Central pontine myelinolysis

related topics
{disease, patient, cell}
{rate, high, increase}

Central pontine myelinolysis is a neurologic disease caused by severe damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons.

It can also occur outside the pons.[1] The term "osmotic demyelinization syndrome" is similar to "central pontine myelinolysis", but also includes areas outside the pons.[2]



The most common cause is the rapid correction of low blood sodium levels (hyponatremia).[3]

It has been observed following hematopoietic stem cell transplantation.[4]

It is frequently associated with alcoholism. When alcoholics are treated for hyponatremia, an overly rapid rate of correction can lead to CPM.[5]

Non-alcoholic patients can be affected; these include: -underlying severe liver disease -liver transplant patients -severe burns -malnutrition -anorexia -severe electrolyte disorders -AIDS

It can be associated with Hyperemesis gravidarum.


It can be difficult to identify using conventional imaging techniques.[6]

Imaging by MRI demonstrates an area of high signal return on T2 weighted images.


Frequently observed symptoms in this disorder are acute para- or quadraparesis, dysphagia, dysarthria, diplopia, loss of consciousness, and other neurological symptoms associated with brainstem damage. The patient may experience locked-in syndrome where cognitive function is intact, but all muscles are paralyzed with the exception of eye blinking. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.

Treatment and Prevention

Treatment is supportive only.

To prevent CPM via the most common cause, overly rapid correction of hyponatremia, the hyponatremia should be corrected at a rate not in excess of 10mmol/L/24hr or 0.5 mEq/L/Hr; thus diligently avoiding hypernatremia. Details concerning the etiology and correction of electrolyte disorders are discussed extensively in general medicine texts. Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status. [7][8]

Full article ▸

related documents
Patient-controlled analgesia
Gumma (pathology)
Bipolar spectrum
Mental breakdown
Bipolar I disorder
Paroxysmal attack
Bacillus cereus
Warkany syndrome 2
Kidneys, ureters, and bladder
Shock (circulatory)
Memory consolidation
Entorhinal cortex
Mucous membrane
Urea breath test
Specific phobia
Aldose reductase inhibitor
Pulmonary alveolus