Bilateral Occipital Cortex Research Articles

Inhibition-Related Cortical Hypoconnectivity as a Candidate Vulnerability Marker for Obsessive-Compulsive Disorder

BackgroundObsessive-compulsive disorder (OCD) is a prevalent neuropsychiatric condition, with biological models implicating disruption of cortically mediated inhibitory control pathways, ordinarily serving to regulate our environmental responses and habits. The aim of this study was to evaluate inhibition-related cortical dysconnectivity as a novel candidate vulnerability marker of OCD. MethodsIn total, 20 patients with OCD, 18 clinically asymptomatic first-degree relatives of patients with OCD, and 20 control participants took part in a neuroimaging study comprising a functional magnetic resonance imaging stop signal task. Brain activations during the contrasts of interest were cluster thresholded, and a three-dimensional watershed algorithm was used to decompose activation maps into discrete clusters. Functional connections between these key neural nodes were examined using a generalized psychophysiological interaction model. ResultsThe three groups did not differ in terms of age, education level, gender, IQ, or behavioral task parameters. Patients with OCD exhibited hyperactivation of the bilateral occipital cortex during the task versus the other groups. Compared with control participants, patients with OCD and their relatives exhibited significantly reduced connectivity between neural nodes, including frontal cortical, middle occipital cortical, and cerebellar regions, during the stop signal task. ConclusionsThese findings indicate that hypoconnectivity between anterior and posterior cortical regions during inhibitory control represents a candidate vulnerability marker for OCD. Such vulnerability markers, if found to generalize, may be valuable to shed light on etiological processes contributing not only to OCD but also obsessive-compulsive–related disorders more widely.

Progressive Cortical Thinning in Patients With Focal Epilepsy

It is controversial whether epilepsy is a static or progressive disease. Evidence of progressive gray matter loss in epilepsy would support early diagnosis, rapid treatment, and early referral for surgical interventions. To demonstrate progressive cortical thinning in patients with focal epilepsy distinct from cortical thinning associated with normal aging. A case-control neuroimaging study was conducted from August 3, 2004, to January 26, 2016, among 190 patients with focal epilepsy at a tertiary epilepsy referral center (epilepsy data) and 3 independent comparison cohorts matched for age and sex (healthy volunteer data; n = 141). Two or more high-resolution T1-weighted magnetic resonance imaging scans at least 6 months apart (mean [SD] interval, 2.5 [1.6] years). Global and vertexwise rate of progressive cortical thinning. A total of 190 people with focal epilepsy (99 women and 91 men; mean [SD] age, 36 [11] years; 396 magnetic resonance imaging scans) were compared with 141 healthy volunteers (76 women and 65 men; mean [SD] age, 35 [17] years; 282 magnetic resonance imaging scans). Widespread highly significant progressive cortical thinning exceeding normal aging effects, mainly involving the bilateral temporal lobes, medial parietal and occipital cortices, pericentral gyri, and opercula, was seen in 146 individuals with epilepsy (76.8%; 95% CI, 58%-95%). The mean (SD) annualized rate of global cortical thinning in patients with epilepsy was twice the rate of age-associated thinning observed in healthy volunteers (0.024 [0.061] vs 0.011 [0.029] mm/y; P = .01). Progression was most pronounced in adults older than 55 years and during the first 5 years after the onset of seizures. Areas of accelerated cortical thinning were detected in patients with early onset of epilepsy and in patients with hippocampal sclerosis. Accelerated thinning was not associated with seizure frequency, history of generalized seizures, or antiepileptic drug load and did not differ between patients with or without ongoing seizures. Progressive atrophy in temporal (n = 101) and frontal (n = 28) lobe epilepsy was most pronounced ipsilaterally to the epileptic focus but also affected a widespread area extending beyond the focus and commonly affected the contralateral hemisphere. For patients with temporal lobe epilepsy, accelerated cortical thinning was observed within areas structurally connected with the ipsilateral hippocampus. Widespread progressive cortical thinning exceeding that seen with normal aging may occur in patients with focal epilepsy. These findings appear to highlight the need to develop epilepsy disease-modifying treatments to disrupt or slow ongoing atrophy. Longitudinal cortical thickness measurements may have the potential to serve as biomarkers for such studies.

Resting-state functional hypoconnectivity of amygdala in clinical high risk state and first-episode schizophrenia.

