Sleep and Dreaming

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Sleep and Dreaming
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Stages of Sleep

• EEG records and behavioral observations indicate
  that the sleep of many species, including
  humans,exhibits a pattern of distinct stages and
  two distinct categories slow-wave sleep (SWS)
  and rapid-eye-movement sleep (REM).

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Stages of Sleep Human SWS stages may be
distinguished on the basis of EEG
characteristics Stage 1 SWS contains vertex
spikes, stage 2 SWS contains sleep
spindles, stage 3 SWS is marked by the appearance
of large delta waves, and in stage 4 SWS delta
waves are present at least 50 of the time. The
progression through the stages is marked by
decreasing fre- quency and increasing amplitude
in the EEG.
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Stages of Sleep-REM REM sleep is characterized
by a return to fast, desynchronized EEG activity
resembling the awake state, complete loss of
muscle tone, and rapid eye movements.
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Stages of Sleep Human sleep exhibits an
alternating cycle of REM and SWS every 90-110
minutes. Sleep cycle length is shorter in smaller
animals. Some species of mam- mals do not display
REM sleep at all, and some, notably the dolphin,
sleep only one cerebral hemi- sphere at a time.
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Stages of Sleep Vivid dreaming involving imagery
occurs during REM sleep dreaming during SWS
tends to involve vague thoughts. Nightmares are
associated with REM, whereas night terrors are
associated with stages 3 and 4 SWS.
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Braun et al. (1997)

• 37 male volunteers
• Measured rCBF using PET during different stages
  of sleep.

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Fig. 3 Brain map illustrating decreases in rCBF
during slow wave sleep (SWS), when compared with
pre-sleep wakefulness as baseline. The
statistical parametric (SPMZ) map illustrating
changes in rCBF is displayed on a standardized
MRI scan. The MRI data were transformed linearly
into the same stereotaxic (Talairach) space as
the SPMZ data. Using Voxel View Ultra (Vital
Images, Fairfield, Ia., USA), SPM and MRI data
were volume-rendered into a single
three-dimensional image. The volume sets are
truncated and displayed at selected planes of
interest. Planes of section are located at 27 mm
(A),0 mm (B), 113 mm (C) and 127 mm (D) relative
to the anterior commissuralposterior commissural
line. Values are Z-scores representing the
significance level of changes in normalized rCBF
in each voxel the range of scores is coded in
the accompanying colour table, with light purple
designating significant negative Z-scores of 4.5
and below. Significant decreases in rCBF during
SWS were observed in centrencephalic structures
including pons (A,arrowhead), midbrain (B, short
arrow), basal ganglia (B, long arrow C, medium
arrowhead), thalamus (C, short arrow), caudal
orbital cortexbasal forebrain (B, small
arrowhead) and cerebellum (A, arrow). Similar
decreases were also found in paralimbic regions
of interest including anterior insula (B, medium
arrowhead) and anterior cingluate cortices (C and
D, small arrowheads). SWS was associated with
significant reductions in rCBF in heteromodal
association cortices of the orbital (B, medium
arrow), dorsolateral prefrontal (C, medium arrow
D, small arrow) and inferior parietal lobes (D,
medium arrow), but not in unimodal (visual or
auditory) occipitotemporal sensory cortices (see
Table 1).
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SWS minus Wakefulness
Pons
Basal Ganglia
Frontal
Basal Forebrain
Cingulate
B.G.
B.F.
Cerebellum
Midbrain
Thalamus
Parietal
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Fig. 4 Brain map illustrating increases in rCBF
during REM sleep when compared with slow wave as
baseline, prepared using methods outlined in the
legend to Fig. 3. Values are Z-scores
representing the significance level of changes in
normalized rCBF in each voxel the range of
scores is coded in the accompanying colour table,
with red designating Z-scores of 3.5 and above.
Planes of section are located at 25 mm (A), 11
mm (B), 18 mm (C) and 127 mm (D) relative to the
anterior commissuralposterior commissural line.
Significant increases in rCBF during REM sleep
were observed in centrencephalic structures
including pons (A, arrowhead), midbrain (B, long
arrow), basal ganglia (B, short arrow C, small
arrowhead), thalamus (C, medium arrowhead) and
caudal orbital cortexbasal forebrain (B, medium
arrowhead). Increases were also found in
paralimbic regions including the anterior insula
(B, small arrowhead), anterior cingluate (C,
small arrow D, medium arrow) and mesial temporal
(parahippocampal) cortices (B, medium arrow). REM
sleep was associated with significant elevations
in rCBF in unimodal sensory cortices including
inferior visual association fusiforminferotempor
al (B, large arrowhead) and lateral occipital (C,
long arrow) and auditory association cortices
(C, medium arrow), as well as the medial
prefrontal cortex (D, small arrow). On the other
hand, activity in heteromodal association
cortices of the orbital, dorsolateral prefrontal
and inferior parietal lobes, did not differ from
levels observed during SWS (see Table 2).
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REM minus SWS
Cingulate
B.G.
Midbrain
Thalamus
Pons
Frontal
Temporal
Occipital
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Fig. 5 Brain map illustrating increases in rCBF
during post-sleep wakefulness when compared with
REM sleep as baseline, prepared using methods
outlined in the legend to Fig. 3. Values are
Z-scores representing the significance level of
changes in normalized rCBF in each voxel the
range of scores is coded in the accompanying
colour table, with red designating Z-scores of
3.5 and above. Planes of section are located at
25 mm (A), 5 mm (B), 19 mm (C) and 127 mm (D)
relative to the anterior commissuralposterior
commissural line. The rCBF in heteromodal
association cortices of the orbital (B, small
arrow), dorsolateral prefrontal (C and D, small
arrows), and inferior parietal lobes (D, medium
arrow), which had decreased at the onset of SWS
and remained depressed during REM
sleep, increased significantly during the
transition from REM sleep to post-sleep
wakefulness. Similar increases were seen in the
cerebellar hemispheres (A, small arrow). Activity
in centrencephalic, paralimbic and post-rolandic
sensory association cortices, on the other
hand,was relatively higher during REM sleep than
during post-sleep wakefulness (see Table 3).
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Wakefulness minus REM
Frontal
Cerebellum
Parietal
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Why Do We Sleep?

