Mania following use of ibogaine: A case series

Tabernanthe iboga, a West African shrub, contains the hallucinogenic indole ibogaine. Use of ibogaine has expanded outside indigenous contexts for reasons including treatment of opiate withdrawal and detoxification, often in unregulated clinics in countries such as Mexico and Canada. The extracted text reports survey and ethnographic estimates indicating growing non‑indigenous use (for example, a non‑scientific HuffPost/YouGov poll showed 17% support for legalization, and an ethnographic estimate suggested several thousand people had taken ibogaine outside Africa, with about 53% using it for opioid dependence). Known adverse effects in the literature include cardiac toxicity leading to sudden death (attributed to QT prolongation), seizures, vestibular toxicity, ataxia and vomiting, but prior to this report mania had not been documented as an outcome. This paper presents a case series describing three patients who developed manic syndromes temporally associated with unregulated ibogaine ingestion. The authors aim to document these occurrences, summarise clinical features and course, and discuss implications for clinicians encountering new‑onset mania in the context of ibogaine exposure and opiate treatment histories.

The study is reported as a case series comprised of three patients who presented to a psychiatric emergency department with manic symptoms after using ibogaine. Information available in the extracted text consists of individual case presentations including clinical history, collateral reports, physical examination findings, routine laboratory tests and urine toxicology, psychiatric diagnoses assigned by treating clinicians, treatments provided in hospital, and short‑term outcomes. Marta and colleagues also reviewed relevant prior literature to place these cases in context. The paper does not provide a formal methods section detailing case identification criteria, time period of case ascertainment, ethical approvals, or systematic data‑extraction procedures. Toxicological confirmation of ibogaine itself was not available in any case; routine hospital toxicology panels were used and reported where noted. Where collateral history was available it was incorporated into the case narratives; in one case collateral contact was refused. The authors acknowledge that objective verification of ibogaine ingestion was limited by timing of presentation and the lack of readily accessible assays outside specialised laboratories.

Three cases are presented, each diagnosed by treating clinicians as bipolar I disorder, most recent episode mania, following reported ibogaine ingestion. Case 1 (Mr A): A 36‑year‑old man with ADHD and polysubstance dependence, primarily opiates, presented with prominent manic symptoms after taking ibogaine two months earlier. Family reported he did not sleep for 14 days. Symptoms included irritability, grandiose delusions, rapid tangential speech and aggression. He had a prior single ibogaine exposure without neuropsychiatric effects. Workup included physical examination and routine labs; findings were notable only for patellar hyperreflexia and a positive urine test for benzodiazepines administered in the ED. He had been treated at an outside residential programme and discharged against medical advice the day before presentation. In the reporting facility divalproex ER was titrated to 1,500 mg daily, risperidone to 2 mg twice daily, quetiapine was discontinued due to insomnia, and 80 mg atomoxetine was given for ADHD symptoms. After a 13‑day hospitalisation he showed marked improvement and was discharged. Case 2 (Ms B): A 35‑year‑old woman with a history of opiate dependence in sustained remission presented after 3–4 weeks of symptoms beginning the day she ingested ibogaine in an unstructured setting. Her husband and mother described 4–5 days of little to no sleep, aggression, impulsivity, psychomotor agitation, hallucinations, pressured and tangential speech, and hyper‑religious and bizarre delusions. She had been stabilised at a nearby hospital on antipsychotics (quetiapine, risperidone, olanzapine; doses not specified) and discharged, but she self‑discontinued medication and later decompensated. Urine toxicology was positive for methadone; on a subsequent ED visit tests were positive for methadone, opiates and benzodiazepines (the latter given in ED). During a short admission she was titrated to a therapeutic dose of olanzapine with partial response, discharged to family care, then returned with further persecutory delusions and was again diagnosed with mania; she was transferred to another facility and lost to follow‑up. Case 3 (Mr C): A 40‑year‑old man with no known psychiatric history reported a two‑week history of distractibility, irritability, grandiosity, decreased need for sleep, racing thoughts and suicidal ideation following ingestion of ibogaine in Mexico for spiritual reasons. He also reported ingesting an unknown quantity of psilocybin mushrooms after his return and continued daily marijuana use. Physical and laboratory testing were notable only for cannabinoids on urine screen. He refused treatment while detained involuntarily, was diagnosed with bipolar I disorder, and left hospital after six days still symptomatic and declining offered treatments. Across the three cases onset of symptoms was reported from hours to days after ingestion. Collateral evidence suggested absence of prior manic episodes in two cases (Mr A and Ms B). Routine testing did not identify amphetamine or cocaine metabolites in any case. The authors report they could not objectively verify ibogaine ingestion due to timing and lack of specific assays.

Marta and colleagues interpret these three presentations as demonstrating a temporal association between ibogaine ingestion and subsequent onset of mania. They note no prior reports of mania following ibogaine use in the literature they reviewed, although reduced need for sleep and isolated reports of psychosis or prolonged mental health problems after ibogaine have been described. The authors argue the presentations differ from classic hallucinogen‑induced psychosis because of the manic phenomenology and temporal pattern, and because stimulant-related laboratory findings were absent. The researchers acknowledge potential alternative explanations and important limitations. Opiate withdrawal might have contributed in two cases (Mr A and Ms B) but not in the third. Co‑ingestion of psilocybin and heavy marijuana use in Mr C represent confounding exposures, and collaborative history was unavailable for that case. Objective toxicological confirmation of ibogaine was lacking for all three patients; the authors explain that assays require specialised liquid‑chromatography/mass‑spectrometry techniques not performed here. They also suggest prior studies may have missed similar events due to small sample sizes and exclusion of people with psychiatric histories. Clinical implications highlighted by the authors include the need for clinicians assessing new‑onset mania to obtain detailed substance use and treatment histories, specifically asking about ibogaine and opiate treatments. The discussion emphasises the risks associated with unregulated ibogaine provision, including lack of pharmaceutical and procedural standardisation, and advises clinicians to be prepared to discuss the limited evidence base, safety concerns and paucity of high‑quality data regarding ibogaine with patients considering its use.