Abstracts

Rationale: Gamma-aminobutyric acid (GABA) receptor agonists that are used as anticonvulsants primarily target GABA-A receptors. In contrast, the antispasticity drug baclofen primarily targets GABA-B receptors and demonstrates proconvulsive properties, as indicated by reports of baclofen-induced seizures in the literature. Here we report a case of baclofen overdose which resulted in sustained nonconvulsive status epilepticus (NCSE). Methods: 53-year-old woman overdosed on baclofen, which she was prescribed 3 months ago after lumbar spine surgery. Emergency responders found her unresponsive with an empty bottle of baclofen. On admission, she was confused with 7-mm non-reactive pupils, no spontaneous movements, and diffuse hypotonia and hyporeflexia. Brain CT was normal and MRI showed chronic microvascular changes. EEG revealed diffuse high-voltage rhythmic spikes, sharp waves, and slow waves consistent with NCSE. Serum baclofen level was 0.39 ug/ml 26 hours post-ingestion, corresponding to a peak serum level of 1.56 ug/ml 2 hours post-ingestion. This baclofen level translates to 300-360 mg of baclofen ingested. Intravenous levetiracetam (2g load, then 1g q12) was administered and EEG was continuously monitored. The EEG normalized in 24 hours and the patient was completely asymptomatic in 48 hours. Results: The clinical presentation (confusion, bilateral mydriasis, diffuse hypotonia, and hyporeflexia) and the extrapolated serum baclofen level indicate baclofen toxicity. In the absence of a witness or a clue (e.g. empty bottle), baclofen toxicity can easily escape diagnosis because routine toxicology will not detect baclofen and because the average physician is unlikely to be aware of baclofen's proconvulsive effects. Conclusions: The proconvulsive property of baclofen is poorly understood. One hypothesis is that baclofen activates the postsynaptic GABA-B receptors of inhibitory interneuron resulting in decrease inhibition and enhanced excitability of excitatory neurons.