Observations on Treatment With IbogaineDaniel Luciano, M.D.
Department of Neurology, The Hospital for Joint Diseases
NYU School of Medicine, New York, NY
The American Journal on Addictions, 7(1):89-90, 1998
SIR: Approximately 1 year ago, I was given the opportunity to be present while three addicted patients were administered ibogaine hydrochloride (NIH 10567, Endabuse) by the medical staff of Centro Medico Paitilla, in Panama City (Drs. Edgardo Della Serra and Ezekiel Jethmal). This agent is a hallucinogenic indole alkaloid reported to be effective in the treatment of addiction to multiple drugs of abuse, including opiates, stimulants, and alcohol.1,2 It has also been utilized in the psychotherapeutic milieu, largely for its abreactive properties.3 I would like to relate my observations as a neurologist concerning clinical and EEG examinations performed during and after treatment.
The study was a collaborative effort between NDA International (Staten Island, NY), CITA (Centro Internacional para el Tratamiento de Addiciones), and the University of Miami. Patients had been obtained via private application to NDA International. The study was approved by the Institutional Review Board of Centro Medico Paitilla, and all patients signed informed consent. All three were addicted to cocaine (intranasal, intravenous [IV], or crack: 0.5-8 gm/day), one to heroin (1 gm/day IV), and two to alcohol. Screening medical and psychiatric examinations were performed, as well as laboratory exams, including ECG, EEG, and MRI.
Patients initially received a 1 mg/kg test dose of ibogaine. The next day, they were premedicated with domperidone 10 mg to prevent nausea/vomiting and were then administered ibogaine hydrochloride in capsule form (20-25 mg/kg). General medical monitoring was continuous, and neurologic/EEG studies were performed intermittently over 24 hours. Patients were kept in a quiet, darkened room and generally remained lying in bed. Despite treatment with domperidone, movement-induced vomiting occurred in two patients 1 hour after ingestion. Based on the estimated amount of ibogaine lost, they were given additional doses to ensure a total dose of 20-25 mg/kg. Regarding neurological signs: all patients developed transient cerebellar dysfunction within 2 hours, which was variably expressed as nystagmus, intention tremor without dysmetria, and gait ataxia. Signs were present but improved at 8 hours. Visual hallucinosis with eyes closed was seen in only one patient. Reality-testing remained normal in all, and there were no signs or symptoms of anxiety or thought disorder. Routine EEG studies were normal in all cases, during and after treatment. No general medical or ECG abnormalities were seen. At 24 hours after treatment, all neurologic examinations were normal, and patients did not have subjective or objective signs of withdrawal or craving.
Ibogaine has been touted as a potential cure for addictions to multiple drugs of abuse, eliminating withdrawal symptoms and craving after a single administration. Clearly, more extensive prospective testing will be needed to establish the validity of this claim. My observations suggest that ibogaine causes transient vestibulocerebellar dysfunction, not unlike other soporifics, and is generally well tolerated, except that it may produce prominent movement-induced nausea and vomiting occurring relatively early after ingestion.
References1.Lotsof HS: Ibogaine in the treatment of chemical dependence disorders: clinical perspectives. Bulletin of the Multidisciplinary Association of Psychedelic Studies 1995; 5:16-27
2.Sheppard SG: A preliminary investigation of ibogaine: case reports and recommendations for further study. J Subst Abuse Treat 1994; 11:379-385
3.Naranjo C: The Healing Journey: New Approaches to Consciousness. New York, Pantheon, 1973
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