Multiple Sclerosis: A Neurological Enigma

Multiple sclerosis is a neurological immune-mediated disease that affects the brain and spinal cord. It is an unpredictable, often disabling disease that disrupts the flow of information within the brain and between the brain and the body.
MS affects one in every 500 persons, women twice as frequently as men. It is more common in young adults, and causes a variety of neurological deficits (visual loss, paralysis, sensory loss, ataxia, brainstem signs, psychiatric disorders, and dementia). Many MS cases evolve over a long period (20-30 years) with remissions and exacerbations. Some cases have an acute, even fatal course, and others go into a relentlessly progressive phase after a period of remissions and exacerbations.
MS involves an immune mediated process that develops when a previous viral injury to the nervous system has occurred in a genetically susceptible individual. B lymphocytes, plasma cells, and activated T cells, along with pro-inflammatory cytokines, cause inflammation, oligodendrocyte injury, and demyelination. Early inflammation and demyelination lead to irreparable axonal degeneration and scarring (Huether & McCance, 2012).
MS not only causes focal inflammatory changes but also causes diffuse injury throughout the central nervous system called MS lesions or plaques. MS lesions can occur anywhere in gray or white matter with localized areas of demyelination, changes in the components of myelin, damage to oligodendrocytes, extensive loss of neurons over time, and atrophy of the brain. Even normal appearing white matter is microscopically very abnormal. The multi-focal, multi-staged features of MS lesions in established disease produce symptoms that are multiple and variable (Huether & McCance, 2012).

Multiple sclerosis can minimally affect some people while others experience a rapid