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At least 469 records · Page 26Linked to original sources
PubMed1992

White matter lesions on magnetic resonance imaging in clinically diagnosed Alzheimer's disease. Evidence for heterogeneity.

In a prospective magnetic resonance imaging (MRI) study we evaluated the prevalence and severity of white matter changes in 29 patients with Alzheimer's Disease (AD) and 24 age-matched healthy elderly, all without cerebrovascular risk factors. The AD patients were divided into two groups according to age at onset of symptoms, one with presenile onset AD (n = 13) and one with senile onset AD (n = 16), who were matched for dementia severity. Signal hyperintensities were rated using a semiquantitative scoring method, separately in the periventricular region (PVH) and in the lobar white matter (WMH), as well as in the basal ganglia (BGH) and in the infratentorial region (ITFH). Cortical atrophy as a parameter of grey matter involvement was rated on a 0 (absent) to 3 (severe) scale. We found PVH, WMH and BGH scores to be significantly higher in senile onset AD patients than in age-matched controls. By means of multiple linear logistic regression we found that PVH, WMH and BGH scores were significantly dependent on the diagnosis of senile onset AD, while the PVH score also showed a significant age dependency. Cortical atrophy did not differ significantly between presenile onset AD and senile onset AD patients. These results indicate that presenile onset AD and senile onset AD patients differ with respect to white matter involvement, but not with respect to grey matter involvement on MRI. Since cerebrovascular risk factors were excluded these findings may indicate that senile onset AD patients display more small vessel involvement (arteriolosclerosis) than presenile onset AD patients, suggesting additional (microvascular) factors for the dementia syndrome in senile onset AD. Our data lend support to the growing body of evidence that AD is heterogeneous, consisting of at least two types. Based on our findings two forms can be distinguished: (i) a 'pure' form of the disease, usually with early disease onset, and no more white matter changes than normal for age; (ii) a 'mixed' form, usually with disease onset later in life, and showing more white matter changes on MRI than normal for age.

Aged↗
PubMed1993

Differences in the fatty acid composition of the grey and white matter of different regions of the brains of patients with Alzheimer's disease and control subjects.

In the present study, a comparison was made of the fatty acid composition of the grey and white matter of the frontal, parietal and parahippocampal regions of post-mortem brains of patients who had died with Alzheimer's disease (n = 15) and control postmortem subjects (n = 10). Diagnosis of Alzheimer-type disease was based on the presence of senile plaques and neurofibrillary tangles in post-mortem sections. Several highly significant and specific differences were observed between the two groups. Adrenic acid (22:4 n-6) was three to four times higher in the grey matter but lower in the white matter in each of the three regions in the Alzheimer brains than in the control group. These alterations were compensated by reciprocal changes in 18:0 in the grey matter and 16:1 fatty acids in the white matter. There was no significant difference in the proportion of other fatty acids, including those of the n-6 and n-3 series, in either the grey or the white matter of any of the three regions of the two groups, except for a higher proportion of 22:6 n-3 in the parietal white matter in the Alzheimer patients. There was no significant relationship between the levels of the individual fatty acids and age at death. It is suggested that the alterations in the fatty acid composition observed in the brains of Alzheimer patients may be caused by an aberration in the system by which essential fatty acids are transported into the brain.

Aged↗
PubMed1998

Imaging axonal damage of normal-appearing white matter in multiple sclerosis.

The current study was designed to determine the relative distribution of decreases of N-acetylasparate (NAA), a marker of axonal damage, between lesions and normal-appearing white matter of patients with established multiple sclerosis and to test for associations between changes in the ratio of NAA to creatine/phosphocreatine (NAA:Cr) in those compartments and changes in disability. Data were collected from a 30-month longitudinal study of 28 patients with either a relapsing course with partial remissons and no progression between attacks (relapsing/remitting) (11 patients) or a course of progressively increasing disability, following a period of relapsing/remitting disease (secondary progressive) (17 patients). Proton magnetic resonance spectroscopic imaging (MRSI) and conventional MRI examinations were performed at 6-8-month intervals with concurrent clinical assessments of disability. General linear models were used to test associations between MRSI, MRI, lesion volume and clinical data. Analysis confirmed that the NAA:Cr ratio is lower in lesions than in the normal-appearing white matter (-15.3% in relapsing/remitting multiple sclerosis and -8.8% in secondary progressive multiple sclerosis). The lower NAA:Cr ratio per unit lesion volume previously observed for secondary progressive relative to relapsing/remitting patients was found to result from a lower ratio (8.2%, P < 0.01) in the normal-appearing white matter rather than from any differences within lesions. The importance of changes in the normal-appearing white matter was emphasized further with the observation that the NAA:Cr ratio in the normal-appearing white matter accounted for most of the observed 15.6% (P < 0.001) decrease in the NAA:Cr ratio in the brains of relapsing/remitting patients over the period of study. The decrease in the NAA:Cr ratio in normal-appearing white matter correlated strongly (P < 0.001) with changes in disability in the relapsing/remitting subgroup. These results add to data suggesting that axonal damage or loss may be responsible for functional impairments in multiple sclerosis. The accumulation of secondary axonal damage in the normal-appearing white matter may be of particular significance for understanding chronic disability in this disease.