Resting-state functional hypoconnectivity of the amygdala with several brain regions has been identified in patients with schizophrenia. However, little is known about it in individuals at clinical high risk state. Treatment-seeking, drug-naive young adults were recruited for the study. The participants included 33 adults at Clinical High Risk (CHRs), 31 adults with first-episode schizophrenia (FSZs), and 37 age-, gender-, and education-matched healthy controls. All the participants were subjected to resting-state functional magnetic resonance imaging scans. Seed-based voxel-wise amygdala/whole-brain functional connectivity (FC) was calculated and compared. In the CHR group, the right amygdala showed decreased FC with clusters located in the left orbital, right temporal, insular, and bilateral frontal and cingulate areas. In the FSZ group, the right amygdala showed decreased FC with clusters located in the right temporal, insular, cingulate, and frontal areas. Exactly 30% of the voxels showing decreased FC in the FSZ group coincided with those in the CHR group. No difference in FC was identified between the CHR and FSZ groups. Voxel-wise FC values with the left or right amygdala in the bilateral occipital cortex were negatively correlated with the PANSS total score in the FSZ group. Resting-state functional hypoconnectivity of the amygdala is a valuable risk phenotype of schizophrenia, and its distribution, rather than degree, distinguishes CHR state from schizophrenia. This particular hypoconnectivity in CHRs and FSZs is relatively independent of the symptomatology and may reflect a dysfunctional dopamine system.

Prism adaptation effect on neural activity and spatial neglect depend on brain lesion site

Prism adaptation (PA) is one of the few rehabilitation techniques for spatial neglect that directly targets physiological mechanisms underlying space representation, but its efficacy and neural mechanisms remain unresolved. Using PA and fMRI in patients with spatial neglect after an acute right-hemispheric stroke, we previously observed post-PA increases in activity in bilateral parietal, frontal, and occipital cortex during specific visuo-spatial tasks (bisection and visual search). However, given a key role of parietal areas for PA in healthy individuals, we hypothesized that such activation might differ according to the site of brain damage. We studied a group of 10 patients with focal right hemisphere stroke and spatial neglect at baseline and after PA, who were divided in two groups (5 patients with frontal and 5 patients with parietal strokes). We compared their behavioural performance and brain activation patterns during fMRI. At the behavioural level, frontal and parietal patients showed similar neglect signs on visuo-spatial tasks before PA, but frontal patients showed larger benefit from PA. Differences were also observed in cortical activity, with enhanced recruitment of right parietal areas in frontal patients and less consistent patterns in parietal patients. Furthermore, fMRI analysis during PA itself (divided in 5 successive periods) showed differential activations between group in anatomically preserved pathways, including occipital areas and cerebellum, that preceded changes in parietal areas and were specific to frontal patients. These data accord with the hypothesis that intact cerebello-parietal connections may underpin improvement of spatial neglect after PA. Altogether, these results provide important insights on brain networks involved in spatial cognition and may allow an optimal selection of patients benefiting from PA after right hemispheric stroke.

Altered cognitive control network is related to psychometric and biochemical profiles in covert hepatic encephalopathy

The cognitive control network (CCN) is a network responsible for multiple executive functions, which are impaired in covert hepatic encephalopathy (CHE). We aimed to use functional connectivity (FC) magnetic resonance imaging to test the hypothesis that CHE manifested with disconnection within the CCN, which is associated with impaired neuropsychiatric and biochemical profiles. CHE was detected with abnormally low psychometric hepatic encephalopathy scores (PHES) (total cut-off score <−4). Two seeds in the dorsal anterior cingulate cortex (dACC) and the dorsolateral prefrontal cortex (DLPFC) were used to calculate the FC map within the CCN. Pearson correlation analysis was performed between the CCN and psychometric, biochemical profiles including ammonia, Interleukin (IL)-6, and tumor necrosis factor (TNF)-α. Eighteen CHE, 36 non-HE (NHE) cirrhotic patients and 36 controls were studied. Significant differences in FC were noted among groups, which revealed CHE patients had a lower FC in the bilateral lateral occipital cortex (seed in the bilateral dACC) and in the right lateral occipital and precuneus cortices (seed in the left DLPFC) (P < 0.05, corrected) compared with NHE. Progressively decreased FC in the left precentral gyrus within the CCN was noted from control, NHE to CHE. PHES positively and biochemistry negatively correlated with FC in the CCN. In conclusion, CHE patients showed aberrant FC within the CCN which is correlated with both cognitive dysfunction and biochemical profiles. Ammonia and pro-inflammatory cytokines may contribute to the occurrence of aberrant connectivity. Impaired FC within the CCN may serve as a complementary biomarker for CHE.

