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Parkinson's hemp treatment

The team led by the Czech doctor Evžen Růžička conducted a study last year on patients with Parkinson's disease.

Kamila Schwubová-Tomsová, Mladý svět, 27.4.04, (from the ZDN Information Service - Health and Medicine)
(Article extract)

The team led by the Czech doctor Evžen Růžička conducted a study last year on patients with Parkinson's disease. Six hundred of them sent an anonymous questionnaire. More than three hundred responses returned, with eighty-five patients responding that they had tried marijuana.

"About half of them observed an improvement in their condition, such as a reduction in shaking, a relaxation of muscle hardening, a slowing of the movements or a reduction in unwanted movements," Růžička comments on the results.

The questionnaire was mostly filled out by older people, the average age was 65,7 years. "There's no clear evidence that hemp cures Parkinson's disease, but it's one reason to continue the research," the doctor concluded.

Note: The following study is just such a sequel. The summary of the results can be found in the discussion.

Study: Parkinson's syndrome and hemp: quantitative analysis of 11-nor-delta-9-THC acid in patients' urine.

Autoren: Venderová Kateřina, Růžička Evžen, Voříšek Viktor, Višňovský Peter, Department of Pharmacology and Toxicology, Faculty of Pharmacy of Charles University, Hradec Králové, Neurological Clinic of 1. Faculty of Medicine of the Charles University and General University Clinic, Prague, Department of Clinical Toxicology and Mass Spectrometry, Institute of Clinical Biochemistry and Diagnostics, University Hospital in Hradec Králové


From the results of the previous questionnaire study it appears that taking small doses of hemp improves the symptoms of PS, especially bradykinesis. This improvement has been described significantly more frequently by patients who took hemp for a longer period of time (at least 3 months). To demonstrate that our patients are actually taking hemp, we have a quantitative analysis of 8-nor-delta-11-tetrahydrocannabinoleic acid (9-nor-delta-11-THCOOH) in selected patients (n = 9) by GC / MS performed in a urine sample (based on observation of m / z 371 as a selected substance for the purpose of quantification after silylation of the original molecule 11-nor-delta-9-THCOOH using the separation on the THC II screen as described previously Extraction of cannabinoids using SPEC C-18-I cartridges).

All samples tested were positive. All regular cannabis users measured 11-nor-delta-9-THCOOH in urine greater than 60 ng / ml (n = 3) showed improvement in bradykinesis, 2 improved rigidity, and both dyskinesia suffering patients alleviated this complication. One of the patients even stated that taking hemp allowed him to reduce the dosage of levodopa. On the other hand, a patient who ingested hemp irregularly did not experience improvement, although he was found to have the second highest level of 11-nor-delta-9-THCOOH in the urine (132,3 ng / ml). These results support our hypothesis that the long-term and regular use of cannabinoids is important for alleviating the symptoms.

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Introduction: Parkinson's syndrome and hemp

Common cannabis (cannabis sativa) is the main representative of cannabis plants (cannabaceae). This family is characterized by the content of substances with terpenoid structure called cannabinoids. The best-known herbal cannabinoid is Delta-9-tetrahydrocannabinol, which is also responsible for most of the psychoactive effects of this plant. These and other effects of cannabinoids are produced by the activation of the specific so-called cannabinoid receptors. These are classic receptors coupled with G protein.

So far, two types of cannabinoid receptors have been described. While the cannabinoid receptors CB1 are localized in the CNS (especially in the basal ganglia, cortex, cerebellum, and hippocampus areas) and peripheries (eg, in the gastrointestinal tract), the CB2 receptors are located on the cells of the immune system. For these receptors, there are natural ligands in the body called endocannabinoids. Although new potential endocannabinoids are being discovered, only anandamide (N- (2-hydroxyethyl) arachidonamide), 2-arachidonoylglycerol (glycerol-O-arachidonate) and noladin ether (ethers of glycerol arachidonate) have so far been recognized.

With regard to the density of CB1 receptors and the concentration of endocannabinoids in some structures of the CNS, not only the physiological role of the cannabinoid system is considered, eg mobility control, coordination of movements and processes of learning and memory, but also often also on the possible contribution of this system to the pathophysiology of some neurological and psychiatric disorders, and thus to the potential use of these substances, which intervene at the level of the cannabinoid system, in pharmacotherapy.

One of these disorders is Parkinson's syndrome (PS) and dyskinetic damage caused by anti-Parkinsonian therapy (1,2). From the results of our previous questionnaire study, it seems that taking small doses of hemp improves symptoms of PS, especially bradykinesis. According to the patients' claims, there was an improvement on average after 1,7 months (3).

In order to prove that our patients are actually taking hemp, we have made a quantitative determination of the main metabolite Delta-9-THC, 11-nor-delta-9-tetrahydrocannabinoleic acid (11-nor-delta-9-THCOOH) in selected patients. performed in a urine sample.

Methodology: Parkinson's syndrome and hemp

Patients from Prague, Hradec Králové and the surrounding area were included in the test group, who in the questionnaire showed an interest in further cooperation, often taking hemp, signing the enlightened consent and being sufficiently mobile (n = 8). First we performed a preliminary enzymoimmunochemical screening (EMIT II plus cannabinoid assay, Dade Behring, USA) and then a quantitative analysis of the urine by GC / MS (ion trap spectrometry Magnum, ThermoFinnigan, capillary column DB1ms (30m; 0,25 mm; 0,25 mm JW Scientific-Agilent, USA) based on the observation of m / z 371 as a selected substance for the purpose of quantification after silylation of the original molecule 11-nor-delta-9-THCOOH using separation on the THC II screen silicatic agent: bis (trimethylsilyl) trifluoroacetamide + trimethylchlorosilane 99: 1; standards: Drugs of abuse control S1, S2 and S3 (Bio-Rad) For the extraction of cannabinoids we used SPEC-C-18-I Cartridges (Ansys, Inc., USA) and a vacuum extractor Supelco Visiprep 24.

