Interactive mobile application for Parkinson's disease deep brain stimulation (MAP DBS): An open-label, multicenter, randomized, controlled clinical trial.

INTRODUCTION: Deep brain stimulation (DBS) is an effective treatment for Parkinson's disease (PD), but its efficacy is tied to DBS programming, which is often time consuming and burdensome for patients, caregivers, and clinicians. Our aim is to test whether the Mobile Application for PD DBS (MAP DBS), a clinical decision support system, can improve programming. METHODS: We conducted an open-label, 1:1 randomized, controlled, multicenter clinical trial comparing six months of SOC standard of care (SOC) to six months of MAP DBS-aided programming. We enrolled patients between 30 and 80 years old who received DBS to treat idiopathic PD at six expert centers across the United States. The primary outcome was time spent DBS programming and secondary outcomes measured changes in motor symptoms, caregiver strain and medication requirements. RESULTS: We found a significant reduction in initial visit time (SOC: 43.8 ± 28.9 min n = 37, MAP DBS: 27.4 ± 13.0 min n = 35, p = 0.001). We did not find a significant difference in total programming time between the groups over the 6-month study duration. MAP DBS-aided patients experienced a significantly larger reduction in UPDRS III on-medication scores (-7.0 ± 7.9) compared to SOC (-2.7 ± 6.9, p = 0.01) at six months. CONCLUSION: MAP DBS was well tolerated and improves key aspects of DBS programming time and clinical efficacy.

Telepsychiatry for patients with movement disorders: a feasibility and patient satisfaction study.

BACKGROUND: Telemedicine is a convenient health service delivery modality for patients with movement disorders, including Parkinson's disease (PD), but is currently underutilized in the management of associated psychiatric symptoms. This study explored the feasibility of and patient satisfaction with telepsychiatry services at an academic movement disorders center. METHODS: All patients seen by telepsychiatry between January and December 2017 at the UCSF Movement Disorders and Neuromodulation Center were invited to participate. Participation was voluntary. Patients received an initial survey after the first telepsychiatry visit and satisfaction surveys after each visit. Survey responses were collected online via Research Electronic Data Capture (REDCap). Frequencies were calculated for categorical variables, and means and standard deviations were generated for continuous variables. RESULTS: Thirty-three patients (79% with PD; 72% Medicare recipients; 64% men; mean age, 61.1 ± 10.5 years; mean distance to clinic, 79.9 ± 81.3 miles) completed a total of 119 telepsychiatry and 62 in-person visits. Twenty-two initial surveys and 50 satisfaction surveys (from 21 patients) were collected. Patients were very satisfied with the care (95%), convenience (100%), comfort (95%), and overall visit (95%). Technical quality was somewhat lower rated, with 76% patients reporting they were very satisfied, while 19% were satisfied. All patients would recommend telemedicine to friends or family members. CONCLUSIONS: Telepsychiatry is a feasible option for patients with movement disorders, leading to high patient satisfaction and improved access to care. Technical aspects still need optimization. Whenever available, telepsychiatry can be considered in addition to in-person visits. Future studies with larger samples should explore its impact on patient care outcomes and caregiver burden.

TRPA1 contributes to cold hypersensitivity.

TRPA1 is a nonselective cation channel expressed by nociceptors. Although it is widely accepted that TRPA1 serves as a broad irritancy receptor for a variety of reactive chemicals, its role in cold sensation remains controversial. Here, we demonstrate that mild cooling markedly increases agonist-evoked rat TRPA1 currents. In the absence of an agonist, even noxious cold only increases current amplitude slightly. These results suggest that TRPA1 is a key mediator of cold hypersensitivity in pathological conditions in which reactive oxygen species and proinflammatory activators of the channel are present, but likely plays a comparatively minor role in acute cold sensation. Supporting this, cold hypersensitivity can be induced in wild-type but not Trpa1(-/-) mice by subcutaneous administration of a TRPA1 agonist. Furthermore, the selective TRPA1 antagonist HC-030031 [2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide] reduces cold hypersensitivity in rodent models of inflammatory and neuropathic pain.