Insomnia Insomnia

30 Bonnet and Arand
chronic caffeine use. Respective means for baseline, early caffeine, late caffeine,
and withdrawal were 10.7, 17.9, 13.4, and 11.3 minutes, respectively. Again, these
increased SLs were similar to those seen in insomnia patients compared with normal
subjects.
The MMPI is a nontransparent measure of relatively stable personality characteristics.
It was administered before caffeine use and at the end of the caffeine administration
primarily because it has been used as a measure in many previous
insomnia studies. At baseline, as expected, all of the MMPI values were characteristic
of normal young adults. However, after 1 week of caffeine administration,
there was movement toward increased pathology on all the clinical scales except
masculine–feminine scale, and the change was statistically significant for the Psychasthenia
(anxiety) scale. These findings were also surprising because they indicated
that even stable aspects of personality could shift significantly toward
pathology in a short period secondary to a relatively simple physiological manipulation.
As can be seen in Table 2, subjects given caffeine had significant changes in the
direction of patients with chronic insomnia on MSLT, metabolic rate, negative
moods, and personality. The data indicate that chronic hyperarousal with no predisposing
psychological component can produce the typical pattern of poor sleep,
mood change, and personality change commonly seen in patients with psychophysiological
insomnia. However, it could not be determined from these data if the mood
and personality symptoms were produced by the hyperarousal or were secondary
from the poor sleep also produced.
Effects of Poor Sleep
It has been implied that increased physiological arousal, possibly even as an
innate phenomenon, produces an environment in which an individual is prone to
report insomnia. Many patients with insomnia, however, feel that their sleep is the
central problem, and that poor sleep leads to symptoms of fatigue and dysphoria.
To test whether the insomnia sleep pattern by itself could produce hyperarousal and
the other symptoms of primary insomnia, the poor sleep found in patients with
insomnia was produced for 1 week in normal young adults, and subjects were followed
for the development of insomnia symptoms (36). Patients with primary
insomnia were identified based on the same report of poor sleep and polysomnographic
criteria as used for insomnia patients who participated in the metabolic
studies reported earlier and the sleep parameters of those patients were used
in a yoke control fashion to produce comparable sleep in a group of matched normal
sleepers. It was hypothesized that if the yoked normal sleepers developed the
spectrum of secondary symptoms seen in the patients with “true” insomnia after
sleeping like the patients, then those symptoms could be seen as secondary to the
poor sleep. On the other hand, if the yoked normal sleepers did not develop the
symptoms seen in the true patients with insomnia, then some factor other than poor
sleep itself would be responsible for those secondary symptoms.