Theme : Dreams
Isolated Sleep Paralysis: A Web Survey
Giorgio Buzzi and Fabio Cirignotta
Sleep Medicine Unit, Department of Neurology, S. Orsola-Malpighi Hospital,
University of Bologna, Italy
Abstract
Isolated Sleep Paralysis (SP) occurs at least once in a lifetime in 40-50%
of normal subjects, while as a chronic complaint it is an uncommon and
scarcely known disorder. A series of messages written by subjects who
experienced at least one episode of SP, containing more or less detailed
descriptions of this disorder, were collected from the Sleep Web site
of the University of California in Los Angeles between January 1996 and
July 1998. Two hundred and sixty-four messages fulfilling the International
Classification of Sleep Disorders (ICSD) (Thorpy, 1990) minimal criteria
for SP were analyzed. A wide spectrum of severity was evident, with a
frequency of episodes ranging from one in a lifetime to almost every night,
and a variety of emotional and hallucinatory experiences associated with
SP episodes were reported. Clinical similarities between the recurrent
form of isolated SP and channelopathies (in particular, periodic paralyses)
are discussed. An activation of limbic system structures is suggested
in order to explain some of the most common subjective experiences associated
with SP.
Current Claim: Isolated Sleep Paralysis may occur with a wide spectrum
of severity, including a recurrent form which closely resembles the ion-channel
pathologies, and it is often accompanied by stereotyped subjective experiences
which suggest an activation of limbic system structures.
Activate the ShortNotes by clicking on this link. Your notes will be stored
in this area and automatically retrieved upon your next visit.
Sleep Paralysis (SP) and hallucinations in the wake-sleep (hypnagogic)
or sleep-wake (hypnopompic) transition can occur separately or in association,
and they seem to share a common neurophysiopathologic substrate, as shown
by polysomnographic registrations of such events occasionally captured
in a laboratory. In either case, clinical and electrophysiologic assessment
evidences a mixed pattern of REM sleep phase and wakefulness (Takeuchi
et al., 1994; Dyken et al., 1998). REM sleep is a brain-activated state,
characterized by a desynchronized electroencephalographic activity resembling
that of wakefulness. Bursts of phasic events, such as REMs (rapid eye
movements) and MEMA (middle ear muscular activity), are also present and
seem to be related to ponto-geniculo-occipital (PGO) spikes, which originate
in the mesopontine region and propagate to the cerebral cortex. REM sleep
phasic activities are supposed to underlie the hallucinoid imagery of
dreams. In particular, PGO spikes project to the visual lateral geniculate
nucleus and occipital cortex and may trigger the visual imagery of dreams
(Steriade and McCarley, 1990). In spite of this high brain activation,
REM sleep differs from wakefulness because of muscular atonia, with abolished
H-reflex, caused by inhibitory postsynaptic potentials in spinal motoneurons.
Furthermore, late cerebral responses to somatosensory stimulation (P100,
P200, P300) disappear during REM sleep (Goff et al., 1966; Velasco et
al., 1980). SP differs from normal REM sleep since there is not such blocking
of exteroceptive stimulation, and waking consciousness is largely retained
(Hishikawa and Kaneko, 1965). SP may occur in an isolated form in otherwise
healthy individuals, as well as in a familial form transmitted genetically
and as one of the classical symptom tetrad of narcolepsy. Isolated SP
occurs at least once in a lifetime in 40-50% of normal subjects, while
as a chronic complaint it is much less common, affecting 3-6% of survey
respondents, many of whom had rare episodes (Thorpy, 1990). The aim of
this study is to contribute to a better clinical characterization of this
still poorly understood disorder.
Activate the ShortNotes by clicking on this link. Your notes will be stored
in this area and automatically retrieved upon your next visit.
We collected all the messages regarding "Sleep Paralysis" posted
on the Sleep Home Pages Web site (http://www.sleephomepages.org), between
January 1996 and July 1998. In these messages, subjects who experienced
at least one episode of SP described their experiences in a more or less
detailed fashion. Since all the messages were written freely, following
the original one posted by a doctor in physics affected by this condition,
not all subjects gave complete information. It is possible that a few
messages, in a random way, escaped the collection.
