Sleep, 17(8):723-732
© 1994 American Sleep Disorders Association and Sleep Research Society
Motor Dysfunction and Sleep
Motor Dysfunction During Sleep in
Posttraumatic Stress Disorder
*tRichard J. Ross, tWilliam A. Ball, tDavid F. Dinges, tNancy B. Kribbs,
HAdrian R. Morrison, §Steven M. Silver and *Francis D. Mulvaney
*Research Service, Philadelphia Veterans Affairs Medical Center, Philadelphia, Pennsylvania, U.S.A.;
tDepartment of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U.S.A.;
:f:Department of Animal Biology, University of Pennsylvania School of Veterinary Medicine,
Philadelphia, Pennsylvania, U.S.A.; and
§Coatesville Veterans Affairs Medical Center, Coatesville, Pennsylvania, U.S.A.
Summary: A subjective disturbance of sleep, including the occurrence of repetitive, stereotypical anxiety dreams,
is characteristic of posttraumatic stress disorder (PTSD). The phenomenology of the PTSD anxiety dream has
seemed most consistent with an underlying rapid eye movement (REM) sleep dysfunction. However, motor behavior
reportedly can accompany PTSD dreams, and normal REM sleep typically involves a nearly total paralysis of the
body musculature. As a means of understanding this discrepancy, anterior tibialis muscle activity during sleep was
studied in a group of Vietnam combat veterans with current PTSD and in an age-matched normal control group.
The PTSD subjects had a higher percentage of REM sleep epochs with at least one prolonged twitch burst; they
also were more likely to have periodic limb movements in sleep, during nonrapid eye movement sleep. Both these
forms of muscle activation also have been observed in REM behavior disorder (RBD), a parasomnia characterized
by the actual enactment of dream sequences during REM sleep. The identification ofRBD-like signs in PTSD adds
to the evidence for a fundamental disturbance of REM sleep phasic mechanisms in PTSD. Key Words:Posttraumatic
stress disorder-REM behavior disorder-Muscle twitch bursts-Periodic limb movements-Nightmares.
Posttraumatic stress disorder (PTSD) is a mental
disorder that occurs commonly in people who have
experienced a psychologically traumatic event (1). It
is characterized by the intrusive reexperiencing of the
event. In what generally is thought to be a large number
of patients, the reexperiencing takes the form of repetitive, stereotypical anxiety dreams (2). Largely because the content of the PTSD anxiety dream resembles traditionally described rapid eye movement (REM)
sleep, rather than nonrapid eye movement (NREM)
sleep mentation, we have argued that PTSD may involve a fundamental REM sleep disturbance (3). Some,
but not all, polysomnographic investigations have provided evidence for REM sleep abnormalities in PTSD
(3). We have reported on a group of Vietnam combat
veterans with current PTSD who had elevated tonic
and phasic REM sleep measures compared to an age-
Accepted for publication July 1994.
Address correspondence and reprint requests to Richard J. Ross,
M.D., Ph.D., Psychiatry Service (116A), Philadelphia Veterans Affairs Medical Center, University and Woodland Avenues, Philadelphia, PA 19104, U.S.A.
and sex-matched normal control group (4). The persistence during a subsequent recording night of elevated REM sleep phasic activity, in the form of rapid
eye movements (REMs), suggested the particular importance of disturbed REM sleep phasic mechanisms
in the pathophysiology of PTSD (4).
Normal REM sleep is characterized by a near atonia
of the body musculature. However, the REM sleep of
patients with REM sleep behavior disorder (RBD)
manifests a profound increase in phasic limb twitch
activity. Vivid, dysphoric dreams can be an associated
symptom of RBD (5,6). We wondered whether Vietnam combat veterans with PTSD, studied polysomnographically, would show unusual phasic limb muscle
activation during REM sleep, perhaps even RBD. Because RBD patients may also show motor dysregulation during NREM sleep, in the form of periodic limb
movement disorder (PLMD) (5), we also considered
the possibility that an increased occurrence of these
periodic limb movements would be detected in PTSD
subjects.
