Tải bản đầy đủ - 0trang
12 Use It or Lose It
little mention of the accompanying ‘cognitive load’, but instead tend to
attribute the effect largely to improvements with the brain’s blood supply
and aspects of the brain’s chemistry. However, at least one recent major
review of this area  has been much more guarded about why some
cognitive functions improve with exercise while others are insensitive.
For example, although a year-long indoor walking programme in healthy
older adults  pointed to (working) memory improvements, and to better physical fitness, there were no improvements to be seen with measures
of executive function. Here, walking was monotonous, on an indoor circular track and, interestingly, it was noted  that with more environmental stimulation, these improvements may well have been greater.
Apparent benefits for the brain of exercise alone, usually soon disappear
when the regimen is ended  and exercise taken to excess can be counterproductive, as the brain goes into a protective mode  that can be interpreted as a sign of improving brain health, which is not necessarily the
case. On the other hand, brisk walking regimens and jogging can improve
sleep quality and subjectively determined sleep in poor sleepers .
Despite physical exercise alone seeming to be able to reverse some detrimental effects of ageing on those aspects of memory that focus on the
hippocampus  (Sect. 10.7), the same benefits are seen with a variety
of non-exercise ‘cognitive stimulations’  in normal healthy individuals, in particular, those activities involving novel experiences undertaken
daily over several weeks as, for example, in taxi drivers learning new
routes , with these improvements maintained for several months
after training. Although healthy older people usually show obvious associations between their levels of physical fitness and cognitive function,
including executive skills, all of this usually comes with a more mentally
and physically active and outgoing lifestyle as well as with a positive attitude to one’s life.
12.3 Boosting SWS
Sleep, particularly SWS and 1 Hz EEG activities, indicates the enhancing
of brain plasticity , and these activities, and probably other (yet to
be determined) aspects of the sleep EEG, can provide useful markers of
the effects of this increased brainwork in terms of ‘use it or lose it’ for the
ageing brain. However, more needs to be known about how long-term
daily regimens of cognitive stimulation with and without accompanying physical exercise compare with each other. To date, such findings
have been incidental as, for example, seen with a major study  of
age-related cognitive decline linked to structural changes within the
frontal cortex, and accompanied by diminished SWS. The investigators
concluded  that these findings could be improved by behavioural
interventions. Moreover, there is evidence  that three hours of daily
structured but engaging social and physical activity in healthy elderly
people leads to increased SWS, with improvements to memory-oriented
tasks. However, this intervention  only lasted for two weeks, and it
is not clear what would happen if this and similar activities were to be
continued in the long term.
Interestingly, we  have found that older people who naturally and
habitually have more SWS are more flexible in their thinking, have better executive skills, and thus seem to have a ‘younger brain’ for their age.
But simply using what might be viewed as more artificial methods to
increase SWS in the sleep of the older person, is not necessarily a good
sign of a more active waking brain, unless there is evidence of cognitive improvement. Certain drugs can also elevate SWS, as can shortterm increases in waking brain temperature (thus increasing the brain’s
metabolic rate) but without any improvements to waking behaviour, cf.
. Nevertheless, a 30-minute warm bath in the evening, to increase
both body and brain temperature not only increases SWS that night,
but generally improves nighttime sleep in those healthy elderly with
Of course, getting out and about, outdoors, and encountering daylight, will help synchronise the circadian clock and the timing of sleep,
as well as have a daytime alerting effect and reduce the extent of daytime
naps and thus promote better nighttime sleep.
Finally, increased levels of ß-amyloid in the cortex are associated
with dementia. There is new evidence  that in older people these
levels in areas of the prefrontal cortex are correlated with diminished
amounts of SWS, especially its 1 Hz component, as well as with impaired
hippocampus-dependent memory consolidation. However the extent to
Use It or Lose It
which there is any cause and effect, here, remains a matter for speculation, as might the benefits of the ‘getting out and about’ enhancement of
SWS in older age have in offsetting progression of this ß-amyloid. But
clearly this is a potentially worthwhile area of further investigation.
