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Background Heart rate variability (HRV) decreases in Parkinson’s disease (PD) and it can be considered a marker for cardiovascular dysautonomia. The purpose of this pilot study is to evaluate long-term time-domain analysis of HRV of PD patients and compare the results with those of matched healthy individuals. Methods Idiopathic PD patients without comorbidity impairing HRV, and age-matched healthy individuals were recruited in a pilot study. A long-term time domain analysis of HRV using 24-h ambulatory ECG was performed. Results Overall, 18 PD patients fulfilling inclusion criteria completed the evaluation (mean age was 55.6 ± 8.8, disease duration: 5.0 ± 4.7). Mean SCOPA-AUT score was 10.1 ± 7.3. Patients were on Hoehn & Yahr stage 1–2 and mean Levodopa Equivalent Dose (LED) was 311 ± 239.9. Mean of the 5-min standard deviation (SD) of R-R intervals distribution (SDNN) for all 5 min segments of the entire recording (ISDNN) was significantly lower in patients compared to controls. ISDNN was significantly different between Parkinson’s disease patients and healthy controls. Conclusions In our population characterized by mild to moderate disease severity, time-domain assessment of HRV seemed to be a potential tool to characterize cardiovascular dysautonomia. Decrease of ISDNN in PD may reflect an autonomic derangement extending all day and night long.

Background Autonomic nervous system dysfunction, common in patients with Parkinson’s disease (PD), causes significant morbidity and it is correlated with poor quality of life. To assess frequency of urinary symptoms in patients with PD, without conditions known to interfere with urinary function. Methods Non-demented PD patients were consecutively enrolled from the outpatients clinic of our department. Scales investigating motor and non-motor symptoms were carried out. Evaluation of urinary dysfunctions was carried out using the AUTonomic Scale for Outcomes in Parkinson’s disease (SCOPA-AUT) questionnaire. Patients underwent noninvasive urological studies (nUS), including uroflowmetry and ultrasound of the urinary tract. Results Forty-eight (20 women, 42%) out of 187 PD patients met the inclusion criteria and were enrolled in the study. Mean SCOPA-AUT score was 14.1 ± 6.9 (urinary symptoms subscore 5.2 ± 3.8). Among those evaluated by the SCOPA-AUT scale, the urinary symptoms were among the most common complaints (93.8%). At nUS mean maximum flow rate (Qmax) was 17.9 ± 9.1 ml/s, and mean postvoid residual (PVR) urine volume was 24.4 ± 44.1 ml. Ultrasound investigation documented prostate hypertrophy in 12 male patients (42.8%). Urinary items of the SCOPA-AUT (SCOPA-U subscore) correlated with measures of disease severity only in female patients. Conclusion Urinary symptoms and abnormal findings in nUS are common in PD. Though nigrostriatal degeneration might be responsible for urinary symptoms also in the early-intermediate stage of the disease, when urinary dysfunction occurs other medical conditions need to be excluded.

Background: Autonomic symptoms and sleep disorders are common non-motor symptoms of Parkinson disease (PD), which are correlated with poor quality of life for patients. Purpose: To assess the frequency of autonomic symptoms in a consecutive series of PD patients and to correlate them with other motor and non-motor symptoms. Methods: All consecutive non-demented PD patients who underwent an extensive evaluation including Hoehn and Yahr staging, Unified Parkinson’s Disease Rating Scale, Beck’s Depression Inventory, Neuropsychiatric Inventory, PDQ-39 Scale, the Parkinson’s diseases Sleep Scale, the Epworth Sleepiness Scale and SCOPA-AUT scale were enrolled. Comorbidity has been also considered. Supine to standing position blood pressure and cardiac frequency changes were also measured. Results: 135 PD patients were included (mean age at interview 67.7; mean disease duration: 5.3 years). Patients were stratified according to mean SCOPA-AUT scale score (13.1). Those with higher SCOPA-AUT scale score were significantly older, had longer disease duration, worse disease stage, worse quality of sleep, were more severely affected, and were also taking a higher dosage of levodopa. At multivariate analysis, older age, longer disease duration, and worse quality of sleep were independently associated with higher SCOPA-AUT scale scores. Conclusions: Our results remark the role of autonomic symptoms in PD. In our patient population, characterized by mild to moderate disease severity, most of the patients complained of autonomic nervous system involvement (84 %). A significant association between autonomic symptoms and sleep disorders was also observed.

Dear Editor, We have read with interest comments by Solla et al. [1] regarding our Letter to the Editor published in NeurologicalSciences titled ‘‘Insidious onset of Pisa Syndrome afterrasagiline therapy in a patient with Parkinson’s Disease’’[2]. We thank the authors for their interest in our paper, but we think it is necessary to make some clarifications regarding the temporal relationship between the onset of Pisa Syndrome (PS) and rasagiline therapy. PS occurred in fact after and not before rasagiline treatment as stated by Solla et al. In particular, PS occurred after a time interval of 6–12 months and anyway after rasagiline was added to patient’s therapy. This long time interval is one of the elements that makes the case interesting (time period longer than previously described). Temporal relationship is fundamental for the interpretation of clinical and electrophysiological findings in our case. Rasagiline is an inhibitor of monoamine oxidase type B, and although different mechanisms of action have been advocated, its effect is primarily dopamine mediated [3]. This means that occurrence of Pisa syndrome in our case was likely related not only to the specific mechanisms of action of the drug but also to increased dopamine extracellular levels at the striatal synapses, and thus to the total dopamine agonism load. To conclude, though it is likely that concomitant use of other antiparkinsonian drugs could have contributed to the onset of PS in our patient, it is noteworthy that PS was not evident before rasagiline was started, it became evident after rasagiline was initiated, and it was not anymore evident after rasagiline was stopped.

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