In this article, we present a further analysis of polysomnograms on which we previously have reported
723
R. J. ROSS ET AL.
724
(4). We first compare motor activity during sleep between the group of PTSD subjects and the group of
age- and sex-matched normal control subjects, focusing specifically on 1) the frequency ofleg muscle twitch
bursts in REM sleep and 2) the number of periodic
limb movements in NREM sleep. Finding that leg
muscle twitch bursts during REM sleep were more
prominent in the PTSD subjects, we then ask how such
bursts were distributed over the course of an REM
sleep period and what temporal relation, ifany, existed
between limb twitch bursts and REM activity. Finally,
we report that leg muscle twitch bursts, like REMs,
remained elevated on a subsequent recording night,
providing additional evidence for a fundamental disturbance of REM sleep phasic event generation in
PTSD.
METHODS
Subjects
Twelve male U.S. military veterans who had seen
combat during the Vietnam War were recruited from
the in-patient general psychiatry unit and the out-patient psychiatry clinic of the Philadelphia Veterans Affairs Medical Center (V AMC, Philadelphia, PA), and
the residential PTSD treatment unit at the Coatesville
Veterans Affairs Medical Center (Coatesville, PA). They
were administered selected components of the Structured Clinical Interview for DSM-III-R, Non-Patient
Version (SCID-NP- V) (7), and all met criteria for lifetime and current PTSD. In addition, nine had a history
of major depression, five currently met the criteria for
major depression, two had panic disorder, six had agoraphobia, two had generalized anxiety disorder, and
one fulfilled the criteria for hypomania. All subjects
were evaluated medically and found to be free of any
significant physical problem. None had abused alcohol
or any other substance during the preceding 5 weeks,
nor had any received a psychotropic drug during the
prior 2 weeks. However, seven had a history of alcohol
abuse, and one of them reported consuming 2.0 oz. of
alcohol a week before the study. One subject without
a history of alcohol abuse had drunk 0.5 oz. of alcohol
11 days prior to the study. Urine specimens for toxicology screening were obtained on each study night.
The data from one of the PTSD subjects were not
scored because he had a lengthy nocturnal coughing
episode, which was thought to have disturbed his sleep.
Ten healthy, male military veterans, two of whom
had served in Vietnam, were recruited as control subjects from among hospital employees and by advertising in local newspapers. None had any major medical
illness or met the criteria for any psychiatric disorder
included in the modified SCID-NP-V. Furthermore,
Sleep, Vol. 17, No.8, 1994
none reported any problem consistent with a dyssomnia or parasomnia. Two had consumed in the range of
1.0-4.0 oz. alcohol within the prior 2 weeks (> 3 days
earlier). A urine toxicology screen was performed on
each study night. Clinically significant sleep apnea unexpectedly was detected in one control subject, whereas
another was found retrospectively to be a "short sleeper" (8) with a history of alcoholism; their records were
not tabulated.
Procedure
All subjects provided informed consent and were
treated in accordance with the ethical standards of the
Subcommittees on Human Studies of the Philadelphia
and Coatesville Veterans Affairs Medical Centers. Remuneration was provided at the protocol's completion.
The subjects were asked to retire at their usual bedtimes, and they either woke spontaneously or were
awakened by the polysomnographer at their typical
wake-up times. Inpatients from the Coatesville VAMC
traveled an hour back and forth between Coatesville
and Philadelphia, generally via public transportation.
With both groups of subjects, the 1st night was considered to be adaptational and was not formally analyzed. The PTSD subjects were monitored on 2 subsequent study nights, whereas the control subjects (for
reasons pertaining to ease of recruitment) had 1 study
night. This report describes differences in REM sleep
phasic leg activity (RPLA) between 11 PTSD (41.1 ±
3.5 years, mean age ± SD) and eight control (43.9 ±
2.8 years) subjects on the 2nd night of polysomnographic monitoring and explores any relationship between RPLA and REM activity on the 2nd night. Finally, in the PTSD subjects alone, the stability of a
measure of RPLA from the 2nd to the 3rd night (n =
10) is investigated.
