Cannabinoids reduce levodopa-induced dyskinesia in Parkinson’s disease: A pilot study

Sieradzan, Katarzyna; Fox, Susan H.; Hill, Michael P.; Dick, Jeremy; Crossman, Alan R.; Brotchie, Jonathan M.

doi:10.1212/wnl.57.11.2108

Cited by 325 publications

(218 citation statements)

References 6 publications

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“…A small but class III randomized double-blind study using nabilone (synthetic Δ 9 -THC) showed a significant reduction in Rush score on levodopa-induced dyskinesias in 7 patients, observed and measured with the Rush dyskinesia scale [16], and 2 reported improvement in dystonia occurring in the off period for dopa. In a study of 17 patients using the oral preparation Cannador (2.5 mg Δ 9 -THC/1.25 mg CBD) no improvement was noted in dyskinesias as measured in Q32-34 of the Unified Parkinson's disease rating scale scale (the primary outcome), or other scales including Parkinson Disease Questionnaire-39 scale, nor was there a dose response [17].…”

Section: Dyskinesias From Levodopa (In Advanced Pd)mentioning

confidence: 99%

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Koppel

2015

Neurotherapeutics

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Cannabis has been used for many medicinal purposes, including management of spasms, dystonia, and dyskinesias, with variable success. Its use for tetanus was described in the second century BCE, but the literature continues to include more case reports and surveys of its beneficial effects in managing symptoms of hyperkinetic movement disorders than randomized controlled trials, making evidence-based recommendations difficult. This paper reviews clinical research using various formulations of cannabis (botanical products, oral preparations containing Δ 9 -tetrahydrocannabinol and/or cannabidiol) and currently available preparations in the USA (nabilone and dronabinol). This has been expanded from a recent systematic review of cannabis use in several neurologic conditions to include case reports and case series and results of anonymous surveys of patients using cannabis outside of medical settings, with the original evidence classifications marked for those papers that followed research protocols. Despite overlap in some patients, dyskinesias will be treated separately from dystonia and chorea; benefit was not established beyond individual patients for these conditions. Tics, usually due to Tourettes, did respond to cannabis preparations. Side effects reported in the trials will be reviewed but those due to recreational use, including the dystonia that can be secondary to synthetic marijuana preparations, are outside the scope of this paper.

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Section: Dyskinesias From Levodopa (In Advanced Pd)mentioning

confidence: 99%

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Koppel

2015

Neurotherapeutics

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“…This stimulation may also change the reuptake of GABA in striatal references. 21 It also reduces glutamate release in basal ganglia. 22 In PD, CB1 receptors are increased in basal ganglia and treatment with levodopa restores the levels to normal numbers.…”

Section: Introductionmentioning

confidence: 99%

Depression in Parkinson's disease is related to a genetic polymorphism of the cannabinoid receptor gene (CNR1)

et al. 2005

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Depression is a common symptom in Parkinson's disease (PD) and it is present in up to 40% of the patients. The cause of depression in PD is thought to be related to disturbance of monoamine neurotransmission. The endogenous cannabinoid system mediates different brain processes that play a role in the control of behaviour and emotions. Cannabinoid function may be altered in neuropsychiatry diseases, directly or through interactions with monoamine, GABA and glutamate systems. For this reason, we have investigated whether there is a genetic risk factor for depression in PD linked to the polymorphisms of CB1 receptor gene. Depression was more frequent in patients with PD than in controls with osteoarthritis. The presence of depression did not correlate with the stage of the disease but it was more frequent in patients with pure akinetic syndrome than in those with tremoric or mixed type PD. The CB1 receptor gene polymorphism (AAT)n is considered to modify the transcription of the gene and, therefore, it may have functional relevance. We analysed the length of the polymorphic triplet (AAT)n of the gene that encodes CB1 (CNR1) receptor in 89 subjects (48 PD patients and 41 controls). In patients with PD, the presence of two long alleles, with more than 16 repeated AAT trinucleotides in the CNR1 gene, was associated with a reduced prevalence of depression (Fisher's exact test: P ¼ 0.003). This association did not reach significant differences in the control group, but the number of control individuals with depression was too small to allow for statistical analysis. Since the alleles with long expansions may have functional impact in cannabinoid neurotransmission, our data suggest that the pharmacological manipulation of cannabinoid neurotransmission could open a new therapeutic approach for the treatment of depression in PD and possibly in other conditions.

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“…Presently, only two small-scale clinical trials have shown that marijuana was ineffective in reducing Parkinsonian tremor, but recently a randomized, double blind, placebo-controlled, cross-over trial with the cannabinoid receptor agonist nabilone showed an improvement in L-DOPA-induced dyskinesia in patients with PD (Sieradzan et al, 2001). This obviously contrasts the animal studies that suggest that CB 1 receptor antagonists may be used to reduce the adverse actions of L-DOPA.…”

Section: Parkinson's Diseasementioning

confidence: 95%

Biosynthesis of endocannabinoids and their modes of action in neurodegenerative diseases

et al. 2003

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Endocannabinoids are thought to function as retrograde messengers, which modulate neurotransmitter release by activating presynaptic cannabinoid receptors. Anandamide and 2-arachidonoylglycerol (2-AG) are the two best studied endogenous lipids which can act as endocannabinoids. Together with the proteins responsible for their biosynthesis, inactivation and the cannabinoid receptors, these lipids constitute the endocannabinoid system. This system is proposed to be involved in various neurodegenerative diseases such as Parkinson's and Huntington's diseases as well as Multiple Sclerosis. It has been demonstrated that the endocannabinoid system can protect neurons against glutamate excitotoxicity and acute neuronal damage in both in vitro and in vivo models. In this paper we review the data concerning the involvement of the endocannabinoid system in neurodegenerative diseases in which neuronal cell death may be elicited by excitotoxicity. We focus on the biosynthesis of endocannabinoids and on their modes of action in animal models of these neurodegenerative diseases.

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Cannabinoids reduce levodopa-induced dyskinesia in Parkinson’s disease: A pilot study

Cited by 325 publications

References 6 publications

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics

Depression in Parkinson's disease is related to a genetic polymorphism of the cannabinoid receptor gene (CNR1)

Biosynthesis of endocannabinoids and their modes of action in neurodegenerative diseases

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