-
|
- mise à jour
du
- 12 novembre
2026
- Tremor
Other Hyperkinet Mov (N
Y)
- 2026;16:57
|
- Revisiting
Parakinesia Brachialis Oscitans:
- You Yawn,
I Move! A Scoping Review
- Vasireddy RP, Vivanco RA, Koppanatham A,
Lenka A
|
|
- Tous
les articles sur la parakinésie brachiale
oscitante
-
- All
articles about parakinesia brachialis
oscitans
-
- Parakinesia brachialis oscitans (PBO) is a
rarely reported phenomenon in which a paretic
limb moves involuntarily during yawning. The
literature consists predominantly of case
reports and small series, with limited
comparative evidence.
-
- Methods: The authors conducted a
PRISMA-ScR-guided scoping review of PubMed,
Embase, and Web of Science from inception to 28
August 2026, with backward citation searching.
Eligible reports described one or more patients
with an involuntary, stereotyped, yawn-locked
movement of a paretic limb after a focal central
nervous system lesion, with the lesion site
reported on neuroimaging. Data included
demographics, movement description, latency,
lesion site, etiology, and outcome.
-
- Results: Twenty-two reports
describing 31 patients met the inclusion
criteria. Most patients were men (67.7%), with a
mean age of 56.1 years. PBO involved the upper
limb alone in 29 patients (93.5%). Acute
ischemic stroke was the most common etiology
(83.9%). Lesions were often seen in the internal
capsule (44.4%) and the corona radiata or
subcortical white matter (40.7%). Onset ranged
from immediate to four months after the lesion.
Complete resolution was documented in 10
patients (32.3%), PBO persisted for up to three
years in five, and outcome was not reported in
15 (48.4%).
-
- Discussion: PBO is associated with
focal lesions affecting distributed voluntary
motor-control networks, frequently involving
subcortical motor pathways. Although no
mechanism has been established, the observations
suggest a release of preserved brainstem and
extrapyramidal circuits. Outcome was unreported
in almost half the cases; prospective,
standardized reporting is needed to clarify its
course and prognostic significance.
-
- La parakinésie brachiale oscillante
(PBO) est un phénomène rarement
rapporté, caractérisé par
des mouvements involontaires d'un membre
parétique lors d'un bâillement. La
littérature se compose principalement de
rapports de cas et de petites séries,
avec des données comparatives
limitées.
-
- Méthodes : les auteurs ont
mené une revue de la littérature
guidée par les critères PRISMA-ScR
sur PubMed, Embase et Web of Science, couvrant
la période allant de leur création
au 28 août 2026, avec une recherche
rétrospective des citations. Les rapports
éligibles décrivaient un ou
plusieurs patients présentant un
mouvement involontaire,
stéréotypé et lié au
bâillement d'un membre parétique
à la suite d'une lésion focale du
système nerveux central, le site de la
lésion étant rapporté par
neuroimagerie. Les données comprenaient
les caractéristiques
démographiques, la description du
mouvement, le délai d'apparition, la
localisation de la lésion,
l'étiologie et l'issue.
-
- Résultats : Vingt-deux
rapports décrivant 31 patients
répondaient aux critères
d'inclusion. La plupart des patients
étaient des hommes (67,7 %), avec un
âge moyen de 56,1 ans. Le PBO touchait
uniquement le membre supérieur chez 29
patients (93,5 %). L'AVC ischémique aigu
était l'étiologie la plus
fréquente (83,9 %). Les lésions
étaient souvent observées dans la
capsule interne (44,4 %) et dans la couronne
rayonnée ou la substance blanche
sous-corticale (40,7 %). L'apparition variait
d'immédiate à quatre mois
après la lésion. Une
résolution complète a
été documentée chez 10
patients (32,3 %), la PBO a persisté
jusqu'à trois ans chez cinq d'entre eux,
et l'évolution n'a pas été
rapportée chez 15 (48,4 %).
-
- Discussion : La PBO est
associée à des lésions
focales affectant les réseaux de
contrôle moteur volontaire, impliquant
fréquemment les voies motrices
sous-corticales. Bien qu'aucun mécanisme
n'ait été établi, ces
observations suggèrent une
libération des circuits
préservés du tronc
cérébral et des circuits
extrapyramidaux. L'évolution n'a pas
été rapportée dans
près de la moitié des cas ; des
rapports prospectifs et standardisés sont
nécessaires pour clarifier son
évolution et sa signification
pronostique.
