Surprise result in caffeine trial for Parkinson’s patients

By Eleanor McDermid, Senior MedWire Reporter

Caffeine treatment may improve motor symptoms in patients with Parkinson's disease (PD), research suggests.

The randomized, controlled trial was actually designed to assess the effects of caffeine on excessive daytime sleepiness in PD patients. The study failed to support a benefit for caffeine in this indication, however, and motor severity was only a secondary endpoint.

"Nevertheless, these findings are noteworthy, the first to suggest antiparkinsonian effects of caffeine in a randomized clinical trial," says Michael Schwarzschild (Massachusetts General Hospital, Boston, USA) in an editorial accompanying the study in Neurology.

He adds: "Although current data do not warrant a recommendation of caffeine as a therapeutic intervention in PD, they can reasonably be taken into consideration when discussing dietary caffeine use."

The 61 study participants took caffeine 100 mg twice daily for 3 weeks and 200 mg twice daily for another 3 weeks, or matching placebo. Over this period the Unified Parkinson's Disease Rating Scale (UPDRS) score improved by an average of 4.69 points among patients taking caffeine relative to those taking placebo.

Also, the objective motor component improved by 3.15 points, and the effect was evident after 3 weeks of 100 mg caffeine, at which point the motor component had improved by 2.96 points in the caffeine group relative to the placebo group. Caffeine had significant effects on the bradykinesia and rigidity UPDRS subcomponents, without having an adverse effect on tremor, report Ronald Postuma (McGill University, Montreal, Canada) and colleagues.

There was a nonsignificant improvement in somnolence outcomes in the intent-to-treat analysis, with a 1.71-point improvement on the Epworth Sleepiness Scale among patients in the caffeine versus the placebo group. After excluding protocol violations, this became a "modest" although significant 1.97-point improvement.

The beneficial effects of caffeine are thought to occur via adenosine receptor antagonism. Schwarzschild notes that other, more specific adenosine A2A receptor antagonists in development reportedly have antiparkinsonian benefits, but says: "Such benefits should be substantial to offset the unmatchable advantages of caffeine's long-term safety experience and cost."

However, he adds that patients may become tolerant to the motor benefits of caffeine, whereas no study to date has shown such an effect for the specific adenosine A2A receptor antagonists. Ultimately, head-to-head trials may be needed, he concludes.

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