Sleep, 20(11 ):972-981
© 1997 American Sleep Disorders Association and Sleep Research Society
Parasomnias
A Parasomnia Uverlap Disorder Involving Sleepwalking,
Sleep Terrors, and REM Sleep Behavior Disorder in 33
Polysomnographically Confirmed Cases
*Carlos H. Schenck, *Jeffrey L. Boyd and tMark W. Mahowald
Minnesota Regional Sleep Disorders Center;
Departments of *Psychiatry and tNeuro!ogy, Hennepin County Medical Center; and
University of Minnesota Medical School, Minneapolis, Minnesota, U.S.A.
Summary: A series of 33 patients with combined (injurious) sleepwalking. sleep terrors, and rapid eye movement
(REM) sleep behavior disorder (viz. "parasomnia overlap disorder") was gathered over an 8-year period. Patients
underwent clinical and polysomnographic evaluations. Mean age was 34 ± 14 (SD) years; mean age of parasomnia
onset was IS ± 16 years (range 1-66); 70% (n = 23) were males. An idiopathic subgroup (n = 22) had a
significantly earlier mean age of paras omnia onset (9 ± 7 years) than a symptomatic subgroup (n = II) (27 ± 23
years, p = 0.002), whose parasomnia began with either of the following: neurologic disorders, n = 6 [congenital
Mobius syndrome, narcolepsy, multiple sclerosis, brain tumor (and treatment), brain trauma, indeterminate disorder
(exaggerated startle response/atypical cataplexy)]; nocturnal paroxysmal atrial fibrillation, n = I; posttraumatic stress
disorder/major depression, n = I; chronic ethanol/amphetamine abuse and withdrawal, n = I; or mixed disorders
(schizophrenia, hrain trauma, substance abuse), n = 2. The rate of DSM-III-R (Diagnostic and Statistical Manual,
3rd edition, revised) Axis I psychiatric disorders was not elevated; group scores on various psychometric tests were
not elevated. Forty-five percent (n = IS) had previously received psychologic or psychiatric therapy for their
parasomnia, without benefit. Treatment outcome was available for n = 20 patients; 90% (n = 18) had subst&ntial
parasomnia control with bedtime clonazepam (n = 13), alprazolam and/or carbamazepine (n = 4), or self-hypnosis
(n = I). Thus, "parasomnia overlap disorder" is a treatable condition that emerges in various clinical settings and
can be understood within the context of current knowledge on parasomnias and motor control/dyscontrol during
sleep. Key Words: Parasomnias-Sleepwalking-Sleep terrors-REM sleep behavior disorder-Neurologic disorders-Psychiatric disorders-Nocturnal paroxysmal atrial fibrillation.
The tenn "parasornnia" refers to physical disturbances during sleep that involve the skeletal motor
and/or autonomic nervous systems (1). Knowledge on
the parasornnias, based on polysorrmographic (PSG) documentation (2-5), has expanded considerably over recent
years, as new disorders have been identified [e.g. rapid
eye movement (REM) sleep behavior disorder (RBD)
(6,7), REM sleep-related asystole (8), episodic nocturnal
wanderings (9,10), nocturnal dissociative disorders
(11,12), nocturnal paroxysmal dystonia (13)], and as previously known disorders have been recognized to occur
more frequently, across a broader age group, and with
more serious consequences than previously recognized
Accepted for publication August 1997.
Address correspondence and reprint requests to Carlos H.
Schenck, M.D., Hennepin County Medical Center, Department of
Psychiatry (844), 701 Park Avenue South, Minneapolis, MN 55415,
U.S.A.
[e.g. sleepwalking (SW), sleep terrors (ST) (11 ,14-17),
nocturnal eating disorders (18-20), etc. (21)].
Adults with parasomnias often report bizarre nocturnal experiences involving behavioral, perceptual,
emotional, and dreamlike disturbances that may erroneously suggest a psychiatric disorder. RBD, for example, with its violent behaviors and shouting,
screaming, and swearing, is especially prone to misdiagnosis (6,7,22). However, RBD is rarely a manifestation of a psychiatric disorder but rather is a physiologic disorder of REM sleep in which the customary,
active paralysis of REM sleep ("REM atonia") is
compromised and/or the REM sleep-related phasic
motor system is overactivated, resulting in behavioral
release and attempted dream enactment (22-25). In
more than half of reported cases in the world literature,
RBD is causally associated with a neurologic disorder,
972
973
PARASOMNIA OVERLAP DISORDER
usually a neurodegenerative disorder or narcolepsy
(25). An animal model of RBD exists, in which lesions
to the dorsolateral pons in the brain stem release elaborate and aggressive behaviors during (unequivocal)
REM sleep (26-28).
