Poor sleep in old age linked to hardened brain arteries

New York, Jan 15 (IANS) Poor sleep quality in elderly people is linked with more severe arteriosclerosis — thickening and hardening of the walls of the arteries — in the brain as well as a greater burden of oxygen-starved tissue (infarcts) in the brain, says a new study.

The condition can contribute to the risk of stroke as well as cognitive impairment, the study warned.

“The forms of brain injury that we observed are important because they may not only contribute to the risk of stroke but also to chronic progressive cognitive and motor impairment,” said Andrew Lim, an assistant professor at the University of Toronto, in Canada.

Sleep monitoring may potentially be another way to identify old age people who might be at risk of stroke, the findings suggested. Fragmented sleep occurs when sleep is interrupted by repeated awakenings or arousals.

The study revealed that greater sleep fragmentation was associated with 27 percent higher odds of having hardened brain arteries. Researchers examined autopsied brains of 315 people (average age 90, 70 percent women). Their sleep was disrupted on average almost seven times each hour.

In all, 29 percent of the patients had suffered a stroke, while 61 percent had signs of moderate to severe damage to their blood vessels in the brain.

Moreover, for each additional two arousals during one hour of sleep, researchers reported a 30 percent increase in the odds that subjects had visible signs of oxygen deprivation in their brain.

These findings were independent of other cardiovascular risk factors, such as body mass, smoking history, diabetes, and hypertension, or other medical conditions such as Alzheimer’s disease, pain, depression or heart failure, researchers said.

The study also pointed out that further work is needed to clarify whether brain blood vessel damage is a consequence or a cause of sleep fragmentation and the role of specific contributors to sleep fragmentation such as sleep apnea and the underlying biological mechanisms.

The findings were reported in the American Heart Association’s journal Stroke.

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