Insidious onset of Pisa syndrome after rasagiline therapy in a patient with Parkinson’s disease

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Insidious onset of Pisa syndrome after rasagiline therapy in a patient with Parkinson’s disease

N.A

Pisa syndrome after rasagiline therapy in a patient with Parkinson’s disease

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

Pisa syndrome after rasagiline therapy in a patient with Parkinson’s disease

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

Vitamin D and Parkinson’s Disease

Vitamin D is a fat-soluble secosteroid, traditionally considered a key regulator of bone metabolism, calcium and phosphorous homeostasis. Its action is made possible through the binding to the vitamin D receptor (VDR), after which it directly and indirectly modulates the expression of thousands of genes. Vitamin D is important for brain development, mature brain activity and associated with many neurological diseases, including Parkinson’s disease (PD). High frequency of vitamin D deficiency in patients with Parkinson’s disease compared to control population was noted nearly twenty years ago. This finding is of interest given vitamin D’s neuroprotective effect, exerted by the action of neurotrophic factors, regulation of nerve growth or through protection against cytotoxicity. Vitamin D deficiency seems to be related to disease severity and disease progression, evaluated by Unified Parkinson’s Disease Rating Scale (UPDRS) and Hoehn and Yahr (H&Y) scale, but not with age of PD onset and duration of disease. Additionally, fall risk has been associated with lower vitamin D levels in PD. However, while the association between vitamin D and motor-symptoms seems to be possible, results of studies investigating the association with non-motor symptoms are conflicting. In addition, very little evidence exists regarding the possibility to use vitamin D supplementation to reduce clinical manifestations and disability in patients with PD. However, considering the positive balance between potential benefits against its limited risks, vitamin D supplementation for PD patients will probably be considered in the near future, if further confirmed in clinical studies

Urological dysfunctions in patients with Parkinson’s disease: clues from clinical and non-invasive urological assessment

Abstract 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