SW and ST (along with "confusional arousals") are
parasomnias involving disorders of arousal from nonREM (NREM) sleep (1,29-31). SW and ST frequently
co-occur in adults presenting to a sleep disorders center because of sleep-related injury (11). Various medical disorders, medications, and organic factors have
been linked with SW and ST (1,31). Psychopathology
in adults with SW or ST has been reported in two
studies that used the Minnesota multiphasic personality inventory (MMPI) (32,33). A more recent study,
however, of adult clinical referrals with ST revealed
generally intact MMPI profiles (34). A report on sleeprelated injury included MMPI data on 36 adults with
SW andlor ST; two-thirds were found to have nondeviant personality traits; most did not have a current
DSM-III (Diagnostic and Statistical Manual, 3rd edition) Axis 1 disorder (11). A report on six adults with
ST revealed a current or past DSM-III-R (Diagnostic
and Statistical Manual, 3rd edition, revised) Axis 1
disorder in each patient (35).
We now report a parasomnia overlap disorder involving SW, ST, and RBD.
METHODS
Clinical evaluation
Over an 8-year period (1988-1996), 33 cases of parasomnia overlap disorder were diagnosed, comprising
approximately 21 % of all RBD cases and 28% of all
SW1ST cases seen at our center during that time period. One author (C.H.S.) evaluated 25 of the 33 patients, and another author (M.W.M.) evaluated six. The
clinical evaluation included review of medical records,
neurologic exam, and patient interviews that were usually attended by bedpartners andlor family members.
. All patients, except one, completed a structured questionnaire that covered a current review of systems, and
sleep-wake, medical, psychiatric, psychosocial, and
family histories. The questionnaire contained 40 questions on lifetime use of prescription and over-the-counter medications and on use or abuse of alcohol and
psychoactive substances. Nine questions from the
Michigan alcoholism screening test (36) were included.
Patients were administered a validated, computerized diagnostic interview schedule (C-DIS) for DSMIII (or DSM-III-R) diagnoses (37); MMPI; Beck depression inventory (BDI); and symptom checklist-90
(SCL-90). [The C-DIS was not completed by n = 10
patients: a child, a schizophrenic patient, n = 3 with
brain disorders, n = 5 who were evaluated previously
by a semistructured interview for DSM-III diagnoses
(11)].
MMPI profiles were clinically interpreted by the
chief psychologist at our hospital, who was blind to
medical and sleep histories but who was aware of the
age, sex, and sleep center referral source. The MMPI
profiles were later interpreted blindly for this study by
the current chief psychologist (J.L.B.). Two clinical
groups had their MMPls selected for comparative analysis: the idiopathic parasornnia overlap disorder group
and an injurious NREM sleep parasomnia comparison
group (two NREM sleep parasomnia comparison patients per each idiopathic parasomnia overlap disorder
patient). The groups were matched for gender, age (±5
years), and predominant NREM sleep parasomnia subtype (SW, ST, or mixed SW/ST). The MMPls of the
two groups were randomly intermixed before they
were interpreted (by 1.L.B.), who was blind to sleep
disorder diagnoses, medical history, and purpose or
methods of the study. The comparison parasomnia
MMPls were selected, without identified bias, after
finding the most recent suitable comparison patients in
our files.
Polysomnographic evaluation
Hospital-based, overnight PSG studies used standard monitoring and scoring procedures (38), with allowance for loss of REM atonia. PSG studies included
continuous audio-visual monitoring that was viewed
by the sleep lab technologists during the PSG studies
and subsequently reviewed by a sleep medicine specialist. Figure lA-C depicts the montage for the electrooculogram, electroencephalogram (EEG; with fast
paper speeds of 15 mm1second, and 30 mm1second for
5 minutes every hour, to facilitate detection of epileptiform activity), submentalllimb electromyograms
(EMGs), and cardiorespiratory monitoring. An experienced clinical polysomnographer (usually MWM) interpreted each PSG study. Urine toxicology screening
was performed for patients with either a positive or
suspected history of alcohol or drug abuse. A multiple
sleep latency test (MSLT) (39) was completed for patients suspected to have excessive daytime sleepiness.
