Multiple Sclerosis | Symptoms, Diagnosis, Treatment and Management

Multiple sclerosis (MS) is an inflammatory, demyelinating disease principally affecting young adults, characterized pathologically by presence of numerous area of demyelination of central nervous system (CNS) and clinically by neurological symptom which have a tendency toward remission and exacerbation.
The etiology remains unresolved, though evidence suggest that an environmental agent, most likely viral may be responsible in a genetically susceptible person.

Immunological mechanisms suggested by
- Presence of T and B lymphocytes and macrophages in areas of recent demyelination.
- Detection of Interleukin – 2 (IL – 2) receptors on lymphocytes.
- Cell mediated and humoral immunological abnormalities in the tissue, CSF and peripheral blood.
Inflammation – an earliest detectable event presenting as an increase in permeability of blood – brain barrier is seen in association with inflammation.

Onset – common mode of onset are
- Spinal cord involvement
  - Sudden onset of weakness or paresis of lower limb.
  - Impairment of cutaneous sensation in lower limbs and trunk.
- Brain stem symptoms such as vertigo, diplopia (double vision) and ataxia.

Motor symptoms – weakness of legs commonly seen weakness of one leg after excretion with recovery after rest but with subsequent progression.
Sensory changes – paraesthesia (sensory loss) is commonly seen. Pain is usually rare in MS. There may be impairment of postural or vibration sense.
Ocular symptom – unilateral retro – bulbar neuritis, diplopia and nystagmus (side to side movement of eyeball) are common.
Mental symptom – emotional changes, euphoria, delusions, and dementia is seen.
Uhthoff’s phenomenon – characterized by worsening of weakness or vision with heat e.g. hot bath or exercise.

CSF – increase in total protein up to 1g/lit.
Evoked potentials – visual evoked potential often delayed.
MRI – is almost useful investigation. Areas of demyelinating plaques visible on MRI imaging with gadolinium contrast.

No effective curative treatment available.

Treatment modifying course of disease
- Short course of cyclophosphamide.
- Cytokines and cytokine inhibitors.

Treatment of acute relapse with corticosteroids (methyl prednisolone). ACTH to shorten duration of acute relapse.

Symptomatic treatment
- Local nerve block with botulinum toxin incase of spasticity.
- Isoniazid with pyridoxine in tremors.
- Tricyclic anti – depressants for chronic dysaesthetic pain.
- Oxybutynin for urinary frequency and urgency.
- Desmopressin for nocturia (frequent urination at night).

June 16, 2009 | Filed Under Neurological Disorders

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