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
18 novembre 2023
 Neurology: Clinical Practice
Parakinesia Brachialis Oscitans
in a Patient With a First Manifestation
of Multiple Sclerosis
Manuel Salavisa, Bader Mohamed, Kimberley Allen-Philbey,
Andrea M. Stennett, Thomas Campion, Klaus Schmierera
Centre for Neuroscience (MS, BM, KA-P, KS), Surgery and Trauma, The Blizard Institute, Queen Mary University of London


Tous les articles sur la parakinésie brachiale oscitante 
All articles about parakinsia brachialis oscitans
Parakinesia brachialis oscitans (PBO) is the involuntary movement of an otherwise paretic upper limb triggered by yawning. We describe the first case of PBO in a patient with a first manifestation of tumefactive multiple sclerosis (MS).
A 35-year-old man presented to the emergency department with a first episode of generalized seizure. Neurologic examination revealed left-sided spastic hemiparesis, predominantly affecting his upper limb. Brain MRI showed a tumefactive right hemisphere lesion consistent with demyelination. CSF did not document unmatched oligoclonal bands.
Two weeks after admission and, despite being unable to voluntarily raise his left arm, the patient noticed a repeated and reproducible involuntary raise of this limb upon yawning, consistent with PBO. In the following weeks, the phenomenon diminished both in fre- quency and movement amplitude alongside motor recovery. An MRI performed 2 months later showed progression of the demyelinating lesion load and confirmed a diagnosis of MS.
PBO is an example of autonomic voluntary motor dissociation and reþects the interplay between loss of cortical inhibition of the cerebellum in the setting of functional spinocerebellar pathways. Clinicians should be aware of this transient phenomenon which should not be mistaken as a chronic movement disorder or focal epileptic seizures.

Recognizing the pattern of limb movement in the context of yawning as its predicable trigger is key in diagnosing PBO and sets it apart from potential confounders such as focal epileptic seizures. PBO may arise from any structural lesion disrupting descending cortico-ponto-cerebellar tracts in the setting of preserved spino- cerebellar pathways.
La parakinésie brachialis oscitans (PBO) est le mouvement involontaire d'un membre supérieur parétique déclenché par un bâillement. Ces auteurs décrivent le premier cas de PBO chez un patient présentant une première manifestation de sclérose en plaques (SEP) tumorale.
Un homme de 35 ans s'est présenté aux urgences pour un premier épisode de crise épileptique généralisée. L'examen neurologique a révélé une hémiparésie spastique du côté gauche, affectant principalement le membre supérieur. L'IRM cérébrale a montré une lésion tumorale de l'hémisphère droit correspondant à une démyélinisation. Le LCR n'a pas révélé de bandes oligoclonales.
Deux semaines après son admission et bien qu'il soit incapable de lever volontairement son bras gauche, le patient a remarqué une élévation involontaire répétée et reproductible de ce membre lors d'un bâillement, ce qui correspond à la PBO. Au cours des semaines suivantes, le phénomène a diminué à la fois en fréquence et en amplitude de mouvement, parallèlement à la récupération motrice. Une IRM réalisée deux mois plus tard a montré une progression de la charge lésionnelle démyélinisante et a confirmé le diagnostic de SEP.
Le PBO est un exemple de dissociation motrice volontaire autonome et reflète l'interaction entre la perte d'inhibition corticale du cervelet dans le cadre de voies spinocérébelleuses fonctionnelles. Les cliniciens doivent être conscients de ce phénomène transitoire qui ne doit pas être confondu avec un trouble chronique du mouvement ou des crises épileptiques focales.
In some cases of hemiplegia, the initiation of yawning is associated with an involuntary upward movement of the otherwise paralyzed arm, a phenomenon described in the medical literature as parakinesia brachialis oscitans.
Previously, this rare phenomenon has been essentially reported in the context of stroke, namely those affecting the internal capsule region. We report a case of parakinesia brachialis oscitans in a patient presenting with a pseudotumoral form of multiple sclerosis.
