Gray Matter In Subjects Research Articles

Cortical-Subcortical morphometric signature of hot water epilepsy patients

BackgroundCortical and subcortical grey matter (GM) morphometric changes have been demonstrated Temporal Lobe Epilepsy (TLE) or Idiopathic Generalized Epilepsies (IGE). Hot Water Epilepsy (HWE) has not hitherto been studied in these perspectives. PurposeTo investigate the cortical and subcortical grey matter in subjects with HWE in terms of thickness, volume, and surface area using Surface-Based Morphometry (SBM). To assess relationships of SBM-derived metrics with clinical variables. Materials and MethodsNinety-nine people with HWE and 50 age-matched healthy controls underwent high resolution volumetric MRI brain. These were processed with FreeSurfer to obtain SBM parameters i:e cortical thickness, cortical volume, and Cortical surface area. Volumes of seven subcortical GM structures (hippocampus, globus pallidus, nucleus ambiguous(NA), caudate nucleus, putamen, thalamus, and amygdala) were computed. Intergroup morphometric differences and their correlation with epilepsy-specific clinical variables were calculated. ResultsSBM revealed a global reduction in bihemispheric cortical thickness and left hemispheric cortical volume. Besides, a regional difference in the morphometric measures was noted in temporo-limbic, parietal, pre-cuneus, and the cingulate region. Reduced volume of thalami and left caudate alongside an increased volume of the bilateral amygdala, bilateral nucleus ambiguous (NA), right caudate, and putamen was the other cardinal observation. ConclusionHWE subjects show alterations in the morphometry of the cortical ribbon and the subcortical grey matter. The temporal semiology, ‘reflex nature’ pathophysiology correlates involvement of temporo-limbic structures/somatosensory cortex, while the involvement of structures like pre-cuneus, posterior cingulate, and frontal regions are in agreement with functional networks related loss of awareness. That bilateral amygdala swelling occurs in HWE is a novel observation and may signal that it could be a distinct variant of Mesial TLE.

Associations Between the Subjective Cognitive Decline-Questionnaire's Scores, Gray Matter Volume, and Amyloid-β Levels.

Exploring the relationship between Alzheimer's disease (AD) biomarkers and subjective cognitive decline (SCD) is needed for better defining its clinical meaning in preclinical AD (preAD). To assess the association between the Subjective Cognitive Decline Questionnaire (SCD-Q), gray matter (GM), and cerebrospinal fluid amyloid-β (Aβ). 56 cognitively healthy older adults and their informants answered the SCD-Q. Correlations between GM and SCD-Q scores were explored using structural voxel-based morphometry models including Aβ levels. SCD-Q*Aβ vectors were calculated with higher scores reflecting higher SCD and cerebral amyloid, simultaneously. Subjects were classified according to their perception of cognitive worsening in the last two years, exploring for GM differences between-groups. Higher self-reported SCD-Q scores correlated with reduced GM in the right frontal lobe and increased volumes in the occipital lobe, calcarine sulcus, fusiform gyrus, and cerebellum, while higher informant's scores correlated with increased GM in the right middle temporal gyrus. Correlations were more significant for SCD-Q language items, self-complaints, and more positive than negative correlations were found. The SCD-Q*Aβ vectors were negatively associated with GM both in self and informant's reports. Finally, lower Aβ levels related to lower GM in subjects who noticed cognitive worsening, but related to higher GM in subjects who have not noticed this decline. Our results suggest that SCD-Q scores relate with incipient brain changes that may be due to preAD. Independent studies are needed to confirm our observations.

The anterior hypothalamus in cluster headache.

Objective To evaluate the presence, localization, and specificity of structural hypothalamic and whole brain changes in cluster headache and chronic paroxysmal hemicrania (CPH). Methods We compared T1-weighted magnetic resonance images of subjects with cluster headache (episodic n = 24; chronic n = 23; probable n = 14), CPH ( n = 9), migraine (with aura n = 14; without aura n = 19), and no headache ( n = 48). We applied whole brain voxel-based morphometry (VBM) using two complementary methods to analyze structural changes in the hypothalamus: region-of-interest analyses in whole brain VBM, and manual segmentation of the hypothalamus to calculate volumes. We used both conservative VBM thresholds, correcting for multiple comparisons, and less conservative thresholds for exploratory purposes. Results Using region-of-interest VBM analyses mirrored to the headache side, we found enlargement ( p < 0.05, small volume correction) in the anterior hypothalamic gray matter in subjects with chronic cluster headache compared to controls, and in all participants with episodic or chronic cluster headache taken together compared to migraineurs. After manual segmentation, hypothalamic volume (mean±SD) was larger ( p < 0.05) both in subjects with episodic (1.89 ± 0.18 ml) and chronic (1.87 ± 0.21 ml) cluster headache compared to controls (1.72 ± 0.15 ml) and migraineurs (1.68 ± 0.19 ml). Similar but non-significant trends were observed for participants with probable cluster headache (1.82 ± 0.19 ml; p = 0.07) and CPH (1.79 ± 0.20 ml; p = 0.15). Increased hypothalamic volume was primarily explained by bilateral enlargement of the anterior hypothalamus. Exploratory whole brain VBM analyses showed widespread changes in pain-modulating areas in all subjects with headache. Interpretation The anterior hypothalamus is enlarged in episodic and chronic cluster headache and possibly also in probable cluster headache or CPH, but not in migraine.