- Introduction
- Parakinesia brachialis oscitans (PBO) is a
rarely reported neurological phenomenon in which
involuntary movements emerge in a paretic limb
during yawning. Although similar observations in
hemiplegia were described long before the
phenomenon was named, from Erasmus Darwin in
1794 and Abercrombie in the 19th century [1,
2], the term parakinesia brachialis oscitans
was formally introduced by Walusinski et al.
[1]. PBO usually emerges hours to months
after a precipitating brain lesion, most
frequently a cerebrovascular event [1,
3]. The movement is most consistently
described as shoulder abduction while starting
to yawn and followed by spontaneous return to
rest upon completion of yawning [1, 4].
While upper-limb involvement predominates,
lower-extremity manifestations have been
reported in a minority of cases [2,
5].
-
- Although it is a rarely reported phenomenon,
PBO has meaningful clinical implications. Its
stereotyped, yawn-locked pattern has to be
distinguished from a focal motor seizure and
from other involuntary movements of a paretic
limb, a distinction that relies on clinical
observation [3]. It may also be read as
a return of voluntary movement: de Lima et al.
described a patient who regarded his own PBO as
a sign of impending functional improvement
[5]. Therefore, the importance of clear
communication about their nature and
significance in patient counseling should be
underscored.
-
- The current literature on PBO consists
predominantly of isolated case reports and small
case series, with no systematic synthesis of
lesion sites, etiologies, and reported course
across them. This scoping review systematically
identifies and synthesizes published PBO cases
to characterize their clinical features,
underlying etiologies, and neuroanatomical
correlates, to provide a more coherent
descriptive framework for this rarely reported
phenomenon.
-
- Clinical Description and Duration of
Parakinesia brachialis oscitans
- PBO manifested in the upper limb alone in 29
cases (93.5%), while combined upper and lower
limb involvement was observed in the remaining
two cases. Limb involvement was left-sided in 19
cases (61.3%) and right-sided in 12 (38.7%), and
was contralateral to the lesion in all 31
patients. PBO was present at the initial
presentation in nine cases (29%) and within
1&endash;7 days in an additional 11 cases
(35.5%). Onset between more than one week and
one month was reported in five cases (16.1%),
and beyond one month in two cases (6.5%).
Latency was not specified in four cases (12.9%).
The longest reported latency was four months.
One case reported botulinum toxin use for
spasticity, followed by eventual resolution of
PBO. Complete resolution was documented in ten
patients (32.3%), occurring within one week in
four cases and after more than one week in four,
and at an unspecified interval in two.
Improvement without resolution was reported in
one patient (3.2%), and PBO persisted at last
follow-up in five (16.1%). The longest reported
persistence of PBO was three years. Outcome
duration was not specified in 15 cases
(48.4%).
-
- Lesion Etiology and Neuroanatomical
Localization
- Anatomical involvement could be determined
in 27 of the 31 cases; in the remaining four the
report named only a vascular territory.
Involvement was most frequent in the internal
capsule (12 cases, 44.4%) and the corona radiata
or subcortical white matter in 11 (40.7%),
followed by the basal ganglia in eight (29.6%),
the cortex in six (22.2%), the brainstem in four
(14.8%) and the thalamus in one (3.7%). A
vascular territory was named by the source
authors in only 12 of the 26 patients with an
ischemic lesion (46.2%), and was the middle
cerebral artery in eleven and the posterior and
middle cerebral arteries together in one. These
frequencies describe lesion involvement rather
than independent anatomical localization,
because categories were not mutually exclusive
and several cases had multifocal lesions. The
predominant underlying etiology was acute
ischemic stroke (83.9%). Less frequent causes
were intracerebral hemorrhage (9.7%) and
multiple sclerosis or other inflammatory
etiologies (6.5%).
-
- Discussion
- In this scoping review of 22 reports
describing 31 patients, PBO has been reported in
patients with acute motor weakness attributable
to disruption of voluntary motor control
pathways. Acute ischemic stroke was the most
common etiology in 26 patients. Among the 27
patients for whom an anatomical structure was
reported, the lesion most often involved the
internal capsule or the corona radiata and
adjacent subcortical white matter.
