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Dreaming

ContentsHistory of the Study of DreamsThe Interpretation of DreamsThe Psychology of DreamsDreams, Psychopathology, PsychotherapyDreaming and Psychiatric DisordersNeurobiology of Dreaming

History of the Study of DreamsR Cartwright, Rush University Medical Center, Chicago, IL, USA

ã 2013 Elsevier Inc. All rights reserved.

GlossaryActivation-synthesis theory: Hobson and McCarley theory

that dreams are initially random images that acquire

meaning following arousal.

Atonia: Abrupt loss of muscle tone at the onset of rapid eye

movement (REM) sleep.

Dream: A hallucinatory experience during sleep consisting

of visual images related in a story-like structure, which are

accepted as reality at the time.

EMs: Eye movements during a REM period, which vary in

speed and density. These may relate to the visual content of

the dream.

Imagery rehearsal therapy: A treatment program for

the control of nightmares through practice during

waking of pleasant visual images.

Incorporation: Inclusion in the dream report of an

external stimulus.

Mood regulation function: Dream reports

are initially negative in emotion and progressively

become more positive at the end of the

night.

Nightmares: Strongly unpleasant dreams that

awaken the dreamer with full recall of the dream

story.

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S

The Early History of Laboratory Investigation of Dreams

Dreams have been a source of interest throughout human

history. However, much of this literature does not meet the

criteria of being a ‘study.’ This article will cover only investiga-

tions that test a hypothesis. Such studies began in the mid-

1950s when laboratory-monitored sleep proved dreams could

be elicited reliably by awakening sleepers from a specific neu-

rophysiological state known as rapid eye movement (REM)

sleep. This article will cover some highlights of the research

that followed.

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Hypothesis: Dreams are Related to REM SleepCharacteristics

Early sleep studies, and more recent brain imaging work, hy-

pothesized that REM sleep determines the psychological char-

acteristics of dreams. The first such study hypothesized that

body movement within a REM period would disrupt the

continuity of the reported dream story. REM periods were

divided into those that were continuous and those that were

interrupted by a body movement. The dream reports from

these episodes were judged as being either a continuous narra-

tive or one with an abrupt change to another story. The data

analysis showed that REM periods, free of body movement,

yield continuous dream reports while those with one or more

body movements were associated with reports of unrelated

dreams. This established that REM sleep is typically free of

body movements and that their presence interferes with

dream continuity. This study led to the addition of a chin

muscle monitor, in recognition that loss of muscle tone is a

reliable signal of the onset of REM sleep and thus the likely

presence of dreaming.

Another hypothesis tested whether the reported dream is

related to the type of eye movements (EMs) that precede the

awakening. The EMs were divided into those that were large

(high amplitude) and dense (occurring in bursts) versus those

that were slower and sparser. A significant association was found

between the activity of the EMs and a dream story in which the

ncyclopedia of Sleep http://dx.doi.org/10.1016/B978-0-12-378610-4.00028-0

Dreaming | History of the Study of Dreams 125

dreamer was engaged in some activity. As per reports following

sparse EMs, the dreamer was passive or was ‘just observing.’

Studies correlating REM characteristics and dream features

waned following the publication of the Hobson and McCarley

activation-synthesis theory of dream construction. These neu-

roscientists had located the cells involved in initiating REM

sleep to be in the pons, an area at the base of the brain. They

argued that as this excitation traveled upward through the

occipital cortex, random visual images were stimulated. These

acquired meaning only during arousal when the higher brain

areas attempt to make sense of these inherently meaningless

images. Later, brain imaging studies, using positron emission

tomography (PET) scans and functional magnetic resonance

imaging (fMRI), identified patterns of brain areas that are more

or less active in REM sleep than in waking, or in nonrapid eye

movement (NREM) sleep and the relation of these to the

known function of these brain areas. These studies added

specificity to the description of REM as a highly activated

brain state. Finding strong activity in the limbic and paralimbic

cortex (the amygdala, hypothalamus, the anterior cingulate)

supports that dreams are more likely to involve negative emo-

tions. The deactivation of the prefrontal cortex accounts for the

difficulty remembering dreams and the weakening of reality

testing (accepting the dream as if real). Dream reports collected

during these imaging studies verified that dreams were being

experienced during a specific pattern of increased and de-

creased brain activity in healthy persons but these varied in

different clinical samples. This moved the dream interpretation

question back from being a waking afterthought to being due

to the particular brain areas active in the REM state.

Hypothesis: Dream Images are Internally Generated

Early experiments attempted to test whether the images reported

in dreams could be influenced by applying a variety of external

stimuli during an ongoing REM episode. They first used an

auditory tone, a flashing light, and a spray of water, followed

by a doorbell to awaken the sleeper to report their experience.

None of these stimuli was ‘markedly effective’ in modifying the

ongoing dream. Another study used auditory stimuli of spoken

proper names, two of which were emotionally salient and two

were neutral. The finding was that half of the dream reports

showed some effect although this was not by a direct inclusion

of the names but by a similarity in sound of a word in the report

to the stimulus name (via assonance). Familiar names, their

own or those of ex-girlfriends, were more likely to have an effect

on the dream content than neutral names. The finding that

emotional stimuli have more effect on dream content than

those neutral in tone has been a repeated finding.

To test whether the auditory stimuli had more effect on

dreams than the visual, because the receptor organs (ears)

were open in sleep while the eyes were not, volunteers were

tested while sleeping with their eyes taped open. Once REM

was identified, an experimenter held up an object in front of

the sleeper’s eyes, before they were awakened to give a dream

report. Judges attempted to match these reports to the stimulus

object. As they were not able do this at a rate better than

chance, the conclusion was that dream images are internally

generated and only on rare occasions are external stimuli re-

sponsible for some element of a dream.

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Hypothesis: Dreams are Related to Each Other Withinthe Night

Testing the relation of dreams to each other found these were

not obviously similar within the night nor did all the dreams of

a night make up one continuous story. The conclusion was that

dreams are independent stories but with some elements in

common, and that those that were similar were not always

found in reports from adjacent REM periods. Since in only a

few cases was the same theme expressed throughout all the

dreams of a night, it was concluded that, at the level of the

manifest content, dreams are not related to each other. This

raised the question of whether the experimental awakenings

were disrupting a natural continuity of the dreams. Further

study showed the amount of time spent awake for the sleeper

to report their dream was negatively related to the continuity

between that dream and the report from the next REM awak-

ening. The longer the time awake, the less the continuity was.

Although awakenings from REM yielded a report of dream-

ing 80% of the time, those from nonrapid eye movement

(NREM) sleep yielded widely varied percentages of dream re-

ports. The highest percent was found at sleep onset. More

typically, NREM reports differed in quality from REM reports.

They were described as less imagistic and more thought-like,

less emotional and more pleasant than the highly emotional,

unpleasant reports from REM. To test whether the failure to

find continuity between dreams of the same night was because

the dream theme was set prior to the first REM, the next

investigation collected samples from both NREM and REM

sleep, sampling all Electroencephalography (EEG) stages of

sleep. Sleepers were awakened either 30 or 90min following

sleep onset by a coin toss. The coin toss was repeated following

each report to determine the timing of the next awakening.

This resulted in 6–9 reports each night in random sequences of

various sleep stages. The reports were examined for repeated

images or themes in the manifest content. Sometimes, the

initial report was from a NREM stage before any REM had

occurred. Repeated elements were found in different sequences

of sleep stages. Testing continuity of the sleeping mind using

this random awakening schedule presents a real difficulty:

repeated elements may be present but missed if the random

protocol skipped a time when reports were most connected.

