Spectrum of pathological changes observed in Osmotic Demyelination syndrome includes Central pontine myelinolysis and extra-pontine myelinolysis, which can be reported on computed tomography.
WD of MCPs can also occur after pontine hemorrhage and central pontine myelinolysis, not only pons infarction.[6] Moreover, in clinical practice, WD may mimic ischemic cerebrovascular disease due to similar signals on MRI,[6] especially in patients with multiple vascular risk factors.
Central pontine myelinolysis (CPM) was originally described as a complication of rapid correction of hyponatremia, particularly in the setting of malnutrition, alcohol abuse, and liver disease [9,10].
To evaluate alcohol's central nervous system effects, researchers distinguish "uncomplicated alcoholism" (i.e., alcohol use disorder [AUD]) from the various clinically diagnosable consequences of chronic alcohol consumption, including Wernicke's encephalopathy (WE), Korsakoff's syndrome (KS), hepatic encephalopathy (HE), central pontine myelinolysis (CPM), alcoholic cerebellar degeneration (ACD), alcohol-related dementia (ARD), and Marchiafava-Bignami disease (MBD).
Patients with possible hyponatraemic encephalopathy should be urgently treated according to the protocols of management of severe hyponatraemia but caution must be taken to avoid rapid correction of chronic hyponatraemia, which might put patients at risk for central pontine myelinolysis.
An MRI scan of the brain may reveal complications such as central pontine myelinolysis. Its use is also important in atypical cases of acute nonalcoholic WE.
Hypernatremia is hazardous during liver transplantation, particularly in patients with low serum sodium levels who are at risk of central pontine myelinolysis due to rapid correction of hyponatremia.
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