Results: Parkinson's syndrome and hemp

All samples tested were positive (see table). All patients who regularly used hemp and measured levels of 11-nor-delta-9-THCOOH in urine greater than 60 ng / ml (n = 3) showed improvement in bradykinesis. By contrast, in the subgroup of patients with lower concentrations of this urinary metabolite, only one such improvement occurred (P <0,05). One of the patients even stated that taking hemp allowed him to reduce the dosage of levodopa. It is interesting to note that a patient who did not regularly take hemp (but ingested one day before taking it) did not experience any change in symptoms or dyskinesia during use, even though he had the second highest concentration of 11. nor-delta-9-THCOOH was found in urine (132,3 ng / ml).

Discussion: Parkinson's syndrome and hemp

These results are consistent with the results obtained from the questionnaire part of the study. It seems, therefore, that cannabinoids have a positive effect on bradykinesis in particular, and that regular, long-term use of hemp is important for influencing the symptoms of PS. There are several possible explanations for this finding. According to an experiment in healthy rats, the influence of delta-9-THC on mobility depends on the dose used: low doses tend to dampen locomotor activity, higher ones stimulate it, but after very high doses catalepsy follows (4) ,

Given that cannabinoids are highly lipophilic substances with a few days elimination half-life (5-6), the later onset of action in this case can be attributed to the gradual accumulation of doses in the organism. Further possible explanations include regulation of expression of mRNA for the CB1 receptor (7), a change in the coupling of the CB1 receptor (8) or its desensitization (9) due to a long-term application of low hemp doses.

Although it appears that the improvement of some symptoms (especially bradykinesis) in regular users is related to the level of the main metabolite delta-9-THC in the urine, we must also consider the effects of other herbal cannabinoids, namely the effects of delta -9-THC itself change significantly (10, 11). An example may be cannabidiol, which indirectly affects the CB receptors by inhibiting the reuptake and degradation of anandamide. Cannabidiol also activates the vanilloid receptors (VR1), which are also found in the basal ganglia and appear to play a role in the control of mobility (12, 13).
Supported by CEZ Grant: J13 / 98: 11600004

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Literature:
1. Sieradzan KA, Fox SH, Hill M, Dick JP, Crossman AR, Brotchie JM. Cannabinoids reduce levodopa-induced dyskinesia in Parkinson's disease: a pilot study. Neurology 2001; 57: 2108 2111.
2. Breadchiech JM. Adjunct to dopamine replacement: a pragmatic approach to reducing the problem of dyskinesia in Parkinson's disease. Mov Disord 1998; 13: 871 876.
3. Venderová K, Růžička E, Višňovský P. Cannabis and Parkinson's disease: subjective improvement of symptoms and drug-induced dyskinesias. Mov Dis 2002; 17 (Suppl.5): S77.
4. Sanudo-Pena MC, Romero J, Seale GE, Fernandez-Ruiz JJ, Walker JM. Activational role of cannabinoids on movement. Eur J Pharmacol 2000; 391: 269 274.
5. Johansson E, Agurell S, Hollister LE, Halldin MM. Prolonged apparent half-life of delta-1-tetrahydrocannabinol in plasma of chronic marijuana users. J Pharm Pharmacol 1988; 40: 374-375.
6. Consroe P, Kennedy K, Schram K. Assay of plasma cannabidiol by capillary gas chromatography / ion trap mass spectroscopy following high-dose daily oral administration in humans. Pharmacol Biochem Behav 1991; 40: 517 522.
7. Zhuang S, Kittler J, Grigorenko EV et al. Effects of long-term exposure to delta9-THC on expression of cannabinoid receptor (CB1) mRNA in different rat brain regions. Brain Res Mol Brain Res 1998; 62: 141 149.
8. Romero J, Garcia L, Fernandez-Ruiz JJ, Cebeira M, Ramos JA. Changes in rat brain cannabinoid binding sites after acute or chronic exposure to their endogenous agonist, anandamide, or to delta-9-tetrhydrocannabinol. Pharmacol Biochem Behav 1995; 51: 731 737.
9. Sim LJ, Hampson RE, Deadwyler SA, Childers SR. Effects of chronic treatment with delta9-tetrhydrocannabinol on cannabinoid-stimulated [35S] GTPgammaS autoradiography in rat brain. J Neurosci 1996; 16: 8057 8066.
10. Formukong EA, Evans AT, Evans FJ. Inhibition of the cataleptic effect of tetrahydrocannabinol by other constituents of Cannabis sativa L. J Pharm Pharmacol 1988; 40: 132 134.
11. Bornheim LM, Kim KY, Li J, Perotti BY, Benet LZ. Effect of cannabidiol pretreatment on the kinetics of tetrahydrocannabinol metabolites in mouse brain. Drug Metab Dispos 1995; 23: 825 831.
12. Mezey E, Toth ZE, Cortright DN et al. Distribution of mRNA for vanilloid receptor subtype 1 (VR1), and VR1-like immunoreactivity, in the central nervous system of the rat and human. PNAS 2000; 97: 3655 3660.
13. Di Marzo V, Lastres-Becker I, Bisogno T et al. Hypolocomotor effects in capsaicin and two long chain capsaicin homologues. European Journal of Pharmacology 2001; 420: 123 131.

Source: www.tigis.cz

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