Postural tachycardia syndrome (PoTS) is a poorly understood but important cause of orthostatic intolerance resulting from cardiovascular autonomic dysfunction. PoTS is distinct from the syndromes of autonomic failure usually associated with orthostatic hypotension, such as pure autonomic failure and multiple system atrophy. Individuals affected by PoTS are mainly young (aged between 15 years and 40 years) and predominantly female. The symptoms--palpitations, dizziness and occasionally syncope--mainly occur when the patient is standing upright, and are often relieved by sitting or lying flat. Common stimuli in daily life, such as modest exertion, food ingestion and heat, are now recognized to be capable of exacerbating the symptoms. Onset of the syndrome can be linked to infection, trauma, surgery or stress. PoTS can be associated with various other disorders; in particular, joint hypermobility syndrome (also known as Ehlers-Danlos syndrome hypermobility type, formerly termed Ehlers-Danlos syndrome type III). This Review describes the characteristics and neuroepidemiology of PoTS, and outlines possible pathophysiological mechanisms of this syndrome, as well as current and investigational treatments.

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Many factors influence the outcome of head-up tilt (HUT) test leading to wide variability in sensitivity, specificity and reproducibility of this investigation [1]. Here, we report on an unexpectedly increased proportion of positive HUT test results associated with a change in Autonomic laboratory site and use of a new tilt table. HUT test protocol with pharmacologic provocation is used at our laboratory and did not change after moving. It consists of 5-min supine rest, followed by 30 min of passive 60°HUT, sublingual administration of 0.5 mg of glyceryl trinitrate while tilted up and further 15 min of 60°H UT. A positive outcome is defined as development of presyncopal symptoms or disturbance of consciousness associated with a drop in blood pressure, upon which the patient is tilted down. When the test is terminated on the patients' request due to nonspecific symptoms, the test is categorised as non-interpretable.Tilt tables in both the old and the new laboratory have footplate support. In the old laboratory patients' arms were held at the side of the body, blood pressure was measured with an arm sphygmomanometer at 2-min intervals, ECG and breathing were monitored continuously. Tilt table was lifted and lowered manually in approximately 2 s. In the new laboratory, left arm is held outstretched at heart level, supported on a soft pad. Beat-to-beat blood pressure is measured using TaskForce monitor (CN Systems, Austria), ECG and breathing are monitored continuously. The new electrically driven table is lifted and lowered in 16 s. Temperature and humidity of both investigation rooms are kept within the same limits, both rooms have windows and a waiting room with chairs. Tests are performed by the same two technicians and evaluated by the same physicians.All together, 550 cases were included in the basic analysis: 75 consecutive HUT results from the first May 2008 and 200 from the first September 2008 onward (old laboratory group) and the same number from corresponding periods in 2009 (new laboratory group). Demographic data, test outcomes, blood pressure and heart rate (HR) changes were compared between the groups. For the evaluation of asystole rates, 865 consecutive tests were reviewed from each laboratory.Average age was similar in both groups (51.0 ± 19.0 years in the old and 50.0 ± 16.8 years in the new laboratory, p [ 0.05), so were the proportion of men (36.0 and 38.7%, respectively) and blood pressure values at 2-min intervals. Proportion of positive results was significantly higher in the new laboratory group in both the unmedicated phase and after pharmacologic provocation (p \ 0.001, Fig. 1). Resting supine HR (69.9 ± 19.0 and 68.3 ± 11.6 beats/min) and average HR increase from baseline to second minute of HUT (12.6 ± 7.5 and 11.8 ± 10.2 beats/min) did not differ between groups (p [ 0.05). In contrast, HR increase in the tenth minute of HUT was lower in the old laboratory group (10.3 ± 8.7 beats/min) than in the new laboratory group (13.3 ± 11.7 beats/min, p = 0.001). In the extended sample of 865 case...

Background: Based on the promising results from preclinical studies, bee venom has been investigated as a neuroprotective agent in Parkinson's disease. Objective: To assess if longstanding exposure to bee venom is associated with decreased risk for Parkinson's disease among beekeepers. Methods: Questionnaire gathering information about diagnosis of Parkinson's disease and exposure to bee stings was posted to 6500 members of Slovenian beekeepers' organisation.Results: We received 1298 responses (response rate 20.1%). Twenty beekeepers, all older than 60 years, were diagnosed with Parkinson's disease. The prevalence of Parkinson's disease in beekeepers aged ≥60 years was 3.9%, which is above the reported 0.6-1.3% prevalence of PD in this age group in European population. There was no difference in parameters reflecting bee venom exposure between beekeepers with and without Parkinson's disease. Conclusions: Continuous exposure to bee venom does not affect neurodegeneration to the extent where it could prevent the expression of Parkinson's disease.