Insomnia in Peri-Menopausal and Post-Menopausal Women
by Andrew D. Krystal, M.D., M.S.
| Geriatric Times |
 |
May/June 2001 |
|
Vol. II |
|
Issue 3 |
As women age, there is a gradual decrease in ovarian function that culminates
in the onset of menopause. Menopause is defined as the time of the final
menstrual period and occurs at a mean age of 51 years (Krystal et al., 1998).
During the peri-menopausal period of diminished ovarian production of estrogen
and progesterone occurring prior to menopause, women frequently begin to
experience a number of associated symptoms. These symptoms include insomnia,
night sweats, hot flashes, vaginal dryness, urinary frequency, palpitations,
headaches, vertigo, anxiety, dysphoria, irritability, forgetfulness and an
inability to concentrate. These symptoms may persist after menopause
(Chakravarti et al., 1977; Gambrell, 1986; Sharma and Saxena, 1981). The
centrality of insomnia is evident from data suggesting that it is experienced
by 30% to 63% of peri- and post-menopausal women. In some studies it is the
most common symptom experienced (Krystal et al., 1998; von Muhlen et al.,
1995).
Despite the frequency of insomnia in peri- and post-menopausal women, there
is a surprising lack of research studies in this area (Krystal et al., 1998).
In this brief article, the available literature on the pathophysiology,
diagnosis and treatment of insomnia in peri- and post-menopausal women will be
reviewed.
It is first necessary to determine whether there is evidence for an insomnia
syndrome that is specifically linked to the changes of the
peri-/post-menopausal period. Attribution of insomnia to peri-/post-menopausal
changes is clouded by the fact that the incidence of insomnia complaints among
all women over 30 is 26% to 45% (Krystal et al., 1998). One important
contributing factor is that a number of sleep disorders that can cause insomnia
(restless legs syndrome, periodic movements of sleep and sleep apnea) increase
in frequency with advancing age (Ancoli-Israel et al., 1981; Fry, 1987).
Despite these considerations, there does appear to be evidence that in many
women, insomnia is specifically linked to peri-/post-menopausal changes. A
number of studies indicate an association between nighttime vasomotor changes
(often manifested in night sweats) caused by diminished ovarian hormone
production and sleep disruption (Campbell and Whitehead, 1977; Coope, 1996;
Woodward and Freedman, 1994).
Hormone replacement therapy has also been found to lead to improvement in
both polysomnographic evidence of insomnia and vasomotor symptoms (Campbell,
1976; Regestein et al., 1981). In contrast, subjective complaints of insomnia
not associated with polysomnographic evidence of increased frequency of
arousals tend not to respond to hormonal therapy, as is also the case for
non-vasomotor symptoms. Therefore, these may not be due to diminished hormone
production (Campbell, 1976; Fry, 1987; Regestein et al., 1981). This
non-hormonally related insomnia is of unclear origin, and there are a number of
possible etiologies, including: 1) a period of insomnia due to vasomotor events
that led to behavioral conditioning causing a persistent psychophysiologic
insomnia independent of the vasomotor events (Krystal et al., 1998); 2)
unresolved grief associated with menopausal changes (Thomson and Oswald, 1977;
U.S. Department of Health and Human Services [HHS], 1993); or 3) insomnia not
related to menopausal status (Krystal et al., 1998).
Proper management of a peri-/post-menopausal woman with insomnia is highly
dependent upon determining the correct etiology for the insomnia, since the
optimal treatment differs greatly with different etiologies (Krystal et al.,
1998). In order to sort out this differential diagnosis, it is crucial to take
a careful history.
While this may appear straightforward, insomnia may sometimes be the first
or only presenting symptom. It should also be noted that individuals suffering
from insomnia often do not mention this to their health care practitioners.
Because of the very high incidence of insomnia in peri-/post-menopausal women,
it seems justified to ask patients about their sleep or even consider
implementing routine screening for insomnia using an instrument such as the
Insomnia Symptom Questionnaire (Krystal et al., 1998).