All patients satisfied recognized diagnostic criteria for
Sw, ST, and RBD (1,24).
RESULTS
Clinical data
Twenty-seven (82%) of the patients were physician
referred (16 by primary physicians, 8 by psychiatrists).
Four patients were referred while being committed to
Sleep, VoL 20, No, 11, 1997
C. H. SCHENCK ET AL.
974
A
21 y.o. female
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FIG. 1. Three forms of sleep-related motor dyscontrol are demonstrated during one night of polysomnographic monitoring in a youngadult woman with childhood-onset idiopathic parasomnia overlap disorder. During stage 3/4 non-rapid eye movement sleep (A), there is
well-established electroencephalographic (EEG) delta wave activity (channels 3,4, I 0-17) until a sudden, spontaneous, confusional arousal
occurs. A technician notes that the head is raised while the patient looks around (with a bewildered stare and confused manner) before
resuming sleep within 15 seconds. Later, from a well-established epoch of tonic rapid eye movement (REM) sleep (B), characterized by
absence of eye movements (1,2), low-voltage desynchronized EEG activity (3,4,10-17), and generalized muscle atonia (5-9), the patient
Sleep, Vol. 20, No. 11, 1997
975
PARASOMNIA OVERLAP DISORDER
C
21 y.o. female
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E1·A1 ..../'-~
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Continued.
a psychiatric hospital or residential facility. Among the
adults, 56.3% (18/32) were married or widowed,
31.2% (10/32) were single, and 12.5% (4/32) were divorced. Ninety-one percent (n = 29) were high-school
graduates, and 65.6% (n = 21) had college or more
advanced education. Eighty-one percent (n = 26) were
employed, students, or retired; 15.6% (n = 5) were
disabled [psychiatric (n = 3) or medical (n = 2) disorder]. Forty-five percent (n = 15) had previously received treatment for a presumed psychological (e.g.
stress) or psychiatric basis of their parasomnia but
without benefit in controlling the parasomnia.
Table 1 shows that two-thirds of the group had an
idiopathic disorder, with a significantly younger mean
age of onset (childhood) than that of the symptomatic
subgroup (early adulthood). Each subgroup had a comparable male preponderance. Age of onset spanned
most age groups. There were three significant clusters
in age of parasomnia onset: 1) childhood, n = 20 (11
male, n ~ 16 idiopathic), mean age 5.4 :t 2.0 years
(range 1-10); 2) adolescence, n = 6 (5 male, n = 5
idiopathic), mean age 15.7 :t 2.7 years (range 13-20);
3) adulthood, n = 6 (all male, n = 5 symptomatic),
mean age 44.3 :t 14.7 years (range 28-66). Comparisons of ages of onset by t test revealed significant
differences: childhood vs. adolescence, t = 10.15, degrees of freedom (df) = 24, p < 0.001; adolescence
vs. adulthood, t = 4.27, df = 10, p < 0.002.
Mean age of parasomnia onset was not significantly
different between males and females: 18.9 (:t18.7) vs.
7.3 (±3.4) years (t test, t = 1.72, df = 27, P = 0.096).
However, the males exhibited a much broader range in
the age of parasomnia onset (0.75-66 years) than the
females (5-14 years).
Symptomatic parasomnia overlap disorder
Four categories were identified, with neurologic disorders being most common, as shown in Table 1. Pertinent vignettes are now provided for all 11 patients.
Neurologic disorders (n = 6)
The patient with congenital Mobius syndrome (i.e.
agenesis or aplasia of some or most of the motor nuclei
of brain stem cranial nerves; musculoskeletal defects
are variably present) was mainly affected by predominantly left-sided sixth and seventh cranial nerve palsies and knee/ankle defects. The patient with narcolepsy had the tandem emergence in early childhood of
a parasomnia and the narcoleptic tetrad (1) (excessive
daytime sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations). A 34-year-old man had experienced the fulminant onset of multiple sclerosis (MS),
panic disorder, and a parasomnia 6 years previously.
suddenly jumps up in bed, and then jumps out of bed, as the EEG shifts into alpha rhythm and the patient awakens to report a dream.