12.4 ‘Fresh Air’
Much can be said for the Victorian belief that exercise should be relaxing and not taxing, as advocated, for example by the pronouncements in
1900 by Dr James Sawyer in his article, “Causes and Cure of Insomnia”,
published in the British Medical Journal (8 December 1900, p. 627) that,
“Daily bodily exercise in the open air but always short of great fatigue must
be enjoined. What is called carriage exercise is better than no outdoor change
at all, but walking is far better exercise and cycling better still, and riding
on horseback the best of all. A worn and worrying man habitually wrapt up
in an absorbing torture of self-consciousness and sleeping badly, must come
out of himself with the saving graces when he mounts a cycle or horse’s back.”
And finally, “Gardening in the open air, not in conservatories or hothouses
affords good exercises and it is very efficient in keeping up objective attention.”
As sleeplessness-cum-insomnia was generally thought at the time to be
a problem for those with more cultured and educated minds, one must
sympathise for the horseless, poor worker whose ‘gardening’ comprised
struggling to grow a few vegetables in a meagre plot of land, so as to
supplement the family’s food supply.
We might smile at this naivety and that ‘gardening makes good sport’
but, nevertheless, these words of Dr Sawyer are wiser than they may seem,
as not only does all this outdoor activity also expose one to daylight, but
varied and active gardening will indeed ‘exercise the brain’, to create more
brainwork, and in doing so may further improve sleep and SWS. Hence,
many of us need to be more ‘ecological’ with our sleep and wakefulness,
get out and about more, even commune with nature, take more of those
relaxing baths, contemplate the wisdom of Emerson, and maybe cancel
that subscription to the gym.
1. Halàsz P et al. 2014 Two features of sleep slow waves: homeostatic and reactive aspects. Sleep Med, 15: 1184–1195.
2. Horne JA 2013 Exercise benefits for the aging brain depend on the accompanying cognitive load: insights from sleep electroencephalogram. Sleep Med
3. Fabel K, Kempermann G. 2008 Physical activity and the regulation of neurogenesis in the adult and aging brain. Neuromol Med 10: 59–66.
4. Kraft E. 2012 Cognitive function, physical activity, and aging: possible biological links, implications for multimodal interventions. Neuropsychol Dev
Cogn B Aging Neuropsychol Cogn. 19(1-2):248–263.
5. Lista I, Sorrentino G. 2010 Biological mechanisms of physical activity in
preventing cognitive decline. Cell Mol Neurobiol 30:493–503.
6. Angevaren M et al 2008 Physical activity and enhanced fitness to improve
cognitive function in older people without known cognitive impairment.
Cochrane Database Syst Rev 16: CD005381.
7. Voss MW et al 2012 The influence of aerobic fitness on cerebral white matter integrity and cognitive function in older adults: Results of a one-year
exercise intervention. Hum Brain Mapp. 34:2972–2985.
8. Rhyu IJ et al 2010 Effects of aerobic exercise training on cognitive function
and cortical vascularity in monkeys. Neurosci 167:1239–1248.
9. Secher NH et al 2008. Cerebral blood flow and metabolism during exercise:
implications for fatigue. J Appl Physiol. 104:306–314.
10. Oudegeest-Sander MH et al 2013 Impact of physical fitness and daily
energy expenditure on sleep efficiency in young and older humans.
11. Fotuhi M et al 2012. Modifiable factors that alter the size of the hippocampus with ageing. Nat Rev Neurol. 8:189–202.
12. Woollett K, Maguire EA. 2011 Acquiring “the knowledge” of London’s layout drives structural brain changes. Curr. Biol. 21: 2109–2114.
13. Mander BA et al 2013 Prefrontal atrophy, disrupted NREM slow waves and
impaired hippocampal-dependent memory in aging. Nat Neurosci.
14. Landsness EC et al 2009 Sleep-dependent improvement in visuomotor
learning: a causal role for slow waves. Sleep; 32:1273–1284.
12 Use It or Lose It
15. Naylor E et al 2000 Daily social and physical activity increases slow-wave
sleep and daytime neuropsychological performance in the elderly. Sleep.
