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Introduction: Changes in human behaviour and lifestyle over the last century have resulted in a dramatic increase in the incidence of diabetes worldwide. Neuropathy is a common and costly complication of both type 1 and type 2 diabetes. The prevalence of neuropathy is estimated to be about 8% in newly diagnosed patients and greater than 50% in patients with long-standing disease. There are two main types of diabetic neuropathies, named as sensorimotor and autonomic neuropathies. Sensorimotor neuropathy is marked by pain, paraesthesia and sensory loss, and autonomic neuropathy may contribute to myocardial infarction, malignant arrhythmia and sudden death. Methods: In this article we reviewed the pathogenesis, clinical manifestations diagnosis and treatment of diabetic neuropathies. Conclusion: Sensorimotor and autonomic neuropathies (cardiovascular, gastrointestinal and genitourinary autonomic neuropathies) are common in diabetic patients. Apart from strict glycaemic control, no further therapeutic approach exists in the prevention of this phenomenon. Intensive diabetes therapy, intensive multifactorial cardiovascular risk reduction and lifestyle intervention are recommended in patients with cardiovascular autonomic neuropathy. Gastroparesis is the most debilitating complication of gastrointestinal autonomic neuropathy and genitourinary autonomic neuropathy can cause sexual dysfunction and neurogenic bladder; these conditions are hard to manage. The symptomatic treatment of sensory symptoms includes tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors, gabapentin, pregabalin and opioids. Other treatment strategies are not so effective.

This longitudinal MRI study found clinically silent brain white matter hyperintensities to be predominantly progressive in nature. The absence of a control group precludes definitive conclusions about the nature of these changes or if their degree is beyond normal aging.

Sleep problems are one of the most common non-motor symptoms of Parkinson's disease (PD). The Parkinson's disease Sleep Scale 2 nd version (PDSS-2) was published in 2011 showing satisfactory clinimetric results. We performed an independent testing of the scale adding further information on its clinimetric properties.In this nationwide study 537 PD patients were enrolled. Besides PDSS-2, we assessed Patient's Global Impression-Severity (PGI) scale on sleep disturbances, Non-motor Symptoms Scale and MDS-UPDRS.Following the Classical Theory of Tests we performed descriptive data analysis, factor analysis, reliability, validity and precision measurements. Subsequently, we evaluated cut-off value for detecting clinically meaningful sleep problems based on receiver operating characteristics analysis.Based on the PGI scale, 161 patients (30.0%) did not reported any sleep problems. Factor analysis revealed almost the same factor structure described by the original PDSS-2 validation study. Cronbach's alpha was 0.863 and all item had good item-total correlation. PDSS-2 demonstrated high convergent validity with Non-Motor Symptoms Scale and Clinical Global Impression-Severity and non-motor part of MDS-UPDRS, and divergent validity with age, gender, education-level, disease-duration and Hoehn-Yahr Stages.Presence of sleep problems was identified by scores >10.5 points on PDSS-2 (sensitivity: 85.3%, specificity: 60.8%, diagnostic accuracy: 78.1%); whereas scores >19.5 points indicated marked sleep-related problems (specificity: 68.5%, sensitivity: 78.0%, diagnostic accuracy: 74.3%).Independent and cross-cultural validation of patient reported outcomes is essential to confirm or reject the findings obtained by the developers of the scale. Our results demonstrate that fundamental clinimetric properties of the PDSS-2 are satisfactory.

Abstract.Background: Sleep problems are among the most common non-motor symptoms of Parkinson's disease (PD). The PD Sleep Scale 2nd version (PDSS-2) improved the original PDSS by adding more items on different aspects of sleep problems, making it a more robust tool to evaluate the severity of sleep disturbances. However, previous studies on deep brain stimulation (DBS) have not used the PDSS-2. Objective: To determine if the PDSS-2 could detect improvement reliably in sleep problems after bilateral subthalamic nucleus DBS for PD. Methods: In this prospective study, 25 consecutive patients undergoing DBS implantation were enrolled. Patients were examined twice: 1 week prior to the DBS implantation (baseline) and 12 months postoperatively. Severity of PD symptoms were assessed by the Movement Disorders Society Unified PD Rating Scale (MDS-UPDRS) and the Non-Motor Symptoms Scale (NMSS). Presence and severity of sleep disturbances were specifically measured by PDSS-2. Results: Total score of MDS-UPDRS improved from 81 (median, interquartile-range: 63-103) to 55 points (median, IQR: 46-75, p < 0.001). Health-related quality of life, measured by PDQ-39, also improved from 29 (IQR: 18-40) to 15 (IQR: 9-28) points (p = 0.002). Most domains of NMSS also improved. At baseline 13 patients reported sleep problems, but 1 year after DBS implantation only 3 did (p = 0.012). Although only 6 out of 15 items showed a significant decrease after DBS implantation, the total score of PDSS-2 decreased from 24 (IQR: 17-32) to 10 (IQR: 7-18) points (P < 0.001). Conclusions: Based on our results, PDSS-2 can detect improvements in sleep quality reliably after DBS implantation.