Parietal Association Cortex Research Articles

Disruption in cerebellar and basal ganglia networks during a visuospatial task in cervical dystonia.

Although dystonia is traditionally conceptualized as a basal ganglia disorder, increasing interest has been directed at a different neural network node, the cerebellum, which may play a significant role in the pathophysiology of dystonia. Abnormal sensorimotor processing and disturbed motor schemes, possibly attributable to cerebellar changes, remain unclear. We sought to characterize the extent of cerebellar dysfunction within the motor network using functional MRI activation analysis, connectivity analysis, and voxel-based morphometry in cervical dystonia patients (n = 25, 15 women, mean age 45.8 years) and healthy volunteers (n = 25, 15 women, mean age 44.7 years) in a visuospatial task requiring predictive motor timing. Cervical dystonia patients showed decreased activation in the posterior cerebellar lobules as well as in the premotor areas, the associative parietal cortex, and visual regions. Patients also had decreased cerebellar connectivity with bilateral basal ganglia structures and the dorsolateral prefrontal cortex. This promotes the view that dystonia results from miscommunication between the basal ganglia and cerebellar loops, thus providing new insights into the brain regions essential for the development of cervical dystonia. © 2017 International Parkinson and Movement Disorder Society.

Distribution of Alox15 in the Rat Brain and Its Role in Prefrontal Cortical Resolvin D1 Formation and Spatial Working Memory

Docosahexaenoic acid (DHA) is enriched in membrane phospholipids of the central nervous system (CNS) and has a role in aging and neuropsychiatric disorders. DHA is metabolized by the enzyme Alox15 to 17S-hydroxy-DHA, which is then converted to 7S-hydroperoxy,17S-hydroxy-DHA by a 5-lipoxygenase, and thence via epoxy intermediates to the anti-inflammatory molecule, resolvin D1 (RvD1 or 7S,8R,17S-trihydroxy-docosa-Z,9E,11E,13Z,15E,19Z-hexaenoic acid). In this study, we investigated the distribution and function of Alox15 in the CNS. RT-PCR of the CNS showed that the prefrontal cortex exhibits the highest Alox15 mRNA expression level, followed by the parietal association cortex and secondary auditory cortex, olfactory bulb, motor and somatosensory cortices, and the hippocampus. Western blot analysis was consistent with RT-PCR data, in that the prefrontal cortex, cerebral cortex, hippocampus, and olfactory bulb had high Alox15 protein expression. Immunohistochemistry showed moderate staining in the olfactory bulb, cerebral cortex, septum, striatum, cerebellar cortex, cochlear nuclei, spinal trigeminal nucleus, and dorsal horn of the spinal cord. Immuno-electron microscopy showed localization of Alox15 in dendrites, in the prefrontal cortex. Liquid chromatography mass spectrometry analysis showed significant decrease in resolvin D1 levels in the prefrontal cortex after inhibition or antisense knockdown of Alox15. Alox15 inhibition or antisense knockdown in the prefrontal cortex also blocked long-term potentiation of the hippocampo-prefrontal cortex pathway and increased errors in alternation, in the T-maze test. They indicate that Alox15 processing of DHA contributes to production of resolvin D1 and LTP at hippocampo-prefrontal cortical synapses and associated spatial working memory performance. Together, results provide evidence for a key role of anti-inflammatory molecules generated by Alox15 and DHA, such as resolvin D1, in memory. They suggest that neuroinflammatory brain disorders and chronic neurodegeneration may ‘drain’ anti-inflammatory molecules that are necessary for normal neuronal signaling, and compromise cognition.

Representing Spatial Information in the Parietal Association Cortex

Several clinical studies have shown that the parietal association cortex plays an important role in spatial perception. Electrophysiological studies on behaving monkeys initiated in the 1970s have revealed the presence of neurons in the parietal association cortex whose activity is related to spatial vision. Herein, we review previous studies on non-human primates and we present an overview of the neuronal representation of spatial information in the parietal association cortex.

