Central pontine myelinosis
Classification and external resources
ICD-10	G37.2
ICD-9	341.8
DiseasesDB	2198
MedlinePlus	000775
eMedicine	neuro/50
MeSH	D017590

It has been suggested that this article or section be merged with Central pontine myelinolysis. (Discuss)

Central pontine myelinolysis or osmotic demyelination syndrome is a demyelinating lesion in the brain that occurs with rapid correction of hyponatremia (low sodium levels in the blood). It is characterized by acute paralysis, dysphagia (difficulty swallowing), and dysarthria (diffuculty speaking), and other neurological symptoms.

It is most common in patients with chronic hyponatremia, which is usually caused by alcoholism. The prognosis is poor.

Central pontine myelinolysis is a complication of treatment of patients with profound, life-threatening hyponatraemia (low sodium). It occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatraemia who have made intracellular adaptations to the prevailing hypotonicity. Individuals with hyponatremia should receive no more than 8-10mmol of sodium per day to prevent central pontine myelinosis.

Contents 1 Pathology 2 Prevention 3 Management 4 Prognosis 5 References

[edit] Pathology

The currently accepted theory states that the brain cells adjust their osmolarities by changing levels of certain osmolytes like Inositol, Betaine, Glutamine etc. In hyponatremia the levels of these osmolytes fall, preventing entry of free-water into cells. The reverse is true for hypernatremia. So rapid correction of Sodium in hyponatremia would cause the extra cellular fluid to be relatively hypertonic. Free-water would then move out of the cells. This leads to a central pontine myelinolysis, manifesting as the paralyses.

The demyelination of the axons (nerve fibers in the brain) damages them.^[1]

In the context of chronic low plasma sodium, the brain's cells (neurons and glia) adapt by taking in a small amount of water; the net effect is to move water out of the interstitium and equilibrate (or nearly so) the intracellular and extracellular tonicities. The chronic hyponatremia is thus compensated.

With correction of the hyponatremia with intravenous fluids, the intra- and extra-cellular tonicities are again changed, this time in the opposite direction. With the use of intravenous hypertonic saline, the correction can be too quick, not allowing enough time for the brain's cells to adjust to the new tonicity. With a rise in extracellular tonicity, the cells compensate by losing a small amount of water. This loss will continue until the intra- and extra-cellular tonicities are equal. If hypertonic therapy continues or is too rapid, the extracellular tonicity will continue to drive water out of the brain's cells, leading to cellular dysfunction and the condition of central pontine myelinolysis.

Rapid correction of hypernatremia causes water to move into cells, leading to multiple cerebral hemorrhages, equally catastrophic as osmotic demyelination.

[edit] Prevention

This being a potentially avoidable disaster, following recommendations may be adhered to while maintaining sodium levels:

• Hyponatremia: Correction rate=0.5-1.0meq/L/hr, with not more than 12meq/l correction in 24 hrs. If the patient has seizures (or [Na⁺]<115), correction can be attempted at up to 2meq/L/hr, but only till seizure activity lasts and [Na⁺] reaches above 125-130 meq/L.

• Hypernatremia: Correct at 0.5meq/L/hr. Not more than 12 meq/L/24hrs.

[edit] Management

Once demyelination has begun, there is no specific treatment. Care is supportive, with the goal of preventing complications like aspiration pneumonia or deep vein thrombosis. Alcoholics are usually given vitamins to correct for other deficiencies.

Research has led to improved outcomes.^[2] Animal studies suggest inositol reduces the severity of osmotic demyelination syndrome if given prior to rapid correction of chronic hyponatraemia.^[3] Further study is required prior to its application in humans for this indication.

[edit] Prognosis

The prognosis is overall poor. Some patients die. Most survive, however, and of the survivors, approximately one-third recover; one-third are disabled but are able to live independently; one-third are severely disabled.^[4] Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis and locked-in syndrome.^[5] Some improvements may be seen over the course of the first several months after the condition stabilizes.

The extent of recovery depends on how many axons were damaged.^[1]

[edit] References

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