A Voxel-Based Morphometry Study in AlzheimerÂ’s Disease and Mild Cognitive Impairment

Objectives: A number of structural magnetic resonance imaging (MRI) studies have demonstrated grey matter (GM) atrophy in subjects with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). We used a voxel-based morphometric (VBM) approach to evaluate the patterns of atrophy in GM in subjects with AD and MCI in comparison to control subjects. Methods: We performed brain MRI with VBM analysis in 53 subjects with AD, 32 subjects with MCI, and 32 normal elderly controls. Results: In the AD group, we found GM atrophy in the left cingulate gyrus, left dorsal posterior cingulate cortex, left inferior temporal gyrus, and right supramarginal gyrus compared to control subjects, and in the right inferior frontal gyrus, right orbitofrontal area, left uncus, left ventral entorhinal cortex, and left inferior temporal gyrus compared to subjects in the MCI group. There were no significant differences in GM loss between MCI and control subjects. Conclusion: We demonstrated the involvement of GM in AD, but not in MCI. The pattern of GM volume reductions can help us understand the underlying pathologic mechanisms in AD and MCI.

Surface-based analysis reveals regions of reduced cortical magnetization transfer ratio in patients with multiple sclerosis: a proposed method for imaging subpial demyelination.

The in vivo detection of subpial cortical gray matter lesions in multiple sclerosis is challenging. We quantified the spatial extent of subpial decreases in the magnetization transfer ratio (MTR) of cortical gray matter in subjects with multiple sclerosis, as such reductions may indicate regions of cortical demyelination. We exploited the unique geometry of cortical lesions by using two-dimensional parametric surface models of the cortex instead of traditional three-dimensional voxel-wise analyses. MTR images were mapped onto intermediate surfaces between the pial and white matter surfaces and were used to compute differences between secondary-progressive MS (n = 12), relapsing-remitting MS (n = 12), and normal control (n = 12) groups as well as between each individual patient and the normal controls. We identified large regions of significantly reduced cortical MTR in secondary-progressive patients when compared with normal controls. We also identified large regions of reduced cortical MTR in 11 individual patients (8 secondary-progressive, 3 relapsing-remitting). The secondary-progressive patients showed larger areas of abnormally low MTR compared with relapsing-remitting patients both at the group level and on an individual basis. The spatial distributions of abnormal MTR preferentially involved cingulate cortex, insula, and the depths of sulci, in agreement with pathological descriptions of subpial gray matter lesion distribution. These findings suggest that our method is a plausible in vivo imaging technique for quantifying subpial cortical demyelinating lesions in patients with multiple sclerosis and, furthermore, can be applied at the typical clinical field strength of 1.5 T.

Magnetic resonance morphometry of the loss of gray matter volume in Parkinson's disease patients.

Voxel-based morphometry can be used to quantitatively compare structural differences and func-tional changes of gray matter in subjects. In the present study, we compared gray matter images of 32 patients with Parkinson's disease and 25 healthy controls using voxel-based morphometry based on 3.0 T high-field magnetic resonance T1-weighted imaging and clinical neurological scale scores. Results showed that the scores in Mini-Mental State Examination and Montreal Cognitive Assessment were lower in patients compared with controls. In particular, the scores of visuospa-tial/executive function items in Montreal Cognitive Assessment were significantly reduced, but mean scores of non-motor symptoms significantly increased, in patients with Parkinson's disease. In dition, gray matter volume was significantly diminished in Parkinson's disease patients compared with normal controls, including bilateral temporal lobe, bilateral occipital lobe, bilateral parietal lobe, bilateral frontal lobe, bilateral insular lobe, bilateral parahippocampal gyrus, bilateral amygdale, right uncus, and right posterior lobe of the cerebellum. These findings indicate that voxel-based phometry can accurately and quantitatively assess the loss of gray matter volume in patients with Parkinson' disease, and provide essential neuroimaging evidence for multisystem pathological mechanisms involved in Parkinson's disease.

