Sleep paralysis

DEFINITION AND CLINICAL PRESENTATION

  • A transient state of inability to move and to speak at sleep onset (hypnagogic form) or on awakening (hypnopompic form).
  • Patients are subjectively awake and engaged in a mental struggle to move and to cry, but they appear to be sleeping and sometimes dreaming.
  • It is commonly associated with intense fear and anxiety.
  • Duration of the experience: 1 to several minutes (termination is spontaneous, or induced by touch from another person).
  • Patients may or may not be able to open their eyes; ocular movements, however, are intact.
  • Patients may feel unable to breathe; respiratory movements, however, are intact.
  • A chest pressure (a crushing weight, the feeling of being pushed down into the bed) is commonly experienced when the subject is lying in the supine position (on his or her back).
  • Sleep paralysis may be accompanied by hallucinatory experiences, including (ref. 3):
    • The incubus: an hallucination of being suffocated by a demon sitting on the patient’s chest;
    • The intruder: the feeling that a malevolent being (often unseen) is present in the room;
    • Unusual bodily experiences, including the feeling of flying, floating, leaving one’s own body or seeing one’s own body from another location (“out-of-body experiences”).
  • Isolated sleep paralysis: sleep paralysis as an isolated complaint in otherwise healthy individuals;
  • Familial sleep paralysis: like the former, but transmitted genetically;
  • Narcoleptic sleep paralysis: sleep paralysis as a symptom of narcolepsy.

References.
1. American Sleep Disorders Association: ICSD- International Classification of Sleep Disorders: Diagnostic and Coding Manual. Diagnostic Classification Steering
Committe, Thorpy MJ (Chairman). Rochester, MN, American Sleep Disorder Association, 1990.
2. Hishikawa Y. Sleep Paralysis. In: Guilleminault C, Dement WC, Passouant P, eds. Narcolepsy. New York: Spectrum, 1976, pp 97-124.
3.Cheyne JA, Rueffer SD, and Newby-Clark IR. Hypnagogic and hypnopompic hallucinations during sleep paralysis: neurological and cultural
construction of the night-mare. Conscious Cogn 1999, 8: 319-337.

 

PATHOPHYSIOLOGY

  • Sleep paralysis is supposed to occur when the sleeping subject becomes aware during REM sleep muscular atonia.
    • REM sleep atonia: a generalized state of paralysis which occurs during REM sleep.
    • This is a physiologic phenomenon which occurs 4-6 times every night (in concomitance with every REM sleep phase), aimed at preventing the sleeping subjects from enacting their dreams.
    • Usually, the sleeping subjects are unaware of this physiologic state of paralysis.
  • Studies on narcoleptic patients have shown that sleep paralysis is usually associated with Sleep Onset REM sleep (SOREM) episodes (ref. 1,2).
    • In the normal sleep cycle, the first REM sleep phase usually starts about 90 minutes after the sleep onset.
    • A SOREM episode is defined as a REM sleep episode that occurs within 20 minutes from the sleep onset.
    • The level of consciousness in SOREM episodes is higher than in REM sleep occurring later in the sleep cycle; motor inhibition is much stronger in SOREM episodes than during REM sleep occurring later in the sleep cycle.
  •  In normal (non-narcoleptic) subjects, isolated sleep paralysis has been elicited by a nocturnal sleep interruption schedule (ref. 3,4). In these studies, too, sleep paralysis was associated with SOREM episodes. Most SOREM episodes, however, were not associated with the experience of sleep paralysis.
  • SOREM episodes, which are characterized by strong motor inhibition and relatively high levels of consciousness, are a prerequisite for the occurrence of sleep paralysis. Other- yet unidentified- factors, however, must be involved.

References.

1. Hishikawa Y. Sleep Paralysis. In: Guilleminault C, Dement WC, Passouant P, eds. Narcolepsy. New York: Spectrum, 1976, pp 97-124..
2. Hishikawa Y, Shimizu T. Physiology of REM sleep, cataplexy, and sleep paralysis. Adv Neurol 1995; 67: 245-271.
3. Takeuchi T, Miyasita A, Sasaki Y, Inumami M, and Fukuda K. Isolated sleep paralysis elicited by sleep interruption. Sleep 1992, 15: 217-225.
4. Takeuchi T, Fukuda K, Sasaki Y, Inugami M, and Murphy TI. Factors related to the occurrence of isolated sleep paralysis elicited during a multi-phasic sleep-wake schedule. Sleep 2002, 25: 89-96.

 

PSYCHOPHYSIOLOGY

  • Sleep paralysis is a “dissociated state”, since it is characterized by the simultaneous presence of elements of two different states: REM sleep and waking. Polysomnographic recordings show abundant alpha waves activity (the waking electroencephalographic activity) intruding into REM sleep; or the persistence of REM atonia (motor inhibition) into waking (ref.1).
  • Different from normal REM sleep, in sleep paralysis waking consciousness is largely retained:
    • Patients are aware of themselves and of their surroundings;
    • Under experimental conditions, during sleep paralysis the individuals perceived and remembered all of the stimuli (flashes of light at random intervals) applied by the researchers (ref. 2).
  • REM sleep mental activity, however, may coexist with the above mentioned waking consciousness. It has been suggested that the characteristic formal aspects of hallucinations associated with sleep paralysis (for example: the incubus, the intruder, etc) correspond to characteristic aspects of physiological brain activation during REM sleep (ref. 3,4).

References.

