We report the case of a 23-year-old French Canadian woman who presented at the Emergency Room in summer 2006 with paranoid delusions and auditory hallucinations. Her previous history included two brief psychotic episodes induced by substances (amphetamines and marijuana). During these previous psychotic episodes, she exhibited ideas of reference and visual hallucinations which had responded well to olanzapine, an atypical antipsychotic.

In the last six months, she had shown bizarre behaviour, had been more isolated and apathetic, and unable to participate in daily chores. Her motivation had declined. She had gradually withdrawn from significant social relationships and stopped working. She described feeling anxious on a regular basis with no apparent reason. This was confirmed by family members accompanying her. The patient reported occasional use of GHB, but as her initial accounts of drug use were contradictory, the product used could not be positively identified and frequency of use remained unknown at the time.

Upon admission, the patient appeared perplexed and entertained the unsubstantiated fear that someone would try to kill her. She was under the impression that her whole entourage was speaking ill of her behind her back. She was whispering for fear of being heard, and attacked. She reported not having slept in days. She also mentioned visual hallucinations, claiming to have seen tigers in her apartment. The toxicology urine screen was negative. No evidence of depressive or manic symptoms was found. Patient history and physical examination indicated no general medical condition.

The initial suspicion of a schizophrenic disorder was in accordance with the terms of this diagnosis as described in the DSM-IV: The patient presented an acute psychotic break (hallucinations and delusions, part of Criterion A of the DSM-IV diagnosis), preceded by a prodrome of negative symptoms (prolonged apathy and lack of motivation, part of Criterion A), lasting six months (Criterion C), with a significant decline in social and occupational functioning (Criterion B). Mood disorders were excluded (Criterion D). Substance-induced and general medical condition-induced psychoses were excluded as unlikely (Criterion E). The patient was thus prescribed olanzapine 10 mg at bed time.

A few hours after her admission, she started presenting labile vital signs (Figure 1 and 2): tachycardia (range 160-120 beat/min) and hypertension (range 183/95-139/88 mmHg) that lasted for 24 hours. The patient’s temperature was not taken. She also suffered from severe agitation and anxiety, showed disorganized speech and behaviour, had insomnia, and possibly visual hallucinations. Restraints and confinement had to be used to protect the patient from injury, and a cumulative dose of 7 mg lorazepam p.o. over 24 hours was necessary to stabilize her. At this point, we suspected a withdrawal delirium, either from ethanol or GHB because of the autonomic system instability. Olanzapine was discontinued (of which she had received a single dose). Apart from lorazepam, she did not require any further drug treatment. Her confusion resolved in less than 72 hours. She suffered from a complete amnesia of the episode.

At this point, the patient revealed that she had been using GHB daily for the last six months as a self-medication to treat insomnia and anxiety. She denied using any other drug or medication during that time, including alcohol. She had developed a dependence to GHB as evidenced by increased anxiety, tremor and insomnia whenever she skipped a dose, and also by the increasing amount of time spent seeking and using GHB. She also admitted to often being very sedated while using GHB, a frequent state which resulted in a general lack of motivation and interest. One day prior to her admission, the patient had decided to put an end to her GHB use, an abrupt interruption which provoked the onset of intense anxiety and paranoid delusions within 18 hours, followed by disorganisation, and auditory and visual hallucinations within 24 hours.