Functionally Separable Font-invariant and Font-sensitive Neural Populations in Occipitotemporal Cortex.

Reading relies on the rapid visual recognition of words viewed in a wide variety of fonts. We used fMRI to identify neural populations showing reduced fMRI responses to repeated words displayed in different fonts ("font-invariant" repetition suppression). We also identified neural populations showing greater fMRI responses to words repeated in a changing font as compared with words repeated in the same font ("font-sensitive" release from repetition suppression). We observed font-invariant repetition suppression in two anatomically distinct regions of the left occipitotemporal cortex (OT), a "visual word form area" in mid-fusiform cortex, and a more posterior region in the middle occipital gyrus. In contrast, bilateral shape-selective lateral occipital cortex and posterior fusiform showed considerable sensitivity to font changes during the viewing of repeated words. Although the visual word form area and the left middle occipital gyrus showed some evidence of font sensitivity, both regions showed a relatively greater degree of font invariance than font sensitivity. Our results show that the neural mechanisms in the left OT involved in font-invariant word recognition are anatomically distinct from those sensitive to font-related shape changes. We conclude that font-invariant representation of visual word form is instantiated at multiple levels by anatomically distinct neural mechanisms within the left OT.

Cortical thinning and flattening in schizophrenia and their unaffected parents.

Background: Schizophrenia is a neurodevelopmental disorder with high heritability. Widespread cortical thinning has been identified in schizophrenia, suggesting that it is a result of cortical development deficit. However, the findings of other cortical morphological indexes of patients are inconsistent, and the research on their relationship with genetic risk factors for schizophrenia is rare.Methods: In order to investigate cortical morphology deficits and their disease-related genetic liability in schizophrenia, we analyzed a sample of 33 patients with schizophrenia, 60 biological parents of the patients, as well as 30 young controls for patients and 28 elderly controls for parents with age, sex and education level being well-matched. We calculated vertex-wise measurements of cortical thickness, surface area, local gyrification index, sulcal depth, and their correlation with the clinical and cognitive characteristics.Results: Widespread cortical thinning of the fronto-temporo-parietal region, sulcal flattening of the insula and gyrification reduction of the frontal cortex were observed in schizophrenia patients. Conjunction analysis revealed that patients with schizophrenia and their parents shared significant cortical thinning of bilateral prefrontal and insula, left lateral occipital and fusiform regions (Monte Carlo correction, P<0.05), as well as a trend-level sulcal depth reduction mainly in bilateral insula and occipital cortex. We observed comprehensive cognitive deficits in patients and similar impairment in the speed of processing of their unaffected parents. Significant associations between lower processing speed and thinning of the frontal cortex and flattening of the parahippocampal gyrus were found in patients and their parents, respectively. However, no significant correlation between abnormal measurements of cortical morphology and clinical characteristics was found.Conclusion: The results suggest that cortical morphology may be susceptible to a genetic risk of schizophrenia and could underlie the cognitive dysfunction in patients and their unaffected relatives. The abnormalities shared with unaffected parents allow us to better understand the disease-specific genetic effect on cortical development.

Reduced lateral occipital gray matter volume is associated with physical frailty and cognitive impairment in Parkinson's disease.