In conclusion, there were nights with little or no repeated ele-

ments and others when these were plentiful in both NREM and

REM sleep. During nights when these were frequent, they were

also the most vivid and memorable of the reported dream but

were embedded into distinctly independent contexts, suggesting

that they were driven by intense preoccupations (possibly pre-

conscious day residues), which then interfaced in sleep with

ongoing unconscious (latent) dream thoughts. The conclusion

was that there is an interaction of preconscious and unconscious

streams of thought throughout sleep but that the methods used

to analyze dreams were not appropriate to identify these.

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Hypothesis: Dreams Relate to the PresleepWaking State

The findings of the TV study reported above pushed the ques-

tion of how dreams are constructed back still earlier to examine

126 Dreaming | History of the Study of Dreams

the influence of the emotional state of the participants before

they fell asleep. It was clear that there was also a need for more

subtle and more systematic methods to measure dream con-

tent. The most comprehensive and influential of the scales

developed were those of Hall and Van de Castle. These allowed

studies to compare dream reports of various groups on stan-

dardized measures. Differences were found between the

dreams of men and women, older and younger age groups,

ethnic groups, and many clinical groups such as alcoholics and

nondrinkers. Studies of the relation between the prior waking

psychological state and the dreams of the night began to use

the Hall and Van de Castle scales for standardizing the dream

content and various personality tests for measuring waking

traits and states. The presleep emotional state of the volunteer

was then manipulated using stimuli chosen to be emotion

invoking or bland, and reports from the following dreams

were analyzed using the new content scales. One study used

two episodes of a TV series, one very violent and the other a

comedy. The order of these was counterbalanced on two sleep

nights. Reports were collected from both REM and NREM sleep

episodes to explore the differences in the influence of these

movies on the different sleep stages, as well as the relation to

the waking personality characteristics. The aggressive film pro-

duced longer and more imaginative, more vivid, and emo-

tional REM reports than did the comedy movie. However,

these film differences were not found between the reports

collected from NREM sleep. The correlation of dream charac-

teristics and the waking personality tests showed an ‘extremely

consistent pattern of correlations between the clinically ori-

ented scales and dream-like features of the reports.’ The imag-

inativeness of the person in waking was highly correlated with

that aspect of the dream reports. There were no significant

direct incorporations of either film into the sleep reports.

Why the aggressive film had a clear impact on REM reports

but not on those from NREM and why, despite the increase in

vivid, imaginative, emotional REM dreams after the violent

film, were the dreams not more violent or unpleasant? The

explanation offered was that the violent film had a general

effect and not a specific one, and that the general emotional

arousal stimulated the viewers’ personal emotional memories

to be displayed during REM sleep.

To focus the waking attention to a specific drive, the next

study included a physiological measure of sexual arousal dur-

ing the exposure to a pornographic film. This study examined

the effects of this on the dreams of adult men over five nights of

REM collections. The first night was a control to assess the

baseline rate of sexual dreams. The following day, the partici-

pants wore a penile strain gauge to measure their response to

the movie shown before their second night. The dream reports

were analyzed using the Hall and Van de Castle norms for the

frequency of common words in the dream reports of a similar

sample of adult men. Judges first rated these words for sym-

bolic sexual reference, for example, balls, nuts, shaft, and foun-

tain. The judges agreed on ten words as having symbolic sexual

meaning and ten others were chosen to refer to the laboratory

setting. There was a marked increase in the symbolic words in

the dream reports over the rate expected from the norms. That

this might represent a latent response to the sexual film was

supported by a significant increase in ‘No recall’ reports on

Night 2, and an increase in number of dreams with one charac-

ter, indicating a possible suppression response to two-person

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interactions. On the final night, Night 5, the recall rate returned

to the baseline control level and the number of dreams with two

characters was significantly higher than on the control night.

In summary, the findings of an immediate increase in fail-

ure to recall from REM awakenings and lack of any direct

incorporation into dreams of the arousing movie suggested

an inhibiting effect possibly related to the presleep interactions

with the laboratory personnel, two attractive female techni-

cians, with whom they had some bodily contact during the

application of the electrodes. This appears to have raised anxiety

about having, or reporting, explicit dreams leading to both a

dampening of recall and increased number of dreams with only

one character. The conclusion was that although the sexual

movie produced an immediate physiological arousal response

in waking, it was inhibited from direct expression in sleep on

Night 2. On the following Night 3, the number of symbolic

sexual words in the dream reports hit the highest peak. Over the

next three nights, there was a gradual return to the baseline recall

rate. The laboratory situation appeared to have a powerful inhi-

biting effect on the drive aroused by watching the movie.

Finding that the planned effect of experimental stimuli

often had a minimal effect and that the social context may

have a more powerful, unanticipated effect on dream content,

there was a shift in research strategy toward more naturalistic

studies. Dreams following natural disasters, such as the 9/11

terrorist attack, the holocaust, bereavement, divorce, kidnap-

ping, rape, and living under missile attacks, have all been

studied. The landmark study of this kind chose an inherently

emotion arousing event, elective surgery, to study the effect on

dreams. Patients were recorded for four nights before and three

nights after surgery. Rating scales were constructed for analyz-

ing the dreams including degree of recall, anxiety, and involve-

ment. The general conclusion was that the surgeries meant

different things to different patients. The initial dreams never

dealt with the surgery directly but as has been seen before there

were many transformations to represent this event symboli-

cally. Most apparent was that the dreams demonstrated the

participant’s attempts to integrate the present stressful event

into their individual adaptive strategies that had worked for

them in the past. If this has a learning effect on future coping,

longer follow up would be needed.

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Hypothesis: Dreams Effect Postsleep PsychologicalFunctioning

Studies of the effect of dreams on changing the waking mood

have examined both healthy persons and those with clinical

diagnoses. One study of a healthy, high functioning sample

used the Profile of Mood States (POMS) test before and after

sleep for two nights with REM interruptions for collecting

dreams on the second night. The sleepers rated the emotional

quality of each dream immediately following their report as

positive/pleasant, neutral, or negative/unpleasant. The sample

was divided on the presleep mood score into those who had

little or no elevation on the Depression Mood Scale and those

who had a mild elevation of this negative mood. The Not

Depressed (ND) group had twice as many positive dreams as

negative and the Mildly Depressed (MD) had an equal number

of positive and negative dreams. To test whether dreams regulate

moodwithin sleep, the average ratings of dream affect in the first

Dreaming | History of the Study of Dreams 127

half of the night was compared to the average of those in the

second. The ND had more positive than negative dreams in

both halves. The MD had a high proportion of negative dreams

in the first half-night, with a marked decrease in the last half and

the opposite pattern for positive dreams; with few at the begin-

ning of the night and a high proportion at the end of the night.

The conclusion that sleep generally improves morning

mood was confirmed by a lower depression score following

both nights. Whether this effect is related to the intervening

dreams was supported by the finding that the affect in first

dreams of the night was significantly correlated to the previous

waking mood. Even when this mood was only mildly un-

happy, negative dreams dominate in the first dream reports

and then decrease in the second half-night. The natural se-

quence appears to be that the emotional state before sleep is

continued into sleep onset, stimulating a network of memories

associated with similar feeling. The varied dream scenarios or

‘contexts’ appear to dissipate the negative mood, which in turn

accounts for the improved morning mood in healthy persons.

If this is a natural function in well-adjusted adults, do dreams

display dysfunctions in those not emotionally fit?

Hypothesis: Dreams Differ in Psychiatric Patients

The ‘naturalistic’ studies, particularly of sleep during or after

traumatic events, brought attention to the study of nightmares.