A careful history will also rule out an underlying sleep disorder. When
restless legs syndrome is the cause of the insomnia, the patient will have a
history of trouble falling asleep due to an uncomfortable, crawling feeling in
the legs associated with the need to walk (Fry, 1987). Similarly, periodic
movements of sleep are typically associated with a history of the bed partner
noticing twitching movements throughout the night. The reports of the bed
partner are also helpful in identifying sleep apnea. They generally will
provide a history of loud snoring and episodes of stopping breathing at night.
A history of morning headaches and dry mouth and daytime sleepiness is also
commonly present.
Despite efforts to identify these disorders by taking a careful history,
some individuals -- roughly 10% in the elderly -- may have clinically
significant periodic movements of sleep or sleep apnea when there is nothing in
the history to suggest their presence (McCall et al., 1992). Because such cases
can only be picked up with polysomnography, it is prudent to refer patients for
polysomnography when all the usual treatments fail.
The history should also help to identify if the onset of insomnia symptoms
coincided with the onset of vasomotor symptoms. In this case, a referral for
hormone replacement therapy is appropriate (Krystal et al., 1998).
If hormone replacement does not work, behavioral conditioning should be
considered. Behavioral sleep therapy will break the association of anxiety and
alertness with the attempts to sleep, alter the expectations of poor sleep and
correct aberrant sleep hygiene practices. In circumstances where the insomnia
is associated with peri-menopausal symptoms but vasomotor symptoms are absent,
or the onset of the insomnia occurred at a different time than clear vasomotor
symptoms, other etiologies should be explored (Krystal et al., 1998).
In addition, it is very important to explore the patient's reactions to
their hormonal changes to determine if unresolved grief may be a contributing
factor (HHS, 1993). A referral for grief-oriented psychotherapy should be
considered in these cases (Krystal et al., 1998).
In some cases, sedative/hypnotic medications may be very helpful. These
should generally be reserved for cases when all other attempts to treat the
underlying cause of the insomnia have failed or because hormone replacement
therapy is not possible (e.g., there is a high risk of cancer) (Krystal et al.,
1998).
Because the course of medication is likely to be relatively long-term,
sedative/hypnotic medications -- such as the benzodiazepines and chloral
hydrate -- that lead to significant tolerance and withdrawal should be avoided.
Zaleplon (Sonata) and zolpidem (Ambien) are better in this regard than the
older benzodiazepines and could be considered. The sedating antidepressants
have excellent tolerance and withdrawal profiles, but have significantly more
side effects and a greater likelihood of next-day sedation and, therefore, may
not be tolerated by many patients. There is one report of the use of trazodone
(Desyrel) in this setting (Pansini et al., 1995), but there has been no
systematic study of treatment with a sedative/hypnotic medication in this
population. On the basis of the above considerations, I use the protocol listed
in the Table in order to assess and treat women with
insomnia who may be peri-/post-menopausal.
There are substantial gaps in the available information as to how to best
manage insomnia in women of peri-/post-menopausal age. For example, a way to
determine definitively if peri-menopausal hormonal changes are present is
glaringly absent. Leutenizing hormone levels appear to increase during
vasomotor events, however, this occurs so sporadically that it has not proven
useful as a screening test (Krystal et al., 1998).
Additional work is also needed to determine if, and in what conditions,
polysomnography, including skin conductivity and temperature recording, may be
useful to determine if nighttime sleep disruptions are due to vasomotor events
and whether hormone replacement therapy actually eliminates nighttime vasomotor
events (Krystal et al., 1998). Additional studies would also be helpful to
determine if behavioral sleep therapy following unsuccessful hormone
replacement therapy results in resolution of symptoms. Finally, further
research on sedative/hypnotic medication is needed.
In summary, some progress has been made about how to manage insomnia in
peri-/post-menopausal women, however, a review of the literature illustrates
that a great deal more research is needed in order to optimize diagnosis and
treatment.
Dr. Krystal is professor of psychiatry and behavioral
sciences at Duke University Medical Center. He is also director of the Duke
Clinic Sleep Disorders Research Laboratory.
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