Sleep disturbance -- especially waking frequently during the night -- was associated with an increased incidence of cerebral vessel damage and other brain insults related to stroke in an autopsy study of elderly people who had their sleep quality monitored prior to death.

Researchers examined brain autopsy findings from participants in the Rush University Memory and Aging Project. All study participants had undergone at least 1 week of around-the-clock monitoring aimed at quantifying sleep quality and circadian rhythms.

Each additional two arousals during a single hour of sleep was associated with a 30% increase in the odds of showing visible signs of severe cerebral small vessel thickening, reported Andrew Lim, MD, of Sunnybrook Health Science Center in Toronto, and colleagues in Stroke.

Elderly people are at high risk for both stroke and sleep disturbances. Getting too little sleep has been linked to an increased risk for stroke in several studies, but important histopathologic pathologies in the brain can not be identified in living patients, the researchers wrote.

"Some cerebrovascular pathologies, such as arteriolosclerosis, cerebral amyloid angiopathy, and microscopic infarcts, can only be quantified by histopathology and with few exceptions, their associations with sleep are unknown. This is important because these pathologies contribute not only to clinical stroke but also to chronic progressive cognitive and motor impairment," the researchers wrote.

They used the sleep study data to test their hypothesis that elderly people who experience greater sleep fragmentation also have more evidence of severe arteriolosclerosis and other brain pathologies such as atherosclerosis, cerebral amyloid angiopathy, and macroscopic and microscopic infarcts.



A total of 315 Rush Memory and Aging Project participants were included in the study. The mean age of the participants at death was 90.4 and 70% were female. Twenty-nine percent had experienced a stroke and 61% had one or more moderate to severe vascular abnormalities.

The authors reported that greater sleep fragmentation was associated with more severe arteriolosclerosis (odds ratio 1.27, 95% CI 1.02-1.59, P=0.03 per 1 standard deviation [SD] greater sleep fragmentation).

Also, sleep fragmentation was also associated with a greater incidence of subcortical macroscopic infarcts (OR 1.31, 95% CI 1.01-1.68, P=0.04).

Associations were similar for lacunar (≥1 mm, OR 1.30, 95% CI 1.00–1.68) and nonlacunar (<1 mm, OR 1.36, 95% CI 0.96–1.88) infarcts.

The associations were independent of established cardiovascular risk factors, such as obesity, smoking history, diabetes, and hypertension and other medical conditions such as Alzheimer's disease, depression, and heart failure.

"In models adjusted for pulmonary and renal function, the associations between sleep fragmentation and arteriolosclerosis were minimally attenuated," the researchers wrote. "Similarly, in models adjusted for circadian irregularity, dementia, coronary disease, and renal function, the associations with subcortical infarcts were minimally attenuated."

Sleep monitoring may be useful for identifying seniors at risk for stroke, but more research is needed to determine if these cerebrovascular pathologies are caused by sleep fragmentation or if they are a consequence, Lim noted in a written press statement.

"There are several ways to view these findings: sleep fragmentation may impair the circulation of blood to the brain, poor circulation of blood to the brain may cause sleep fragmentation, or both may be caused by another underlying risk factor," he said.

The observational design of the study, along with the lack of data on sleep apnea and limb movement during sleep were cited by the researchers as study limitations, along with the fact that several covariates, including heart disease, smoking, and diabetes status were self reported by the study participants.

"Notwithstanding these limitations, these data show that greater sleep fragmentation is associated with more arteriolosclerosis and macroscopic subcortical infarct pathology," the researchers wrote. "Further work is needed to clarify whether these are consequences or causes of sleep fragmentation, the role of specific contributors to sleep fragmentation (e.g., sleep apnea), and underlying biological mechanisms."

If you have any questions, please click:http://www.medicalequipment-msl.com/