Neuroanatomy of the Parietal Association Areas

The parietal association cortex comprises the superior and inferior parietal lobules, the precuneus and the cortices in the intraparietal, parietooccipital and lunate sulci. By processing somatic, visual, acoustic and vestibular sensory information, the parietal association cortex plays a pivotal role in spatial cognition and motor control of the eyes and the extremities. Sensory information from the primary and secondary somatosensory areas enters the superior parietal lobule and is transferred to the inferior parietal lobule. Visual information is processed through the dorsal visual pathway and it reaches the inferior parietal lobule, the intraparietal sulcus and the precuneus. Acoustic information is transferred posteriorly from the primary acoustic area, and it reaches the posterior region of the inferior parietal lobule. The areas in the intraparietal sulcus project to the premotor area, the frontal eye fields, and the prefrontal area. These areas are involved in the control of ocular movements, reaching and grasping of the upper extremities, and spatial working memory. The posterior region of the inferior parietal lobule and the precuneus both project either directly, or indirectly via the posterior cingulate gyrus, to the parahippocampal and entorhinal cortices. Both these areas are strongly associated with hippocampal functions for long-term memory formation.

In vivo cortical spreading pattern of tau and amyloid in the Alzheimer disease spectrum.

To determine the in vivo cortical spreading pattern of tau and amyloid and to establish positron emission tomography (PET) image-based tau staging in the Alzheimer disease (AD) spectrum. We included 195 participants (53 AD, 52 amnestic mild cognitive impairment [MCI], 23 nonamnestic MCI, and 67 healthy controls) who underwent 2 PET scans ((18) F-florbetaben for amyloid-β and (18) F-AV-1451 for tau). We assumed that regions with earlier appearances of pathology may show increased binding in a greater number of participants and acquired spreading order of tau accumulation by sorting the regional frequencies of involvement. We classified each participant into image-based tau stage based on the Z score of the composite region for each stage. Tau accumulation was most frequently observed in the medial temporal regions and spread stepwise to the basal and lateral temporal, inferior parietal, posterior cingulate, and other association cortices, and then ultimately to the primary cortical regions. In contrast, amyloid accumulation was found with similar frequency in the diffuse neocortical areas and then finally spread to the medial temporal regions. The image-based tau stage correlated with the general cognitive status, whereas cortical thinning was found only in the advanced tau stages: medial temporal region in stage V and widespread cortex in stage VI. Our PET study replicated postmortem spreading patterns of tau and amyloid-β pathologies. Unlike the diffuse accumulation of amyloid throughout the neocortex, tau spreading occurred in a stepwise fashion through the networks. Image-based tau staging may be useful for the objective assessment of AD progression. Ann Neurol 2016;80:247-258.

Frontoparietal cortex and cerebellum contribution to the update of actual and mental motor performance during the day.

Actual and imagined movement speed increases from early morning until mid-afternoon. Here, we investigated the neural correlates of these daily changes. Fifteen subjects performed actual and imagined right finger opposition movement sequences at 8 am and 2 pm. Both actual and imagined movements were significantly faster at 2 pm than 8 am. In the morning, actual movements significantly activated the left primary somatosensory and motor areas, and bilaterally the cerebellum; in the afternoon activations were similar but reduced. Contrast analysis revealed greater activity in the cerebellum, the left primary sensorimotor cortex and parietal lobe in the morning than in the afternoon. Imagined movements in the morning significantly activated the parietal association cortices bilaterally, the left supplementary and premotor areas, and the right orbitofrontal cortex and cerebellum. In the afternoon, the frontal lobe was significantly activated with the right cerebellum. Contrast analysis revealed increased activity in the left parietal lobe in the morning than in the afternoon. For both tasks, speed in the morning was significantly related to the BOLD signal in the brain areas resulted more active. These findings suggest that motor performance is continuously updated on a daily basis with a predominant role of the frontoparietal cortex and cerebellum.

Implications of Lateral Cerebellum in Proactive Control of Saccades.

