Central pontine myelosis

A brain cell dysfunction caused by the destruction of the myelin sheath covering nerve cells in the pons and other areas of the brainstem.

The damage of the myelin sheath that covers nerve cells prevents signals from being properly transmitted in the nerve, decreasing the nerve’s ability to communicate with other cells.

Most common cause is a rapid rise in the body’s sodium levels, that occurs when a person is treated for hyponatremia in a very rapid fashion.

Can also occur with the rapid correction of hypernatremia.

Has been observed following hematopoietic stem cell transplantation.

This process does not occur spontaneously.

Related to alcoholism, liver disease, and malnutrition, liver transplantation, severe thermal injury, anorexia, AIDS and hyperemesis gravidarum.

Symptoms include: confusion, delirium, impaired balance, impaired swallowing, hallucinations, lethargy, impaired speech and enunciation, tremors, and acute paraparesis and quadrparesis of extremities, face.

All muscles may be paralyzed except for eye blinking.

Neurologic findings occur as a result of rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.

Clinically patients may have spastic quadriplegia, upper motor neuron findings, and abnormal reflexes, and confusion.

Brain MRI may have brainstem abnormalities demonstrated an area of high signal return on T2 weighted images.

Treatment is focused on relieving symptoms, since once demyelination has begun, there is no specific treatment.

Hyponatremia should be corrected at a rate not in excess of 0.5 mEq/L/H.

Controlled treatment of low sodium levels may reduce the risk.

Nerve damage is long-lasting.

While some patients die, most survive and approximately one-third recover, one-third are disabled, and one-third are severely disabled.

Persistent disabilities range from tremors and ataxia, spastic quadriparesis and locked-in syndrome.

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