Aspartic Acid↗
PubMed2003

Dissociations of cerebral cortex, subcortical and cerebral white matter volumes in autistic boys.

High-functioning autistic and normal school-age boys were compared using a whole-brain morphometric profile that includes both total brain volume and volumes of all major brain regions. We performed MRI-based morphometric analysis on the brains of 17 autistic and 15 control subjects, all male with normal intelligence, aged 7-11 years. Clinical neuroradiologists judged the brains of all subjects to be clinically normal. The entire brain was segmented into cerebrum, cerebellum, brainstem and ventricles. The cerebrum was subdivided into cerebral cortex, cerebral white matter, hippocampus-amygdala, caudate nucleus, globus pallidus plus putamen, and diencephalon (thalamus plus ventral diencephalon). Volumes were derived for each region and compared between groups both before and after adjustment for variation in total brain volume. Factor analysis was then used to group brain regions based on their intercorrelations. Volumes were significantly different between groups overall; and diencephalon, cerebral white matter, cerebellum and globus pallidus-putamen were significantly larger in the autistic group. Brain volumes were not significantly different overall after adjustment for total brain size, but this analysis approached significance and effect sizes and univariate comparisons remained notable for three regions, although not all in the same direction: cerebral white matter showed a trend towards being disproportionately larger in autistic boys, while cerebral cortex and hippocampus-amygdala showed trends toward being disproportionately smaller. Factor analysis of all brain region volumes yielded three factors, with central white matter grouping alone, and with cerebral cortex and hippocampus-amygdala grouping separately from other grey matter regions. This morphometric profile of the autistic brain suggests that there is an overall increase in brain volumes compared with controls. Additionally, results suggest that there may be differential effects driving white matter to be larger and cerebral cortex and hippocampus-amygdala to be relatively smaller in the autistic than in the typically developing brain. The cause of this apparent dissociation of cerebral cortical regions from subcortical regions and of cortical white from grey matter is unknown, and merits further investigation.

Autistic Disorder↗
PubMed2005

Quantitative diffusion tensor imaging in cerebral palsy due to periventricular white matter injury.

Periventricular white matter injury (PWI) is a major form of brain injury observed in congenital hemiparesis. The aim of this study is to determine the usefulness of diffusion tensor imaging (DTI) and fibre tracking in delineating the primary and secondary degenerative changes in cerebral white matter and deep grey matter in patients with spastic cerebral palsy due to PWI and to look for any possible reorganization of the axonal architecture. Five hemiparetic cerebral palsy patients (median age 14 years) with known PWI were prospectively studied with DTI of the brain at 1.5T and quantitatively compared with five age and sex matched controls. Fibre tracts for various corticofugal, thalamocortical and association tracts were generated and analysed for the DTI fibre count and for diffusion parameters. A region of interest based analysis was performed for the directionally averaged mean diffusivity (D(av)) and fractional anisotropy (FA) values in various white matter locations in the brain and the brainstem and in the deep grey matter nuclei. Group statistics were performed for these parameters using Mann-Whitney U-test comparing the affected sides in patients with either side in controls and the unaffected side in hemiparetics. There was significant reduction in DTI fibre count on the lesional side involving corticospinal tract (CST), corticobulbar tract (CBT) and superior thalamic radiation in the patient group compared with controls. Also there was an increase in DTI fibre count in the unaffected side of the hemiparetic patients in CST and CBT, which reached statistical significance only in CBT. The corpus callosum, cingulum, superior longitudinal fasciculus and middle cerebellar peduncle failed to show any significant change. ROI measurements on the primary site of white matter lesion and the thalamus revealed a significant increase in D(av) and decrease in FA, suggesting primary degeneration. The CST in the brainstem, the body of corpus callosum and the head of caudate and lentiform nuclei showed features of secondary degeneration on the affected side. The CST on the unaffected side of hemiparetics was found to have a significant decrease in D(av) and an increase in FA. Thus the degeneration of various motor and sensory pathways, as well as deep grey matter structures, appears to be important in determining the pathophysiological mechanisms in patients with congenital PWI. Also evidence suggesting the reorganization of sensorimotor tracts in the unaffected side of spastic hemiparetic patients was noted.

