The abundance of CB1 receptors in basal ganglia and reports of animal studies showing the involvement of cannabinoids in the control of movement suggest that cannabinoids would be useful in treating movement disorders in humans. Marijuana or CB1 receptor agonists might provide symptomatic relief of chorea, dystonia, some aspects of parkinsonism, and tics. However, clinical evidence is largely anecdotal; there have been no well-controlled studies of adequate numbers of patients. Furthermore, nonspecific effects might confound interpretation of results of studies. For example, the anxiolytic effects of cannabinoids might make patients feel that their condition is improved, despite the absence of measurable change in their condition.
Compared to the abundance of anecdotal reports concerning the beneficial effects of marijuana on muscle spasticity, there are relatively few claims that marijuana is useful for treating movement disorders. This might reflect a lack of effect or a lack of individuals with movement disorders who have tried marijuana. In any case, while there are a few isolated reports of individuals with movement disorders who report a benefit from marijuana, there are no published surveys indicating that a substantial percentage of patients with movement disorders find relief from marijuana. Existing studies involve too few patients from which to draw conclusions. The most promising reports involve symptomatic treatment of spasticity. If the reported neuroprotective effects of cannabinoids discussed in chapter 2 prove to be therapeutically useful, this could benefit patients with movement disorders, but without further data such a benefit is highly speculative. Since stress often transiently exacerbates movement disorders, it is reasonable to hypothesize that the anxiolytic effects of marijuana or cannabinoids might be beneficial to some patients with movement disorders. However, chronic marijuana smoking is a health risk that could increase the burden of chronic conditions, such as movement disorders.
Cannabinoids inhibit both major excitatory and inhibitory inputs to the basal ganglia. This suggests that a cannabinoid agonist could produce opposite effects on movement, depending on the type of transmission (excitatory or inhibitory) that is most active at the time of drug administration. This property could be used to design treatments in basal ganglia movement disorders, such as Parkinson's disease where either the excitatory subthalamic input becomes hyperactive or the inhibitory striatal input becomes hypoactive. The dose employed would be a major factor in the therapeutic uses of cannabinoids in movement disorders; low doses should be desirable, while higher doses could be expected to aggravate pathological conditions. Thus, there is a clear reason to recommend pre-