During a subsequent epoch of phasic REM sleep (C), characterized by dense REMs (1,2), low-voltage de synchronized EEG activity (3,4,1017), and preservation of the customary background muscle atonia of REM sleep (REM atonia) (5), there is excessive leg twitching (8,9)
that often occurs in high-voltage bursts.
Sleep, Vol. 20, No. 11, 1997
976
C. H. SCHENCK ET AL.
TABLE 1.
Classification of parasomnia overlap disorder involving sleepwalking, sleep terrors, and RBD in 33 patients
Gender
Classification
Males
Females
Age
(mean years:!:: SD)
Age of parasomnia onset
(mean years :!:: SD)"
Total (n = 33)
Idiopathic (n = 22)
Symptomatic (n = II)'
Neurologic (n = 6)d
Cardiologic (n = I)e
Psychiatric (n = 2)1
Mixed (n = 2)"
23 (69.7%)
15 (fiS.2%)
8 (72.7%)
10 (30.3%)
7 (31.8%)
3 (27.3%)
33.8 :!:: 13.9 (range 5-72)
30.6 :!:: 12.7 (range 5-63)
40.3 :!:: 14.6 (range 23-72)
14.6 :!:: 16.3 (range 1-66)
8.8 :!:: 6.7" (range 1-28)
27.3 :!:: 23.5" (range 5-66)
RBD, rapid eye movement (REM) sleep behavior disorder.
" In n = 28, ages of onset of NREM sleep parasomnias (sleep terrors, sleepwalking) and RBD were indistinguishable by history. In n =
5, NREM sleep paras omnia began at a mean age of 4.6 :!:: 0.9 years. and RBD began at a mean age of 29.2 :!:: 15.3 years (range 16-55).
In these five patients, age of NREM parasomnia onset (i.e. age of initial parasomnia onset) was used in calculating the age of paras omnia
onset for the entire group of 33.
b Significantly different ages of parasomnia onset between the idiopathic and symptomatic groups (t test, t = 3.47, df = 31, P = 0.002).
, Onset linked with onset of neurologic, medical, or psychiatric disorder (n = 1, indeterminate age of onset).
d Congenital Mobius syndrome (n = 1), narcolepsy (n = 1), multiple sclerosis (n = I), brain tumor and tumor treatment (n = I), traumatic
brain injury (n = I). indeterminate neurologic disorder (n = 1).
e Nocturnal paroxysmal atrial fibrillation (n = I).
fPosttraumatic stress disorder and major depression (n = 1), chronic ethanol and amphetamine abuse and withdrawal (n = I).
g Traumatic brain injury, and chronic ethanol abuse and withdrawal (n = I); schizophrenia, antipsychotic and anticholinergic pharmacotherapy, chronic ethanol and cocaine abuse (n = I).
A 24-year-old man developed a fourth ventricle astrocytoma 9 years previously. After surgical resection!
irradiation, he suddenly developed both an explosive
daytime behavioral dyscontrol disorder, requiring
long-term psychiatric confinement, and a violent nocturnal parasomnia. A 50-year-old man fell off a train
in an occupational accident 1 year previously and sustained a major concussion with cerebral contusion, loss
of consciousness for > 10 minutes, and a L5 vertebral
compression fracture. A violent parasomnia developed
soon thereafter.
A 72-year-old man developed a violent parasomnia
subsequent to developing an indeterminate neurologic
disorder characterized by exaggerated startle responses, with episodic hand clenching and total body
shaking; atypical cataplexy [sudden, spontaneous
(without emotional trigger), bilateral loss of muscle
tone, but without altered consciousness]. A waking 16channel EEG (paper speed 30 mm/second) performed
at another hospital at the time of one of these episodes
revealed the following: posterior rhythm was organized, synchronous, and symmetric, with low voltage
and a rate of 9-10 Hz. There was a moderate amount
of background theta, delta, and beta activity seen bilaterally. Photic stimulation did not induce any spikes,
or sharp or slow waveforms, but did induce mild, bilateral frontotemporal slowing. No sleep was obtained
during the waking EEG. Finally, there was no history
of excessive daytime sleepiness.
Cardiologic disorder (n
= 1)
A 54-year-old man precipitously developed an injurious parasomnia 4 years previously in conjunction
Sleep, Vol. 20, No. 11, 1997
with the onset of exclusively nocturnal paroxysmal
atrial fibrillation (confirmed by 24-hour cardiac Holter
monitoring). The arrhythmia eventually was controlled
1 year before referral with antiarrhythmic medications,
but the parasomnia persisted unabated.