Inclusion Criteria
We followed the minimal criteria of the ICSD (1990): A (a complaint of
inability to move the trunk or limbs at sleep onset or upon awakening)
+ B (presence of brief episodes of partial or complete skeletal muscle
paralysis) + E (not associated with other medical or psychiatric disorders);
the latter criterion has been applied as far as possible according to
the available data. On the other hand, all participants reported a substantially
stereotyped symptomatology (a disorder arising at sleep onset or on awakening,
characterized by skeletal muscle paralysis associated with a high level
of alertness, with sparing of ocular movements and a cessation that occurs
in seconds or minutes when spontaneous, or suddenly when the patient is
touched by a relative) that seems to warrant a sufficient diagnostic certainty.
Activate the ShortNotes by clicking on this link. Your notes will be stored
in this area and automatically retrieved upon your next visit.
We collected 337 messages about SP; of these, 73 were rejected according
to either criterion E of ICSD (exclusion of other medical or psychiatric
disorders), or because they didn't concern the matter of the study (e.g.,
questions, explanations given by "experts," suggestions for
new researches on the topic), or because they were replies from authors
of previous messages. Two hundred and sixty-four messages containing more
or less detailed descriptions of SP were retained for analysis.
Epidemiological Characteristics
Most authors are Americans, but Canadians, Australians and Europeans are
also represented. Males are by far prevalent, but it's not possible to
provide definite data because several subjects signed their messages with
a pseudonym. Eighty-two patients declared their age, which is so distributed:
14-19 years, 18 patients; 20-29 years, 37 patients; 30-39 years, 20 patients;
>39 years, 7 patients.
Only six subjects reported that they had received a defined or possible
diagnosis of narcolepsy by qualified physicians; all the others reported
SP as the only significant complaint. Anyway, since the messages were
written freely and no patient was clinically or polysomnographically examined
in this study, it is not impossible that a diagnosis of narcolepsy could
have been considered for some other case.
Natural History of the Disease
Tables 1-4 show data regarding the age of onset, the frequency and time
of occurrence (sleep onset or awakening) of the episodes and the reported
precipitating factors.
Only a minority of patients reported that they had one or a few episodes
through their life; all the others reported a recurring disease, with
a highly variable frequency ranging from a few episodes per year to almost
every night. In most cases, the onset of the disease occurs during childhood
or adolescence; the course is sometimes characterized by clusters of episodes
alternating with even long periods of remission, with episodes often decreasing
in frequency in adulthood. The length of single episodes is subjectively
estimated in seconds or a few minutes in almost all cases. The time of
occurrence (sleep onset or awakening) is available, though not always
certain, for 112 patients. As shown in Table 3, there seems to be a prevalence
of hypnopompic episodes, with attacks occurring in the middle of the night
or at the end of nocturnal sleep. Eight patients (3%) had SP only in the
course of diurnal nap. Twenty-nine patients (11%) reported that sometimes
SP can occur more consecutive times at every attempt to fall asleep. In
this case, the first episode can be either hypnagogic or hypnopompic.
Sometimes the only way to stop this phenomenon involves definitively interrupting
sleep for some time; that is to say, the patient has to completely awaken
(for example: getting up after the first episode, walking around, getting
a drink of water, etc.) before falling back to sleep again.
Subjective Experiences During SP
One hundred and ten subjects (41.6%) reported that, before they had access
to reliable information about SP by means of "Web Forums" and
sleep medicine Web sites, they had no idea about the nature of the phenomenon.
In particular, 56 patients thought they were the only ones to have such
a disease, 18 patients thought that it was a psychiatric illness, 11 patients
were afraid of being "possessed by the devil" or "visited
by spirits," while 17 patients told their experiences to friends
and 8 patients told their physicians. As a result, no one believed them
or gave them reliable explanations. Several patients were convinced that
SP and related experiences were not simply a physical phenomenon, but
that they fell into the realm of the paranormal. Twenty-five reported
that they used to pray during the episode, getting a great help from this
practice.
Table 5 shows the most common subjective experiences related to SP. Each
episode may occur with different characteristics in the same patient.
