Multiple sclerosis (MS) is an immune-mediated inflammatory disease that
attacks myelinated axons in the central nervous system, destroying the myelin and the axon in variable degrees and producing significant physical disability. MS is more predominant in women compared to men. In most cases, the disease follows a relapsing-remitting pattern, with short-term episodes of neurologic deficits that resolve completely or almost completely. A minority of patients experience steadily progressive neurologic deterioration. The cause of MS is not known, but it likely involves a combination of genetic susceptibility and a presumed nongenetic trigger such as viral infection and low vitamin D levels that together result in a self-sustaining autoimmune disorder that leads to recurrent immune attacks on the CNS. Four disease courses have been identified in multiple sclerosis which are clinically isolated syndrome (CIS), relapsing-remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS). CIS is a first episode of neurologic symptoms caused by inflammation and demyelination in the central nervous system. The episode, which by definition must last for at least 24 hours, is characteristic of multiple sclerosis but does not yet meet the criteria for a diagnosis of MS because people who experience a MRI 1 reveals multiple lesions with high T2 signal intensity and one large CIS may or may not go on to develop MS. RRMS is white matter lesion. These demyelinating lesions may sometimes the most common disease course and is mimic brain tumors because of the associated edema and inflammation. characterized by clearly defined attacks of new or increasing neurologic symptoms. These attacks also called relapses or exacerbations are followed by periods of partial or complete recovery (remissions). During remissions, all symptoms may disappear, or some symptoms may continue and become permanent. PPMS is characterized by worsening neurologic function (accumulation of disability) from the onset of symptoms, without early relapses or remissions. SPMS follows an initial relapsing-remitting course. Most people who are diagnosed with RRMS will eventually transition to a secondary progressive course in which there is a progressive worsening of neurologic function (accumulation of disability) over time. Clinical manifestations in early stages of MS are blurring of vision, in coordination, abnormal sensation whereas in later stages MS can cause blindness, paraplegia & incontinence due to spinal cord involvement. Ataxia and Charcot triad of dysarthria in MS is due to spinal and cerebellar involvement. Other symptoms such as fatique, depression, heat intolerance and euphoria are also seen in MS.
A diagnosis of MS is done by identifying the clinical manifestation followed
by CT and MRI scans to identify the area of demyelination. Also, if MRI is not available a lumbar puncture can be performed and CSF obtained is evaluated for oligoclonal bands and intrathecal immunoglobulin G (IgG) production.
Disease modifying treatments are approved. Suppression of relapses and
their surrogates (new lesions on imaging) have been used as the endpoints for evaluating efficacy of these drugs. Suboptimal response is indicated by an unchanged relapse rate or ongoing MRI activity after continuous therapy for at least 6 months compared with pre-treatment. The patient should first be evaluated to identify secondary causes for suboptimal response including noncompliance or the development of neutralising antibodies to interferon-. First line treatments are interferon-s and glatiramer acetate have been used as first line DMTs for RRM. Second line treatments are Natalizumab which reduces the rate of disability progression, the annualised relapse rate and the number of new lesions on MRI. its use is limited due to the potentially devastating complication of progressive multifocal leukoencephalopathy due to a brain infection with JC virus. Symptomatic treatment are used to treat troublesome symptoms cause by MS and to improve quality of life.
If left untreated, more than 30% of patients with MS will develop
significant physical disability within 20-25 years after onset. Several of the disease-modifying agents used in MS have slowed disability progression within the duration of research trials; whether these effects will be maintained over longer periods is not known. Less than 5-10% of patients have a clinically milder MS phenotype, in which no significant physical disability accumulates despite the passage of several decades after onset (sometimes in spite of multiple new lesions seen on MRI). Detailed examination of these patients in many instances reveals some degree of cognitive deterioration. REFERENCES.
1. Multiple Sclerosis Society of Australia: www.msaustralia.org.au