In stroke patients, involuntary movements
can occur both in the acute and chronic phase.
Here, we describe one such involuntary movement
consistent with the rare phenomenon of
parakinesia brachialis oscitans (PBO). PBO has
been reported in ischaemic and haemorrhagic
strokes involving the anterior circulation;
however, this is only the second time this
phenomenon is being reported in posterior
circulation stroke in the English literature.
Chez les patients ayant subi un AVC, des
mouvements involontaires peuvent survenir tant
à la phase aiguë que à la
phase chronique. Les auteurs décrivent
ici un de ces mouvements involontaires,
compatible avec le phénomène rare
de parakinesia brachialis oscitans (PBO). Des
cas de PBO ont été
rapportés dans des accidents vasculaires
cérébraux ischémiques et
hémorragiques impliquant la circulation
antérieure. Cependant, ce n'est que la
deuxième fois que ce
phénomène est rapporté dans
les accidents vasculaires
cérébraux de la circulation
postérieure dans la littérature
Abnormal and often bizarre involuntary
movements can occur in the acute or late setting
of an ischaemic stroke. Clinicians need to be
aware of these to avoid mis- diagnosis. Here, we
present a rare phenomenon termed "parakinesia
brachialis oscitans" (PBO) in a patient with an
acute ischaemic stroke involving the
A 53-year-old woman was admitted with a
history of noticing weakness on the left side of
her body after getting up from her sleep. She
was a poorly controlled diabetic and
hypertensive. There was no past history of
stroke or transient ischaemic attacks.
On examination, she was fully conscious,
orientated and obeying commands. The language
functions were normal. There was no sensory,
motor or visuo-spatial neglect. The cranial
nerve examination showed a mild lower motor
neurone type of facial weakness on the right
side. The muscle tone on the left side was
reduced. The power in the left upper limb was
grade 1/5 and grade 0/5 in the lower limbs. The
sensory examination was normal. MRI showed an
acute infarct in the right pons and upper
medulla with restricted diffusion on
diffusion-weighted images and high signals on
the T2 and T2 FLAIR images. The CT angiogram
showed extensive intracranial atherosclerosis
with involvement of the bilateral cavernous
segments of the internal carotid arteries and
the bilateral middle cerebral and anterior
She had presented outside the window period
of thrombolysis and was conservatively managed.
On the second day after admission, the power
improved to grade 2/5 in the upper limb.
The patient also mentioned that she felt her
left upper limb was lifted up whenever she
yawned. On observing the patient, it was
confirmed that during yawning her left
upper limb was involuntarily lifted up above her
head. After the cessation of yawning, the
limb power returned to its earlier power of 2/5.
This involuntary movement occurred every time
the patient yawned. The patient's level of
consciousness was preserved before, during and
after these movements. There were no other
concomitant movements noticed either of the face
or of the lower limbs. No involuntary move-
ments were seen on the stroke-unaffected right
These findings were consistent with the rare
phenomenon of PBO, which is the involuntary
movement of a paralysed upper limb induced by
the act of yawning. During her hospital stay,
the patient continued to improve and was able to
ambulate with one person's support by 8 days.
The parakinesia was observed for 3 days and had
disappeared by the time of her discharge.
Yawning is a poorly understood phenomenon,
which has been observed even during foetal life
. It is observed not only in humans
but also in non-human primates and other
vertebrates and usually occurs after waking up
and before falling asleep. A typical yawn lasts
5 s  and consists of an initial
reflexive wide opening of the mouth accompanied
by a slow and deep inhalation through the open
mouth and nose, which is followed by a slow
expiration . During a yawn, a
reflexive retroflexion of the head and arm
elevation can occur.
The neurophysiological basis of
yawning is not well understood. The
paraventricular nucleus (PVN) of the
hypothalamus is considered as the supratentorial
control centre . The hypothalamus
exerts its influence on the lower centres
through the paraventriculo-spinal pathway. This
pathway connects the PVN and other hypothalamic
areas with preganglionic sympathetic and
parasympathetic neurones of the dorsal vagal
complex and thoracic spinal cord .
The lower centres for yawning include the
motor nuclei of the V, VII, IX, XI and XII
cranial nerves. However, there is a neocortical
control mechanism on the hypothalamic PVN for
helping us control yawning in socially
inappropriate situations. Walusinski 
in 2014 proposed an exciting new hypothesis,
according to which yawning switches the
default-mode network to the attention network by
activating cerebrospinal fluid flow, thus
clearing somnogens from the brain and reducing
Abnormal yawning can be seen in many
neurological disorders. It can be a premonitory
symptom in migraine; peri-ictal yawning
can occur in seizures; and spontaneous
yawning can be seen in persistent
vegetative state, traumatic brain injury and
brain tumours. Excessive yawning has been noted
to occur in patients with amyotrophic lateral
sclerosis (especially with bulbar-onset
amyotrophic lateral sclerosis) .
Excessive yawning can herald a
posterior circulation stroke . In
ischaemic anterior circulation strokes with
cortical dysfunction, excessive yawning has been
observed , and one possible
explanation is that the hypothalamus is released
from the neocortical control mechanism. Studies
 have shown that involvement of the
insula and caudate nucleus has the strongest
correlates for causing excessive yawing
in patients with anterior circulation strokes.
In patients with bilateral anterior opercular
syndrome (Foix-Chavany-Marie syndrome) having
paralysis of the voluntary facial and pharyngeal
innervation, yawning can occur despite weakness
In some cases of hemiplegia, yawning can
cause involuntary movement of a paralysed upper
limb. This phenomenon was termed PBO
. It has been noted in both
ischaemic and haemorrhagic strokes involving the
middle cerebral artery territory, particularly
the lenticulostriate branches . A
case of PBO in a case of right-sided pontine
infarction due to basilar artery thrombosis was
also noted .
The exact mechanism which causes this
phenomenon is not clear. Walusinski et al.
 proposed a model where the
cortico-neocerebellar tract (corticospinal and
corticonuclear pathways) of the extrapyramidal
system is damaged, which in turn disinhibits the
spino-archeocerebellar tract, enabling the
lateral reticular nucleus to fire, resulting in
motor stimulation of the arm.
To the best of our knowledge, this is only
the second case in the English literature to
report this phenomenon in a case of posterior
circulation ischaemic stroke.
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