The reported frequencies were calculated according to the number of patients
that experienced a specific symptom at least once.
More than two in three subjects reported feelings of panic/fear/terror
during the episodes. This sensation can be very intense and persist in
patients' memories for years. Many subjects reported that, in spite of
the recurrence of episodes and of the awareness that the event would stop
with no harm within seconds or a few minutes, the experience was always
as terrifying as it was the first time (Appendix I, 1-3). Some patients,
however, get used to the episodes and find them no longer terrifying but
simply annoying. A few subjects enjoyed the episodes and tried to study
them or to use them as a "launching pad" toward some particular
states of consciousness, i.e., "lucid dreaming" and "out-of-body
experiences."
Approximately one in three patients reported that during some SP episodes
they felt a "presence" in the sleeping environment. In most
cases this was not reported as a visual experience but as a dim perception;
only 15 patients referred to it as a "dark," "shadowy"
or "black" figure. In almost all cases the "presence"
had a definite "evil" character and it was felt as a threat
(Appendix I, 4-5).
Less than one in three patients perceived, during some episodes, an acoustic
hallucination described as a "buzzing sound," "loud ringing,"
"rumble noise" or something of this sort. These sounds often
represented the first sign of a forthcoming episode. Their emotional intensity
can be so high that some subjects consider them the most characterizing
element of the experience and particularly, if the patient struggles to
move, they can change into a sense of vibration of the whole body or into
a physically painful sensation (Appendix I, 6-7).
The other subjective sensations more frequently reported were: pressure
on the body; physical contact; "phantom movements;" "floating;"
"out-of-body experiences;" dyspnea/apnea; and visual hallucinations
or acoustic hallucinations (other than the sounds reported above). Table
5 reports their respective frequencies.
A series of motor and sensitive/sensorial hallucinations may sometimes
mimic sleep-related epileptic seizures (Table 6). Such "paroxysmal
hallucinations" are vividly perceived during sleep and they suddenly
stop at the moment of full awakening.
Finally, many patients reported that they can distinctly see the sleeping
environment during SP; nevertheless, in most cases this seems to be an
oneiric-though extremely detailed-experience, as results from some patients
who note that such "vision" occurs with eyes still closed, or
from others who note some small but significant differences from their
"real" environment. One subject has even conceived little experiments,
putting some objects in unusual places and concluding, not having identified
them during the experience, that what is "seen" must be stored
in the patient's memory of the surroundings (Appendix I, 11-13).
Activate the ShortNotes by clicking on this link. Your notes will be stored
in this area and automatically retrieved upon your next visit.
Our study leads us to some general observations about this peculiar condition.
First, it is noteworthy that more than 40% of patients reported that they
had no idea (or had wrong/irrational ideas) about the nature of the disease,
conjecturing a mental disease or spiritual/paranormal phenomena before
they found a scientific explanation through the Internet sleep Web sites
and Discussion Forums. A similar way of thinking had previously been described
among subjects affected by SP in developing countries, where patients
rarely spontaneously volunteer these fears and doctors pay them scant
attention (Ohaeri, 1992).
A second surprising datum of this survey deals with the high number of
patients reporting isolated SP as a chronic condition, with a frequency
ranging from a few episodes per year to almost every night. According
to ICSD (Thorpy, 1990), SP as a chronic complaint affects only 3-6% of
individuals; reported data seem particularly representative of such a
restricted group of patients. This population has probably been selected
because of a bias due to the kind of disease that is likely to induce
a patient to perform personal research on the topic. This could explain
the very low presence, in this survey, of narcoleptics (who are more likely
to consult qualified physicians and to get adequate information on their
condition) and the surprisingly high ratio among subjects with recurrent
attacks (who are more likely to search for information) and subjects having
had only one or very few episodes.
Since this study was based upon a series of messages written freely by
subjects who seemed to experience the same disorder, but no patient was
examined, it is possible that not all the collected stories of "isolated
SP" represented the same pathophysiologic phenomenon. In Table 7,
the conditions that could mimic isolated SP are listed. Though some of
the collected stories could be of doubtful interpretation, in most cases
the disorders listed in Table 7 could be ruled out with a high degree
of certainty on the grounds of the information given by the subjects.
