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Cortical Demyelination (cortical + demyelination)

Distribution by Scientific Domains

Medical Sciences	87%

Selected Abstracts

Propagation of spreading depression inversely correlates with cortical myelin content,

ANNALS OF NEUROLOGY, Issue 3 2009
Doron Merkler MD
Objective Cortical myelin can be severely affected in patients with demyelinating disorders of the central nervous system. However, the functional implication of cortical demyelination remains elusive. In this study, we investigated whether cortical myelin influences cortical spreading depression (CSD). Methods CSD measurements were performed in rodent models of toxic and autoimmune induced cortical demyelination, in neuregulin-1 type I transgenic mice displaying cortical hypermyelination, and in glial fibrillary acidic protein,transgenic mice exhibiting pronounced astrogliosis. Results Cortical demyelination, but not astrogliosis or inflammation per se, was associated with accelerated CSD. In contrast, hypermyelinated neuregulin-1 type I transgenic mice displayed a decelerated CSD propagation. Interpretation Cortical myelin may be crucially involved in the stabilization and buffering of extracellular ion content that is decisive for CSD propagation velocity and cortical excitability, respectively. Our data thus indicate that cortical involvement in human demyelinating diseases may lead to relevant alterations of cortical function. Ann Neurol 2009;66:355,365 [source]

Evidence for synaptic stripping by cortical microglia

GLIA, Issue 4 2007
Bruce D. Trapp
Abstract Recent studies have described significant demyelination and microglial activation in the cerebral cortex of brains from multiple sclerosis patients. To date, however, experimental models of cortical demyelination or cortical inflammation have not been extensively studied. In this report we describe focal cortical inflammation induced by stereotaxic injection of killed bacteria (BCG), followed 1 month later by subcutaneous injection of the same antigen, a protocol that overcomes the immune privilege of the cortex. Intracerebral BCG injection produced focal microglial activation at the injection site (termed acute lesion). Ten days after peripheral challenge (termed immune-mediated lesion), larger areas and higher densities of activated microglia were found near the injection site. In both paradigms, activated microglia and/or their processes closely apposed neuronal perikarya and apical dendrites. In the immune-mediated lesions, ,45% of the axosomatic synapses was displaced by activated microglia. Upon activation, therefore, cortical microglial migrate to and strip synapses from neuronal perikarya. Since neuronal pathology was not a feature of either the acute or immune-mediated lesion, synaptic stripping by activated microglia may have neuroprotective consequences. © 2006 Wiley-Liss, Inc. [source]

3 Tesla and 7 Tesla MRI of multiple sclerosis cortical lesions

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2010
Emma C. Tallantyre BM
Abstract Cortical lesions are prevalent in multiple sclerosis but are poorly detected using MRI. The double inversion recovery (DIR) sequence is increasingly used to explore the clinical relevance of cortical demyelination. Here we evaluate the agreement between imaging sequences at 3 Tesla (T) and 7T for the presence and appearance of individual multiple sclerosis cortical lesions. Eleven patients with demyelinating disease and eight healthy volunteers underwent MR imaging at 3T (fluid attenuated inversion recovery [FLAIR], DIR, and T1 -weighted magnetization prepared rapid acquisition gradient echo [MP-RAGE] sequences) and 7T (T1 -weighted MP-RAGE). There was good agreement between images for the presence of mixed cortical lesions (involving both gray and white matter). However, agreement between imaging sequences was less good for purely intracortical lesions. Even after retrospective analysis, 25% of cortical lesions could only be visualized on a single MRI sequence. Several DIR hyperintensities thought to represent cortical lesions were found to correspond to signal arising from extracortical blood vessels. High-resolution 7T imaging appeared useful for confidently classifying the location of lesions in relation to the cortical/subcortical boundary. We conclude that DIR, FLAIR, and MP-RAGE imaging sequences appear to provide complementary information during the detection of multiple sclerosis cortical lesions. High resolution 7T imaging may facilitate anatomical localization of lesions in relation to the cortical boundary. J. Magn. Reson. Imaging 2010;32:971,977. © 2010 Wiley-Liss, Inc. [source]

Propagation of spreading depression inversely correlates with cortical myelin content,

Extensive Cortical Remyelination in Patients with Chronic Multiple Sclerosis

BRAIN PATHOLOGY, Issue 2 2007
Monika Albert MD
Recent studies revealed prominent cortical demyelination in patients with chronic multiple sclerosis (MS). Demyelination in white matter lesions is frequently accompanied by remyelination. This repair process, however, often remains incomplete and restricted to the lesion border. In the present study, we examined the frequency and extent of remyelination in cortical and white matter lesions in autopsy brain tissue of 33 patients with chronic MS. The majority of patients (29 of 33) harbored cortical demyelination. Remyelination of cortical lesions was identified light microscopically by the presence of thin and irregularly arranged myelin sheaths, and confirmed by electron microscopy. Extensive remyelination was found in 18%, remyelination restricted to the lesion border in 54%, and no remyelination in 28% of cortical lesions. A direct comparison of the extent of remyelination in white matter and cortical lesions of the same patients revealed that remyelination of cortical lesions was consistently more extensive. In addition, g-ratios of fibers in areas of "normal appearing cortex" yielded values consistent with remyelination. Our data confirm the high prevalence of cortical demyelination in chronic MS and imply that the propensity to remyelinate is high in cortical MS lesions. [source]

Grey matter pathology in multiple sclerosis

ACTA NEUROLOGICA SCANDINAVICA, Issue 2006
L. Bö
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. [source]