechinus variegatus eggs and find the sequence 94% identical to the effector domain of rab3 in Stronglocentrotus purpuratus. Then, with synthetic peptides to different regions of the rab3 protein, we find that cortical granule exocytosis is inhibited in eggs injected with effector domain peptides, but not with peptides from the hypervariable region or with a scrambled effector peptide. Additionally, effector-peptide-injected eggs injected with IP3 are blocked in their ability to exocytose cortical granules, suggesting that the inhibition is directly on the membrane fusion event and not the result of interference with the signal transduction mechanism leading to calcium release. We interpret these results to mean that rab3 functions in the regulation of cortical granule exocytosis following vesicle docking. Copyright 1998 Academic

The Unique Brain Anatomy of Meditation Practitioners: Alterations in Cortical Gyrification

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Luders, Eileen; Kurth, Florian; Mayer, Emeran A.; Toga, Arthur W.; Narr, Katherine L.; Gaser, Christian

2012-01-01

Several cortical regions are reported to vary in meditation practitioners. However, prior analyses have focused primarily on examining gray matter or cortical thickness. Thus, additional effects with respect to other cortical features might have remained undetected. Gyrification (the pattern and degree of cortical folding) is an important cerebral characteristic related to the geometry of the brain’s surface. Thus, exploring cortical gyrification in long-term meditators may provide additional clues with respect to the underlying anatomical correlates of meditation. This study examined cortical gyrification in a large sample (n = 100) of meditators and controls, carefully matched for sex and age. Cortical gyrification was established by calculating mean curvature across thousands of vertices on individual cortical surface models. Pronounced group differences indicating larger gyrification in meditators were evident within the left precentral gyrus, right fusiform gyrus, right cuneus, as well as left and right anterior dorsal insula (the latter representing the global significance maximum). Positive correlations between gyrification and the number of meditation years were similarly pronounced in the right anterior dorsal insula. Although the exact functional implications of larger cortical gyrification remain to be established, these findings suggest the insula to be a key structure involved in aspects of meditation. For example, variations in insular complexity could affect the regulation of well-known distractions in the process of meditation, such as daydreaming, mind-wandering, and projections into past or future. Moreover, given that meditators are masters in introspection, awareness, and emotional control, increased insular gyrification may reflect an integration of autonomic, affective, and cognitive processes. Due to the cross-sectional nature of this study, further research is necessary to determine the relative contribution of nature and nurture to

POSTPARTUM DEPRESSION – THE CENTRAL PROBLEM OF MENTAL HEALTH OF EARLY MOTHERHOOD

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N. A. Kornetov

2015-01-01

irritability as during the postpartum depression and in its residual period. They can cause child abuse. This paper also presents current data on the epidemiology, etiology, risk factors for postpartum depression, its clinical manifestations, the influence of untreated maternal depression on child development, therapy and educational modules to spread multidisciplinary and inter-agency approach in perinatal mental health problems.

Beta-amyloid deposition and cognitive function in patients with major depressive disorder with different subtypes of mild cognitive impairment: {sup 18}F-florbetapir (AV-45/Amyvid) PET study

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Wu, Kuan-Yi; Liu, Chia-Yih; Chen, Chia-Hsiang; Lee, Chin-Pang [Chang Gung Memorial Hospital and Chang Gung University, Department of Psychiatry, Tao-Yuan (China); Chen, Cheng-Sheng [Kaohsiung Medical University Hospital and College of Medicine, Kaohsiung Medical University, Department of Psychiatry, Kaohsiung (China); Hsiao, Ing-Tsung; Hsieh, Chia-Ju; Yen, Tzu-Chen; Lin, Kun-Ju [Chang Gung Memorial Hospital, Department of Nuclear Medicine and Molecular Imaging Center, Kuei Shan Hsiang, Taoyuan (China); Chang Gung University, Department of Medical Imaging and Radiological Sciences and Healthy Aging Research Center, Tao-Yuan (China)

