Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal

mystery of yawning 











mise à jour du
1 janvier 2022
Parakinesia Brachialis Oscitans:
Old Sign, New Findings
Isis Claire Z.Y. Lim, Shermyn Neo
Department of Medicine, YongLoo Lin School of Medicine,
National University of Singapore (I.C.Z.Y.L.).
Department of Neurology, National Neuroscience Institute, Singapore (S.N.).


Tous les articles sur la parakinésie brachiale oscitante 
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A65-year-old male smoker with a history of hypertension and hyperlipidemia, presented within 3 hours of onset of left-sided hemiplegia, dysarthria, facial droop, and hemiataxia. His National Institutes of Health Stroke Scale score was 7, and a non contrast computed tomography of his brain was normal. He was treated with intravenous r-tPA (recombinant tissue-type plasminogen activator) 3.5 hours from onset. Multiphasic computed tomography angiography did not reveal any large vessel occlusion. Despite treatment, his hemiplegia worsened, resulting in a 2 point increase in National Institutes of Health Stroke Scale 2 hours post-r-tPA administration.
Magnetic resonance imaging confirmed an acute infarct in the right corona radiata and internal capsule without hemorrhagic conversion. The stroke work-up was significant for LDL-C (low-density lipoprotein cho- lesterol) of 162 mg/dL, hemoglobin A1c of 5.8%, and unremarkable echocardiography and telemetry.
Fourteen hours post-r-tPA, the patient reported that he was able to lift his left paretic arm off the bed, but only when yawning. He demonstrated this by simulating a yawn, which resulted in antigravity left shoulder abduction. The simulated yawn generated a smaller amplitude upper limb movement compared with an involuntary one (Video S1), and he had no control over the direction and amplitude of the movement. The arm returned to its original position on the bed at the end of each yawn. There were no associated lower limb movements during these episodes.
He received dual antiplatelet therapy and a course of rehabilitation, with improved National Institutes of Health Stroke Scale of 3 at 3 months. Power had improved to 3+ in the left upper limb and 4+ in the left lower limb. The involuntary movement in his left arm with yawning gradually disappeared with recovery of motor power.
The involuntary antigravity movement of an otherwise plegic arm during yawning has been described in case reports as early as 1844, and the term parakinesia brachialis oscitans (PBO) was first coined by Walusinski.1
Described in both the flaccid and spastic phases of poststroke recovery, the onset of PBO is variable and can occur fromwithin1 day of the infarct to as late as 4 monthsafter.2 The majority of cases report shoulder abduction occurs exclusively at the onset of a yawn. The arm then returns to a resting position as the yawn subsides.1,3 While PBO usually involves the upper extremity, lower extremity movements have also been described.3,4 Furthermore, PBO can be unpleasant as some patients find it distressing as it can give them a false sense of hope.5
PBO is thought to be a form of parakinesia as there appears to be an automatic-voluntary dissociation, whereby voluntary movement of the paretic limb is not possible but can be triggered by yawning, an automatic activity. Another classic example of automatic-voluntary dissociation is the Foix-Chavany-Marie syndrome, where biopercular lesions lead to the loss of voluntary movements of the facial, pharyngeal, lingual, and masticatory muscles. However, movements in these muscles can be triggered by emotions through the activation of alternative pathways from the amygdala and lateral hypothalamus to
Although various articles have proposed different mechanisms for this phenomenon, the prerequisite condition for PBO seems to be consistent, it requires an interruption of the corticospinal and corticopontocerebellar pathways, and the preservation of spinocerebellar pathways. Interruption of the corticopontocerebellar pathway allows the release of subcortical structures from cortical inhibition, while preservation of spinocerebellar pathways allow phylogenetically primitive structures to modulate movement in response to yawning. Most commonly, the lesion responsible for PBO is found at the level of corticopontine pathway where it passes through the internal capsule. Distal cortical lesions without the involvement of the corticopontine pathway do not cause PBO as there is no interruption of cortical modulating inhibitory influence on the cerebellum and spinal motor neurons.1
Two Main Theories Have Been Proposed for the Pathophysiology of PBO
1. Emotional motorsystem: A distinct set of descending fiber tracts within the brain stem separate from the pyramidal tracts, is proposed to facilitate an integrated discharge of the bulbar reticular formation in response to an emotional state. In this theory, yawning is thought to represent a somatic manifestation of a disinterested emotional state. During a yawn, there is co-activation of bulbar and motor neurons in the brain stem, resulting in stretching movements in the upper limb via intact reticulospinal tracts.6
2. Proprioceptive loop theory: The theory proposes that the strong contraction of respiratory muscles during a yawn sends a proprioceptive signal antidromically to the anterior spinal horn, cerebellum, and finally the lateral reticular nucleus in the medulla via the ventral spinocerebellar tract. A motor signal from the lateral reticular nucleus is then formulated in response and travels through the extrapyramidal pathways of the cerebellum, back to the anterior horn cell from C4 to C8, resulting in the involuntary movement of the paralyzed upper limb. In this case, yawning is thought to be an exteriorization of a homeostatic arousal mechanism and is frequently observed poststroke. A limitation of this theory is that it does not explain the lower limb movements observed in some case reports.1 Our patient_s ability to trigger the involuntary movement in his plegic arm with a simulated yawn supports the proprioceptive loop theory.
PBO has been observed in both ischemic and hemorrhagic infarcts, and in other nonvascular neurological
conditions like the bulbar form of amyotrophic lateral sclerosis and brain stem tuberculoma.2 Clinically, this phenomenon is not uncommon, occurring in up to 78.6% of anterior circulation strokes.4 While there are several case reports of PBO in posterior circulation infarcts in the literature,2 it is unclear why it is less commonly reported in infarcts in this territory. A plausible explanation is that spinocerebellar pathways are often disrupted in these cases and, therefore, the prerequisite conditions for PBO are not met. The large muscle bulk in the lower limbs may account for less frequent involvement in PBO.4
The neurophysiology of yawning is not well understood. It is a stereotyped phenomenon, observed in both mammalian and nonmammalian animals and is sometimes accompanied by elevation of the arms (pan- diculation). The hypothalamic paraventricular nucleus controls the lower motor centers in the brain stem that are involved in yawning, and stimulation of its oxytocin neurons by dopamine or its agonists (eg, apomorphine injections) triggers yawning and erection.7
Excessive yawning poststroke is a well-recognized clinical sign&emdash;it may herald brain stem ischemia with dener- vation hypersensitivity of a putative brain stem yawn center in posterior circulation infarcts,8 and in anterior circulation infarcts with insula and caudate nucleus lesions, the severity of yawning correlates with clinical (National Institutes of Health Stroke Scale) and radiological (apparent diffusion coefficient values) markers of stroke severity.9 A hypothesis that yawning switches the default-mode network to the attentional network by activating cerebrospinal fluid flow and clearing somnogens from the brain and reducing sleepiness has been proposed as part of the aforementioned homeostatic arousal mechanism.10
Current studies suggest that the increased brain stem monoaminergic activation associated with yawning permits movements that are otherwise absent in those with corticospinal tract lesions8; however, the use of dopaminergic medications has not proven effective in motor rehabilitation poststroke. It does raise the possibility that in patients with intact spinoreticulocerebellar pathways (of which PBO may be a clinical indictor of), the use of dopaminergic agents may aid in motor rehabilitation. A previous study did not identify a prognostic value for PBO in recovery; although 32/40 stroke patients had PBO, and only 2 attained useful hand function while 25% remainedplegic.6
In this case report, we present a case of post ischemic stroke PBO, with a patient who was able to trigger involuntary movements in an otherwise plegic arm by simulating a yawn. This provides further evidence for the proprioceptive loop theory to explain the pathophysiology behind this unique condition. We propose that fur- ther studies can be done to investigate how to fully use the potential of this neurological pathway to initiate early rehabilitation for patients poststroke, and evaluate the clinical outcomes of patients who exhibit this phenomenon. Finally, neurologists should be familiar with involuntary movements that can occur after a stroke, so as to not mistake them for abnormal movement disorders and subject patients to unnecessary investigations.

