Hallucinogen Persisting Perception Disorder After Ibogaine Treatment for Opioid Dependence

This case study (n=1) describes one participant who took ibogaine in a study to treat their opioid use disorder (SUD) and subsequently suffered from hallucinogen persisting perception disorder (HPPD).

Abstract

“Ibogaine is a naturally occurring alkaloid in the root bark of the African shrub Tabernanthe iboga. Studies show positive effects of a single dose of ibogaine on withdrawal symptoms, drug self-administration, and craving in animal models of substance use disorders and human case studies. Ibogaine is increasingly used as a remedy for substance use disorders in the lay-scene. However, ibogaine (either ingested as the root bark or in more purified form) has well-known dose-dependent adverse effects. These effects include among others ataxia and potentially lethal cardiac dysrhythmias. Here we report a case of hallucinogen persisting perception disorder (HPPD) that occurred after ibogaine treatment in a patient with opioid use disorder who participated in a phase II safety trial on ibogaine. Potential treatment options and existing literature on HPPD are discussed.“

Authors: Thomas Knuijver, Maarten Belgers, Wiebren Markus, Robbert-Jan Verkes, Toon van Oosteren & Arnt Schellekens

Summary

Ibogaine, a naturally occurring alkaloid in the root bark of the African shrub Tabernanthe iboga, has well-known dose-dependent adverse effects, including ataxia and potentially lethal cardiac dysrhythmias. A patient with opioid use disorder experienced hallucinogen persisting perception disorder.

A 31-year-old man with an opioid use disorder was admitted to a high-care medical facility to participate in a phase II clinical trial on ibogaine treatment for opioid dependence. He had a history of heroin dependence since he was 18 years old and received extensive treatment in the last 7 years.

To the Editors:

Ibogaine treatment and cessation of morphine was followed by no withdrawal symptoms. A mild ataxia was observed during the treatment, but faded within 24 hours.

A patient who had experienced ibogaine reported disturbing recurrence of images, which he had never experienced before. The re-experiences caused intense emotions of rejection, shame, and guilt, which were managed with support in a clinical setting and after a week administration of buprenorphine/naloxone 16/4 mg daily.

The patient received EMDR therapy to treat his HPPD, which helped to reduce the intrusive memories and negative feelings associated with them. However, he relapsed in heroin use 2 weeks after EMDR treatment.

We report a case of re-experiencing of perceptual alterations after an ibogaine treatment that caused clinically significant distress and met the criteria for HPPD. The differential diagnoses included delirium during opioid withdrawal, trigger of preexisting psychopathology, or persisting ibogaine-induced psychotic symptoms or prolonged oneirogenic experiences.

The optimal therapeutic dose of ibogaine-HCl is not known, but the psychotropic effects of ibogaine occur at commonly applied doses, similar to the dose in our case. The visual experiences persisted for nearly 5 weeks.

HPPD can occur after the use of other hallucinogens, including LSD, psilocybin, cannabis, and ecstasy. It is not well defined what causes HPPD, but it is likely caused by an overactivation of predominantly visual neural pathways that worsens anxiety after ingestion of arousal-altering drugs.

Pharmacological treatment options for HPPD include benzodiazepines, antipsychotics, serotonergic agents, adrenergic agonists or reuptake inhibitors, and opioid antagonists. EMDR therapy was successfully applied to treat HPPD-related distress, without a clear effect on craving and not preventing relapse.

In summary, this case illustrates the importance of psychiatric monitoring during and after treatment with ibogaine, and the successful use of EMDR therapy in HPPD-related stress.