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les articles sur la parakinésie brachiale
oscitante
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articles about parakinesia brachialis
oscitans
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- Parakinesia Brachialis Oscitans (PBO) is a
rare post-stroke phenomenon characterized by
abnormal, involuntary movement in a paralyzed
limb triggered by yawning. The authors present
the case of a male patient, age 57 years, who
was admitted with right hemiparesis, dysarthria,
and facial weakness. Brain magnetic resonance
imaging revealed an infarction in the left pons.
One week following the stroke, the patient began
to experience involuntary elevation of his
paretic arm and, to a lesser extent, his leg,
triggered specifically by yawning. Based on
these observations, they diagnosed with PBO.
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- The characteristic movement pattern of
elevation of the upper limb during yawning was
consistent with the typical presentation of PBO.
The patient was reassured about the benign
nature of his condition and continued his
rehabilitation program. This phenomenon occurs
due to a dissociation between autonomic and
voluntary motor control, reflecting a disruption
of cortical inhibition of the cerebellum, while
sparing functional spinocerebellar pathways.
Given the potential for confusion with focal
seizure activity, especially during the acute
phase of a stroke, a high index of suspicion is
necessary to distinguish PBO from other
neurologic disorders.
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- Correctly identifying PBO can guide accurate
diagnosis and appropriate management preventing
unnecessary investigations and facilitating
better outcomes in post-stroke care.
La parakinésie brachiale oscitante (PBO)
est un phénomène rare survenant
après un AVC, caractérisé
par des mouvements anormaux et involontaires
d'un membre paralysé,
déclenchés par un
bâillement. Les auteurs présentent
le cas d'un patient de sexe masculin,
âgé de 57 ans, admis pour une
hémiparésie droite, une dysarthrie
et une faiblesse faciale. L'IRM
cérébrale a
révélé un infarctus au
niveau du pont gauche. Une semaine après
l'AVC, le patient a commencé à
présenter une élévation
involontaire de son bras parétique et,
dans une moindre mesure, de sa jambe,
déclenchée spécifiquement
par le bâillement.
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- Sur la base de ces observations, un
diagnostic de PBO a été
posé. Le schéma moteur
caractéristique, consistant en une
élévation du membre
supérieur lors du bâillement,
correspondait à la présentation
typique du PBO. Le patient a été
rassuré quant à la nature
bénigne de son état et a poursuivi
son programme de rééducation. Ce
phénomène résulte d'une
dissociation entre le contrôle moteur
autonome et volontaire, reflétant une
perturbation de l'inhibition corticale du
cervelet, tout en épargnant les voies
spinocérébelleuses fonctionnelles.
Compte tenu du risque de confusion avec une
activité épileptique focale, en
particulier pendant la phase aiguë d'un
AVC, un indice de suspicion élevé
est nécessaire pour distinguer le PBO
d'autres troubles neurologiques.
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- Une identification correcte du PBO permet
d'établir un diagnostic précis et
une prise en charge appropriée,
évitant ainsi des examens inutiles et
favorisant de meilleurs résultats dans la
prise en charge post-AVC.
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The term
parakinesia brachialis oscitans (PBO) was first
introduced by Walusinski et al.,1 who
described the phenomenon of abnormal,
involuntary movement in a paralyzed limb
triggered by yawning following a stroke. The
basal ganglia and internal capsule are the
primary brain areas implicated in this
condition.1,2 PBO is a rare phenomenon, with
only a limited number of cases reported in the
literature, and several aspects of this
intriguing clinical condition remain
unresolved.3,4 Despite its recognition in the
medical literature since the mid-1800s, PBO
remains an enigma. Its pathophysiology is still
hypothetical, with no consensus on whether it
results from a released brainstem reflex, a
disinhibited sensory-motor loop, or another
mechanism entirely. The heterogeneity of lesion
sites associated with PBO from the cerebral
cortex to the pons adds further complexity to
any unifying theory. Knowledge of its natural
history is fragmentary, based almost exclusively
on single case reports with limited follow-up.
Consequently, clinicians lack clear guidance on
management, and issues such as the necessity of
counseling, the role of any pharmacological
agent, or the impact on rehabilitation outcomes
remain unexplored.