1. Takeuchi T, Miyasita A, Sasaki Y, Inumami M, and Fukuda K. Isolated sleep paralysis elicited by sleep interruption. Sleep 1992, 15: 217-225.
2. Hishikawa Y. Sleep Paralysis. In: Guilleminault C, Dement WC, Passouant P, eds. Narcolepsy. New York: Spectrum, 1976, pp 97-124.
3. Cheyne JA, Newby-Clark IR, and Rueffer SD. Sleep paralysis and associated hypnagogic and hypnopompic experiences. J Sleep Res 1999, 8: 313-317.
4. Cheyne JA, Rueffer SD, and Newby-Clark IR. Hypnagogic and hypnopompic hallucinations during sleep paralysis: neurological and cultural construction of the night-mare. Conscious Cog 1999, 8: 319-337.

 

EPIDEMIOLOGY AND CULTURAL INTERPRETATIONS

  • Sleep paralysis has been recognized across different ethnic groups and it is highly colored by indigenous cultural beliefs. Sleep paralysis and associated hallucinatory experiences are supposed to be the basis of worldwide cultural accounts of nocturnal assaults by evil beings which sit on the helpless sleepers’ chest and suffocate them (ref. 1):
    • incubus (Middle Ages in Europe);
    • old hag (Newfoundland);
    • kanashibari (Japan);
    • ghost oppression (Hong Kong Chinese); etc.
  • Recent surveys yield consistent prevalence rates of 25-40 % for isolated sleep paralysis (ref. 2-6). In many of these studies, most subjects reported a single or a few life events.
    A surprisingly lower rate of 6.2% has been reported in a large study in the general population in Germany and Italy (ref. 7).
  • The experience rate of sleep paralysis has been reported to be higher in shift workers and in nurses (ref 6).
  • A significant association of sleep paralysis with panic disorder and agoraphobia has been reported in African Americans (ref. 8).
  • Isolated cases show no sexual predominance. Women are affected more often than men in the familial form (ref. 9).
  • The prevailing concept is that the majority of cases with sleep paralysis have their onset during adolescence, but in a study investigating the prevalence of mental disorders in Chinese elderly in Hong Kong, the authors found a bimodal distribution of onset of sleep paralysis with peak during adolescence and after age 60 y (the latter probably due to the increased nocturnal sleep disturbances and arousal in the elderly) (ref. 10).

References.

1. Cheyne JA, Rueffer SD, and Newby-Clark IR. Hypnagogic and hypnopompic hallucinations during sleep paralysis: neurological and cultural
construction of the night-mare. Conscious Cogn 1999, 8: 319-337.
2. Fukuda K, Miyasita A; Inugami M, Ishihara K. High prevalence of isolated sleep paralysis: kanashibari phenomenon in Japan. Sleep 1987; 10: 279-286.
3. Ohaeri JU. The prevalence of isolated sleep paralysis among a sample of Nigerian civil servants and undergraduates. Afr J Med Med Sci. 1997 Mar-Jun;26 (1-2) : 43-5.
4. Cheyne JA, Newby-Clark IR, and Rueffer SD. Sleep paralysis and associated hypnagogic and hypnopompic experiences. J Sleep Res 1999, 8: 313-317.
5. Wing YK, Li RHY, Fong SYY. Sleep paralysis in Hong Kong Chinese. J Sleep Res 2000, 9 (S1)
6. Kotorii T, Kotorii T, Uchimura N, Hashizume Y, Shirakawa S, Satomura T, Tanaka J, Nakazawa Y, Maeda H. Questionnaire relating to sleep paralysis. Psychiatry Clin Neurosci 2001;55:265-6.
7. Ohayon MM, Zulley J, Guilleminault C, Smirne S. Prevalence and pathologic associations of sleep paralysis in the general population. Neurology 1999; 52: 1194-1200.
8. Friedman S, Paradis C. Panic disorder in African-Americans: symptomatology and isolated sleep paralysis. Cult Med Psychiatry. 2002 Jun;26(2):179-98.
9. American Sleep Disorders Association: ICSD- International Classification of Sleep Disorders: Diagnostic and Coding Manual. Diagnostic Classification
Steering Committe, Thorpy MJ (Chairman). Rochester, MN, American Sleep Disorder Association, 1990.
10. Wing YK, Chiu H, Leung T, and Ng J. Sleep paralysis in the elderly. J Sleep Res 1999, 8: 151-155.

 

SLEEP PARALYSIS AND NARCOLEPSY

  • The classical symptom tetrad of Narcolepsy (ref. 1, 2):
    • excessive daytime sleepiness, most typically in the form of sleep attacks;
    • cataplectic attacks: brief episodes of sudden, bilateral loss of muscle tone triggered by intense emotion (typically, by laughing or by telling or hearing a joke). The muscle weakness may be partial or complete, and may involve some or all muscles (knees, face and neck are predominantly involved in partial attacks);
    • Sleep paralysis;
    • Hypnagogic (at sleep onset) and hypnopompic (on awakening) hallucinations.
  • Sleep paralysis occurs in about 60% of patients with narcolepsy (ref. 3); its frequency varies from a few life events to daily episodes (ref. 1, 3).
  • The prevalence of sleep paralysis in the general population is 25-40% according to most studies ; in those studies, however, most subjects reported a single or a few life events; on the contrary, in a recent review on Narcolepsy (ref. 2) the authors state that in most narcoleptic patients sleep paralysis is infrequent, “occurring as much as once or twice a week” (which would be considered as severe sleep paralysis, according to the international criteria for isolated sleep paralysis).

References.