Psychiatric and mixed disorders (n = 4)
A 46-year-old man developed a violent parasomnia
3 years previously together with the emergence of
posttraumatic stress disorder (PTSD) and major depression that were related to the Vietnam war. A 40year-old man, with childhood-onset SW, developed
RBD 11 years before referral at the time of initiating
long-term abstinence from ethanol and amphetamine
abuse. A 32-year-old woman had a childhood-onset
parasomnia that subsequently became aggravated by a
traumatic brain injury resulting in coma of several
days' duration and by chronic ethanol abuse and repeated withdrawal states. A 32-year-old man developed schizophrenia and a parasomnia during adolescence (or earlier), with subsequent exacerbations of
both conditions associated with repeated ethanol and
cocaine abuse and withdrawal states.
Thus, 54.5% (6/11) of patients in the symptomatic
paras omnia overlap group had a precipitous onset of
their parasomnia, which was twice the rate of 27.3%
(6/22) found in the idiopathic group.
Parasomnia history
In combination with RBD, n = 16 had SW, n = 15
had SW and ST, n = 1 had ST, and n = 1 had indeterminate SW vs. ST. A parasomnia episode that in-
977
PARASOMNIA OVERLAP DISORDER
TABLE 2.
Polysomnographic (PSG) measures from 26 patients with parasomnia overlap disorder
Consecutive night PSG studiesa
Measures
TST (minutes)
% Sleep efficiency"
Sleep latency (minutes)
REM sleep latency (minutes)"
Number of awakenings
% Stage I sleep (of TST)
% Stage 2 sleep (of TST)
% Stage 3/4 sleep (of TST)
% REM sleep (of TST)
(n
First night
(n = 14)
Total PSG studies
40; n = 26 first night PSGs)
=
432.8
85.1
13.5
80.6
8.9
6.9
50.5
18.8
23.8
:!:
:!:
:!:
:!:
:!:
:!:
:!:
:!:
+
86.5 (7.2 hours)
10.7
14.7
28.4
6.0
4.0
8.6
7.3
6.2
443.1
88.2
14.4
86.4
9.2
6.3
52.2
18.5
23.0
:!:
:!:
:!:
:!:
:!:
:!:
:!:
:!:
103.6 (7.4 hours)
8.3
18.9
34.8
6.5
3.8
8.4
8.0
+ 6.6
Second night
(n = 14)
427.1 :!:
89.6:!:
11.5 :!:
80.7 :!:
8.2 :!:
5.1 :!:
50.3 :!:
20.2:!:
24.4 +
65.8 (7.1 hours)
8.5
12.2
29.0
6.4
2.4
9.5
7.3
5.6
TST, total sleep time; REM, rapid eye movement.
a Paired t test did not reveal any significant first night vs. second night differences in mean scores of sleep measures.
" Defined as time asleep (minutes)ltime in bed (minutes).
'Defined as latency to 5 continuous minutes of REM sleep, less any intervening wakefulness. Data on n = 35 PSG studies (n = 5
excluded because of outlying REM sleep latencies of 171-297 minutes).
All values. shown as mean:!: standard deviation. Of the total group of n = 33 patients, n = 7 were excluded from this table because of
promment dIsturbance of sleep architecture.
volved either a ST, or leaving the bed, or injuring oneself/bedpartner had occurred at least weekly in n = 19
and at least monthly in n = 14.
Forty-one percent (13/32, n = 1 unknown) had left
their homes during SW episodes, and 50% (16/32) had
either jumped or punched through windows during SW
or ST episodes. Repeated sleep-related injuries to self
and/or bedpartner had occurred in 90.9% (30/33) of
patients: n = 30 had sustained multiple ecchymoses,
n = 16 had sustained lacerations, and n = 3 had sustained fractures. Two patients required emergency surgical repair of an 80% tear of a triceps muscle, and of
lacerated hand tendons.
These patients usually did not experience sleep-deprivation symptoms from their parasomnia activity.
Marital relations were occasionally strained because of
spousal sleep disruption or injury from the patient's
parasomnia. However, in no instance did the spouse
believe that the patient was intentionally engaging in
this activity.
