I have been reading about cases where patients were diagnosed with central pontine myelinolysis. I found out that conditions predisposing patients to this problem include alcoholism, liver disease, malnutrition, and hyponatremia. There I found also that risk factors for central pontine myelinolysis in the hyponatremic patient include development of hypernatremia during some other treatment. I found this topic interesting so I would like to hear more about this disease. Could you explain more about this to me?
I have to say that contemporary physicians recognize that central pontine myelinolysis occurs inconsistently as a complication of severe and prolonged hyponatremia, particularly when it is corrected too rapidly. Standard of care requires judicious treatment of electrolyte disturbances to reduce the risk for osmotic myelinolysis. Central pontine myelinolysis is concentrated, frequently symmetric, noninflammatory demyelination within the central basis pontis. In at least 10% of these patients, demyelination also occurs in extrapontine regions, including the mid brain, thalamus, basal nuclei, and cerebellum. Problem with this disease is that the exact mechanism that strips the myelin sheath is unknown. One theory proposes that in regions of compact interdigitation of white and gray matter, cellular edema results in compression of fiber tracts and induces demyelination. As you have already heard, prolonged hyponatremia followed by rapid sodium correction results in edema. During the period of hyponatremia, the concentration of intracellular charged protein moieties is altered. That is why the term osmotic myelinolysis is more appropriate than central pontine myelinolysis. This is worth only for demyelination occurring in extrapontine regions after the correction of hyponatremia.