1. Bassetti C and Aldrich MS. Narcolepsy. Neurol Clin 1996, 14: 545-571.
2. Overeem S, Mignot E, van Dijk JG, and Lammers GJ. Narcolepsy: clinical features, new pathophysiologic insights, and future perspectives. J Clin Neurophysiol 2001,18: 78-105.
3. Thorpy M. Current concepts in the etiology, diagnosis and treatment of narcolepsy. Sleep Medicine 2001, 2: 5-17.

 

SLEEP PARALYSIS AND THE PERIODIC PARALYSES

  • According to The International Classification of Sleep Disorders: “Hypokalemic periodic paralysis is perhaps the only condition that closely mimics sleep paralysis. The attacks usually occur during rest; paralysis occurs on awakening as in true sleep paralysis. (…) the condition has a familial transmission, shows low serum potassium levels during attacks, may be provoked by high carbohydrate meals or alcohol, and is readily reversed by correcting hypokalemia”.
  • In general: sleep paralysis usually lasts a few minutes, and disappears spontaneously or upon external stimulation (touch or movement induced by another person); the periodic paralyses usually last several hours, and they never disappear upon external stimulation. Some cases, however, may be difficult to classify. The following message was submitted by a family doctor to the PPA (Periodic Paralysis Association) Online Ask-the Experts tool:
  • “ My patient is 65 and in reasonable general health. She was diagnosed at the (… Institute in …) with sleep paralysis attacks some 10-15 years ago, but had been having them since her 20s, in typical form. She does not have hallucinations or other frightening phenomena, and has no psychiatric history or current symptoms, and is not prone to somatic symptoms. There is no family history of anything similar. Her thyroid function is normal and I don’t think it would be possible to check electrolytes during an attack. Mrs H describes her attacks as always occurring in the daytime, usually in the evening if she falls asleep in a chair, and never in the mornings. She sleeps well at night and wakes normally. If she sleeps deeply in her chair, on waking she is unable to do more than open her eyes and feels as though there is a heavy pressure on her chest preventing deep inspiration. She is unable to speak at first and then only whispering. It makes no difference if she is shaken, spoken to etc, which is alarming for others as well as herself. It takes her 30-45 min to recover. This happens once or twice a month and she does not connect it with any particular food types, nor with exercise, only with being overtired. She does not have any other episodes of muscle weakness to suggest a myotonia.” See the section Diagnosis for diagnostic workup in such cases.
  • An alteration of REM sleep homeostasis (possibly leading to abnormal REM sleep phenomena, such as sleep paralysis and sleep-related hallucinations) may be associated with the Periodic Paralyses.
  • The Periodic Paralyses are characterized by episodes of muscular weakness associated with changes in the serum potassium levels and, therefore, with possible alterations in extracellular neuronal potassium conductance. Two studies in rats (ref 1, 2) suggest that alterations in neuronal potassium conductance may influence REM sleep homeostasis. This, in turn, may result in abnormal REM sleep expression.
  • The case of a man with sporadic Hyperkalemic Periodic Paralysis who presented with episodes resembling sleep paralysis has been reported (ref. 3). Polysomnographic recordings demonstrated the presence of sleep onset REM periods (SOREMPs). Treatment with a diuretic which decreases serum potassium resolved all the clinical symptoms and a new polysomnographic study showed the absence of SOREMPs. According to the authors, this case suggests that SOREMPs in this patient may be explained by an increased extracellular potassium conductance related to Hyperkalemic Periodic Paralysis.
  • In a survey conducted among the members of the Periodic Paralysis Listserv (web site: http://www.hkpp.org/ ), we found that subjects with Periodic Paralysis were more likely to report nightmares/abnormal dreams, sleep related hallucinations and sleep paralysis as compared with control groups (ref. 4). This study supports the hypothesis that an alteration of REM sleep homeostasis may occur in subjects with Periodic Paralysis.
    See a more detailed description of this study on the Periodic Paralysis News Desk at:
    http://www.hkpp.org/physicians/sleep.html
  • Finally, it should be noted that sleep paralysis and the Periodic Paralyses share some common clinical characters, including the periodic occurrence, the possible influence of genetic factors (the familial form of sleep paralysis: ref.5) and the presence of similar precipitating factors (stress, fatigue, alcohol, sleep schedule alterations). The Periodic Paralyses are now known to belong to the family of the ion channel disorders (disorders of membrane excitability resulting from a number of different alterations of ion conductance), so one may question if a ion channel disorder may be involved in the recurrent form of sleep paralysis too.

References.
1. Benington JH, Woudenberg MC, Heller HC. Apamin, a selective SK potassium channel blocker, suppresses REM sleep without a compensatory rebound. Brain Res 1995; 692: 86-92.
2. Gandolfo G, Schweitz H, Lazdunski M, Gottesmann C. Sleep cycle disturbances induced by apamin, a selective blocker of Ca2+ activated K+ channels. Brain Res 1996; 736: 344-347
3. Iranzo AI and Santamaria J. Hyperkalemic Periodic Paralysis associated with multiple sleep onset REM periods. Sleep 1999; 22 (8): 1123-1124.
4. Buzzi G, Mostacci M, Sancisi E, Cirignotta F. Sleep complaints in periodic paralyses: a web survey. Funct Neurol 2001; 17 (3): 245-252.
5. Dahlitz M and Parkes JD. Sleep paralysis. Lancet 1993; 341: 406-407.