Standard techniques were used to record the polysomnogram on a Grass 78E polygraph run continuously at 10 mm/second. Electroencephalographic activity recorded from the C 3 and Oz leads was referenced
to the mastoid region bilaterally. Chin muscle activity
was monitored, and the electrocardiogram was recorded. Electrooculographic activity recorded between a
point above the nasion and points below the left and
right outer canthi, respectively, indicated eye movements. For the purpose of detecting RPLA and periodic
limb movements, recordings were made of both right
and left anterior tibialis muscle activity. The pre sleep
ankle flexion, used to assess the magnitudes of RPLA
as well as periodic limb movements, was obtained by
instructing the subject to dorsiflex his feet (9). During
the adaptation night in 11 subjects, a nasal thermistor
was placed to register nasal airflow and reveal any sleep
apnea episodes. The eight subjects who were unmon-
MOTOR DYSFUNCTION DURING SLEEP IN PTSD
725
record (10). Essentially a movement was required to
be between 0.5 second and 5.0 seconds in duration, to
be of an amplitude ;:::1/2 that of the pre sleep ankle flexion response, and to be part of a train of at least four
consecutive movements separated by a minimum of
4 but not more than 90 seconds. The time spent asleep
Data analysis
(TSA) also was calculated for each record, and the PLM
The records were scored by a technician trained in index (number of periodic limb movements/TSA) was
the interpretation of polysomnographic data, accord- obtained.
ing to the criteria of Rechtschaffen and Kales (9). A
blind rater who rescored nine of the records, chosen Statistical analysis
at random, achieved 85.5% agreement. For each 2nd
The SPSS/PC+ system was used for all data analnight record, the number of REMs during REM sleep
was counted manually by a rater blind to subject iden- yses. The RPLA and the PLM indices from the 2nd
tity. REM sleep time was calculated, and the average night in the PTSD and control groups were compared
REM density (no. REMs/REM sleep time) was com- by t tests, with 0.05 (two-tailed) as the accepted level
puted. In order to detect any relationship between of significance. To remove the proportionality between
RPLA and REMs, average REM density also was cal- the mean and standard deviation, in each case, we
culated separately for the total numbers of REM sleep elected to first apply an appropriate logarithmic transepochs with and without RPLA. Finally, the number formation, 10glO(x + 1), to the data. For the withinof REM sleep epochs manifesting RPLA, without a subject comparisons of average REM density between
coincident REM, was counted and expressed as a per- RPLA and non-RPLA-containing REM sleep epochs
centage of the total number of RPLA-containing ep- from the 2nd night, paired t tests were used; a twoochs; for the purposes of this analysis, coincident REMs way (group x RPLA condition) ANOVA with repeated
were defined as those occurring within 10 seconds of measures on the RPLA condition also was carried out.
The logarithmically transformed data tabulated from
the RPLA.
A phasic leg movement was defined as activity in successive quartiles of 2nd night REM sleep periods
either leg channel that was;::: 1.5 seconds in duration were analyzed by a two-way (group x quartile) ANOand ;::: 1/2 the amplitude of the pre sleep ankle flexion VA with repeated measures on the quartile. The RPLA
response. For each 2nd night record, phasic leg move- indices from the 2nd and 3rd nights in the PTSD group
ments were counted manually by a rater blind to sub- were compared by a t test.
ject identity, and the percent of REM sleep epochs
containing at least one such movement was computed
RESULTS
(RPLA. index). Phasic leg movements in each 3rd night
The RPLA index was significantly higher in the PTSD
record were counted by a rater aware that only PTSD
subjects compared to the normal control subjects [4.6
subjects were represented.
Movements during REM sleep that were part of a ± 4.8 (SD) vs. 1.3 ± 0.8, p < 0.05]. An example of
movement arousal, defined as "any increase in EMG RPLA in a PTSD subject is shown in Fig. 1.
The PLM index also was significantly higher in the
on any channel, which is accompanied by a change in
pattern on any additional channel" (9), were not count- PTSD subjects (11.2 ± 10.6 vs. 0.9 ± 2.4, p < 0.02).
ed as RPLA. Hence, RPLA cannot be taken as an Figure 2 illustrates periodic limb movements in a PTSD
indicator of a shift in behavioral state toward greater subject. Periodic limb movements did not extend into
arousal. RPLA also was distinguished from 1) move- REM sleep in any subject.
When the average REM density was calculated sepment time, which is a specific epoch score to be used
when more than 1/2 the epoch (15 seconds, at a paper arately for the total numbers of REM sleep epochs with
speed of 10 mm/second) is obscured by movement and without RPLA, no significant difference was noted
artifact, and 2) body movement, which implies a dis- in the group of PTSD subjects (8.6 ± 7.0 vs. 6.2 ±
crete, substantial spatial displacement of the body of 2.9, p > 0.25), in the group of normal control subjects
(3.2 ± 5.5 vs. 4.2 ± 2.8, p > 0.65), or in the two
no particular duration (9).
