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I. Multiple Sclerosis (MS)

MS is characterized by more than one episode of neurologic deficits separated in time, attributable to CNS white matter lesions that are separated in space. Lesions initially involve destruction of myelin; axonal damage may occur later in the process. Inflammatory brain lesions appear to arise from autoimmune responses involving activated lymphocytes and monocytes.
Age of onset: 20-50 years of age, usually; more common in women
Pathogenesis: The lesions of MS are caused by a cellular immune response that is inappropriately directed against the components of the myelin sheath. One of the early events in the development of a new lesion is an increase in permeability of the blood-brain barrier associated with inflammation, generally in a perivenous distribution. Demyelination occurs early in the inflammatory phase, and apoptosis of oligodendrocytes has been documented at an early stage. Both CD4+ and CD8+ lymphocytes are present in active lesions. The regression of symptoms has been attributed to the resolution of inflammatory edema, to partial remyelination, and/or to redistribution of sodium channels to enhance conduction in demyelinated axons.  

- The clinical diagnosis is based on clinical history, MRI, and/or CSF analysis. The relapsing forms are considered clinically definite when neurologic dysfunction becomes "disseminated in space and time." On MRI, findings of multifocal lesions of various ages, especially those involving the periventricular white matter, brainstem, cerebellum, and/or spinal cord white matter, support the clinical impression. The presence of gadolinium-enhancing
lesions on MRI indicates current sites of presumed inflammatory demyelination (active lesions).


T2 weighted MRI image (horizontal section) showing demyelinating plaques as bright areas around the lateral ventricles. 

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