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Insomnia,
i.e. insufficient or poor quality sleep, can manifest as a primary
disorder or as secondary to other circumstances, including disease/illness.
As a symptom, insomnia is self-reported but sleep behavior can
be assessed physiologically. While PSG is not essential for the
clinical determination of insomnia, it enriches research insights.
Perceptional and physiological indicators of sleep quality do
not always match, leading to type diagnoses of psychophysiological-type
and sleep state misperception-type insomnia and leaving an open
door to the study of potential reasons for the mismatch. Because
sleep quality is partially seen as a function of environmental
conditioning, methodological issues related to PSG measurement
include interfering with natural or usual sleep by the instrumentation
or measuring in a laboratory versus the usual sleeping environment
and allowing for adaptation to the measurement prior to assuming
the data is a reflection of typical sleep. Relatively high variability
in intra-as well as inter-individual night-to-night sleep patterns
pose other challenges to capturing and explaining insomnia.
Insomnia is logically viewed within a stress framework. It emerges
under conditions of emotional distress and environmental duress
and is manifested in people who exhibit hyper-aroused and hyper-activated
stress indicators, often in a sustained (trait-type) way. This
would support a view of primary insomnia as a stress-related disorder
rather than a sleep-related disorder, implicating the importance
of testing biobehavioral and environmental manipulation treatments.
PSG sleep patterns are synchronized with stress and trophic neuroendocrine
function. For example, early phase nighttime sleep (longer SWS
epochs than in later phase) normatively coincides with suppressed
hypothalamic-pituitary-adrenal (HPA) activity (nadirs of ACTH
and cortisol) but peaks of growth hormone. During late phase sleep
(longer epochs of REM sleep), cortisol activity escalates to reach
maximal output shortly after awakening. Stress physiology has
been linked with general host defense alterations, including immune
changes and an influential role for quality sleep is emerging.
Also relevant is the argument that sleep be considered part of
the acute-phase response to infection, mediated by cytokines (especially
interleukin-1, tumor necrosis factor-alpha and interleukin-6),
as reviewed by Benca and Quintas (1997). Increases in sleep accompany
infectious illness and the amount of deep sleep during infection
has been related to mortality rates in animals. Separating out
the features of sleep loss from sleep depth or continuity as affecting
host defense or health/wellness status remains methodologically
challenging.
Since sleep, stress physiology and immune function are inextricably
intertwined, understanding this complex interaction likely is
the key to new understandings about disease /health and illness/wellness.
Given the circular or spiral-- rather than linear-- interrelationships
of stress, sleep, and health, the search for evidence to clarify
postulated connections between them constitutes far reaching and
intriguing investigative challenges. (Benca
and Quintas, 1997).
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