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Periodic movements in sleep (nocturnal myoclonus) Relation to sleep disorders.

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Periodic Movements in Sleep
(Nocturnal Myoclons): Relation
to Sleep Disorders
Richard M. Coleman, PhD,” Charles P. Pollak, MD, and Elliot D. Weitzman, M D
Periodic movements in sleep (PMS) are stereotvped, repetitive, nonepilqmbrm m o v e m e e h e lower ext r e e s . A total of 409 sleep disorder patients were studied with all-night polysomnogram recording,, and 53
(13%) had PMS. Such movements occurred in a wide variety of sleep-wake disorders in addition to insomnia. The
prevalence and magnitude of PMS were not statistically greater in patients with insomniac disorders than in those
with syndromes of excessive daytime sleepiness or other sleep-wake disorders. The results suggest that although
isassociated with
PMS is responsible for disturbed sleep in relatively few patients, chrongsleep-wakdturbance
PMSaniimay lead to the development of these movements.
Coleman RM, Pollak CP, Weitzman ED: Periodic movements in sleep (nocturnal myoclonus):
relation to sleep disorders. Ann Neurol 8:416-421, 1980
Periodic movements in sleep (PMS) are stereotyped,
repetitive, nonepileptiform movements of one or
both lower extremities occurring primarily in nonREM (NREM) sleep. Patients with the restless legs
syndrome may also experience PMS while they are in
a state of relaxed wakefulness just prior to falling
asleep at night. Typically, the movements consist of
dorsiflexion of the foot, extension of the big toe, and
often flexion of the lower leg at the knee and hip.
The duration of the movement complex is usually
between 1.5 and 2.5 seconds; the time course, pattern, and stereotypy of these movements are not
truly myoclonic. The movements recur approximately every 30 seconds, sometimes over a period of
hours, and their remarkable periodicity (Fig 1)clearly
distinguishes them from other types of movements
during sleep. Unlike most movement disorders (e.g.,
parkinsonism or chorea), PMS is initiated rather than
inhibited by sleep. These movements are important
in the diagnosis and treatment of sleep-wake disorders since they have been reported to be a cause of
sleep disturbance in 10 to 2096 of patients with a
primary complaint of insomnia [5].
Although Willis [22] described restless leg movements (voluntary movements to relieve uncomfortable paresthesias,in the calf muscles) in relation to
insomnia almost 300 years ago, Symonds [17]
published the first paper suggesting the presence
of periodic movements occurring during sleep.
Symonds, however, lacked polygraphic and video
monitoring and did not make direct observations of
sleep and movements in the 5 patients he reported; it
is therefore uncertain what type of movements they
actually had. Review of his clinical descriptions suggests that his 5 cases may have included examples of
restless legs syndrome, sleep starts, and myoclonic
epilepsy, as well as PMS. Symonds introduced the
term nocturnal myoclonus for this wide assortment of
movements associated with the complaint of insomnia and considered the disorder to be an “epileptic
Periodic movements in sleep are to be differentiated from “sleep starts” (hypnic jerks), which are
nonperiodic myoclonic movements, generally of the
trunk and all extremities simultaneously, occurring at
sleep onset and frequently associated with the perception of falling. These body jerks are also not accompanied by epileptic activity on the electroencephalogram (EEG) [151. Such sudden movements
occurring at the transition between waking and sleep
can be considered normal since most normal adults
indicate that they have experienced them, usually on
multiple occasions. Lugaresi et a1 [13, 143, the first to
record PMS polygraphically in patients complaining
From the Sleep-Wake Disorders Center, Department of Neurulogy, Montefiore Hospital and Medical Center and the Albert
Einstein College of Medicine, Bronx, NY.
Received Oct 5, 1979, and in revised form Feb 19, 1980. Accepted for publication Feb 23, 1980.
*Current address: Stanford Sleep Research Center, Department of
Psychiatry, Stanford University Medical Center, Stanford, CA
Address reprint requests to Elliot D. Weitzman, MD, Department of Neurology, Montefiore Hospital and Medical Center,
1 1 1 E 210th St, Bronx, N Y 10467.
