By Alan Z. Segal, MD
Associate Professor of Clinical Neurology, Weill Cornell Medical College
Dr. Segal reports no financial relationships relevant to this field of study.
Synopsis: The presence of white matter infarcts and cerebral microbleeds is associated with disruption of sleep but not total sleep time.
Source: Zuurbier LA, et al. Cerebral small vessel disease is related to disturbed 24-h activity rhythms: A population-based study. Eur J Neurol 2015; July 24. doi:10.1111/ene.12775 [Epub ahead of print].
As the brain ages, its ability to generate deep, slow-wave sleep declines. Chronic illness may accelerate this process. Equally important is our circadian rhythm, which drives multiple endocrine axes and acts as a counterbalance to sleep. The circadian process allows us to stay awake into the evening (when sleep propensity is increasing) and to sleep into the morning hours (when sleep propensity is waning). Because of these factors, it is possible that it is the timing of our sleep, rather than its quantity or quality, that defines the physiological benefits of our slumber.
In the present study, the authors used an actigraph, a movement sensor with an accelerometer not unlike a “Fitbit,” to measure patients’ activity. Worn on the wrist, an actigraph produces an imperfect characterization of sleep, since the sedentary awake state would decrease actigraphic output and a state of active movement during sleep would augment actigraphy. Subjects (n = 970) were middle-aged and drawn from a large cohort of patients in the Rotterdam Community Study. Each subject underwent an MRI to evaluate white matter lesion (WML) volume and the presence of cerebral microbleeds (CMBs) and lacunar infarcts.
It was shown that disruption of overall daily actigraphy correlated with WML volume and CMBs but not lacunar infarcts. Importantly, sleep itself did not affect these imaging parameters. Sleep duration, wake after sleep onset, and subjective ratings of sleep quality did not show any consistent effects. Although it is thought to be important that bed and wake times be consistent, actigraphy only correlated with “intraday” 24-hour readings, not day-to-day changes. Erratic, fragmented sleep habits were deleterious, whether they were the same each day or randomly changed for every 24-hour period.
As the authors note, it is not clear if changes in the brain are producing these circadian changes or whether disorders of circadian rhythms affect the brain. Damage to subcortical fibers, including periventricular tracts, may affect coordination between the cortex and hypothalamus (supraoptic and suprachiasmatic nuclei).
Actigraphy is not an accurate reflector of sleep and neither is it as precise a marker of circadian rhythms as body temperature or melatonin levels. There is little doubt, however, that a robust circadian rhythm is a marker of health. Robust circadian rhythms have been shown to be predictive of other important endpoints such as overall mortality, heart disease, and mood disorders.
The difficulty, however, is accurately discerning the directionality of these effects. Circadian rhythms wane as we age and deteriorate with dementia and chronic disease. It is not known, however, whether circadian rhythms protect against damage to the nervous system or rather if they are an early sensitive marker of neurodegenerative disease. Further study is needed to clarify this “chicken or egg” problem.