Multiple Sclerosis Overview and Epidemiology

Study Notes

Multiple sclerosis (MS) is a common, disabling neurological disease, mainly affecting young adults.
Approximately 85,000 people in the UK have MS, though recent data suggests the figure is closer to 100,000. Globally, about 2,500,000 people have MS.
Women are twice as likely to be diagnosed with MS than men.
Diagnosis typically occurs between the ages of 20 and 40.

The prevalence of MS increases the further away you get from the equator.
Some ethnic groups, such as Māori in New Zealand, have a lower prevalence of MS.
Migration patterns affect MS risk. Adults who move from low-risk areas to high-risk areas retain the original area's risk, while those migrating as children acquire the risk of the new area.

MS is believed to be a complex interplay of genetics, infection, lack of sunlight exposure, diet, and environmental factors.
Chance also plays a role.

Structure of a Neuron: Includes dendrites, cell body, nodes of Ranvier, axon, myelin sheath, and the axon terminal.
Healthy vs Damaged Nerve: Illustrations show healthy nerves with intact myelin sheaths, contrasted with damaged nerves exhibiting demyelination.
Pathological Description: MS is a progressive autoimmune disease that targets CNS myelin. Demyelination occurs as plaques in the white matter, mainly around ventricles of the brain, optic nerves, and spinal cord tracts.
Stages of Lesions: Early lesions exhibit a marked inflammatory response, destroying myelin and oligodendrocytes (cells that produce myelin) with relatively intact axons and cell bodies. Older lesions show macrophage infiltration, astrocyte proliferation, and fibrous tissue development. Eventually, a fibrous scar forms, with no potential for recovery.
Late Stage Damage: Axonal damage is a characteristic feature in the later phases of the disease. This damage is likely responsible for the more progressive and chronic forms of MS. Findings visible on MRI include brain atrophy, degeneration of ascending and descending tracts, and ventricular dilation.

Diagnosis relies on a combination of clinical signs, MRI scans, lumbar punctures, and visual evoked potentials.

Benign: Relatively stable course with minor symptoms over time.
Relapsing-remitting: Characterized by clearly defined relapses followed by periods of remission (recovery).
Secondary progressive: Starts with a relapsing-remitting pattern then transitions to a steady worsening of disabilities.
Primary progressive: Symptoms gradually worsen from the outset without distinct relapses or remissions.

Disease-modifying drugs: Examples include Beta Interferons 1a (Avonex, Rebif), Beta Interferon 1B (Betaferon), Glatiramer acetate (Copaxone). These medications can reduce the frequency of relapses in RRMS by about 30% over 2 years.
Steroids: Such as methylprednisolone, used to reduce inflammation.