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MARIJUANA AND TOURETTE'S SYNDROME
Journal of Clinical Psychopharmacology, Vol. 8/No. 6, Dec 1988
Although a variety of pharmacological agents have been reported to
attenuate symptoms of Tourette's syndrome (TS), the pathophysiology of this
disorder remains unknown. Apart from the presence of disabling motor and
vocal tics, TS patients often experience behavioral disturbances including
obsessive compulsive thoughts, anxiety, depression, abnormal sleep
disturbances. (1) Drug abuse to obtain relief from the chronic anxiety may
be common among these patients. (2) (3) We recently encountered three
patients with TS who experienced incomplete responses to conventional
anti-TS drugs but noted a significant amelioration of symptoms when smoking
The first patient was a 15-year-old boy who, in addition to motor
tics, had obsessive compulsive and self-mutilatory behavior improved with
administration of imipramine (37.5 mg/day) combined with the oral opiate
receptor antagonist naltrexone (dose range 50 to 100 mg/day). During
recreational use of marijuana (1 to 2 cigarettes/day), he noted general
relaxation and marked lessening in his urge to tic. According to the
patient's mother, motor tics had decreased by about 50% and there was also
some reduction in the frequency of the self-mutilatory behavior. The
patients had been smoking marijuana for 4 weeks, and upon discontinuation,
noted rebound exacerbation of symptoms within 12 hours.
The second patient, age 17, had had severe motor tics since the age
of 7 years. He had frequent jerk-type movements of his neck muscles
associate with infrequent vocalizations during stressful situations. His
management had been difficult as he was unable to tolerate haloperidol or
clonidine. Administration of naltrexone (150 mg/day) reduced his anxiety
level and the urge to tic; this was the only drug he could tolerate. On
several occasions, he had smoked marijuana and noted generalized relaxation
accompanied by reduction in the severity of the motor tics and improvement
in attention span. He volunteered that smoking one cigarette reduced the
frequency of his motor tics by about 60% to 70%, which was sustained over
The third patient was a 39-year-old man who had had symptoms of TS
since the age of 9 years. His symptoms included frequent jerking-type
movements of his neck and upper extremity muscles, facial grimacing,
frequent blinking, and leg jerking. Vocalizations were not noted except
during extreme anxiety. In addition he was troubled by chronic insomnia
and hypersexuality. He reported no benefit from haloperidol, clonidine, or
benzodiazepines but experienced some relief after consuming large amounts
of ethanol. He also admitted that marijuana smoking (1/2 to 1
cigarette/day) produced relaxation with subsequent reduction in the
severity of the motor tics along with marked attenuation of his
From 1842 to the turn of this century, several reports in the
literature have indicated that marijuana smoking was used extensively as an
analgesic, sedative, and hypnotic agent. (4) Moreover, oral cannabis
preparations were useful in the management of diverse neurological
conditions including convulsions and chorea. (5) Much more recently it was
reported anecdotally that patients with dystonia improved with their
alleged cannabis smoking. (6) The cannabis constituent cannabidiol was
reported efficacious in reducing symptoms of dystonia. (7,8) and
Huntington's chorea. (9) In experimental animals, cannabidiol has been
shown to exert anticonvulsant and antianxiety properties and affect
apomorphine-induced turning behavior in rats. (10) The latter report
suggested that cannabidiol exerts antidyskinetic effects through modulation
of striatal dopaminergic activity. Tetrahudrocannabinol (THC, the active
compound of marijuana) may exert GABA-ergic as well as antiserotonergic
effects. (11) A recent report has demonstrated that THC reduces opiate
receptor binding sites and modulates opiod receptors in a noncompetitive
manner. (12) THC may also exert effects on the cholinergic system. (13)
Considering evidence that marijuana may exert effects on a large
number of neurotransmitters, it is difficult to speculate on its mode of
action in attenuating symptoms of TS. It is reasonable to assume that the
effects of marijuana in TS may be largely related to its anxiety-reducing
properties, although a more specific antidyskinetic effect cannot be
excluded. Should marijuana compounds prove to have specific actions in TS,
chemical modifications which eliminate the psychoactive properties while
retaining the antiduskinetic effects (e.g., cannabidiol) could promise a
new class of drugs useful in the management of TS. Further studies are
clearly needed in both the clinical and basic laboratory realms to further
characterize the effects of cannabinoids in TS.
Reuven Sandyk, MD, MSc
Gavin Awerbuch, MD
University of Arizona
1. Brunn RD. Gilles de la Tourette Syndrome: an overview of clinical
experience. J Am Acad Child Psychiatry 1984;23: 125-33.
2. Mesulam MM. Cocaine and Tourette's syndrome. N Engl J Med 1986; 315:
3. Sandyk R, Gillman MD. Gilles de la Tourette syndrome following
alcohol withdrawal. Br J Addict 1985; 80: 213-4.
4. Consroe P, Snider SR. Therapeutic potential of cannabinoids in
neurological disorders. In: Mechoulam R, ed. Cannabinoids as therapeutic
agents. Boca Raton, FL: CRC Press, 1986: 21-49.
5. O'Shaughnessy R. On the preparation of the indian hemp or gunjah
(cannabis indica): the effects on the animal system in health and their
utility in the treatment of tetanus and other convulsive diseases. Trans
Med Phys Soc Bombay 1842; 8: 421-61.
6. Marsden CD. Treatment of torsion dystonia. In: Barbeau A, ed.
Disorders of movement, current status of modern therapy, Vol. 8.
Philadelphia: Lippincott, 1981: 81-104.
7. Snider SF, Consroe P. Treatment of Meige's syndrome with cannabidiol.
Neurology 1984; 34 (Suppl): 147.
8. Consroe P, Sandyk R, Snider SR. Open label evaluation of cannabidiol
in dystonic movement disorder. Int J Neurosci 1986; 30: 277-80.
9. Sandyk R, Consroe P, Stern LZ, Snider SR. Effects of cannabidiol in
Hungtington's disease. Neurology 1986; 36 (suppl): 342.
10. Conti LH, Johannesen J, Musty RE, Consroe P. Anti-dyskinetic effects
of cannabidiol. Proceedings of the International Congress on Marijuana.
Melbourne, Australia: Melbourne University Press 1987: 21.
11. Revuelta AV, Cheney DL, Wood PL, Costa E. Gabergic mediation in the
inhibition of hippocampal acetylcholine turnover rate elicited by
delta-9-tetrahudrocannabidiol. J Clin Pharmacol 1979; 18: 525-30.
12. Vaysse PJJ, Gardner EL, Zukin RS. Modulation of rat brain opiod
receptors by cannabinoids. J Pharmacol Exp Ther 1987; 241: 534-9.
13. Revuelta AV, Moroni F, Cheney DL, Costa E. Effect of cannabinoids on
the turnover rate of acetylcholine in rat hippocampus, striatum and cortex.
Naunyn Schmiedebergs Arch Pharmacol 1978; 304: 107-11.
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