Although several lines of evidence establish the involvement of the medial and vestibular parts of the cerebellum in the adaptive control of eye movements, the role of the lateral hemisphere of the cerebellum in eye movements remains unclear. Ascending projections from the lateral cerebellum to the frontal and parietal association cortices via the thalamus are consistent with a role of these pathways in higher-order oculomotor control. In support of this, previous functional imaging studies and recent analyses in subjects with cerebellar lesions have indicated a role for the lateral cerebellum in volitional eye movements such as anti-saccades. To elucidate the underlying mechanisms, we recorded from single neurons in the dentate nucleus of the cerebellum in monkeys performing anti-saccade/pro-saccade tasks. We found that neurons in the posterior part of the dentate nucleus showed higher firing rates during the preparation of anti-saccades compared with pro-saccades. When the animals made erroneous saccades to the visual stimuli in the anti-saccade trials, the firing rate during the preparatory period decreased. Furthermore, local inactivation of the recording sites with muscimol moderately increased the proportion of error trials, while successful anti-saccades were more variable and often had shorter latency during inactivation. Thus, our results show that neuronal activity in the cerebellar dentate nucleus causally regulates anti-saccade performance. Neuronal signals from the lateral cerebellum to the frontal cortex might modulate the proactive control signals in the corticobasal ganglia circuitry that inhibit early reactive responses and possibly optimize the speed and accuracy of anti-saccades. Although the lateral cerebellum is interconnected with the cortical eye fields via the thalamus and the pons, its role in eye movements remains unclear. We found that neurons in the caudal part of the lateral (dentate) nucleus of the cerebellum showed the increased firing rate during the preparation of anti-saccades. Inactivation of the recording sites modestly elevated the rate of erroneous saccades to the visual stimuli in the anti-saccade trials, while successful anti-saccades during inactivation tended to have a shorter latency. Our data indicate that neuronal signals in the lateral cerebellum may proactively regulate anti-saccade generation through the pathways to the frontal cortex, and may inhibit early reactive responses and regulate the accuracy of anti-saccades.

Age-related differences in the neural correlates of trial-to-trial variations of reaction time

Intra-subject variation in reaction time (ISVRT) is a developmentally-important phenomenon that decreases from childhood through young adulthood in parallel with the development of executive functions and networks. Prior work has shown a significant association between trial-by-trial variations in reaction time (RT) and trial-by-trial variations in brain activity as measured by the blood-oxygenated level-dependent (BOLD) response in functional magnetic resonance imaging (fMRI) studies. It remains unclear, however, whether such “RT-BOLD” relationships vary with age. Here, we determined whether such trial-by-trial relationships vary with age in a cross-sectional design. We observed an association between age and RT-BOLD relationships in 11 clusters located in visual/occipital regions, frontal and parietal association cortex, precentral/postcentral gyrus, and thalamus. Some of these relationships were negative, reflecting increased BOLD associated with decreased RT, manifesting around the time of stimulus presentation and positive several seconds later. Critically for present purposes, all RT-BOLD relationships increased with age. Thus, RT-BOLD relationships may reflect robust, measurable changes in the brain-behavior relationship across development.

Functionally Brain Network Connected to the Retrosplenial Cortex of Rats Revealed by 7T fMRI.

Functional networks are regarded as important mechanisms for increasing our understanding of brain function in healthy and diseased states, and increased interest has been focused on extending the study of functional networks to animal models because such models provide a functional understanding of disease progression, therapy and repair. In rodents, the retrosplenial cortex (RSC) is an important cortical region because it has a large size and presents transitional patterns of lamination between the neocortex and archicortex. In addition, a number of invasive studies have highlighted the importance of the RSC for many functions. However, the network based on the RSC in rodents remains unclear. Based on the critical importance of the RSC, we defined the bilateral RSCs as two regions of interest and estimated the network based on the RSC. The results showed that the related regions include the parietal association cortex, hippocampus, thalamus nucleus, midbrain structures, and hypothalamic mammillary bodies. Our findings indicate two possible major networks: a sensory-cognitive network that has a hub in the RSCs and processes sensory information, spatial learning, and episodic memory; and a second network that is involved in the regulation of visceral functions and arousal. In addition, functional asymmetry between the bilateral RSCs was observed.