By analogy with a group of neuromuscular diseases called "periodic
paralyses," we could define "Periodic Isolated Sleep Paralysis"
(PISP), the recurrent disorder reported by most patients of the present
study.
While in narcoleptic patients the hypnagogic form of SP is largely prevalent
(Thorpy, 1990; Hishikawa, 1976), isolated SP seems to be more often hypnopompic
(Table 3), with episodes occurring at the end of nocturnal sleep or in
the middle of the night. From a physiopathological point of view, this
observation somehow challenges the current interpretation of SP as due
to the marked dissociation between the level of alertness and skeletal
muscle atonia during sleep onset REM periods (SOREMPs) (Hishikawa, 1976;
Hishikawa and Shimizu, 1995). Furthermore, while some hypotheses have
been formulated about the neural and biochemical anomalies accounting
for the occurrence of SOREMPs in narcoleptic patients (Hishikawa and Shimizu,
1995), at present nothing is known about the mechanisms underlying anomalies
of REM-wakefulness transition in the middle or end of the night. From
an etiopathogenetical point of view, some clues might come from some evident
clinical similarities between PISP and a group of neurologic disorders
known as "channelopathies" (which comprise periodic paralyses,
some kinds of migraine and of epilepsy and some episodic movement disorders).
Such similarities appear in the periodic occurrence, the possible influence
of genetic factors, and the presence of similar precipitating factors
(Ptácek, 1998) (Table 8). The episodic occurrence of periodic paralyses
and, in general, of channelopathies suggests the existence of some biologic
anomaly that must be mild enough to let patients be perfectly normal between
attacks. Certain factors can push the patient "beyond the border"
and induce an attack. Known precipitating factors include stress, physical
fatigue, and some foods and drinks. Such analogies seem to suggest that
all these conditions share a common physiopathologic basis (Ptácek,
1998).
In particular, Hypokalemic Periodic Paralysis (HypoKPP), which is due
to mutations in a gene of calcium channel in skeletal muscle, is cited
by the ICSD (Thorpy, 1990) as "...the only condition that closely
mimics sleep paralysis. The attacks usually occur during rest; paralysis
occurs on awakening as in true sleep paralysis." Furthermore, several
patients with an established diagnosis of HypoKPP report that during their
attacks (and not at other times) they present vivid lucid dreams and frank
hallucinations closely resembling the ones which occur during SP (Appendix
II, Hypokalemic Periodic Paralysis Resource Page). This seems to suggest
a disorder of REM sleep regulating mechanisms during some HypoKPP episodes.
We could speculate that in some cases of HypoKPP, the ion-channel anomalies
responsible for muscle weakness may somehow also affect the neural systems
regulating REM sleep and trigger dissociated REM episodes during the attacks.
This would be a further link between SP and periodic paralyses.
A second bias affecting this study is due to the fact that the epidemiologic
characteristics of patients are influenced by the kind of subject who
can have access to an American sleep medicine Web site; that is to say,
it is a population made up mainly of young American males. Subjective
experiences associated with SP may be influenced by cultural factors,
as appears from the different interpretation and denomination of such
experiences, i.e., "old hag," "Kanashibari," etc.
(Dahlitz and Parkes, 1993). In the present survey, such cultural influences
can be found in some reports of "alien abduction" beside more
traditional "visits" by "spirits" and "demons"
(Appendix I, 14). The central subjective experience associated with SP,
however, seems to be highly stereotyped through all ages and countries,
and consists of feelings of fear or terror and of a threatening presence,
while the subject believes to see, quite distinctly, his surroundings.
