SAN DIEGO — Patients with Parkinson’s disease who have higher levels of slow-wave, or deep, sleep show significantly higher performance on a variety cognitive measures compared with those who have lower slow-wave sleep levels, despite no differences between the groups’ subjective measures of daytime sleepiness.
“We found that sleep has a significant influence on cognitive performance in Parkinson’s disease,” said first author, Amy W. Amara, MD, from the University of Alabama, Birmingham, in presenting the findings here at the ANA 2017: 48th Annual Meeting of the American Neurological Association.
“These findings suggest that interventions to improve sleep might improve cognitive function as well.”
Sleep dysfunction is common in Parkinson’s disease, resulting from multifactorial causes ranging from nocturnal motor symptoms of the disease to side effects from various drugs.
To take a closer look at the quality of sleep — specifically the role of deep, or slow-wave, sleep, defined as non–rapid eye movement (REM) stage 3 sleep — in cognitive measures in Parkinson’s disease, Dr Amara and her colleagues enrolled 32 patients with Parkinson’s disease. They underwent polysomnography and subsequently were evaluated for sleepiness and psychomotor skills.
The patients were categorized as having high slow-wave sleep, defined as more than 10% of the time in non-REM stage 3, or having low slow-wave sleep, defined as 10% or less time in non-REM stage 3 sleep.
Age, education, and disease severity did not differ between the two groups, but there were more women in the high slow-wave sleep than the low slow-wave sleep group.
Despite the differences in time spent in deep sleep, no differences were seen between the two groups’ subjective measures of daytime sleepiness, assessed on the Epworth Sleepiness Scale, or in their reports of sleep quality, assessed on the Pittsburgh Sleep Quality Index.
There were, however, important differences in neurocognitive measures: Patients with high slow-wave sleep showed significantly faster reciprocal reaction time on the Psychomotor Vigilance Task (P = .04), and they performed significantly better on measures of global cognition, including the Montreal Cognitive Assessment (P = .04), attention/working memory (Stroop color naming: P = .0006; word naming: P = .0025; letter number sequencing: P = .031).
In addition, patients with higher slow-wave sleep had higher scores in executive function (Trails B-A: P = .01; Stroop inhibition: P = .0052), as well as one of the two measures of language (Controlled Oral Word Association: P = .021).
Findings on memory and visuospatial function assessments did not significantly differ between groups, and none of the results changed after controlling for sex.
In an opinion statement published in July in Current Treatment Options in Neurology, Dr Amara and her colleagues further discussed sleep disruption in Parkinson’s disease and the potential treatments.
“While the optimal treatment for insomnia in Parkinson’s disease has not been established, available strategies include cognitive-behavioral therapy, medications with soporific properties, and light therapy,” they wrote.
Safety measures, clonazepam, and melatonin are the mainstays of treatment for REM sleep behavior disorder, while continuous positive-airway pressure is an effective treatment for sleep-disordered breathing in Parkinson’s disease, they said.
Another notable sleep disturbance in Parkinson’s disease is circadian rhythm disturbance.
“Circadian disruption has emerged as an important etiology of impaired sleep-wake cycles in Parkinson’s disease, and circadian-based interventions hold promise for novel treatment approaches,” they said.
The new study adds to the understanding of how Parkinson’s disease is affected by such sleep disturbances, commented Kathleen Poston, MD, associate professor of neurology and neurological sciences and neurosurgery at Stanford University Medical Center, in California, who co-moderated the session.
“Insomnia is a common nonmotor symptom in Parkinson’s disease, which patients often discuss with their physicians,” she told Medscape Medical News.
“This study adds to our understanding of insomnia in Parkinson’s by identifying a specific part of sleep, known as slow-wave-sleep, that seems to be specifically impacted in patients with Parkinson’s disease.”
Dr Poston noted that a wide range of factors can have cognitive effects in Parkinson’s disease, and the study doesn’t necessarily imply causation of poor slow-wave sleep on low cognitive scores. However, it raises important issues for further study.
“Cognitive performance is extremely multifactorial, and researchers have just begun to understand all of the different genetic, biological, and clinical factors that impact low cognitive performance,” Dr Poston said.
“Sleep is often implicated as one of those potential causes, and this study supports that idea. Further, it supports the idea that the connection between sleep and cognition is important to study in the future.”
The authors and Dr Poston have disclosed no relevant financial relationships.
ANA 2017: 48th Annual Meeting of the American Neurological Association. Abstract S272. Presented October 15, 2017.
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