Case Report
A 35-year-old man with a medical history of autism spec- trum disorder and mild learning difficulties was brought to the hospital by ambulance after a first episode of generalized tonic-clonic seizure. The patient recalled noticing brief spells of intermittent left arm twitching in the 3 days leading up to hospital admission, followed by brief spells of tran- sient left arm weakness, particularly affecting his grip and dexterity.
He denied concurrent headaches or any other symptoms suggestive of acute neurologic change. His family denied any change in his behavior or increased cognitive difficulties. On initial examination, he was alert and complained of severe back pain.
Neurologic examination revealed left-sided spastic hemiparesis, predominantly affecting his upper limb with a Medical Research Council (MRC) grade 3 weakness noted in left shoulder ab- duction and grade 2 in left wrist dorsiþexion. Reþexes were pronounced on the left, with extensor plantar response. The sensory and cerebellar examination results were normal, as was the cranial nerve examination. No involuntary movements or signs of epileptic activity were noted at this stage.
Because of the rapid onset of left-sided hemiparesis, stroke was suspected, and he was referred for acute CT of the head. This revealed an ill-defined right hemispheric supra- tentorial hypodensity with mild rim enhancement after contrast administration (Figure, A). A brain tumor or ab- scess was suspected, and the patient was immediately referred for a brain MRI. An EEG demonstrated focal right- sided frontal and temporal slowing with no epileptiform discharges.
MRI confirmed a 47-mm oval-shaped hyperintense lesion in the right centrum semiovale on T2-weighted scans, with incomplete (C-shaped) peripheral enhancement after gadolinium- diethylenetriamine penta-acetic acid injection (Figure, B and C). The lesion exerted subtle mass effect on the adjacent ven- tricular system. In addition, a smaller frontal juxtacortical lesion with the same characteristics was noted, both sharing a typical "central vein sign" visible on the susceptibility-weighted se- quences (Figure, D and E). Both diffusion-weighted imaging and apparent diffusion coefficient sequences were negative for brain ischemia. Spinal MRI imaging showed no signal changes within the cord (Figure, F). CSF studies revealed <1 white blood cells/mm3. Glucose (3.8 mmol/L) and protein (279 mg/L) were within normal range. Testing for oligoclonal bands (OCB) was negative in the serum and CSF. The CSF neurofilament light (NfL) chain level was significantly elevated to 2527 pg/mL (age-adjusted reference <380 pg/mL). Serum AQP4 and MOG antibodies were negative. The presentation and findings at this stage were deemed compatible with a fulminant first manifes- tation of inþammatory demyelination not fulfilling McDonald 2017 criteria for a diagnosis of multiple sclerosis (MS).
A diagnosis of clinically isolated syndrome of demyelination was made, and the patient was given oral methylprednisolone 500 mg for 5 days. He was subsequently enrolled into Attack MS, a placebo-controlled clinical trial of natalizumab within 14 days of symptom onset (NCT05418010).
Two weeks after symptom onset and shortly after discharge from inpatient admission, the patient reported that, despite being unable to hold up is left arm voluntarily, this would occur spontaneously on yawning (Video 1). He described that each episode of yawning would predictably produce an abduction movement of the arm with associated distal high amplitude postural left hand tremor, followed by a return to the resting position on yawning cessation. There was no associated left lower limb movement during these episodes. The patient was unable to reproduce the phenomenon of parakinesia brachialis oscitans (PBO) voluntarily by simulating yawning.
Over the following weeks, the patient noticed a gradual reduction in the frequency and amplitude of PBO, concurrent with an improvement of voluntary movements with his left-sided limbs. However, in the context of subacute worsening of his neurologic symptoms, PBO re-emerged. Follow-up brain MRI performed 2 months after clinical onset demonstrated new lesions accrual in a periventricular and juxtacortical distribution (Figure, G) in keeping with a diagnosis of MS. The original large right hemi- spheric lesion had reduced in size. The patient continues to be followed up in the context of his trial participation.