Such experiences suggest an activation of limbic system structures during
SP. In fact, either the terror, which is not simply due to the awareness
of paralysis, since most patients keep on experiencing it though they
have become aware that the disease is not harmful and it will stop in
a few seconds or minutes, or the feeling of an impending threat suggest
an involvement of structures (the amygdala in particular) controlling
emotions and individual attention/surprise/defense reactions (Davis, 1997;
Sleep Paralysis Page, 1998) (Table 9). Also, the acoustic hallucinations
("buzzing sound," "loud ringing," etc.) perceived
by approximately one third of the patients during SP may be explained
in a similar way, according to a hypothesis on "phantom sounds"
(Hazell, 1995; Dauman, 1998). According to this theory, tinnitus would
take rise as a "pathologic product" of a reflex of protection
against impending dangers. Such a reflex is supposed to be a phylogenetic
inheritance of a mechanismof vital importance for wild animalsof
individuation and amplification of even minimal noises which could represent
a threat, during nighttime in particular. In support of their theory,
the authors emphasize that tinnitus often starts or increases during states
of alertness or anxiety disorders. Finally, as noted above, the reported
"distinct vision" of surroundings during SP seems to be, in
most cases, an oneiric experience based upon a recollection of information
stored in the patient's memory and involving, once more, an activation
of specific areas within the limbic system (LeDoux, 1993).
Recent reports suggest an activation of the limbic system during physiologic
REM sleep (Nofzinger et al., 1997; Braun et al., 1998). We could speculate
that the arising of a high level of alertness while limbic structures
maintain a condition of activation different from that of normal wakefulness
causes the typical, stereotyped subjective experiences of SP. These hypotheses
can find validation only in more sophisticated research.
APPENDIX I
Examples from the Examined Cases
"Nothing I have ever encountered in my life has ever come close to
the absolutely unreal feeling of terror that grabbed me the night when
I had my S.P. experience."
"I was filled with the most awful terror I have ever experienced."
"...and it is always just as terrifying as it has ever been."
"I often feel a sense of an evil presence when I have one of these
episodes."
"I always felt a 'presence' in my bedroom during this stage, however
I could not identify it clearly."
"They always start with this buzzing sound getting gradually louder
and suddenly I'm trapped."
"...the ringing or buzzing sensation in my ears. This occurs just
before the paralysis occurs. I've found that if I can wake up then, I
can prevent the paralysis from occurring."
"Sometimes I get up and move, only suddenly to wake up in my bed
like I didn't ever leave. Maybe what they call astral travel? It is hard
to articulate the experience."
"I too have floated around the room during some of the paralysis
occurrences and then the next day tried to explain it to someone only
to get strange looks and people thinking I'm nuts."
"I looked down and realized that I could see my body below me. I
was on the ceiling."
"I think I'm awake, so I look at my alarm clock to check, and if
the bright green LED is not there, then I immediately know that is a sleep
disorder experience...my bedroom seems the same as it is during waking,
only the lights don't work."
"I have some awareness that my eyes are closed, but I can see my
surroundings very clearly. My bedroom is exactly as it is in reality."
"I usually end up on the ceiling looking at myself in bed...I've
placed things on top of the wardrobe to try to see (while I'm on the ceiling),
because I need some evidence that what I'm feeling is real or a hallucination.
So far I haven't been able to identify anything, so I guess what you see
is just stored in the memory of your surroundings."
"Lately I have been having sleep paralysis dreams about aliens abducting
me. It feels so real, I try to scream but I can't move!"
APPENDIX II
Vivid Dreams and Hallucinations in Course of Hypokalemic Periodic Paralysisa
"The lucid dreams serve as a 'warning system' as I recognize from
the character of the dream that I am entering an episode, and that I need
to awaken and get some potassium."
"The hallucinations generally occur only when I awaken completely
paralyzed, and thus they resemble in some ways a sleep paralysis. I have
never found these frightening, as many people seem to do, but then I usually
believe I am awake and I am doing something when in fact I am totally
inert."
"I am one that has tremendous hallucinations when I am in an abortive
attack...I have had an imaginary choir of children come to sing to me
when I was not feeling well and too weak to get out of bed."
"I have very vivid dreams when I'm going into an episode...I'll realize
that I'm going into an episode and I'll wake myself up enough to flail
around to get my husband's attention."
aInformation achieved from members of the HypoKPP On-line Support Group;
the group can be contacted at the address reported on the Hypokalemic
Periodic Paralysis Resource Page (see References).
1. Braun AR, Balkin TJ, Wesensten NJ, Gwadry F, Carson RE, Varga M, Baldwin
P, Belenky G, Herscovitch P. Dissociated pattern of activity in visual
cortices and their projections during human rapid eye movement sleep.
