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© Springer Nature Switzerland AG 2019
F. R. Pérez-López (ed.), Postmenopausal Diseases and Disorders,
https://doi.org/10.1007/978-3-030-13936-0_17
P. Polo-Kantola (*)
Department of Obstetrics and Gynecology, Turku University Hospital and University
of Turku, Turku, Finland
e-mail: paivi.polo@tyks.
T. Saaresranta
Sleep Research Centre, Department of Pulmonary Diseases and Clinical Allergology,
University of Turku, Turku, Finland
Division of Medicine, Department of Pulmonary Diseases, Turku University Hospital,
Turku, Finland
Department of Pulmonary Diseases and Clinical Allergology, University of Turku,
Turku, Finland
e-mail: tasaare@utu.
L. Lampio
Department of Obstetrics and Gynecology, Helsinki University Hospital, Helsinki, Finland
e-mail: lmlamp@utu.
17
Sleep andSleep Disturbances
inClimacteric Women
PäiviPolo-Kantola, TarjaSaaresranta, andLauraLampio
17.1 The Importance ofSleep
Good and sufficient sleep is necessary for good quality of life [1, 2] and health.
Chronic sleep disturbances are associated with both physical and mental neg-
ative health consequences, like with cardiovascular diseases [3–6], diabetes
[7, 8], depression [9], and cognitive impairment [10, 11]. In addition, sleep
disturbances are related to increased work absenteeism [12–15], poor work
performance [16, 17], accidents, and increased healthcare costs [18, 19]. Sleep
disturbances increase in prevalence during climacteric [20, 21], thus influenc-
ing in health-related quality of life, work productivity, and healthcare utiliza-
tion [22].
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262
17.2 The Sleep Regulation andMeasuring theSleep Quality
The sleep-wake cycle is regulated by two biological processes, which interact
and balance each other, the circadian process C and homeostatic process S [23].
Circadian rhythm (circa dia) is an approximately 24-h regulation cycle of the body’s
internal processes and alertness levels [24]. Sleep-wake homeostasis, process S, is an
internal mechanism that produces a pressure to sleep and regulates sleep intensity;
i.e., the longer awake, the stronger the need to sleep, and vice versa. Several brain
areas are involved in regulation of sleep, most importantly the medulla oblongata,
pons, formation reticularis, midbrain, thalamus, hypothalamus, preoptic area, basal
forebrain, hippocampus, and cerebral cortex. Of neurotransmitters, adenosine and
nitric oxide [25] and gamma-aminobutyric acid (GABA), hypocretin, and histamine
[26] are critical for sleep regulation. Also various hormones, such as growth hor-
mone, cortisol, melatonin, prolactin, and ovarian hormones, are involved [27–34].
Sleep quality is divided to subjectively reported sleep quality (subjective sleep
quality) and objectively measured sleep quality (sleep architecture). Subjective
sleep quality and daytime consequences (fatigue, tiredness, reduced attention, cog-
nition or memory impairment, mood disturbance, or irritability) are evaluated with
structured questionnaires or sleep diaries. Subjective sleep quality is most com-
monly worsened by insomnia symptoms (e.g., difculty initiating or maintaining
sleep, or too early morning awakening) but sometimes by sleep disordered breath-
ing (SDB) or restless legs syndrome (RLS) as well. One or more insomnia symp-
toms which occur at least three times per week during at least 1month with daytime
symptoms are required for the denition of insomnia disorder [35]. Generally, older
age, female sex, and lower socioeconomic status, as well as previously diagnosed
insomnia, positive family history of insomnia, and poor perceived mental and gen-
eral health are risk factors for insomnia [36–39]. Also several systemic diseases and
the use of medicaments may induce sleep disturbances [40, 41].