Unveiling the mystery of déjà vu

Deja vu is an eerie experience that is characterized by the recognition of a situation concurrent with the awareness that this recognition is inappropriate. This feeling of irrelevant familiarity is a common phenomenon occurring both in clinical (mainly epileptic) and nonclinical population. Despite numerous theories have been suggested as to what nonpathological deja vu is and what causes it, until now no ultimate explanation has been generally accepted. We investigated differences in brain morphology between healthy subjects with and without deja vu using a novel multivariate neuroimaging technique, Source-Based Morphometry. The analysis revealed a set of cortical (predominantly mesiotemporal) and subcortical regions in which there was significantly less gray matter in subjects reporting deja vu. In these regions gray matter volume was inversely correlated with the frequency of deja vu. Our results demonstrate for the first time a structural correlate of deja vu in healthy individuals and implicate a direct pathogenetic link between nonpathological and epileptic deja vu. We hypothesize our findings reflect an alteration of hippocampal function and postnatal neurogenesis in subjects with deja vu. ∗Speaker †Corresponding author: mbrazd@med.muni.cz sciencesconf.org:escan2012:4032

Reduced volume in the anterior internal capsule but its maintained correlation with the frontal gray matter in subjects at ultra-high risk for psychosis

The anterior limb of the internal capsule (ALIC), which interconnects with the frontal cortex and thalamus, is volumetrically altered in schizophrenia patients. However, it is unclear whether an abnormal ALIC volume is apparent prior to the onset of schizophrenia and whether this aberrant ALIC volume is related to the frontal gray matter in individuals at ultra-high risk (UHR) for psychosis. We used magnetic resonance imaging of 43 UHR subjects, 36 schizophrenia patients, and 42 healthy controls to investigate manually traced ALIC volumes. Additionally, we evaluated the correlation between the ALIC volume and the frontal gray matter. Significantly reduced ALIC volumes were observed in the UHR and schizophrenia groups compared to the healthy controls. However, the volume of the frontal gray matter was decreased only in the schizophrenia group. A positive correlation between the volumes in the ALIC and frontal gray matter found in healthy controls was maintained only in UHR subjects. In addition, a negative correlation between the total scores on the Positive and Negative Syndrome Scale and the ALIC volumes was observed only in schizophrenia patients. An aberrant ALIC volume but its maintained correlation with the interconnecting frontal lobe was present prior to the onset of full psychosis, indicating the prodromal phase of psychosis.

Unveiling the mystery of déjà vu: The structural anatomy of déjà vu

Déjà vu (DV) is a widespread, fascinating and mysterious human experience. It occurs both in health and in disease, notably as an aura of temporal lobe epilepsy. This feeling of inappropriate familiarity has attracted interest from psychologists and neuroscientists for over a century, but still there is no widely agreed explanation for the phenomenon of non-pathological DV. Here we investigated differences in brain morphology between healthy subjects with and without DV using a novel multivariate neuroimaging technique, Source-Based Morphometry. The analysis revealed a set of cortical (predominantly mesiotemporal) and subcortical regions in which there was significantly less gray matter in subjects reporting DV. In these regions gray matter volume was inversely correlated with the frequency of DV. Our results demonstrate a structural correlate of DV in healthy individuals for the first time and support a neurological explanation for the phenomenon. We hypothesis that the observed local gray matter decrease in subjects experiencing DV reflects an alteration of hippocampal function and postnatal neurogenesis with resulting changes of volume in remote brain regions.

NPY mRNA expression in the prefrontal cortex: Selective reduction in the superficial white matter of subjects with schizoaffective disorder

BackgroundAlterations in the inhibitory circuitry of the dorsolateral prefrontal cortex (DLPFC) in schizophrenia include reduced expression of the messenger RNA (mRNA) for somatostatin (SST), a neuropeptide present in a subpopulation of γ-aminobutyric acid (GABA) neurons. Neuropeptide Y (NPY) is expressed in a subset of SST-containing interneurons and lower levels of NPY mRNA have also been reported in schizophrenia spectrum disorders. However, whether the alterations in these two transcripts identify the same, particularly vulnerable, subset of GABA neurons has not been examined. MethodsWe used in situ hybridization to quantify NPY mRNA levels in DLPFC gray and white matter from 23 pairs of subjects with schizophrenia or schizoaffective disorder and matched normal control subjects; results were compared to those from a previous study of SST mRNA expression in the same subjects. ResultsIn contrast to SST mRNA, NPY mRNA levels were not significantly lower in the gray matter of subjects with schizophrenia or schizoaffective disorder. However, NPY, but not SST, mRNA expression was significantly lower in the superficial white matter of subjects with schizoaffective disorder. ConclusionThese findings suggest that the alterations in SST-containing interneurons in schizophrenia and schizoaffective disorder are selective for the subset that do not express NPY mRNA, and that lower NPY mRNA expression in the superficial white matter may distinguish subjects with schizoaffective disorder from those with schizophrenia.

