Study Cites Factors Associated With Sleep Benefit In Parkinson’s Disease

sleep study

Parkinson’s patients who have had the disease for a long time, who do not sleep very efficiently, and have higher motor impairment are more likely to experience sleep benefit — the phenomenon in which Parkinson’s patients wake up feeling better before taking medication.

The study with that finding, “The related factors of sleep benefit in Parkinson’s disease: A systematic review and meta-analysis,” was published recently in PLOS One.

Sleep benefit is, as the investigators wrote, “a fascinating, but mysterious phenomenon.” It is reported to happen in between a third and half of Parkinson’s patients.

The phenomenon is essentially when a person wakes up from sleep and feels better, with fewer disease symptoms. This is particularly puzzling for clinicians because, at least in theory, just waking up is often when a person has no medications helping them along. So, what could cause sleep benefit?

Researchers still are not sure. Some reports suggest that, although patients may report feeling better, they do not actually perform better on objective motor control tests. aAs such, it might all be psychological.

Still, the team wondered whether patient characteristics — from age and sex to sleep patterns and disease score — might predict which patients would experience sleep benefit.

After a search of the existing scientific literature, the investigators identified seven studies reporting on sleep benefit that included more than 1,300 Parkinson’s disease patients. Using the data from these studies, the authors looked for statistical trends to see which patient traits might be associated with experiencing sleep benefit.

Most of the factors they looked at, including sex, age at diagnosis, and sleep length, did not have a significant association with sleep benefit. However, the investigators did identify three factors that were predictive of experiencing sleep benefit: having had Parkinson’s for a long time; having a low sleep efficiency; and having a high score on the MDS-UPDRS-Ⅲ, a scale used to assess the severity of Parkinson’s motor symptoms, while on medication.

These results might let researchers determine which patients are most likely to experience sleep benefit, though what causes this phenomenon is still pretty much unknown.

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Cognitive Performance in Parkinson’s Linked to Sleep Efficiency, Study Shows

sleep study

University of São Paulo researchers have found that Parkinson’s patients with dementia sleep less and less efficiently, which affects their overall cognitive performance.

The study with that finding, “Global cognitive performance is associated with sleep efficiency measured by polysomnography in patients with Parkinson’s disease,” was published in Psychiatry and Clinical Neurosciences.

Non-motor complications associated with Parkinson’s disease, including cognitive impairment and sleep disturbances, can drastically affect patients’ quality of life.

Evidence suggests an interaction between sleep disorders and cognition. For instance, sleep after learning helps memory consolidation.

In addition, people with obstructive sleep apnea syndrome or chronic insomnia have cognitive abnormalities, which could be reversed after proper treatment of the underlying sleep disturbance.

Although there is still no consensus about whether sleep disorders are associated with cognitive dysfunction, studies suggest an association and add that rapid eye movement (REM) sleep behavioral disorder may be associated with increased risk for cognitive decline. REM is a sleep stage in which the eyes move rapidly in various directions.  During sleep, the body cycles between intervals of basic states: REM sleep and non-REM sleep.

Researchers in Brazil now examined a possible association between clinical variables, cognitive status and the presence of sleep abnormalities and symptoms in Parkinson’s patients.

Investigators performed detailed clinical and cognitive assessment in 79 patients. Participants were mostly men (61%), 51-72 years old, and a disease duration varying between 3.9 and 13.9 years.

Based on cognitive diagnosis, researchers categorized patients as those with normal cognition (29 patients), mild cognitive impairment (39 patients) or dementia (11 patients).

Within two weeks after initial medical evaluation, participants were submitted to an overnight polysomnography, meaning they had their brain waves, blood oxygen level, heart rate, breathing patterns, and eye and leg movements monitored while they were asleep.

Compared to Parkinson’s patients with normal cognition, the dementia group was older, had more severe disease, and more difficulty performing daily activities. Dementia patients also took higher daily levodopa-equivalent dose than participants without abnormalities.

Patients with dementia had lower sleep efficiency, less total sleep time and lower number of sleep state changes, in comparison to the normal cognition group.

Researchers also found an association between sleepiness, measures of obstructive sleep apnea and sleep symptoms, which were assessed by the Parkinson’s Disease Sleep Scale and the Pittsburgh Sleep Quality Index.

“Concerning sleep disorders and sleep symptoms, [there was] no significant differences between groups in the proportion of cases with obstructive sleep apnea, chronic insomnia, [REM sleep behavioral disorder] and [restless legs syndrome]. We also did not observe significant differences between scores of patients in the three groups about excessive daytime sleepiness, quality of sleep and general sleep-related symptoms. There was also no significant differences in the number of sleep disorders between the groups,” authors wrote.

There was a significant association between overall (aka “global”) cognitive performance and wakefulness and the number of sleep state changes during sleep.

“However, we did not find any other association between sleep disorders or symptoms and cognitive status or cognitive performance of patients with Parkinson’s,” researchers wrote.