These fear-inducing dreams lead to an interruption of sleep, an

awakening with full recall of the dream. These are the most

disturbing symptom of posttraumatic stress disorder (PTSD),

the most long lasting symptom and the one most difficult to

treat. The PTSD diagnosis includes not only distressing dreams

but in some exact replications of the traumatic event. Treat-

ments that train patients to control their dreams have become

the behavioral treatment of choice. To test whether dreamers

are capable of controlling their dreams, Imagery Rehearsal

Therapy, a brief clinical program, was developed. This begins

by training nightmare patients to rehearse a positive image of

their choice during waking. Next step is to write out their

nightmare but to change the ending to one they prefer. That

this trains nightmare control is being reported in some studies

based on self-report.

Dreams have also been studied in major depression since

these patients show abnormalities of REM sleep and dream

reports that are both brief and bland in feeling when the

depression is severe. Moderate depression is characterized by

dreams with negative feelings, which fail to reduce, in fact

increase, in frequency within the night. Those whose within-

sleep pattern of dream affect resembles that of healthy samples,

with decreasing negative and increasing positive dreams within

the night, are more likely to remit without treatment within a

year. This finding has been confirmed in several studies leading

to the first verified function of dreams: dreaming performs a

mood regulatory function.

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The Future of Dream Research

As reviewed here, studies of the last 60 years have freed dreams

of being seen as meaningless accompaniments of REM sleep.

Partly, this is due to recent studies of patients with brain

injuries, seizure disorders, and psychosurgeries who report

changes in their dreaming. Solms reported almost 1000 cases

experiencing a cessation of dreaming following a focal fore-

brain lesion. Many of these were confirmed as ‘dreamless’ by

the REM awakening method. In these cases, the pontine brain

stem was completely spared and REM sleep was intact. Further,

he found that dreaming can be initiated by a forebrain mech-

anism independent of the REM state in those with nocturnal

seizures occurring in NREM sleep, which are experienced as

nightmares. Comparing a large sample of patients who

reported changes in their dream experience and a healthy

control sample, Solms identified the brain areas that had

been damaged or surgically removed and the patients’ experi-

ence of changes in their dreams, to map the structures respon-

sible for specific characteristics of dreams, for example, the

presence of color or of people. This led him to conclude that

dreaming and REM sleep are controlled by different mecha-

nisms; with REM initiated from the pons and dreaming from

the forebrain. What is common is that dreaming occurs not

only in sleep when the brain is highly activated as it is in REM

but also in the transitions between waking and sleep; at sleep

onset in NREM and at the end of the sleep cycle just prior to

waking. This allows clinical intervention for control of night-

mares, to target sleep onset.

The other major conclusion from this review is that dreams

are strongly influenced by the waking emotional state, which is

not expressed directly but in sensory images drawn from asso-

ciated memory networks. These will be displayed in a sequence

of dreams that function to down-regulate negative mood.

Given these studies, it should be possible to estimate the health

of this function by collecting only two samples: the first from

sleep onset and the second from the end of sleep. This would

avoid disrupting the sleep with REM awakenings andminimize

the laboratory effect.

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See also: Critical Theoretical and Practical Issues: Future ofSleep Research; The Function of Sleep; Dreaming: Dreaming andPsychiatric Disorders; Dreams, Psychopathology, Psychotherapy;Neurobiology of Dreaming; The Interpretation of Dreams; ThePsychology of Dreams; Instrumentation and Methodology:Neuroimaging and Sleep; Nocturnal Penile Tumescence; PsychiatricAssociations of Sleep Loss/Deprivation: Changes in Affect;Personality and Psychopathic Changes

Further Reading

Cartwright R (1990) A network model of dreams. In: Bootzin RR, Kihlstrom JF, andSchacter DL (eds.) Sleep and Cognition, pp. 179–189. Washington, DC: AmericanPsychological Association.

Cartwright R (1991) Dreams that work: The relation of dream incorporation to adaptationto stressful events. Dreaming 1: 3–9.

Cartwright R (2005) Dreaming as a mood regulation system. In: Kryger M, Roth T, andDement W (eds.) Principles and Practice of Sleep Medicine, 4th edn., pp. 565–572.Philadelphia, PA: Elsevier Saunders.

Cartwright R (2010) The Twenty-four Hour Mind: The Role of Sleep and Dreaming inOur Emotional Lives. New York, NY: Oxford University Press.

Cartwright R, Bernick N, Borowitz G, and Kling A (1969) The effects of an erotic movieon the sleep and dreams of young men. Archives of General Psychiatry20: 262–271.

128 Dreaming | History of the Study of Dreams

Dement W and Kleitman N (1957) The relation of eye movement during sleep to dreamactivity: An objective method for the study of dreaming. Journal of ExperimentalPsychology 53: 330–346.

Dement W and Wolpert E (1958) Relationships in the manifest content of dreamsoccurring on the same night. The Journal of Nervous and Mental Disease126: 568–578.

Ellman SJ and Antrobus JS (1991) The Mind in Sleep: Psychology andPsychophysiology, 2nd edn. New York, NY: John Wiley & Sons.

Foulkes D (1985) Dreaming: A Cognitive-Psychological Analysis. Hinsdale, NJ:Lawrence Erlbaum Associates.

Foulkes D and Vogel G (1965) Mental activity at sleep onset. Journal of AbnormalPsychology 70: 231–243.

Hall CS and Van de Castle R (1966) The Content Analysis of Dreams. New York, NY:Appleton-Century-Crofts.

Hartmann E (2002) Dreaming. In: Lee-Chiong T, Sateia MJ, and Carskadon MA (eds.)Sleep Medicine, pp. 93–98. Philadelphia, PA: Hanley & Balfus.

Hobson JA and McCarley RW (1997) The brain as a dream-state generator:An activation-synthesis hypothesis of the dream process. The American Journal ofPsychiatry 134: 1335–1348.

Koulack D (1993) Dreams and adaptation to contemporary stress. In: Moffitt A,Kramer M, and Hoffman R (eds.) The Functions of Dreaming, pp. 321–340.Albany, NY: State University of New York Press.

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Krakow B, Hollifeld M, and Schrader R (2000) A controlled study of imagery rehearsalfor chronic nightmares in sexual assault survivors with PTSD: A preliminaryreport. Journal of Traumatic Stress 13: 589–609.

Kramer M (1993) The selective mood regulatory function of dreaming: An updateand revision. In: Moffitt A, Kramer M, and Hoffman R (eds.) The Functions ofDreaming, pp. 139–195. Albany, NY: State University of New York Press.

Lavie P and Kaminer H (1991) Dreams that poison sleep: Dreaming in holocaustsurvivors. Dreaming 1: 11–21.

Nofzinger EA, Mintun MA, Wiseman M, Kupfer D, and Moore RY (1997) Forebrainactivation in REM sleep: An FDG PET study. Brain Research 770: 192–201.

Solms M (1997) The Neuropsychology of Dreams: A Clinico-Anatomical Study.Mahwah, NJ: Lawrence Erlbaum Associates.

Solms M (2003) Dreaming and REM sleep are controlled by different brainmechanisms. In: Pace-Schott E, Solms M, Blagrove M, and Harnad S (eds.)Sleep and Dreaming: Scientific Advances and Reconsiderations, pp. 51–58.New York, NY: Cambridge University Press.

Stickgold R (2003) Memory, cognition and dreams. In: Maquet P, Smith C, and Stickgold R(eds.) Sleep and Brain Plasticity, pp. 17–39. New York, NY: Oxford University Press.

Strauch I and Meier B (1996) In Search of Dreams: Results of Experimental DreamResearch. Albany, NY: State University of New York Press.