To investigate the distribution of RPLA over the groups combined (6.3 ± 6.8 vs. 5.4 ± 3.0, p > 0.53).
course of REM sleep periods on the 2nd night, each The two-way (group x RPLA condition) ANOVA
REM sleep period was divided into quartiles and the showed a higher REM density in the PTSD group
[F(I, 17) = 4.45, p < 0.05]; there was no main effect
RPLA index was calculated for individual quartiles.
Standard criteria were used to count the total num- of RPLA condition [F(1, 17) = 0.20, p > 0.65], and
ber of periodic limb movements in each 2nd night there was no significant interaction of subject group
itored showed no evidence of sleep apnea; there was
no sign of excessive sleep fragmentation in the form
of an unusual number of stage changes or movement
arousals.
Sleep, Vol. 17, No.8, 1994
R. J. ROSS ET AL.
726
L.O.C. - Nasion
C3- A I +A2
~/I~!'IIv~'''''''j'vW''''\I'~"'\/\ j\.J\yj'." \'
ChinEMG
'; ;:,"('" ,\,J''V\.'_--''\J,,\;,j' .,,'lA:
"/.,"'"'
of· •
Left Anterior Tibialis
IliJht Anterior TibiaJis
lOOuV I
I
2 sec
FIG. 1. Polygraphic recording of an REM sleep epoch in a PTSD subject. RPLA is evident in the right anterior tibialis muscle channel.
L.O.c. and R.O.C. are left and right outer canthi, respectively. e3 , A" A2 , and 0, are left central, left and right auricular, and midline
occipital electrode placements, respectively.
and RPLA condition [F( 1,17) = 1.28, p > 0.25]. Thus,
in a PTSD subject who otherwise displayed RPLA,
dense eye movements could be observed in isolation
(Fig. 3). Conversely, RPLA sometimes appeared when
eye movement activity was absent (Fig. 4). The percentage of RPLA-containing epochs that lacked coincident eye movements varied from 0 to 67 among all
the subjects, with a mean of 24 ± 27 (SD).
The one anxiety dream that was reported by a PTSD
subject emerged from an REM sleep episode with an
RPLA index of 15.6 and an REM density of 17.6 (Fig.
5). None of the control subjects was awakened by an
anxiety dream.
A comparison of RPLA in the PTSD and control
groups, with an analysis by quartiles of the REM sleep
period, is presented in Fig. 6. There was a trend towards a higher RPLA index in the PTSD group [F( 1,17)
= 3.77, p < 0.07]; there was no main effect of quartile
Righ-t-An-tert-'-or-n-l-bialia-'--·-----1-)-oo-.u-v-----------:-'2-sec-':-· . · ..· .--....
FIG. 2. Polygraphic recording of an NREM sleep epoch in a PTSD subject. Periodic limb movements are evident in the left anterior
tibialis muscle channel. Abbreviations as in Fig. 1.
Sleep, Vol. 17, No.8, 1994
MOTOR DYSFUNCTION DURING SLEEP IN PTSD
727
.,
Chin EMG
Left Anterior Tibialis
1
100
,.V
,.c
Right Anterior Tibialis
2
FIG. 3. Polygraphic recording of an REM sleep epoch with dense rapid eye movements, but no coincident RPLA, in a PTSD subject.
Abbreviations as in Fig. I.
[F(3,51) = 0.46, p > 0.70], nor was there a significant
interaction of subject group and quartile [F(3,51) =
0.48, p > 0.65].
The RPLA index in the PTSD subjects remained
high on the 3rd (5.4 ± 5.2) compared to the 2nd (4.6
± 4.8) night (p > 0.7).
DISCUSSION
We have argued that the essential pathophysiology
of PTSD might involve disordered REM sleep mechanisms (3). Previously, we have emphasized an increase in REM sleep phasic activity in the form of
REMs (4). Here we suggest that another REM sleep
phasic event, RPLA, also may be recruited at a greater
frequency in subjects with PTSD. The persistence of
high RPLA on the 3rd recording night in the PTSD
subjects adds to the evidence for a fundamental phasic
REM sleep disturbance in PTSD.