TABLE 3. Abnormal motorlbehavioral findings during
polysomnographic monitoring oj 33 patients with parasomnia overlap disorder
Abnormal findings
REM sleepa
Excessive, phasic EMG twitching
Augmentation of submental EMG tone
Gross behavioral emergence
Non-REM sleep (stages 3/4)"
Gross behavioral emergence
Frequency % (n)
87.9 (29)
51.5 (17)
42.4 (14)
75.8 (25)
REM, rapid eye movement; EMG, electromyographic.
REM sleep: shouting, swearing; throwing punches; kicking; supine running behaviors; jumping from bed.
b Non-REM sleep: screaming (sleep terror); throwing punches;
kicking; sitting or jumping up; walking or running in bed or out of
bed.
a
Medical history and caffeine consumption
Medical history in the idiopathic group (n = 22)
included closed head injury without sequelae (n = 7),
migraine or tension headaches (n = 4), and miscellaneous non severe disorders (n = 9).
The extent of coffee consumption was tabulated because caffeine abuse has been implicated in a case of
RBD (40). The mean number of cups of coffee consumed daily was 5.3 ± 7.2 (n = 31, one child and one
adult with unknown consumption were excluded). Two
major subgroups were identified: a high coffee consumption group (n = 6), with a mean 18.2 ± 7.2 cups/
day (range 10-30); and a moderate coffee consumption group (n = 25), with a mean 2.3 ± 1.9 cups/day
(range 0-7), which was virtually identical to the mean
daily coffee consumption of two large normative
groups of males and females in the U.S. (41,42). The
six patients in the group with high coffee consumption
(caffeine abuse?) declined to substantially reduce coffee intake.
Polysomnographic data
Table 2 contains the sleep architecture and related
PSG data, which are unremarkable apart from a slightly reduced sleep efficiency. The distribution of sleep
stages is not perturbed, and a "first-night effect" (43)
is not present in the 14 pairs of two-consecutive-night
PSG studies. Urine toxicology screening was conducted for 12 patients: one patient, with schizophrenia,
tested positive (cocaine). Table 3 describes the motor
and behavioral abnormalities documented during the
PSG studies.
An important contrast in paras omnia-related autonomic nervous system functioning was routinely notSleep. Vol. 20. No. II. 1997
978
C. H. SCHENCK ET AL.
ed: tachycardia rarely accompanied REM sleep behavioral release (including shouting) in RBD [a typical
finding in RBD (44) that reflects the sympathetic paresis of REM sleep (45)]; in contrast, there was impressive autonomic activation (tachycardia, tachypnea,
diaphoresis) during each ST episode [a hallmark feature of ST (1)].
The EEG during ST and SW episodes ranged from
no evidence of wakefulness (e.g. persistence of delta
waves); to mixed sleep-wakefulness (e.g. admixture of
delta and either alpha wave or low-voltage, desynchronized activity); to frank EEG wakefulness, but
usually without conscious awareness. EEG epileptiform activity was not detected during any PSG study.
Periodic limb movements (PLM) of NREM sleep
(1) and obstructive sleep apnea (1) were present in six
and three patients, respectively. An MSLT was performed on 51.5% (n = 17) of patients. Objective hypersomnolence (viz. mean sleep latency :5.7 minutes)
was detected in n = 4: n = 1 had narcolepsy, and n
= 3 had idiopathic hypersomnia (1).
Treatment outcome
Treatment outcome, ranging from 6 months to 9
years (mean 2.2 ± 2.5 years), was available for 20
patients (the others were not followed at our center);
n = 18 (90%) reported full/substantial control of injurious nocturnal behaviors with either bedtime clonazepam (0.25-4.0 mg), n = 13; alprazolam (1-3 mg)
and/or carbamazepine (0.5-1.5 gm), n = 4; or selfhypnosis (46), n = 1. The initial recommended treatment for the 5-year-old child consisted of hypnosis
with guided imagery rehearsal.
Psychometric and psychiatric data
The mean BDI score was not elevated (4.4 ± 5.1),
nor was the mean SCL-90 global severity index score
elevated (0.38 ± 0.33, with comparable scores in all
nine subscales). These tests were completed by 26 patients.
Sixteen of 22 patients with idiopathic parasomnia
overlap disorder completed valid MMPls. Mean ages
of male patients (n = 9) and male comparison patients
(n = 18) were 30.4 ± 7.3 and 30.6 ± 5.7 years, respectively. Mean ages of female patients (n = 7) and
female comparison patients (n = 14) were 25.9 ± 4.4
and 26.5 ± 5.6 years, respectively.