Witkin HA and Lewis HB (1967) Experimental Studies of Dreaming. New York, NY:Random House.

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SleepwalkingV Jain, Stanford Sleep Medicine Center, Redwood City, CA, USA

Published by Elsevier Inc.

GlossaryParasomnias: Undesirable movements and behaviors that

occur during entry into sleep, within sleep, or in the setting

of arousals from sleep.

Sleep diaries: Records kept by the patient or family

member/partner that indicate sleep onset and offset

times, including naps and awakenings overnight; these

data are often helpful in determining whether

parasomnia episodes are triggered by relative sleep

deprivation.

Sleepwalking: Complex behaviors usually initiated during

arousals from sleep culminating in ambulation during an

altered state of consciousness and impaired judgment; also

referred to as somnambulism.

20

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Description

Sleepwalking is characterized by complex behaviors that are

typically initiated during arousals from sleep and result in

ambulation. The activity can vary from simple events such as

sitting up in bed to more complex movements such as walking

or even ‘bolting’ from the room. These episodes can last from a

few seconds to several minutes long. Patients are generally

difficult to arouse during these periods, and if they are able to

be awakened, patients are often in a confused state. Many

patients typically have their eyes open and have a ‘glassy-

eyed’ appearance during sleepwalking episodes. As these events

typically occur because of arousals from slow-wave sleep, they

generally occur during the first half of the sleep period.

While some patients may have little memory of the event,

most patients generally have nomemory of the event the follow-

ing morning. Patients may be able to recall emotions or impres-

sions from the event. Symptoms of tachycardia, sweating, or the

expression of fear is generally not displayed in patients during an

episode. The absence of autonomic symptoms and screaming is

what can differentiate a sleepwalking episode from sleep terrors.

Sleepwalking is a subset of a larger group of parasomnias.

Parasomnias are undesirable movements and behaviors that

occur during entry into sleep, during sleep, or with arousals

from sleep. Parasomnias are subdivided into several categories:

(1) disorders of arousal from non-REM sleep, (2) parasomnias

associated with REM sleep, and (3) other parasomnias.

The disorders of arousal include confusional arousals, sleep-

walking, and sleep terrors. The disorders of arousal tend to

occur in stage N3 sleep and therefore typically occur in the

first third of the night.

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Risk Factors

There are a number of factors that may predispose a patient to

sleepwalking. There is a strong genetic influence in the devel-

opment of sleepwalking. Generally, if one or both parents have

had a history of sleepwalking, the child is at a significantly

increased risk of developing sleepwalking episodes as well. The

Finnish Twin Cohort study published by Hublin et al. reported

a concordance rate of 55% for monozygotic and 35% for

dizygotic twins for sleepwalking in childhood. Bakwin et al.

also published a twin study that reported a six-time greater

concordance for sleepwalking among monozygotic twins

than in dizygotic twins.

Factors such as sleep deprivation, fever, head injury, alcohol

abuse, hyperthyroidism, and other conditions have also been

shown to induce sleepwalking. The use of certain medications,

including lithium, tricyclic antidepressants (TCAs), phenothi-

azines, zolpidem, and other benzodiazepine receptor agonists,

can also precipitate these events. Studies have also shown that

sleep-disordered breathing in children, that is, obstructive

sleep apnea (OSA), may trigger sleepwalking due to the fre-

quent arousals associated with respiratory events. Effective

treatment of OSA may reduce the frequency of sleepwalking

episodes in some patients.

Overall, sleepwalking has been reported to have a 2%

prevalence in the general population. Sleepwalking tends to

be more prevalent in childhood, peaking around age 8, and

generally resolves with puberty although episodes have been

described in adults. While de novo sleepwalking can occur in

adulthood, many adults who sleepwalk first exhibited sleep-

walking behavior in childhood. The persistence of sleepwalk-

ing into adulthood has been associated with underlying

psychopathology in a significant number of patients.

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Diagnosis and Differential Diagnosis

The most important initial approach to diagnosing sleepwalk-

ing is to obtain a careful and detailed history from the patient

and their bed partner, parent, or caregiver. Information regard-

ing the frequency, timing, and duration of the episodes should

be obtained. It may be helpful to have patients keep a sleep

diary to document this information. Detailed descriptions of

any motor behavior should be obtained and the patient should

be questioned about sensory symptoms. The clinician should

pay particular attention to the patient’s past medical history,

family history, and medication list to look for any precipitating

factors outlined above. If the patient relays a history of associ-

ated snoring or apnea, they should also be evaluated for

underlying sleep-disordered breathing.

While not required for a diagnosis, overnight polysomno-

graphy (PSG) can also be a valuable tool in the evaluation of

sleepwalking. Although rare, the occurrence of a complex

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Descriptions of Parasomnias | Sleepwalking 203

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behavior during PSG can support the diagnosis. While not

pathognomonic for sleepwalking, several PSG findings have

been thought to be associated with disorders of arousals.

Patients with sleepwalking have been found to have an

increased number of arousals from slow-wave sleep when

compared to matched controls. It has also been suggested that

patients with a higher percentage of slow-wave sleep are at

higher risk for disorders of arousals. However, studies of sleep-

walkers have revealed that many have the same if not lower

slow-wave sleep activity when compared to matched controls.

Also, arousals during slow-wave sleep can be seen in disorders

other than sleepwalking such as OSA and periodic limb move-

ments in sleep (PLMS). Hypersynchronous delta (HSD) activity

has been documented just before sleepwalking episodes in sev-

eral studies. HSD waves consist of two or more high amplitude

delta frequency waves that precede an arousal or complex be-

havior during sleep. Although sleepwalkers have been found to

have higher ratios of HSD during slow-wave sleep, this finding

has not been confirmed inmore recent studies. Finally, as sleep-

disordered breathing has been postulated as a possible trigger

for sleepwalking, evidence of OSA on PSG should prompt treat-

ment with nasal continuous positive airway pressure (nCPAP),

as successful treatment has been reported to decrease or elimi-

nate the occurrence of sleepwalking.

The differential diagnosis of sleepwalking includes other

NREM parasomnias such as confusional arousals and night

terrors and other sleep disorders, including nightmare disor-

ders, rapid eye movement sleep behavior disorder (RBD), noc-

turnal seizure activity, epileptic events, and sleep-related panic

attacks. Sleepwalking can be differentiated from sleep terrors

by the lack of autonomic hyperactivity and loud scream during

nocturnal episodes. Nightmare disorder and RBD both occur

within REM sleep and are more common in the second half of

the night. Also, children who are aroused from a nightmare

generally become alert quickly and may often provide a de-

tailed description of their dream content. If there is concern

regarding epileptic activity, nocturnal PSG should be

performed with an expanded seizure montage. Patients with

sleep-related panic attacks typically develop autonomic activa-

tion following arousal from sleep and lack the confusion and

amnesia seen in sleepwalkers.LS

E

Management

Management of sleepwalking should focus on both attempting to

eliminate the occurrence of the events andmitigating the adverse

effects of a potential episode. Patients with other sleep, medical,

or psychiatric disorders should obtain appropriate treatment for

the underlying disorder. Next, patients should be provided reas-

surance and counseling regarding safety precautions in the home.

Patients and their parents, bed partners, or caregivers should be

reassured that many arousal disorders decline in frequency, as a

child enters adolescence. The clinician should ensure that

counseling regarding environmental protection is provided.