The concurrent diagnoses present in many of the
PTSD subjects must be considered as potential confounders of this interpretation of our results. Certainly
as manifested in Vietnam War veterans, PTSD frequently is diagnosed together with other mental disorders (11). Alcohol abuse, of which seven of the PTSD
subjects had a history, may disturb sleep for many
months after withdrawal and detoxification, although
this has not been observed consistently (12, 13). A slowwave sleep deficit, along with a fragmentation of REM
sleep periods, is the most replicated finding following
prolonged abstinence. Although we saw neither abnormality in this group ofPTSD subjects, efforts should
be made in future sleep studies to include PTSD populations without a high prevalence of substance abuse
disorders (4). In other investigations, PTSD subjects
should be compared to control subjects with a history
of alcoholism.
Major depression commonly is diagnosed together
with PTSD (11,14), and prominent REM sleep abnormalities first were described in depressed subjects
(15,16). Generally, REM latency is abbreviated, REM
sleep distribution is shifted toward the earlier part of
the night, and REM density (at least during the first
REM sleep period) is elevated. Nine of the PTSD subjects had a history of major depression, and five met
the criteria for current major depression. We have used
several lines of reasoning to argue that current major
depression is not an essential covariate determining
the increase in REM density in this group (4). To our
knowledge, RPLA has neither been sought nor detected
in patients with major depression, preventing us from
definitively ruling out major depression as a factor in
Sleep. Vol. 17. No.8. 1994
R. J. ROSS ET AL.
728
, L.O.C. - Nasion
~------­
Nasion - R.O.C.
~.~~
C 3 - Al + ~
Chin EMG
Left Anterior Tibialis
100 llV
I
',~I ~·+I---Mt..~~-------------------
.
Right Anterior Tibialis
2 sec
FIG. 4. Polygraphic recording of an REM sleep epoch with RPLA, but no coincident rapid eye movements, in a PTSD subject. Abbreviations as in Fig. 1.
of men with RBD, Schenck et al. (6) found that 36.8%
of REM sleep epochs that otherwise displayed chin
atonia contained a muscle twitch burst ::::2.0 seconds
in duration.
Although the people in whom RBD was described
originally
were elderly men with demonstrable central
Motor control during normal REM sleep
nervous system pathology, a more common idiopathic
It is important to place our findings in the context form of the disorder, with presumably more subtle
of what is understood about normal REM sleep motor physio-anatomical abnormalities such as might exist
function. In the normal adult, spinal motoneurons are in PTSD, has been delineated (20). Furthermore, RBD,
postsynaptically inhibited during REM sleep by path- like PTSD, displays a high prevalence of vivid, dysways originating in the caudal brainstem, so that there phoric dreams, and there have been reports of overis skeletal muscle atonia (17). Barrages of excitation whelmingly stressful experiences precipitating RBD
from supraspinal regions intermittently override this (20). No instance of actual RBD was observed in our
powerful motoneuronal inhibition, producing phasic group of PTSD subjects, but other experiments using
twitches ofthe extraocular muscles and the distal mus- a stimulus probe such as REM sleep deprivation might
cles of the extremities (17). Thus, isolated motor unit be expected to yield such examples.
action potentials can be a prominent feature of normal
REM sleep; however, bursts of motor unit action potentials (>600 msec in duration), such as we have ob- Relation between RPLA and nightmares in PTSD
served in our PTSD subjects, rarely occur (18).
Posttraumatic anxiety dreams, which occasionally
have been observed under polysomnographic monitoring (21,22), can emerge from REM sleep. Some of
RBD-like findings in PTSD
these REM sleep-related anxiety dreams have been
The current group of PTSD subjects had an RPLA found to occur in close temporal association with moindex elevated above the control level (4.6 vs. 1.3). tor activity (22). The only true nightmare [defined as
Limb twitch bursts in RBD appear to occur at a con- a long, frightening dream that awakens one during REM
siderably higher frequency in the upper compared with sleep (23)] that we observed in 32 nights of sleep in 11
the lower extremities (19), which suggests that an arm- PTSD subjects emerged from an REM sleep episode
derived RPLA index might have been even higher than with an exceedingly high RPLA index (Fig. 5). This
the leg measure used in our subjects. Recording from finding is consistent with the notion of a linkage bethe upper as well as the lower extremities in a group tween RPLA and nightmares. How the neural mech-
explaining the current results. It will be important in
future polysomnographic studies to include more subjects with no history of a mood disorder (4).
