Abstract
Parakinesia Brachialis Oscitans (PBO) is a rare post-stroke phenomenon characterized by abnormal, involuntary movement in a paralyzed limb triggered by yawning. We present the case of a male patient, age 57 years, who was admitted with right hemiparesis, dysarthria, and facial weakness. Brain magnetic resonance imaging revealed an infarction in the left pons. One week following the stroke, the patient began to experience involuntary elevation of his paretic arm and, to a lesser extent, his leg, triggered specifically by yawning. Based on these observations, he was diagnosed with PBO. The characteristic movement pattern of elevation of the upper limb during yawning was consistent with the typical presentation of PBO. The patient was reassured about the benign nature of his condition and continued his rehabilitation program. This phenomenon occurs due to a dissociation between autonomic and voluntary motor control, reflecting a disruption of cortical inhibition of the cerebellum, while sparing functional spinocerebellar pathways. Given the potential for confusion with focal seizure activity, especially during the acute phase of a stroke, a high index of suspicion is necessary to distinguish PBO from other neurologic disorders. Correctly identifying PBO can guide accurate diagnosis and appropriate management preventing unnecessary investigations and facilitating better outcomes in post-stroke care.
The term parakinesia brachialis oscitans (PBO) was first introduced by Walusinski et al.,1 who described the phenomenon of abnormal, involuntary movement in a paralyzed limb triggered by yawning following a stroke. The basal ganglia and internal capsule are the primary brain areas implicated in this condition.1,2 PBO is a rare phenomenon, with only a limited number of cases reported in the literature, and several aspects of this intriguing clinical condition remain unresolved.3,4 Despite its recognition in the medical literature since the mid-1800s, PBO remains an enigma. Its pathophysiology is still hypothetical, with no consensus on whether it results from a released brainstem reflex, a disinhibited sensory-motor loop, or another mechanism entirely. The heterogeneity of lesion sites associated with PBO from the cerebral cortex to the pons adds further complexity to any unifying theory. Knowledge of its natural history is fragmentary, based almost exclusively on single case reports with limited follow-up. Consequently, clinicians lack clear guidance on management, and issues such as the necessity of counseling, the role of any pharmacological agent, or the impact on rehabilitation outcomes remain unexplored.5
Herein, we report a case of PBO following a pontine infarction and discuss the clinical features, video-e electroencephalogram (EEG) correlates, and proposed pathophysiological mechanisms. This report aims to increase clinical awareness of this phenomenon and contribute to the growing body of literature by highlighting its occurrence in a brainstem stroke, thereby expanding the spectrum of associated lesion locations.
Case Report
We present the case of a male patient, age 57 years, a smoker with a history of hypertension, who was brought to the emergency room with right-sided hemiparesis, dysarthria, and facial weakness of 12-hours’ duration. Upon initial assessment, his National Institutes of Health Stroke Scale score was 5, with right arm and leg drift, facial weakness, and dysarthria. Over the next few hours, his weakness progressed, with the right arm showing 0/5 strength, and the right leg exhibiting 3/5 strength. He was found to have flaccid paralysis of the right side, with mild dysarthria and right upper-motor neuron-type facial weakness (Video 1: Demonstrates right arm complete paralysis along with 2/5 power in right leg; available at https://youtu.be/BgmZQXQRJ-w). Magnetic resonance imaging revealed an old infarction and an acute infarction in the left pons. A computed tomography angiogram showed a faint irregularity at the basilar artery, likely due to atherosclerosis (Figure 1).
Axial Diffusion weighted magnetic resonance image shows (a) left pontine multifocal restriction; (b) corresponding high signal intensity in FLAIR sequence; (c, d) computed tomography angiogram shows faint irregularity at the basilar artery.
One week after the stroke, the patient began to notice involuntary elevation of his paretic arm and leg during yawning. The involuntary movements were stereotyped, occurring with every yawn. There was no observed variability in the pattern (shoulder abduction, elbow/finger flexion, hip flexion), although the intensity of the movement varied from one episode to the next.
These episodes were captured on video electroencephalogram (EEG), which showed the right arm lifting with elbow and finger flexion, accompanied by slight abduction, returning to the paretic position at the end of the yawn. There was also slight flexion of the right hip during yawning (Video 2 & Video 3: Demonstrate right arm lifting with elbow and finger flexion, accompanied by slight abduction, returning to the paretic position at the end of the yawn; Video 2 is available at https://youtu.be/4WUBA3uvxM4; Video 3 is available at https://youtu.be/etDXu1EtBSI). The EEG during these episodes was unremarkable, with no associated epileptiform activity associated with the arm-raising movements (Figure 2). The patient initially perceived these involuntary movements as a sign of improving weakness. We conducted a counseling session to explain that this phenomenon, while interesting, is part of the post-stroke recovery process and should not be mistaken for the restoration of true motor function. He participated in a comprehensive inpatient stroke rehabilitation program consisting of daily physical therapy (focusing on bed mobility, transfers, and gait training) and occupational therapy (focusing on activities of daily living), provided 5 days a week during his 2-week inpatient stay. His weakness showed only gradual, albeit minimal, improvement with therapy, and he continued to require assistance with activities of daily living. In addition to the National Institutes of Health Stroke Scale, functional status was assessed using the Barthel Index,6 which improved from 35/100 on admission to 45/100 at discharge, indicating severe dependency with modest gains. By 3 months, his motor power showed minimal improvement (right arm remained 0/5, right leg improved to 4/5), and his Barthel Index score was 60/100, reflecting continued severe disability but further gains in self-care. The patient was followed for 3-months post-stroke. The PBO episodes persisted throughout his inpatient stay and were still present, though with subjectively reduced frequency, at his 1-month outpatient follow-up. By the 3-month follow-up, the patient reported the movements had significantly diminished in frequency and were no longer a noticeable occurrence, with the frequency decreasing over time in parallel with the subacute phase of stroke recovery.