Interestingly, the onset ranged from the acute
phase of injury to four months after the lesion,
and the clinical course varied from self-limited
resolution within one week to persistent
symptoms for at least three years. However, the
outcome was not reported in 15 patients. The
clinical impact of this phenomenon on patients'
quality of life remains unknown, but no included
report assessed it formally.
-
- Neuroanatomical and Pathophysiological
Mechanisms
- PBO has been reported almost exclusively in
the setting of acute or subacute focal brain
injury, involving the descending motor pathways,
such as in the internal capsule. In this sample,
the lesions were predominantly supratentorial
and subcortical with the internal capsule
involved in 44.4% and the corona radiata and
adjacent subcortical white matter in 40.7% of
the 27 patients. This distribution is compatible
with the hypothesis that interruption of
corticospinal output, rather than a single-site
injury, is the shared substrate, but a
case-based literature cannot establish which
structures are necessary or sufficient. Reports
of PBO resolving as strength improves are
consistent with a state-dependent phenomenon,
although this cannot be concluded from the
present data: PBO persisted for one to three
years in 5 patients (16.1%), complete resolution
was documented in only 10 (32.3%), and outcome
was not reported at all in 15 (48.4%). Observed
resolution proportions should not be interpreted
as estimates of the natural history of PBO
because follow-up was unavailable or
incompletely reported in nearly half of cases
and follow-up duration varied
substantially.
-
- Lim and Neo [9] have proposed at
least two hypotheses to explain how yawning
triggers this release phenomenon: the emotional
motor system and the proprioceptive loop
theories (Figure 2). Neither has been tested
directly in patients with PBO. The emotional
motor system theory highlights that yawning is a
coordinated somatic expression of emotional
disengagement, leading to co-activation of
bulbar and motor neurons. These neurons allow
involuntary, stretch-like limb movements via
intact reticulospinal pathways when the
corticospinal tract is injured [10, 11].
The proprioceptive loop theory proposes that
yawning induces a contraction of the respiratory
muscles, which sends afferent signals through
the ventral spinocerebellar tract to the spinal
cord, cerebellum, and the lateral reticular
nucleus in the medulla. This triggers an
efferent response that travels along
extrapyramidal pathways back to the cervical
spinal cord (C4&endash;C8), which may produce
involuntary upper-limb movement [1].
However, this explanation does not fully account
for lower limb involvement reported in some
cases, a limitation raised by de Lima et al
[5]. Lastly, some studies indicate that
yawning is associated with monoaminergic
activation in the brainstem, which may
facilitate residual motor responses in patients
with corticospinal tract injuries [12,
13]. Lim and Neo proposed that dopaminergic
agents may support recovery in patients with PBO
in whom spinoreticular-cerebellar pathways are
intact. However, this benefit has not been
translated into post-stroke rehabilitation
studies [9]. Moreover, it remains
unclear why not all patients with focal brain
injury and limb weakness develop PBO.
-
- The common denominator in both theories is
an imbalance of the descending control pathways.
Töpper et al. described involuntary
stretching during yawning as an automatic motor
pattern normally suppressed by an intact
corticospinal tract, reappearing when that tract
is interrupted, characteristically as spasticity
and pathological reflexes return [10].
This timing is not universal: in a prospective
series of 75 patients with internal capsule
stroke, yawning-associated limb movements were
more frequent in those with hypotonia than
hypertonia (87% versus 61%) [2]. Blin et
al. reached a comparable conclusion
pharmacologically: apomorphine-induced yawning
reproduced the same stereotyped arm movement in
their patient, which they attributed to release
of basal ganglia projections onto brainstem
motor centers, while a simulated yawn and
passive head and neck movement did not
[14]. Töpper et al. noted that an
intact basal ganglia projection is nonetheless
not a prerequisite, since yawning with
associated limb stretching has been observed
after bilateral midbrain infarction
[10]. A comparable release of an
automatic motor pattern has been demonstrated
experimentally in chronic hemiparetic stroke,
where head rotation modulates flexion synergy
torques in the paretic limb, reproducing the
asymmetric tonic neck reflex and implicating
increased reliance on ipsilateral reticulospinal
pathways once corticospinal drive is lost
[15]. Consistent with a proximally
weighted brainstem drive, yawning-associated
movements in hemiplegic limbs occur far more
often at proximal than distal joints
[2]. PBO is compatible with an altered
interaction between impaired corticospinal
control and relatively preserved brainstem and
extrapyramidal pathways, although the specific
circuit remains unidentified.