Safety measures include locks on doors and windows, sleeping

on the first level of the home, gates across stairs, removing sharp

objects from the bedroom, avoiding bunk beds, and placing

padding or mattresses next to the bed. Emphasis should also be

placed on sleep hygiene, as sleep deprivation, irregular sleep

E

schedules, and unfamiliar sleep environments can increase sleep-

walking episodes. If inciting agents are noted on the medication

list, the precipitating agent should be avoided and the patient

should be providedwith a therapeutic alternative. If sleepwalking

activity remains problematic, pharmacologic therapy with ben-

zodiazepines, TCAs, and selective serotonin reuptake inhibitors

may provide benefit. Clonazepam at a dose of 0.5–2.0mg ad-

ministered at bedtime has been successful at controlling sleep-

walking activity.

Conclusion

In conclusion, sleepwalking is a common parasomnia that is

most prevalent in children. There is a strong genetic influence,

and many factors can precipitate sleepwalking episodes. The

diagnosis can be obtained from a careful and detailed history.

In more complicated cases, PSG may be used. Clinical suspicion

of any underlying etiology warrants appropriate evaluation and

treatment. The management of sleepwalking is typically straight-

forward with reassurance and counseling on safety precautions.

Finally, in refractory cases, pharmacotherapy may be warranted.

See also: Descriptions of Parasomnias: Confusional Arousals;Parasomnias in Children; Sleep Terrors.

Further Reading

AASM (2005) International Classification of Sleep Disorders: Diagnostic and CodingManual, 2nd edn. Westchester, IL: American Academy of Sleep Medicine.

Avidan AY and Kaplish N (2011) The parasomnias: Epidemiology, clinical features anddiagnostic approach. Clinics in Chest Medicine 31: 353–370.

Bakwin H (1970) Sleepwalking in twins. The Lancet 2: 466–467.Barabas G, Ferrari M, and Matthews WS (1983) Childhood migraine and

somnambulism. Neurology 33: 948–949.Berry R (2012) Fundamentals of Sleep Medicine, pp. 567–592. Philadelphia PA:

Elsevier Saunders.Broughton RJ (1968) Sleep disorders: Disorders of arousal? Enuresis, somnambulism,

and nightmares occur in confusional states of arousal, not in "dreaming sleep".Science 159: 1070–1078.

Broughton R (2000) NREM parasomnias. In: Kryger MHRT and Dement WC (eds.)Principles and Practice of Sleep Medicine, pp. 693–706. Philadelphia, PA: W.B.Saunders.

Chokroverty SHW and Walters AS (2003) An approach to the patient with movementdisorders during sleep and classification. In: Chokroverty SHW and Walters AS(eds.) Sleep and Movement Disorders, pp. 201–218. Philadelphia, PA:Butterworth-Heinemann.

Espa F, Dauvilliers Y, Ondze B, Billiard M, and Besset A (2002) Arousal reactions insleepwalking and night terrors in adults: The role of respiratory events. Sleep25: 871–875.

Goodwin JL, Kaemingk KL, Fregosi RF, et al. (2004) Parasomnias and sleepdisordered breathing in Caucasian and Hispanic children – the Tucson children’sassessment of sleep apnea study. BMC Medicine 2: 14.

Guilleminault C, Palombini L, Pelayo R, and Chervin RD (2003) Sleepwalking andsleep terrors in prepubertal children: What triggers them? Pediatrics111: e17–e25.

Hublin C, Kaprio J, Partinen M, et al. (1997) Prevalence and genetics of sleepwalking:A population-based twin study. Neurology 48: 177–181.

Kales JD, Kales A, Soldatos CR, Chamberlin K, and Martin ED (1979) Sleepwalking andnight terrors related to febrile illness. The American Journal of Psychiatry136: 1214–1215.

Kales A, Soldatos CR, Bixler EO, et al. (1980) Hereditary factors in sleepwalking andnight terrors. The British Journal of Psychiatry 137: 111–118.

V

204 Descriptions of Parasomnias | Sleepwalking

Laberge L, Tremblay RE, Vitaro F, and Montplaisir J (2000) Development ofparasomnias from childhood to early adolescence. Pediatrics 106: 67–74.

Mahowald M (2002) Arousal and sleep-wake transition parasomnias.In: Lee-Chiong TLSM and Carskadon MA (eds.) Sleep Medicine, pp. 207–213.Philadelphia, PA: Hanley and Belfus.

Mindell JA and Owens J (2003) Sleepwalking and sleep terrors. A Clinical Guide toPediatric Sleep. Philadelphia, PA: Lipincott Williams &Wilkins.

ELSE

Pesikoff RB and Davis PC (1971) Treatment of pavor nocturnus and somnambulism inchildren. The American Journal of Psychiatry 128: 778–781.

Robinson A and Guilleminault C (2003) Disorders of arousal. In: Chokroverty SHW andWalters AS (eds.) Sleep and Movement Disorders, pp. 265–272. Philadelphia, PA:Butterworth-Heinemann.

Rosen GM, Ferber R, and Mahowald MW (1996) Evaluation of parasomnias in children.Child and Adolescent Clinics of North America 5: 601–616.

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En

Special Conditions, Disorders, and Clinical Issues of SRMD

ContentsGender Differences in Sleep-Related Movement DisordersSleep-Related Movement Disorders in ChildrenAge-Related Changes in PLMS Characteristics of RLS PatientsMedication Effects and Sleep-Related Movement DisordersRestless Legs Syndrome in Internal MedicineImpact of Psychiatric Disorders on Sleep-Related Movement Disorders

Gender Differences in Sleep-Related Movement DisordersB Phillips, University of KY College of Medicine, Lexington, KY, USA; UK GSH Hospital, Lexington, KY, USA

ã 2013 Elsevier Inc. All rights reserved.

GlossaryPeriodic limb movements (PLMs): Stereotyped

and repetitive limb movements that occur during

sleep.

Periodic limb movement disorder (PLMD): A sleep

disorder characterized by stereotyped and repetitive

limb movements that occur during sleep at the rate of

more than 15 times per hour in adults (or more than five

times per hour in children) and is associated with sleep

disturbance and/or daytime fatigue or sleepiness.

Sleep-disordered breathing (SDB): This describes a group

of disorders characterized by abnormalities of respiratory

pattern (pauses in breathing) or the quantity of ventilation

during sleep.VIER

cyclopedia of Sleep http://dx.doi.org/10.1016/B978-0-12-378610-4.00404-6

E

Restless Legs Syndrome

Clinical Features

Restless legs syndrome (RLS) is a sleep-related movement dis-

order whose cardinal feature is unpleasant leg sensations, typ-

ically occurring at night, that interfere with sleep. The sensation

is probably most aptly described as a powerful urge to move

the legs; it is rarely described as painful, and the possibility

of neuropathy should be considered when the discomfort

presents primarily as pain. There is a circadian variation in

symptoms, with greatest intensity typically occurring between

10 p.m. and 2 a.m. Symptoms are worse at rest and improve

with movement or stimulation, including walking, rubbing,

and stretching. The distressing sensations most typically in-

volve the legs, but can also occur in the arms. Because of the

nature and timing of RLS symptoms, patients with RLS may

present with sleep-onset insomnia.

Diagnosis

The diagnosis of RLS is made by history and physical exami-

nation based on criteria listed in Table 1.

Thus, the diagnosis is based on subjective criteria alone, and

polysomnography (PSG) is not generally necessary. The

ELS

specificity of these criteria is not ideal, but careful application

of the first four features, accompanied by a physical examina-

tion (to rule out neuropathy and vascular disease), is fairly

specific for RLS. The differential diagnosis includes cramps,

positional discomfort, vascular leg disease, and neuropathy.

Adding response to dopaminergic medication to the essential

criteria improves diagnostic accuracy.

