The use of AT is common in patients with PD. The age at onset of PD is the most potent predictor of AT use. There is no association between the use of AT and the severity of PD. The widespread and largely unexamined use of AT for PD requires more attention. This should be directed at testing their safety and efficacy and improving physician and patient knowledge about the potential benefits, costs, limitations, and risks of AT.

Cardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.

Background and Purpose-Vasospasm after aneurysmal subarachnoid hemorrhage (SAH) remains a leading cause of death and disability after aneurysm rupture. Decreased availability of nitric oxide (NO) may be crucial in its pathogenesis. We hypothesized that endothelial NO synthase (eNOS) polymorphisms may determine susceptibility to vasospasm in SAH patients. Methods-We conducted a prospective cohort study of SAH patients and determined vasospasm by cerebral angiography.We genotyped 3 eNOS polymorphisms: an intron 4 variable-number tandem-repeat, a promoter single-nucleotide polymorphism (Ϫ786T3 C SNP), and a coding SNP in exon 7 (894G3 T encoding E298D). Using multivariable logistic regression, we quantified the association of eNOS polymorphisms in patients with vasospasm confirmed by cerebral angiography. Results-For the eNOS promoter Ϫ786T3 C SNP, the presence of the CC genotype compared with any T genotype (CT or TT) was associated with increased odds of vasospasm (odds ratioϭ2.97, 95% CIϭ1.32 to 6.67, Pϭ0.008). No association with vasospasm was observed for the eNOS 894G3 T or variable-number tandem-repeat polymorphisms. Conclusions-These findings suggest that genetic variation influencing NO regulation contributes to the risk of angiographic vasospasm in patients with SAH. The specific role of the promoter SNP (Ϫ786T3 C) may determine the effect of NO regulated by this pathway, distinct from other known eNOS polymorphisms.