-
- Clinical Implications of Parakinesia
Brachialis Oscitans
- PBO is brief and occurs only with a yawn, so
whether it is detected depends largely on
someone being present when the patient yawns; it
is likely documented most often in stroke units
and inpatient rehabilitation wards. The small
number of published cases therefore does not
accurately estimate the prevalence of the
phenomenon. Although not specifically in PBO, a
prospective observational study found
yawning-associated movements of the hemiplegic
limbs in 78.6% of the 75 patients with internal
capsule stroke, a figure close to that of an
earlier survey of 40 hemiplegic patients [2,
7]. Recognition of the stereotyped,
yawn-locked pattern and return of the limb to
rest is important for an accurate diagnosis and
differentiation from other involuntary movements
of a paretic limb (Supplementary Table 4) or
yawning-related movement disorders
(Supplementary Table 5) [16].
Importantly, the phenomenology reported under
the term PBO is itself broader than the classic
description: de Lima et al. reported
yawning-induced upper limb movement in one
patient in whom only the lower limb was paretic
and in another in whom no hemiparesis was
present, describing both as variants
[5].
-
- Appropriate counseling for patients and
caregivers is also important to avoid leading to
false expectations of functional improvement,
which has not been established. Although
initially noted that PBO does tend to diminish
as motor recovery occurs [1], associated
movements in the hemiplegic arm were
subsequently judged to have no prognostic value
[2]. A recent retrospective study has
now examined whether PBO carries prognostic
information: among patients with acute ischemic
stroke matched on baseline severity, those with
PBO had higher motor recovery scores at three
months than those without, and PBO resolving
within one month was associated with higher
scores than persistent PBO [17].
Although promising, PBO cannot yet be used as a
prognostic marker until prospective data are
available.
-
- Strengths, Limitations, and Future
Directions
- This scoping review represents, to our
knowledge, the most comprehensive synthesis of
published PBO cases to date. We provided a
structured overview of the characteristic
presentation, lesion localization, timing, and
reported course of this phenomenon. Its
limitations arise from the evidence base and
from the review process. The evidence base is
small and unevenly reported: motor severity,
imaging detail and follow-up were documented
inconsistently, and lesion site was frequently
given only as a vascular territory, which
restricted anatomical coding to 27 of the 31
patients. Sex distribution, laterality, latency
and outcome are reported as observed
frequencies, without inference about sex or
hemispheric predominance. Because case reports
favor unusual or well-documented presentations,
the published literature is unlikely to reflect
either the true frequency of PBO or the range of
its outcomes. Within the review process,
inclusion was restricted to English-language
reports, which excluded three reports and may
have introduced a language bias to which a small
evidence base is particularly vulnerable; no
formal critical appraisal was undertaken,
consistent with PRISMA-ScR guidance.
-
- Future studies should emphasize prospective
case follow-up, standardized reporting, and
advanced neuroimaging approaches, such as
diffusion and functional connectivity
techniques, to better elucidate the neural
substrates of yawning-associated motor release.
While no treatments have been shown to modify
PBO, rehabilitative strategies that reinforce
voluntary motor control, such as mirror therapy,
may warrant exploratory investigation.
-
- Conclusion
- PBO is a rarely reported yawning-induced
motor phenomenon characterized by stereotyped,
involuntary limb movements associated with focal
lesions affecting distributed voluntary
motor-control networks, frequently involving
subcortical motor pathways. The literature
suggests a release-facilitated activation of
brainstem and extrapyramidal pathways following
loss of corticospinal control, although no
mechanism has been established. Clinically,
recognition of PBO is important to avoid
misdiagnosis as focal seizures or
misinterpretation as evidence of returning
volitional movement. Improved recognition and
systematic reporting will be critical to
improving understanding of PBO mechanisms,
prognosis, and likely implications for
neurorehabilitation.
|
|