Epidemiology

In population-based surveys, typically conducted by phone, the

prevalence of any degree of RLS symptoms is estimated to be

somewhere between10%and 15% for all adults,with lower rates

in the young and higher in the elderly. However, the prevalence

of RLS varies considerably with different criteria for frequency

and severity. For example, in the restless legs syndrome preva-

lence and impact Restless Legs Epidemiology Symptoms and

Treatment (REST) study, RLS symptoms were endorsed by 7.2%

of the survey population. However, symptoms occurring at least

twice perweekwere reported by only 5%of the subjects andwere

moderately or severely distressing in only 2.7%.

The rate of RLS may be lower in Asian than in European

populations, but the prevalence in African Americans is similar

to that of Caucasians.

109

Table 1 Diagnostic criteria for RLS in adults

A. The patient reports an urge to move the legs, usually accompanied orcaused by uncomfortable and unpleasant sensations in the legs.

B. The urge to move or the unpleasant sensations begin or worsenduring periods of rest or inactivity such as lying or sitting.

C. The urge to move or the unpleasant sensations are partially or totallyrelieved by movement, such as walking and stretching, or at least aslong as the activity continues.

D. The urge to move or the unpleasant sensations are worse, or onlyoccur, in the evening or night.

E. The condition is not better explained by another current sleepdisorder, medical or neurological disorder, mental disorder,medication use, or substance use disorder.

From American Academy of Sleep Medicine (2005) International Classification of

Sleep Disorders: Diagnostic and Coding Manual, 2nd edn., p. 180. Westchester, IL:

American Academy of Sleep Medicine.

110 Special Conditions, Disorders, and Clinical Issues of SRMD | Gender Differences in Sleep-Related Movement Disorders

Gender Differences for RLS

RLS affects women disproportionately. A consistent finding in

the literature about RLS is that women are 1.5–2 times as likely

as men are to report RLS symptoms. Studies in both children

and adolescents have demonstrated that this difference does

not usually develop until the second or third decade of life.

However, after the third decade, women are about twice as

likely as men to endorse RLS symptoms, and the likelihood

of having RLS may be related to pregnancy. Pregnancy is an

important risk factor for RLS, both during the pregnancy and in

subsequent years. About a fourth of pregnant women experi-

ence RLS symptoms, which typically peak in severity in the

third trimester and resolve promptly after delivery. Lower he-

moglobin, mean corpuscular volumes, and serum folate levels

appear to be risk factors for RLS in pregnancy. With aging, the

risk of RLS is fairly level for men, but it increases for women,

proportionate to parity. In one study, nulliparous women had

the same risk for RLS as did men up to the age of 64. However,

for women who had borne children, the risk of RLS increased

with the number of children. A woman with one child had

twice the risk of RLS as a nulliparous woman and the risk

increased with additional children. Indeed, a recent publica-

tion by Pantaleo et al. indicated that pregnancy accounts for

almost all of the gender differences reported in overall RLS

prevalence.

The gender difference in RLS symptoms appears to be

present for both primary and secondary RLS. In a large cross-

sectional study of patients with end-stage renal disease (ESRD),

women were much more likely than men were to endorse RLS

symptoms. Other associated factors for RLS in ESRD include

lower hemoglobin, worse subjective and objective sleep qual-

ity, excessive daytime sleepiness, use of sleeping pills, depres-

sive symptoms, and higher risk of both obstructive sleep apnea

and hypertension.

RLS is frequently reported to occur with antidepressant use.

It appears likely that the association between RLS and antide-

pressant use varies by gender and by type of antidepressant.

Indeed, antidepressants were more strongly associated with

RLS for men than for women in one study. But analyses of

individual agents showed that fluoxetine was more strongly

associated with RLS in women than in men, whereas use of

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paroxetine, citalopram, and amitriptyline was more likely

to be associated with RLS symptoms in men.

Augmentation (worsening of symptoms despite treatment)

occurs in a large percentage of patients treated with levodopa.

Data on the prevalence of augmentation with dopamine ago-

nists are still scant, but this phenomenon has been documen-

ted to occur with these agents. One study reported a prevalence

rate of about 12% with dopamine agonists, with low ferritin

being the primary associated risk. In that study, there were no

gender differences in the rate of augmentation.

Associative, Predisposing, and Precipitating Factors

Two recent genome-wide association studies have reported

positive association with sequence variants in or around spe-

cific genes on chromosomes 6p, 2p, and 15q and having

symptoms of RLS (and periodic limb movements). Serum

ferritin levels are lower in those with the genetic variant that

predisposes to RLS, which supports the hypothesis that iron

depletion or dysfunction is somehow involved in the patho-

genesis of the disease. Dopamine deficiency or dysfunction is

also in the pathophysiology of RLS, and one unifying hypoth-

esis is that impairment of dopamine transport or function in

the central nervous system due to reduced iron may contribute

to the development of this disorder.

Primary RLS occurs without a known predisposing or exac-

erbating condition, is more likely to have earlier age of onset,

and is likely to be familial. RLS can also be ‘secondary’ to

another condition, including especially iron deficiency, preg-

nancy, and renal failure.

A large group of conditions has now been reported to be

associated with RLS. Many of these conditions and disorders

also lack objective diagnostic criteria, such as attention deficit

hyperactivity disorder, depression, and fibromyalgia, and

many occur with increased frequency in women.

Complications and consequencesIndividuals with RLS are at increased risk for mood distur-

bance, according to cross-sectional studies. This is not neces-

sarily a causal relationship; mood disturbance could contribute

to endorsement of RLS symptoms. Like RLS, depression occurs

with increased frequency inwomen compared tomen and could

partly account for the increased prevalence of RLS symptoms in

women. The effects of RLS symptoms on daytime function are

not clear. RLS has variously been reported to be associated with

daytime sleepiness as well as not to impair daytime sleepiness

and alertness. It does, however, appear to adversely affect quality

and quantity of nocturnal sleep. RLS appears to be associated

with many significant medical conditions and may be a marker

for poor overall health. Indeed, one study has reported an in-

creased risk of death in individuals with RLS.

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Management

Nonpharmacologic treatmentElimination of factors that may cause or contribute to RLS

may make a difference. Several medications have been linked

to both RLS and periodic limb movements, and the data

are particularly strong for the association between RLS and

antidepressants. Lifestyle relates to RLS symptoms: increased

Special Conditions, Disorders, and Clinical Issues of SRMD | Gender Differences in Sleep-Related Movement Disorders 111

weight, caffeine intake, and smoking have been associated

with increased likelihood of endorsing RLS symptoms. RLS

is also associated with earning a lower income, sedentary

lifestyle, and reduced alcohol consumption. Nonpharmaco-

logic measures therefore should include education, moderate

exercise, smoking cessation, caffeine reduction or elimina-

tion, and discontinuation of exacerbating medications if it is

safe to do so. Some have found that working at night and

sleeping in the day has helped. Iron supplementation should

be given to those who are iron deficient.

Pharmacologic treatmentDopamine receptor agonists are the first-line treatment and

are the only agents that are Food and Drug Administration

(FDA)-approved for RLS. The two dopamine receptor agonists

available for this purpose in the United States are ropinirole

and pramipexole; both are FDA-approved. Pramipexole is ren-

ally excreted, and the dose is 0.125–0.75mgday�1 in single or

divided doses, averaging 0.25mgday�1. Ropinirole is hepati-

cally excreted, and the effective dose is in the range of 1.5–6mg

day�1 in single or divided doses, averaging about 2mgday�1.

The main side effects of these agents are nausea, vomiting,

orthostasis, dizziness, sleepiness, insomnia, and compulsive

behavior. Because of delays in absorption, these agents

work best if given at least an hour before symptom onset

typically occurs.

