Background
Insomnia is one of the most common nonmotor features of Parkinson's disease (PD). However, there are few practical guidelines for providers on how to best evaluate and treat this problem.
Methods and Findings
This review was developed to provide clinicians with a pragmatic approach to assessing and managing insomnia in PD. Recommendations were based on literature review and expert opinion. We addressed the following topics in this review: prevalence of insomnia in PD, sleep–wake mechanisms, theoretical models of insomnia, risk factors, assessment, pharmacologic and nonpharmacologic treatments. Insomnia treatment choices may be guided by PD severity, comorbidities, and patient preference. However, there is limited evidence supporting pharmacotherapy and nonpharmacologic treatments of insomnia in PD.
Conclusions
We provide a pragmatic algorithm for evaluating and treating insomnia in PD based on the literature and our clinical experience. We propose personalized insomnia treatment approaches based on age and other issues. Gaps in the existing literature and future directions in the treatment of insomnia in PD are also highlighted.
Introduction
Sleep-related breathing disorders are common after TBI. To date, two single site studies have reported divergent findings in post-TBI patients with one reporting predominantly obstructive sleep apnea (OSA, Holcomb et al., 2016) and the other central sleep apnea (CSA, Webster and Bell, 1998). The purpose of this analysis is to explore prevalence, demographics, and injury characteristics of patients with a clinical diagnosis of CSA in a recently-completed multicenter comparative-effectiveness trial during inpatient rehabilitation following moderate to severe TBI.
Methods
Participants in a six-center diagnostic comparative effectiveness trial underwent Level-1 polysomnography (PSG) during inpatient rehabilitation for TBI. Studies were scored at a centralized scoring center by one of two certified PSG technicians with final interpretation by a board-certified sleep medicine physician.
Results
21 of 248 (8.5%) participants evidenced elevated CSA indices >5. Predominant CSA was rare (n=3 [1.2%], age range: 36-59; 100% male; 33-52 days post-TBI). One participant was on opioid, anti-depressant and antiepileptic drugs, one was on an antiepileptic, and another was on an opioid. PAP therapy was not initiated during PSG thus there was no treatment-emergent CSA. All had a central apnea-hypopnea index (AHI) in the moderate to severe range (29-49). Two out of the three had a GCS <8 and one participant had a GCS of 14.
Conclusion
In this multi-center clinical trial, predominant CSA was rare. The common practice of reducing polypharmacy in order to minimize sedation and optimize mental status in specialized inpatient brain-injury rehabilitation programs may contribute to the low CSA incidence in this cohort. Attention to medication side-effects and their influence on sleep-related breathing should be routinely considered.
Support
PCORI (CER-1511-33005), GDHS (W91YTZ-13-C-0015) for DVBIC, NIDILRR (90DPTB0008-03-00; 90DPTB0013-01-00).
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