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Osmotic demyelination may occur as a complication when patients undergo rapid electrolyte imbalance correction, which causes myelin sheath deterioration. The risk of this occurring increases when patients have underlying medical conditions such as burns, chronic alcoholism, or malnutrition. Symptoms of osmotic demyelization depend on which neurons are damaged, and some patients experience headaches while others suffer impaired mobility. Diagnostic testing generally pinpoints the affected area. There is no cure and treatment usually consists of symptomatic relief and possibly physical therapy.
The white matter of the brain and spinal column consist of a fatty whitish colored substance covering the bundles of nerve cells. If damage or deterioration of this insulating material occurs, chemical and electrical transmissions fail to travel down the axon to the synapses between the cells. Similar to an electrical cord losing its outer insulation, arcing or shorting may occur. In nerve cells, this action may cause inappropriate or nonexistent signal transmission.
Rapidly changing sodium levels commonly cause osmotic demyelination. Patients diagnosed with hyponatremia, or low salt levels, are frequently given hypertonic solutions containing the electrolyte. When infusion occurs too rapidly, the body does not have a chance to equalize the salt levels in the blood, the extracellular spaces, and the intracellular spaces. Researchers believe hypernatremic solutions adversely affect myelin, causing it to deteriorate.
Physicians also see the condition in patients who receive treatment for hypernatremia. Reducing serum salt levels too rapidly causes cells to release sodium ions in an attempt to correct the imbalance. Cells dehydrate and shrink, causing possible demyelination. Similarly, patients undergoing dialysis for end stage renal disease may experience osmotic demyelination from electrolyte imbalances or blood gas changes. Other medical conditions that may contribute to the syndrome include liver failure, organ transplants, and prolonged diuretic use.
In the brain, osmotic demyelination may occur in the pons, the basal ganglia, and the thalamus. Areas around the ventricles are another location sometimes affected. Patients suffering demyelination in these regions may experience nausea, vomiting, and confusion or loss of consciousness. If the condition occurs in the spinal column, patients suffer Parkinsonian type tremors or coordination difficulty on both sides of the body. Limbs can also become flaccid and patients may have difficulty swallowing or speaking.
Physicians consider osmotic demyelination a medical emergency and perform physical assessments, blood work, and imaging studies, which determine blood abnormalities and the site of demyelination. Patients may receive infusion corrections to prevent further myelin damage. In some instances, patients fully recover. In others, the damage is permanent. Depending on the location of the impairment, some patients improve with physical therapy, while others require lifelong assistance with daily activities.