16. Anderson C & Horne JA 2003 Pre-frontal cortex: links between low frequency delta EEG in sleep and neuro-psychological performance in healthy,
older people. Psychophysiology, 40: 349–357.
17. Liao WC. 2002 Effects of passive body heating on body temperature and
sleep regulation in the elderly: a systematic review. Int J Nursing Studies. 32:
18. Mander BA et al 2015. ß-amyloid disrupts human NREM slow waves and
related hippocampus-dependent memory consolidation. Nat Neurosci.
Online advance publication.
REM Sleep: Food for Thought?
During our lifespan, REM sleep (REM) is most prolific 1–2 months
before birth, occupying about half of the roughly 18 hours of the baby’s
daily sleep in utero, where REM probably provides essential, artificial
stimulation for the developing brain in the absence of stimulation from
the outside world. Soon after birth, with the baby being bombarded with
real sensory stimulation, much of REM disappears, much more than
non-REM, to be replaced by wakefulness. However, we adults retain a
higher proportion of REM within sleep than do most other mammals;
this is about 20 % of sleep compared with around 5–15 % for other
mammals. One reason is that we adults resemble our infants more than
any other ape. The retention of marked infant characteristics into adulthood, known as ‘neoteny’, is seen not only in our overall body shape and
general anatomy, but in our remarkable ability to maintain a high degree
of learning, even into old age, and for our cortex to continue adapting
to new experiences and ‘rewire’ itself accordingly. This may help explain
our relatively high amounts of REM in adulthood, to the extent that
some of this REM still falls into the category of ‘dispensability’, like that
© The Editor(s) (if applicable) and The Author(s) 2016
J. Horne, Sleeplessness, DOI 10.1007/978-3-319-30572-1_13
of infants. Our adult REM predominates towards the end of a night’s
sleep, particularly as the usually last REM period (REMP, see hypnogram
in Sect. 6.1) when sleep is less essential, and it is this last REMP which
seems to be most dispensable.
REM is a complex and intriguing aspect of our sleep, and is not simply a platform for dreaming, especially as different parts of the brain are
involved in REM and dreaming, and thus the two phenomena are not
really synonymous. REM can appear in the absence of dreaming, or at
least dreaming as we know it, especially when one considers the predominance of REM in utero.
The eponymous bursts of rapid eye movements (rems), characterising
REM, which are absent from non-REM, typically appear every minute
or so, lasting for about 15 seconds at a time, followed by a period of
inactivity. Although rems are mostly ‘saccadic’, that is with the eyes moving together, darting from side to side as in wakefulness, these bursts are
largely random, seeming to have little or nothing to do with the dream
imagery. The rems per minute, known as ‘REM density’, are greatest during this last REMP, when dreams are also at their most vivid and intense.
In fact, almost half of a whole night’s worth of rems are found here, and
it seems that this overall increased intensity in rems and dreaming may be
a means for maintaining sleep as an alternative to wakefulness when there
is little real need to wake up.
Interestingly, something similar to bursts of rems occurs concurrently
within the ears during rems, called ‘middle ear muscle activity’ (MIMA),
and is also found frequently during wakefulness to ‘tone up hearing’,
and is comparable with ‘pricking up one’s ears’. Bursts of rems and
MIMAs reflect the phasic component of REM, largely emanating from
more ‘basic’ brain structures well below the cortex, where this is seen in
the ‘sub-cortical’ EEG as bursts of pontine-geniculate-occipital (PGO)
waves. These, together with rems and MIMAs seem to resemble an alerting response, in redirecting attention to a new stimulus.
I liken dreaming to the ‘cinema of the mind’, with what seems to be
increasingly appealing dreams in successive REMPs, when dreams jump
from one intriguing scene to another, maybe distracting us from waking.
