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. 2011 Aug;163(7):1365–1378. doi: 10.1111/j.1476-5381.2011.01365.x

Table 1.

Summary of effects observed with pharmacological manipulation of the cannabinoid system in basal ganglia disorders

Neurological disorder Symptom relieving effects Effects on disease progression
Huntington's disease –TRPV1 agonists reduce hyperkinesia in animal models (Lastres-Becker et al., 2003) –CB2 agonists reduce inflammatory events and excitotoxicity in animal models (Palazuelos et al., 2009; Sagredo et al., 2009)
–CB1 agonists produce only modest effects in animal models (Lastres-Becker et al., 2003), whereas the data in patients are controversial (Müller-Vahl et al., 1999; Curtis and Rickards, 2006; Curtis et al., 2009) –Cannabidiol and Δ9-THC reduce oxidative stress in animal models (Lastres-Becker et al., 2004; Sagredo et al., 2007)
–CB1 agonists may also reduce excitotoxicity in animal models (Pintor et al., 2006; Blázquez et al., 2011), but they are lost during the progression of the disease
Parkinson's disease –CB1 antagonists reduce bradykinesia in animal models (Fernández-Espejo et al., 2005; González et al., 2006; Kelsey et al., 2009) but not in patients (Mesnage et al., 2004) –Antioxidant cannabinoids are neuroprotective in animal models (Lastres-Becker et al., 2005; García-Arencibia et al., 2007)
–CB1 agonists may reduce tremor in animal models (Sañudo-Peña and Walker, 1997) but the issue is not clear in patients (Consroe, 1998; Sieradzan et al., 2001; Carroll et al., 2004) –CB2 agonists may reduce inflammatory events in animal models (Price et al., 2009; García et al., 2011)
Tourette's syndrome –Plant-derived cannabinoids and analogues reduce tics in patients (reviewed in Müller-Vahl, 2009)
Dystonia –Classic and non-classic cannabinoid agonists have antidystonic effects in animals models and patients (reviewed in Fernández-Ruiz and González, 2005)
Dyskinesia –CB1 agonists or antagonists attenuate levodopa-induced dyskinesia in animal models and patients (reviewed in Fabbrini et al., 2007)

Δ9-THC, Δ9-tetrahydrocannabinol.