J R Soc Med 2002;95:591-597
doi:10.1258/jrsm.95.12.591
© 2002 Royal Society of Medicine
What does brain damage tell us about the mechanisms of sleep?
B M Evans FRCP
Department of Clinical Neurophysiology, Mapother House, King's College
Hospital, Denmark Hill, London SE5 0RS, UK
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Figure 1. Arousal and arousal inhibitory mechanisms of brainstem (vertical section
of monkey brain). C=cortex; CC=corpus callosum; CB=cerebellum;
MB=mid-brain; T=thalamus; RF=reticular formation. (a) Reticular
activating mechanism. Arrows show sensory input from spinal cord and mid-brain
into reticular substance of mid-brain nuclei, which then form relays in the
thalamus. Fibres of the thalamo-cortical radiation reach all areas of the
cortex. (b) Arousal inhibitory mechanism. Reticular formation input
remains the same as in (a) but the upward flow into the thalamus is
partly blocked in relation to the thalamic sleep spindles (S). The cortex
shows slow and very slow activity (SD). The slowest waves are related to the
sleep spindle
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Figure 2. Relation between sleep spindles (ss) and cyclical alternating pattern in
early sleep. The bar graph shows the intervals between the onsets of 1148
sleep spindles; pooled data from 32 individuals in stage 2-3 sleep. The
preferred interval is between 3 and 5 s. The line graph shows the interval
between the onsets of 1463 episodes of higher arousal activity in stage 1
sleep; pooled data from 52 individuals. The preferred interval is about 16 s
with subpeaks at shorter and longer intervals (the subpeaks were consistent
during collection of the data). The intervals between the subpeaks are at
about 4 s—i.e. similar to the intervals between sleep spindles
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Figure 3. Polygraphic record at 1.5 cm/s showing intermittent arousal activity of
early sleep (stage 1). The upper 14 traces show the EEG with alternating
periods of faster activity (dark areas associated with higher arousal). The
intervals between the onsets of the higher arousal periods are shown by the
figures at the top. (These are the intervals used in the line graph of Figure
3.) Channel 17 is an electrocardiogram; channel 18 is respiration showing
periodic apnoea, each group of breaths associated with higher arousal. Below
is a heart rate graph showing intermittent heart rate increases with each
arousal
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Figure 4. Recordings from a patient aged 66 with subarachnoid haemorrhage from
anterior communicating aneurysm. Above: channels 1-3 show EEG at
1.5 cm/s. Low voltage slower activity is followed, at the time of a
spontaneous arousal, by flattening of the EEG and then by slow waves with
muscle artefact. Channel 4, respiration from a thermistor in the nose, channel
5, electrocardiogram. Note marked increase in respiratory and heart rates at
the moment of arousal and a wandering pacemaker during the period of lower
arousal. Below: graphs of respiration rate (R.R.) and heart rate
plotted at 1 s intervals. This shows that arousal events are occurring about
every 4 min. Open blocks above the respiration graph illustrate periods of
higher arousal in the EEG. Filled areas below the heart rate graph illustrate
periods when wandering pacemaker was evident. Short arrows show the section of
the cardiorespiratory graphs associated with the EEG polygraph above. X marks
a stimulus
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Figure 5. Recording from boy aged 16 with closed head injury. Above:
two pieces of polygraph, A and B. Channels 1-5 EEG; channel 6, surface
electromyogram (E.M.G.) from right leg; channel 7, electrocardiogram; channel
8, respiration from thermistor in nose. Section A is taken from a spontaneous
arousal accompanied by a decerebrate spasm and shows change in the EEG from
low voltage to higher voltage slow waves and marked increase in muscle
activity and heart and respiration rate. Section B is taken from a brief
arousal after the spasm shown in section A had subsided. EEG shows a brief
burst of slow waves with an associated muscle spasm with heart and respiratory
rate increases. Below: graph of the heart rate. Short arrows, A and
B, mark the periods of the graph related to the polygraphic traces shown
above. Open blocks illustrate occurrence of EEG change; closed blocks
illustrate muscle spasms
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