CONVULSIONS ASSOCIATED WITH ANALYTICALLY CONFIRMED PHENIBUT INGESTION Elamin MEMO1, Dunn M2, Hill SL1,2, Thomas SHL1,2 1 National Poisons Information Service (Newcastle Unit), Newcastle upon Tyne, UK 2 Medical Toxicology Centre, Newcastle University, Newcastle upon Tyne, UK. Introduction Phenibut is a neuropsychotropic drug structurally similar to γ–aminobutyric acid (GABA) and baclofen (Figure: 1). It is a GABA mimetic, primarily at GABAB receptors, with good blood-brain penetration1. Developed in Russia over fifty years ago, phenibut is used for its anxiolytic and cognition enhancing effects. We report a case of analytically confirmed phenibut ingestion associated with acute toxicity including convulsions. Figure: 1 Chemical Structure of GABA, Phenibut and Baclofen Progression A post-seizure 12 lead ECG revealed a borderline prolonged QTc of 475msecs at 75bpm. The following day T-wave inversion was noted in V3 and a QTc of 509msecs at 87bpm. These changes normalised by discharge. His confusion slowly improved with normalisation of his conscious level over the next 48 hours. On recovery he confirmed ingesting a ‘‘teaspoonful’’ of phenibut to improve his motivation and energy; ‘‘Online instructions’’ had recommended a dose of ‘‘1/4 spoonful’’. His regular medications included gabapentin for back pain (started 6 years previously), which he denied taking in excess. Presentation A 71 year old male with a background of myalgic encephalopathy, lumbar spondylosis and depression was admitted with vomiting, agitation, hallucinations and a reduced conscious level (Glasgow Coma Score 10/15 [E=3,V=1,M=6]). He received 1mg lorazepam iv for agitation. Despite this he developed a generalised tonic-clonic seizure which was terminated with a further 3mg of iv lorazepam. He remained haemodynamically stable with BP 103/52mmHg and heart rate of 67bpm. He was admitted to intensive care for observation without requiring circulatory or ventilatory support. Initial hyponatraemia (126 mmol/L) corrected over the first 24 hours of his admission without active intervention. Other blood tests were unremarkable. X Analytical confirmation Phenibut was identified from a serum sample by Liquid Chromatography-Mass Spectrometry. A novel, non-targeted data independent analytical technique was employed using a LC-QqTOF high-resolution tandem mass spectrometer, providing highly selective MS/MS mass spectra of all analytes. Discussion and conclusions Limited information has been published in English on adverse effects following therapeutic dose or overdose of phenibut. Tonic-clonic seizures have been described after presumed use without analytical confirmation2, whereas analytically confirmed recreational use of phenibut has been associated with fluctuating levels of consciousness, agitation, somnolence, dystonia and dilated pupils, with some cases requiring intubation and critical care admission3,4. This reported case indicates that phenibut toxicity may be associated with convulsions, however further information on clinical features of phenibut toxicity is required. References Lapin I. Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug. CNS Drug Rev. 2001;7:471-81. Marraffa JM, Nacca NE, Stork CM, Hodgman MJ. Phenibut: One poison center’s experience. Clin Toxicol (Phila). 2014;52:736–737. Wong A, Little M, Caldicott D, Easton C, Andres D, Greene SL. Multiple intensive care admissions associated with analytically confirmed recreational use of phenibut (β-phenyl-γ-aminobutyric acid) purchased over the Internet. Clin Toxicol (Phila). 2015;53:784-784. Downes MA, Berling IL, Isbister GK. Acute behavioural disturbance associated with phenibut purchased via an Internet supplier. Clin Toxicol (Phila). 2015;53:636-638. The National Poisons Information Service is commissioned by Public Health England on behalf of UK Health Departments