Sleep. Vol. 17. No, 8. 1994
MOTOR DYSFUNCTION DURING SLEEP IN PTSD
729
L.O.C. - Nasion
Nasion - R.O.C_
Chin EMG
til
i
--------~----~I~,~,-,~~~,~·,-,----------------~!I+t--~I~W~"--~------~r~t'~~H
Left Anterior Tibialis
1
I'
100
.~,~ ... ;v
Riqht Anterior Tibialis
•. .
rl
~. ~rtt--
'2 sec~
I
FIG. 5. Polygraphic recording in a PTSD subject of an REM sleep epoch from an REM sleep episode that culminated in an arousal out
of a nightmare. Abbreviations as in Fig. 1.
anisms underlying RPLA might actually contribute to
disturbed dreaming in PTSD remains a matter for
speculation. As one example, the activation-synthesis
hypothesis of the origin of dream mentation posits the
faithful elaboration by forebrain circuitry of a cognitive
structure for streams of brain stem afferent activity (24).
Could then abnormal patterns of central motor activation in PTSD be translated at higher cortical levels
into vivid, terrifying dream imagery?
As in RBD, where a substantial dissociation between
REM sleep limb twitch bursts and saccadic eye movements has been observed (19), no clear temporal relation between these two REM sleep phasic events was
demonstrated in our subjects. In neither the PTSD nor
the control group did REM sleep epochs with RPLA
show a higher average REM density than did nonRPLA epochs (Fig. 3). Conversely, RPLA could be
observed when the eye movement channels were relatively silent (Fig. 4). Yet the REM sleep episode out
of which the single nightmare in a PTSD subject occurred had an exceedingly high REM density as well
as RPLA index (Fig. 5). This suggests that, as a nightmare unfolds, diverse REM sleep phasic processes,
which otherwise can be uncoupled, are recruited en
masse.
Relation between RPLA and exaggerated startle in
PTSD
Signs of "hyperarousal", including an exaggerated
startle response, figure prominently in the PTSD symptom complex. Indeed, specific abnormalities of startle
behavior in PTSD subjects have been identified by
several groups of investigators (25,26). Ornitz and Pynoos (26) found impaired startle inhibition in children
with PTSD and suggested that it might result from a
long-lasting alteration in the brainstem circuitry controlling startle modulation.
Studies in the cat have suggested that the muscle
twitches seen during REM sleep may be manifestations
of an endogenously activated startle reflex (27,28). Recently, we have demonstrated that some normal cats
display the acoustic startle response during REM sleep
(29), as do all cats that have received bilateral lesions
of the dorsolateral pontine tegmentum and then show
spontaneous behavior in REM sleep (REM sleep without atonia) (30). Largely on the basis of such investigations, we have proposed that startle abnormalities
during waking, as well as nightmares during sleep, might
be explained as dysfunctional REM sleep manifestations in PTSD (3).
Sleep, Vol. 17, No.8, 1994
R. J. ROSS ET AL.
730
O. '2
0.08
x
o
w
0.04-
Z
<!:
-.J
0.00
(L
n:::
o
PTSD
(N •
11)
Control
(N - 8)
1
2
:3
4
REM SLEEP PERIOD (BY QUARTIL[S)
FIG. 6.
RPLA index over quartiles of the REM sleep period in PTSD and normal control subjects.
Our current report of an excess ofleg muscle twitch
bursts during REM sleep in a group of PTSD subjects
is consistent with the view that an REM sleep-related
startle mechanism has an essential role in PTSD symptomatology. PTSD occurring in the aftermath of an
overwhelming psychological stressor could reflect plasticity in brainstem systems controlling REM sleep phasic activity. Such systems might be related to the startle-modulating pathways discussed by Ornitz and
Pynoos (26). Consistent with this speculation is the
report that lesions of the pedunculopontine tegmental
nucleus in the rat disrupted prepulse inhibition of
acoustic startle (31); cholinergic neurons of the pedunculopontine tegmental nucleus have a significant role
in the phasic as well as the tonic activational processes
of REM sleep (32,33).
