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We report two cases of central pontine myelinolysis (CPM) following liver transplantation. The incidence may well be underestimated as in the past the diagnosis of CPM was based on postmortem findings. Malnutrition, poor clinical condition, encephalopathy are common features of transplanted patients developing CPM. The clinical course is characterized by a biphasic pattern; after normal recovery from anesthesia, there is a subsequent and gradual deterioration in the neurological state. The complex syndrome associates loss of consciousness, flaccid quadriplegia and pseudobulbar palsy. Among the many factors suspected of inducing CPM, a rapid correction of natremia (> 12 mmole/l/day) seems most probable. With regards to liver transplantation, CPM presents rather specific problems. Delaying transplantation to correct hyponatremia carries a risk of severe hepatic encephalopathy. On the other hand, the intraoperative compensation of blood losses with high sodium content blood products tends to induce an abrupt rise in sodium serum concentration. Moreover, renal capacity to excrete sodium is often impaired, due to hepatic insufficiency and surgical procedure. Transplantation should not be delayed, but as infusion of large amounts of sodium cannot be avoided (fresh frozen plasma, human albumin, red blood cells), natremia may be controlled by continuous veno-venous hemofiltration with low sodium content substitution fluids.

A 81 year-old female, weighing 56 kgs, had taken carbamazepine (10.2 mg/kg/day) for simple partial motor seizures of recent onset during 15 days. EEG recording showed slow waves on the left hemisphere. CT was normal. The seizures were controlled for a few days and then reappeared beginning as simple partial seizures and progressing to impairment of consciousness. The patient became confused. On admission she was severely confused. Neurological examination was otherwise normal. Plasma sodium level was 134 meq/l and CBZ plasma level was 4.3 micrograms/ml. EEG showed high voltage bilateral delta waves and a left focus. The drug was withdrawn with relief of clinical symptoms and to a lesser extent, of EEG abnormalities. Phenytoin encephalopathy is a well known pathological entity but to our knowledge there has been no report of carbamazepine encephalopathy with neither excessive plasma level of the drug nor water intoxication. An idiosyncratic reaction is considered likely.