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- Herein, we report a case of PBO following a
pontine infarction and discuss the clinical
features, video-e electroencephalogram (EEG)
correlates, and proposed pathophysiological
mechanisms. This report aims to increase
clinical awareness of this phenomenon and
contribute to the growing body of literature by
highlighting its occurrence in a brainstem
stroke, thereby expanding the spectrum of
associated lesion locations.
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- Case Report
- We present the case of a male patient, age
57 years, a smoker with a history of
hypertension, who was brought to the emergency
room with right-sided hemiparesis, dysarthria,
and facial weakness of 12-hours' duration. Upon
initial assessment, his National Institutes of
Health Stroke Scale score was 5, with right arm
and leg drift, facial weakness, and dysarthria.
Over the next few hours, his weakness
progressed, with the right arm showing 0/5
strength, and the right leg exhibiting 3/5
strength. He was found to have flaccid paralysis
of the right side, with mild dysarthria and
right upper-motor neuron-type facial weakness
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- Magnetic resonance imaging revealed an old
infarction and an acute infarction in the left
pons. A computed tomography angiogram showed a
faint irregularity at the basilar artery, likely
due to atherosclerosis.
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- One week after the stroke, the patient began
to notice involuntary elevation of his paretic
arm and leg during yawning. The involuntary
movements were stereotyped, occurring with every
yawn. There was no observed variability in the
pattern (shoulder abduction, elbow/finger
flexion, hip flexion), although the intensity of
the movement varied from one episode to the
next.
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- These episodes were captured on video
electroencephalogram (EEG), which showed the
right arm lifting with elbow and finger flexion,
accompanied by slight abduction, returning to
the paretic position at the end of the yawn.
There was also slight flexion of the right hip
during yawning (Video 2 & Video 3:
Demonstrate right arm lifting with elbow and
finger flexion, accompanied by slight abduction,
returning to the paretic position at the end of
the yawn; Video 2 is available at
https://youtu.be/4WUBA3uvxM4; Video 3 is
available at https://youtu.be/etDXu1EtBSI). The
EEG during these episodes was unremarkable, with
no associated epileptiform activity associated
with the arm-raising movements (Figure 2). The
patient initially perceived these involuntary
movements as a sign of improving weakness. We
conducted a counseling session to explain that
this phenomenon, while interesting, is part of
the post-stroke recovery process and should not
be mistaken for the restoration of true motor
function. He participated in a comprehensive
inpatient stroke rehabilitation program
consisting of daily physical therapy (focusing
on bed mobility, transfers, and gait training)
and occupational therapy (focusing on activities
of daily living), provided 5 days a week during
his 2-week inpatient stay. His weakness showed
only gradual, albeit minimal, improvement with
therapy, and he continued to require assistance
with activities of daily living. In addition to
the National Institutes of Health Stroke Scale,
functional status was assessed using the Barthel
Index,6 which improved from 35/100 on admission
to 45/100 at discharge, indicating severe
dependency with modest gains. By 3 months, his
motor power showed minimal improvement (right
arm remained 0/5, right leg improved to 4/5),
and his Barthel Index score was 60/100,
reflecting continued severe disability but
further gains in self-care. The patient was
followed for 3-months post-stroke. The PBO
episodes persisted throughout his inpatient stay
and were still present, though with subjectively
reduced frequency, at his 1-month outpatient
follow-up. By the 3-month follow-up, the patient
reported the movements had significantly
diminished in frequency and were no longer a
noticeable occurrence, with the frequency
decreasing over time in parallel with the
subacute phase of stroke recovery.