Neurostructural correlates of consistent and weak handedness

ABSTRACTVarious cognitive differences have been reported between consistent and weak handers, but little is known about the neurobiological factors that may be associated with this distinction. The current study examined cortical structural lateralization and corpus callosum volume in a large, well-matched sample of young adults (N = 164) to explore potential neurostructural bases for this hand group difference. The groups did not differ in corpus callosum volume. However, at the global hemispheric level, weak handers had reduced or absent asymmetries for grey and white matter volume, cortical surface area, thickness, and local gyrification, relative to consistent handers. Group differences were also observed for some regional hemispheric asymmetries, the most prominent of which was reduced or absent gyrification asymmetry for weak handers in a large region surrounding the central sulcus and extending into parietal association cortex. The findings imply that variations in handedness strength are associated with differences in structural lateralization, not only in somatomotor regions, but also in areas associated with high level cognitive control of action.

Topology of genetic associations between regional gray matter volume and intellectual ability: Evidence for a high capacity network

Intelligence is associated with a network of distributed gray matter areas including the frontal and parietal higher association cortices and primary processing areas of the temporal and occipital lobes. Efficient information transfer between gray matter regions implicated in intelligence is thought to be critical for this trait to emerge. Genetic factors implicated in intelligence and gray matter may promote a high capacity for information transfer. Whether these genetic factors act globally or on local gray matter areas separately is not known.Brain maps of phenotypic and genetic associations between gray matter volume and intelligence were made using structural equation modeling of 3T MRI T1-weighted scans acquired in 167 adult twins of the newly acquired U-TWIN cohort. Subsequently, structural connectivity analyses (DTI) were performed to test the hypothesis that gray matter regions associated with intellectual ability form a densely connected core.Gray matter regions associated with intellectual ability were situated in the right prefrontal, bilateral temporal, bilateral parietal, right occipital and subcortical regions. Regions implicated in intelligence had high structural connectivity density compared to 10,000 reference networks (p=0.031). The genetic association with intelligence was for 39% explained by a genetic source unique to these regions (independent of total brain volume), this source specifically implicated the right supramarginal gyrus.Using a twin design, we show that intelligence is genetically represented in a spatially distributed and densely connected network of gray matter regions providing a high capacity infrastructure. Although genes for intelligence have overlap with those for total brain volume, we present evidence that there are genes for intelligence that act specifically on the subset of brain areas that form an efficient brain network.

Regional mosaic genomic heterogeneity in the elderly and in Alzheimer's disease as a correlate of neuronal vulnerability.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by fibrillary aggregates of Aβ peptide and tau protein. The distribution of these pathological hallmarks throughout the brain is not random; it follows a predictive pattern that is used for pathological staging. However, most etiopathogenetic concepts, irrespective of whether they focus on Aβ or tau pathology, leave a key question unanswered: what is the explanation for the different vulnerabilities of brain regions in AD? The pattern of regional progression of neurofibrillary degeneration in AD to some extent inversely recapitulates ontogenetic and phylogenetic brain development. Accordingly, degeneration preferentially affects brain areas that have recently been acquired or restructured during anthropoid evolution, which means that the involvement of a neurodevelopmental mechanism is highly likely. Since evolutionary expansion of the neocortex is based on a substantial extension of the mitotic activity of progenitor cells, we propose a conceptual link between neurogenesis in anthropoid primates and a higher risk of accumulating mitotic errors that give rise to genomic aberrations commonly referred to as DNA content variation (DCV). If increased rates of DCV make neurons more vulnerable to AD-related pathology, one might expect there to be a higher rate of DCV in areas that are affected very early during the course of AD, as compared to areas which are hardly affected or are affected only during the most advanced stages. Therefore, in the present study, we comparatively analyzed the DCV in five different cortical areas that are affected during the early stage (entorhinal cortex), the intermediate stage (temporal, frontal, and parietal association cortex), and the late stage (primary sensory occipital cortex) of AD in both normal elderly subjects and AD patients. On average, we observed about 10% neuronal mosaic DCV in the normal elderly and a two- to threefold increase in DCV in AD patients. We were able to demonstrate, moreover, that the neuronal DCV in the cerebral cortex of the normal elderly as well as the increased neuronal DCV in AD patients are not randomly distributed but instead show systematic regional differences which correspond to differences in vulnerability. These findings provide additional evidence that mosaic genomic heterogeneity may play a key role in AD pathology.