416 0364-5134/80/100416-06$01.25 @ 1979 by Elliot D. Weitzman
Fig 1. Polysomnogram of PMS from the right and ltft legs
during 2 minutes of stage 3 sleep in a 47-year-old man with
chronic insomnia. The surface E M G is obtained from skin
electrodes overlying the anterior tibialis mu.&. ROCILOC
represents an eye movement channel from electrodes placed at the
outer ranthi of both eyes.
of restless legs s y n d r o m e and chronic insomnia, suggested that such m o v e m e n t s m i g h t be a specific cause
of insomnia. The p r e s e n t study evaluated t h e frequency of occurrence as well as the quantitative
characteristics of PMS i n 409 consecutive patients in
a large sleep disorders c e n t e r .
Observations were made during a 22-month period at the
Sleep-Wake Disorders Center at Montefiore Hospital on
441 unselected, successive patients with a variety of
sleep-wake complaints. Of these, 409 completed a full
clinical evaluation consisting of a detailed clinical history,
physical and neurological examinations, psychological tests
and interviews, and polygraphic monitoring (polysomnogram) of standard clinical sleep disorder functions 12 I]. To
record PMS, each patient was monitored for EEG, electrooculography (EOG), chin electromyography (EMG),
electrocardiography (EKG), and bipolar surface EMG of
the left and right anterior tibialis muscles: respiration was
also recorded. In most patients video recordings of the actual movements during sleep were obtained by means of a
time-lapse technique. One to three nights of these
polysomnographic recordings were obtained for each patient, and the recordings were scored for stages of sleep in
20-second epochs according to the Rechtschaffen and
Kales manual [16]. A diagnosis of primary sleep-wake disorder was made by the clinic physician independently of
the PMS experimental protocol. Patierits were then
classified as having a disorder of insomnia, a disorder of
excessive daytime sleepiness, o r one of a variety of specific
other disorders. Within each of these three groups, a more
detailed diagnosis was then made.
Since a clear description of PMS had not been previously
agreed upon, on the basis of our experience we defined a
PMS as anterior tibialis muscle EMG activity lasting 0.5 to
4 seconds in association with at least five consecutive
movements having an interevent interval between 20 and
40 seconds. Each such event was called a movement event
(ME). Synchronous discharges (<4 seconds) from both leg
muscles were also counted as an ME. Individual MEs separated by greater than 60 seconds were excluded. For the
purpose of this analysis, patients with 40 or more MEs
during a night's sleep were diagnosed as having PMS.
Four movement indices were devised in order to rate the
severity of PMS: (1) the total number of MEs shown by a
patient for the total recording time during one night's
polysomnogram; (2) the number of MEs per hour of total
recording time (i.e., from lights-off to lights-on); (3) the
number of MEs per hour of total sleep time; and ( 4 ) the
number of MEs per hour of NREM sleep. The fourth
criterion is the best index of severity since PMS is almost
entirely confined to NREM sleep.
In addition, the recordings of 10 patients with PMS were
studied in detail to enable evaluation of the periodicity of
movements. A total of 14 polysomnograms were quantified
such that all time intervals between consecutive MEs were
measured (in seconds). These extensive data were then
analyzed with several computer programs specifically developed to describe and display the periodic pattern of the
Sleep stage data (21 variables) were compared between
all patients with PMS and the same number of patients
without PMS ("controls") matched for age, sex, and final
diagnosis. Correlations were also made between the
movement indices and the sleep variables. In addition, the
PMS patients and the matched controls were evaluated o n
15 scales of the Minnesota Multiphasic Personality Inventory (MMPI) (7 PMS patients did not complete t h e
MMPI due to such reasons as lack of fluency in English o r
dementia associated with aging).
A careful analysis of case histories for all PMS patients
was catalogued along 35 measures. Five of these
measures-age, sex, duration and type of chief complaint,
and final diagnosis-were compared statistically berween
the PMS patients and the entire non-PMS clinic population.