 

DIAGNOSIS

  • Typical story and no other complaints generally, further investigation is not needed
  • sleep paralysis associated with daytime sleepiness and/or with disrupted nocturnal sleep  consider narcoleptic syndrome or other sleep disorders (such as sleep apnea or periodic limb movements during sleep) which cause REM sleep deprivation, thus predisposing the patient to enter REM sleep prematurely (SOREM).
    Diagnostic workup: neurologic examination; sleep studies
  • “sleep paralysis” of abnormal length (more than 10-15 minutes), or “sleep paralysis” that does not end upon external stimulation (touch or movement induced by another person)  consider a periodic paralysis .
    Diagnostic workup: neurologic examination; serum potassium level during an attack; neurophysiological testing (prolonged exercise test)
  • “sleep paralysis” associated with jerking-shaking-trembling movements, or “sleep paralysis” followed by confusion after awakening  consider brain attacks (seizure disorders or –more questionably- ischemic attacks) during sleep.
    Diagnostic workup: neurologic examination; EEG; brain imaging.
    Note that sleep paralysis may be associated with unusual bodily sensations, including “jerking-shaking-trembling” sensations,
    but these are just hallucinatory experiences; if the involuntary movements are real -based on physical evidence, or on witness
    information -, the diagnosis of sleep paralysis can’t be made.

 

PREVENTION AND TREATMENT

  • Sleep paralysis and sleep-related hallucinations occur predominantly in the supine position (ref. 1-3), therefore people suffering from sleep paralysis should try to avoid the supine sleeping position. However, most subjects find themselves in the supine position during sleep paralysis regardless of the usually preferred sleeping position (ref. 3,4).
  • Sleep paralysis is also facilitated by sleep disruption and wake-sleep schedule alterations (which, in turn, may be facilitated by stress and by drinking beverages containing caffeine and alcohol in the late evening).
    See for example http://watarts.uwaterloo.ca/~acheyne/prevent.html
    Sleep disorders which may cause sleep disruption –such as obstructive sleep apnea, or periodic limb movements during
    sleep- should be researched in subjects with recurrent episodes of sleep paralysis.
  • Sleep paralysis has also been associated with periods of shift work or rapid time zone change (jet lag) (ref. 5).
  • Some patients have noted that repeated efforts to move, or attempting to move one’s fingers or toes, or vigorous eye movements may help to abort the paralytic state.
  • Many experiencers, however, suggest that the best way to manage sleep paralysis is to let it go, without trying to struggle against it (personal observations).
  • When a pharmacologic treatment is needed, tricyclic antidepressants (e.g., imipramine, clomipramine) or selective serotonine reuptake inhibitors (e.g., fluoxetine, paroxetine) are the most effective treatment, since they are potent REM sleep inhibitors (ref. 6).

References.

6. Dahmen N and Kasten M. REM-associated hallucinations and sleep paralysis are dependent on body posture. J Neurol 2001; 248: 423-424.
7. Dahmen N, Kasten M, Muller MJ, Mittag K. Frequency and dependence on body posture of hallucinations and sleep paralysis in a community sample. J Sleep Res 2002; 11 (2): 179.
8. Cheyne JA. Situational factors affecting sleep paralysis and associated hallucinations: position and timing effects. J Sleep Res 2002; 11 (2): 169-177.
9. Fukuda K, Ogilvie RD, Chilcott L, Vendittelli AM, Takeuchi T. The prevalence of sleep paralysis among Canadian and Japanese college students. Dreaming 1998; 8: 5959.
10. Synder S. Isolated sleep paralysis after rapid time zone change (“jet lag”) syndrome. Chronobiol 1983; 10: 377-379.
11. Overeem S, Mignot E, van Dijk JG, and Lammers GJ. Narcolepsy: clinical features, new pathophysiologic insights, and future perspectives. J Clin Neurophysiol 2001,18: 78-105.

 

KINDS OF EXPERIENCE (EXAMPLES)

Common sleep paralysis:

“Occasionally, during sleep, I start to wake up…or try to force myself to wake up…during these episodes, I can hear what is going on around me…but I’m unable to move or open my eyes… I’m not completely awake…but I’m not really asleep either…it’s an extremely frightening and stressful incident, when it occurs…and I’m wondering if this is normal??? not being able to move is almost painful…as I can feel my muscles fighting to move, and can’t”.

Hallucinatory sleep paralysis (two examples from the literature):

Herman Melville. Moby-Dick. “… I opened my eyes and the before sunlit room was now wrapped in outer darkness. Instantly I felt a shock running through all my frame; nothing was to be seen and nothing was to be heard; but a supernatural hand seemed placed in mine. My arm hung over the counterpane, and the nameless, unimaginable silent form or phantom, to which the hand belonged, seemed closely seated by my bedside. For what seemed ages piled on ages, I lay there, frozen with the most awful fears, not daring to drag away my hand; yet ever thinking that if I could but stir it one single inch, the horrid spell would be broken”.

see: Herman J. An instance of sleep paralysis in Moby-Dick. Sleep 1997; 20 (7): 577-579

Guy de Maupassant. Le Horla. “I sleep—for a while—two or three hours—then a dream—no—a nightmare seizes me in its grip, I know full well that I am lying down and that I am asleep . . . I sense it and I know it . . . and I am also aware that somebody is coming up to me, looking at me, running his fingers over me, climbing on to my bed, kneeling on my chest, taking me by the throat and squeezing . . . squeezing . . . with all its might, trying to strangle me. I struggle, but I am tied down by that dreadful feeling of helplessness which paralyzes us in our dreams. I want to cry out—but I can’t. I want to move——I can’t do it. I try, making terrible, strenuous efforts, gasping for breath, to turn on my side, to throw off this creature who is crushing me and choking me—but I can’t! Then, suddenly, I wake up, panic-stricken, covered in sweat. I light a candle. I am alone”.