Entorhinal tau deposition is associated with parietal association cortex hypometabolism in clinically normal older individuals

Entorhinal tau deposition is associated with parietal association cortex hypometabolism in clinically normal older individuals

Human Brain Representations of Haptic and Visual Textures

We present a literature review of functional brain imaging studies of haptic and visual texture perception, and highlight our ongoing functional magnetic resonance imaging (fMRI) experiment of the crossmodal links between vision and touch. In the fMRI experiment, the subjects viewed or touched a piece of wool or denim cloth. A multivoxel pattern analysis of whole-brain fMRI activity revealed the crossmodal nature of natural texture perception. Visual texture representations were found in the somatosensory and association cortices as well as the visual cortex, while haptic texture representations were found in the visual cortex and association cortices as well as the somatosensory cortex. Furthermore, shared visuo-haptic representations were found in the parietal association, somatosensory, and visual cortices. These results that suggested the crossmodal transfer of texture information across functionally segregated sensory and associative brain regions are discussed in relation to previous findings on texture perception and aesthetic texture or shitsukan.

Brain structure-function associations in multi-generational families genetically enriched for bipolar disorder.

Recent theories regarding the pathophysiology of bipolar disorder suggest contributions of both neurodevelopmental and neurodegenerative processes. While structural neuroimaging studies indicate disease-associated neuroanatomical alterations, the behavioural correlates of these alterations have not been well characterized. Here, we investigated multi-generational families genetically enriched for bipolar disorder to: (i) characterize neurobehavioural correlates of neuroanatomical measures implicated in the pathophysiology of bipolar disorder; (ii) identify brain-behaviour associations that differ between diagnostic groups; (iii) identify neurocognitive traits that show evidence of accelerated ageing specifically in subjects with bipolar disorder; and (iv) identify brain-behaviour correlations that differ across the age span. Structural neuroimages and multi-dimensional assessments of temperament and neurocognition were acquired from 527 (153 bipolar disorder and 374 non-bipolar disorder) adults aged 18-87 years in 26 families with heavy genetic loading for bipolar disorder. We used linear regression models to identify significant brain-behaviour associations and test whether brain-behaviour relationships differed: (i) between diagnostic groups; and (ii) as a function of age. We found that total cortical and ventricular volume had the greatest number of significant behavioural associations, and included correlations with measures from multiple cognitive domains, particularly declarative and working memory and executive function. Cortical thickness measures, in contrast, showed more specific associations with declarative memory, letter fluency and processing speed tasks. While the majority of brain-behaviour relationships were similar across diagnostic groups, increased cortical thickness in ventrolateral prefrontal and parietal cortical regions was associated with better declarative memory only in bipolar disorder subjects, and not in non-bipolar disorder family members. Additionally, while age had a relatively strong impact on all neurocognitive traits, the effects of age on cognition did not differ between diagnostic groups. Most brain-behaviour associations were also similar across the age range, with the exception of cortical and ventricular volume and lingual gyrus thickness, which showed weak correlations with verbal fluency and inhibitory control at younger ages that increased in magnitude in older subjects, regardless of diagnosis. Findings indicate that neuroanatomical traits potentially impacted by bipolar disorder are significantly associated with multiple neurobehavioural domains. Structure-function relationships are generally preserved across diagnostic groups, with the notable exception of ventrolateral prefrontal and parietal association cortex, volumetric increases in which may be associated with cognitive resilience specifically in individuals with bipolar disorder. Although age impacted all neurobehavioural traits, we did not find any evidence of accelerated cognitive decline specific to bipolar disorder subjects. Regardless of diagnosis, greater global brain volume may represent a protective factor for the effects of ageing on executive functioning.