2016-06-15

The objective of this study was to evaluate the amyloid burden, as assessed by {sup 18}F-florbetapir (AV-45/Amyvid) positron emission tomography PET, in patients with major depressive disorder (MDD) with different subtypes of mild cognitive impairment (MCI) and the relationship between amyloid burden and cognition in MDD patients. The study included 55 MDD patients without dementia and 21 healthy control subjects (HCs) who were assessed using a comprehensive cognitive test battery and {sup 18}F-florbetapir PET imaging. The standardized uptake value ratios (SUVR) in eight cortical regions using the whole cerebellum as reference region were determined and voxel-wise comparisons between the HC and MDD groups were performed. Vascular risk factors, serum homocysteine level and the apolipoprotein E (ApoE) genotype were also determined. Among the 55 MDD patients, 22 (40.0 %) had MCI, 12 (21.8 %) non-amnestic MCI (naMCI) and 10 (18.2 %) amnestic MCI (aMCI). The MDD patients with aMCI had the highest relative {sup 18}F-florbetapir uptake in all cortical regions, and a significant difference in relative {sup 18}F-florbetapir uptake was found in the parietal region as compared with that in naMCI subjects (P < 0.05) and HCs (P < 0.01). Voxel-wise analyses revealed significantly increased relative {sup 18}F-florbetapir uptake in the MDD patients with aMCI and naMCI in the frontal, parietal, temporal and occipital areas (P < 0.005). The global cortical SUVR was significantly negatively correlated with MMSE score (r = -0.342, P = 0.010) and memory function (r = -0.328, P = 0.015). The negative correlation between the global SUVR and memory in the MDD patients remained significant in multiple regression analyses that included age, educational level, ApoE genotype, and depression severity (β = -3.607, t = -2.874, P = 0.006). We found preliminary evidence of brain beta-amyloid deposition in MDD patients with different subtypes of MCI. Our findings in MDD patients support the

Surface-Based Regional Homogeneity in First-Episode, Drug-Naïve Major Depression: A Resting-State fMRI Study

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Hui-Jie Li

2014-01-01

Full Text Available Background. Previous volume-based regional homogeneity (ReHo studies neglected the intersubject variability in cortical folding patterns. Recently, surface-based ReHo was developed to reduce the intersubject variability and to increase statistical power. The present study used this novel surface-based ReHo approach to explore the brain functional activity differences between first-episode, drug-naïve MDD patients and healthy controls. Methods. Thirty-three first-episode, drug-naïve MDD patients and 32 healthy controls participated in structural and resting-state fMRI scans. MDD patients were rated with a 17-item Hamilton Rating Scale for Depression prior to the scan. Results. In comparison with the healthy controls, MDD patients showed reduced surface-based ReHo in the left insula. There was no increase in surface-based ReHo in MDD patients. The surface-based ReHo value in the left insula was not significantly correlated with the clinical information or the depressive scores in the MDD group. Conclusions. The decreased surface-based ReHo in the left insula in MDD may lead to the abnormal top-down cortical-limbic regulation of emotional and cognitive information. The surface-based ReHo may be a useful index to explore the pathophysiological mechanism of MDD.

MicroRNA-338 modulates cortical neuronal placement and polarity.

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Kos, Aron; de Mooij-Malsen, Annetrude J; van Bokhoven, Hans; Kaplan, Barry B; Martens, Gerard J; Kolk, Sharon M; Aschrafi, Armaz

2017-07-03

The precise spatial and temporal regulation of gene expression orchestrates the many intricate processes during brain development. In the present study we examined the role of the brain-enriched microRNA-338 (miR-338) during mouse cortical development. Reduction of miR-338 levels in the developing mouse cortex, using a sequence-specific miR-sponge, resulted in a loss of neuronal polarity in the cortical plate and significantly reduced the number of neurons within this cortical layer. Conversely, miR-338 overexpression in developing mouse cortex increased the number of neurons, which exhibited a multipolar morphology. All together, our results raise the possibility for a direct role for this non-coding RNA, which was recently associated with schizophrenia, in the regulation of cortical neuronal polarity and layer placement.

Gossip spread in social network Models

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Johansson, Tobias

2017-04-01

Gossip almost inevitably arises in real social networks. In this article we investigate the relationship between the number of friends of a person and limits on how far gossip about that person can spread in the network. How far gossip travels in a network depends on two sets of factors: (a) factors determining gossip transmission from one person to the next and (b) factors determining network topology. For a simple model where gossip is spread among people who know the victim it is known that a standard scale-free network model produces a non-monotonic relationship between number of friends and expected relative spread of gossip, a pattern that is also observed in real networks (Lind et al., 2007). Here, we study gossip spread in two social network models (Toivonen et al., 2006; Vázquez, 2003) by exploring the parameter space of both models and fitting them to a real Facebook data set. Both models can produce the non-monotonic relationship of real networks more accurately than a standard scale-free model while also exhibiting more realistic variability in gossip spread. Of the two models, the one given in Vázquez (2003) best captures both the expected values and variability of gossip spread.

Perineural spread in head and neck tumors.

