http://journal.frontiersin.org/article/10.3389/fneur.2014.00287/full?
Thomas Kantermann1,2*, Andreas Meisel3,4, Katharina Fitzthum3,4, Thomas Penzel5, Ingo Fietze5 and Lena Ulm3,4,6
- 1Chronobiology Unit, Groningen Institute for Evolutionary Life Sciences, University of Groningen, Groningen, The Netherlands
- 2Clinical Centre, Institute for Occupational, Social and Environmental Medicine, Ludwig-Maximilians University Munich, Munich, Germany
- 3NeuroCure Clinical Research Center, Charité – Universitätsmedizin Berlin, Berlin, Germany
- 4Department of Neurology, Center for Stroke Research Berlin, Charité – Universitätsmedizin Berlin, Berlin, Germany
- 5Center of Sleep Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany
- 6Centre for Clinical Research, The University of Queensland, Herston, QLD, Australia
Introduction
The onset of vascular events exhibits a circadian
(about 24-h) pattern, with a prominent peak in the morning hours and a
second, smaller peak in the early evening (1–4).
This phenomenon is thought being caused by diurnal variations in
underlying pathophysiological mechanisms, e.g., platelet aggregation,
blood pressure, and catecholamine concentrations (3, 5).
Several animal studies demonstrated that cerebrovascular events, in
turn, also impact circadian rhythms and sleep architecture (6–9).
Longer latencies to fall asleep, fragmented sleep, NREM sleep
instability, and hypersomnia have also been described in stroke
patients, indicating changes in sleep homeostasis and circadian
rhythmicity after stroke (10, 11).
Two studies with small sample sizes provided some evidence of altered
timing in urinary melatonin as a marker of disturbed circadian rhythms
in stroke patients (12, 13).
However, knowledge on the interplay between sleep homeostasis, the
circadian timing of sleep, and vascular events is still incomplete.
The circadian timing of sleep is regulated by an internal clock, which is synchronized (entrained) by light to the 24-h day (14, 15). The relation between external (local) and internal (circadian) time is called phase of entrainment (16)
and people that differ in this trait are referred to as different
chronotypes. Chronotype can easily be assessed with the Munich ChronoType Questionnaire [MCTQ; (16)]
as the mid-point of sleep on work-free days (MSF), corrected for sleep
deficit accumulated across the workweek (MSF sleep corrected; MSFsc). MSFsc as a measure for internal time allows calculating the internal time point of a physiological event (17, 18).
Social jetlag (the difference between MSF and mid-sleep on workdays,
MSW) is a surrogate measure for circadian rhythm disruption and has been
linked to elevated heart rate in shift-workers (19), smoking (20), and depression (21).
To date, no study has assessed phase of entrainment (chronotype) and
social jetlag before and after stroke to compare the impact of stroke in
relation to internal time.
The current study was the first to investigate
associations between stroke onset and severity and internal time before
and after stroke. We hypothesized that (a) there is a correlation
between chronotype (MSFsc) and stroke onset, (b) experiencing
a stroke results in chronotype changes, and (c) the impact of stroke
varies with the internal time point a stroke happened.
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