A 29-y-old man had taken small daily doses of barbiturates as hypnotics (50 mg pentobarbital, 30 mg phenobarbital) for 4y with no evident intoxication. When he attempted suicide by ingestion of 15 g amobarbital, treatment with charcoal hemoperfusion resulted in rapid disappearance of drug from the blood. Generalized convulsions and delirium ensued; these were responsive to phenobarbital. An electroencephalogram (EEG) showed diffuse 5-Hz theta activity. Tc-99m hexamethylpropyleneamineoxime (HMPAO) single photon emission computed tomographic (SPECT) imaging of the brain demonstrated a diffuse bilateral decrease in blood flow to the cerebral cortex. These investigations were performed interictally on day4 without sedative drugs, prior to initiation of anticonvulsants, and at a time when barbiturates were no longer detected in the serum. An EEG on day 15 no longer showed abnormal slowing. On the other hand, Tc-99m HMPAO SPECT of the brain demonstrated residual cerebral hypoperfusion on day 20, with nearly full recovery of cerebral perfusion on day 51. Barbiturate withdrawal syndrome is presumed to require a history of abuse; however in patients with a history of treatment with barbiturates physicians treating acute barbiturate poisoning should be alert for the possibility of barbiturate withdrawal syndrome even in the absence of barbiturate abuse.