MIT Encyclopedia of the Cognitive Sciences - Cryptome

As a function of the circadian rhythm generated by the
suprachiasmatic nucleus of the hypothalamus, all vertebrate
animals show prominent rest-activity cycles with an
endogenous period of about one day. Corresponding to
the increased complexity of the supervening thalamocortical
brain and the greater sophistication of their thermoregulatory
capacity, the vertebrate mammals link active sleep
control mechanisms in the lower brain stem to the circadian
cycle. The result is a stereotyped sequence of events
that is coordinated throughout the brain so as to alter
every aspect of cognition in a dramatic and sometimes
paradoxical fashion. The most surprising aspect of this
automatic sequence of events is the regular recurrence of
periods of brain activation and rapid eye movement
(REM) in sleep that is associated in humans with hallucinoid
DREAMING.
Waking, with all of its cognitive components, is an
actively maintained brain state in which the thalamocortical
circuitry is kept open and receptive to information
from within and without by the depolarization of reticular
thalamic neurons by cholinergic and aminergic modulatory
elements of the brain stem. This activation, together
with its specific neuromodulatory effects, renders the forebrain
capable of sensation, perception, ATTENTION, orientation,
emotion, and stimulus evaluation in terms of past
experience, and deliberate action. Whenever the brain
stem neuromodulatory influence declines to a critical
level, the thalamocortical system tends to oscillate, producing
its own endogenous rhythm of electroencephalographic
(EEG) spindles and slow waves which are incompatible
with waking conscious experience because the
inputs to and outputs from the cortex are blocked and
intracortical communication is preempted. Cognitive func-
Sleep 773
Figure 1. Sleep cycle schematic. The states of
waking, NREM, and REM sleep have behavioral,
polygraphic, and psychological manifestations that
are depicted here. In the behavioral channel,
posture shifts—detectable by time-lapse
photography or video—can be seen to occur during
waking and in concert with phase changes of the
sleep cycle. Two different mechanisms account for
sleep immobility: disfacilitation (during stages I–
IV of NREM sleep) and inhibition (during REM
sleep). In dreams, we imagine that we move, but we
do not. The sequence of these stages is
schematically represented in the polygraph channel
and sample tracings are also shown. Three
variables are used to distinguish these states: the
electromyogram (EMG), which is highest in
waking, intermediate in NREM sleep, and lowest
in REM sleep; and the electroencephalogram
(EEG) and electrooculogram (EOG), which are
both activated in waking and REM sleep, and
inactivated in NREM sleep. Each sample record is
about 20 sec long. Other subjective and objective
state variables are described in the three lower
channels. (From J. A. Hobson and M. Steriade
(1986), Neuronal basis of behavioral state control.
In V. Mountcastle and F. E. Bloom, Eds.,
Handbook of Physiology: The Nervous System.
Vol. 4, pp. 701–823.)
tion is thus progressively obtunded as this progressive
brain deactivation proceeds in nocturnal sleep. This is
reflected by the shift from stage I to stage IV of so-called
non-REM (NREM) sleep from the depths of which human
subjects are very difficult to rouse. Even when verbally
responsive they may then show marked sleep inertia with
persistent slow waves in the EEG and an inability to perform
even trivially simple cognitive tasks such as serial
seven subtraction. This sleep inertia process is greatest in
the first two NREM cycles of the night and is intensified in
postdeprivation recovery sleep.
Recent POSITRON EMISSION TOMOGRAPHY (PET) studies
of human NREM sleep have revealed decreased blood flow
in the brain stem reticular formation, the subthalamus, and
in frontal cortical regions denoting the massive deactivation
of these structures in NREM sleep. Animal studies further
confirm this deactivation process at the level of individual
neurons, many of which decrease their rate of firing by as
much as 50 percent. There is also a 50 percent decline in the
output of the wake state neuromodulatory chemicals acetylcholine,
norepinephrine, and serotonin. It is for all these reasons
that the NREM sleeping brain is such a poor cognitive
instrument and it is the carryover of these effects into subsequent
waking that so severely impairs problem-solving
behavior upon arousal from deep NREM sleep. That this
cognitive impairment may nonetheless be beneficial is suggested
by the finding that complex DECISION MAKING is
more efficient during waking that follows nights with uninterrupted
NREM sleep.
After sixty to seventy minutes of deep NREM sleep subjects
show a reversal of these oscillatory EEG patterns and
the brain spontaneously reactivates. Together with the EEG
desynchronization is an activation of the upper brain’s