2 - RESTRICTED SLEEP: NEUROBEHAVIORAL AND PHYSIOLOGICAL EFFECTS
Sleep Deprivation in Adults
Studies on the effects
of sleep loss on neurobehavioral functions, especially neurocognitive
performance, have two primary emphases: (a) specification of
the properties of tasks (e.g., cognitive versus physical; long
versus short duration) that make them sensitive to sleep loss;
and (b) specification of the aspects of performance (e.g., cognitive
processing speed versus accuracy, declarative versus implicit
memory processes) that are impacted by sleep loss. Underlying
this research has been controversy regarding the likely nature
of sleep loss-induced performance deficits (e.g., whether they
reflect true deficits in physiological function of the brain,
a motivational effect reflecting reprioritization of the reinforcement
hierarchy, an initiation of sleep onset mechanisms in the face
of waking performance, or some combination of these processes).
This controversy has not been resolved due to lack of a basic
understanding of the function(s) of sleep, the physiological
processes affecting recuperation during sleep, and the neurobiology
Implicit in this
research has been the assumption that total and partial sleep
deprivation produce qualitatively similar decrements in brain
function and/or motivation levels that differ only in degree.
As a result, the overwhelming majority of studies in which the
relationship between sleep and performance have been explored
have utilized the more efficient total sleep deprivation procedures,
and very few studies have examined the effects of chronic sleep
restriction. Further, of these few studies only a very small
subset have included adequate and objective verification of
compliance with the sleep restriction regimen being studied.
sleep deprivation is more pervasive than total sleep deprivation.
Epidemiological studies suggest that mean sleep duration has
decreased substantially as proportionally more people are awake
more of the time. These decreases are due, in part, to expanded
possibilities for nighttime activities that accompanied the
introduction of electric light and other technologies, and to
the more recent trend toward expansion of both manufacturing
and service sectors to 24 hour-per-day operations. Sleep restriction
appears to be an almost inevitable consequence of nighttime
Because of the scarcity
of chronic sleep restriction experiments despite a wealth of
total sleep deprivation/performance studies, theoretical and
practical questions remain: (a) What are the physiological processes
mediating neurobehavioral performance deficits resulting from
sleep loss? (b) What accounts for the wide individual differences
that emerge in the ability to maintain performance during s
leep loss? (c) Do the physiological and neurobehavioral responses
to chronic partial sleep loss differ from those resulting from
total sleep loss? (d) Relative to the adverse neurocognitive
and physiological effects of sleep loss, is there habituation/adaptation
or potentiation/sensitization to repeated exposure to sleep
loss? (e) Are there physiological and/or behavioral adaptations
or dysfunctions in sleep or circadian physiology in response
to chronic sleep restriction (e.g., a change in sleep itself
or the brain's recovery response to chronically inadequate sleep)?
(f) Are the neurobehavioral and physiological effects of chronic
partial sleep loss different at different circadian phases?
(g) What are the physiological processes that affect restoration
of cognitive performance capacity during recovery sleep, and
are these processes reflected in any currently measured sleep
parameters? (h) How much recovery sleep is required following
chronic partial sleep loss vs. total sleep deprivation? (i)
What are the effects on neurobehavioral functions of long term
(weeks, months, years) exposure to a typical work or school
schedule of 5 or more days of sleep restriction followed by
2 days of recovery?