Altered synchrony and loss of consciousness during frontal lobe seizures

ObjectiveLoss of consciousness (LOC) in frontal lobe epilepsy (FLE) has been rarely specifically studied until now. In this study we evaluated the LOC in a population of patients with FLE and studied the relationship between changes in synchrony and degree of LOC. Methods24 patients undergoing stereoelectroencephalography (SEEG) during pre-surgical evaluation of FLE were studied. The LOC intensity was scored using the Consciousness Seizure Scale (CSS). For each studied seizure (n=52), interdependencies between signals recorded from 5 brain regions were estimated as a function of time by using non-linear regression analysis (h2 coefficient). ResultsSeizures were divided into 3 groups according to the CSS scale: group A (no LOC) with a score ⩽2, group B (intermediate or partial LOC) with a score ranging from 3 to 5, and group C (maximal LOC) with a score ⩾6. The majority of seizures in FLE patients disclosed significant LOC, particularly for patients with prefrontal lobe seizures. Mean correlation values were significantly different between groups A and C (p<0.001), the maximal values of synchrony being observed in group C. Differences were significant for interaction affecting the external prefrontal cortex (p=0.004) (p=0.01) and the parietal cortex. In addition, a significant correlation was found between CSS scores and correlations values (h2) of the prefrontal and the parietal region but not with the premotor cortex. ConclusionsThis study indicates that in FLE, prefrontal seizures frequently alter consciousness. As in other focal seizures, LOC appears to be related to changes in synchrony in prefrontal and parietal associative cortices. SignificanceLOC in FLE is frequent and as in other focal epilepsies is related to an alteration of prefrontal–parietal network.

Neuro-anatomic mapping of dopamine D1 receptor involvement in nicotine self-administration in rats

Dopaminergic signaling has long been known to be a critical factor in nicotine addiction, as well as other drugs of abuse. Dopaminergic projections from the VTA to the nucleus accumbens and prefrontal cortex have been well established to be critical to the reinforcing effects of these drugs. However, other projections of dopamine neurons are likely to have significant roles in this process. Also, the relative contributions of D1 and D2 dopamine receptors in drug addiction and its treatment remain to be fully understood. In this study, we examined the effects of blocking D1 and D2 receptors in the nucleus accumbens shell (AcS), anterior cingulate cortex (ACC), and parietal association cortex (PtA) on nicotine self-administration in rats. Female Sprague–Dawley rats were fitted with jugular catheters and allowed to self-administer nicotine (0.03 mg/kg/infusion) on an FR1 schedule. Rats were fitted with bilateral infusion cannulae to allow infusion of D1 or D2 antagonists (SCH-23390 or haloperidol) into each targeted brain area. Acute local infusions of SCH-23390 (1–4 μg/side) into the AcS and PtA significantly reduced nicotine self-administration by up to 75%. SCH-23390 infusion into the ACC was less effective with only suggestive non-significant reductions of nicotine self-administration. Acute, local infusions of haloperidol (0.5–2 μg/side) in any of the brain regions targeted did not have significant effects on nicotine self-administration. These results demonstrate a more significant role for D1 receptor mechanisms in the process of nicotine reinforcement and help provide a more detailed neuroanatomic map of nicotine dependence in the brain.

Schmahmann's syndrome - identification of the third cornerstone of clinical ataxiology.