Video-EEG Recording During PBO. A 10-second epoch of EEG (longitudinal bipolar montage) captured during a typical PBO episode. The vertical line marks the clinical onset of the involuntary arm movement. The tracing demonstrates normal background activity with no evidence of epileptiform discharges, spike-wave activity, or electrographic seizure pattern, confirming the non-epileptic nature of the phenomenon. (A) Yawn with right sided body movement at 7:40 AM; (B) Yawn with right upper and lower limb movement at 8:01 AM.
Discussion
These involuntary movements have been described in the literature since 1844, though the term parakinesia brachialis oscitans (PBO) was first introduced by Walusinski et al.2 PBO has been observed in both the flaccid and spastic phases of post-stroke recovery. While the exact mechanism remains unclear, topographical studies suggest several brain regions may be involved, including the brainstem and areas supplied by the middle cerebral artery, particularly the internal capsule and corona radiata. In one reported case, the involuntary movement was also associated with a tremor.5 The entire movement typically lasts around 5 seconds. While PBO is most commonly observed shortly after the acute stroke (usually within the first week), late onset during the spastic phase has also been reported. There is no clear age or gender predilection, although most reported cases of PBO have involved men.7 In most instances, shoulder abduction occurs at the onset of yawning and returns to the resting position as the yawn subsides.2,3
While the upper extremity is most commonly affected, some reports also document involvement of the lower extremity.3 In addition to being potentially mistaken for a stroke-related seizure, PBO can be distressing, as it may create a false sense of hope for recovery.5 Some patients are able to intentionally suppress these movements, which generally diminish as motor function is regained in the affected limb, typically within the first 6 months. However, in some cases, PBO persists for a more prolonged period.3 While the majority of reported PBO cases have been attributed to ischemic stroke, the phenomenon has also been observed in the setting of hemorrhagic stroke, amyotrophic lateral sclerosis (ALS), and brainstem tuberculoma.1,2,7
Our findings are consistent with a recent report by Chowdhury et al.4 which also described PBO in the acute post-stroke. However, the present case offers several distinct contributions. First, the index patient in Chowdhury et al. had a middle cerebral artery territory infarct, a classic location for PBO. In contrast, our patient’s infarct was localized to the pons. This difference is clinically significant as it supports the hypothesis that disruption of the corticopontocerebellar pathway at the brainstem level is sufficient to produce the phenomenon, not just lesions in the basal ganglia or internal capsule. Second, we provide a more detailed account of the patient’s longitudinal clinical course, including specific functional outcome measures (Barthel Index) and the positive impact of targeted patient counseling, which adds practical guidance for clinicians.
The exact pathophysiological mechanism of PBO remains largely uncertain.2,7 The most commonly proposed explanation is that PBO reflects the activation of a proprioceptive loop. In this model, strong contraction of the respiratory muscles during yawning generates a proprioceptive signal, which travels via the spinocerebellar tract to the medullary lateral reticular nucleus. From there, the signal is relayed through extrapyramidal pathways to the cervical anterior horn cells, leading to involuntary movement of the affected upper limb.7 A key element in this process is the disruption of the corticopontocerebellar pathway, which results in the disinhibition of the proprioceptive loop, ultimately triggering the manifestation of PBO. Another proposed pathophysiological mechanism involves cortical damage that leads to disinhibition of subcortical structures, potentially releasing the reticular formation in the brainstem. This release may activate motor pathways, with stimuli such as yawning serving as a trigger.7 Additionally, some researchers suggest an “emotional motor system” could contribute to the movement of the paralyzed upper limb, with yawning acting as a trigger due to its association with emotional states such as drowsiness.7
Our patient developed PBO one week after experiencing a lacunar infarct in the left pons, which led to disruption of the descending pyramidal tracts. Given the location of the infarct, it is likely that the corticospinal, corticobulbar, and corticopontocerebellar pathways were affected. However, the most plausible explanation for the occurrence of PBO in this case is the preservation of the proprioceptive loop, which operates independently of these pathways. Despite the damage to the corticospinal and related pathways, the proprioceptive signal may have been able to travel through the intact spinocerebellar tract, ultimately leading to activation of the motor pathways and triggering involuntary movements. This suggests the proprioceptive loop remains functional even in the presence of significant corticospinal tract damage.
The prognosis of PBO is generally benign and self-limiting. In most reported cases, including ours, the involuntary movements tend to decrease in frequency and intensity over time, often resolving within the first 6-months post-stroke.7 This improvement may parallel the resolution of local post-stroke diaschisis or the establishment of compensatory inhibitory mechanisms. The persistence of PBO does not appear to negatively impact overall functional motor recovery, which remains dependent on the severity of the initial corticospinal tract damage.
Conclusion
A better understanding of PBO could inform rehabilitation strategies for stroke survivors, potentially by targeting and utilizing preserved extrapyramidal pathways. Neurologists should remain vigilant in recognizing these involuntary movements to prevent misdiagnosis as abnormal movement disorders, thereby avoiding unnecessary investigations and facilitating more accurate patient management.
Acknowledgments
This study made use of the computational resources and technical services of the Scientific & High-Performance Computing Center at Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia. The authors would like to acknowledge the assistance of Ms. Theophil Lorenzo in recording the video.
Footnotes
Disclosures: The authors received no financial support for the research, authorship, and/or publication of this article. The authors declare no conflicts of interest related to this work. Data will be available upon appropriate request.
Ethics Approval: The application reviewed and approved at Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia, Institutional Review Board (IRB). IRB number IRB-2024-01-678.
- Received August 31, 2025.
- Revision received March 12, 2026.
- Accepted April 8, 2026.