 

False awakenings:

“ I don’t think my eyes were open, but I could “see” (feel?) myself lying in bed. Then I would get up and turn on the light and walk around the room, only to then realize that I was still asleep. I tried several times to get up, but each time I would realize I was still asleep. Then, when I would “get up” I would try to jump up and down, because I thought it would feel different if I was awake, and I could test, but every time, I was still asleep. I don’t know how, but I eventually woke up, and realized I had been asleep for maybe 15 to 20 minutes”.

“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 it 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”.

Comment. All the above reported experiences occur during REM sleep atonia (motor inhibition), but they are characterized by different levels of alertness and lucidity. In common sleep paralysis, the subject is almost completely alert and lucid; hallucinatory sleep paralysis is characterized by a “double consciousness”, since the individuals experience a simultaneous perception of dream-like imagery and of the sleeping environment; in false awakenings, the level of lucidity is still lower, since the subjects are somehow aware of their surroundings, but they are not aware of being paralysed. The concept of “metachoric” hallucination was suggested to indicate a kind of hallucination in which “the entire visual environment is replaced by a hallucinatory one, although this may provide a precise replica of the physical world” (Green C. Waking dreams and other metachoric experiences. Psychiatr J Univ Ott 1990; 15: 123-128). This may occur either during sleep paralysis, or during false awakenings.

 

While Sleep Paralysis is NOT an ion channelopathy and is unrelated to periodic paralysis, we encounter numerous visitors inquiring about this problem.  As such, Dr. Giorgio Buzzi, an Italian neurologist, has graciously provided the PPA with some basic information and answers to frequently asked questions on sleep paralysis.

For more information, please see here

which gives excellent descriptions of hypnagogic hallucinations.  Click the links “auditory hallucinations” and “visual hallucinations”. You’ll find lots of information about these often so frightening and realistic phenomena.

You may read the results of a survey that Dr. Buzzi made a few years ago about sleep paralysis and associated experiences at the following address:

http://www.sro.org/2000/Buzzi/61/

Inability to breathe, and “a wind rushing loudly” past your ears are often associated with sleep paralysis. Just like other sensations possibly associated with sleep paralysis, these are unpleasant (for many patients they are really frightening) but not harmful phenomena. Many experiencers suggest that the best way to manage sleep paralysis is to let it go, without trying to struggle against it.  SP may be an isolated phenomenon in otherwise healthy individuals, or it may be facilitated by concomitant disorders which cause a disruption of sleep architecture. The occurrence of SP in the periods when you have trouble with breathing may suggest a concomitant respiratory disorder during sleep (for example, sleep apnea syndrome), which should be investigated by means of a polysomnographic recording.
The episodes of inability to move while “awake and very aware” sound like episodes of sleep paralysis (SP),
a sleep disorder which consists of a period of inability to perform voluntary movements either at sleep onset (hypnagogic form) or upon awakening (hypnopompic form).

Sleep paralysis (SP) is often reported as a frightening experience, particularly if the patient senses
difficulty in being able to breathe; moreover, some people also exepriences vivid and terrifying hallucinations during the episodes. Anyway, it’s a not-harmful incident that always stops within seconds or a few minutes. Many experiencers suggest that the best way to manage SP is to let it go, without trying to struggle against it. According to recent studies, 20-40% of normal people experiences SP at least once, and 3-6% experience it as a recurrent disorder. 
Though no specific pharmacologic treatment exists, small doses of tryciclic antidepressants or of the new SSRI (serotonergic) antidepressants may help in some cases. This is not due to the antidepressant effect of these drugs, but to their effect of inhibiting REM sleep. In fact,
although the cause of sleep paralysis is not fully understood, polysomnographic studies have shown that most often it occurs during a REM phase at sleep onset.

