%0 Journal Article
%T An Interesting Case of Barbiturate Automatism and Review of Literature
%A Sankalp Gokhale
%A Ciro Ramos-Estebanez
%J Case Reports in Neurological Medicine
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/713065
%X A 48 year old man with a diagnosis of HIV infection since 1993, on highly active anti-retro viral therapy (HAART) with stable CD4 count and undetectable viral load for years and seizure disorder presented with recurrent drowsiness. His seizures were well controlled on phenobarbitone for years. Repeated laboratory evaluation demonstrated toxic levels of phenobarbitone in his blood. A thorough clinical, psychiatric, laboratory and imaging evaluation did not reveal any obvious etiology for the recurrent barbiturate intoxication in this man. Our findings suggest the possible diagnosis of barbiturate drug automatism in this patient. Though drug automatism is a controversial entity, it merits continued attention. There are recent reports of similar phenomenon with newer sedative agents such as Zolpidem. It is important to be aware of this phenomenon as a possible explanation for recurrent intoxication with barbiturates without a clear etiology for drug overdose. 1. Case Report We report a case of 48-year-old man with a diagnosis of HIV infection since 1993, on HAART (abacavir, lopinavir-ritonavir, and stavudine) with a recent CD4 count of 692, and undetectable viral load for years type II diabetes, and generalized tonic-clonic, complex partial and motor seizures since childhood. His seizures had been well controlled on phenobarbital, levetiracetam, and zonisamide for many years. Prior Electroencephalograms (EEGs) had evidenced right temporal discharges without clinical seizure activity. His brain magnetic resonance imaging had remained normal. He resides at a group home, where he was responsible for taking his medications. The patient presented with repeated admissions due to changes in mental status. He consistently became somnolent, arousable to voice, and able to follow simple commands. He had symmetrical fine and course nystagmus. His tone was flaccid and reflexes were diminished with upgoing toes. Initially his phenobarbital level was 65.5£¿mcg/mL (therapeutic level: 15¨C40£¿mcg/mL). It increased to 120£¿mcg/mL during readmission a day after discharge. Once his levels trended down to 23.3£¿mcg/mL, he was discharged from the hospital and further assistance with medications was initiated at his group home. Several days later, his phenobarbital level was 51.3£¿mcg/mL. He reported that he was taking phenobarbital at the prescribed doses and denied overdosing himself. He was continued on phenobarbital 120£¿mg/day. At discharge his phenobarbital level was 41.3£¿mcg/mL. Hours later, the levels peaked at 112£¿mcg/mL. Finally, we increased his zonisamide dosing and
%U http://www.hindawi.com/journals/crinm/2013/713065/