Research on sleep
loss countermeasures in healthy adults, including pharmacological
and non-pharmacological interventions such as napping strategies,
is also of increasing practical and theoretical relevance. There
is a need for experiments on the efficacy, long-term effectiveness,
and safety of repeated use of traditional stimulants (e.g.,
caffeine, d-amphetamine, methylphenidate) and novel wake-promoting
agents (e.g., modafinil) for maintenance of performance in healthy
adults engaged in emergency and/or continuous operations. Complementary
studies of sleep-inducing and/or phase-shifting drugs (e.g.,
benzodiazepine agonists, melatonin) to enhance sleep and subsequent
alertness/performance (e.g., for those engaged in shift work,
transmeridian travel, or recovery from continuous operations)
will likewise continue to expand from the clinical to the operational
and sleep scheduling will constitute at least part of any comprehensive
strategy to maintain alertness and performance during extended
continuous operations. Cell phones, beepers, and other communication
devices can put some workers in a perpetual "on-call"
status in which sleep might be interrupted by need for rapid
decisions and/or other duty-related tasks. Studies of sleep
inertia (and sleep inertia countermeasures), therefore, will
be of increasing relevance and importance. Finally, the physiological
effects of acute and chronic sleep loss in vital organ systems
other than the brain have only just begun to be explored.
In The Last 5 Years
- Functional brain
imaging studies and EEG brain-mapping studies show that the
patterns of functional connectivity between brain regions evident
during performance of specific cognitive tasks are altered by
sleep loss. This suggests that maintenance of performance during
sleep loss may depend upon regional functional plasticity.
- Recent experiments
have documented precise dose-response effects of chronic sleep
restriction on waking neurobehavioral and physiological functions,
suggesting that the cumulative waking neurocognitive deficits
and state instability that develop from chronic sleep loss have
a basis in a neurobiological process that can integrate homeostatic
pressure for sleep across days.
- There have been
increased efforts to determine the roles of REM and nonREM sleep
in memory consolidation, although definitive evidence for such
relationships remains elusive.
- Plasticity in visual
cortices during a critical period in kittens is NREM sleep-dependent.
This suggests that one function of sleep is to facilitate the
functional organization of the brain, and that there are sleep-dependent
aspects of putatively related processes such as LTP and DNA
- Genetic array techniques
have identified the patterns of gene expression that characterize
and differentiate sleep and wakefulness. This information will
help in understanding the most basic cellular processes mediating
performance and alertness deficits following sleep loss, and
the restoration of performance capacity and alertness during
- Studies have identified
those aspects of performance that are most susceptible to sleep
inertia, their differential time courses, and have begun to
identify sleep inertia countermeasures (e.g., caffeine).
- Determine the physiological
and behavioral processes mediating the state instability (manifested
as increased variability in alertness and neurobehavioral performance)
that result from acute versus chronic sleep loss. Compare these
processes with those mediating the alertness and performance
deficits that characterize pathologies such as Narcolepsy, Sleep-Disordered
Breathing ( Section V), and closed head injury.
- Identify the full
range of psychological, behavioral, and physiological (e.g.,
endocrine, immune, cardiovascular, liver, muscle, etc.) consequences
of long-term cumulative partial sleep deprivation and their
- Discover the physiological
processes mediating restoration/recovery of alertness and performance
by sleep. This includes elucidation of the basic mechanisms
that contribute to the time course of recovery within and between
days, as well as determining whether there are longer-duration
time constants for reversal of the cumulative neurobehavioral
deficits that accrue during chronically restricted sleep.
- Determine whether
and how factors such as cognitive activity/workload and physical
activity/work modulate sleepiness.
- Identify factors
that account for individual differences in sleep need, and in
the apparent differential vulnerability among people with similar
sleep needs in their neurocognitive and physiological responses
to sleep deprivation. The stability and reliability of these
individual differences need to be established and, once established,
a search for stable and reliable biological and behavioral predictors
is needed to establish a phenotype that can then be investigated.
- Determine the physiological
basis and behavioral characterization of sleep inertia effects,
and study the comparative effects of possible countermeasures
for sleep inertia.
- Assess the physiological
modulation of sleepiness by stimulant and wake- promoting pharmacological
agents, focusing on their sustained efficacy and safety for
acute and chronic sleep deprivation, the impact of repeated
dosing, and the effect of these agents on recovery sleep homeostasis
and on the "recycle rate" (the speed with which full
recovery from sleep loss is achieved, preparing the individual
for initiation of another episode of sleep restriction/deprivation).