To investigate the structural changes of the brain that correlate with physical frailty and cognitive impairments in Parkinson's disease (PD) patients. Sixty-one PD patients and 59 age- and sex-matched healthy controls were enrolled. For each participant, a frailty assessment using Fried's criteria and comprehensive neuropsychological testing using the Wechsler Adult Intelligence Scale-III and Cognitive Ability Screening Instrument were conducted, and structural brain MR images were acquired for voxel-based morphometric analysis. The neuropsychological testing includes various tests in these five domains: attention, executive, memory, speech and language, and visuospatial functions. Exploratory group-wise comparisons of gray matter volume (GMV) in the PD patients and controls were conducted. Voxel-wise multiple linear regression analyses were conducted for physical frailty-related and cognitive impairment-related GMV changes in the PD patients. Voxel-wise multiple linear regressions were also performed with the five cognitive domains separated using the same model. The PD patients exhibited diffuse GMV reductions in comparison to the controls. In the PD patients, physical frailty-related decreases in GMV were observed in the bilateral frontal and occipital cortices, while cognitive impairment-related decreases in GMV were observed in the bilateral frontal, occipital, and temporal cortices. These regions overlap in the lateral occipital cortex. After the five domains of cognitive functions were analyzed separately, physical frailty-related decreases in GMV still overlap in lateral occipital cortices with every domain of cognitive impairment-related decreases in GMV. Reduced GMV in the lateral occipital cortex is associated with cognitive impairment and physical frailty in PD patients. • Physical frailty in PD was associated with decreased GMV in the frontal and occipital cortices, while cognitive impairment was associated with decreased GMV in the frontal, temporal, and occipital cortices. • Physical frailty and cognitive impairment were both associated with decreased GMV in the lateral occipital cortex, which is part of the ventral object-based visual pathway. • Decreased GMV in the lateral occipital cortex may serve as a potential imaging biomarker for physical frailty and cognitive impairment in PD.

Cerebral blood flow changes after a day of wake, sleep, and sleep deprivation

Elucidating the neurobiological effects of sleep and wake is an important goal of the neurosciences. Whether and how human cerebral blood flow (CBF) changes during the sleep-wake cycle remain to be clarified. Based on the synaptic homeostasis hypothesis of sleep and wake, we hypothesized that a day of wake and a night of sleep deprivation would be associated with gray matter resting CBF (rCBF) increases and that sleep would be associated with rCBF decreases. Thirty-eight healthy adult males (age 22.1 ± 2.5 years) underwent arterial spin labeling perfusion magnetic resonance imaging at three time points: in the morning after a regular night's sleep, the evening of the same day, and the next morning, either after total sleep deprivation (n = 19) or a night of sleep (n = 19). All analyses were adjusted for hematocrit and head motion. rCBF increased from morning to evening and decreased after a night of sleep. These effects were most prominent in bilateral hippocampus, amygdala, thalamus, and in the occipital and sensorimotor cortices. Group × time interaction analyses for evening versus next morning revealed significant interaction in bilateral lateral and medial occipital cortices and in bilateral insula, driven by rCBF increases in the sleep deprived individuals and decreases in the sleepers, respectively. Furthermore, group × time interaction analyses for first morning versus next morning showed significant effects in medial and lateral occipital cortices, in anterior cingulate gyrus, and in the insula, in both hemispheres. These effects were mainly driven by CBF increases from TP1 to TP3 in the sleep deprived individuals. There were no associations between the rCBF changes and sleep characteristics, vigilant attention, or subjective sleepiness that remained significant after adjustments for multiple analyses. Altogether, these results encourage future studies to clarify mechanisms underlying sleep-related rCBF changes.

Altered spatial and temporal concordance among intrinsic brain activity measures in schizophrenia

Various data-driven voxel-wise measures derived from resting-state functional magnetic resonance imaging (rs-fMRI) have been developed to characterize spontaneous brain activity. These measures have been widely applied to explore brain functional changes in schizophrenia and have enjoyed significant success in unraveling the neural mechanisms of this disorder. However, their spatial and temporal coupling alterations in schizophrenia remain largely unknown. To address this issue, 88 schizophrenia patients and 116 gender- and age-matched healthy controls underwent rs-fMRI examinations. Kendall's W was used to calculate volume-wise (across voxels) and voxel-wise (across time windows) concordance among multiple commonly used measures, including fractional amplitude of low frequency fluctuations, regional homogeneity, voxel-mirrored homotopic connectivity, degree centrality and global signal connectivity. Inter-group differences in the concordance were investigated. Results revealed that whole gray matter volume-wise concordance was reduced in schizophrenia patients relative to healthy controls. Although two groups showed similar spatial distributions of the voxel-wise concordance, quantitative comparison analysis revealed that schizophrenia patients exhibited decreased voxel-wise concordance in gray matter areas spanning the bilateral frontal, parietal, occipital, temporal and insular cortices. In addition, these concordance changes were negatively correlated with onset age in schizophrenia patients. Our findings suggest that the concordance approaches may provide new insights into the neural mechanisms of schizophrenia and have the potential to be extended to neuropsychiatric disorders.