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Brea Álvarez, B; Tuñón Gómez, M

2014-01-01

Perineural spread is the dissemination of some types of head and neck tumors along nervous structures. Perineural spread has negative repercussions on treatment because it requires more extensive resection and larger fields of irradiation. Moreover, perineural spread is associated with increased local recurrence, and it is considered an independent indicator of poor prognosis in the TNM classification for tumor staging. However, perineural spread often goes undetected on imaging studies. In this update, we review the concept of perineural spread, its pathogenesis, and the main pathways and connections among the facial nerves, which are essential to understand this process. Furthermore, we discuss the appropriate techniques for imaging studies, and we describe and illustrate the typical imaging signs that help identify perineural spread on CT and MRI. Finally, we discuss the differential diagnosis with other entities. Copyright © 2013 SERAM. Published by Elsevier Espana. All rights reserved.

When Cognitive Decline and Depression Coexist in the Elderly: CSF Biomarkers Analysis Can Differentiate Alzheimer's Disease from Late-Life Depression.

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Liguori, Claudio; Pierantozzi, Mariangela; Chiaravalloti, Agostino; Sancesario, Giulia M; Mercuri, Nicola B; Franchini, Flaminia; Schillaci, Orazio; Sancesario, Giuseppe

2018-01-01

Late-life depression (LLD) and Alzheimer's Disease (AD) are the two most frequent neuropsychiatric disorders affecting elderly. LLD and AD may clinically present with depressive and cognitive symptoms. Therefore, when cognitive decline is coupled with depression in the elderly, the differential diagnosis between LLD and AD could be challenging. The aim of the present study was to evaluate in a population of elderly patients affected by depression and dementia the usefulness of CSF AD biomarkers (tau proteins and β-amyloid 42 -Aβ 42 ) and 2-[18F]fluoro-2-deoxy-d-glucose positron emission tomography (18FFDG-PET) in early differentiating LLD from AD. Two hundred and fifty-six depressed and demented patients, after performing CSF AD biomarkers and 18FFDG-PET, were distributed in two groups on the basis of the current diagnostic guidelines for AD ( n = 201) and LLD ( n = 55). Patients were then observed for 2 years to verify the early diagnosis. After the 2 year follow-up we compared AD and LLD patients' CSF and 18FFDG-PET data obtained at baseline to a group of age- and sex-matched controls. We found CSF Aβ 42 levels significantly higher in LLD compared to AD patients. Remarkably, CSF Aβ 42 levels of LLD patients (range between 550 and 1204 pg/mL) did not overlap with those of AD patients (range between 82 and 528 pg/mL). Moreover, we documented no differences in CSF AD biomarkers (Aβ 42 and tau proteins) when comparing LLD patients to controls. In addition, AD patients showed the significant reduction of 18FFDG-PET uptake in temporo-parietal regions compared to both controls and LLD. Conversely, LLD and control groups did not differ at 18FFDG-PET analysis, although LLD patients showed heterogeneous patterns of glucose hypometabolism involving cortical and subcortical brain areas. It is noteworthy that at the end of the clinical follow-up, patients owing to AD group showed the expected significant decline of cognitive performances, whereas patients assigned to LLD

When Cognitive Decline and Depression Coexist in the Elderly: CSF Biomarkers Analysis Can Differentiate Alzheimer's Disease from Late-Life Depression

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Claudio Liguori

2018-02-01

Full Text Available Late-life depression (LLD and Alzheimer's Disease (AD are the two most frequent neuropsychiatric disorders affecting elderly. LLD and AD may clinically present with depressive and cognitive symptoms. Therefore, when cognitive decline is coupled with depression in the elderly, the differential diagnosis between LLD and AD could be challenging. The aim of the present study was to evaluate in a population of elderly patients affected by depression and dementia the usefulness of CSF AD biomarkers (tau proteins and β-amyloid42–Aβ42 and 2-[18F]fluoro-2-deoxy-d-glucose positron emission tomography (18FFDG-PET in early differentiating LLD from AD. Two hundred and fifty-six depressed and demented patients, after performing CSF AD biomarkers and 18FFDG-PET, were distributed in two groups on the basis of the current diagnostic guidelines for AD (n = 201 and LLD (n = 55. Patients were then observed for 2 years to verify the early diagnosis. After the 2 year follow-up we compared AD and LLD patients' CSF and 18FFDG-PET data obtained at baseline to a group of age- and sex-matched controls. We found CSF Aβ42 levels significantly higher in LLD compared to AD patients. Remarkably, CSF Aβ42 levels of LLD patients (range between 550 and 1204 pg/mL did not overlap with those of AD patients (range between 82 and 528 pg/mL. Moreover, we documented no differences in CSF AD biomarkers (Aβ42 and tau proteins when comparing LLD patients to controls. In addition, AD patients showed the significant reduction of 18FFDG-PET uptake in temporo-parietal regions compared to both controls and LLD. Conversely, LLD and control groups did not differ at 18FFDG-PET analysis, although LLD patients showed heterogeneous patterns of glucose hypometabolism involving cortical and subcortical brain areas. It is noteworthy that at the end of the clinical follow-up, patients owing to AD group showed the expected significant decline of cognitive performances, whereas patients assigned to

Connections underlying the synthesis of cognition, memory, and emotion in primate prefrontal cortices.

