Restorative Sleep (Part 1)
Questions about Restorative Sleep in the General Population
Maurice M. Ohayon, MD, DSc, PhD,
Stanford Sleep Epidemiology Research Center
Restorative sleep has been scantly studied in the general population although this issue has an important role in several medical conditions such as heart disease, fibromyalgia and chronic fatigue syndrome and various sleep disorders. Little is known about:
- How to define Restorative sleep?
- How is it different and more specific than chronic fatigue syndrome, fibromyalgia, etc?
- Is Non- Restorative sleep to be considered as one of the insomnia symptoms?
- Is it a separate clinical or diagnostic entity?
- Admitting that we have a clear definition, how frequent is this symptom in the general population?
- Who is the most affected (age, sex, comorbidity)?
- What are the associated factors?
- What are the daytime, social professional and familial consequences of NRS?
- What are the medical needs of individuals complaining of NRS?
- What is the naturalistic way of these individuals to complain and to deal with their general practitioner?
- What kind of treatment are they taking? For how long?
- What is the level of satisfaction with their treatment and general practitioner?
The Interrelationship of Insomnia, Sleep Fragmentation, and Metabolic Rate in Sleep Restoration.
Michael H. Bonnet, Ph.D
Dayton VA Medical Center, Dayton
This work will include data showing increased 24-hour metabolic rate in patients with psychophysiological insomnia (compared to matched controls) and increased metabolic rate in normals during fragmented sleep. A third study of mine that showed increased metabolic rate after chronic caffeine administration (and additionally, normal sleepers with this increased metabolic rate developed a symptom complex similar to that seen in patients with psychophysiological insomnia). However, this complex differed from that seen after pure sleep deprivation or experimental sleep fragmentation. In a final study, metabolic rate during sleep was varied by administering caffeine prior to nocturnal sleep. Ss were sleep deprived following sleep at different metabolic rates to see if the 'high metabolic rate' sleep produced increased sensitivity to sleep deprivation. Few significant effects were found.
Conclusions are that insomnia patients have increased metabolic rate and that this can be related to fatigue, anxiety, and poor sleep but not to excessive sleepiness or performance similar to that seen after sleep deprivation. Normals with highly fragmented sleep develop excessive sleepiness but do not develop mood changes or other typical symptoms seen in insomnia patients.
Pharmacological Enhancement of Slow Wave Sleep and the Restorative Capacity of Sleep
James Walsh, PhD
St. Luke's Hospital
Several pharmacological agents with different mechanisms of action increase slow wave sleep (SWS) as measured classically or in a more quantitative fashion as NREM slow wave activity (SWA). Studies with three SWS-enhancing drugs conducted to evaluate the impact of enhanced slow wave sleep (SWS) on established consequences of sleep restriction in healthy adults have demonstrated that pharmacological SWS enhancement reduces selective aspects of the behavioral, psychological, and physiological impact of sleep restriction. In one investigation, SWS enhancement during sleep restriction reduced the homeostatic response to sleep loss during recovery sleep. These findings suggest that pharmacologic SWS enhancement in healthy individuals intensifies some of the processes of physiologic sleep related to the construct of restoration.