Dreams comprise a jumble of waking encounters, thoughts and emotions
and, as Freud noted, ‘we dream as we think’, although I doubt whether
REM Sleep: Food for Thought?
attempts at dream interpretation are the ‘royal road to unconsciousness’
as he believed. As dreams are largely a mixture of personal experiences
and thoughts, one must be sceptical about attempts by others to ‘interpret’ them, without knowledge of these experiences. Nevertheless, dreams
are quite emotive, and may somehow help consolidate waking memories
having particular emotional significance . However, as we typically
dream for about 90 minutes in total during the course of a night’s sleep,
and as much of dreaming seems to be nonsense, there is little opportunity
to remember a dream unless we immediately wake up out of one, when
little more than the previous few minutes can usually be recalled, even
then, and is soon forgotten.
Recently, there has been much interest in what is known as the ‘default
mode network’ of linked areas within the waking brain, largely identified by fMRI findings, with this network becoming most active during
daydreaming  as well as during REM, but being less active during
As noted earlier (Sect. 6.3), by extending sleep, as with a lie-in, and
when not making up for previously lost sleep, the next, hitherto usually absent REMP (at around 7 hours’ sleep), is even longer albeit not
so intense in terms of REM density, suggesting that sleep has probably
reached saturation. Nevertheless, if after waking up in the morning at
the normal time, feeling refreshed and sleep satiated, we then decide to
return to sleep, it is likely that another REM will reappear within 10
minutes of any sleep onset. This is known as a ‘SOREMP’—sleep onset
REM period. These otherwise absent examples of ‘extra REM’ seem to
help sleep ‘coast along’, especially as this extra REM does not subtract
from the ensuing night’s amount of REM, nor change rem density. Thus,
this particular REM seems quite surplus to requirements.
Another notable characteristic of REM is its associated atonia, a temporary paralysis of limb, trunk and facial muscles, preventing us from
moving and thus physically enacting a dream. Sometimes, when woken
up suddenly from a frightening nightmare, this atonia remains for a short
while, often causing further alarm, especially as this also prevents speech.
Known as ‘isolated sleep paralysis’, it is unlikely to be symptomatic of
narcolepsy (see Sect. 9.5). This atonia may well have roles other than just
safeguard the dreamer, as there may be a need for the brain to generate
this physical movement during REM, to be blocked by the paralysis.
Interestingly, if healthy sleepers are woken as soon as they enter REM,
then get up and quietly walk around for about 15 minutes to return to
sleep, and if this process is repeated whenever REM reappears that night,
then there is little recovery of this lost REM (‘REM rebound’) the following night and, perhaps surprisingly, there is little by way of increased
daytime sleepiness, cf. . However, it is not known to what extent all
this could be replicated into a second night and beyond. Nevertheless,
substitution of REM by waking movement, with no subsequent REM
rebound, has also been reported by several animal studies, cf. .
13.2 REM Wakefulness
REM is both a light and deep form of sleep, inasmuch that during REM we
can hear what is going on around and unconsciously determine whether
to wake up and respond to a noise or ignore it. This mechanism centres
on the limbic system of the brain, most notably the amygdala, which in
wakefulness is largely concerned with assessing the emotional significance
of whatever is sensed. Throughout REM the amygdala remains active
and can ‘decide’ whether a sound warrants a rapid awakening with full
alertness or being blocked out. In this latter respect, REM seems to be a
‘deep’ form of sleep, allowing sleep to continue, and this is why a familiar
train thundering by on a nearby railway is unlikely to cause an awakening during REM, whereas whispering a familiar name or the whimper of
a child will cause an immediate awakening and rapid alertness. On the
other hand, during SWS such arousals are largely a matter of the loudness of the sound rather than its meaning, requiring much more stimulation for an awakening, followed by grogginess and ‘sleep inertia’ lasting
for several minutes (see Sect. 11.5). ’Light sleepers’ are more reactive to
sounds, especially during REM, and as they are more liable to wake up,
so are they more likely to know they have been dreaming, unlike the
‘sounder sleeper’ who slumbers on, unable to remember their dreams.
Brain imaging using fMRI during REM also shows the activities of
several other major brain areas to be similar to those of wakefulness, apart
from the default mode network and the amygdala, which are in contrast
REM Sleep: Food for Thought?
with non-REM and quite different from SWS . This similarity is also
apparent in the EEGs of REM and relaxed wakefulness, where for many
mammals REM is also known as ‘paradoxical sleep’ as the EEG appears to
be like that of wakefulness, while the animal is clearly asleep.
