Abstract
Multiple sclerosis (MS) is an inflammatory relapsing or progressive disorder of central nervous system white matter. Several mechanisms may be important to MS plaque formation: autoimmunity, infection, bystander demyelinisation and heredity. Although convincing proof is lacking, dietary factors and toxin exposure have been hypothesized.
MS can cause a wide variety of clinical features. Sensory symptoms are the most common presenting manifestation of in MS (numbness, paresthesias, burning and hyperesthesias). Pyramidal tract dysfunction is common in MS and causes weakness, spasticity, and loss of dexterity, hyperreflexia, and Babinski sign. Exercises or heat frequently worsens subtle deficits. The initial symptom of MS is optic neuritis (14-23% of patients). Cerebellar pathways are frequently involved during the course of MS, but predominant cerebellar syndrome is uncommon at onset. Fatigue is a pervasive symptom among MS patients that is not related to disability or depression. The temporal course of MS can be described by one of four categories: relapsing-remitting (RR), secondary progressive (SP), primary progressive (PP) and progressive relapsing (RR) and benign (BN). The term “clinical isolated syndrome” (CIS) refers to patients presenting with their first episode of demyelination. After 5-10 years of follow-up, the majority of patients with any asymptomatic cerebral lesions will develop definite MS (treatment implication). The diagnosis of MS is based on the demonstration of white matter lesions disseminated in time and space in the absence of another identifiable explanation. An international expert panel proposed new diagnostic criteria for MS in 2001 (Mc Donald at all). MRI of the head is the most sensitive test for MS and dissemination in time and space demonstrated by serial MRIs separated by at least 3 months would clarify the diagnosis.