Coleman et al: Periodic Movements in Sleep
Of the 409 patients studied, 53 exhibited PMS; the
distribution of their diagnoses and primary complaints did not differ from that of the entire sleep
disorders study population. A time-sequence computer program that we developed provided a description of the temporal progression of intermovement event intervals throughout the night (Fig 2).
Analysis of 14 polysomnograms (in 10 patients) revealed that movements typically occur in epochs
lasting 10 or more minutes (mean, 45 minutes).
Within each epoch the intervals between consecutive
movements were calculated, combining the data from
the left and right legs. A grand mean of 26 seconds
was found for the 6,502 intervals on the 14 subjectnights. The intermovement interval was generally
stable within separate epochs, although the mean
interval differed slightly between epochs. Furthermore, the interval remained fairly stable during two
consecutive nights in the 4 patients studied. Even
when the right and left legs did not move synchronously, the mean intermovement time interval was almost identical in the two legs during the same epoch.
One patient had a unique pattern of alternating left
and right leg movements (Fig 3).
Two types of movement patterns could be identified from the computer histogram analysis: one
(type A) showed little variation about a mean interval
(Fig 2A), whereas the other (type B, Fig 2B) showed
considerable variation around the mean intervals for
both the entire night and individual epochs. A
significant negative correlation between the movement indices and sleep efficiency (total sleep time/
total recording time) was found only for type B, suggesting that the more invariant the periodic movements, the less disturbed the patient's sleep.
Tables 1 and 2 show the final diagnostic categories
of the 53 patients with PMS and the 409 consecutive
patients. The final sleep disorder diagnoses were distributed equally among patients with insomnia and
those with excessive daytime sleepiness. This distribution held true for severe cases (patients averaging
greater than 50 MEs per hour of NREM sleep) as
well as for mild ones. Therefore, regardless of sever-
Annals of Neurology
Vol 8 No 4 October 1980
30 35
Inter - Movement Interval (seconds)
F i g 2. Histograms of the intermovement event interval (IMEI).
Abscissa represents the IMEI from 1 to 60 seconds: ordinate,
the frequency of occurrence of each IMEI. Each histogram is for
an entire night's recording. (A)Type A IMEI i n a 47-year-old
man with drug dependency and insomnia. (B) Type B IMEl
in a 72-year-old man with narcolepsy-cataplexy. This subject
demonstrated considerable variation about the mean interval
for each epoch and for the entire night.
F i g 3. PMS alternating between the left and right legs during
stage 3 sleep i n a 52-year-old patient with narcolepsycaataplexy. The IMEI ranges from 21 t o 26 seconds for the
right leg, from 23 to 24 seconds for the left leg, and from 10 to
14 seconds for all movementJ together.
CAC 4 0 0 uv
PAPER SPEED = 15 rnm/sec
Inter - Movement lntervol (seconds)
Table 1 . Final Diagnosis of Patients
with Periodic Movements in Sleep
Type of Sleep Disorder
I nsomnias
Restless legs syndrome
Drug dependence
Anxiety neurosis
Excessive daytime sleepiness
Narcolepsy -cataplexy
Obstructive apnea
Central apnea
Mild apnea
Questionable narcolepsycataplexy
Other disorders
Miscellaneous disorders
Circadian phase shift
Nocturnal seizures
Depression-restless legs syndrome
Nocturnal hallucinosis
Chronic sleep deprivation
Asymptomatic nocturnal myoclonus
Sleep apnea
Other hypersomnias
Other disorders
x2 = 4.70 (NS)
No. with
No. of
ity, PMS occurred with equal frequency in insomniac
and hypersomniac conditions. Table 1 also demonstrates that in addition to insomnia and sleep apnea
[12], PMS was associated with several conditions not
previously recognized: it occurred in patients with
narcolepsy-cataplexy syndrome (including patients
not using imipramine), delayed sleep phase syndrome, nocturnal epilepsy, nocturnal hallucinosis,
depression, and asymptomatic PMS (1 patient, who
came to the clinic because of his wife’s complaint of
being “kicked” during the night). The major subjective complaints of the PMS patients were nocturnal
(45%) or early morning (11%) awakening, sleeponset difficulty (43%), and daytime sleepiness
(42%). Since no significant differences were found
when the four myoclonic indices were compared in
five diagnostic and three chief complaint groups, the
severity of PMS was not related to the complaint or
the diagnosis.
