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BY: Mevinder Jit Kaur

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
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.

1. Multiple Sclerosis Society of Australia: www.msaustralia.org.au

2. http://emedicine.medscape.com/article/1146199-overview#a1

3. Benjamin K-T Tsang, Richard Macdonell, Multiple sclerosis Benjamin K-T

Tsang Diagnosis,

management and prognosis, Australian Family Physician Vol. 40, No. 12,
December 2011