Science 1998; 279(5347): 91-5.
2. Dahlitz M, Parkes JD. Sleep Paralysis. Lancet 1993; 341-406.
3. Dauman R. Acouphènes: mécanismes et approche clinique.
In: Encycl Méd-Chir Elsevier, Paris, Oto-rhino-laryngologie, 20-180-A-10,
Neurologie: 17-018-D-10, 1998, pp. 7.
4. Davis M. Neurobiology of fear responses: the role of the amygdala.
J Neuropsychiatry Clin Neurosci 1997; 9(3): 382-402.
5. Dyken ME, Yamada T, Lin-Dyken DC, Yeh M. Sleep Paralysis: a REM sleep
phenomenon as documented with simultaneous clinical and electrophysiologic
assessment. Sleep 1998; 21(Suppl 3): 541.K5 (Abstract).
6. Goff WR, Allison T, Shapiro A, Rosner BS. Cerebral somatosensory responses
evoked during sleep in man. Electroencephalogr Clin Neurophysiol 1966;
21: 1-9.
7. Hazell JW. Models of tinnitus: generation, perception, clinical implications.
In: Vernon JA, Moller AR, eds. Mechanisms of Tinnitus. Boston: Allyn and
Bacon, 1995, pp. 57-72.
8. Hishikawa Y. Sleep Paralysis. In: Guilleminault C, Dement WC, Passouant
P, eds.Narcolepsy. New York: Spectrum, 1976, pp. 97-124.
9. Hishikawa Y, Kaneko Z. Electroencephalographic study on narcolepsy.
Electroencephalogr Clin Neurophysiol 1965; 18: 249-59.
10. Hishikawa Y, Shimizu T. Physiology of REM sleep, cataplexy, and sleep
paralysis. Adv Neurol 1995; 67: 245-71.
11. Hypokalemic Periodic Paralysis Resource Page (Accessed January 30,
1999). Http://www.calexplorer.com/ushkpp.html.
12. LeDoux JE. Emotional memory systems in the brain. Behav Brain Res
1993; 58(1-2): 69-79.
13. Nofzinger EA, Mintun MA, Wiseman M, Kupfer DJ, Moore RY. Forebrain
activation in REM sleep: an FDG PET study. Brain Res 1997; 770 (1-2):
192-201.
14. Ohaeri JU. Experience of isolated sleep paralysis in clinical practice
in Nigeria. J Natl Med Assoc 1992; 84(6): 521-3.
15. Ptàcek LJ. The place of migraine as a channelopathy. Curr
Opin Neurol 1998; 11: 217-26.
16. Sleep Paralysis Page (Revised August 20, 1998). Http://www.arts.uwaterloo.ca/~acheyne/S_P.html.
17. Steriade M, McCarley RW. Brainstem Control of Wakefulness and Sleep.
NY: Plenum Press, 1990.
18. Takeuchi T, Miyasita A, Inugami M, Sasaki Y, Fukuda K. Laboratory-documented
hallucination during sleep-onset REM period in a normal subject. Percept
Mot Skills 1994; 78: 979-85.
19. Thorpy MJ, ed. International Classification of Sleep Disorders: Diagnostic
and Coding Manual. Rochester: Diagnostic Classification Steering Committee-American
Sleep Disorders Association, 1990.
20. Velasco F, Velasco M, Cepeda C, Munoz H. Wakefulness-sleep modulation
of cortical and subcortical somatic evoked potentials in man. Electroencephalogr
Clin Neurophysiol 1980; 48: 64-72.
We thank the members of the HypoKPP Online Support Group (in particular,
Mrs. Deborah Cavel-Greant) for providing helpful information and Dr. Anna
Maria Buzzi for revising the English text.
Original address of this text :
http://www.sro.org/bin/article.dll?Paper&1818&0&0
Please copy this address to the address bar of your
internet browser and press the "enter" key.
(We prefer not to put actual links because
often page locations change and then our log files get cluttered with
error messages
- if the address does not work try to find it from the homepage of the
website in question).
|