The team believes the association with the number of state changes during sleep may be because Parkinson’s disease patients with dementia slept less than the other subsets and as such, had less time to change between sleep states.

“We hope that, in the near future, new prospective controlled studies, with more significant numbers of patients, could evaluate, in detail, the relationship of different variables related to sleep with cognitive functions in this specific population,” researchers concluded.

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Parkinson’s Study Analyzes Levodopa‐induced Dyskinesia’s Effect on Sleep

sleep study

When a person is awake, brain circuit activity is constantly “on.” This activity needs to be normalized during sleep. Researchers now report that neuronal activity in Parkinson’s disease patients with levodopa-induced dyskinesia fails to decrease during sleep.

The study, “Levodopa-induced dyskinesia in Parkinson’s disease: sleep matters,” was published in Annals of Neurology.

The brain’s structure and functional networks are constantly changing/evolving in a biological process scientists call “neuronal plasticity,” which affects the brain’s learning and memory abilities.

Levodopa (L-Dopa), one of the main therapies used to treat Parkinson’s symptoms, “successfully controls motor symptoms for several years and then induces motor fluctuation and abnormal involuntary movements, i.e. levodopa-induced dyskinesias (LIDs),” researchers wrote.

This long-term, therapy-related complication results in important functional disability, often requiring complex pharmacological or surgical interventions.

Although LDIs are believed to be associated with changes in neuronal plasticity in the striatum — a brain area involved in multiple aspects of cognition — studies have demonstrated abnormal motor cortex plasticity in LID patients. The motor cortex is the brain area involved in the planning, control, and execution of voluntary movements.

In addition, changes in cortical slow wave activity (SWA) — the major characteristic of deep sleep key for both cortical restructuring and functioning, which, in turn, supports cognition — have been described in animal models of Parkinson’s disease with LID.

SWA increases with wake duration, peaks in early sleep, and declines in late sleep. Animal studies have shown that “rodents exposed to combined levodopa treatment and sleep deprivation developed earlier and more severe LID than animals that were not sleep deprived,” authors noted.

The team at Neurocenter of Southern Switzerland investigated if sleep could influence clinical presentation of Parkinson’s in humans, as previously observed in animals.

A total of 27 Parkinson’s patients (50-65 years old) were divided into three groups:

  • de novo: seven recently diagnosed patients who had received only azilect (rasagiline, by Teva) as dopaminergic therapy;
  • advanced: nine subjects without LID using their usual therapy, but demonstrating the end-of-dose or wearing-off phenomenon;
  • dyskinetic: 11 advanced patients with LID.

Seven healthy and age-matched participants also were recruited as controls.

Researchers evaluated subjects’ mood and sleep complaints as well as their Parkinson’s motor symptoms, using a series of rating scales, and asked them to maintain regular sleep-wake schedules.

A wristwatch-like device was attached to individuals’ non-dominant wrist to monitor their sleep/wake cycles for one week. This method is known as actigraphy. Because of technical failure, one patient from each of the Parkinson’s groups could not undergo rest/activity cycles monitoring.

Additionally, participants were submitted to whole night video polysomnography-high-density electroencephalogram (EEG) recording, meaning those studied had their brain waves, blood oxygen level, heart rate, breathing patterns, eye and leg movements monitored while they were asleep. Recording data was corrupted by artifacts in two de novo patients and one dyskinetic participant, and as a result was excluded from the SWA analysis.

Subjects were followed for at least six months.

Results showed there was a decline in SWA in the de novo, advanced and control groups, but not in dyskinetic patients, who had their SWA persistently elevated during the night.

In accordance, all groups except the dyskinetic one, manifested a significant decrease in SWA between early and late sleep, further supporting the investigators’ hypothesis that dyskinetic patients have their much-needed overnight brain activity normalization process compromised.

In all Parkinson’s patients, total sleep time and sleep efficiency were negatively correlated with disease duration, which is consistent with previous studies.

However, “while the correlation between [deep sleep] and disease duration was positive in both [de novo and advanced] patients, it was surprisingly negative in [dyskinetic] patients,” researchers wrote.

A possible explanation is there may be biological compensatory mechanisms in the de novo and advanced sample that can be compromised in the dyskinetic one, making dyskinetic patients unable to sleep efficiently as disease progresses.

Because levodopa dose influences dyskinesia onset, investigators performed a correlation analysis between sleep parameters and levodopa-equivaled daily dose.

A negative correlation of total sleep time and sleep efficiency with levodopa-equivalent daily dose was observed in all patients with motor fluctuations, i.e., in both advanced and dyskinetic groups. Importantly, slow wave (or deep) sleep was negatively correlated with levodopa-equivalent daily dose only in patients  experiencing LID.

“In conclusion, these results support our preclinical findings of a clear association between sleep and LID at the electrophysiological, behavioral, and biochemical levels,” researchers wrote.

“Although our findings do not imply a causative role for the lack of SWA reduction in the emergence of LID … they do suggest an association between sleep and some clinical [features] of PD and suggest a relationship between sleep disruption and LID,” they concluded.

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