With dreams often being emotional, and as REM can be a light sleep,
it is surprising that we do not wake up more frequently from them.
Despite such dream content, the actual emotional response is blocked,
as there is no physiological arousal such as rapid rises in heart rate and
blood pressure, as would happen in wakefulness. Although, if the dream
develops into a nightmare and an awakening, these responses are triggered immediately. This blocking of responses is, again, largely under the
control of the amygdala which, during wakefulness, also helps us to deal
with threats and fears , as do the activities of other parts of the limbic
system, notably the orbitofrontal region (see Fig. 10.1) of the frontal
cortex which tones down more basic emotions into more acceptable ways
. The Appendix also gives examples of the effects on behaviour when
this region is destroyed as a result of trauma, often leading to uninhibited
and impaired social responses. The orbitofrontal region also happens to
be active in REM, but not in non-REM.
Other key brain regions similarly active during both REM and wakefulness are the anterior cingulate cortex (ACC) and the hippocampus
[4, 7]. In wakefulness the ACC helps resolve indecisions or conflicts
between competing behavioural responses and in working out the payoffs, especially in terms of curiosity versus risk . Inasmuch as curiosity
can bring us into threatening situations, the amygdala and orbitofrontal
cortex seem to contribute to the final decision on what to do. The hippocampus, mentioned earlier (Sect. 10.7), within the context of memory,
not only is critical to the formation of long-term (‘episodic’) memories
associated with personal events, experiences and related emotions, but
also enables the navigating around our environment, with the creation of
‘mental maps’ (largely utilising hippocampal ‘place neurones’), as well as
with helping to integrate these memories.
In conjunction with other brain regions also active in REM, these mental maps might be created for the location of places having strong positive
or negative emotional associations. Which brings me back to that atonia
of REM, and the suppression of intended movements, as these might be
integral to the creation of mental maps during REM. In wakefulness,
locomotion is indeed integral to brain plasticity (see Sect. 12.1), including this mental mapping . One might even speculate that the atonia
of REM is somehow ‘rehearsing’ the physical movements between these
more emotionally driven mapping points.
Whilst the role of REM in the more ‘standard’ forms of memory,
outlined in Sect. 10.7, remains debatable , impressive evidence is
accumulating that REM helps us cope with and stabilise the emotional
memories of wakefulness [7, 10–13], not only in terms of what has happened recently, but also in preparation for the future. The term used is
‘fear extinction’, that is, the lessening of more fearful or apprehensive
events, and maybe their locations, thus enabling one better able to deal
with similar encounters in the future. However, in these respects there
remains the puzzle of explaining the value of what must be the ‘surplus’
REM, seen in extended sleep and those SOREMPs.
Most antidepressant medicines reduce REM by at least 30 % (about
30 minute per night) [14, 15], with more extreme cases  of at least
50 % REM reductions for over 6 months. This absent REM seems largely
replaced by interim wakefulness throughout the night, which may well
be compensatory. It should be noted that this form of REM suppression
is diffuse throughout the night, and not just a termination of the last
REMP. Although there is some increase in REM (‘REM rebound’) when
medication ceases, this only lasts a few days and, clearly, only represents
a small fraction of the REM that has been lost. Interestingly, these longterm partial losses of REM do not seem to cause memory impairments.
As REM suppression is immediate when these medications are given,
their beneficial effects on depression tend to take 2–4 weeks before
becoming evident. So, the extent to which REM and dream loss are therapeutic remains a matter for conjecture, and it should be noted that most
antidepressants are associated with changes to non-REM as well as with
REM . On the other hand, when severely depressed patients have
their night sleep reduced to about 4 hours, thus losing the last one or two
REMPs, there is often an immediate but temporary mood-improving
effect the next day, which relapses on the return to normal sleep. But we
cannot be certain that it is the loss of REM itself which is the key to this
temporary mood improvement.