Cannabidiol (CBD) a nonpsychoactive cannabinoid of Cannabis, was given to 5 patients with dystonic movement disorders in a preliminary open pilot
study. Oral doses of CBD rising from 100 t 600 mg/day over a 6 week period
were administered along with standard medication. Dose-related improvement in dystonia was observed in all patients and ranged from 20 to 50%. Side-effects of CBD were mild and included hypotension, dry mouth,
psychomotor slowing, lightheadedness, and sedation. In 2 patients with
coexisting Parkinsonian features, CBD at doses over 300 mg/day exacerbated the hypokinesia and resting tremor. CBD appears to have antidystonic and Parkinsonism-aggravating effects in humans. 

As early as 1842, O’Shaughnessy reported that oral Cannabis blocked tetanic
convulsions and reduced muscular spasms in his patients afflicted with
epilepsy, tetanus or rabies, while in 1890 Reynolds claimed that oral
Cannabis was useful in the management of “choreoid and epileptoid clonic
spasms.” During the latter 19th century, Cannabis was commonly employed as a general antispasmodic agent, and several recent reports appear to provide some justification for this use. In 1981, Petro and Ellenberger reported that delta-9-tetrahydrocannabinol (THC), the major psychoactive cannabinoid of Cannabis, reduced spasticity of multiple sclerosis, and in 1983 Cliffored reported that THC reduced tremor in a few patients with the same disease. Also in 1980 Cunha et al. reported that cannabidiol (CBD), a
major nonpsychoactive cannabinoid of Cannabis, prevented convulsions in
epileptic patients who were largely refractory to standard antiepileptic
drugs. 
Recently, it has been mentioned that patients with idiopathic
dystonia (a group of disorders characterized by abnormal movements and
postures produced by prolonged spasms of muscle contractions) improved with Cannabis smoking (Marsden, 1981). In addition, findings of potent effects of cannabinoids on reserpine-induced hypokinesia in rats led to the
suggestion that cannabinoids might have antidystonic properties in humans
(Moss et al., 1984). In light of the above, we initiated an open trial of
CBD in a patient with Meige’s syndrome (Blepharospasm-oromandibbular
dystonia) (Snider & Consroe, 1984) and a patient with levodopa-induced
dystonia (Snider & Consroe, 1985). We now present the results of our
preliminary open study of oral CBD in these two cases and in three
additional patients with primary dystonia. 

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