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Barbas, H

2000-07-15

Distinct domains of the prefrontal cortex in primates have a set of connections suggesting that they have different roles in cognition, memory, and emotion. Caudal lateral prefrontal areas (areas 8 and 46) receive projections from cortices representing early stages in visual or auditory processing, and from intraparietal and posterior cingulate areas associated with oculomotor guidance and attentional processes. Cortical input to areas 46 and 8 is complemented by projections from the thalamic multiform and parvicellular sectors of the mediodorsal nucleus associated with oculomotor functions and working memory. In contrast, caudal orbitofrontal areas receive diverse input from cortices representing late stages of processing within every unimodal sensory cortical system. In addition, orbitofrontal and caudal medial (limbic) prefrontal cortices receive robust projections from the amygdala, associated with emotional memory, and from medial temporal and thalamic structures associated with long-term memory. Prefrontal cortices are linked with motor control structures related to their specific roles in central executive functions. Caudal lateral prefrontal areas project to brainstem oculomotor structures, and are connected with premotor cortices effecting head, limb and body movements. In contrast, medial prefrontal and orbitofrontal limbic cortices project to hypothalamic visceromotor centers for the expression of emotions. Lateral, orbitofrontal, and medial prefrontal cortices are robustly interconnected, suggesting that they participate in concert in central executive functions. Prefrontal limbic cortices issue widespread projections through their deep layers and terminate in the upper layers of lateral (eulaminate) cortices, suggesting a predominant role in feedback communication. In contrast, when lateral prefrontal cortices communicate with limbic areas they issue projections from their upper layers and their axons terminate in the deep layers, suggesting a role in

Anterior Cortical Development During Adolescence in Bipolar Disorder.

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Najt, Pablo; Wang, Fei; Spencer, Linda; Johnston, Jennifer A Y; Cox Lippard, Elizabeth T; Pittman, Brian P; Lacadie, Cheryl; Staib, Lawrence H; Papademetris, Xenophon; Blumberg, Hilary P

2016-02-15

Increasing evidence supports a neurodevelopmental model for bipolar disorder (BD), with adolescence as a critical period in its development. Developmental abnormalities of anterior paralimbic and heteromodal frontal cortices, key structures in emotional regulation processes and central in BD, are implicated. However, few longitudinal studies have been conducted, limiting understanding of trajectory alterations in BD. In this study, we performed longitudinal neuroimaging of adolescents with and without BD and assessed volume changes over time, including changes in tissue overall and within gray and white matter. Larger decreases over time in anterior cortical volumes in the adolescents with BD were hypothesized. Gray matter decreases and white matter increases are typically observed during adolescence in anterior cortices. It was hypothesized that volume decreases over time in BD would reflect alterations in those processes, showing larger gray matter contraction and decreased white matter expansion. Two high-resolution magnetic resonance imaging scans were obtained approximately 2 years apart for 35 adolescents with bipolar I disorder (BDI) and 37 healthy adolescents. Differences over time between groups were investigated for volume overall and specifically for gray and white matter. Relative to healthy adolescents, adolescents with BDI showed greater volume contraction over time in a region including insula and orbitofrontal, rostral, and dorsolateral prefrontal cortices (p adolescence in BDI in anterior cortices, including altered developmental trajectories of anterior gray and white matter. Published by Elsevier Inc.

A failure of suppression within the default mode network in depressed adolescents with compulsive internet game play.

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Han, Doug Hyun; Kim, Sun Mi; Bae, Sujin; Renshaw, Perry F; Anderson, Jeffrey S

