‘There is preliminary evidence that alterations in sleep stage transitions and sleep instability, and other physiological mechanisms, such as heart rate variability and altered cortisol profiles, may be evident.’ –Jackson & Bruck, 2012
The fatigue experienced by CFS/ME patients is separate from the expression of sleepiness; sleep disorders may be comorbid and occur at the same rate as in the general population, and does not differ in those with comorbid psychiatric conditions (therefore are not secondary to depression).
‘Pain and fatigue symptoms, similar to those reported in CFS/ME and FM, have been induced in healthy individuals by disrupting SWS. Thus, it has been posited that the physiological arousals that are observed during sleep reflect a vigilant nocturnal state that contributes to daytime fatigue, pain, and hypersensitivity, and subjective feelings of non-restorative sleep.’
An increased number and duration of intermittent awakenings have been reported; CFS/ME patients may have differential parasympathetic activity at sleep onset, which may contribute to delayed sleep latency. Stage 3 sleep or slow wave sleep (SWS) is typically observed for approximately a fifth of the sleep period in young healthy individuals. A number of studies have reported reduced time in SWS in CFS/ME patients relative to controls, and between monozygotic twins discordant for CFS/ME. These effects are independent of depression and FM. The appearance of alpha-delta sleep, or alpha intrusions, during SWS has been reported in some early studies of CFS/ME patients but is now debated. Reduced REM sleep in CFS/ME patients is reported in some studies; statistically controlling for medication use removed the difference, suggesting that medications used by these patients may play a role in some sleep architecture differences previously reported.
While objective sleep parameters do not clearly predict subjective reports of sleep disturbance, other physiological measures may have more promise for detection of alterations in CFS/ME patients’ sleep, such as stage shifts and dynamic stage transitions. The relative frequency of REM to NREM transition is lower in CFS/ME, while there are significantly more transitions from REM and stage 1 sleep to wakefulness. more microarousals have been observed in CFS/ME patients. Cyclic alternating pattern (CAP) is an EEG-derived measure of sleep instability, which is reflected as periodic EEG activity during NREM sleep. Despite having similar NREM sleep times, CFS/ME patients had higher CAP rates than matched controls, indicating higher NREM sleep instability in their CFS/ME patients.
In some CFS/ME patients, the autonomic dysfunction observed during waking also transfers into sleep, such as hypotension and reduced heart rate variability (HRV). Decreased HRV is thought to reflect a persistent state of autonomic hypervigilance. HRV may be the best predictor of subjective sleep quality in CFS/ME patients.
Likewise, Cardiopulmonary coupling (CPC) is another emerging technique, used as a measure of sleep quality and stability based solely on the electrocardiogram (ECG) signal, using heart rate (R-R interval) and respiration dynamics to generate a spectrogram of cardiopulmonary coupling. There is preliminary evidence that sleep quality and stability measured by CPC is poor in CFS/ME patients, with reduced high-frequency coupling and increased low-frequency coupling.
One theory for the non-restorative sleep experienced in insomnia suggests that negative cognitions trigger autonomic arousal during wakefulness that transfers into sleep. Nocturnal arousal is often treated by reducing hyperarousability and cognitions during the day, using cognitive behavioral therapy or mindfulness based techniques.
Dysregulation of the HPA has been examined using salivary cortisol profiling in a few studies. Given that CFS/ME is 2 to 3 times more prevalent in women, it has been proposed that sex differences in hypocortisolism may explain the increased risk of CFS in women.
Pacing with a heart rate monitor to improve HRV may be a way of improving sleep, especially as poor quality sleep may follow overexertion as a symptom of PEM.
Management: during the later stages of a crash, for example, heart rate may be not be at resting until the second half of an 8 hour sleep. This results in the requirement for an extended sleep duration for it to be restorative. This can then cause the sleep-wake rhythm to cycle around the clock as it is more than 24hrs (16hours wake 10 hours sleep). This is on top of the tendency towards delayed latency sleep onset following exertion or stimulation. The sleep hr/HRV relationship can show a reliable pattern during overexertion, PEM and recovery; see relevant heart rate monitoring documents for sleep heart rate graph examples.
Regarding recommendations to force patients to stay awake:
– Sleep deprivation is a mast cell deregulator, MCAS is implicated in ME/CFS
– sleep quality and regulation improves with rest and worsen with stress
For some examples interpreting nervous system activity during sleep, see this document