cbd movement disorders

Cbd movement disorders

Without clinical trial data however, we do not know whether CBD is safe and effective for a particular symptom, and if it is, what CBD formulation and dosage is best to be used for a particular symptom.

APDA Parkinson’s Treatments Use of Cannabidiol (CBD) for PD symptoms

People with PD are already using CBD in various forms for all sorts of symptoms of PD including insomnia, anxiety, tremor, dystonia and pain.

What evidence is available for the use of CBD for PD?

The FDA is aware that patients are frustrated that our understanding of how best to use CBD remains minimal because of the lack of clinical trials. In 2015, the FDA changed some of their regulations to make it easier to study CBD in clinical trials.

It is not just the Parkinson’s disease community that has taken an interest in CBD. There are countless health claims that CBD is helpful for a whole host of conditions. Clinical trial evidence to support the use of CBD however, is minimal. The only FDA-approved indication for CBD is to reduce seizure frequency in certain rare and severe forms of childhood epilepsy. A purified form of CBD, sold under the brand name Epidiolex® was tested in a well-designed clinical trial in order to gain this approval. (Three other cannabis related drug products that are not CBD, but rather synthetic THC, also have FDA approval and are used to treat loss of appetite and weight loss in patients with HIV, and severe nausea and vomiting due to chemotherapy).

This has not dimmed the enthusiasm of millions of CBD users for a wide range of medical conditions.

Understanding CBD

More recently, I have received many inquiries specifically about the use of cannabidiol or CBD, for symptoms of PD. So today I’ll take a more in-depth look at CBD to help you better understand what it is and its possible use for symptoms of PD.

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We also don’t know the side effect profile of CBD in people with PD. At baseline, people with PD may have various non-motor symptoms that may make them more prone to side effects from CBD, including fatigue and nausea.

Several studies in animal models of both PD and HD suggest that cannabinoid-based therapies may attenuate neurodegeneration ( Table 2 ). Indeed, on October 7, 2003, U.S. Health and Human Services was granted U.S. Patent 6630507, which lists the use of cannabinoids found within the cannabis sativa plant as useful in certain neurodegenerative diseases such as PD, Alzheimer’s disease and dementia caused by human immunodeficiency virus. 141 Cannabinoids may offer neuroprotection through both receptor-mediated and receptor-independent mechanisms. Cannabinoids are capable of reducing oxidative damage by acting as scavengers of reactive oxygen species (ROS) and enhancing endogenous antioxidant defenses. 19 This property appears to be independent of CB1 and CB2 receptor modulation and restricted to certain cannabinoids, including CBD, THC, cannabinol, CP55,940, and the anandamide analogue AM404. 20–22 CB2 agonists exert anti-inflammatory effects by inhibiting reactive microglia and cytokine release. 20, 23–25 Lastly, CB1 agonists reduce excitotoxicity by suppressing glutamatergic activity, subsequent calcium ion influx, and nitric oxide production. 26, 27 However, in one study, both a CB1 agonist, THC, and a selective CB1 antagonist, rimonabant, exacerbated malonate-induced striatal lesions. 28

While cannabinoids appear to be well tolerated when used in moderation, AEs are clearly a major concern. In the systematic review of CB studies conducted by the AAN 6.9% (95% CI 5.7%–8.2%) of participants stopped their medication due to AEs. 8 AEs include ataxia, nausea, impaired short-term memory, stroke, cognitive impairment, dry mouth, suicidal ideation, hallucinations, dizziness, fatigue, behavioral or mood changes, impaired motor skills, increased weakness, heart rate and appetite. 8, 100, 101 Marijuana use is also associated with an increased risk of chronic anxiety, depression and psychosis, though causality has not been established. 102 Except for ataxia, there have been no documented cases of movement disorders induced by cannabis use. However, there has been one case report of propriospinal myoclonus possibly induced by cannabis, 103 but this form of myoclonus is often of psychogenic origin. 104

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Table 1

It has been hypothesized that CB1 agonists reduce overactivity of the globus pallidus interna (GPi) and improve dystonia by reducing GABA reuptake. 73 In support of this idea, the CB1 and CB2 agonist WIN55,212-2 produces antidystonic effects in a mutant hamster model of dystonia, increases the antidystonic efficacy of benzodiazepines and is reversed by rimonabant, a selective CB1 antagonist. 74, 75 Animal models suggest that cannabinoids may reduce MS-related tremor, an effect that appears to be selectively mediated by CB1 receptors. 92

Multiple Sclerosis-related Tremor

In contrast, 4 controlled clinical studies of cannabinoids reported no benefit for motor symptoms, mixed results regarding LID and quality of life. 59–61, 140 ( Table 4 ) A small (N=5) randomized, double-blind, placebo-controlled crossover trial, assessed the efficacy of 0.03 mg/kg nabilone, a CB1 and CB2 agonist for LID given in a split dose 12 and 1 hour prior to a levodopa challenge. 61 They found a significant reduction in LID versus placebo on the Rush Dyskinesia Disability Scale and total LID time. Nabilone did not diminish the antiparkinsonian actions of levodopa or improve parkinsonian symptoms although 2 patients reported improvements in painful off-period dystonia. A larger (N=17) 4-week randomized double-blind crossover study of twice daily Cannador, an oral cannabis extract containing 1.25 mg CBD and 2.5 mg THC, titrated Cannador up to 0.25 mg/kg THC for LID. 59 Although the blinding seemed to be compromised (71% correct identification of treatment), Cannador failed to improve LID on multiple outcomes, including a non-significant worsening on their primary outcome (UPDRS dyskinesia items) and the Rush Dyskinesia scale. There were no significant changes for other secondary outcomes including motor symptoms (Part 3 UPDRS), quality of life (PDQ-39) or sleep. Another small (N=8) 16-day randomized placebo-controlled trial assessing the efficacy of 20 mg daily oral rimonabant (CB1 antagonist) showed no effect on parkinsonian motor symptoms or LID as measured by the UPDRS and a standardized videotape procedure. 60 Examination of data suggested a trend towards worsening in motor scores but the small sample size and other methodological issues prevent any meaningful conclusions. Most recently, 21 PD patients were randomized to placebo, CBD 75mg/day or CBD 300 mg/day for a 6-week trial. 140 No significant changes were found for the total UPDRS or any subscales or measures of neuroprotection (serum brain derived neurotrophic factor levels or putamen magnetic resonance spectroscopy). Improvements were noted for the total PDQ-39 score and stigma and activities of daily living subscores for the CBD 300 mg/day group. Despite the low sample size and quality of these studies, the data suggest cannabinoid agonists and antagonists are probably ineffective for both LID and motor symptoms although further study using different doses, formulations or target symptoms (e.g. dystonia, psychosis, sleep) may be justified. While there were no serious adverse events reported, side effects included hypotension, vertigo, visual hallucinations, dizziness and somnolence.

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