2016-04-01

Individuals who are chronic, compulsive video game players experience an elevated incidence of major depression. Excessive or problematic game play can interact with depression clinically, and may magnify impulsive behavior associated with video gaming. Functional brain imaging was performed during a Wisconsin Card Sorting Test (WCST) task in 42 healthy control and 95 volunteers seeking treatment for compulsive video game playing, including 60 participants without major depression (pure internet gaming disorder, pure IGD) and 35 participants comorbid with major depression (IGD+MDD). In response to the WCST in contrast to fixation, activation was observed in canonical brain attentional networks including bilateral intraparietal sulcus, frontal eye fields, and middle temporal cortical regions as well as dorsolateral prefrontal, inferior parietal and anterior insula, anterior cingulate cortex in all participants. For WCST>Fixation contrasts, the IGD+MDD group exhibited greater relative activation within the left hippocampus, compared to healthy control participants. For WCST>Fixation contrasts, the IGD+MDD group exhibited greater relative activation within the left hippocampus and the right parahippocampal gyrus immediately posterior to the hippocampus, compared to the pure IGD group. In cohorts of individuals with a history of compulsive internet game play, individuals with depression showed failure to suppress default mode network activity during an attentionally demanding task, compared to individuals without depression, including comparison groups with and without a history of compulsive video gaming. This reduced suppression of the brain regions within the default mode network may be a consequence of depressive neurophysiology or represent a predisposition for depression within compulsive game players. Copyright © 2016 Elsevier B.V. All rights reserved.

Depression (Major Depressive Disorder)

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... generally miserable or unhappy without really knowing why. Depression symptoms in children and teens Common signs and ... in normal activities, and avoidance of social interaction. Depression symptoms in older adults Depression is not a ...

Imprinting and recalling cortical ensembles.

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Carrillo-Reid, Luis; Yang, Weijian; Bando, Yuki; Peterka, Darcy S; Yuste, Rafael

2016-08-12

Neuronal ensembles are coactive groups of neurons that may represent building blocks of cortical circuits. These ensembles could be formed by Hebbian plasticity, whereby synapses between coactive neurons are strengthened. Here we report that repetitive activation with two-photon optogenetics of neuronal populations from ensembles in the visual cortex of awake mice builds neuronal ensembles that recur spontaneously after being imprinted and do not disrupt preexisting ones. Moreover, imprinted ensembles can be recalled by single- cell stimulation and remain coactive on consecutive days. Our results demonstrate the persistent reconfiguration of cortical circuits by two-photon optogenetics into neuronal ensembles that can perform pattern completion. Copyright © 2016, American Association for the Advancement of Science.

Development of Pistachio (Pistacia vera L.) spread.

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Shakerardekani, Ahmad; Karim, Roselina; Ghazali, Hasanah Mohd; Chin, Nyuk Ling

2013-03-01

Pistachio nut (Pistacia vera L.) is one of the most delicious and nutritious nuts in the world. Pistachio spreads were developed using pistachio paste as the main component, icing sugar, soy protein isolate (SPI), and red palm oil (RPO), at different ratios. The highest mean scores of all the sensory attributes were depicted by spreads that were made without addition of SPI. It was found that the work of shear was 0 to 11.0 kg s for an acceptable spread. Sensory spreadability, overall texture, spreadability, and overall acceptability were negatively correlated (R > 0.83) with the work of shear of spreads. The findings indicated that the presence of RPO had a direct effect on the viscoelastic behavior of the pistachio spreads. The a values, which are related to the green color of the pistachio product ranged from 1.7 to 3.9 for spread without addition of RPO, and 4.0 to 5.3 in the presence of RPO. The development of pistachio spread would potentially increase the food uses of pistachio and introduce consumers with a healthier snack food. © 2013 Institute of Food Technologists®

Nonlinear Recurrent Dynamics and Long-Term Nonstationarities in EEG Alpha Cortical Activity: Implications for Choosing Adequate Segment Length in Nonlinear EEG Analyses.

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Cerquera, Alexander; Vollebregt, Madelon A; Arns, Martijn

2018-03-01

Nonlinear analysis of EEG recordings allows detection of characteristics that would probably be neglected by linear methods. This study aimed to determine a suitable epoch length for nonlinear analysis of EEG data based on its recurrence rate in EEG alpha activity (electrodes Fz, Oz, and Pz) from 28 healthy and 64 major depressive disorder subjects. Two nonlinear metrics, Lempel-Ziv complexity and scaling index, were applied in sliding windows of 20 seconds shifted every 1 second and in nonoverlapping windows of 1 minute. In addition, linear spectral analysis was carried out for comparison with the nonlinear results. The analysis with sliding windows showed that the cortical dynamics underlying alpha activity had a recurrence period of around 40 seconds in both groups. In the analysis with nonoverlapping windows, long-term nonstationarities entailed changes over time in the nonlinear dynamics that became significantly different between epochs across time, which was not detected with the linear spectral analysis. Findings suggest that epoch lengths shorter than 40 seconds neglect information in EEG nonlinear studies. In turn, linear analysis did not detect characteristics from long-term nonstationarities in EEG alpha waves of control subjects and patients with major depressive disorder patients. We recommend that application of nonlinear metrics in EEG time series, particularly of alpha activity, should be carried out with epochs around 60 seconds. In addition, this study aimed to demonstrate that long-term nonlinearities are inherent to the cortical brain dynamics regardless of the presence or absence of a mental disorder.

