In November, 2007, early afternoon, a 17-year-old unconscious male patient was admitted to our paediatric emergency department. Third-party history from his co-workers and company physician revealed that the young man collapsed suddenly without any obvious triggers while standing at his workbench in a metal processing factory. He had been completely unconscious for about 1 min; later he was still somnolent but reacted when loudly addressed. There had been no suggestion of a seizure, such as convulsions, tongue biting, or enuresis. Medical history was reported to be unremarkable and there was no knowledge of him taking recreational drugs, medication, or alcohol. There was a family history of epilepsy. On arrival at our hospital, he responded to painful stimuli; heart rate, blood pressure, and respiration were normal. His pupils were moderately dilated and reactive to light. Perioral myoclonia was present. Further clinical examination was unremarkable, but a small glass bottle with a clear fl uid and a 1 mL syringe were found in his belongings (fi gure). Laboratory blood test results including blood-gas analysis and ammonia were within normal ranges. Toxicological analysis of urine was negative for common drugs. CT of the head was normal. The somnolence was fi rst suspected to be post-ictal, although an electroencephalogram (EEG) did not show any seizure activity. Without any specifi c treatment, our patient regained consciousness within 3 h after admission. He could not recall the events that had passed, reported feeling well, and denied any recreational drug use. He stated that the bottle of liquid in his bag was used for cleaning work equipment. Toxicological testing supported this explanation as the liquid was found to be a mixture of long-chain alcohol compounds–widely used in cleaning liquids. Further investigations, including MRI of the brain and a sleep-deprived EEG, showed no abnormalities. The next day he had polydipsia and was sweating excessively. We suspected that these were detoxifi cation symptoms. He admitted that immediately before his collapse he had ingested 2·5 mL of the fl uid from the glass bottle diluted in a soft drink; he stated that the fl uid was γ-butyrolactone (GBL). We monitored him for 2 more days; he underwent psychological assessment, and was discharged in good clinical condition. His parents were informed of the events, and further consultation for drug counselling was arranged. GBL, a pro-drug of γ-hydroxybutyric acid (GHB), has emerged as a major recreational drug during the past 10 years. It is used because of its uninhibiting eff ects, but also as a sleep aid, muscle building, and weight-loss agent. Furthermore, GBL and GHB are used as date-rape drugs because the colourless liquids can easily be added to a drink to induce sedation and anterograde amnesia in the victim. Drug users take GBL orally in volumes of only 1 to 2 mL normally measured by a syringe to obtain these small doses and then dilute it in water or other drinks. Accidental overdosage can happen easily and typically causes sudden unconsciousness followed by abrupt awakening after a few hours (‘fast-in, fast-out’), because of prompt drug resorption and short half-life of about 30 min. Toxicity can be confi rmed by gas chromatography-mass spectrometry. GHB is restricted by controlled substances legislation; its precursors can be legally obtained. Information about the prevalence of GBL/GHB abuse is limited. European surveys estimate an ever-in-lifetime use of 3%, increasing to 19% in some groups, such as people attending nightclubs. GBL toxicity should be considered in any patient who presents with rapid onset of coma of unknown cause. Since there is only a short time frame (<12 h) for chemical detection of GBL, blood or urine samples should be analysed as soon as possible. There is no specifi c antidote for GBL/GHB overdose and patients usually recover rapidly. However, fatalities can occur.