Adolescent↗
PubMed2026

Dose-dependent white matter changes associated with repetitive head impacts in former American football players.

Repetitive head impacts sustained during American football have been associated with neuropathological changes such as white matter shear injuries. However, the impact of specific factors, such as age of first exposure and cumulative head impact burden, on white matter integrity remains unclear. This study investigated in vivo white matter microstructural changes using diffusion tensor imaging and tract-based spatial statistics in 165 male former American football players (mean age 57.3 years, range 45-74) and 52 unexposed asymptomatic male controls (mean age 59.4 years, range 45-74) in the DIAGNOSE CTE Research Project. Compared to controls, former football players exhibited significantly higher fractional anisotropy (FA) in 1.97% of the white matter skeleton (1552 voxels; Cohen's d = 0.587) and higher tissue-corrected FA (FAt) in 1.48% of the white matter skeleton (1004 voxels; Cohen's d = 0.616). No significant differences were observed for mean diffusivity, axial diffusivity, radial diffusivity, or free water between football players and controls. Among football players, there were no significant differences in the white matter microstructure between players diagnosed with traumatic encephalopathy syndrome and those without the diagnosis. Lower FA was significantly associated with older age (P < 0.00001) and an earlier age of first exposure to tackle football (P < 0.01), while lower FAt was associated with greater cumulative head impact burden, specifically higher linear acceleration (P < 0.04) and rotational force (P < 0.02). This study highlights the influential role of exposure factors on white matter microstructure in former American football players, as well as the utility of diffusion tensor imaging to aid in characterizing the long-term effects of repetitive head impacts in contact sport athletes.

American football↗
PubMed1998

A profile of cortical gray matter volume deficits characteristic of schizophrenia.

Quantitative magnetic resonance imaging (MRI) studies from our laboratory have reported that patients with schizophrenia show a widespread cortical gray matter volume deficit, which is especially pronounced in the prefrontal and anterior superior temporal cortices. The present study compared two separate samples of schizophrenic patients -- 71 men from a Veterans Administration (VA) hospital and a sample of 57 severely ill men from a state hospital (SH) -- in an effort to test whether the pattern of brain volume abnormalities previously observed in VA schizophrenic patients can be generalized to other groups of schizophrenic patients. MRI-derived brain volumes of gray matter, white matter and sulcal cerebrospinal fluid (CSF) in six cortical regions, and CSF in the lateral and third ventricles were computed. All MRI volumes were adjusted for normal variation in head size and age and were expressed as standardized Z-scores, which also permitted structures of different sizes to be compared directly. The two schizophrenic groups displayed similar patterns of volume abnormalities: cortical gray matter but not white matter volume deficits that were widespread but especially notable in the prefrontal and temporal regions. The regional gray matter deficits in the SH group were generally greater than those in the VA group, particularly in the prefrontal and posterior superior temporal regions. Both schizophrenic groups had abnormally large volumes of the cortical sulci and lateral and third ventricles; however, the SH group showed greater enlargements, the most prominent occurring in the ventricles and temporal sulci. The overlapping patterns of cortical gray matter deficits in the two groups provide evidence for generality of this pattern of regional brain volume abnormalities in schizophrenia.

Adult↗
PubMed2004

Differential vulnerability of anterior white matter in nondemented aging with minimal acceleration in dementia of the Alzheimer type: evidence from diffusion tensor imaging.

