Sleep
Paralysis
as an Anomalous REM State
REM and Dreaming: A major distinction of sleep
states, for
close to a half century, has been accepted between REM and NREM sleep
(Aserinsky & Kleitman, 1953; Jouvet, 1967). REM periods are
characterized
by desynchronized cortical characterized by low-voltage fast EEG
patterns
with synchronized hippocampal activity characterized by slow (4-8 Hz)
theta
activity (e.g., Culebras, 1994). It is also widely accepted that
dreaming is
more common and more vivid during REM than during NREM sleep (Dement
&
Kleitman, 1957). In addition to the characteristic desynchronized
cortical
low-voltage fast EEG activity, there are numerous physiological,
behavioral,
and sensory features associated with REM such as muscle atonia, gating
of
sensory input, rapid eye and middle ear movements, as well as heart
rate and
respiration changes (Carskadon & Dement, 1989; Symons,
1993).
Within REM periods a distinction is sometimes made between a
background
tonic state (TREM) and bursts of phasic REM (PREM) every 16-120
seconds and
lasting from 2-9 seconds (Aserinsky, 1971, Molinari & Foulkes,
1969).
Specifically, PREM is characterized by bursts of rapid eye and middle
ear
movements and characteristic cortical and hippocampal EEG patterns.
PREM is
associated with, and may be preceded by, ponto-geniculo-occipital EEG
waves
(PGO spikes in animal preparations) originating in the bilateral,
dorsolateral pons and projecting rostrally through the lateral
geniculate
nucleus and other thalamic nuclei (Hobson, Alexander, Frederickson,
1969). It
has been conjectured that the most vivid dreams, or most vivid events
within
dreams, are associated with PREM (Molinari and Foulkes, 1969).
REM and SP: SP has also been associated with REM states,
particularly with
sleep-onset and sleep-offset REM (SOREM) (Nan'no, Hishikawa, &
Koida,
1970). In both REM dreams and SP hallucinations a general atonia is
maintained during REM by marked and sustained hyperpolarization of the
motoneurons (Chase & Morales, 1989). One likely
function of the general
atonia is the prevention of the physical enactment of the motor
components of
dreaming. There are at least two major traditional hypotheses
concerning the
connection between neurophysiological events and visual imagery in
dreams.
The visual imagery of dreaming may arise either from the direct
stimulation
of visual areas of the cortex during the PGO spike, in which case the
rapid
eye movements may reflect attempts to scan the images (Ladd, 1892;
Roffwarg,
Dement, & Muzio, 1962), or conversely, the mages may be produced
by the oculomotor
impulses in response to direct stimulation from the gigantocellular
pontine
reticular field (Hobson & McCarley, 1977; McCarley & Hobson,
1979).
REM is thought to be generated in the lateral portions of the
nucleus
reticularis pontis oralis (RPO) immediately ventral to the locus
ceruleus in
the pontine reticular formation. The neurotransmitters in this region
have
not been clearly determined, but are neither cholinergic nor
monoaminergic.
The RPO receives projections from cholinergic regions in the
laterodorsal
tegmental nucleus (LDT) and the pedunculopontine tegmental nucleus
(PPT) as
well as from ventromedial portions of the medulla. The RPO, LDT, and
PPT are
collectively thought to be part of the REM-on neural population
(Steriade
& McCarley, 1990). These populations are hypothesized to interact
with
REM-off noradrenergic neurons in the locus ceruleus and seratonergic
neurons
in the raphe system. These latter populations are most active during
waking
and least active during REM. Interactions between the REM-on and
REM-off
populations are thought to control REM onset and offset (Steriade
&
McCarley, 1990).