It is unlikely that PMS occurs as a side effect of any
class of medication, since a variety of different drugs
were used by the patients. The case history analysis
revealed that 40 of the 53 PMS patients were taking
at least one medication on a regular basis at the time
of evaluation: 24 were using hypnotics, 8 were using
stimulants, and several were using tricyclic antidepressants, major tranquilizers, diuretics, or chronic
Twenty of 44 PMS patients had hypertension
(arterial blood pressure > 140/90 on at least two
recordings). This high percentage is probably due to
the 9 PMS patients with sleep apnea, a syndrome
commonly associated with hypertension r201. Neurological examination was essentially normal, although unsustained ankle clonus, absent reflexes, hyperreflexia, and tremor were minor, isolated findings
distributed among 10 PMS patients. Four out of 20
examined had an elevated blood urea nitrogen concentration (>20 mg/dl). Uremia has been reported to
be associated with restless legs syndrome and PMS
No. of
Other disorders
x2 = 3.15 (NS)
No. of
“Sample population = 409 patients with sleep-wake disorders.
bOverall mean frequency = 13%.
Coleman et al: Periodic Movements in Sleep 419
I21. However, none of these patients were diagnosed
as having renal insufficiency.
A standard clinical EEG was normal in 10 of 13
PMS patients recorded; it showed an epileptic abnormality in 2 patients and mild, diffuse slowing in 1.
Twenty-one of the 53 PMS patients had a sleeprelated EEG abnormality such as alpha-delta sleep,
REM spindles, excessive beta activity, or seizure activity [20]. Except for the seizure activity, these abnormalities reflect chronically disturbed sleep.
Data on familial history of PMS or restless legs
syndrome were difficult to obtain, and only 2 patients
were certain that relatives also had PMS.
Nine patients who could delineate the start of their
PMS (confirmed by a spouse’s report) had a 0.93 correlation ( p < 0.01) between the duration in years of
the chief complaint and PMS, suggesting that PMS
may be a primary cause of sleep disturbances in those
patients who are very aware of their nocturnal leg
movements. Other major complaints were nocturnal
awakenings (in 45% of PMS patients), sleep-onset
difficulty (43961, early morning awakening (1l%),
and daytime sleepiness (42%).There were no differences in the distribution for gender or duration of
chief complaint. The mean age of PMS patients (47
years) was significantly ( p < 0.01) greater than that of
non-PMS patients ( 4 1 years). An analysis of variance
of 2 1 sleep measures demonstrated only one
significant difference between the 53 PMS patients
and the 53 non-PMS controls. This was “sleep efficiency,’’ i.e., total sleep time divided by the total recording time. The average for PMS patients was
69%, while that for the matched controls was 74% (p
< 0.05). There were no significant interactions between a specific sleep-wake diagnosis and the presence of PMS on any sleep variable. Stage 3 and 4
sleep, total minutes and percentage, and number of
awakenings of at least 10 seconds’ duration per night
(30 versus 27) were also almost identical. PMS patients showed a trend toward an increased sleep latency (time elapsed from iights-off until the first 10
minutes of consolidated sleep; 39 minutes versus 2 5 )
and increased REM latency (time elapsed from sleep
onset to onset of the first REM period; 142 minutes
versus 113), but these differences did not achieve
significance. A significant positive correlation ( Y =
0.26) was found for duration of the chief complaint
and movement indices. Significant negative correlations were found for total recording time ( Y =
-0.36), total sleep time ( r = -0.31), and minutes of
REM sleep (r = -0.25) in relation to the movement
indices (p < 0.05, one-tailed t test), suggesting that
patients with many movements (i.e., severe cases)
have decreased total sleep times and REM sleep and
tend to have chronic sleep complaints.
