The study drew on a large national cohort assembled from the Finnish Parkinson’s Association, an organization with roughly 7,500 members, of whom 5,373 were registered as Parkinson’s patients. From this registry, the researchers randomly selected 1,500 individuals and mailed a structured sleep questionnaire to 1,447 eligible participants between 2010 and 2011. Every included patient had a Parkinson’s diagnosis confirmed by a neurologist in accordance with national clinical guidelines consistent with the Gelb diagnostic criteria. The questionnaire incorporated validated sleep items from the Basic Nordic Sleep Questionnaire, a well-established instrument for quantifying subjective sleep complaints. A follow-up questionnaire was sent in 2014 to 2015, and after reminders and telephone contact, 183 participants provided complete data at both time points, forming the analytical cohort for the longitudinal comparison.

The researchers measured an unusually broad set of sleep domains at both time points. Daytime sleepiness was assessed with the Epworth Sleepiness Scale, restless legs syndrome with the international four-item diagnostic criteria, and REM sleep behavior disorder symptoms with the REM Sleep Behavior Disorder Screening Questionnaire, on which a score of six or higher suggests the disorder. Sleep apnea risk was screened with the STOP questionnaire, insomnia symptoms were captured through difficulty initiating sleep, nocturnal awakenings, early morning awakenings, and non-restorative sleep, and circadian timing was estimated from midsleep, the midpoint between sleep onset and wake time. The team also recorded medication use, converting self-reported drugs into levodopa equivalent doses, and screened depressive symptoms with Rimon’s Brief Depression Scale, an instrument deliberately designed to exclude insomnia items so that sleep complaints would not inflate depression scores.

Over the five-year interval, mean disease duration in the cohort rose from 5.5 to 9.7 years, mean levodopa equivalent dose increased from 607.8 to 732.6 milligrams, and the proportion of sedentary participants nearly doubled from 9.0 to 18.0 percent. Against this backdrop of advancing disease, the sleep data told a nuanced story. Total sleep time edged up only trivially, from 7.0 to 7.2 hours, a change that was not statistically significant. Individual insomnia symptoms, including trouble falling asleep, frequent night awakenings, early morning awakening, and unrefreshing sleep, showed no significant deterioration, and a composite measure capturing any insomnia symptom or regular use of sleep medication remained flat. Daytime fatigue and hallucinations were likewise stable, a finding that contrasts with several earlier reports describing insomnia as a progressively worsening complaint in Parkinson’s disease.

In sharp contrast, the symptoms tied to REM sleep pathology advanced markedly. The proportion of participants who talked in their sleep at least once a week nearly doubled, rising from 17.4 to 30.4 percent. Weekly nightmares increased from 14.8 to 24.6 percent. The mean REM Sleep Behavior Disorder Screening Questionnaire score climbed from 4.4 to 5.3 points, and the share of participants crossing the screening threshold of six or more rose from 28.9 to 39.9 percent. REM sleep behavior disorder, in which patients act out their dreams because the normal muscle paralysis of REM sleep fails, is recognized as a core prodromal feature of synucleinopathies, the family of neurodegenerative diseases that includes Parkinson’s, and it is strongly linked to later cognitive decline and a more aggressive disease course. The authors argue that the longitudinal rise in these symptoms reflects active progression of REM sleep pathology rather than an incidental annoyance.

Daytime sleepiness also worsened in clinically meaningful ways. The proportion of participants with an Epworth Sleepiness Scale score above 10, the conventional cutoff for excessive sleepiness, increased from 30.6 to 38.8 percent, while severe sleepiness, defined as a score above 15, rose from 8.9 to 14.8 percent. Daily napping grew from 21.4 to 31.7 percent of the cohort, likely mirroring the rising sleepiness. Prevalence of restless legs syndrome climbed from 21.0 to 31.2 percent, an increase the authors note is broadly consistent with cross-sectional studies showing elevated restless legs frequency in more advanced Parkinson’s disease. Because restless legs syndrome shares dopaminergic pathways with Parkinson’s itself, the rise alongside increasing levodopa doses could reflect inadequate treatment or, importantly, augmentation, a paradoxical worsening of symptoms caused by long-term dopaminergic therapy itself.

To understand what drove the worsening sleepiness, the researchers built multivariate logistic regression models with excessive daytime sleepiness as the outcome. Three factors emerged as independent predictors: higher depression scores, use of dopamine agonists, and high risk of sleep apnea on the STOP questionnaire. Dopamine agonist use carried an odds ratio of 3.92, meaning users faced nearly four times the odds of excessive sleepiness compared with non-users after adjustment. Notably, neither levodopa nor MAO inhibitor use was associated with sleepiness, and age, total sleep time, and REM behavior disorder screening score were not independently predictive. The authors emphasize that this pattern highlights the need to investigate secondary, potentially treatable causes, such as undiagnosed sleep apnea or depression, before attributing sleepiness solely to disease progression.

The study has important strengths and candidly acknowledged limitations. Its prospective design with a five-year interval and consistent use of a validated questionnaire at both time points allow genuine longitudinal inference across multiple sleep domains simultaneously, something most prior studies, which typically examined single symptoms in cross-sectional or short-term designs, could not provide. However, the follow-up sample of 183 is small relative to the baseline cohort of 611, and the analysis was restricted to participants with complete data at both points. Those who completed follow-up were younger, had shorter disease duration, higher body mass index, and better quality of life than those excluded, indicating a healthy-survivor effect that likely makes the reported changes conservative underestimates of true progression. The questionnaire-based approach also means that REM sleep behavior disorder and sleep apnea were identified through surrogate markers rather than video-polysomnography, the gold standard, and Parkinson’s diagnoses were self-reported as neurologist-confirmed without record re-verification.

Despite these caveats, the selective pattern of progression carries a clear clinical message. Sleep in Parkinson’s disease is not a single monolithic complaint that simply deepens over time; it is a collection of distinct disorders evolving on different trajectories, some driven by neurodegeneration, some by medication, and some by comorbid conditions. The stability of insomnia and total sleep time suggests that these features may reflect aging and individual vulnerability more than disease progression, whereas the rise in REM-related behaviors, sleep talking, and nightmares tracks the underlying neurodegenerative process and, as the team’s earlier work in this same cohort showed, is associated with increased mortality. The authors conclude that multi-domain sleep assessment should be routine in Parkinson’s care, and that sleep talking and REM behavior disorder screening scores deserve attention not merely as symptoms to soothe but as markers of disease progression with genuine prognostic weight. For patients and clinicians alike, the message is that worsening sleep deserves careful, domain-specific evaluation rather than a one-size-fits-all response.

Subject of Research: Longitudinal changes in sleep characteristics and sleep disorders over five years in Parkinson's disease

Article Title: Changes in sleep characteristics in Parkinson’s disease: a prospective 5-year follow-up study

Article References: Partinen, E., Ylikoski, A., Hublin, C., & Partinen, M. (2026). Changes in sleep characteristics in Parkinson’s disease: a prospective 5-year follow-up study. Journal of Clinical Sleep Medicine, 22(1), Article 166. https://doi.org/10.1007/s44470-026-00169-6

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00169-6

Keywords: Parkinson's disease, sleep disorders, excessive daytime sleepiness, REM sleep behavior disorder, sleep talking, nightmares, restless legs syndrome, insomnia, dopamine agonists, sleep apnea, prospective cohort study, daytime napping