Central pontine myelinolysis


Central pontine myelinolysis

Description, Causes and Risk Factors:

Abbreviation: CPM.

Central pontine myelinolysis is a demyelinating disease of the pons characterised by loss of myelin and oligodendroglia with relative neuron sparing. This condition classically occurs in alcoholics, malnourished or chronically debilitated adults and usually occurs in the hospital setting, a few days following rapid correction of hyponatremia.

Central pontine myelinolysis

The pathophysiological mechanism is unknown. Since both the pontine and extrapontine sites involved have a rich grey and white matter interface, it has been hypothesised that a rapid osmotic change causes an endothelial injury in the more vascular grey and white matter which induces the release of myelinolytic factors that damage the adjacent white matter. The term osmotic myelinolysis is currently favoured for this condition.

The most common cause is the too rapid correction of low blood sodium levels (hyponatremia). It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It has been observed following hematopoietic stem cell transplantation.

CPM may also occur in patients affected by

    Severe liver disease.

  • Liver transplant.

  • Alcoholism.

  • Severe burns.

  • Malnutrition.

  • Anorexia.

  • Severe electrolyte disorders.

  • AIDS.

  • Hyperemesis gravidarum.

The exact incidence of central pontine myelinolysis is unknown. A study by Singh demonstrated that central pontine myelinolysis was present in 29% of postmortem examinations of liver transplant patients. Two thirds of these patients had serum sodium fluctuations of only ± 15-20 mEq/L. Central pontine myelinolysis occurs more frequently in females than in males.

The prognosis is overall poor. While some patients die, most survive and of the survivors, approximately one-third recover; one-third are disabled but are able to live independently; one-third are severely disabled. Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis and locked-in syndrome. Some improvements may be seen over the course of the first several months after the condition stabilizes.

Symptoms:

The initial symptoms may be weakness, confusion and dysarthria.In severe cases there is spastic quadriparesis and pseudobulbar palsy.This may evolve within 3 - 10 days into a locked-in-state (pseudo coma).Additional symptoms often arise over the next 1—2 weeks including impaired thinking, weakness, paralysis in the arms and legs, stiffness, impaired sensation, and difficulty with coordination. At its most severe, myelinolysis can lead to coma, "locked-in" syndrome, and death.

Diagnosis:

Cerebral spinal fluid (CSF) probably is not necessary when the etiology and diagnosis are obvious. CSF studies may demonstrate increased opening pressure, elevated protein, or mononuclear pleocytosis.

MRI is the imaging modality of choice. According to one study, serial brain imaging is of value because a substantial proportion of patients have normal findings on initial MRI.Typically, T2-weighted MRI images demonstrate hyperintense or bright areas where demyelination has occurred and has been caused by relatively increased water content in those regions. MRI or CT imaging of the brain stem may not reveal an obvious anatomic disturbance. A thorough neurologic exam therefore is indispensable.

Electroencephalography in central pontine myelinolysis may demonstrate diffuse bihemispheric slowing. Brainstem-evoked potentials may reveal abnormalities when neuroimaging is unrevealing.

Relative preservation of axons and surrounding neurons within areas of demyelination and an associated reduction in oligodendroglia is present.

Treatment:

Treatment is supportive only. Correction rate is controversial. Diligently avoid hypernatremia. It is advised to study details concerning the etiology and correction of electrolyte disorders.

Patients with alcoholism should receive vitamin supplementation. Formally evaluate their nutritional status.

Once medically stable, the patient should be evaluated by a neuro rehabilitation specialist and, if appropriate, transferred for further inpatient recovery-oriented therapy.

Patients who survive central pontine myelinolysis likely require extensive and prolonged neurorehabilitation. Incorporate occupational, physical, speech, and language therapists early in the care of such patients. Swallowing studies are necessary to evaluate for dysphagia and determine the risk for aspiration pneumonia.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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