Psychedelic Research

Ms. A was an 18-year-old female patient admitted to our psychiatric emergency service with acute onset of agitation, disorganization, and hallucinating behavior after smoking cannabis. A few days after admission, her former boyfriend disclosed that she had also unknowingly smoked the leaves and leaf extracts of S. divinorum, which had been added to her marijuana cigarette, for the first time. The patient had a long history of use of cannabis but had never experienced a psychotic episode.

Ms. A was admitted to a general psychiatric ward with the presumptive diagnosis of a substance-induced psychotic disorder (ICD-10 criteria) and subsequent schizophrenia-spectrum disorder. After showing more and more self-mutilating behavior, with massive disorganization, disorientation and the intention to quit treatment, she was legally committed to a closed ward for involuntary treatment. There was no response to antipsychotic treatment with intramuscular olanzapine (up to 30 mg/day) or intravenous haloperidol (up to 15 mg/day), and Ms. A remained highly psychotic, with disordered thinking, thought blocking, derealization or delusional perceptions, and slow speech.

During one of the following nights, Ms. A showed a marked decrease of alertness that required an immediate transfer to an intensive care unit. Because of a developing toxic psychosis with stupor and catatonic excitement, potential neuroleptic associated elevation of creatine kinase to 2055 U/L, and the lack of efficacy of the ongoing antipsychotic medication, further treatment was required. Ms. A then underwent 2 rounds of emergency electroconvulsive therapy (ECT), but these were discontinued after she developed recurrent self-limited asystolias with a maximum duration of 5 seconds. Although there was no further ECT treatment, Ms. A experienced recurrent cardiac arrhythmias that required a temporary external cardiac pacemaker.

A recurring acute agitation led to a traumatic amputation of a 1 cm × 1 cm part of Ms. A’s tongue with a subsequent aspiration leading to a temporary intubation and ventilation. Shortly after that, Ms. A developed elevated temperature and a drop in blood pressure that required catecholamine treatment. Within hours, the abdomen became tense and inflated, and the ultrasound and x-ray showed signs of peritonitis and an atony of the bowels. A following explorative laparatomy showed multiple segmental necroses of the distal small intestine and the ascending colon, so that these parts had to be removed surgically. Thereafter we started a serum-blood-level controlled antipsychotic treatment with clozapine up to 300 mg (reaching serum drug levels of 355 μg/L clozapine and 148 μg/L norclozapine). Slowly but surely, Ms. A’s psychopathology improved, her psychotic symptoms disappeared, and she was relocated to the psychiatric department. As she requested termination of the clozapine treatment, we shifted to a low-dose treatment with olanzapine, 7.5 mg/day. Ms. A was then discharged in stable psychiatric condition. After the long course of the disease and the devastating somatic consequences, Ms. A and her parents decided to institute legal proceedings against the former friend of the patient who was accused of having administered S. divinorum unbeknownst to the patient.

Another potential risk of hallucinogen administration is provoking the onset of prolonged psychosis, lasting days or even months (Strassman, 1984). Although determining causation is difficult, it appears that individuals who experience such reactions have premorbid mental illness before taking hallucinogens. However, it is unknown whether the precipitation of psychosis in such susceptible individuals represents a psychotic reaction that would have never occurred in the absence of hallucinogen use, or whether it represents an earlier onset of a psychotic break that would have inevitably occurred (Grinspoon and Bakalar, 1979; Strassman, 1984). Unlike acute psychological distress, these cases will be extremely rare in well-selected and well-prepared participants.