330 Insomnia
bene“ts for clinical insomnia. Because melatonin and valer-
ian are not regulated by the Food and Drug Administration,
an important concern surrounds the lack of information avail-
able to the consumer about the substances used to in their
preparation. The remainder of this section focuses on benzo-
diazepines and newer hypnotic drugs.
Evidence for Efficacy
Placebo-controlled clinical studies have documented the
acute effects of benzodiazepine-receptor agents on sleep
(Holbrook, Crowther, Lotter, Cheng, & King, 2000; Nowell
et al., 1997). Hypnotic medications improve sleep continuity
and ef“ciency through a reduction of sleep onset latency
and time awake after sleep onset. They also increase total
sleep time and reduce the number of awakenings and stage
shifts through the night. Their effects on sleep stages vary
with the speci“c class of medications. All benzodiazepine-
receptor agents increase stage 1 and stage 2 sleep and reduce
REM and slow-wave (stages 3 and 4) sleep. These latter
changes are less pronounced with the newer hypnotics
(e.g., zolpidem, zopiclone). In a recent meta-analysis of
22 placebo-controlled trials (n1894), benzodiazepines and
zolpidem were found to produce reliable improvements of
sleep-onset latency (mean effect size of 0.56), number of
awakenings (0.65), total sleep time (0.71), and sleep quality
(0.62) (Nowell et al., 1997). Thus, hypnotic medications are
ef“cacious for the acute and short-term management of in-
somnia. However, because the median treatment duration in
controlled studies is only one week (range of 4 to 35 days),
and follow-ups are virtually absent, the long-term ef“cacy of
hypnotic medications remains unknown.
Risks and Limitations
The main limitations of hypnotic medications are their
residual effects (e.g., daytime sedation, cognitive and psy-
chomotor impairments, anterograde amnesia), which are more
pronounced with long-acting agents (e.g., ”urazepam,
quazepam) and in older adults (Monti & Monti, 1995). The
use of long-acting benzodiazepines is associated with an in-
creased rate of falls and hip fractures (Ray, 1992) and motor
vehicle accidents in the elderly (Hemmelgarn, Suissa, Huang,
Boivin, & Pinard, 1997). When used on a prolonged basis,
hypnotics may lead to tolerance and it may be necessary to in-
crease the dosage to maintain therapeutic effects. This toler-
ance effect, however, varies across agents and individuals and
some people may remain on the same dosage for prolonged
periods of time. Whether this prolonged usage is a sign of con-
tinued effectiveness or of fear of discontinuing the medication
is unclear. Rebound insomnia is a common problem associ-
ated with discontinuation of benzodiazepine-hypnotics; it is
more pronounced with short-acting drugs and can be attenu-
ated with a gradual tapering regimen. Zolpidem and zopiclone
may produce less rebound insomnia upon discontinuation
(Monti & Monti, 1995; Wadworth & McTavish, 1993). Fi-
nally, prolonged usage of sleep-promoting medications, pre-
scribed or over-the-counter, carry some risk of dependence
(APA, 1990); this dependency is often more psychological
than physical (Morin, 1993). Psychological interventions
have been found effective in assisting prolonged users of ben-
zodiazepines to discontinue their drugs (Morin et al., 1998).
In summary, hypnotic medications are effective for the
short-term treatment of insomnia; they produce rapid bene“ts
which last several nights and, in some cases, up to a few
weeks. There is, however, little evidence of sustained bene“ts
upon drug discontinuation or of continued ef“cacy with
prolonged usage. In addition, all hypnotics carry some risk of
dependence, particularly with prolonged usage. The primary
indication for hypnotic medications is for situational sleep
dif“culties; their role in the clinical management of recurrent
or chronic insomnia is still controversial.Psychological TherapiesMore than a dozen psychological interventions (mostly
cognitive-behavioral in content) have been used for treating
insomnia. Treatment modalities that have been adequately
evaluated in controlled clinical trials include stimulus control
therapy, sleep restriction, relaxation-based interventions,
cognitive therapy, and sleep hygiene education. The main
focus of these treatments is to alter the presumed perpetuat-
ing factors of chronic insomnia. As such, they seek to modify
maladaptive sleep habits, reduce autonomic and cognitive
arousal, alter dysfunctional beliefs and attitudes about sleep,
and educate patients about healthier sleep practices (see
Table 14.3). As for most cognitive-behavioral interventions,
the format of insomnia treatment is structured, short-term,
and sleep-focused. Treatment duration typically lasts 4 to 6
hours and is implemented over a period of 4 to 8 weeks. A
summary of these treatments is provided below; more exten-
sive descriptions are available in other sources (Espie, 1991;
Hauri, 1991; Lichstein & Morin, 2000; Morin, 1993).Relaxation-Based InterventionsRelaxation is the most commonly used nondrug therapy for in-
somnia. Among the available relaxation-based interventions,
some methods (e.g., progressive-muscle relaxation, autogenic
training, biofeedback) focus primarily on reducing somatic