White matter microstructural integrity was assessed using diffusion tensor imaging (DTI) in 25 young adults, 25 nondemented older adults, and 25 age-matched older adults with dementia of the Alzheimer type (DAT). For each individual, measures of anisotropy and diffusivity were obtained from atlas-transformed images in the anterior and posterior callosum and in the frontal, parietal, temporal and occipital white matter. These data revealed age differences in anisotropy and diffusivity in all assessed regions. Age effects were greater in the anterior as opposed to the posterior corpus callosum and greater in the frontal white matter than in the temporal, parietal and occipital white matter, suggesting age-associated differences in white matter that exhibit a roughly anterior-to-posterior gradient. In contrast, individuals with early-stage dementia exhibited minimal, if any, additional change in anterior regions but did show greater deterioration of white matter in posterior lobar regions. Taken collectively, these results indicate that nondemented aging is characterized by significant changes in white matter most prominently in anterior brain regions. The dissociation between the regional effects of age and dementia status suggests that the mechanisms underlying age-associated cognitive decline are likely distinct from those underlying DAT.

Adult↗
PubMed1997

Developmental neuropathology and impact of perinatal brain damage. II: white matter lesions of the neocortex.

The neuropathology and developmental impact of acute, subacute, and chronic white matter lesions has been studied in infants who survived (days, weeks, months, or years) this type of perinatal brain damage. The study emphasizes the survival of the developing gray matter overlying extensive white matter lesions (multicystic encephalopathy, porencephaly, and hydranencephaly ex-vacuo). Although partially isolated from afferent inputs (corticipetal fiber destruction) and unable to reach other cortical centers (corticofugal fiber destruction), this overlying gray matter is able to survive because neither its independent leptomeningeal blood supply nor its intrinsic anastomotic vasculature are affected by the underlying lesion. Moreover, the postinjury structural and functional development of this partially isolated gray matter is altered. Some of its axotomized pyramidal neurons are transformed into local-circuit interneurons, some of its interneurons are structurally and functionally enlarged (hypertrophy), and its intracortical neuropil (deprived of afferent synaptic terminals) increases by an expansion of intrinsic terminals (hypertrophy). An attempt has been made to correlate these postinjury alterations with the pathogenesis of the ensuing neurologic sequelae (7 infants develop epilepsy). The study proposes that neurological sequelae (e.g. epilepsy and cerebral palsy) following perinatal white matter lesions are a direct consequence of the postinjury gray matter transformations.

Brain Damage, Chronic↗
PubMed2005

Relation between short-term fine-particulate matter exposure and onset of myocardial infarction.

BACKGROUND: Epidemiologic studies have reported increases in the incidence of cardiovascular morbidity and myocardial infarction (MI) associated with increases in short-term and daily levels of fine-particulate matter air pollution, suggesting a role for particulate matter in triggering an MI. METHODS: We studied the association between onset time of MI and preceding hourly measures of fine-particulate matter using a case-crossover study of 5793 confirmed cases of acute MI. We linked data from a community-wide database on acute MI from 1988-1994 in King County, Washington, with central site air pollution monitoring data on fine-particulate matter determined by nephelometry. We compared air pollution exposure levels averaged 1 hour, 2 hours, 4 hours, and 24 hours before MI onset to a set of time-stratified referent exposures from the same day of the week in the month of the case event. RESULTS: : The estimated relative risk for a 10-microg/m increase in fine-particulate matter the hour before MI onset was 1.01 (95% CI=0.98-1.05). Analyses of pollutant levels at the other time points demonstrated a similar lack of association. No increased risk was found in all cases with preexisting cardiac disease (odds ratio = 1.05; 0.95-1.16). Stratification by known cardiovascular risk factors (hypertension, diabetes, and smoking status) also did not modify the relation between fine-particulate matter and MI onset. CONCLUSION: Although a very small effect cannot be excluded, there was no consistent association between ambient levels of fine-particulate matter and risk of MI onset.

Aged↗
PubMed2006

The relationship between frontal gray matter volume and cognition varies across the healthy adult lifespan.