Equilibrium spreading pressure and Langmuir–Blodgett film formation of omega-substituted palmitic acids

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Snow, Arthur W., E-mail: arthur.snow@nrl.navy.mil; Jernigan, Glenn G.; Ancona, Mario G.

2014-04-01

Langmuir–Blodgett isotherms and equilibrium spreading pressures were measured for compounds of the series X–(CH{sub 2}){sub 15}COOH, X = CH{sub 3}, SH, OH, F, Cl, Br. Only the CH{sub 3} and F terminated compounds formed monolayers with sufficient stability for accurate isotherm measurement, film transfer and X-ray photoelectron spectroscopic analysis. The presence of the terminal heteroatom substituents significantly diminished the stability of the L–B film and depressed the equilibrium spreading pressures (20 °C) from 15.4 mN/m for the CH{sub 3} terminated compound to a range of 0.95 to 0.08 mN/m for the other members of the series. These characteristics are attributed to the monolayer film being in a metastable state and the dipole moment of the heteroatom terminal group increasing the monolayer film kinetic instability by facilitating the formation of three-dimensional structures. - Highlights: • Compound series X–(CH{sub 2}){sub 15}COOH, X = CH{sub 3}, SH, OH, F, Cl, Br was analyzed. • Only-CH{sub 3} and-F terminated compounds form stable Langmuir–Blodgett films. • Heteroatom terminal groups promote kinetic instability in Langmuir–Blodgett films. • X-ray photoelectron spectra analyzed for molecular orientation and packing density.

Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX

DEFF Research Database (Denmark)

Christensen, Thomas; Jørgensen, M B; Diemer, Nils Henrik

1993-01-01

or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal...... infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions...

Neuregulin 3 Mediates Cortical Plate Invasion and Laminar Allocation of GABAergic Interneurons

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Giorgia Bartolini

2017-01-01

Full Text Available Neural circuits in the cerebral cortex consist of excitatory pyramidal cells and inhibitory interneurons. These two main classes of cortical neurons follow largely different genetic programs, yet they assemble into highly specialized circuits during development following a very precise choreography. Previous studies have shown that signals produced by pyramidal cells influence the migration of cortical interneurons, but the molecular nature of these factors has remained elusive. Here, we identified Neuregulin 3 (Nrg3 as a chemoattractive factor expressed by developing pyramidal cells that guides the allocation of cortical interneurons in the developing cortical plate. Gain- and loss-of-function approaches reveal that Nrg3 modulates the migration of interneurons into the cortical plate in a process that is dependent on the tyrosine kinase receptor ErbB4. Perturbation of Nrg3 signaling in conditional mutants leads to abnormal lamination of cortical interneurons. Nrg3 is therefore a critical mediator in the assembly of cortical inhibitory circuits.

Early development of synchrony in cortical activations in the human.

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Koolen, N; Dereymaeker, A; Räsänen, O; Jansen, K; Vervisch, J; Matic, V; Naulaers, G; De Vos, M; Van Huffel, S; Vanhatalo, S

2016-05-13

Early intermittent cortical activity is thought to play a crucial role in the growth of neuronal network development, and large scale brain networks are known to provide the basis for higher brain functions. Yet, the early development of the large scale synchrony in cortical activations is unknown. Here, we tested the hypothesis that the early intermittent cortical activations seen in the human scalp EEG show a clear developmental course during the last trimester of pregnancy, the period of intensive growth of cortico-cortical connections. We recorded scalp EEG from altogether 22 premature infants at post-menstrual age between 30 and 44 weeks, and the early cortical synchrony was quantified using recently introduced activation synchrony index (ASI). The developmental correlations of ASI were computed for individual EEG signals as well as anatomically and mathematically defined spatial subgroups. We report two main findings. First, we observed a robust and statistically significant increase in ASI in all cortical areas. Second, there were significant spatial gradients in the synchrony in fronto-occipital and left-to-right directions. These findings provide evidence that early cortical activity is increasingly synchronized across the neocortex. The ASI-based metrics introduced in our work allow direct translational comparison to in vivo animal models, as well as hold promise for implementation as a functional developmental biomarker in future research on human neonates. Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.

