Sleep disturbances are common
Sleep disturbances are so common in CFS/ME that most doctors will not even
make the diagnosis if a patient reports having normal, restful sleep. Virtually every
CFS/ME patient has some trouble sleeping. Usually, problems consist of either
sleeping too little or sleeping too much. In either case the quality of sleep is poor.
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Non-restorative sleep
Although sleep disturbances can take many forms, the outcome is always the
same—waking up tired. Nonrestorative sleep is a hallmark symptom of CFS/ME
and is a condition that acts as a catalyst. Because poor sleep exacerbates other
symptoms (pain, emotional swings, flu-like symptoms, fatigue) it is a focal point for
treatment.
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Sleep is complex; relies on hypothalamus
The chemical recipe for sleep is complex, and the timing of hormones, such as
melatonin, amines, and other substances that send messages throughout the body
must be perfect. Body temperature must be lowered, metabolism slowed, appetite
inhibited, hormones released, elimination down regulated, and immune system
upregulated. Think of it as a symphonic orchestra, with the hypothalamus as the
conductor.
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Common sleep disorders
Any chronic alteration in normal sleep patterns is referred to as a sleep
disorder. Common sleep disorders include insomnia (inability to fall or stay asleep),
malsomnia (excessive light sleep or broken sleep), hypersomnia (excessive sleep),
hypnagogic sleep (a state of being half awake, half asleep), and nightmares.
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Altered brain waves in ME; research studies
Most researchers agree that the sleep disturbance in CFS/ME is caused by an
alteration in the normal brain wave patterns required for deep, restful sleep. Dr.
Russell Poland has proposed that in CFS/ME the normal pattern of sleep phases is
interrupted by alpha wave spikes (around 10 Hz); that is, when you should be in
deep, restoring stage four sleep, your brain waves are acting as though you are
awake ( CFIDS Chronicle , Summer 1993). (It should be mentioned that alpha spikes
are common in many autoimmune disorders.) Another CFS/ME anomaly is the
presence of excess theta waves, which cause the sleeper to remain in a light sleep
state. Dr. Jay Goldstein has theorized that the brain wave disturbances are the
result of alterations in hypothalamic function ( CFIDS Chronicle , Fall 1991).
In 1993 Krupp et al conducted sleep studies (polysomnography) in a group of
72 CFS patients with sleep disturbances. In 10 of 16 (62.5%) patients, the
researchers found clinically significant sleep abnormalities. The disorders included
periodic movement disorder, excessive daytime sleepiness, apnea, and narcolepsy.
A subsequent study in 1997 by Fischler et al revealed a lower ratio of stage 4
sleep, which would explain why sleep is nonrestorative in CFS/ME patients. The
researchers also found sleep initiation problems and sleep maintenance
disturbances. In keeping with the lower percentage of deep sleep they found a
higher percentage of stage 1 (light) sleep and a lower percentage of stage 2 sleep. All
of these finding confirm a significant disturbance in the sleep architecture of
CFS/ME patients.
Cytokines
The cause of the dysregulation may be attributable to excess cytokines acting
to stimulate the sympathetic nervous system (which is regulated by the
hypothalamus). Many studies have found increased inflammatory cytokines in the
plasma of patients with CFS/ME, including IL-6 and IL-1. Research indicates that
IL-1 plays a role in the regulation of non-REM sleep by increasing delta waves,
which may lead to hypersomnia and daytime sleepiness.
Interestingly, the only study which has actually measured cytokine levels of
CFS/ME patients during sleep found not pro-inflammatory activity, but anti-
inflammatory activity. In 2010 Nakamura et al found that in both CFS/ME and FM
patients, increases in IL-10 levels correlated with fragmented sleep. The
researchers concluded that “alterations in the balance of Th1 and Th2 cytokines
toward a Th2 or sleep-disrupting response suggests a possible role for cytokine-
induced, disturbed sleep in the pathogenesis of both syndromes.”
Low acetylcholine?
But cytokines are only one player in sleep disturbances. In 1996 Dr. Ernir
Snorrason, Dr. Arni Geirsson and Dr. Kari Stefansson tested Galantamine, a
selective acetylcholinesterase inhibitor, as a treatment for CFS/ME. The
researchers theorized that a deficit in acetylcholine was responsible for many
CFS/ME symptoms. Interestingly, the increase in acetylcholine, a neurochemical
generally associated with arousal, resulted in a 70% improvement of sleep
disturbances. Later studies conducted by Khan et al confirming hyper-
responsiveness to acetylcholine seem to bear out the hypothesis that low levels of
acetylcholine may contribute to sleep disturbance.