The involuntary movement of a paralysed
upper limb following the act of yawning was
described by Walusinski et al1 2 as parakinesia
brachialis oscitans (PBO). This under-recognised
phenomenon is scantily described in the
literature, in most cases secondary to
haemorrhagic or ischaemic stroke. The precise
physiopathology remains unclear, and from a
topographic standpoint, lesions have been
described in the brainstem or areas supplied by
the middle cerebral artery (MCA). Here we
describe a case of PBO observed during
thrombolytic therapy (TPA) in a patient with
left MCA, which resolved within 24 h, although
there was no motor neurological improvement.
CASE PRESENTATION A 60-year-old man,
right-handed, presented with sudden onset of
aphasia and right-sided weakness. Medical
history was positive for hypertension and
myocardial infarction 10 years before. Brain CT
scan was normal upon admission. Within 4 h of
symptom onset, intravenous TPA was initiated.
During the infusion and the following hours, the
patient was drowsy and yawned deeply in an
abnormally frequent and repeated way. At the
beginning of each yawn, the right arm
involuntarily rose with flexion of the elbow and
adduction, remaining still for a couple of
seconds, and slowly returning to its primary
rest position. During the initial 24 h, this
phenomenon occurred repeatedly, disappearing
thereafter. After TPA infusion, the neurological
deficits remained unchanged with mild
improvement during the following days. A
follow-up CT scan, performed 24 h after
treatment revealed a large ischaemic stroke in
the left MCA territory (figures 1 and 2).
INVESTIGATIONS
Additional investigations included
transthoracic, transoesophageal and carotid
Doppler ultrasound, showing no significant
abnormalities. Transcranial Doppler ultrasound
scan showed subtle asymmetry of velocity between
the MCA (R>L).
OUTCOME AND FOLLOW-UP
The patient was discharged with NIHSS 15,
reaching a score of 12 on clinical follow-ups.
Since then, no further episodes of PBO have been
detected. DISCUSSION Since the early 19th
century, a few cases of movements of a paralysed
arm during yawning have been reported; however,
the term PBO has only recently been coined.1
'Parakinesia' is defined as an abnormal
involuntary movement that replaces a normal
movement. Differing from synkinesia, which
involves involuntary muscle contraction that
accompanies voluntary movements, parakinesia
refers to a reflex movement.1 2 Parakinesia may
appear right after the event's onset, during the
flaccid phase, or later, during the spastic
phase, while synkinesia occurs more often during
the spastic phase. The aetiology of the motor
deficit is variable in the literature, including
ischaemic or haemorrhagic stroke, amyotrophic
lateral sclerosis or brainstem tuberculoma. Two
main locations are closely linked to this
abnormal movement: a lesion in the MCA
territory, leading to infarction in the internal
capsule and basal ganglia or a pontomedullary
lesion.
Classically, yawning is thought to recruit
specific control systems, including the
paraventricular nucleus of the hypothalamus, the
locus coeruleus and reticular activating system
and the brainstem including the nuclei of
cranial nerves (V, VII, IX, X, XI, XII and
C1&endash;C4). Neocortical brain areas possibly
have an inhibitory effect on these systems. In
the case of specific MCA strokes, these systems
become abnormally excitable, leading to
repetitive yawning.3 In addition, Walusinski et
al4 also argued that a lesion in the internal
capsule affecting inhibitory pathways liberates
certain subcortical structures that coordinate
the massive inspiration of yawning and the motor
control associated with quadrupedal
locomotion.
To date, there have been no cases of PBO
reported during thrombolysis. Our patient
presented an infarction of the MCA territory, a
location that is known to be associated with
PBO. The phenomenon was short-lived (not
observed after the first 24 h) with no
significant improvement of hemiplegia. It is
possible that the relatively short duration of
PBO was influenced by thrombolysis. Lesions
generally reflect substantial disruption of
energy metabolism, which leads to irreversibly
damaged tissue. But the mechanisms also generate
oxygen radicals and provoke changes in calcium
homeostasis or adenosine, during the
thrombolysis itself. This metabolic process may
secondarily alter the arousal response to
stimulation of the cortex by the reticular
activating system of the brainstem, which can
trigger recurrent yawning. The literature
describes additional cases in which the duration
was not specifically described.1 4&endash;6
Further studies are necessary to determine the
exact physiopathological basis involved in PBO
during stroke and the implications of
thrombolytic therapy.
Blin O, Rascol
O, AzulayJ, Serratrice G, Nieoullon A. A
single report of hemiplegic arm stretching
related to yawning: further investigation using
apomorphine administration. J Neurol Sci
1994;126(2):225-7.
Topper
R, Mull M, Nacimiento W. Involuntary
stretching during yawning in patients with
pyramidal tract lesions: further evidence for
the existence of an independent emotional motor
system. Eur J Neurol 2003;10(5): 495-9.