OBJECTIVE: Age-associated decline in gray matter brain volume and cognitive function in healthy adults has been reported in the literature. The goal of the current study is to examine the relationship between age-related changes in regional gray matter volumes and cognitive function in a large, cross-sectional sample of healthy adults across the lifespan. METHODS: Magnetic resonance imaging and cognitive assessment were conducted on 148 adults aged 21-76 years. Multiple regression analyses examining the effect of age were performed on magnetic resonance image-derived gray matter brain volumes and standardized cognitive summary scores of attention and executive function. Regression was also performed to test the effect of age, gray matter volumes, and their interaction on the prediction of cognitive performance. RESULTS: Age significantly predicted performance on tests of attention (F [1, 146]=50.97, p <0.01, R2=0.26) and executive function (F [1, 146]=126.19, p <0.01, R2=0.46) and gray matter volumes for frontal subregions (lateral, medial, orbital), hippocampus, amygdala, and putamen (F [2, 145]=45.34-23.96, p <0.01-0.02). Lateral frontal (beta=-1.53, t=-2.16, df=131, p <0.03) and orbital frontal (beta=1.24, t=2.08, df=131, p <0.04) regions significantly predicted performance on tests of attention. Lateral frontal (beta=-1.69, t=-2.83, df=131, p <0.01) and the interaction between age and lateral frontal volume (beta=3.76, t=2.49, df=131, p <0.02) significantly predicted executive function. CONCLUSIONS: The findings confirm age-associated decline in cognitive function and gray matter volumes, particularly in anterior cortical brain regions. Furthermore, the association between lateral frontal gray matter volume and the ability to successfully plan, organize, and execute strategies varies as a function of age across the healthy adult lifespan.

Adult↗
PubMed2003

Large-scale structure and matter in the Universe.

This paper summarizes the physical mechanisms that encode the type and quantity of cosmological matter in the properties of large-scale structure, and reviews the application of such tests to current datasets. The key lengths of the horizon size at matter-radiation equality and at last scattering determine the total matter density and its ratio to the relativistic density; acoustic oscillations can diagnose whether the matter is collisionless, and small-scale structure or its absence can limit the mass of any dark-matter relic particle. The most stringent constraints come from combining data on present-day galaxy clustering with data on CMB anisotropies. Such an analysis breaks the degeneracies inherent in either dataset alone, and proves that the Universe is very close to flat. The matter content is accurately consistent with pure cold dark matter, with ca. 25% of the critical density, and fluctuations that are scalar only, adiabatic and scale invariant. It is demonstrated that these conclusions cannot be evaded by adjusting either the equation of state of the vacuum, or the total relativistic density.

Journal Article↗
PubMed2004

Dark matter particle production in b-->s transitions with missing energy.

Dedicated underground experiments searching for dark matter have little sensitivity to GeV and sub-GeV masses of dark matter particles. We show that the decay of B mesons to K(K(*)) and missing energy in the final state can be an efficient probe of dark matter models in this mass range. We analyze the minimal scalar dark matter model to show that the width of the decay mode with two dark matter scalars B-->KSS may exceed the decay width in the standard model channel, B-->Knunu , by up to 2 orders of magnitude. Existing data from B physics experiments almost entirely exclude dark matter scalars with masses less than 1 GeV. Expected data from B factories probe the range of dark matter masses up to 2 GeV.

Journal Article↗
PubMed1997

Creating connected representations of cortical gray matter for functional MRI visualization.

We describe a system that is being used to segment gray matter from magnetic resonance imaging (MRI) and to create connected cortical representations for functional MRI visualization (fMRI). The method exploits knowledge of the anatomy of the cortex and incorporates structural constraints into the segmentation. First, the white matter and cerebral spinal fluid (CSF) regions in the MR volume are segmented using a novel techniques of posterior anisotropic diffusion. Then, the user selects the cortical white matter component of interest, and its structure is verified by checking for cavities and handles. After this, a connected representation of the gray matter is created by a constrained growing-out from the white matter boundary. Because the connectivity is computed, the segmentation can be used as input to several methods of visualizing the spatial pattern of cortical activity within gray matter. In our case, the connected representation of gray matter is used to create a flattened representation of the cortex. Then, fMRI measurements are overlaid on the flattened representation, yielding a representation of the volumetric data within a single image. The software is freely available to the research community.

Cerebral Cortex↗
PubMed1992

Morphological spectrum, distribution and clinical correlation of white matter lesions in AIDS brains.

This paper analyses the histopathological characteristics and the topographical distribution of 'pure' HIV-associated white matter lesions of the brain in 18 AIDS patients at autopsy; it includes a time-controlled correlation of neuropathology to clinical staging of the AIDS dementia complex. Three distinct lesion types can be delineated: 1 Vacuolar myelin damage (n = 15) in the hemispheric and interhemispheric white matter, in projection fibre tracts, and in intracerebral segments of cranial nerves III, VII, and VIII; 2 Angiocentric foci (n = 14), disseminated randomly in the white matter; 3 HIV leukoencephalopathy (n = 14), as previously defined, seen predominantly in the hemispheric white matter. As a sole lesion type, HIV leukoencephalopathy is found in two cases, while vacuolar myelin damage and angiocentric foci always occur in combination with one or both other types of pathology. Patients with advanced AIDS-dementia complex consistently show severe and combined white matter pathologies at autopsy. We conclude that, in addition to the previously defined features of diffuse HIV leukoencephalopathy, vacuolar myelin damage and angiocentric foci are significant and frequent components of white matter pathology in AIDS autopsies. This reflects the multitude of pathogenetic factors which co-operate in damaging the brain in AIDS. The advanced AIDS dementia complex correlates with the combined and severe white matter lesions.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Contributors to white matter damage in the frontal lobe in Alzheimer's disease.