Here are some suggestions in order to prevent sleep paralysis (from a work of Dr. J.A. Cheyne, Dpt. of Psychology, University of Waterloo). Stress: Among the most common precursors of sleep paralysis are stress and sleep disturbances. These two often occur together. Indeed, a reasonable hypothesis is that the effects of stress on sleep paralysis are mediated through disruption of sleep. In any case our respondents very frequently mention, quite spontaneously, that they experienced more than usual amounts of stress during bouts of sleep paralysis. Some older respondents have mentioned that they had experienced sleep paralysis many years ago, but had gone for many years without any problems until they began to experience family-, professional-, or job-related stress. Knowing that one’s sleep paralysis may be caused by stress may seem of limited utility. One is almost certatinly already highly motivated to reduce high levels of stress and likely would have done so if it were easily done. Realizing, however, that the stress may be mediated through sleep disturbances at least affords one some strategies of dealing with stress-related sleep paralysis even if one cannot eliminate the stress itself. Periods of stress are often associated with insomnias, including difficulty falling asleep, multiple and prolonged wakings during the night, and early waking. The first likely leads simply to a general sleep deprivation, while the later two may have a relatively greater impact on deep sleep and REM sleep. Since sleep paralysis is thought to be a REM-related problem, not being able to remain asleep for sufficient periods to accumulate normal REM may predispose one to enter REM prematurely, as it were, immediately upon falling asleep and hence cause the person to experience sleep paralysis. The most direct way of coping with this is to maintain a regular schedule and maintain one’s normal times of retiring and rising. These are frequently disrupted during periods of
stress. Eating large amounts late into the evening, drinking beverages containing caffeine and alcohol, and excessive smoking are common reactions to stressful conditions and can be quite disruptive both of sleep in general and of the normal sequencing of sleep periods more specifically. Clearly avoiding any of these, especially in the late evening, will help prevent sleep loss and hence bouts of sleep paralysis. A serious Sleep Debt debt, which tends to take a greater toll on REM, might well contribute to increased incidence of SP.
Sleeping position: It has been long suspected, and frequently reported, that lying in the supine (face-up) position seems to be associated with sleep paralysis. In our own work we have found that lying in the supine position is five times more likely during sleep paralysis that it is during normal sleep. If one is trying to avoid sleep paralysis then avoiding the supine position is strongly advised. For people who normally sleep in this position changing may prove difficult. However, sleeping on one’s back appears to be relative rarely in our (Canadian) samples, with only 10%-15% of people reporting that they normally sleep in this position. Since, about 60% of sleep paralysis episodes are reported to occur in the supine position obviously many people who are experiencing sleep paralysis are in, for them, an unusual position. It should be noted, however, that many people who report normally sleeping in the supine position also report experiencing sleep paralysis in this position, so we cannot conclude that the supine position is associated with sleep paralysis simply because it is unusual.
We have recently come up with a new and intriguing finding regarding finding. It turns out that the prone position (sleeping face-down) is completely neutral with regard to sleep paralysis. About 15% of people
report sleeping in this position and about the same percent report experiencing sleep paralysis in that position. Sleeping on one’s side during sleep paralysis is, however, extremely uncommon, with only about 5% of people reporting this. This finding is especially striking when one realizes that this is the most commonly reported normal sleeping position in our samples. According to these reports people are ten times more likely to be on their sides during sleep than during sleep paralysis. These findings
should certainly encourage people to try to sleep on the side, especially during bouts of sleep paralysis. Of course, we cannot know yet whether there is a causal relation. It may simply be that whatever state predisposes one to sleep paralysis may also bias one to lying in the supine position. Nonetheless, if I were having difficulty falling asleep because of recurring episodes of sleep paralysis I would certainly elect to lie on my side.

Other sleep disorders that may facilitate the occurrence of sleep paralysis are narcolepsy or other conditions that may disrupt the sleep architecture.

Sleep paralysis and sleep-related hallucinations may occur in an isolated form in otherwise healthy individuals, in a familial form transmitted genetically, and as a part of narcoleptic syndrome (the other symptoms of narcolepsy are: excessive daytime sleepiness with sleep attacks; and cataplexy, i.e. sudden loss of bilateral muscle tone provoked by strong emotion).

 

Differential Diagnosis:

Sleep-related “muscle jerks” may be a physiologic phenomenon which occur at sleep onset (“sleep starts” or “hypnic jerks”), or a pathologic phenomenon which may recur through the sleep (“periodic limb movements in sleep” or “nocturnal myoclonus”).
Sleep starts are sudden, brief contractions of the legs, sometimes involving the arms and head, which occur
at sleep onset. They are sometimes associated with the subjective impression of falling, a sensory flash, or a visual hypnagogic dream or hallucination. Sleep starts are an essentially universal component of the sleep-onset process (although often they are not recalled), but they are enhanced by stimulants (such as caffeine) and by anxiety.
Sleep starts should be differentiated from nocturnal myoclonus (a synonym is “Periodic Limb Movements in Sleep, PLMS”).
The latter is a sleep disorder characterized by involuntary movements in sleep that usually affect the leg(s) alone or leg(s) more than arm(s). They are typically characterized by repetitive stereotypic dorsiflexions of the big toe accompanied by flexions of the ankles, knees, and thighs that recur at intervals of 5-90 seconds with a duration of 0.5-5 seconds. While sleep starts generally occur only during the sleep onset process, nocturnal myoclonus may recur through the sleep and may cause a disrupted sleep pattern.
More uncommon causes of sleep-related muscle jerks include “fragmentary myoclonus”; “propriospinal myoclonus”; and muscle jerks of epileptic nature.
Therefore, the nature of your disorder should be investigated by means of a polysomnographic recording (more than a single recording may be necessary, if the disorder does not recur every night).

Cataplexy (cataplexy, which is a symptom of narcolepsy, is a sudden weakness -or full paralysis- triggered by emotions)  Compare this to sleep paralysis, which can have terrifying hypnagogic (that means sleep-related) hallucinations. Many individuals who experience this disorder avoid talking about it because they believe that people will think they are crazy. However, this is neither a symptom of psychiatric disorder, nor a spiritual or paranormal phenomenon. It’s only a sleep disorder with a fairly well known physiopathologic explanation (hallucinoid imagery -typical of the REM sleep phase- which intrudes into wakefulness).
Therefore, please consider discussing with your treating physician the possibility of undergoing a sleep study in order to rule out other possibly associated sleep disorders.

Dr. Buzzi reports an analysis of 264 cases of sleep paralysis with associated hypnagogic hallucinations available at  Sleep Research Online at:  http://www.sro.org/2000/Buzzi/61/

If there is shaking that genuinely occurs during sleep, a sleep-related seizure may trigger an abnormal arousal leading to sleep paralysis and, subsequently, to the convulsive manifestations.  If there is no actual shaking, it has been suggested that REM sleep-related myoclonic jerks may trigger motor hallucinations (such as the feeling of shaking) during sleep paralysis episodes. An acurate history, EEG, and a video-monitored polysomnographic recording can help to clarify the nature of these sleep-related attacks.