Cortical inactivation by cooling in small animals

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Ben eCoomber

2011-06-01

Full Text Available Reversible inactivation of the cortex by surface cooling is a powerful method for studying the function of a particular area. Implanted cooling cryoloops have been used to study the role of individual cortical areas in auditory processing of awake-behaving cats. Cryoloops have also been used in rodents for reversible inactivation of the cortex, but recently there has been a concern that the cryoloop may also cool non-cortical structures either directly or via the perfusion of blood, cooled as it passed close to the cooling loop. In this study we have confirmed that the loop can inactivate most of the auditory cortex without causing a significant reduction in temperature of the auditory thalamus or other sub-cortical structures. We placed a cryoloop on the surface of the guinea pig cortex, cooled it to 2°C and measured thermal gradients across the neocortical surface. We found that the temperature dropped to 20-24°C among cells within a radius of about 2.5mm away from the loop. This temperature drop was sufficient to reduce activity of most cortical cells and led to the inactivation of almost the entire auditory region. When the temperature of thalamus, midbrain, and middle ear were measured directly during cortical cooling, there was a small drop in temperature (about 4°C but this was not sufficient to directly reduce neural activity. In an effort to visualise the extent of neural inactivation we measured the uptake of thallium ions following an intravenous injection. This confirmed that there was a large reduction of activity across much of the ipsilateral cortex and only a small reduction in subcortical structures.

Brain cortical thickness in male adolescents with serious substance use and conduct problems.

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Chumachenko, Serhiy Y; Sakai, Joseph T; Dalwani, Manish S; Mikulich-Gilbertson, Susan K; Dunn, Robin; Tanabe, Jody; Young, Susan; McWilliams, Shannon K; Banich, Marie T; Crowley, Thomas J

2015-01-01

Adolescents with substance use disorder (SUD) and conduct problems exhibit high levels of impulsivity and poor self-control. Limited work to date tests for brain cortical thickness differences in these youths. To investigate differences in cortical thickness between adolescents with substance use and conduct problems and controls. We recruited 25 male adolescents with SUD, and 19 male adolescent controls, and completed structural 3T magnetic resonance brain imaging. Using the surface-based morphometry software FreeSurfer, we completed region-of-interest (ROI) analyses for group cortical thickness differences in left, and separately right, inferior frontal gyrus (IFG), orbitofrontal cortex (OFC) and insula. Using FreeSurfer, we completed whole-cerebrum analyses of group differences in cortical thickness. Versus controls, the SUD group showed no cortical thickness differences in ROI analyses. Controlling for age and IQ, no regions with cortical thickness differences were found using whole-cerebrum analyses (though secondary analyses co-varying IQ and whole-cerebrum cortical thickness yielded a between-group cortical thickness difference in the left posterior cingulate/precuneus). Secondary findings showed that the SUD group, relative to controls, demonstrated significantly less right > left asymmetry in IFG, had weaker insular-to-whole-cerebrum cortical thickness correlations, and showed a positive association between conduct disorder symptom count and cortical thickness in a superior temporal gyrus cluster. Functional group differences may reflect a more nuanced cortical morphometric difference than ROI cortical thickness. Further investigation of morphometric differences is needed. If replicable findings can be established, they may aid in developing improved diagnostic or more targeted treatment approaches.

The cortical representation of sensory inputs arising from bone.

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Ivanusic, Jason J; Sahai, Vineet; Mahns, David A

2009-05-07

In the present study, we show that sensory information from bone reaches the discriminative areas of the somatosensory cortices by electrically stimulating the nerve to the cat humerus and recording evoked potentials on the surface of the primary (SI) and secondary (SII) somatosensory cortex. The SI focus was located over the rostral part of the postcruciate cortex, caudal to the lateral aspect of the cruciate sulcus. The SII focus was identified on the anterior ectosylvian gyrus, lateral to the suprasylvian sulcus. These foci were located adjacent to, or within areas that responded to stimulation of the median, ulnar and/or musculocutaneous nerves. The latency (6-11 ms) to onset of cortical responses in SI and SII were indistinguishable (unpaired t-test; P>0.05), and were consistent with activation of A delta fibers in the peripheral nerve. The amplitudes of the cortical responses were graded as a function of stimulus intensity, and may reflect a mechanism for intensity coding. We did not observe long latency cortical responses (50-300 ms) that would be consistent with C fiber activation in the peripheral nerve, and provide evidence that this may be attributable to inhibition of cortical responsiveness following the initial A delta response. Our finding of discrete, short latency evoked potentials (presumably of A delta origin) in the primary and secondary somatosensory cortices, following stimulation of a nerve innervating bone, may reflect a mechanism for the discriminative component of bone pain.

Paradiaphyseal calcific tendinitis with cortical bone erosion.