Abnormal brain processing of gentle touch in anorexia nervosa

Body image disturbance is a core symptom in anorexia nervosa (AN). Recent research suggests that abnormalities in touch perception may contribute to the disease mechanisms in AN. Here, we used functional magnetic resonance imaging (fMRI) to study possible abnormalities in cortical processing of affective touch in AN. Gentle skin strokes were applied to the right forearm during fMRI scanning in women diagnosed with AN (n = 25) and in matched healthy controls (HC; n = 25). Blocks of skin stroking were alternated with blocks of static skin indentation. Participants provided ratings of the pleasantness of skin stroking stimulation. AN participants perceived skin stroking as significantly less pleasant than HC. We observed no group differences for the contrast between skin stroking and skin indentation in primary tactile regions. We did find, however, significantly less activity in the AN group in areas including left caudate nucleus. Also, we found less activity in the AN group in bilateral lateral occipital cortex for the main effect of skin stroking. Our results suggest that abnormal functioning of the dorsal striatum could affect evaluation of pleasant tactile stimuli, and that abnormal functioning of the lateral occipital cortex might be related to disturbed body image perception.

Sex-Related Reserve Hypothesis in Alzheimer’s Disease: Changes in Cortical Thickness with a Five-Year Longitudinal Follow-Up

Sex effects on the progression of Alzheimer's disease (AD) have received less attention than other demographic factors, including onset age and education. The aim of this study was to investigate whether sex affected cortical thinning in the disease progression of AD. We prospectively recruited 36 patients with early-stage AD and 14 people with normal cognition. All subjects were assessed with magnetic resonance imaging at baseline, Year 1, Year 3, and Year 5. We performed cortical thickness analyses using surface-based morphometry on magnetic resonance imaging. Women with AD showed more rapid cortical thinning in the left dorsolateral frontal cortex, left superior temporal gyrus, bilateral temporo-parietal association cortices, bilateral anterior cingulate gyri, bilateral medial frontal cortices, and bilateral occipital cortices over 5 years than men with AD, even though there was no difference in cortical thickness at baseline. In contrast, there were no regions of significantly more rapid atrophy in men with AD. Our findings suggest that women deteriorate faster than men in the progression of AD.

Amyloid-β-related and unrelated cortical thinning in dementia with Lewy bodies.

Coexisting Alzheimer's disease (AD) pathology is common in patients with dementia with Lewy bodies (DLB). To evaluate the cortical thinning in patients with DLB considering the effect of amyloid-β (Aβ), we compared the regional cortical thickness between control subjects and patients with DLB with abnormal dopamine transporter imaging. Seventeen (43.6%) of 39 patients with DLB and no control subjects had significant Aβ deposition on 18F-florbetaben positron emission tomography. Compared to control (n= 15), Aβ-negative DLB group (n= 21) had cortical thinning in the bilateral insula, entorhinal, basal frontal, and occipito-parietal cortices. Compared to Aβ-negative DLB, Aβ-positive DLB group (n= 15) had a lower cortical thickness in the AD-prone brain regions in addition to the bilateral occipital, basal frontal, and somatomotor cortices. After controlling for the amount of Aβ deposition, DLB group had cortical thinning in the same regions affected in the Aβ-negative DLB group. In summary, patients with DLB had an Aβ-independent cortical thinning, while Aβ was associated with additional cortical thinning in the AD-prone brain regions and the aggravation of DLB-specific cortical thinning.

Imaging studies of kleptomania in a middle-aged woman with obsessive-compulsive disorder: a case report

A 57-year-old woman who had been arrested for shoplifting visited our hospital. She was diagnosed with kleptomania. She had previously been diagnosed with CREST (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome and obsessive-compulsive disorder. Cranial magnetic resonance imaging showed mild atrophy of the bilateral dorsolateral prefrontal cortices, left hippocampus, and occipital cortex, as well as diffuse mild T2 hyperintensity in the deep and subcortical white matter, including the frontal region. During a single-photon emission computed tomography scan, significant hyperperfusion was observed in the right ventral striatum, including the nucleus accumbens, ventral thalamus, and right ventrolateral prefrontal areas. Patchy hypoperfusion was found in the bilateral posterior cingulate, parietal, and occipital regions. The patient's neurocognitive function was normal, except for slight impairment of her executive function. Her symptoms and neuroimaging findings were not suggestive of a specific neurocognitive disorder. Hyperactivity of the right ventral striatum may contribute to both obsessive-compulsive disorder and kleptomania. Although frontotemporal lobar degeneration is a major neurocognitive disorder related to illegal behaviours, CREST syndrome-induced white matter microstructural damage in the orbitofrontal lobe could have caused our patient's kleptomania.