31Phosphorus magnetic resonance spectroscopy study of tissue specific changes in high energy phosphates before and after sertraline treatment of geriatric depression

We investigated tissue specific differences in markers of energy metabolism, including high energy phosphate compounds (beta and total NTP, PCr) and pH, in older adults with depression compared with healthy controls, before and after a 12-week treatment trial of sertraline. Thirteen older adults, age > or =55, with Major Depressive Disorder (HAMD(17) score of > or =18) were recruited along with ten age-matched controls. The depression subjects had a pre- and post-treatment 4T (31)P-MRS scan using a three-dimensional chemical shift imaging sequence. The extracted brain images were segmented into white matter (WM), gray matter (GM) and CSF. A linear mixed effects model analyzed the effects of pre-treatment and post-treatment depression on phosphorus metabolite concentration estimates (including calculated pH and Mg(++)). Total tissue beta-NTP (-8%, t(18.66) = 3.50; p = 0.0024) and total tissue total NTP (-6%, t(17.41) = 2.68; p = 0.0156) were lower in subjects with geriatric depression compared with healthy controls. Total tissue levels of total-NTP changed significantly with treatment (-2%, t(14.84) = -2.47; p = 0.0259). Total NTP was reduced in the WM, but not the GM, in the pre-treatment depression group (t(51.65) = 4.02; p = 0.0002). Intracellular pH was higher in the GM of subjects with pre-treatment depression (t(1133.84) = -2.10; p = 0.0353) and decreased to approximate control levels after treatment (t(648.86) = -2.53; p = 0.0115). These findings demonstrate bioenergetic changes including tissue specific differences in (31)P-MRS metabolites in geriatric depression. Decreased white matter total NTP may reflect alterations in white matter function.

Gray matter volume differences and the effects of smoking on gray matter in schizophrenia

Objective Many studies have evaluated differences in gray matter volume in schizophrenia, but have not considered the possible effects of smoking, which is extraordinarily common in people with the illness. The present study used voxel-based morphometry (VBM) to examine differences in gray matter in subjects with schizophrenia and evaluate the effects of smoking on this measure. Methods Thirty-two subjects with schizophrenia (14 smokers, 18 non-smokers) and 32 healthy comparison subjects participated in the study. Whole brain, voxel-wise analyses of regional gray matter volume were conducted using voxel-based morphometry (VBM). Results Reduced gray matter was observed in the schizophrenia group in the orbitofrontal cortex, bilateral insula and superior temporal gyri (STG), bilateral dorsolateral prefrontal cortices (DLPFC), medial frontal gyrus, and cingulate gyrus. Within this group, smoking subjects had greater lateral prefrontal and STG gray matter volumes relative to non-smoking subjects. Conclusions The finding of reduced gray matter volume in prefrontal and temporal regions in schizophrenia is consistent with prior anatomical tracing and whole-brain voxel-based studies. Greater gray matter volumes in smoking relative to non-smoking subjects with schizophrenia highlight a potential experimental confound in volumetric studies and suggests that smoking may be associated with a relative preservation of lateral prefrontal and temporal gray matter in schizophrenia.

Brain volume in children with neurofibromatosis type 1: relation to neuropsychological status.

To determine characteristics of brain morphology in children and adolescents with neurofibromatosis type 1 and relate these characteristics to neuropsychological functioning. Neurofibromatosis type 1 is associated with numerous CNS abnormalities and cognitive impairment. Abnormal high signal intensity visible on brain MRI, brain tumors, and macrocephaly are common. Research into links between neuroanatomic and cognitive features has been inconclusive. Fifty-two children and adolescents with neurofibromatosis type 1 were compared with 19 control subjects on several quantitative neuroanatomic and neuropsychological measures. Total brain volume, especially gray matter, was significantly greater for neurofibromatosis type 1 subjects than the control subjects. Group differences in the ratio of gray matter to white matter were more prominent in younger than in older subjects. Volume of gray matter in the subjects with neurofibromatosis type 1 was related to their degree of learning disability. Corpus callosum size was significantly larger for subjects in the neurofibromatosis type 1 group, and diminished performance on measures of academic achievement and visual-spatial and motor skills were associated with greater regional corpus callosum size. Neuroanatomic morphology and the developmental pattern of gray matter and white matter in subjects with neurofibromatosis type 1 differed from in control subjects. Some of these differences are related to the neuropsychological status of the neurofibromatosis type 1 group. We propose that delayed developmental apoptosis results in macrocephaly and a delay in the development of appropriate neuronal connections in children with neurofibromatosis type 1. We further propose that these morphologic delays are related to the cognitive profile of neurofibromatosis type 1.