LAUSR

Introduction Several studies point to the importance that the complex formed by GABA and the benzodiazepine receptor play for cerebral dopaminergic transmission and, hence, to the pathophysiology of psychotic symptoms. The decrease in GABA neuratransmisión or the hypofunction of the system in the hippocampus, cortex and other limbic prefrontal or subcortical regions has consequences as emotional dysregulation, cognitive impairment and development of positive psychotic symptoms. Objectives We intended to show an additional practical example to the limited literature available based on a case linking the emergence of psychotic symptoms due to acute benzodiazepine withdrawal. Methods We present the case of a 21 year old man who was sent to the emergency room of our hospital after an episode of aggressiveness on the street. The patient showed a psychotic schizophrenic syndrome with significant emotional and behavioural impact with aggressive and bizarre movements. In parallel, restlessness, sweating, tremor, increased blood pressure and tachycardia were observed. Symptoms had started abruptly two hours earlier. The patient companion explained that he usually took Alprazolam at an of over 40 mg per day. He had decided to give up this consumption abruptly four days earlier. Discussion GABAergic deficits cause the imbalance between excitatory and inhibitory neurotransmission that may relate the pathophysiology of psychotic symptoms. The dysfunction of the GABAergic cortical interneurons could affect to the modulating response from the association cortex, which, could also relate with the appearance of these symptoms. Conclusion This case could relate a decrease in GABAergic transmission with the appearance of psychotic symptoms. Disclosure of interest The authors have not supplied their declaration of competing interest.