European Psychiatry - Volume 33 - March 2016

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S10 24th European Congress of Psychiatry / European Psychiatry 33S (2016) S8–S11
experiences have been funding cuts and lack of incentives. Some
examples will be presented.
Disclosure of interest The author has not supplied his declaration
of competing interest.
Symposium: making medicines out of illicit
drugs – ECNP symposium hosted by EPA
JS07
Can ecstasy treat the agony of PTSD?
M. Mithoefer
Department of Psychiatry and Behavioral Sciences, Medical
University of South Carolina, Charleston, USA
Introduction Two serotonin reuptake inhibitors (SSRIs) have
received FDA indication for treatment of PTSD, however the
effectiveness of pharmacotherapy for PTSD is limited. Psychother-
apy, including several well established evidence based methods,
is the mainstay of PTSD treatment. Despite advances in this
area, a significant percentage of PTSD patients are refractory
to existing treatments. Recent research has explored the pos-
sibility that certain drugs could increase the effectiveness of
psychotherapy when administered intermittently in conjunction
with psychotherapy sessions. The most robust published. Results
to date using this approach have been in early clinical tri-
als of ± 3,4-methylenedioxymethamphetamine (MDMA)-assisted
psychotherapy. These studies primarily involved civilians with
treatment-resistant, crime-related PTSD. A more recent phase 2
trial, completed in 2015 yielded equally promising. Results in a
cohort of military veterans, police officers and firefighters, mostly
veterans from the wars in Iraq and Afghanistan.
Methodology In these double blind controlled trials subjects with
PTSD refractory to prior treatment are randomized to an active
dose of MDMA or an active or inactive placebo administered
to each individual on only two or three occasions during eight-
hour psychotherapy sessions one month apart, in conjunction
with preparatory and follow-up psychotherapy sessions. Outcome
measures are repeated one or two months after the secondMDMA-
assisted session before the blind is broken. Subjects who were
randomized to full dose MDMA are then eligible for one addi-
tional, open label, MDMA-assisted session. Those randomized to
placebo or a lower dose of MDMA are eligible for three open-label
full dose sessions. Outcome measures are repeated two months
following the third MDMA-assisted session. The primary out-
come measure is the Clinician Administered PTSD Scale (CAPS).
Additional measures include the Beck Depression Inventory-
II (BDI-II), Global Assessment of Functioning (GAF), Pittsburgh
Sleep Quality Index (PSQI) and Posttraumatic Growth Inventory
(PTGI).
Results In the original study comparing MDMA with inactive
placebo along with the same psychotherapy PTSD was resolved
in 83% of the MDMA group vs. 25% of the placebo group receiv-
ing the same therapy. Improvement was maintained for at least
74% of subjects at long-term follow-up a mean of 45 months later.
In a more recent, unpublished, study both the high dose and the
medium dose of MDMA showed large effect sizes in reducing CAPS
scores, and improvements in secondarymeasures: and BDI-II, PSQI,
GAF and PTGI.
Conclusion Evidence in phase II trials suggest that MDMA-
assisted psychotherapy is effective in treating PTSD in both civilians
and veterans who have not responded to established treatments.
Phase III trials are necessary to definitively establish safety and
efficacy of MDMA-assisted psychotherapy for PTSD.
Disclosure of interest The author has not supplied his declaration
of competing interest.
JS08
Treatment of heroin dependence with
ibogaine
A. Schellekens ∗ osteren nuijver . verkes
M. Belgers
1 Radboud University Medical Centre, Donders Centre for
Neuroscience- department of Psychiatry – Nijmegen Institute for
Scientist Practitioners in Addiction, Nijmegen, Netherlands
2 IrisZorg, addiction care, Arnhem, Netherlands
∗ Corresponding author.
Background The use of the hallucinogen ibogaine as an anti-
addiction agent has been described in several case reports, dating
back to the eighties. The anti-addiction properties of ibogaine
have been confirmed in a large body of animal work. Ibogaine
has been shown to be effective in reducing withdrawal sever-
ity and substance use for a variety of substances, including
cocaine and opiates. Animal studies also show some potentially
dangerous adverse reactions, including cerebellar toxicity and
potential cardiac effects. While pharmacological treatment options
for opiate and cocaine dependence are still limited, ibogaine
assisted treatment might be a promising new option. Therefore
more systematic studies on its toxicity and efficacy are warr-
anted. In our studies we address these two research questions:
is ibogaine treatment for opiate dependence safe and effective
for treating opiate withdrawal and relapse prevention? A sec-
ondary objective is to explore the pharmacokinetic properties of
ibogaine.
Methods Animal work: first we performed a systematic review
and meta-analysis of animal studies on ibogaine. Thirty studies
were included in the systematic review, of which 27 could be ana-
lyzed in meta-analysis. Human studies: fifteen opiate dependent
patients will be treated with ibogaine (10mg/kg), on top of treat-
ment as usual. Ibogaine toxicity will be assessed through close
monitoring with electrocardiography, with QTc prolongation as
main outcome measure, repeated assessments of ataxia using the
(SARA) and observation of psychotic symptoms by using the Delir-
ium Observations Scale (DOS). Ibogaine efficacy will be measured,
using repeated evaluations of opiate withdrawal severity (Subjec-
tive OpiateWithdrawal Scale: SOWS; Objective OpiateWithdrawal
Scale: OOWS), craving intensity (using a Visual Analogue Scale) and
substance use, with a six-month follow-up. Clinical observations
in ibogaine treated individuals will be compared with a cohort of
opiate dependent patients treated with a rapid detoxification pro-
cedure. Both acute and long-term effects will be linked with serum
ibogaine and noribogaine levels.
Results Animal work: overall, ibogaine reduced drug self-
administration, particularly during the first 24 hours after
administration. Ibogaine had no effect on drug-induced con-
ditioned place preference. Ibogaine administration resulted in
motor impairment in the first 24 hours after supplementation,
and cerebral cell loss even weeks after administration. Data on
ibogaines effect on cardiac rhythm as well as on its neurophar-
macological working mechanisms are limited. Human studies:
human data are still being collected. Treatment of the first patients
confirmed strong effects of ibogaine on heart rhythm (QTc pro-
longation) and ataxia, while the opiate withdrawal symptoms
were relatively mild. The first observations on the clinical effect of
ibogaine on craving and substance use will also be shared.
Conclusions Based on our meta-analysis of animal data, there is
strong evidence that ibogaine is effective in reducing drug self-
administration in animals. This warrants further studies into the
clinical efficacy of ibogaine in substance dependent patients in
reducing craving and substance use. Our first clinical experiences in