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- Discussion
- These involuntary movements have been
described in the literature since 1844, though
the term parakinesia brachialis oscitans (PBO)
was first introduced by Walusinski et al.2 PBO
has been observed in both the flaccid and
spastic phases of post-stroke recovery. While
the exact mechanism remains unclear,
topographical studies suggest several brain
regions may be involved, including the brainstem
and areas supplied by the middle cerebral
artery, particularly the internal capsule and
corona radiata. In one reported case, the
involuntary movement was also associated with a
tremor.5 The entire movement typically lasts
around 5 seconds. While PBO is most commonly
observed shortly after the acute stroke (usually
within the first week), late onset during the
spastic phase has also been reported. There is
no clear age or gender predilection, although
most reported cases of PBO have involved men.7
In most instances, shoulder abduction occurs at
the onset of yawning and returns to the resting
position as the yawn subsides.2,3
- While the upper extremity is most commonly
affected, some reports also document involvement
of the lower extremity.3 In addition to being
potentially mistaken for a stroke-related
seizure, PBO can be distressing, as it may
create a false sense of hope for recovery.5 Some
patients are able to intentionally suppress
these movements, which generally diminish as
motor function is regained in the affected limb,
typically within the first 6 months. However, in
some cases, PBO persists for a more prolonged
period.3 While the majority of reported PBO
cases have been attributed to ischemic stroke,
the phenomenon has also been observed in the
setting of hemorrhagic stroke, amyotrophic
lateral sclerosis (ALS), and brainstem
tuberculoma
- Our findings are consistent with a recent
report by Chowdhury et al.4 which also described
PBO in the acute post-stroke. However, the
present case offers several distinct
contributions. First, the index patient in
Chowdhury et al. had a middle cerebral artery
territory infarct, a classic location for PBO.
In contrast, our patient's infarct was localized
to the pons. This difference is clinically
significant as it supports the hypothesis that
disruption of the corticopontocerebellar pathway
at the brainstem level is sufficient to produce
the phenomenon, not just lesions in the basal
ganglia or internal capsule. Second, we provide
a more detailed account of the patient's
longitudinal clinical course, including specific
functional outcome measures (Barthel Index) and
the positive impact of targeted patient
counseling, which adds practical guidance for
clinicians.
- The exact pathophysiological mechanism of
PBO remains largely uncertain.2,7 The most
commonly proposed explanation is that PBO
reflects the activation of a proprioceptive
loop. In this model, strong contraction of the
respiratory muscles during yawning generates a
proprioceptive signal, which travels via the
spinocerebellar tract to the medullary lateral
reticular nucleus. From there, the signal is
relayed through extrapyramidal pathways to the
cervical anterior horn cells, leading to
involuntary movement of the affected upper
limb.7 A key element in this process is the
disruption of the corticopontocerebellar
pathway, which results in the disinhibition of
the proprioceptive loop, ultimately triggering
the manifestation of PBO. Another proposed
pathophysiological mechanism involves cortical
damage that leads to disinhibition of
subcortical structures, potentially releasing
the reticular formation in the brainstem. This
release may activate motor pathways, with
stimuli such as yawning serving as a trigger.
Additionally, some researchers suggest an
"emotional motor system" could contribute to the
movement of the paralyzed upper limb, with
yawning acting as a trigger due to its
association with emotional states such as
drowsiness.
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- Our patient developed PBO one week after
experiencing a lacunar infarct in the left pons,
which led to disruption of the descending
pyramidal tracts. Given the location of the
infarct, it is likely that the corticospinal,
corticobulbar, and corticopontocerebellar
pathways were affected. However, the most
plausible explanation for the occurrence of PBO
in this case is the preservation of the
proprioceptive loop, which operates
independently of these pathways. Despite the
damage to the corticospinal and related
pathways, the proprioceptive signal may have
been able to travel through the intact
spinocerebellar tract, ultimately leading to
activation of the motor pathways and triggering
involuntary movements. This suggests the
proprioceptive loop remains functional even in
the presence of significant corticospinal tract
damage.
- The prognosis of PBO is generally benign and
self-limiting. In most reported cases, including
ours, the involuntary movements tend to decrease
in frequency and intensity over time, often
resolving within the first 6-months
post-stroke.7 This improvement may parallel the
resolution of local post-stroke diaschisis or
the establishment of compensatory inhibitory
mechanisms. The persistence of PBO does not
appear to negatively impact overall functional
motor recovery, which remains dependent on the
severity of the initial corticospinal tract
damage.
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- Conclusion
- A better understanding of PBO could inform
rehabilitation strategies for stroke survivors,
potentially by targeting and utilizing preserved
extrapyramidal pathways. Neurologists should
remain vigilant in recognizing these involuntary
movements to prevent misdiagnosis as abnormal
movement disorders, thereby avoiding unnecessary
investigations and facilitating more accurate
patient management.
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