Second edition

18.qxd 3/10/08 9:52 AM Page 586
586 Sleep disorders
individuals will experience some insomnia, but, in the
overwhelming majority, this is transient. In those destined
to develop psychophysiologic insomnia, however, a certain
anxiety appears over whether or not sleep will come. This
anxiety then makes sleep less likely to occur and a vicious
cycle may be established in which a failure to sleep engenders
more anticipatory anxiety, which in turn makes the
insomnia worse. Once this pattern is firmly established, the
bed, rather than being seen as a place for relaxation and
restoration, becomes an anxiety-provoking stimulus in
itself. Interestingly, in such cases patients may sleep better
on the couch or in a hotel. Whether or not other etiologic
factors exist in psychophysiologic insomnia is not clear; a
recent report, however, did note reduced nocturnal melatonin
levels in patients compared with control subjects
(Riemann et al. 2002a).
Idiopathic insomnia is presumed to be secondary to dysfunction
of hypothalamic or brainstem structures involved
in sleep.
Differential diagnosis
Other sleep disorders, discussed in other sections in this
chapter, must be considered, including sleep apnea, restless
legs syndrome, periodic leg movements of sleep, and
the syndrome of painful legs and moving toes.
Depression is perhaps one of the most common causes
of insomnia, and one should always inquire about the presence
of other vegetative symptoms. Generalized anxiety
disorder, post-traumatic stress disorder, and schizophrenia
must also be considered.
Caffeine and other stimulants taken too late in the day
cause insomnia, and insomnia is universal and often very
severe and long-lasting in alcohol withdrawal.
Painful conditions, such as heartburn or arthritis, routinely
disturb sleep.
Finally, one must consider whether the patient suffers
from ‘sleep state misperception’ or is merely an otherwise
normal ‘short sleeper’. Sleep state misperception is said to
exist in cases in which, despite often bitter complaints of
insomnia, polysomnography reveals normal sleep. Before
making this diagnosis, however, it must be borne in mind
that some patients with psychophysiologic insomnia sleep
better when they are away from home. When this is suspected,
it may be appropriate to perform polysomnography
at the patient’s home before making the diagnosis.
‘Short sleepers’ are individuals who, despite getting little
sleep, awake refreshed and have no complaints.
Treatment
Good sleep hygiene is essential. Naps should not be taken,
and patients should get some exercise every day. Caffeine
and other stimulants should be reserved for morning
use only. Evenings should be reserved for relaxing
activities, the bedroom should be darkened and quiet, and
the bed should be reserved for sleep or sexual activity. If
sleep does not come, patients should do something else,
perhaps reading, until drowsiness occurs. Whether insomnia
occurs or not, the wake-up time should be strictly
adhered to.
Should insomnia persist despite good sleep hygiene,
consideration may be given to cognitive behavioral
therapy, which is not only effective acutely (Edinger et al.
2001) but also confers enduring benefits (Backhaus
et al. 2001). Should cognitive behavioral therapy be ineffective
or impractical, pharmacologic treatment may be
considered.
Zolpidem, 10 mg h.s., is effective (Perlis et al. 2004) and
is perhaps the most widely prescribed hypnotic for primary
insomnia; it generally has no residual effects the next day
(Staner et al. 2005) or any rebound insomnia upon discontinuation
after chronic use; there have, however, been rare
reports of somnambulism with zolpidem (Morgenthaler
and Silber 2002, Yang et al. 2005). Eszopiclone is an alternative
choice (Zammit et al. 2004).
Melatonin was effective in one double-blind study
(Zhdanova et al. 2001) but not another (Almeida Montes
et al. 2003), in doses ranging from 0.1 to 6 mg given in the
evening. Ramelteon, a selective melatonin receptor agonist,
also appears to be effective (Erman et al. 2006).
Doxepin, in doses of 25 to 50 mg h.s., is effective, but in
a small minority may be followed by severe rebound
insomnia upon discontinuation after chronic use (Hajak
et al. 2001). Trimipramine, another tricyclic antidepressant,
is also effective in doses of 100–200 mg h.s. (Hohagen et al.
1994, Riemann et al. 2002b), and does not appear to suppress
REM sleep or cause rebound insomnia. Trazodone is
very widely used in doses ranging from 25–100 mg h.s.;
however, there is little evidence for its effectiveness
(Mendelson 2005).
Benzodiazepines (e.g., lorazepam, diazepam) and antihistamines
(e.g., hydroxyzine, diphenhydramine) are often
prescribed, but there are no double-blind studies supporting
their use in primary insomnia.
Choosing among these various agents requires considerable
clinical judgment. Given the excellent tolerability of
melatonin, starting with this agent, using a dose of 3–6 mg
in the evening, is a reasonable choice. At present, there are
no comparative studies of melatonin and ramelteon; the
latter agent, however, represents another reasonable first
choice. Should melatoninergic agents fail, consideration
may be given to zolpidem or eszopiclone; doxepin and
trimipramine, although effective, tend to cause considerable
side-effects. Trazodone should also be considered if
melatoninergic agents fail.
The foregoing discussion of pharmacologic treatment
concerns the psychophysiologic form of primary insomnia;
in cases of idiopathic insomnia in children, melatonin,
5 mg in the evening, appears to be effective (Smits et al.
2001).