In patients with PLMD, blink reflexes, elicited by
electrical stimulation of the supraorbital nerve or mechanical stimulation of the glabellar region and recorded electromyographically from the orbicularis oculi
muscle, have been shown to contain at least three components, compared to the two seen normally (34). Because the blink reflex forms a part of the wide range
of body muscle responses to an abrupt, intense stimulus that defines the startle reflex (35), abnormalities
in a long-latency component of the blink reflex might
indicate some dysfunction of the startle mechanism in
PLMD patients. The elevated PLM index in our group
ofPTSD subjects might reflect the operation of neural
systems that mediate exaggerated startle behavior during waking in PTSD. Supportive of this hypothesis is
the observation that patients with hyperexplexia, a genetic disorder characterized by pronounced startling,
display prominent leg jerks during sleep (36).
Implications of periodic limb movements in PTSD
Evidence for an increased occurrence of PLMD has
Periodic limb movements, as were observed here, been sought previously in major depressive disorder,
are essentially an NREM sleep phenomenon (10). and no heightened prevalence was found (37). This
Therefore, the finding of a heightened PLM index in negative finding supports the view that PTSD is a disthis group ofPTSD subjects suggests the possibility of tinct psychiatric diagnosis with demonstrable validity
some generalized motor dysfunction throughout sleep (38). The likelihood that the depressive mood disturin PTSD.
bance diagnosed in many PTSD patients represents
Sleep, Vol. 17, No.8, 1994
MOTOR DYSFUNCTION DURING SLEEP IN PTSD
something other than DSM-III-R major depression is
heightened by recent biological findings (39, 40). Specifically, urinary cortisol excretion was low in a group
of combat veterans with PTSD, even those with a concurrent diagnosis of major depressive disorder; urinary
cortisol excretion otherwise has been found to be elevated in major depression (41).
Therapeutic considerations
We have argued that the development of successful
pharmacological treatments for PTSD would be facilitated by the elucidation of the pathophysiology ofthe
disorder (3). The results of the current investigation
lead us to propose that insights obtained from either
RBD or PLMD pharmacotherapy might aid in the
design of an effective drug treatment for PTSD.
Although the precise pharmacological mechanisms
remain uncertain, dramatic and sustained improvement in RBD symptomatology has been reported with
the long-acting benzodiazepine, clonazepam (20).
Nightmares as well as overt motor behaviors abate in
frequency and intensity. There has been only one systematic, placebo-controlled trial of any benzodiazepine in the treatment of PTSD; in that study, alprazolam was found to have little therapeutic efficacy (42).
To our knowledge, clonazepam itselfhas not been tried
systematically.
From the opposite perspective, tricyclic antidepressant or monoamine oxidase (MAO) inhibitor administration, as well as alcohol, sedative-hypnotic or psychostimulant withdrawal have been linked to the onset
of RBD (20), and it must be wondered whether such
conditions could exacerbate the sleep and dreaming
problems of PTSD patients. This caution necessitates
a revision of our earlier view that REM sleep-suppressant drugs, in particular the tricyclic antidepressants and MAO inhibitors, could have some therapeutic efficacy in PTSD by way of their effects on REM
sleep (3). Indeed, recent evidence calls into question
the utility of antidepressant drugs in treating PTSD
(43). Perhaps these negative results reflect the drugs'
disruptive effects on the internal structure of REM
sleep, including RPLA.
The optimal pharmacological management ofPLMD
is only partially understood. Some success has been
reported with clonazepam (44), again suggesting the
potential utility of clinical trials with this drug in PTSD.
Positive results with L-DOPA in the treatment of
PLMD raise the possibility of a dopaminergic mechanism in this condition (45) and suggest that the same
neurochemical system might be disturbed in PTSD.
Finally, like RBD, PLMD can be triggered by treatment with a tricyclic antidepressant or an MAO inhibitor or by the withdrawal of alcohol or a sedative-
731
hypnotic agent (46); these situations, which are likely
to be encountered frequently in the course of working
with PTSD patients, ultimately may be recognized to
impact adversely on treatment outcome.
This study was supported by the Department of Veterans Affairs Medical Research Service, MH42903 and F32-MH-09584-01. We are indebted to Patrick
Ciccone, M.D. and Neal Daniels, Ph.D. for subject referrals
and to Mr. James Mamary for assistance with data analysis.
Acknowledgements:
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