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Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion
Clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis, who died during or shortly after the onset of a relapse, raise the possibility of some novel process underlying new lesion formation in multiple sclerosis.
Multiple sclerosis: Distribution of inflammatory cells in newly forming lesions
- A. Henderson, Michael H Barnett, J. Parratt, J. Prineas
- Biology, MedicineAnnals of neurology
- 1 December 2009
The present study was designed to further investigate the inflammatory profile of different regions within rapidly expanding MS lesions and the role of lymphocytes in this process.
Immunopathology of secondary‐progressive multiple sclerosis
Findings suggest that slowly expanding lesions (progressive plaques), in which ongoing myelin breakdown occurs in the absence of florid perivascular cell cuffing or other histological signs of acute inflammation, contribute to disease progression in cases of secondary‐progressive multiple sclerosis.
Chronic relapsing polyneuritis
Multiple sclerosis: remyelination of nascent lesions.
The study provides new evidence that both oligodendrocytes and myelin are destroyed in new lesions, that this activity ceases completely in many lesions within a few weeks, and that remyelination frequently ensues following repopulation of the plaque by oligod endodermictes.
Neuromyelitis optica: a demyelinating disease characterized by acute destruction and regeneration of perivascular astrocytes
The findings raise the possibility that demyelination in MS may be a bystander effect of an astrocyte lesion, i.e. that MS is not a disease primarily of myelin and oligodendrocytes, and add to experimental evidence that the antibody is pathogenic.
Multiple sclerosis. Pathology of recurrent lesions.
- J. Prineas, R. Barnard, T. Révész, E. Kwon, L. Sharer, E. Cho
- PsychologyBrain : a journal of neurology
- 1 June 1993
Of 98 remyelinated plaques examined in 15 patients with multiple sclerosis who died between 27 days and 5 years after clinical onset, 15 showed evidence of a superimposed new demyelinating lesion.
Blood‐Brain Barrier Abnormalities in Longstanding Multiple Sclerosis Lesions. An Immunohistochemical Study
The findings suggest that the blood-brain barrier (BBS) is permanently damaged in many old plaques, although to a degree not often detectable by current gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced magnetic resonance imaging (MRI).
The macrophage in MS: just a scavenger after all? Pathology and pathogenesis of the acute MS lesion
The prephagocytic changes in evolving lesions examined shortly after the onset of an MS relapse raise the possibility that oligodendrocyte cell death and associated changes within the myelin sheath initiate local macrophage scavenger activity, with subsequent amplification of the inflammatory response.
Immunoglobulins and complement in postmortem multiple sclerosis tissue
To identify evidence of a discrete, specific immune response in multiple sclerosis (MS) by analyzing the distribution of immunoglobulins and complement in tissue derived from cases of MS, and from…