SP may reflect an anomaly of the functioning of the monoaminergic
systems
and/or their inhibition of the REM-on cholinergic system. Experimental
and
clinical dissociations have been demonstrated among major components
of
REM: namely, PGO activity, atonia, and EEG desynchronization
(Hishikawa
& Shimizu, 1994). Hishikawa & Shimizu speculate that SP may be
produced by hyperactivation of the Sleep-on populations or, they deem
more
likely, hypoactivation of the Sleep-off populations. That SP may be
alleviated by serotonin and adrenergic reuptake inhibitors is taken to
be
consistent with this hypothesis. Also involved may be suprapontine
systems involving
the reticular system, including the hippocampus and amygdala.
REM SP with HHEs differs from REM dreams in that
during SP
there is little or no blocking of exteroceptive stimulation and there
is no
loss of waking consciousness. SP with HHEs differs from dream
experience in
that the sensory cortex may be receiving both externally and
internally
generated information. The peculiarity of the HHEs in SP may, in part,
be a
result of the brain's attempts to integrate endogenous cortical
arousal
originating in the pons with normal sensory input. A similar
peculiarity may
exist for motor pattern arousal during SP. McCarley and Hobson argue
that,
during dream generation by internal stimulation of motor programs, we
interpret the activity of the pattern generators and their corollary
discharge as movement. The lack of peripheral feedback, though not
normally
necessary for effective control, may contribute to a sense of
unreality to
the apparent movement and hence to the "bizarreness" of dreams.
Pontine activation of motor patterns during SP appears to be less
common in
SP than in dreams, if subjective reports of illusory movement are to
be taken
as evidence. Volitional attempts at movement during SP are common,
however,
and the absence of feedback is most often, though not always,
experienced as
paralysis rather than illusory movement. Thus it appears that, during
SP, the
frontal cortex is more sensitive to the absence of feedback than
during
dreaming. When motor programs are spontaneously
activated during SP these
might be extremely resistant to coherent interpretation am may be
experienced
as very unusual bodily states. In concluding sections we will relate
more
specifically the phenomenology of various HHEs to the underlying
neurophysiology.
A Note on Sleep Paralysis and Narcolepsy
Sleep paralysis is often thought to be associated with
narcolepsy.
Narcolepsy is a condition in which people are overcome with
irresistible
sleep attacks that occur unpredictably and at any time of day. These
sleep
attacks may occur while engaged in conversation, working at a desk,
during
meals, or even driving. These involuntary naps last for about 10 to
20
minutes after which the person will wake up feeling quite refreshed.
The
other major, and perhaps most distinguishing, feature of the
condition is
cataplexy, a sudden loss of muscle tone during excitement or
arousal, such
as laughter. The loss of muscle tone may be partial or complete. In
the
latter case, the person may simply collapse. Although individuals
remain
conscious during a cataplectic episode, they may experience
hallucinations
during prolonged attacks and subsequently fall asleep. Sleep-onset
REM,
sleep paralysis, and hypnagogic hallucinations are often discussed
as
'associated features' of narcolepsy. Not all people with narcolepsy
experience sleep paralysis, however, and, more significantly, not
all
people who experience sleep paralysis have narcolepsy. Indeed, this
should
be quite obvious when one realizes that the prevalence of sleep
paralysis
is 20% to 40%, whereas that of narcolepsy is 0.03% to 0.16%
(ICSD-90).
Moreover, estimates of the prevalence of sleep paralysis among
people with
narcolepsy are quite variable and are in the range of 40% to 60%
(Hishikawa, 1976). Among our own sample of we have found only 1.6%
of SP
experients report that they have been diagnosed with narcolepsy.
Although
this is larger than the percentage in the general population is
obviously a
very small proportion of people who also experience SP. In a recent
report
involving narcoleptic dogs, the authors argue that 'cataplexy and a
dysfunction in the maintenance of and transition between vigilance
states
are central to narcolepsy (Nishino, et al., 2001, p. 445). After
reviewing
literature that suggests that sleep onset REM is associated with
several
other disorders and, as I have noted above, occurs in a substantial
minority of the general population, the authors find little support
for
“the current notion that narcolepsy is a disorder of REM sleep
generation” (p. 445).
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