Use of other agents is off-label and not clearly supported by

the literature. As mentioned, RLS is a particular issue in preg-

nancy. None of the medications commonly used to treat RLS is

safe in pregnancy. For pregnant women, folic acid has been

reported to improve symptoms in those who are folate defi-

cient. Iron replacement may also reduce or eliminate symp-

toms in patients who have serum ferritin levels below 45 mg l�1.

Recently, pneumatic compression devices have been shown to

relieve symptoms in a randomized, double-blinded, sham-

controlled trial.

One consideration in the pharmacologic treatment of RLS

is the rather large placebo effect, which has been reported to be

about 40%. Another consideration in the pharmacologic man-

agement of RLS is the appearance of augmentation. The Inter-

national Restless Legs Study Group has established diagnostic

standards for the dopaminergic augmentation of RLS, based on

usual time of RLS symptom onset each day, number of body

parts with RLS symptoms, latency to symptoms at rest, severity

of the symptoms, time of occurrence, and effects of dopami-

nergic medication on symptoms. In brief, augmentation

may be said to have occurred if the symptoms have spread to

other body parts (e.g., from calves to thighs), occur earlier in

the evening than originally, or increase in severity. Augmenta-

tion occurs frequently with the (off-label) regular use of

carbidopa; it also occurs, but much less frequently, with ropi-

nirole and pramipexole. Evidence-based recommendations for

management of augmentation are lacking, but some suggested

strategies are to take the dose earlier in the day and split the

existing dose into early evening and bedtime doses. Augmen-

tation and progression of the disease are difficult, if not im-

possible, to distinguish. This, coupled with the large placebo

effect associated with any treatment for this condition, results

in the lack of a clear-cut approach to the management of

augmentation.

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Periodic Limb Movements

RLS and periodic limb movements frequently coexist, which

has resulted in much confusion about periodic limb move-

ments. Periodic limb movements of sleep (PLMS), originally

called nocturnal myoclonus, are rhythmical kicking of the

lower extremities. They increase with age and are most com-

monly identified in association with other sleep disorders.

While an overwhelming majority (>80%) of RLS patients

have periodic limb movements, only a fraction of those

individuals who have limb movements during sleep have

RLS. PLMS have also been included in the obstructive sleep

apnea hypopnea syndrome (see Figure 1), the upper airway

resistance syndrome, narcolepsy, and REM sleep behavior

disorder. PLMS are also frequently seen in patients who are

taking antidepressants and probably represent a serotonergic

phenomenon. When patients with complaints of insomnia

or hypersomnia have PLMS and no other sleep disorder or

relevant (e.g., antidepressant) medication use is present,

they may be diagnosed with periodic limb movement disor-

der (PLMD). Such patients are probably rare. Patients with

PLMS associated with RLS symptoms should be treated for

RLS, but there is no evidence to support pharmacologic

treatment of PLMS/PLMD, and there is no agent FDA-

approved for this indication. The revised diagnostic criteria

for PLMD take into account the coexistence of leg jerks with

many medical conditions and medications, and also ‘raise

the bar’ for the ‘abnormal’ number of periodic limb move-

ments from 5 to 15 for adults (Table 2).IE

R

Gender Differences in Periodic Limb Movements

Women may be more likely to have periodic limb movements

than are men because they are more likely to be diagnosed with

depression and to be taking antidepressants. In addition, they

are more likely to have subtle or occult sleep-disordered

breathing (e.g., upper airways resistance syndrome) than are

men, and the resulting arousal-associated leg jerks may be

misdiagnosed as PLMD.

V

Bruxism

Sleep-related bruxism is characterized by repetitive clenching

or grinding of the teeth during sleep. The primary conse-

quences of this are tooth wear and jaw pain. Bruxism prob-

ably has a prevalence of about 15% and is highest in

childhood. Bruxism tends to occur in families. Anecdotally,

bruxism is thought to be associated with anxiety, stress,

tooth malocclusion, or a side effect of medications such as

antidepressants. It has also been reported with sleep apnea,

Huntingdon’s disease, and Parkinson’s disease. Use of

splints or tooth guards, made by a dentist, is the most

common form of treatment, but behavioral therapy, bio-

feedback, botulinum toxin, and correction of misaligned

teeth may also be effective.

There are no reported gender differences in the prevalence,

manifestations, or treatment of bruxism.

Table 2 Diagnostic Criteria for Periodic Limb Movement Disorder

A. Polysomnography demonstrates repetitive, highly stereotyped, limbmovements that are:1. 0.5–5 s2. Of amplitude >25% of toe dorsiflexion during calibration3. In a sequence of four or more movements4. Separated by an interval of more than 5 s (from limb-movement

onset) and less than 90 s (typically an interval of 20–40 s)B. The PLMS index exceeds 5 per hour in children and 15 per hour in

most adult casesC. There is clinical sleep disturbance or a complaint of daytime fatigueD. The PLMS are not better explained by another current sleep disorder,

medical or neurological disorder, mental disorder, medication use, ora substance use disorder

Note: If PLMS are present without clinical sleep disturbance, the PLMS can be noted as

a polysomnographic finding, but criteria are not met for a diagnosis of PLMD.

From American Academy of Sleep Medicine (2005) International Classification of Sleep

Disorders: Diagnostic and Coding Manual, 2nd edn., p. 185. Westchester, IL: American

Academy of Sleep Medicine.

~LEOG

~REOG

~C3A2

0

0

0

0

0

0

0

128

128

128

128

S

S2202 203 203 204

60" 120" 180" 240"

204 205 205 206 206 207 207 208 208 209 209 210 210 211 21S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2 S2

S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S

0

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9098 96 95 95 98 96 98 94 93 93 97 97 99 96 95 94 98 98 98 98 98 969995 959593 93

~C4A1

~O1A2

~O2A1

SAO2

Body

Stage

5 min.

Micro

Chest

ABD

~Chin

~Left Leg

~Right Leg

Flow

Pressure

00

2 S2

Figure 1 In this 5-min, compressed PSG tracing, periodic limb movements are seen in the leg lead channels (‘left leg, right leg’). However,inspection reveals that these leg movements are part of the arousal response to obstructive respiratory events, seen clearly in the respiratorychannel (‘flow, pressure’). This common finding likely accounts for many cases of ‘periodic limb movement disorder (PLMD)’ and is a major reasonwhy the diagnosis of PLMD should be made only after careful exclusion of sleep-disordered breathing, medication side effects, or other causesof movement.

112 Special Conditions, Disorders, and Clinical Issues of SRMD | Gender Differences in Sleep-Related Movement Disorders

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R

Other Sleep-Related Movement Disorders

Other sleep-related movement disorders include leg cramps

and movement disorders due to drugs or medical conditions.

Data about gender differences in these conditions are lacking.

See also: Psychiatric Associations of Sleep Loss/Deprivation:Antidepressant Effects of Sleep Manipulation; Special Conditions,Disorders, and Clinical Issues for Insomnia: GenderDifferences; Special Conditions, Disorders, and Clinical Issuesof SRBD: Gender-Specific Differences in Patients with ObstructiveSleep Apnea–Hypopnea Syndrome; Special Populations Affectedby Sleep Loss/Deprivation: Pregnancy and Postpartum.

Further Reading

Allen RP, Walters AS, Montplaisir J, et al. (2005) Restless legs syndrome prevalenceand impact: REST general population study. Archives of Internal Medicine 165:1286–1292.

American Academy of Sleep Medicine (2005) International Classification of SleepDisorders: Diagnostic and Coding Manual, 2nd edn., p. 185. Westchester, IL:American Academy of Sleep Medicine.

