# Priapism, Ecstasy, and Marijuana: Is There a Connection?

Authors: Quan T. Tran; Robyn A. Wallace; Esther H. A. Sim
Journal: Advances in Urology
 (2008)

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## Abstract

Priapism is a urological emergency with multiple aetiologies including drug induced. Currently, there have been no reports of priapism induced by the combination of ecstasy and marijuana. We speculated on the potential mechanisms for acute drug-induced priapism resulting from ingestion of these two common illicit drugs.


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## Body

## 1. Introduction

Priapism is a urological emergency that, left untreated, may lead to
permanent damage to the corpora
cavernosa resulting in erectile dysfunction. It is
defined as a persistent penile erection greater than four hours in duration,
which is unrelated to sexual stimulation or desire [1]. This condition can be
divided into nonischaemic priapism (high-flow) and ischaemic (low-flow) priapism.
Nonischaemic priapism is rare and often painless; it is thought to occur secondary
to the rupture of a cavernous artery resulting in unregulated flow into the
lacunar spaces and commonly results as a consequence of penile trauma or blunt
perineal injury [2]. Ischaemic priapism is usually due to unremitting corporeal
veno-occlusion resulting in venous stasis within the cavernous tissue and is associated
with pain and tenderness. Prolonged penile veno-occlusion
can result in a comprised
ability to achieve an erection and penile fibrosis [2].We present a case of a previously well 52-year-old Caucasian male
who presented to the department of emergency medicine (DEM) with a four-day
history of persistent erection following a night involving a sexual encounter
and ingestion of ecstasy and marijuana. The next morning after his sexual
encounter, he noticed a prolonged erection, which was progressing in pain. He
had taken only one portion of ecstasy and marijuana but was unable to quantify
the dose. He was not a regular user and had not used ecstasy or marijuana for at
least 12 months. He denied taking other oral, intravenous, or intracavernous drugs.
Other known causes of priapism were excluded. Two days after his sexual
encounter, he presented to his family physician for treatment. Initial
management with oral pseudoephedrine (60 mg) did not resolve his priapism and a
needle aspiration was performed 60 minutes later. However, these measures provided
only minor relief and he presented to DEM two days later.Physical examination at DEM revealed an erect, swollen, and tender
penis. No other abnormalities were detected. Detumescence was achieved by the
attending urologist via insertion of 14-gauge cannulae in each side of the
cavernosa. No intracavernous medications were required. The patient was discharged
and referred to the medical unit to investigate any medical causes of priapism.
After four weeks, there were no additional episodes of priapism. However, the
patient had reported unsatisfactory erections since the incident, which may
have been a consequence of his four-day delayed presentation.


## 2. Discussion

We conducted a PubMed search with priapism and ecstasy (3,4-methlyenedioxymethamphetamine
(MDMA)) and/or marijuana (cannabinoid, cannabis)
and their pseudonyms. Only one case report was found describing a chronic
ecstasy user who developed priapism following one month cessation of ecstasy
use [3]. The present case differs from the latter and suggests that acute
priapism is possible from a single ingestion. No specific association between
priapism and marijuana was found. Therefore, we aimed to explore the acute
relationship between priapism and ecstasy, marijuana, and the possibility of
synergistic activities between these two substances.Dublin and Razack [3] hypothesised
that ecstasy-induced priapism is due to  the effect of ecstasy on serotonin (5-HT). Chronic
use of ecstasy results in reduced serotonin activities and serotonin-related
components of brain neurons [4]. In general, serotonin pathways are considered
to have an inhibitory effect on sexual function [5], and chronic use of ecstasy
may predispose males to priapism as a consequence of the reduced sexual
inhibition [3].However,
ecstasy ingestion often results in the release of 5-HT stores causing an acute
rise in 5-HT concentration [5]. Although
5-HT is primarily inhibitory, stimulation of a subset of 5-HT receptors (i.e., 5-HT1C,
5-HT1D, 5-HT2C) increases erections in animals [6].
Reports of priapism induced by antidepressants such as
trazodone [7], citalopram [8], venlafaxine [9], and sertraline [10] are documented. The proerection
properties of 5-HT2C agonists are thought to be parasympathetically
mediated due to 5-HT2C receptors on the visceromotor neurons of the
sacral parasympathetic nucleus of the spinal cord and on the dorsal gray
commissure and ventral horn motor neuron [11]. Therefore,
acute elevation of 5-HT induced by ecstasy ingestion may facilitate erections.Ecstasy ingestion also results in acute
dopamine (DA) release in the brain. This is thought to occur by diffusion of ecstasy into cerebral neurons stimulating DA release
[5]. Dopamine has facilitative effects on sexual motivation, copulatory
proficiency, and genital reflexes [11]. Clinically, levadopa (a DA precursor)
was found to increase nocturnal erections in elderly males [12]. In addition,
apomorphine, a dopamine (D1, D2) receptor agonist, has
been observed to produce erections in men that were not accompanied by sexual
arousal [13]. It is
thought that the proerection properties of dopaminergic neurons occur by way of activating
oxytocinergic neurons in the paraventricular nuclei and that the release of oxytocin
produces erections [14].Psychotropic drugs have been proposed as a causative agent for priapism [1]. To date, no specific case of priapism and marijuana
was found in the literature. However, we have speculated on
potential cannabinoid properties that may facilitate erections.
Cannabinoids can potentially modulate autonomic blood outflow in
both the central and peripheral nervous systems, and also have
direct effects on the vasculature. The most commonly researched cannabinoid receptor is
CB1 which is mostly found in the central nervous system
but is also present in the peripheral nervous system. In rats,
administered cannabinoids can cause hypotension and bradycardia, which is thought to occur
via inhibition of CB1 mediated prejunctional
sympathetic outflow (inhibition of norepinephrine), and increased
vagal tone [15]. Increased parasympathetic activity would promote
penile tumescence in the sexually aroused male. Furthermore,
cerebral vasorelaxation has been noted as a common effect of
CB1, CB2 and
Δ9-tetrahydrocannabinol, the psychoactive
ingredient of marijuana. The vasorelaxation response has been
suggested to occur by way of hyperpolarization or repolarization
via inhibition of Ca2+ mobilization in vascular smooth
muscle [15]. However, the existence
of cannabinoid receptors within the human penile vasculature
remains unknown.Animal studies have produced contradictory findings. Rat studies have
demonstrated that cannabinoid receptor antagonists have centrally mediated proerection
properties [16]. There is a paucity of studies investigating human erections and marijuana,
and as a result there is insufficient evidence to suggest that marijuana will
cause priapism in humans.Synergist interactions between marijuana and ecstasy have been observed
suggesting that the endocannaboid system is involved with the reinforcing
properties of ecstasy [17]. This relationship may be related to the involvement
of the cannabinoid in the interaction and regulation of DA synthesis and
turnover [18], which is considered the principle neurotransmitter in the reinforcement
pathway. Therefore, it may be possible that the DA pathway is potentiated with
a combination of ecstasy and marijuana, which may also facilitate penile
erections via DA stimulation of oxytocin.


## 3. Conclusion

We concluded that our patient suffered from an ecstasy-induced
priapism, mostly likely mediated via acutely elevated dopamine and serotonin levels,
and that the concentration and interaction of these neurotransmitters may have
been augmented by marijuana. Cessation of these substances has resulted in no
further incidences of priapism. Therefore, illicit drug use is an important
consideration for acute presentations of priapism of unknown aetiology.



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