Recreational physical activity and risk of Parkinson's disease

The purpose of this study was to investigate associations between recreational physical activity and Parkinson's disease (PD) risk. We prospectively followed 143,325 participants in the Cancer Prevention Study II Nutrition Cohort from 1992 to 2001 (mean age at baseline = 63). Recreational physical activity was estimated at baseline from the reported number of hours per week on average spent performing light intensity activities (walking, dancing) and moderate to vigorous intensity activities (jogging/running, lap swimming, tennis/racquetball, bicycling/stationary bike, aerobics/calisthenics). Incident cases of PD (n = 413) were confirmed by treating physicians and medical record review. Relative risks (RR) were estimated using proportional hazards models, adjusting for age, gender, smoking, and other risk factors. Risk of PD declined in the highest categories of baseline recreational activity. The RR comparing the highest category of total recreational activity (men ≥ 23 metabolic equivalent task‐hours/week [MET‐h/wk], women ≥ 18.5 MET‐h/wk) to no activity was 0.8 (95% CI: 0.6, 1.2; P trend = 0.07). When light activity and moderate to vigorous activity were examined separately, only the latter was found to be associated with PD risk. The RR comparing the highest category of moderate to vigorous activity (men ≥ 16 MET‐h/wk, women ≥ 11.5 MET‐h/wk) to the lowest (0 MET‐h/wk) was 0.6 (95% CI: 0.4, 1.0; P trend = 0.02). These results did not differ significantly by gender. The results were similar when we excluded cases with symptom onset in the first 4 years of follow‐up. Our results may be explained either by a reduction in PD risk through moderate to vigorous activity, or by decreased baseline recreational activity due to preclinical PD. © 2007 Movement Disorder Society     

Passive mechanical properties and related proteins change with botulinum neurotoxin A injection of normal skeletal muscle

The effects of botulinum neurotoxin A on the passive mechanical properties of skeletal muscle have not been investigated, but may have significant impact in the treatment of neuromuscular disorders including spasticity. Single fiber and fiber bundle passive mechanical testing was performed on rat muscles treated with botulinum neurotoxin A. Myosin heavy chain and titin composition of single fibers was determined by gel electrophoresis. Muscle collagen content was determined using a hydroxyproline assay. Neurotoxin‐treated single fiber passive elastic modulus was reduced compared to control fibers (53.00 kPa vs. 63.43 kPa). Fiber stiffness and slack sarcomere length were also reduced compared to control fibers and myosin heavy chain composition shifted from faster to slower isoforms. Average titin molecular weight increased 1.77% after treatment. Fiber bundle passive elastic modulus increased following treatment (168.83 kPa vs. 75.14 kPa). Bundle stiffness also increased while collagen content per mass of muscle tissue increased 38%. Injection of botulinum neurotoxin A produces an effect on the passive mechanical properties of normal muscle that is opposite to the changes observed in spastic muscles. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:497–502, 2012     

The partial positive allosteric GABAA receptor modulator EVT 201 is efficacious and safe in the treatment of adult primary insomnia patients

Objective: To evaluate polysomnographic (PSG) and self-reported measures of the efficacy and safety of EVT 201 in patients with primary insomnia.Patients and methods: Following clinical and PSG screening, 75 patients (mean age: 45.1 ± 11.2y; 50f, 25m) meeting DSM-IV criteria for primary insomnia entered this crossover study and were randomly assigned to double-blind treatment sequences of 1.5 mg or 2.5 mg EVT 201, or placebo using a balanced Latin square design. For each study condition study medication was administered on two consecutive nights and PSG and self-reported data were collected. Safety assessments included physical examination, clinical laboratory measures, electrocardiogram, documentation of adverse events, and the digit symbol substitution test (DSST) and self-reported sleepiness/alertness ratings to detect residual sedation. Data were collected at five US sleep laboratories. Efficacy analyses were performed for the 67 patients completing the study. Safety analyses included all 75 randomized patients.Results: On PSG measures compared to placebo, EVT 201 1.5 mg and 2.5 mg increased total sleep time (TST; 33.1, 45.0 min; both p < 0.0001), reduced wake after sleep onset (WASO; −16.7, −25.7 min; both p < 0.0001), reduced latency to persistent sleep (LPS; −17.0, −20.7 min; both p < 0.0001), and reduced the number of awakenings (−1.2, −2.6; both p < 0.0001). Significant reduction of wake time was seen with 1.5 mg during each of the first three quarters of the night (p < 0.0001–0.002), and with 2.5 mg in all four quarters (p < 0.0001–0.0005). Both doses also improved all key self-reported measures of sleep including total sleep time (rTST; 51.9, 51.1 min; both p < 0.0001), wake after sleep onset (rWASO; −29.3, −29.6 min; both p < 0.0001), sleep latency (rSL; −24.0 min, p < 0.004; −25.1 min, p < 0.0002), and number of awakenings (rNAW; −1.1, −1.2; both p < 0.0001). Sleep quality was also improved by both doses. Self-rated sleepiness in the morning did not differ from placebo for either dose; however, there was a small negative effect on the DSST for both doses. Both doses had similar effects on sleep architecture including an increase in Stage 2 sleep and REM latency and a small, but significant decrease in REM (REM −5.7, −8.3 min; p = 0.0175, p = 0.0006). No effect on other sleep architecture parameters, including SWS, was seen. EVT 201 was well tolerated. No serious or unexpected adverse events were reported.Conclusion: This first study of EVT 201 in adult patients with primary insomnia demonstrated improved measures of sleep onset and sleep maintenance, including during the third and fourth quarters of the night. Adverse events were infrequent and all were mild to moderate in severity.     

Hemostatic technique for internal mammary artery anastomotic bleeding

When internal mammary artery is used for myocardial revascularization, a not uncommon occurrence is intraoperative bleeding from the internal mammary artery to coronary artery anastomosis. The conventional method of hemostasis of placing additional sutures across the suture line may produce anastomotic stenosis or may aggravate the bleeding by producing tears, especially as these additional sutures are placed on a beating heart. We describe a simple technique by which hemostasis can be achieved without the risk of anastomotic stenosis or aggravation of the bleeding, as it avoids placing sutures over the anastomotic suture line.     

Muscle dysfunction in male hypogonadism

Twenty-eight consecutive male patients with primary and secondary hypogonadism (14 each) were evaluated clinically and electrophysiologically for muscle dysfunction. Although generalised muscle weakness was initially reported by only 9 patients, on direct questioning, it was recorded in 19. Objective weakness was found in 13 patients and it involved both the proximal and distal limb muscles. Quantitative electromyography showed evidence of myopathy in the proximal muscle in 25 patients, i.e., reduced MUP duration and amplitude with increased polyphasia in the deltoid and the gluteus maximus. There were no denervation potentials. None of the patients showed clinical neuropathy or NCV abnormalities. Thus, the profile of muscle involvement in hypogonadism closely simulates limb-girdle muscular dystrophy and other endocrine myopathies. The incidence of muscle involvement was higher in secondary hypogonadism. Diminished androgens in primary hypogonadism and diminished growth hormone in the secondary hypogonadism are probably responsible for the myopathy.     

Sickle cell trait and stroke in the young adult

Two young patients with sickle cell trait (AS haemaglobinopathy) and ischaemic stroke are reported. The stroke involved the internal carotid artery territory in one and the brainstem in the other. A review of the literature is presented to suggest that the association of sickle cell trait and cerebral infarction is more than coincidental. Haemoglobin electrophoresis should be undertaken routinely in young subjects with ischaemic stroke.