Insomnia Insomnia

Sleep State Misperception 91
arousals during the stimulus (19). Patients with SSM have been shown to have
elevated levels of physiological arousal as measured by 24-hour metabolic rate,
although the increase was less than observed in psychophysioligical insomnia (20).
Patients with SSM have demonstrated increased activity on actigraphy during sleep
(21). The tendency toward mislabeling sleep as wakefulness in insomnia may reflect
elevated levels of CNS arousal, and frequencies that are not normally quantified in
standard polysomnography may be important markers for this elevated arousal. In
one study, patients with insomnia who have low EEG α frequency activity during
sleep were more likely to underestimate total sleep time and overestimate awakenings
compared to patients with insomnia who have higher amounts of α frequency
EEG activity (22). It has also been demonstrated that increased β/γ activity is correlated
with the perception of wakefulness during sleep (23).
Another potential cause of SSM is the misperception or mislabeling of another
bodily state such as fatigue or depression. For instance, in two recent studies, both
nefazodone and fluoxetine alleviated depression and resulted in improvements in
subjective sleep quality, although patients given fluoxetine showed significant
declines in objective sleep characteristics such as increased number of awakenings
and decreased sleep efficiency (24,25). Similarly, no group difference in sleep diary
measures of sleep quality was seen between patients given nefazodone or
paroxetine, despite the declines in objective sleep measures in the patients given
paroxetine (26). Some patients may attribute daytime cognitive difficulties such as
trouble concentrating or memory problems to a poor night’s sleep or sleepiness,
when sleep is adequate and true sleepiness is not present.
Smith and Trinder were able to simulate SSM in 20 healthy volunteers who did
not have insomnia by causing microarousals from sleep through the manipulation
of the sleep environment. The same individuals did not have any misperception
when they were restudied on other nights when the sleep environment was not manipulated
to cause the above mentioned arousals. Hence, the researchers postulated
that the cause of SSM in insomniacs is due at least partly to the increased number of
brief arousals from sleep (27). This sleep misperception as being awake also leads
to the perpetuation of the insomnia because of previous sleep being perceived as
wake time (13).
CLINICAL MANIFESTATIONS
Patients with SSM complain of either longstanding insomnia with difficulty initiating
or maintaining sleep, nonrestorative sleep, or excessive daytime sleepiness
that is not documented by polysomnography and MSLT. The patient must report
that the symptoms were present during the testing. Unique to SSM is the tendency
for patients to report virtually no sleep for days, weeks, or even years. They often
vehemently claim that the essentially normal polysomnographic recordings are in
error. Like other forms of insomnia, clinically significant complaints are accompanied
by reports of waking dysfunction, such as fatigue that impairs social or occupational
function and that the patient believes will improve with treatment.