Central pontine myelinolysis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
It is understood that central pontine myelinolysis is caused by rapid correction of hyponatremia. The CNS is particularly susceptible to reductions in plasma osmolarity, specially during hyponatremia which is the most commonly encountered electrolyte disturbance. When a decrease in the plasma osmolarity happens, neural cells first swell but then they are able to regain their original volume through the release of inorganic and organic osmolytes and exit of osmotically obligated water. A subsequent exposure to hypertonic stress(e.g., correction of hyponatremia with hypertonic I.V. solution's)resulting from a rapid correction of hyponatremia causes the ions to quickly re-enter the intracellular space and compels the water to follow. If the serum sodium levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brain's cells because the brain cells do not have enough time to bring extracellular sudion into the cell, so the water will go out very fast. This can lead to cellular dysfunction and death and finally central pontine myelinolysis.
Pathophysiology
Pathogenesis
- It is understood that central pontine myelinolysis is caused by rapid correction of hyponatremia.[1]
- The CNS is particularly susceptible to reductions in plasma osmolarity, specially during hyponatremia which is the most commonly encountered electrolyte disturbance.
- When a decrease in the plasma osmolarity happens, neural cells first swell but then they are able to regain their original volume through the:[2][3]
- Release of inorganic and organic osmolytes
- Exit of osmotically obligated water
- A subsequent exposure to hypertonic stress(e.g., correction of hyponatremia with hypertonic I.V. solution's)resulting from a rapid correction of hyponatremia causes the ions to quickly re-enter the intracellular space and compels the water to follow.[4]
- If the serum sodium levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brain neurons because the brain cells do not have enough time to bring extracellular sudiom into the cell, so the water will go out very fast instead.[2]
- This can lead to cellular dysfunction and death and finally central pontine myelinolysis.[2]
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Mascarenhas JV, Jude EB (2014). "Central pontine myelinolysis: electrolytes and beyond". BMJ Case Rep. 2014. doi:10.1136/bcr-2013-203516. PMC 3975522. PMID 24682140.
- ↑ 2.0 2.1 2.2 Khosya S, Meena H (2013). "Central pontine myelinolysis". Indian J Med Res. 137 (5): 993–4. PMC 3734697. PMID 23760391.
- ↑ Burg MB, Ferraris JD (2008) Intracellular organic osmolytes: function and regulation. J Biol Chem 283 (12):7309-13. DOI:10.1074/jbc.R700042200 PMID: 18256030
- ↑ Sheikh AB, Afzal RM, Sagheer S, Bukhari MM, Javed A, Nasrullah A et al. z (2018). "The Dilemma of Inadvertent Pontine Demyelinosis: A Review of Literature". Cureus. 10 (8): e3174. doi:10.7759/cureus.3174. PMC 6197531. PMID 30357070.