Abnormalities of cerebral white matter are present in a majority of patients with Alzheimer's disease (AD) and probably contribute to motor dysfunction and cognitive impairment. The white matter abnormalities are usually attributed to degenerative vascular disease and cerebral amyloid angiopathy (CAA) but the evidence is scanty or inconclusive. In the present study we examined sections of frontal lobe from 125 autopsy-confirmed cases of AD and assessed the relationship of degenerative large and small vessel disease, CAA, parenchymal Abeta load and APOE genotype, to several objective measures of white matter damage: extent of immunolabelling for glial fibrillary acidic protein (GFAP), axonal accumulation of amyloid precursor protein (APP), axon density in superficial and deep white matter, and intensity of staining for myelin. We found no association between atherosclerosis, arteriolosclerosis, CAA or APOE genotype and white matter damage. However, labelling of white matter for GFAP correlated strongly with the parenchymal Abeta load (P = 0.0003) and with APP accumulation (P = 0.008). Our findings suggest that severity of frontal white matter damage in AD is closely related to parenchymal Abeta load and that in most cases the contribution of degenerative vascular disease, CAA and APOE is relatively minor.

Alzheimer Disease↗
PubMed1996

Relationship between alcohol withdrawal seizures and temporal lobe white matter volume deficits.

A previous magnetic resonance imaging study from our laboratory reported significant temporal lobe volume deficits in cortical gray matter, white matter, and anterior hippocampus in chronic alcoholic men relative to controls. In the present study, we reexamined these data and asked whether withdrawal seizure history was predictive of either the hippocampal or the extrahippocampal volume deficits. A review of the medical charts indicated that 11 alcoholics had experienced one or more alcohol-related seizures and 35 were seizure-free; no patient had a seizure disorder unrelated to alcohol. The two alcoholic groups did not differ significantly in age, education, alcohol consumption variables, premorbid intelligence, Memory Quotient, Trail Making, or detection of hidden figures. Although each alcoholic group showed significant bilateral volume deficits of the anterior hippocampus and frontal-parietal and temporal gray matter, relative to controls, the seizure group had significantly smaller temporal lobe white matter volumes than either the control or the seizure-free groups; the latter two groups did not differ from each other. Both alcoholic groups, however, had white matter volume deficits in the frontal-parietal region. Thus, the seizure group accounted for the white matter volume deficits in the temporal lobe previously reported in the full sample of alcoholics. It seems, then, that reduced white matter volume in the temporal lobes may be either a risk factor for or sequela of alcohol withdrawal seizures.

Adult↗
PubMed2006

Grey matter pathology in multiple sclerosis.

Although multiple sclerosis (MS) has been considered a white matter disease, MS lesions are known to occur in grey matter. Recent immunohistochemical studies have demonstrated extensive grey matter demyelination in chronic MS. The most common lesion type consists of purely cortical lesions extending inward from the surface of the brain, this lesion subgroup is grossly underestimated by standard histochemical myelin staining methods. Some MS patients have subpial demyelination in all cortical areas of the brain; this pattern has been termed ''general cortical subpial demyelination''. Extensive cortical demyelination is associated with the progressive phases of disease, as less cortical demyelination has been detected in relapsing-remitting MS. The pathology of grey matter lesions differs from that of white matter lesions; grey matter lesions are less inflammatory, with less macrophage and lymphocyte infiltration. In purely cortical lesions there is no significant increase in lymphocytes compared with non-demyelinated adjacent cortical areas in MS patients or cerebral cortex in control patients. Significant axonal transection and neuronal loss have been demonstrated in grey matter MS lesions. Current magnetic resonance imaging (MRI) methods are not sensitive for purely cortical MS lesions. The clinical significance of cortical MS lesions may not be characterised until more sensitive MRI methods are developed.

Cerebral Cortex↗