CPM is a demyelinative lesion in the central pons that was first reported in necropsy cases of alcoholism. Abnormalities in serum electrolytes and serum osmolality have mainly attracted attention and many patients with CPM caused by rapid correction of hyponatraemia have been reported.
We report the case of a pregnant woman of 29 years old and 24 weeks of amenorrhea and without a history of vomiting. The patient presents tetraplegia and respiratory distress. Clinical and biological examination found tetraplegia, bulbar syndrome, dysmetria and pyramidal syndrome with a severe hypokalemia (1.8meq/l), without natremia disorder (142meq/l). After the hypokaliemia correction, we noticed a regression of the motor deficit but a persistence of other signs. A magnetic resonance imaging (MRI) found a hyposignal T1 and hypersignal T2 on pons evoking CPM.
CPM produces neurological symptoms such as quadriparesis, pseudobulbar palsy, oculomotor paresis, and locked in syndrome and psychiatric symptoms such as changes in the level of consciousness and behaviour or cognitive dysfunction. This pathology is seen especially with hyponatremic patients in whom the correction was too fast. Abnormal osmotic pressure and electrolyte abnormalities mainly hypokalaemia and acute changes in the blood glucose concentration have been also suggested. A recent study suggested that CPM tends to occur in hyponatraemia complicated by hypokalaemia because a decreased concentration of Na,K-ATPase in endothelial cell membrane during hypokalaemia may predispose the cell susceptible to injury by osmotic stress associated with the rapid rise in the serum sodium concentration. In our case, natremia was correct.
T Sugimoto, T Murata, M Omori, Y Wada Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa. J Neurol Neurosurg Psychiatry 2003;74:353–355.
© 2012 European Society of Anaesthesiology