• Movement of the paretic arm with yawning poststroke can occur in patients with lesions along the pyramidal tract (most commonly in the internal capsule or the pons). It should not be mistaken for an abnormal movement disorder.
•PBO is an example of an autonomic-voluntary dissociation. The loss of cortical inhibition of the cerebellum
via the corticopontocerebellar pathway, while the spinoarcheocerebellar pathway remains functional, explains the phenomenon.
• This phenomenon fades as the patient progresses in their motor recovery.

1. Walusinski O,Neau J P, Bogousslavsky J. Hand up! Yawn and raise your arm. Int J Stroke.2010;5:21&endash;27.doi:10.1111/j.1747-4949.2009.00394.x
2. Li J-y, Wu, L, Sun, L.-qing,Xiong, J.-mei. Clinical and radiological characteristics of hemiplegic arm raising related to yawning in stroke patient. PLMAJ Med J Chinese People_s Liberation Army.2018;43.doi:10.11855/j. issn.0577-7402.2018.03.09
3. de Lima PM, MunhozRP, Becker N, Teive HA. Parakinesia brachialis osci- tans: report of three cases. Parkinsonism Relat Disord.2012;18:204&endash;206. doi: 10.1016/j.parkreldis.2011.09.020
4. Meenakshisundaram R, Thirumalaikolundusubramanian P, Walusinski O, Muthusundari A, Sweni S. Associated movements in hemiplegic limbs during yawning. Front NeurolNeurosci.2010;28:134&endash;139. doi: 10.1159/000307095
5. Mulley G. Associated reactions in the hemiplegic arm.Scand J Rehabil Med. 1982;14:117&endash;120.
6. To_pper 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;10:495&endash;499. doi: 10.1046/j.1468-1331.2003.00599.x
7. Walusinski O. Yawning in diseases. Eur Neurol. 2009;62:180&endash;187. doi: 10.1159/000228262
8. CattaneoL, CucurachiL, Chierici E, Pavesi G. Pathological yawning as a presenting symptom of brain stem ischaemia in two patients. J Neurol Neurosurg Psychiatry.2006;77:98&endash;100. doi:10.1136/jnnp.2005.075267
9. Krestel H, Weisstanner C, Hess CW, Bassetti CL, Nirkko A, Wiest R. Insular and caudate lesions release abnormalyawning instroke patients. Brain Struct Funct.2015;220:803&endash;812. doi:10.1007/s00429-013-0684-6
10. Walusinski O. How yawning switches the default-mode network to the attentional network by activating the cerebrospinal fluid flow. Clin Anat. 2014;27:201&endash;209. doi: 10.1002/ca.22280