A new study found that patients with 22q11.2 deletion syndrome could exhibit abnormal sleep patterns linked to attention deficits, daytime sleepiness, and psychiatric symptoms often associated with conditions like schizophrenia.
Investigators assessed 37 patients with 22q11.2 deletion syndrome (22q11DS) and 34 healthy controls aged 6 to 36 years. The participants underwent detailed sleep evaluations using EEG and behavioral testing to examine whether changes in sleep—particularly slow-wave activity (SWA)—were associated with clinical symptoms.
SWA, a measure of deep sleep, typically declines from bedtime to morning, reflecting the brain’s restorative processes. In 22q11DS, however, this decline was “blunted,” meaning the reduction in SWA was less pronounced than expected.
“Flatter SWA slopes correlated with reduced SW-density changes,” the study authors reported, indicating inefficient reduction in sleep pressure. They noted that sleep may have been less restorative.
This disruption had measurable consequences. The participants with the flattest SWA slopes scored higher on the Epworth Sleepiness Scale, indicating greater daytime sleepiness, particularly in the morning. These symptoms weren't explained by differences in circadian rhythm preferences, but rather by reduced sleep quality.
The abnormal sleep patterns were also associated with more severe psychiatric symptoms. The participants with disrupted SWA showed increased negative symptoms, including lack of motivation and reduced emotional expression. Neuropsychological testing revealed additional impairments in attention, impulsivity, and processing speed.
Sleep architecture analysis revealed two consistent features in 22q11DS: reduced time in deep sleep (N3%) and increased microarousals during the night. These disruptions were more pronounced in younger participants and were associated with higher apnea-hypopnea index scores, suggesting a possible contribution from undiagnosed obstructive sleep apnea.
To validate these findings outside the lab, the researchers also used wearable headbands to monitor sleep in a naturalistic hotel setting. The same disrupted sleep patterns were observed, strengthening the ecological validity of the results.
Overall, the study suggested that poor sleep quality—especially reduced SWA decline—wasn't merely a byproduct of 22q11DS but may have contributed to the severity of cognitive and psychiatric symptoms. The researchers proposed that interventions targeting sleep, including early screening for sleep apnea, may aid in managing mental health outcomes in this population.
These findings provided early evidence that brain activity during sleep could serve as a measurable indicator of psychiatric risk and cognitive function in patients with 22q11DS.
The authors reported no conflicts of interest.
Source: Psychiatry Research