• Many different functions have been proposed for
  sleep, including bodily restoration, energy
  conservation, predator avoidance, and memory
  consolidation. None of these hypotheses, by
  themselves,appear to account entirely for the
  need to sleep or the dramatic health consequences
  of sleep deprivation.

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Adaptive Response

• Conserves energy
• Avoids predation

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Adaptive Response

• Webb (1975 1982)
• Keeps animals out of harms way when nothing
  important to do
• Sleep may conserve energy when cant find food or
  may do harm to oneself
• Animals that have safe hiding places or are not
  subject to predation will sleep a lot.
• Animals that are subject to predation will not
  sleep as much.

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Sleep is Restorative

• What is effect of sleep deprivation?
• Horne (1978) reviewed over 50 studies of sleep
  deprivation in humans.
• No evidence that sleep deprivation interfered
  with physical activity
• No evidence body was stressed (e.g. no change in
  cortisol or epinephrine)

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Sleep is Restorative

• After staying awake for several days
• perceptual distortions and hallucinations
• Randy Gardner stayed awake for 264 hours with
  only some evidence of perceptual distortions.

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Fatal Familial Insominia

• Die within 7-24 months after beginning of the
  insomina
• Degeneration of the thalamus

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Rechtschaffen et al. (1983 1989 1995)

• Sleep deprived one animal and controlled for the
  amount of exericse the other animal received.

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• Sleep of experimental animal reduced 87
• Sleep of control reduced 31

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• Animals looked sick stopped grooming weak
  uncoordinated
• Lost ability to regulate body temperature
• No obvious signs of inflammation or damage to
  internal organs
• Stress hormones not unusually high
• High calorie diet kept rats awake longer

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• Everson (1995) found evidence of blood infection
  and suggests sleep deprivation disrupts immune
  system.
• Physical exercise and warm baths that raises body
  temperature results in longer sleep

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Basal Forebrain, Preoptic Area Anterior
Hypothalamus

• Involved in thermoregulation
• Warming induces SWS
• When body temperature rises, increase in firing
  rate and animals fall asleep.
• Decreasing body temperature results in activation
  of REM sleep, raising body temperature