Multiple Sclerosis Samira Ghaniwala

Multiple sclerosis is an autoimmune disease caused by activated T cells that gain entry into the central nervous system. The injury results from inflammation and T cell destruction. There are typical symptoms that co relate with the area involved. There are also remissions and relapses which can be triggered by certain factors. Diagnosis of the disease requires visualization of the lesions in the central white matter, on an MRI, Treatment is based on immunosuppressants and steroids to combat inflammation.

"Multiple sclerosis is an acute inflammatory disease that causes focal demyelination of the brain and spinal cord; it also causes axonal loss." (Poser, 2011)

Pathogenesis:

In multiple sclerosis activated T. lymphocytes enter the blood-brain barrier and initiate central nervous system inflammation, by recognizing myelin derived antigens as foreign, on the surface of the central nervous system's antigen presenting cells, the microglia. The resulting inflammation releases cytokines which initiates destruction of the oligodendrocyte-myelin unit by macrophages.

Morphologically, the affected regions show multiple, well circumscribed, slightly depressed, glassy, gray -- tan, irregularly shaped lesions, termed as plaques. These characteristic lesions are inflammatory demyelinations that occur most commonly in the periventricular region, the optic nerves and chiasms, ascending and descending fiber tracts, cerebellum, and spinal cord. Initially, there is accumulation of by activated T. lymphocytes and macrophages, often with prominent perivascular inflammation. After an acute attack, gliosis follows, leaving a shrunken grey scar.

The initial acute clinical signs and symptoms are due to the effects of inflammatory cytokines upon transmission of nervous impulses and not due to the breakdown of myelin. This, along with the role of corticosteroids, may explain why the recovery of acute deficits are prompt. However, when there is breakdown of myelin, resulting from an acute attack, it effects the propagation of impulses or causes a complete block in conduction, lowering the efficiency of the functions of the central nervous system. Moreover, acute inflammatory mediatiors, such as nitrous oxide, also initiate axonal damage, which is a feature of the latter stages of the disease. In acute attacks...

This axonal loss is responsible for the part of the disease where the patient is permanently and progressively disabled.
Etiology and Prevalence:

The etiology of multiple sclerosis involves the role of both, genetic and environmental factors. The disease is more likely to occur in northern Europeans and lesser amongst other racial groups, decreasing in frequency in regions nearing the equator. The lifetime risk of multiple sclerosis in northern Europe is one in eight hundred, increasing to one in fifty, one in twenty and one in three for the offspring, siblings and monozygotic twin partners of affected individuals, respectively. In other areas, such as New Zealand, Spain and Africa, the disease occurs more in those with a Caucasian descent. (D.A, 1996)

Other than the already established candidate genes (DRB, 1.1501, DRB 5.0101, DQA1.0102 AND DQV2.0602) preliminary evidence also associates CD 24 to multiple sclerosis, as a factor, modifying disease progression. These genes are not the causative factors but play a role in modifying the susceptibility of an individual towards multiple sclerosis. (D.A, 1996)

Signs and symptoms:

Signs and symptoms in patients with multiple sclerosis can be broadly classified as, optic neuritis, cervical cord involvement, brainstem manifestations, motor and sensory deficits and cognitive and affective symptoms. (D.A, 1996)

Initially, patients commonly present with the following initial symptoms of, weakness, numbness, tingling, imbalance in a limb; spastic paraparesis; retrobulbar neuritis; diplopia; disequilibrium; or a sphincter disturbance such as urinary urgency or hesitancy. These symptoms show patters of remission and relapse, although examination may reveal a residual deficit even during the latent period. (Tierney, McPhee, & Papadakis, 2004)

This disease takes multiple forms, varying from patient to patient. After the initial attack most patients do not get a second attack for months to years (relapsing-remitting disease). However, the patient eventually relapses and due to incomplete remissions there is increased disability, with weakness, spasticity, and ataxia…