Abstracts

RATIONALE: Ketamine is an NMDA-glutamate antagonist suggested for use in refractory status epilepticus. Experience with use longer than several hours and at anaesthetic concentrations is negligible. We report the long term outcome after five days of therapy in a patient.
METHODS: A 44 year old man with fronto-temporal dementia and epilepsy presented for the third time in a year with multiple generalized tonic-clonic seizures and low serum concentrations of phenytoin and valproic acid. He continued to have periodic bisynchronous frontal sharp waves and complexes for four days despite treatment with phenytoin, valproic acid, and lorazepam. His behavior remained agitated when not sedated. He was then intubated and treated with propofol and ketamine (titrated up to 7.5 mg/kg/hour) with periodic low amplitude sharp transients initially remaining though progressively declining in amplitude over two days. No evidence of hypoxic-ischemic events occurred throughout his course. Ketamine was tapered over three days and the patient was transferred to a rehabilitation facility and later discharged home.
RESULTS: Three months after ketamine treatment the patient has persistent, unimproving appendicular ataxia precluding even simple standing. He had intact coordination prior to admission. The patient was able to run into another patient[ssquote]s room immediately preceding ketamine therapy at a time when he had no convulsive seizures. MRI showed diffuse volume loss especially of the cerebellum. His dementia, initally presenting as personality change, disinhibition and progressive language deficits had appeared stable for two years prior to this episode. PET scanning showed decreased blood flow in bifrontal areas consistent with fronto-temporal dementia. Baseline EEG showed only minimal nonspecific slowing. Correlating with ketamine use, his dementia has abruptly progressed with social withdrawal, and hypoinitiation for all activities. EEG now shows a predominant 5 Hz theta rhythm.
CONCLUSIONS: We suspect that ketamine contributed to this patient[ssquote]s prominent cerebellar deficits, and abruptly augmented his pre-existing cognitive deficits. Animal data on NMDA-antagonist mediated neurotoxicity will be reviewed. Further studies in animal models of prolonged ketamine use at anaesthetic doses are urged prior to human use.
Support: No sources of funding support