Focal myoclonic jerks after acute pontine infarct: A rare encounter

Myoclonus involves sudden, brief, involuntary jerks and can be a manifestation of various neurological conditions, including stroke. Movement disorders arising from cerebrovascular incidents are infrequent but well-documented.[1] While the basal ganglia is associated with such disorders, myoclonus originating from pontine lesions is particularly rare. This report adds to the limited literature on myoclonus secondary to pontine infarcts. A 68-year-old man with diabetes and hypertension presented with sudden onset of episodic, brief, involuntary jerks of the left lower limb from 1 day. On examination, he was conscious with normal vitals. Neurological examination showed left upper motor neuron facial palsy and left upper and lower limb power of 4/5, with mild brisk reflex on the left side with a National Institutes of Health Stroke Scale score of 5. The patient was observed to have brief involuntary jerks of the left lower limb [Video 1A]. These movements were present at rest and were not sensitive to stimulus. The patient maintained preserved awareness during the episodes, and the movements disappeared while walking [Video 1B]. Routine blood investigations were normal. Magnetic resonance imaging (MRI) of the brain revealed acute infarct in the tight hemipontine region [Figures 1 and 2]. Electroencephalogram showed no discharges. He was treated with antiplatelet therapy and statins. Myoclonic jerks were treated with levetiracetam 1 g/day and clonazepam 0.5 mg/day. Over the next 72 hours, the jerks subsided. {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 1","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_s3uhpro0"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} Figure 1: Axial section of brain magnetic resonance imaging. Diffusion-weighted image shows diffusion restriction observed in the right hemipontine regionFigure 2: Axial section of brain magnetic resonance imaging. Apparent diffusion coefficient shows reversal in the right hemipontine regionThe frequency of post-stroke movement disorders is estimated to be between 1% and 4%. These disorders include hemichorea–hemiballism, (most commonly observed in acute stroke), dystonia, tremor, myoclonus, asterixis, myorhythmia, clonic perseveration, posturing from spasticity, and stereotypies. Various studies have reported convulsive-like movements ranging from isolated twitching/clonic movements of the extremities to generalized seizures in pontine ischemia or hemorrhage, as illustrated in Table 1.[2] Subcortical myoclonus is typically associated with lesions in the thalamus, midbrain, and pons.[1] The other unusual presentations include eight-and-half syndrome, pontine warning syndrome, locked-in syndrome, restless leg syndrome, peduncular hallucinosis, palatal myoclonus, and Ondine’s curse syndrome.Table 1: Pontine infraction and hemorrhage with convulsive-like movements (Saposnik et al., 2001)Table 2: Role of various drugs in myoclonus (Kojovic et al.,2011)The exact mechanisms behind pontine stroke-induced myoclonus are not well understood. However, the possible mechanisms include the following: Disruption of brainstem circuits: The pontine infarct likely disrupts pathways involving the dentato-rubro-olivary circuit (Guillain–Mollaret triangle), crucial for coordinating motor control, which could explain the myoclonus[3] Thalamic disinhibition: Brainstem lesions can lead to disinhibition of thalamic nuclei, resulting in increased cortical excitability and involuntary movements[4] The literature on myoclonus in brainstem infarcts is limited. Avanzini et al[5] reported intention tremors with myoclonus secondary to a thalamic angioma. Inoa et al[6]. reported a case of generalized post-stroke myoclonus following a subthalamic nucleus infarct. The effectiveness of various drugs in treating different types of myoclonus varies remarkably as illustrated in Table 2 (Supplementary material).[7] Our patient showed improvement in myoclonic jerks within 72 hours of treatment, suggesting a favorable short-term prognosis [Video 2A and B]. However, long-term management and rehabilitation are necessary to address residual deficits. {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 2","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_oovl9jjm"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} This case highlights the rarity of hyperkinetic movement disorders following a stroke, emphasizing the need to recognize myoclonus as a potential complication of pontine infarcts. Understanding the pathophysiological mechanisms can aid in accurate diagnosis and management, warranting further research to explore the relationship between brainstem lesions and movement disorders. Acknowledgement Nil. Author contribution Research project: Conception: Anish Mehta Organization: Shalini Sachin Execution: Shalini Sachin Review and critique: Manuscript preparation: Anish Mehta, Lakshmi Priya, Pradeep R, Mahendra Javali, Purushottham Acharya Ethical compliance statement The authors confirms that they have read the Journal’s guidelines on ethical publication and affirm that this work is adhering to those guidelines Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.