Central pontine myelinolysis: a rare presentation secondary to hyperglycaemia
Центральный понтинный миелинолиз: редкое проявление, вторичное по отношению к гипергликемии
2015-04-01
SCID: 54.1/4ttwkmux
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central pontine myelinolysisdemyelinationhyperosmolar hyperglycaemiahyperosmolar syndromepseudobulbar affect
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Abstract (AI)
Central pontine myelinolysis (CPM) is classically described as a demyelinating condition that results from the rapid correction of hyponatraemia. CPM has also been reported to arise from hyperglycaemia in association with concomitant acidosis, hypernatraemia and hyperosmolar syndrome. Herein, we report a rare presentation of CPM, which was purely secondary to hyperosmolar hyperglycaemia. The patient presented with ataxia and pseudobulbar affect, which evolved subacutely over a duration of two weeks. It is important to note that, in addition to acute changes in osmolality, a subacute shift secondary to hyperglycaemia may also lead to CPM.
Key Findings
1
CPM may result not only from rapid osmotic changes but also from subacute osmolality shifts caused by hyperglycaemia.
2
Central pontine myelinolysis can rarely occur purely secondary to hyperosmolar hyperglycaemia, without reported concomitant acidosis or hypernatraemia.
3
The patient developed subacute ataxia and pseudobulbar affect over two weeks as manifestations of hyperglycaemia-associated CPM.
4
The report expands recognized CPM triggers beyond rapid correction of hyponatraemia and acute hyperosmolar syndromes.
Research Object
Central pontine myelinolysis secondary to hyperosmolar hyperglycaemia
Research Subject
The subacute development of central pontine myelinolysis due to hyperglycaemia-induced shifts in osmolality, presenting with ataxia and pseudobulbar affect
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2015-04-01
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