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theorize that both these conditions occur to produce RBD.
As already proposed for cats with pontine lesions, disinhi-
bition of selective brainstem motor pattern generators
accounts for the differential release of stereotypical REM
behavior. 15 This same process might produce both the
behavior and dream disorder of RBD. For example, the
generator for violent behavior might become disinhibited
and coactivate both a descending output to the spinal
motor neurons and an ascending output to forebrain
dream-synthesizing centers, thus producing the simultane-
ous movement and dreaming. These two outputs from the
same generator may be isomorphic, so that command for
dream action (fictive movements) is equivalent to command
for actual movements, 144 resulting in acting out of dreams.
In our series of patients with RBD, all who acted vio-
lently during REM sleep also had violent dreams. In fact,
dream recall was most complete following behavioral
enactment. The REM sleep activities we observed in our
patients corresponded to the reported dream mentation.
Most patients repeatedly experienced a typical RBD
nightmare, which consisted of being attacked by animals
or unfamiliar people, few of whom were bizarre in appear-
ance. Characteristically, the dreamer would either fight
back in self-defense or else attempt to lee. Fear, rather
than anger, was the usual accompanying emotion reported.
An ironic situation was produced by RBD when a dream-
ing husband would fight to defend his wife from an aggres-
sor while actually striking her in bed. Her yells would then
awaken him to the unfortunate reality of his violent oneiric
activity. In these patients, medication suppressed both the
vigorous sleep activities and the abnormal dreaming, which
adds further support to the activation-synthesis model.
A singular feature of the dream-enacted episodes in this
group of patients is that customary dreams are generally
not being played out; rather, distinctly altered, stereotypi-
cal, repetitive, and action-packed dreams are put on display.
The violence of the sleep-related behavior is often discor-
dant with the waking personality. The increased aggressive
dream content experienced by patients with RBD is not
associated with increased daytime aggressiveness. 145
were initially thought to have a seizure disorder explaining
the movements during sleep, neither EEG electrical nor
clinical seizure activity has been detected. The conven-
tional scoring parameters of Rechtschaffen and Kales 150
must be modified to allow for the persistence of EMG tone
during epochs that are otherwise clearly REM sleep. These
periods are similar to the “stage 1 REM with tonic EMG”
described by the Japanese, 9 the “stage 1 REM” seen in
delirium tremens, 151 and those recorded in the chronic
pontine-lesioned cats. 3,15,24,93,102-104 There is persistence of
muscle tone during REM sleep, and it may be strikingly
augmented for prolonged periods, occasionally lasting
much of the REM sleep cycle. The onset of a REM sleep
period is often marked by a sudden increase in chin EMG
activity or prominent twitching in conjunction with REMs.
In addition to the intermittent absence of atonia, there
are varying amounts of limb twitching (usually far in excess
of that observed in normal REM sleep), gross body move-
ments, and complex—often violent—activities that corre-
late with reported dream mentation. Tachycardia might
not accompany these impressive movements. A similar lack
of autonomic arousal during REM sleep was observed in
a study of delirium tremens. 151 This likely represents
paresis of the sympathetic nervous system (inactivation of
the locus coeruleus) characteristic of REM sleep. 152 , 153
A curious feature of the chin EMG and extremity move-
ments seen during the REM period is the variability of
involvement and distribution. The chin EMG may be aug-
mented without body movements, or it may be atonic
despite flailing extremities, as shown in Figure 95-3 . The
arms and legs often move independently, necessitating
monitoring of all limbs. Some patients demonstrated per-
sistent (over the span of several years) lateralization of limb
EMG activity or also predominant upper or lower extrem-
ity movements.
Most all patients displayed prominent aperiodic move-
ments of all extremities in every conceivable combination
during all stages of NREM sleep. These aperiodic move-
ments are similar but more intense than the fragmentary
myoclonus described by Broughton and colleagues in
patients with a wide variety of sleep disorders and occa-
sionally as an incidental observation. 154 , 155 Most RBD
patients also showed conventional periodic movements of
sleep, usually involving the legs, infrequently associated
with arousals. Prolonged episodes of aperiodic and peri-
odic movements restricted to the arms were noted occa-
sionally. Figures 95-4 and 95-5 exemplify some of these
dissociated wake-REM states.
Prominent changes in sleep patterns likely representing
variations of RBD have been described in the drug-induced
variety of RWA, 156 , 157 narcolepsy, 75 and Parkinson's
disease. 158 , 159 Figure 95-6 is a dramatic example of venla-
faxine-induced RBD in a 9-year-old boy.
Routine medical history-taking should include questions
that screen for abnormal sleep movements and altered
dreams, especially in older adults, in patients of any age
who have acute or chronic central nervous system disor-
ders—particularly those who have neurologic conditions
that predispose to RBD such as Parkinson's disease or
MSA—or in patients receiving psychoactive medications
known to trigger RBD. The diagnosis of RBD may be
suspected on clinical grounds; however, our experience has
shown that PSG confirmation is mandatory. The com-
plaint of sleep-related injurious or violent activities should
be taken very seriously. Reported injuries in our series
include lacerations and fractures to the patient and bed
partner. RBD has also resulted in subdural hematomas and
other serious injuries. 146-148
Detailed polysomnographic data in these patients have
been reported elsewhere. 10,137,149 The overall sleep archi-
tecture is usually normal, with the expected cycling of
NREM and REM sleep. Most of our subjects had excessive
slow-wave sleep for age. Although some of these patients
The minimum diagnostic criteria for RBD we have formu-
lated can be satisfied in either of two ways. The diagnosis
can be made in patients with a history of problematic sleep
behavior that is harmful or potentially harmful, or that
disrupts sleep continuity, or that is annoying to the patient
or bed partner and that includes excessive augmentation of
chin EMG tone or excessive chin or limb EMG twitching,
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