Araujo SM, de Bruin VM, Nepomuceno LA, et al. (2010) Restless legs syndrome inend-stage renal disease: Clinical characteristics and associated comorbidities.Sleep Medicine 11: 785–790.

Aukerman MM, Aukerman D, Bayard M, Tudiver F, Thorp L, and Bailey B (2006)Exercise and restless legs syndrome: A randomized controlled trial. Journal ofthe American Board of Family Medicine 19: 487–493.

Baughman KR, Bourguet CC, and Ober SK (2009) Gender differences in the associationbetween antidepressant use and restless legs syndrome. Movement Disorders24: 1054–1059.

Benes H, von Eye A, and Kohnen R (2009) Empirical evaluation of theaccuracy of diagnostic criteria for restless legs syndrome. Sleep Medicine10: 524–530.

Special Conditions, Disorders, and Clinical Issues of SRMD | Gender Differences in Sleep-Related Movement Disorders 113

Berger K, Luedemann J, Trenkwalder C, John U, and Kessler C (2004) Sex and therisk of restless legs syndrome in the general population. Archives of InternalMedicine 164: 196–202.

Bjorvatn B, Leissner L, Ulfberg J, et al. (2005) Prevalence, severity and risk factors ofrestless legs syndrome in the general adult population in two Scandinaviancountries. Sleep Medicine 6: 307–312.

Botez MI and Lambert B (1977) Folate deficiency and restless-legs syndrome inpregnancy. The New England Journal of Medicine 297: 670.

Chervin R (2001) Periodic leg movements and sleepiness in patients evaluated forsleep-disordered breathing. American Journal of Respiratory and Critical CareMedicine 164: 1454–1458.

Connor JR, Boyer PJ, Menzies SL, et al. (2003) Neuropathological examinationsuggests impaired brain iron acquisition in restless legs syndrome. Neurology61(22): 304–309.

Dao TT and Lavigne GJ (1998) Oral splints: The crutches for temporomandibulardisorders and bruxism? Critical Reviews in Oral Biology and Medicine 8: 345.

Exar EN and Collop NA (2001) The association of upper airway resistance with periodiclimb movements. Sleep 24: 188–192.

Frauscher B, Gschliesser V, Brandauer E, et al. (2009) The severity range of restlesslegs syndrome (RLS) and augmentation in a prospective patient cohort: Associationwith ferritin levels. Sleep Medicine 10: 611–615.

Garcıa-Borreguero D, Allen RP, Kohnen R, and the International Restless LegsSyndrome Study Group (2007) Diagnostic standards for dopaminergicaugmentation of restless legs syndrome: Report from a World Association ofSleep Medicine-International Restless Legs Syndrome Study Group consensusconference at the Max Planck Institute. Sleep Medicine 8: 520–530.

Hornyak M, Feige B, Voderholzer U, et al. (2007) Polysomnography findings in patientswith restless legs syndrome and in healthy controls: A comparative observationalstudy. Sleep 30: 861–865.

Lee HB, Hening WA, Allen RP, et al. (2007) Race and restless legs syndromesymptoms in an adult community sample in east Baltimore. Sleep Medicine7: 642–645.

Lee HB, Hening WA, Allen RP, et al. (2008) Restless legs syndrome isassociated with DSM-IV major depressive disorder and panic disorder inthe community. The Journal of Neuropsychiatry and Clinical Neurosciences20: 101–105.

Lee KA, Zaffke ME, and Baratte-Beebe K (2001) Restless legs syndrome and sleepdisturbance during pregnancy: The role of folate and iron. Journal of Women’sHealth & Gender-Based Medicine 10: 335–341.

Lettieri CJ and Eliasson AH (2009) Pneumatic compression devices are an effectivetherapy for restless legs syndrome: A prospective, randomized,double-blinded, sham-controlled trial. Chest 135: 74–80.

Littner MR, Kushida C, Anderson WM, and the Standards of Practice Committee of theAmerican Academy of Sleep Medicine (2004) Practice parameters for thedopaminergic treatment of restless legs syndrome and periodic limb movementdisorder. Sleep 27: 557–559.

Lo Coco D, Mattaliano A, Coco AL, and Randisi B (2009) Increased frequency ofrestless legs syndrome in chronic obstructive pulmonary disease patients.Sleep Medicine 10: 572–576.

Mallon L, Broman JE, and Hetta J (2008) Restless legs symptoms with sleepiness inrelation to mortality: 20-year follow-up study of a middle-aged Swedish population.Psychiatry and Clinical Neurosciences 62: 457–463.

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Manconi M, Govoni V, De Vito A, et al. (2004) Restless legs syndrome and pregnancy.Neurology 63: 1065–1069.

Montplaisir J, Michaud M, Denesle R, and Gosselin A (2000) Periodic leg movementsare not more prevalent in insomnia or hypersomnia but are specificallyassociated with sleep disorders involving a dopaminergic impairment. SleepMedicine 1: 163–167.

Pantaleo NP, Hening WA, Allen RP, and Early CJ (2010) Pregnancy accounts formost of the gender difference in prevalence of familial RLS. Sleep Medicine11: 310–313.

Phillips B, Hening W, Britz P, and Mannino DM (2006) Prevalence and correlates ofrestless legs syndrome: Results from the 2005 national sleep foundation poll. Chest129: 76–80.

Phillips B, Young T, Finn L, et al. (2000) Epidemiology of restless legs symptoms inadults. Archives of Internal Medicine 160: 2137–2141.

Pichietti D, Allen RP, Walters AS, et al. (2007) Restless legs syndrome: Prevalenceand impact on children and adolescents – The Peds REST study. Pediatrics120: 253–266.

Rottach KG, Schaner BM, Kirch MH, et al. (2008) Restless legs syndrome as sideeffect of second generation antidepressants. Journal of Psychiatric Research43: 70–75.

Stefansson H, Rye DB, Hicks A, Petursson H, et al. (2007) A genetic risk factor forperiodic limb movements in sleep. The New England Journal of Medicine357: 639–647.

Stehlik R, Arvidsson L, and Ulfberg J (2009) Restless legs syndrome is common amongfemale patients with fibromyalgia. European Neurology 61: 107–111.

Sun ER, Chen CA, Ho G, Earley CJ, and Allen RP (1998) Iron and the restless legssyndrome. Sleep 21: 371–377.

Tan EK, Seah A, See SJ, Lim E, Wong MC, and Koh KK (2001) Restless legssyndrome in an Asian population: A study in Singapore. Movement Disorders16: 577–579.

The National Heart, Lung, and Blood Institute (2008) Restless legs syndrome:Detection and management in primary care. NHLBI-NIH, March 2000. The REMSstudy. Sleep 31: 944–952.

Winkelman JW, Chertow GM, and Lazarus JM (1996) Restless legs syndromein end-stage renal disease. American Journal of Kidney Diseases28: 372–378.

Yang C, White DP, and Winkelman JW (2005) Antidepressants and periodic legmovements of sleep. Biological Psychiatry 58: 510–514.

Yilmaz K, Kilincaslan A, Aydin N, and Kor D (2010) Prevalence and correlates ofrestless legs syndrome in adolescents. Developmental Medicine and ChildNeurology 53(1): 40–47. http://dx.doi.org/10.1111/j.1469-8749.2010.03796.x.

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Relevant Websites

http://www.cdc.gov/sleep/ – The Center for Disease Control’s Public Education site forsleep and its disorders.

http://www.nhlbi.nih.gov/about/ncsdr/patpub/patpub-a.htm – The National Institute ofHealth’s Public Education site for sleep and its disorders.

http://www.rls.org – The Restless Legs Syndrome Foundation Website.

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