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Fritz, P; Bardin, T; Laredo, J D; Ziza, J M; D'Anglejan, G; Lansaman, J; Bucki, B; Forest, M; Kuntz, D

1994-05-01

To determine the clinical, radiologic, and histologic features of calcific tendinitis with cortical bone erosion. The records of 6 patients with paradiaphyseal calcific tendinitis and adjacent bone cortex erosion were reviewed. Calcific tendinitis involved the linea aspera in 4 patients, the bicipital groove in 1 patient, and the deltoid insertion in another. Calcium deposits were associated with cortical bone erosions, revealed on plain radiographs in 4 patients and computed tomography scans in 2. Bone scans were performed in 2 patients and showed local hyperfixation of the isotope. In 4 patients, suspicion of a neoplasm led to a biopsy. Calcium deposits appeared to be surrounded by a foreign body reaction with numerous giant cells. Apatite crystals were identified by transmission electron microscopy and elemental analysis in 1 surgical sample. Paradiaphyseal calcific tendinitis with cortical bone erosion is an uncommon presentation of apatite deposition disease.

Cerebellar Shaping of Motor Cortical Firing Is Correlated with Timing of Motor Actions

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Abdulraheem Nashef

2018-05-01

Full Text Available Summary: In higher mammals, motor timing is considered to be dictated by cerebellar control of motor cortical activity, relayed through the cerebellar-thalamo-cortical (CTC system. Nonetheless, the way cerebellar information is integrated with motor cortical commands and affects their temporal properties remains unclear. To address this issue, we activated the CTC system in primates and found that it efficiently recruits motor cortical cells; however, the cortical response was dominated by prolonged inhibition that imposed a directional activation across the motor cortex. During task performance, cortical cells that integrated CTC information fired synchronous bursts at movement onset. These cells expressed a stronger correlation with reaction time than non-CTC cells. Thus, the excitation-inhibition interplay triggered by the CTC system facilitates transient recruitment of a cortical subnetwork at movement onset. The CTC system may shape neural firing to produce the required profile to initiate movements and thus plays a pivotal role in timing motor actions. : Nashef et al. identified a motor cortical subnetwork recruited by cerebellar volley that was transiently synchronized at movement onset. Cerebellar control of cortical firing was dominated by inhibition that shaped task-related firing of neurons and may dictate motor timing. Keywords: motor control, primates, cerebellar-thalamo-cortical, synchrony, noise correlation, reaction time

[Schizophrenia and cortical GABA neurotransmission].

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Hashimoto, Takanori; Matsubara, Takuro; Lewis, David A

2010-01-01

-synaptic GABA-A receptors. Our recent analyses demonstrated that this pattern exists across diverse cortical areas including the prefrontal, anterior cingulate, primary motor, and primary visual cortices. GABA neurotransmission by PV-containing and SST-containing neurons is important for the generation of cortical oscillatory activities in the gamma (30-100 Hz) and theta (4-7 Hz) bands, respectively. These oscillatory activities have been proposed to play critical roles in regulating the efficiency of information transfer between neurons and neuronal networks in the cortex. Altered cortical GABA neurotransmission appears to contribute to disturbances in diverse functions through affecting the generation of cortical oscillations in schizophrenia.

Retrosplenial cortical thinning as a possible major contributor for cognitive impairment in HIV patients

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Shin, Na-Young [The Catholic University of Korea, Department of Radiology, College of Medicine, Seoul (Korea, Republic of); Hong, Jinwoo; Yoon, Uicheul [Catholic University of Daegu, Department of Biomedical Engineering, College of Health and Medical Science, Gyeongsan-si, Gyeongbuk (Korea, Republic of); Choi, Jun Yong [Yonsei University College of Medicine, Department of Internal Medicine and AIDS Research Institute, Seoul (Korea, Republic of); Lee, Seung-Koo [Yonsei University College of Medicine, Department of Radiology, Seoul (Korea, Republic of); Lim, Soo Mee [Ewha Womans University, School of Medicine, Department of Radiology, Seoul (Korea, Republic of)

2017-11-15

To identify brain cortical regions relevant to HIV-associated neurocognitive disorder (HAND) in HIV patients. HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness. Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills. This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment. (orig.)

Retrosplenial cortical thinning as a possible major contributor for cognitive impairment in HIV patients

International Nuclear Information System (INIS)

Shin, Na-Young; Hong, Jinwoo; Yoon, Uicheul; Choi, Jun Yong; Lee, Seung-Koo; Lim, Soo Mee

2017-01-01

To identify brain cortical regions relevant to HIV-associated neurocognitive disorder (HAND) in HIV patients. HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness. Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills. This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment. (orig.)

Using modern human cortical bone distribution to test the systemic robusticity hypothesis.

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