Group MMPI profiles for male and female patients,
and for male and female comparison NREM parasomnia patients, were highly comparable and within normal limits (viz. T scores <70). The interpretations of
the individual MMPI profiles by the two chief psySleep, Vol. 20, No. 11, 1997
chologists were always congruent: 37.5% (6/16) of
parasomnia overlap patients had mildly/moderately abnormal profiles (anxiety, depression), whereas 71.9%
(23/32) of NREM parasomnia comparison patients had
mildly/moderately abnormal profiles (broad spectrum).
A current or past psychiatric disorder (excluding
simple phobia or nicotine or caffeine dependence) was
present in 33% (n = 11) of patients and included
nonpsychotic mood disorders, anxiety disorders, ethanol/cocaine abuse disorders, and schizophrenia (n =
1). All patients with current psychiatric disorders were
under the care of a psychiatrist; the schizophrenic patient with cocaine abuse was referred for substance
abuse treatment.
DISCUSSION
Clinical profile
A parasomnia overlap disorder has been documented in 33 patients presenting from a broad medical and
psychiatric referral base. The male preponderance, and
the response to benzodiazepine therapy, are typical
both of RBD and of injurious ST and SW (11,25,47).
Although nearly half the patients had received psychological or psychiatric therapy for their parasomnia
without benefit, the rate of benefit of such therapy in
the total parasomnia population is unknown, because
responders would not have presented to a sleep disorders center. A spectrum of parasomnia severity presumably exists throughout the general population.
Literature on parasomnia overlap disorder
At least two other cases of parasomnia overlap disorder have been reported in peer-reviewed journal articles, involving a 49-year-old man with a complex
psychiatric history (48) and a 51-year-old man with
Machado-Joseph disease, an autosomal-dominant,
multisystem neurodegeneration mapped to chromosome 14 (49). Also, a published abstract mentioned
five cases that were unassociated with neurologic disorders and that responded to low-dose bedtime clonazepam therapy (50).
Underlying mechanisms of parasomnia overlap
disorder: REM sleep and RBD
The brain stem (pons and medulla) contains specific
neuronal generators of both REM atonia and phasic
motor activation during REM sleep; descending pathways from these generators impinge on spinal alpha
motoneurons that then control the level of tonic and
phasic skeletal muscle activity (28,51-53). Therefore,
the patients in this report with brain stem disorders,
PARASOMNIA OVERlAP DISORDER
viz. congenital Mobius syndrome, MS, and brain stem
tumor (and its treatment), and also patients with traumatic brain injury, may have developed RBD from
either direct or indirect brain stem involvement. Narcolepsy is a disorder involving REM sleep dysregulation, the onset of which can be linked with RBD
(54,55). Most reported cases of childhood RBD have
occurred with narcolepsy (54); however, the one childhood case in our series did not involve narcolepsy, to
date.
In regards to the elderly man with an exaggerated
startle response and atypical cataplexy, a functionalanatomic link has been identified in animals between
the startle response and REM atonia mechanisms (56);
moreover, disinhibition of the acoustic startle reflex
has been identified in the experimental animal model
of RBD (57).
PTSD and major depression have been linked with
REM sleep dysregulation, although reliable, conclusive findings remain elusive (58,59). Ethanol and amphetamine are REM sleep suppressants, and abstinence
after long-term abuse can lead to a pathologic "REMrebound" state manifesting as RBD (24,60). Psychotropic medications, and caffeine abuse, have been implicated in both RBD (24,25,40,54,60,61) and ST/SW
(20,31,62-65).
In a report on sleep and nocturnal cardiac arrhythmias, in which five different arrhythmias were studied,
only paroxysmal atrial fibrillation (and paroxysmal supraventricular tachycardia) had a significantly close association with REM sleep (66). Thus, for the patient
in our series with nocturnal paroxysmal atrial fibrillation, a primary disturbance of REM sleep may have
manifested both as RBD and as nocturnal cardiac arrhythmia.
Developmental factors must also be considered. In
human sleep-wake ontogeny, REM atonia usually
does not become fully established until the second year
of life, as reviewed by Schenck et al. (6). Some individuals, therefore, may only partially establish REM
atonia, thus rendering them vulnerable to eventually
developing RBD.
