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Examination of the demyelinating lesions in the spinal cord and brain of patients with MS shows myelin loss, destruction of oligodendrocytes, and reactive astrogliosis, often with relative sparing of the axon cylinder.The location of lesions in the CNS usually dictates the type of clinical deficit that results.The T cell receptor recognizes antigen in the context of human leukocyte antigen molecule presentation and also requires a second event (ie, co-stimulatory signal via the B7-CD28 pathway, not shown) for T cell activation to occur.Activated microglia may release free radicals, nitric oxide, and proteases that may contribute to tissue damage.Antibodies against myelin also may be generated in the periphery or intrathecally.Ongoing inflammation leads to epitope spread and recruitment of other inflammatory cells (ie, bystander activation).For example, MS must be distinguished from other neuroinflammatory disorders (see DDx.) Treatment consists of immunomodulatory therapy for the underlying immune disorder and management of symptoms, as well as nonpharmacologic treatments, such as physical and occupational therapy (see Treatment).

(See Workup.) Traditionally, MS could not be diagnosed after only a single symptomatic episode, as diagnosis required the occurrence of repeat clinical attacks suggesting the appearance of lesions separated in time and space; however, recent guidelines allow diagnosis of MS even with a first clinical episode as long as ancillary tests support separation of lesions in time or space.Loss of myelin is demonstrated in this chronic plaque.Note that absence of inflammation may be demonstrated at the edge of chronic lesions.A common misconception is that any attack of CNS demyelination means a diagnosis of acute MS.When a patient has a first attack of demyelination, the physician should not rush to diagnose MS, because the differential diagnosis includes a number of other diseases.

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