Sleep paralysis can occur with other disorders, for example, sleep paralysis associated with a disrupted nocturnal sleep and nightmares. This pattern may occur in several different conditions (including narcolepsy, whose main symptom is daytime sleepiness; nocturnal breathing disorders, such as sleep apnea; and some psychic disorders). In such cases, a thorough medical examination, and -most probably- a polysomnographic recording (i.e., a sleep study) are needed in order to make the correct diagnosis.

cataplectic attacks are brief episodes of sudden, bilateral loss of muscle tone triggered by intense emotion (typically, by laughing or by telling or hearing a joke). The muscle weakness may be partial or complete, and may involve some or all muscles (knees, face and neck are predominantly involved in partial attacks). According to the International Classification of Sleep Disorders, if you have clear-cut cataplectic attacks (diagnosed by a sleep specialist) AND daytime sleepiness, a diagnosis of narcoleptic syndrome can be made even without a polysomnographic study (the combination of daytime sleepiness and cataplectic attacks is diagnostic for narcolepsy). Cataplectic attacks without daytime sleepiness (that is, without narcolepsy) have been described in some extremely uncommon conditions; therefore, if you don’t have narcolepsy, I would search for other possible causes of your symptoms before considering the possibility of cataplectic attacks without narcolepsy.

 

 Dr. Giorgio Buzzi is an Italian neurologist whose main interest is Sleep Medicine. He collaborates with the Sleep Medicine Unit, Department of Neurology, S. Orsola-Malpighi Hospital, University of Bologna, Italy. Dr. Buzzi serves as a member of the PPA Science and Medical Advisory Board, and provides editorial support for this web page.

To ask Dr. Buzzi questions about sleep disorders or sleep-related issues please use our Ask the Experts system.

 

Polsomnography: A Clinical Practice Guideline

This Guideline was developed jointly by the AARC Cardiopulmonary Diagnostics CPG Focus Group and representatives of the Association of Polysomnography Technologists (APT). Both groups have approved its content.

Reprinted from Respiratory Care [Respir Care 1995;40(12):1336-1343]
AARC-APT Clinical Practice Guideline
Polysomnography

PSG 1.0 PROCEDURE:

Polysomnography

 

PSG 2.0 DESCRIPTION/DEFINITION:

Polysomnography refers to the collective process of monitoring and recording physiologic data during sleep. The specific variables monitored during center-based polysomnographic evaluation of sleep-related respiratory disturbances are listed.(1,2) Home-based polysomnography(3) and unattended monitoring systems are not addressed in this guideline.

The variables monitored and recorded during polysomnography include but are not limited to:(4,5)

2.1 global neural electroencephalographic activity (EEG) from electrodes placed on the patient’s scalp;
2.2 eye movements (electro-oculogram, or EOG) from electrodes placed near the outer canthus of each eye;
2.3 submental electromyographic activity (EMG) from electrodes placed over the mentalis, submentalis muscle, and/or masseter regions;
2.4 rhythm electrocardiogram (ECG) with two or three chest leads;
2.5 respiratory effort, by chest-wall and abdominal movement via strain gauges, piezoelectric belts, inductive plethysmography, impedance or inductance pneumography, endoesophageal pressure, or by intercostal EMG;
2.6 nasal and/or oral airflow via thermistor or pneumotachograph;
2.7 oxygen saturation (SpO2) via pulse oximetry;
2.8body position via mercury switches or by direct observation;
2.9limb movements (arms and legs) via EMG;(6)
2.10 recordings of or vibration (frequency and/ or volume) may be recorded;(7)
2.11 end-tidal CO2, transcutaneous CO2, esophageal pH, penile tumescence, and bipolar EEG are beyond the scope and intent of this guideline.
PSG 3.0 SETTING:

Center-based polysomnography is performed within specialized hospital sleep laboratories,(1) appropriately equipped hospital rooms, or stand-alone sleep centers, with a qualified technician in constant attendance.(8)

PSG 4.0 INDICATIONS:

Polysomnography may be indicated in patients(9-12)

4.1with COPD whose awake PaO2 is > 55 torr but whose illness is complicated by pulmonary hypertension, right heart failure, polycythemia, or excessive daytime sleepiness;
4.2with restrictive ventilatory impairment secondary to chest-wall and neuromuscular disturbances whose illness is complicated by chronic hypoventilation, polycythemia, pulmonary hypertension, disturbed sleep, morning headaches, or daytime somnolence and fatigue;
4.3with disturbances in respiratory control whose awake PaCO2 is > 45 torr or whose illness is complicated by pulmonary hypertension, polycythemia, disturbed sleep, morning headaches, or daytime somnolence and fatigue;
4.4with nocturnal cyclic brady- or tachyarrhythmias, nocturnal abnormalities of atrioventricular conduction, or ventricular ectopy that appear to increase in frequency during sleep;
4.5with excessive daytime sleepiness or insomnia;
4.6with snoring associated with observed apneas and/or excessive daytime sleepiness;
4.7with other symptoms of sleep-disordered breathing as described in International Classification of Sleep Disorders;(6)
4.8with symptoms of sleep disorders described in the International Classification of Sleep Disorders.(6)
PSG 5.0 CONTRAINDICATIONS:

There are no absolute contraindications to polysomnography when indications are clearly established.

 

Researchers Discover Heritable Sleep Disorder

August 30, 1999— Researchers studying three families with the same unusual sleep pattern have uncovered the first hereditary sleep disorder in humans caused by a single gene. Neurologist Christopher Jones and Howard Hughes Medical Institute investigator Louis Ptácek, both at the University of Utah, are now searching for the gene that causes the disorder known as familial advanced sleep phase syndrome (FASPS).