Altered Brain Functional Hubs and Connectivity in Type 2 Diabetes Mellitus Patients: A Resting-State fMRI Study.

Type 2 diabetes mellitus (T2DM) affects a vast population and is closely associated with cognitive impairment. However, the mechanisms of cognitive impairment in T2DM patients have not been unraveled. Research on the basic units (nodes or hubs and edges) of the brain functional network on the basis of neuroimaging may advance our understanding of the network change pattern in T2DM patients. This study investigated the change patterns of brain functional hubs using degree centrality (DC) analysis and the connectivity among these hubs using functional connectivity and Granger causality analysis. Compared to healthy controls, the DC values were higher in the left anterior cingulate gyrus (ACG) and lower in the bilateral lateral occipital cortices (LOC) and right precentral gyrus (PreCG) in T2DM patients. The functional connectivity between the left ACG and the right PreCG was stronger in T2DM patients, whereas the functional connectivity among the right PreCG and bilateral LOC was weaker. A negative causal effect from the left ACG to left LOC and a positive effect from the left ACG to right LOC were observed in T2DM patients, while in healthy controls, the opposite occurred. Additionally, the reserve of normal brain function in T2DM patients was negatively associated with the elevated glycemic parameters. This study demonstrates that there are brain functional hubs and connectivity alterations that may reflect the aberrant information communication in the brain of T2DM patients. The findings may advance our understanding of the mechanisms of T2DM-related cognitive impairment.

Functional Neural Correlates of Slower Gait Among Older Adults With Mild Cognitive Impairment.

Subtle, but observable, changes in mobility often exist among older adults with mild cognitive impairment (MCI). Notably, these changes are not inconsequential. Therefore, there is a strong interest to better understand the underlying neural correlates of gait slowing among older adults with MCI. In this study, we aimed to characterize patterns of functional connectivity associated with slower gait speed in older adults with MCI. Forty-nine participants aged 60 years and older with MCI were included in the cross-sectional study. All participants underwent assessments of gait speed and resting state functional magnetic resonance imaging. In this sample of older adults with MCI, slower usual gait was characterized by altered connectivity between the sensorimotor network (SMN) and the frontoparietal network (FPN) (p < .05)-specifically, slower usual gait was associated with greater connectivity between the supplementary motor area (SMA) and the bilateral ventral visual cortices (p = .01); lower connectivity between the SMA and the bilateral superior lateral occipital cortex (p < .01); and lower connectivity between the SMA and the bilateral frontal eye field (p < .01). Altered inter-network functional connectivity between the SMN and FPN may be a neural mechanism for slowing of gait in older adults with MCI.

Abnormal cortical gyrification in criminal psychopathy.

BackgroundPsychopathy is a personality disorder characterized by interpersonal and emotional abnormalities (e.g., lack of empathy and guilt) and antisocial behavior. Psychopathy has been associated with a number of structural brain abnormalities, most notably in orbital frontal and anterior/medial temporal regions, that may underlie psychopathic individuals' problematic behaviors. Past research evaluating cortical structure in psychopathy has considered thickness and volume, but to date no study has investigated differences in cortical gyrification, a measure of cortical complexity thought to reflect early neurodevelopmental cortical connectivity.MethodsWe measured the local gyrification index (LGI) in a sample of 716 adult male inmates and performed a whole brain analysis assessing the relationship between LGI and total and factor scores on the Hare Psychopathy Checklist-Revised (PCL-R).ResultsPCL-R scores were negatively associated with LGI measures within the right hemisphere in the midcingulate cortex (MCC) and adjacent regions of the superior frontal gyrus as well as lateral superior parietal cortex. Additionally, PCL-R Factor 1 scores (interpersonal/affective traits) predicted less LGI within the right MCC and adjacent dorsomedial frontal cortex and greater LGI in bilateral occipital cortex. Scores on PCL-R Factor 2, indicating impulsivity and antisocial behaviors, did not predict LGI in any regions.ConclusionsThese findings suggest that psychopathy, particularly the interpersonal and affective traits, are associated with specific structural abnormalities that form during neurodevelopment and these abnormalities may underlie aberrant brain functioning in regions important in emotional processing and cognitive control.

Prefrontal cortical thickness in motor neuron disease.

