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Multiple Sclerosis (MS)

In This Article

Summary

MS is an inflammatory condition that affects the oligodendrocites of the CNS. Peripheral nerves are not affected.
 
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Epidemiology & Aetiology

  • More common the further away from the equator you are
  • Some genetic factors involved
  • Twice as common in women
  • Mean age of onset 20-45
 
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Pathology

An autoimmune reaction against myelin and oligodendrocites (CNS equivalent of Schwann cells). There is destruction of myelin, and axonal loss. Antibodies to Myelin basic protein seen early on in the disease. Normally, macrophages cannot easily cross BBB, but in MS, they exhibit glycoprotein α4 β1, allowing them to adhere to and cross the endothelium.
Active lesions (plaques) are sites of inflammation, and show up on MRI as white blobs, roughly 2-10mm in size, and can occur anywhere in the CNS, although most commonly occur at the optic nerves, periventricular lesion, brainstem and cerebellar connections.
Conduction loss is probably to blame for most of the symptoms of MS.
 
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Patterns of Disease progression

Progression is extremely variable. Some patients may only ever have one episode (benign MS), whilst other may rapidly get worse with no periods of remission.
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Clinical features

Almost any neurological sign can be present in MS, but some are more common than others. Common examples are below. Usually for motor function, the signs are UMN signs, but there may also be LMN signs.
  • Optic Nueropathy
  • Optic disc swelling
  • Uthoff’s phenomenon – signs worse on hot day or after exercise – heat slows conduction in nerve fibres
  • Relative afferent pupillary defect
  • UMN signs – spasticity, weakness, brisk reflexes
  • Lehrmitte sign – on voluntary flexing of the head, there is an electric shock sensation travelling down the spine and into the limbs.
  • Sensory Signs – numbness and parasthesia
  • Autonomic defects – urinary incontinencem constipation, sexual dysfunction
  • Cerebellar defects – ataxia
  • Fatigue
 
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End-stage Multiple Sclerosis

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Investigations

  • MRI – definitive test. 85% of cases will show plaques on MRI.
  • VEP – visual evoked potentials - can detect lesions in visual pathway. The patient has EEG probes on the skull the measure brain response to visual stimuli. They are then given a visual stimulus, and the time between the visual stimulus and the brain response (on EEG) is measured. If the response is delayed this is evidence of some sort of optic nerve lesion.
  • Oligoclonal bands in CSF Similar to monoclonal bands seen in Lymphoma. However, where monoclonal bands represent massive proliferation of one type of plasma cell (and thus 1 antibody), oligoclonal bands represent massive proliferation of a small number of type of plasma cell. Actually not that useful! – in 80% of cases there will be oligoclonal bands, but these just show that there is a lot of antibody to something  in the CSF.
 
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Diagnosis

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