The MMPI results for 46 PMS and 46 matched
420 Annals of Neurology Vol 8 N o 4 October 1980
non-PMS patients were remarkably similar. The PMS
patients’ scores were significantly ( p < 0.05)elevated
only on the Hypochondriasis and Hysteria scales.
The non-PMS patients’ scores were significantly (p <
0.01) elevated on the Social Introversion scale. Both
groups were above 70 on the Depression scale, the
only score in the psychopathological range. There
was no interaction between the presence of PMS and
the sleep-wake disorder diagnosis for any scale, nor
was there correlation with the movement indices. Insomniacs with PMS have the same degree of
psychopathology as other diagnostic groups and
hence d o not appear to constitute a unique constellation of patients.
The results obtained in this study indicate that nocturnal myoclonus, or PMS, occurs in a wide variety of
sleep-wake disorders. This finding differs from that
of previous studies, which report that nocturnal
myoclonus occurs chiefly in patients with insomnia
and restless legs syndrome. We have previously
monitored nocturnal EMG activity in 8 healthy subjects and 4 patients with a neurological disorder, all
without sleep-wake complaints, and have found no
evidence of PMS [ 181.
These results may be interpreted as indicating that
all patients with PMS have some degree of disrupted
nocturnal sleep (insomnia), although their chief complaint may be excessive daytime sleepiness and their
final diagnosis narcolepsy-cataplexy or sleep apnea
syndrome. Disrupted nocturnal sleep is a frequent
secondary complaint or finding in many such patients. However, since a majority of our PMS patients had a chief complaint other than insomnia, it
would appear that a chronic disturbance of daily
sleep-wake functioning (i.e., circadian slcep-wake
rhythms) may contribute to the occurrence of PMS.
A common theme in all 53 patients was that their
sleep-wake rhythm was chronically disturbed. Additional support for this interpretation is that the PMS
patient group was found to be significantly older than
the patients without PMS. In the elderly, the organization of sleep and waking periods within the 24hour biological day often changes from a monophasic
pattern to a polyphasic one characterized by frequent
napping that is associated with disruption of nighttime sleeping. The predominant findings from sleep
studies in the elderly include a major decrease in
stage 4 sleep, increased awakenings, and lower sleep
“efficiency” [9, 191. This is similar to the pattern of
disturbed sleep in our patients with PMS.
Review of the published literature reveals no clear
evidence that PMS causes insomnia, although the two
are related. TJntil suppression of PMS by a specific
treatment can clearly be shown to ameliorate the as-
sociated insomnia, the conclusion cannot be drawn
that the sleep-related movements actually cause the
sleep complaints. Although many drugs, including
baclofen, methysergide, 5-hydroxytryptophan, clonazepam, and various hypnotics and muscle relaxants, have been utilized in clinical and experimental
trials, none has proved effective in eliminating PMS
[4, 61. Movements similar to PMS have reportedly
been induced in parkinsonian patients receiving high
doses of L-dopa and in narcoleptic patients receiving
high doses of chlorimipramine for the treatment of
cataplexy [8, 111. Both studies suggested that these
drugs precipitated the sleep movements by their effects on central serotonin metabolism.
The neurophysiological mechanism responsible for
PMS is unknown. However, the remarkable periodicity found in all studies including the present
one suggests that there is an underlying central nervous system pacemaker. Several studies carried out
in humans during normal sleep as well as during coma
have reported 20- to 40-second periodicities in blood
pressure (“Mayer Waves”), respiration, intraventricular fluid pressure, pulse frequency, and EEG
arousal [ 3 , 7, 101. Barnes and Birnbaum [l] found a
30-second periodicity in the lumbar monosynaptic
reflex amplitude in decerebrate cats. These results
suggest that chronic disturbance of the temporal organization of the daily sleep-wake schedule and
specific sleep stages might induce o r “disinhibit” an
underlying periodic process in the central nervous
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Coleman et al: Periodic Movements in Sleep 421
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