Underlying mechanisms of parasomnia overlap
disorder: NREM sleep, SW, and ST
Motor dyscontrol during NREM sleep in RBD is
common, as nearly two-thirds of patients have periodic
limb movements, and one-third have nonperiodic
movements (44). Thus, the linking ofNREM paras omnias with RBD in parasomnia overlap disorder may be
another manifestation of generalized NREMIREM
sleep motor dyscontrol (67). A hypothesis has been
formulated proposing that ST may result from anomalous REM sleep intrusion into NREM sleep (68). De-
979
velopmental factors must also be considered, because
disorders of arousal usually emerge in childhood
(1,30,31) but may persist beyond puberty and throughout adulthood (11,14,17).
Besides an animal model for RBD (26), there is another experimental animal model, produced by kainic
acid microinjections into the midbrain reticular core
(69), that may be closely related to the parasornnia
overlap disorder. Within 1 hour of injection, cats in
this model display a repertoire of "hallucinatory-type"
behaviors during wakefulness, with complete unresponsiveness to environmental stimuli, which is identical to the behavioral repertoire displayed during
REM sleep in the cat model of RBD induced by bilateral dorso-Iateral pontine (perilocus ceruleus) lesions (26-28): "Both syndromes share the feature of
occurring in the absence of any outside stimulation. It
is likely that the same mechanism underlies the appearance of these syndromes in spite of the difference
between the polar states of vigilance during which they
occur" (69).
During human SW and ST episodes, as in the midbrain kainic acid animal model, there is usually complete or partial unresponsiveness to environmental
stimuli, the EEG can show full or partial wakefulness
(1), and hallucinations can occur (70). In other words,
a state of increased arousal with motor activation is
associated with attending to endogenous, but not environmental, stimuli.
Two recent lines of evidence (clinical and experimental) implicate the midbrain in abnormal, sleep-related motor phenomena. First, RBD and parkinsonism
(including Parkinson's disease, multiple system atropy,
Lewy body disease, etc.) now appear to be strongly
linked (71-78). Degeneration of the substantia nigra
(SN), a midbrain structure, is a hallmark finding in
Parkinson's disease. Furthermore, two autopsy studies
of RBD patients [one with Lewy body disease (74),
the other with the Lewy body variant of Alzheimer's
disease (79,80)] found severe SN depigmentation in
the first case and decreased SN cell counts in the other
case.
Second, a recent experiment with decerebrated cats
has revealed that dysfunction of the retrorubral nucleus
and the ventral mesopontine junction, induced by either hemorrhagic or N-methyl-D-aspartate lesions, released motor activity (myoclonic twitches, rhythmic
leg movements, spontaneous locomotion) in both sleep
and wakefulness (81). Thus, "degeneration or hypoactivity of this [midbrain] region may contribute to some
movement disorders in waking and sleep" (81). As the
authors noted (81), the retrorubral nucleus and ventral
mesopontine junction contain dopaminergic and glutamatergic neurons; the latter neurons project to the
pontine reticular formation [linked to brain stem 10Sleep, Vol. 20, No. II, 1997
C. H. SCHENCK ET AL.
980
comotor centers (82)], and the former neurons project
to the caudate-putamen (extrapyramidal motor system). These findings may help explain the neurochemical and neuroanatomic mechanisms for the phenomena observed with the midbrain kainic acid cat model
described above.
CONCLUSION
Parasomnia overlap disorder exists within the spectrum of sleep motor dyscontrol disorders and dissociated states of being (67,83). The identification of this
combined NREM-REM sleep disorder suggests that
the basic abnormality of the motor parasomnias may
consist of motor dyscontrol during sleep per se, with
the affected sleep stage( s), and the type of parasomnia,
being influenced by developmental factors (encompassing the entire life cycle) and by various other biological and clinical factors. The natural history, as
yet, is not known. However, patients will need serial
neurologic examinations to detect any delayed emergence of a parkinsonian disorder (76) or other neurologic disorders that are known to be associated with
RBD (25).
Acknowledgements: This work was supported in part
by a grant from Hennepin Faculty Associates (to C.H.S.).
We acknowledge the assistance of Thomas D. Hurwitz,
M.D., Scott R. Bundlie, M.D., Gerald Rosen, M.D., and Paul
Pentel, M.D. We express our appreciation to the sleep laboratory technologists for their expertise and devoted service
to our patients. Zigfried Stelmachers, Ph.D., initially interpreted the MMPls described in this study. Allan Callies performed the statistical analyses.
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