Ptácek and his colleagues concluded that a single gene was responsible for FASPS by studying how the condition was passed along from one generation to the next within the affected families. In this case, inheritance seemed to follow the same simple pattern seen with other single gene traits, such as eye color.
“Our goal is to find the gene that is altered in FASPS and to use it to help us determine how the body’s internal biological clock works,” said Ptácek, whose research team published the findings in the September 1999 issue of the journal Nature Medicine. “Finding this gene might give us important leads not only for treating sleep disorders but also other problems related to human circadian rhythms.”

All creatures—from bacteria to humans—seemingly operate on a biological clock synchronized to a 24-hour day. This internal clock controls a variety of daily biochemical and behavioral cycles—including fluctuations in sleep and wakefulness—that are collectively called circadian rhythms.

People with FASPS have a “fast” biological clock—their internal clock’s “day” is shorter than 24 hours. If left unconstrained by the demands of everyday life, people with a fast clock tend to go to sleep and wake up several hours earlier than normal. For example, the people examined in this study reported that while on vacation they tended to fall asleep earlier and wake up earlier than usual. In comparison, most people stay up later and wake up later while on vacation.

Such large disruptions in circadian rhythms are rare, said Ptácek. “These aren’t diseases per se, and most people just live with this sleep pattern and never see a doctor about it,” he explained.

In this case, however, one woman with a severe circadian disruption did seek help from Jones, a neurologist who specializes in treating sleep disorders. “It turns out that her daughter and grandchild have a similar sleep pattern,” said Ptácek.

Jones approached Ptácek, who studies genetic disorders in humans, and the two scientists led a team that interviewed the woman’s extended family to determine the extent of the problem. During the course of this study, the team found two additional families with members who have FASPS. In total, the researchers found 29 people with the sleep disorder.

Biological monitoring of various hormone levels, body temperature and brain electrical activity confirmed the diagnoses and revealed some interesting changes in sleep patterns. The most notable was a consistent advance of sleep onset and the first incidence of dream sleep by more than three hours.

With the diagnoses confirmed, it was simple matter to create a family tree and map the incidence of FASPS. The results were striking—the researchers discovered that the disorder followed the simple inheritance pattern of traits caused by a single mutant gene. “This is the first Mendelian inherited sleep disorder discovered in humans,” said Ptácek

Eye color is an example of a trait that follows Mendelian inheritance patterns. In the case of eye color, the gene for brown eyes (B) is dominant to the gene for blue eyes (b), which is recessive. A person with brown eyes can be BB or Bb. Only the combination of two recessive genes (bb) results in blue eyes. A brown-eyed (Bb) and a blue-eyed (bb) parent will, on average, have 50 percent brown-eyed and 50 percent blue-eyed children.

In fact, in the three families that Jones and Ptácek studied, half the children of the afflicted parents had the disorder, a classic Mendelian pattern of inheritance.

The fact that FASPS follows the simplest genetic inheritance pattern should simplify the search for the gene involved. “Mapping and cloning a gene can take five years or longer,” said Ptácek. “We hope to have the FASPS gene much sooner than that.”

He added that once the gene is in hand, “we will study the corresponding protein.

 

Sleep and Neuromuscular Disorders

Author: Giorgio Buzzi, M. D.
Note: Dr. Giorgio Buzzi is an Italian neurologist whose main interest is Sleep Medicine. He collaborates with the Sleep Medicine Unit, Department of Neurology, S. Orsola-Malpighi Hospital, University of Bologna, Italy.

Myopathies and neuromuscular junction impairments may represent a threat to the maintenance of normal breathing during sleep (1, 2). myopathies involving the thoraco-abdominal and respiratory accessory muscles will impair breathing during sleep; the problems will systematically worsen during rapid-eye movement (REM) sleep.

Why during sleep During sleep, there is a reduction in ventilation due to sleep state and in response to increased impedance of the respiratory system. However, rib cage activity is maintained, albeit reduced, as is diaphragmatic activity (2).

Why the problems worsen during REM sleep ? During REM sleep, there is an inhibition of somatic motor neurons, which causes further reduction or even complete loss of tone in rib cage and other accessory muscles of respiration, but which leaves the diaphragm relatively unaffected. Thus, any process affecting the diaphragm might cause significant changes in breathing and oxygenation during sleep (2).

Examples of neuromuscular disorders causing sleep-related breathing abnormalities include muscular dystrophies (myotonic dystrophy, Duchenne muscular dystrophy, Thomsen’s disease); congenital myopathies (nemaline myopathy, congenital fiber-type disproportion); metabolic myopathies (mitochondrial myopathy, acid maltase deficit); peripheral neuropathy (Charcot-Marie-Tooth disease) (2).

In addition to sleep related breathing disorders, patients with neuromuscular disease may present a disrupted sleep pattern, with sleep fragmentation and frequent arousals, of unclear origin (7).

When should a sleep disorder be suspected ? It should be suspected in patients complaining of disturbed sleep, early morning headaches, daytime fatigue and hypersomnolence. Such patients should undergo polysomnographic studies.

Below is a compendium of sleep studies in some of the above-mentioned conditions.

Please note the following definitions:

Obstructive sleep apnea is characterized by recurrent episodes of partial or complete upper airway obstruction during sleep, with reduction or complete cessation of airflow despite ongoing inspiratory efforts.