Schmahmann’s syndrome represents a novel clinical condition consisting of a constellation of cognitive and affective deficits following cerebellar disease. The complex was first described in 1998 as cerebellar cognitive affective syndrome (CCAS) on the basis of a careful neurological examination, detailed bedside mental state tests, neuropsychological investigations and anatomical neuroimaging of a group of 20 patients with focal cerebellar disorders. The syndrome was characterized by four clusters of symptoms including: (a) impairment of executive functions such as planning, set-shifting, verbal fluency, abstract reasoning and working memory, (b) impaired visuo-spatial cognition, (c) personality changes with blunting of affect or abnormal behaviour, and (d) language deficits including agrammatism, wordfinding disturbances, disruption of language dynamics and dysprosodia. This complex of neurocognitive and behavioural-affective symptoms was ascribed to a functional disruption of the reciprocal pathways that connect the cerebellum with the limbic circuitry and the prefrontal, temporal and parietal association cortices. With the introduction of Schmahmann’s syndrome, clinical ataxiology has found its third cornerstone, the two others being the cerebellar motor syndrome (CMS) mainly delineated by the pioneer French and English neurologists of the 19th and early 20th century, and the vestibulo-cerebellar syndrome (VCS) consisting of ocular instability, deficits of oculomotor movements and ocular misalignment.

Corpus callosum abnormalities in medication-naïve adult patients with obsessive compulsive disorder

Emerging evidence demonstrates widespread abnormalities involving white matter (WM) tracts connecting different cortical regions in obsessive-compulsive disorder (OCD). The corpus callosum (CC), the largest inter-hemispheric tract connecting the association cortices, has been shown to be affected in OCD. This study examines CC abnormalities in a large sample of medication-naïve OCD patients in comparison to matched healthy controls (HCs). We examined the mid-sagittal area of the CC in medication-naïve OCD patients (n=49) in comparison with age-, sex-, and handedness-matched HCs (n=38). Witelson׳s method was used to measure the sub-regions of the CC – namely, the genu, body, isthmus and splenium – with good inter-rater reliability. The area of the body of the CC and total CC area were significantly larger in OCD patients than in HCs after controlling for age, sex and intracranial area. The Yale–Brown Obsessive-Compulsive Scale (Y–BOCS) compulsion score had a significant negative correlation with the areas of the isthmus and splenium of the CC in addition to the total CC area. The region-specific differences in the body of the CC and the region-specific association of severity score with posterior regions of the CC might be indicative of the involvement of additional areas like the dorsolateral prefrontal cortex, posterior parietal areas, occipital and association cortices in OCD that extend beyond the conventional orbito-fronto-striatal circuitry that is often posited to be involved in OCD.

The value of susceptibility-weighted imaging (SWI) in patients with non-neonatal hypoxic-ischemic encephalopathy

ObjectiveIn susceptibility-weighted imaging (SWI) in the normal brain, cortical veins appear hypointense due to paramagnetic properties of deoxy-hemoglobin. Global cerebral anoxia decreases cerebral oxygen metabolism, thereby increasing oxy-hemoglobin levels in cerebral veins. We hypothesized that a lower cerebral oxygen extraction fraction in comatose patients with non-neonatal hypoxic-ischemic encephalopathy (IHE) produces a pattern of global rarefied or pseudo-diminished cortical veins due to higher oxy-hemoglobin. Purpose(1) To investigate the topographic relationship between susceptibility effects in cortical veins and related diffusion restrictions on diffusion-weighted imaging (DWI) in patients with IHE. (2) To relate imaging findings to patterns of altered resting activity on surface EEG. MethodsTwenty-three IHE patients underwent MRI. EEG patterns were used to classify the depth of coma. Regional vs. global susceptibility changes on SWI and patterns of DWI restrictions were compared with the depth of coma. ResultsAll patients exhibited areas of restricted cortical diffusion and SWI abnormalities. The dominant DWI restrictions encompassed widespread areas along the precuneus, frontal and parietal association cortices and basal ganglia. For SWI, nineteen patients had generalized bi-hemispherical patterns, the EEG patterns correlated with coma grades III–V. Four patients had focal decreases of deoxy-hemoglobin following DWI restrictions; associated with normal EEGs. ConclusionFocal patterns of diamagnetic effects on SWI according to relative decreases in deoxy-hemoglobin due to reduced metabolic demand are associated with normal EEG in IHE patients. Global patterns indicated increased depth of coma and widespread cortical damage. Clinical relevanceThe results indicate a potential diagnostic value of SWI in patients with IHE.