EU_Psychiatry_Mignot_Capasso_quark6.qxp 3/7/08 02:30 Page 44
Insomnia
Diagnosis and Management of Common Sleep Disorders –
An Overview for the Psychiatrist
a report by
Emmanuel Mignot
1
and Robson Capasso
2
1. Howard Hughes Medical Institute Investigator; 2. Post-doctoral Fellow, Sleep Medicine, Stanford Sleep Disorders Center
“Sleep is the golden chain that ties health and our bodies together.” tegmental area (VTA), for example, do not seem to significantly increase
Thomas Dekker overall neuronal activity in wakefulness, but are certainly activated by
specific behaviours in wakefulness and are involved in the wake-
Untreated sleep disorders such as sleep apnoea, restless legs syndrome promoting effects of most stimulants, such as amphetamines,
(RLS) and narcolepsy are common and often undiagnosed. They have methylphenidate and modafinil.
significant effects on quality of life and can even lead to death, for example
in the context of an accident caused by tiredness while driving. A smaller number of systems are sleep-active in the brain: during non-
Furthermore, these disorders can cause symptoms that may be confused rapid eye movement (NREM) sleep, most of the brain activity is decreased
with neuropsychiatric conditions such as depression or schizophrenia or and the EEG is desynchronised, characterised by the appearance of slow
that can contribute to treatment resistance. A number of studies have wave activity. Major sleep-promoting centres include a group of anterior
shown associations between sleep and genuine neuropsychiatric disorders. gamma-aminobutyric acid (GABA)-ergic hypothalamic and basal
forebrain sleep-on networks, including the ventrolateral preoptic (VLPO)
The Basic Neurobiology of Sleep and median preoptic (MnPO) nucleus of the hypothalamus.
3
These
Sleep is not a passive state. The neural substrates underlying sleep states systems strongly inhibit the wake-active systems mentioned above. Of
include sleep- and wake-on neuronal networks. Wake-on-promoting final interest is REM sleep, a paradox as the brain is generally active (most
systems are typically brainstem and hypothalamic systems that project to notably the cortex, with a wave-like desynchronised EEG and associated
the cortex and or the thalamus, which then activates the cortex. These dreaming) while REM and muscle paralysis (atonia) occur. In REM sleep,
include cholinergic ascending systems (pedunculopontine and laterodorsal cholinergic systems and many sleep-on systems are active, but
tegmental areas and basal forebrain), adrenergic locus coeruleus, monoaminergic systems are turned off.
4–6
Most antidepressants are
serotonergic raphe nuclei, hypocretin-containing lateral hypothalamic strong REM sleep suppressants. Sleep and wake tendencies can be seen
systems and histamine-containing tuberomammillary hypothalamic nuclei. as the sum of two processes: homeostatic and circadian. The homeostatic
General brain activation ensues, with high glutamate release and process is a reflection of the sleep debt. It reflects the fact that the longer
electroencephalography (EEG) desynchronisation and consciousness. we are awake, the more sleepy we become. It has been claimed that
Wakefulness is the co-ordinated expression of many behaviours that are adenosine (AD), an inhibitory neuro-transmitter, accumulates in the basal
constantly changing in response to variations in the external and internal forebrain with wakefulness and plays a role in the integration of sleep
milieu. Most likely, each arousal system is particularly active under specific pressure, inhibiting wake-on systems.
2,4–6
Caffeine is a very popular wake-
circumstances, and there is an intense interaction among them.
1,2
promoting agent, and its main mechanism of action is through AD
Dopaminergic cell groups of the substantia nigra (SN) and ventral receptor antagonism. This homeostatic factor interacts with the circadian
process, which has evolved as an adaptation to the solar cycle of light and
dark and is present in almost all mammals.
Emmanuel Mignot is a Howard Hughes Medical Institute
Investigator, a Professor of Psychiatry and Behavioral Sciences
and Director of the Center for Narcolepsy at Stanford
Independently of sleep debt, the circadian clock sends a wake-promoting
University. He is internationally recognised as having signal that peaks in the afternoon (best tracked by body temperature
discovered the cause of narcolepsy. Dr Mignot has received
fluctuations without sleep) so that it opposes the mounting sleep debt that
numerous grants and honours, including National Sleep
Foundation (NSF) awards and the Jacobaeus prize. He is the
results from having been awake since the morning, maintaining alertness
co-author of over 100 original scientific publications and serves
during the day. An opposite interaction occurs during the night so that the
on the Editorial Board of several sleep disorder journals.
tendency to sleep is at its peak in the early hours of the morning, allowing
E:
mignot@stanford.edu
us to sleep longer once the sleep debt has been reduced by the previous
sleep cycles. The suprachiasmatic nucleus (SCN) in the hypothalamus
functions as the main circadian pacemaker, controlling the timing of the
Robson Capasso completed medical school and further
surgical training at the Universidade Federal do Parana in sleep–wake cycle, and is mostly influenced by light and, to a lesser extent,
Curitiba, Brazil. After completion of psychiatry training at
by melatonin, a hormone produced in the night by the pineal gland.
7
This
the University of Miami, he is now pursuing a
post–doctoral fellowship in Sleep Medicine at the Stanford
process may be disrupted in shift workers and when we cross time zones.
Sleep Disorders Center.
This is commonly known as jet-lag, and causes a broad constellation of
symptoms including fatigue, disorientation, irritability (worse in the early
morning of the original time zone) and impaired sleep (worse in the early
evening of the original time zone, sometimes called the forbidden zone).
44 © TOUCH BRIEFINGS 2008
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