Poor Sleep Raises Risk of Dyskinesia With Parkinson’s, Study Finds

Disorder affects more patients with disturbed sleep than without over 3 years

Andrea Lobo avatar

by Andrea Lobo |

Share this article:

Share article via email
This illustration shows two people studying an oversized human brain.

Poor sleep quality is a key factor in developing dyskinesia, the uncontrolled and involuntary movements that can affect people with Parkinson’s disease, a study that followed patients for up to three years suggests.

“[Poor sleep quality] may increase the risk of developing dyskinesia in PD [Parkinson’s disease], implying that therapeutic intervention targeting improving sleep quality may be a promising approach to prevent or delay … dyskinesia,” the researchers wrote.

The study, “High PSQI score is associated with the development of dyskinesia in Parkinson’s disease,” was published in the journal npj Parkinson’s disease.

Recommended Reading

Amneal Seeks Approval of IPX-203 in US to Boost Patient ‘Good On’ Time

Dyskinesia is a complication of long-term use of levodopa, a gold standard of Parkinson’s treatment. Around 40–50% of patients develop dyskinesia within five years after starting treatment, reaching 50–75% of patients after 10 years, the study noted.

Dyskinesia may result from poor sleep affecting the brain

It is thought that dyskinesia is associated with changes in neuronal circuits, and restful sleep — often difficult with Parkinson’s — is crucial for neuronal circuits to function properly.

“Sleep is crucial to keep neural circuit homeostasis, and PD patients often suffer from sleep disturbance … such as long periods spent in bed while not asleep and unable to remain asleep and excessive daytime sleepiness,” the scientists wrote.

Researchers at two hospitals in Shangai, China, investigated the association between sleep quality and dyskinesia among 61 Parkinson’s patients followed for up to 36 months.

These people (67.2% men) had a mean age at disease onset of 61.6, and had been diagnosed with Parkinson’s for a median of 4.5 years when they enrolled in the study. Motor fluctuations were present in 44.3% of the patients, and 31.3% had freezing of gait. None had dyskinesia at enrollment, and all were being treated with levodopa, at a median daily dose of 375 mg.

Over the study’s three years, 20 patients (32.8%) developed dyskinesia. The proportion of those affected by dyskinesia was significantly higher in patients with poor sleep quality compared to those with good quality sleep (48.1% vs. 20.6%, respectively).

Sleep quality was determined using the Pittsburgh Sleep Quality Index, a 19-item and self-reported questionnaire.

A higher risk of dyskinesia also associated with multiple other nonmotor Parkinson’s symptoms, such as higher anxiety levels, and with higher levodopa doses and longer disease duration. Evidence of depressive symptoms, as measured by the Hamilton Depression Rating Scale, was of “borderline significance,” the team noted.

A multivariate analysis — based on the relationship between several variables — examining risk factors for dyskinesia in Parkinson’s, confirmed that poor sleep quality, cognitive difficulties, and longer disease duration were independent predictors of such risk.

“These results highlight the important effect of sleep quality on the risk of dyskinesia,” the researchers wrote.

Good sleep contributes to maintaining cerebral activity, whereas poor sleep or sleep disturbances “could disrupt synaptic plasticity or synaptic homeostasis” in key brain regions, they noted.

Synapses are the junctions between nerve cells that allow them to communicate, synaptic plasticity refers to the ability of synapses to weaken or strengthen over time in response to activity, and synaptic homeostasis refers to this network’s capacity to maintain stability with changes in activity.

The cumulative incidence of dyskinesia rose over follow-up, increasing from 8.2% at 24 months (two years) to 32.8% at 35 months, the researchers reported.

The annual change measured in sleep quality, also tied to greater nonmotor symptoms and anxiety, poorer cognition, and higher levodopa doses, suggests that “patients experienced more impaired mood disturbance and cognitive dysfunction as sleep quality deteriorated,” they added.

Overall, we “found that a high PSQI score [poor sleep quality measure] was a risk factor for the development of dyskinesia in patients with PD, suggesting that therapeutic intervention targeting sleep quality may be a promising approach to prevent or delay the development of dyskinesia,” the researchers concluded.

The team now is planning to use animal models to explore the mechanisms underlying the relationship between sleep and dyskinesia.