Sleep can be objectively measured with polysomnography (PSG), which consists
of an electroencephalogram (EEG), electrooculogram (EOG), and electromyogram
(EMG). Sleep is divided into wake, non-rapid eye movement (NREM) sleep, and
REM sleep. NREM is further divided into stages N1–N3 (former S1–S4). N3 (for-
mer S3 and S4) is also called as slow-wave sleep (SWS) [
42–44] (Fig.17.1). In
addition to the percentages of sleep stages and total sleep time, sleep latency, sleep
efciency, slow-wave activity (SWA), and the number of arousals and awakenings
are typically determined from PSG-measured sleep. The optimal average sleep
duration in order to maintain good health ranges from 7 to 8h [45]. Shorter and
longer sleep durations have been associated with increased morbidity and mortal-
ity in general populations [46–49]. The basic challenge for evaluating sleep quality
and sleep disorders is that the correspondence between subjectively and objectively
measured sleep is not unambiguous [50–53]. However, the individual’s perceptions
of sleep disturbance and daytime consequences are more likely to direct diagnosis
and treatment.
P. Polo-Kantola et al.
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17.3 Subjective Sleep Quality andInsomnia Symptoms
inClimacteric
Sleep disturbances, especially insomnia symptoms, are one of the most bother-
some symptoms in climacteric, being reported by 40–60% of climacteric women
[54]. Both cross-sectional [55–59] and longitudinal [60–63] studies conrm that
the prevalence of perceived sleep disturbances increases in the menopausal transi-
tion, even after controlling for age. A meta-analysis of 24 cross-sectional studies
reported higher odds of experiencing sleep disturbance relative to premenopause in
perimenopausal (1.60), postmenopausal (1.67), and surgically menopausal (2.17)
women [64]. The most common sleep-related complaint is nighttime awakenings
[55, 58, 61, 63], although also difculty falling asleep increases across the meno-
pausal transition [55, 58, 61, 63]. The increase in early morning awakening is shown
to level off from late perimenopause to postmenopause [55, 58, 61, 63]. Although
the insomnia symptoms inevitably increase in climacteric, the research about insom-
nia disorder in climacteric is limited. The phone interview of nearly 1000 women
showed that 26% of perimenopausal women qualied for a DSM-IV diagnosis of
insomnia, with difculty maintaining sleep the most common symptom [65]. As for
increasing follicle-stimulating hormone (FSH), the association with greater odds of
waking up several times was found, whereas decreasing estradiol (E
2
) was associ-
ated with higher odds of difculty falling and staying asleep [61]. Despite this clear
increase in poor sleep quality as women enter climacteric, the severity and persis-
tence of poor sleep, as well as the extent of impairment in daytime function, vary
between women.
Arousal
MT
Wake
REM
S1
S2
S3
S4
00:00 01:00 02:00 03:00 04:00 05:00 06:00
Arousal
MT
Wake
REM
S1
S2
S3
S4
Fig. 17.1 Hypnograms derived from the polysomnograms of the same woman. Premenopausal
situation (upper hypnogram) and perimenopausal situation 6years later (lower hypnogram). Note
especially the sleep fragmentation. MT movement time, S1 stage 1 non-REM sleep, S2 stage 2
NREM sleep, S3 stage 3 NREM sleep, S4 stage 4 NREM sleep. Data from Lampio etal., 2017
17 Sleep andSleep Disturbances inClimacteric Women
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17.4 Sleep Architecture inClimacteric
Even though the evidence for declining subjective sleep quality in climacteric is
strong, polysomnographic (PSG) studies have generally not found a corresponding
negative change in sleep architecture. The observed mismatch between subjective
and objective sleep quality [66] has been explained by a possible inuence of psy-
chological state on sleep quality judgments by affecting the sleep appraisal process
rather than sleep itself [67]. Also, most PSG studies have been cross-sectional with
small sample sizes and differences in denitions of menopausal stages, age ranges,
presence of systemic diseases and sleep disorders, and sleep-recording techniques.
Some studies have found no differences in sleep architecture between pre- and post-
menopausal women [68–72], while a few studies have reported more slow-wave
sleep (SWS) in peri- and postmenopausal women than premenopausal women [59,
73–76]. More SWS could be interpreted as reecting a better sleep pattern, on the
one hand, but alternatively could reect a recovery response to sleep deprivation.
A single study has found more time spent awake and lower sleep efciency in peri-
and postmenopausal women compared to premenopausal women, but all studied
women were insomnia patients [77].