To the best of our knowledge, this is the first reported case of PBO in a patient with MS. Involuntary raising of an otherwise paretic arm during yawning has been described in case re- ports dating back to 1844. However, the term parakinesia brachialis oscitans was only coined by Walusinski in 2005, in a study describing 4 patients presenting with ischemic strokes, all affecting the internal capsular region.1
Our patient had several presenting features unusual for MS, including epileptic seizures at presentation, the tumefactive nature of brain lesions detected, and the absence of OCB in the CSF. These are, however, not uncommon in patients with MS presenting with tumefactive demyelination, as previously described elsewhere.2,3 Further clinical and MRI follow-up in the context of a controlled clinical trial eventually ruled out potential differential diagnoses while fulfilling the McDonald 2017 diagnostic criteria for this condition.
PBO may occur within the first day after cerebral infarction or as late as 4 months after stroke onset2 and has been observed in paretic limbs during both the þaccid and spastic stages of post- stroke recovery. These involuntary and patterned movements usually include a combination of abduction of the shoulder,
þexion of the elbow, and extension of the fingers. Variants in- clude lower limb involvement3 and associated tremor4 such as in our case. Some patients can deliberately suppress their PBO,5 which tends to disappear with recovery of motor function in the affected limb, usually within 6 months, although persistence of PBO beyond this point has been observed.3
The pathophysiology of PBO remains unclear.6,7 The most widely accepted explanation is that PBO reþects a pro- prioceptive loop activation, whereby the strong contraction of respiratory muscles during yawning generates a pro- prioceptive signal through the spinocerebellar tract that reaches the medullary lateral reticular nucleus. This in turn induces a motor signal through extrapyramidal pathways to cervical anterior horn cells, resulting in the involuntary movement of the affected upper limb. The interruption of the cortico-pontocerebellar pathway is thought to be es- sential for the manifestation of PBO because it enables proprioceptive loop disinhibition.
Although previously reported in the context of stroke only, our case demonstrates that PBO may also occur with large inþammatory demyelinating lesions. Mechanistically, we hypothesize that our patient's tumefactive lesion in the right hemisphere temporarily disrupted cortico-ponto-cerebellar and corticospinal pathways releasing subcortical structures from cortical inhibition, thereby enabling the proprioceptive loop disinhibition necessary for the spontaneous yawning- associated upper limb movement to be initiated through intact spinocerebellar pathways.
PBO is clinically relevant because it can potentially be mis- taken for a focal epileptic seizure, particularly in an acute setting. Recognizing the highly stereotyped limb movement pattern in the context of yawning as its predicable trigger is key in diagnosing this condition.
1. Walusinski O, Quoirin E, Neau JP. La parakin´esie brachiale oscitante [Parakinesia
brachialis oscitans]. Rev Neurol (Paris). 2005;161(2):193-200. doi:10.1016/s0035- 3787(05)85022-2
2. Li J-Y, Wu L, Sun L-Q, Xiong J-M. Clinical and radiological characteristics of hemiplegic arm raising related to yawning in stroke patient. Med J Chin PLA. 2018; 43(3):229-233. doi:10.11855/j.issn.0577-7402.2018.03.09
3. de Lima PM, Munhoz RP, Becker N, Teive HA. Parakinesia brachialis oscitans: report of three cases. Parkinsonism Relat Disord. 2012;18(2):204-206. doi:10.1016/ j.parkreldis.2011.09.020
4. Farah M, Barcellos I, Boschetti G, Munhoz RP. Parakinesia brachialis oscitans: a case report. Mov Disord Clin Pract. 2015;2(4):436-437. doi:10.1002/mdc3.12234
5. Chowdhury A, Datta AK, Biswas S, Biswas A. Parakinesia brachialis oscitans &endash; a rare post-stroke phenomenon. Tremor Other Hyperkinetic Mov (N Y). 2022;12(1):6. doi: 10.5334/tohm.680
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(5):495-499. doi:10.1046/j.1468- 1331.2003.00599.x
7. Walusinski O, Neau JP, Bogousslavsky J. Hand up! Yawn and raise your arm. Int J Stroke 2010;5(1):21-27. doi:10.1111/j.1747-4949.2009.00394.x