Glycerol infusion rates warrant caution.

We would like to suggest another factor, namely, that of decreased platelet aggregation, which may contribute to their observation. We studied platelet aggregation in 25 newly diagnosed patients with Parkinson's disease and 25 ageand sex-matched controls. None were diabetic, hypertensive, smokers, or on any treatment. Citrated blood was collected by venipuncture and centrifuged at 20Qg for 10 minutes, and the supernatant platelet-rich plasma was obtained. Platelet counts were measured using a platelet counter (Contraves, Switzerland). No patient had a low platelet count. Platelet aggregation was measured by the Born method using a four-channel aggrerecorder (Daiichi-PA 3220, Kyoto, Japan). Adenosine diphosphate (2.5 ^.M/ml), collagen (2.5 /iM/ml), and epinephrine (3 /xMJ ml) were used as inducers. The stock solution was diluted with 0.85% saline. The aggregation was studied at fixed intervals of 5 minutes for collagen and 10 minutes each for adenosine diphosphate and epinephrine. The absorbance was measured as % aggregation. The results were analyzed statistically using Student's 1 test. Platelet aggregation induced by adenosine diphosphate and epinephrine was significantly decreased (32% and 60%, respectively) in Parkinson's disease cases, while collagen-induced aggregation was unchanged. To the best of our knowledge, these findings have not been recorded elsewhere. We hypothesize that decreased platelet aggregation in Parkinson's patients may be a significant contributory factor for the reduced incidence of ischemic stroke.