Few studies have investigated the association between serum concentration of
FSH and PSG measures. A cross-sectional study of women mostly in the early
menopausal transition without sleep complaints found that higher FSH concentra-
tions were associated with more wakefulness after sleep onset, awakenings, and
arousals, after adjusting for age and BMI [78]. However, in women with insomnia
symptoms, PSG measures did not correlate with FSH, whereas they were associ-
ated with anxiety and symptoms of depression [78]. In a small study with a group of
pre- and postmenopausal women with diagnoses of depression, FSH concentration
was positively associated with wakefulness after sleep onset and negatively associ-
ated with SWS [79]. Further, in another cross-sectional study, a more rapid rate
of FSH change over the previous few years was associated with higher amount of
SWS and longer total sleep time during a subsequent sleep study [
80]. In the only
longitudinal, 6-year follow-up study addressing changes in PSG measures across
the menopausal transition, at follow-up, women had a shorter total sleep time, lower
sleep efciency, more wakefulness after sleep onset, and more awakenings after
adjusting for vasomotor symptoms, BMI, and mood (Fig.17.1). These changes in
sleep were linked with advancing age rather than increased FSH levels. Increasing
FSH was associated with a greater proportion of SWS, presumably reecting an
adaptive change to counteract the age-related sleep fragmentation [73] (Table17.1).
Only limited work about PSG measures in climacteric women with insomnia dis-
order exists. One study showed substantial objective sleep disruption, with a poorer
sleep efciency, more wakefulness after sleep onset, and shorter total sleep time,
matching the subjective poor sleep quality in this group compared to women with-
out insomnia [81]. Further, women with insomnia were more likely to have objec-
tively measured hot ashes, and the presence of hot ashes predicted the number
P. Polo-Kantola et al.
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Table 17.1 Polysomnography sleep studies in menopausal transition
Authors
Study design
Sample
characteristics Findings
Comments
Shaver
etal.
1988 [
72]
Cross-sectional Pre-, peri-, and
postmenopausal
women aged
40–59y (n=76)
No differences in
sleep parameters
between the groups
Peri- and
postmenopausal
women
experiencing hot
ashes had longer
REM latency and
tended to have
lower SE compared
to women without
hot ashes
Young
etal.
2003 [59]
Observational
epidemiologic
study
Pre-, peri-, and
postmenopausal
women, mean age
46.3y, SD 8.1
(n=589)
Peri- and
postmenopausal
women had more
SWS, and
postmenopausal
women had less S2,
and higher SE
compared to
premenopausal
women
Peri- and
postmenopausal
women were more
dissatised with
their sleep quality
compared to
premenopausal
women. No
adaptation night
Sharkey
etal.
2003 [76]
Cross-sectional Pre- and
postmenopausal
women aged
45–56y (n=25)
Postmenopausal
women had more
SWS and less S1
No difference in
subjective sleep
quality. Two
consecutive
laboratory nights
Freedman
etal.
2004 [
71]
Cross-sectional Pre- and
postmenopausal
women with and
without hot ashes,
aged 46–51y
(n=31)
No differences in
sleep parameters
Most awakenings
preceded a hot
ash, but not vice
versa in the three
consecutive
laboratory nights
Kalleinen
etal.
2008 [70]
Cross-sectional Young (aged
20–26y),
premenopausal
(aged 45–51y) and
postmenopausal
(aged 59–71y)
(n=61)
No differences
between pre- and
postmenopausal
women. Young
women had longer
TST, higher SE and
SWA, more SWS,
and less WASO
compared to
pre- and
postmenopausal
women
Postmenopausal
women were less
satised with their
sleep quality
compared to
premenopausal
women. Two
consecutive
laboratory nights
(continued)
17 Sleep andSleep Disturbances inClimacteric Women
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266
Table 17.1
(continued)
Authors
Study design
Sample
characteristics Findings
Comments
Sowers
etal.
2008 [
80]
Sleep was
studied
cross-
sectionally and
FSH annually 7
y prior the
sleep study
At the time of the
sleep study,
women were
premenopausal,
early or late
perimenopausal,
and
postmenopausal,
median age 52y
(n=365)
More rapid rate of
FSH change was
associated with
more SWS and
longer TST
More rapid rate of
FSH change was
associated with
poorer subjective
sleep quality. Two
nights of in-home
PSG
Hachul
etal.
