Insomnia Insomnia

Physiological Basis of Insomnia 35
decreased HFP compared to the good sleepers. These physiological findings in
“preinsomnia” patients suggest that their existing hyperreactivity to sleep-related
stress and caffeine could be secondary to elevated sympathetic nervous system activity,
and this could be a marker for the development of chronic insomnia at a later date.
The finding of elevated physiological activity prior to mood change, personality
change, or complaint of chronic insomnia provides another clue that underlying physiology
could be the key to the later development of additional insomnia symptoms.
DISCUSSION
It is generally accepted that there are changes in several physiological systems
in association with psychophysiological insomnia. The current experiments
attempted to refine our understanding of the relationship among physiological
arousal, poor EEG sleep, psychological status, and subjective report of insomnia.
The finding that experimentally produced chronic physiological arousal in normal
young adults produces the mood and personality changes seen in patients with
insomnia provides a compelling description of how chronic insomnia could develop
in physiologically susceptible individuals. The studies showing that, by itself the
poor sleep of patients with insomnia does not produce the arousal, mood, and personality
characteristics of patients and that the production of much worse EEG
sleep in patients with insomnia does not magnify symptoms leads to the conclusions
that the symptoms produced by chronic physiological arousal were not mediated
by the poor sleep that was produced and the symptom complex that was
associated with psychophysiological insomnia is not really a sleep disorder, but
rather an arousal disorder. Finally, the importance of physiological arousal as the
harbinger of insomnia was enhanced by the finding of elevated heart rate and
abnormal cardiac spectral activity in normal subjects with no sleep complaint who
were found to have EEG-defined SI. These several approaches identify tangible
physiopathology that should be open to identification and amenable to treatment.
We have recognized for many years that some patients have lifelong problems
with excessive sleepiness secondary to disorders such as narcolepsy or idiopathic
hypersomnolance. The extent to which these disorders demonstrate a failure of the
sleep system vs a failure of the arousal system can be debated. Certainly, these
disorders are commonly treated with medications that have direct impact by
increasing central nervous system arousal. Recognition that another group of
patients suffers from the opposite lifelong problem (hyposomnolence or
hyperarousal) has been more difficult. At this point, much work has identified the
physiological markers of chronic hyperarousal in patients. Behavioral relaxation
techniques can provide effective help for patients with some situational
hyperarousal, but as behavioral techniques such as sleep extension eventually fail
in patients with idiopathic hypersomnolance, behavioral techniques may also fail
in patients suffering from chronic hyperarousal. Identifying arousal disorders as a
major component of both hypersomnolance and insomnia can help direct research
toward more effective pharmacological control of the underlying physiologic
arousal disorder.