ObjectiveTo examine whether the distribution of prefrontal cortical thickness in patients with motor neuron disease is normal or bimodal and how it compares to the normal population.Methods158 patients with motor neuron disease (MND) and 86 healthy controls (HC) were enrolled in a prospective, two-center study with a common structural MRI protocol. Cortical thickness measures were extracted for the prefrontal cortex, premotor cortex, motor cortex, and occipital cortex using FreeSurfer, adjusted for age and sex, and tested for normality of distribution.ResultsCortical thickness measures of the bilateral prefrontal, premotor, motor, and occipital cortex were normally distributed in patients and healthy controls. MND-related cortical thinning was observed in the right motor cortex (p = 0.002), reflected in a significantly higher proportion of MND cases being worse than −1 standard deviation of the healthy control mean: 29.1% in the right motor cortex (p = 0.002). Cortical thinning of the left motor cortex was a function of clinical phenotype and physical disability. Left prefrontal cortical thickness was reduced in patients with additional cognitive and/or behavioural deficits compared to MND patients without cognitive deficits. Prefrontal, premotor, motor, and occipital cortical thickness was related to patients' general cognitive abilities.ConclusionThe study shows that prefrontal cortical thickness in MND is normally distributed but shifted towards thinner cortex in MND patients with cognitive and/or behavioural impairment. The distribution of thickness values did not indicate the assumption of a bimodal distribution although patients with comorbid cognitive deficits are more likely to suffer from prefrontal cortical thinning.

Electrocortical N400 Effects of Semantic Satiation.

Semantic satiation is characterised by the subjective and temporary loss of meaning after high repetition of a prime word. To study the nature of this effect, previous electroencephalography (EEG) research recorded the N400, an ERP component that is sensitive to violations of semantic context. The N400 is characterised by a relative negativity to words that are unrelated vs. related to the semantic context. The semantic satiation hypothesis predicts that the N400 should decrease with high repetition. However, previous findings have been inconsistent. Because of these inconsistent findings and the shortcomings of previous research, we used a modified design that minimises confounding effects from non-semantic processes. We recorded 64-channel EEG and analysed the N400 in a semantic priming task in which the primes were repeated 3 or 30 times. Critically, we separated low and high repetition trials and excluded response trials. Further, we varied the physical features (letter case and format) of consecutive primes to minimise confounding effects from perceptual habituation. For centrofrontal electrodes, the N400 was reduced after 30 repetitions (vs. 3 repetitions). Explorative source reconstructions suggested that activity decreased after 30 repetitions in bilateral inferior temporal gyrus, the right posterior section of the superior and middle temporal gyrus, right supramarginal gyrus, bilateral lateral occipital cortex, and bilateral lateral orbitofrontal cortex. These areas overlap broadly with those typically involved in the N400, namely middle temporal gyrus and inferior frontal gyrus. The results support the semantic rather than the perceptual nature of the satiation effect.

Pattern recognition of magnetic resonance imaging-based gray matter volume measurements classifies bipolar disorder and major depressive disorder

BackgroundBipolar Disorder (BD) cannot be reliably distinguished from Major Depressive Disorder (MDD) until the first manic or hypomanic episode. Consequently, many patients with BD are treated with antidepressants without mood stabilizers, a strategy that is often ineffective and carries a risk of inducing a manic episode. We previously reported reduced cortical thickness in right precuneus, right caudal middle-frontal cortex and left inferior parietal cortex in BD compared with MDD. MethodsThis study extends our previous work by performing individual level classification of BD or MDD in an expanded, currently unmedicated, cohort using gray matter volume (GMV) based on Magnetic Resonance Imaging and a Support Vector Machine. All patients were in a Major Depressive Episode and a leave-two-out analysis was performed. ResultsNineteen out of 26 BD subjects and 20 out of 26 MDD subjects were correctly identified, for a combined accuracy of 75%. The three brain regions contributing to the classification were higher GMV in bilateral supramarginal gyrus and occipital cortex indicating MDD, and higher GMV in right dorsolateral prefrontal cortex indicating BD. LimitationsThis analysis included scans performed with two different headcoils and scan sequences, which limited the interpretability of results in an independent cohort analysis. ConclusionsOur results add to previously published data which suggest that regional gray matter volume should be investigated further as a clinical diagnostic tool to predict BD before the appearance of a manic or hypomanic episode.