2009 [
69]
Cross-sectional Early and late
postmenopausal
women aged
50–65y (n=30)
No differences in
sleep parameters
Two consecutive
laboratory nights
Hachul
etal.
2010 [
75]
Cross-sectional Reproductive
(mean age 38.8y
[SD 10.4]) and
postmenopausal
(55.9y [SD 7.9])
women (n=931)
More SWS, less S2
and REM in
postmenopausal
women compared
to reproductive
women; after
adjustment of age
and BMI, only
greater chance of
having AHI >5 for
postmenopausal
No adaptation night
Campbell
etal.
2011 [68]
Cross-sectional Pre-, early peri-,
late peri-, and
postmenopausal
women aged
48–59y (n=321)
No differences in
PSG measures.
Beta EEG power,
indicating arousal,
↑ in late peri- and
postmenopausal
women, but no
difference in delta
EEG power
Beta EEG power
was related to hot
ash frequency.
Three consecutive
in-home PSG-
measurement
nights. Results
adjusted with age
and other
covariates
Xu etal.
2011 [
77]
Cross-sectional Pre-, peri-, and
postmenopausal
women aged
40–59y (n=74)
Longer total wake
time and lower SE
in peri- and
postmenopausal
women compared
to premenopausal
women
All subjects were
insomnia patients.
No differences in
subjective sleep
quality. Three
consecutive
laboratory nights
(continued)
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of PSG awakenings per hour of sleep [81]. According to another study, where sub-
jective sleep quality and PSG measures were compared between premenopausal
and peri-/postmenopausal women with insomnia disorder, subjective sleep quality
and depression were similar between the two groups, whereas peri-/postmenopausal
women had a longer PSG-dened total wake time and lower sleep efciency, sug-
gesting that PSG measures of sleep quality are impacted to a greater extent in peri-/
postmenopausal than in premenopausal women with insomnia disorder [77].
Table 17.1 (continued)
Authors
Study design
Sample
characteristics Findings
Comments
de
Zambotti
etal.
2015 [
78]
Cross-sectional Young (aged
18–27y) and
perimenopausal
women with and
without insomnia
(aged 43–52y)
(n=44)
FSH ↑ was
associated with
WASO, awakenings
and arousals ↑ in
perimenopausal
non-insomniacs,
but not in insomnia
patients in young
women FSH ↑ was
related to WASO
and N1 ↑
In perimenopausal
insomniacs TST
correlated with
anxiety and
depression. No
adaptation night
Hachul
etal.
2015 [
74]
Cross-sectional Reproductive
(mean age 34.6y,
(SD 8.4)), early
(5.22y (5.3)), and
late (63.3y (8.6))
postmenopausal
women (n=535)
More N3, higher
AHI, and lower
SaO
2
in
postmenopausal
women compared
to premenopausal,
no difference
between early and
late
postmenopausal
women
Wide age range
(20–80y), results
were adjusted with
age, BMI, blood
pressure. No
adaptation night
Lampio
etal.
2017 [
73]
6-year
follow-up
At baseline all
women (mean age
46y, SD 0.9) were
premenopausal and
at the follow-up in
different stages of
menopausal
transition (n=60)
Increase in FSH
associated with
SWS ↑, after
controlling for
BMI, vasomotor
and depressive
symptoms
Aging was
associated with
shorter TST, lower
SE, increased
transitions from
SWS to wake,
increased WASO
and amount of
awakenings after
controlling for
confounding
factors
n number, y year, REM rapid-eye movement sleep, SD standard deviation, SWS slow-wave sleep,
S2 stage 2 non-rapid eye movement (NREM) sleep, SE sleep efciency, S1 stage 1 NREM sleep,
FSH follicle-stimulating hormone, TST total sleep time, PSG polysomnography, WASO wake after
sleep onset, N1 stage 1 NREM sleep, N3 stage 3 NREM sleep, SD standard deviation, EEG elec-
troencephalogram, AHI apnea-hypopnea index
17 Sleep andSleep Disturbances inClimacteric Women
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