Abstract

Introduction A 38 year‐old right‐handed female is a fully functional teacher with past medical history of hypertension, type II Diabetes Mellitus, polycystic ovarian syndrome, and infertility. She presented to our emergency department (ER) on the same day she was discharged twice from a local ER for acute onset persistent non‐fluctuating left‐sided weakness and painful bilateral leg spasms that woke her from sleep. Patient had pertinent exam findings of moderate pharyngeal dysarthria, mild right nasolabial flattening, mild weakness of left upper extremity (LUE), and stereotyped, painful tonic extensor posturing of the bilateral lower extremities associated with back arching and extensor response of bilateral toes. NIH Stroke Scale was 10. Methods We conducted a review of patient clinical documentation. Results MRI Brain showed anterior asymmetric bilateral pontine ischemic strokes at the ventral pontomedullary junction. MRA brain with black blood sequencing revealed multifocal vasculopathy at the right V4, mid‐basilar and left M1 segments. An angiogram showed Moya‐moya type collaterals. Tonic posturing and spasms persisted for several hours requiring muscle relaxants and benzodiazepines for symptomatic management. Unfortunately, the patient had worsening LUE weakness, inability to swallow and was found to have total vocal cord paralysis. She was intubated for airway protection and after failing extubation required tracheostomy and percutaneous gastrostomy placement. Initial workup revealed poorly controlled hyperlipidemia (LDL 162) and diabetes (A1c 8.7%), CRP 7–9, hypercoagulable panel and transthoracic echocardiogram were unremarkable. Lumbar puncture was also unremarkable (CSF TNC 2, RBC 3, glucose 116, protein 35, Enterovirus and HSV 1,2 PCR, Streptococcus antigen and VDRL were negative). Anticoagulation was started for an incidental right lower lobe subsegmental pulmonary embolism. Ultimately, the patient was discharged to inpatient rehabilitation (IPR) with a Modified Rankin Scale (mRS) of 4, on day 19th of hospitalization with some improvement in oral intake and decannulation of tracheostomy. Conclusions Movement disorders caused by strokes have been described in the literature. In their majority, they are secondary to a supratentorial injury. There have been some cases published of infratentorial, unilateral lesions that have caused different types of involuntary movements. More specifically, two papers described tonic spasms seen in pontine strokes. To our knowledge, this is a novel description of a case of bilateral pontine ischemic stroke that causes painful tonic spasms associated with decerebrate rigidity or posturing. Our hypothesis is that given the localization of the strokes in the anterior area of the inferior segment of the pons there may be involvement of the corticospinal, corticobulbar, and rubrospinal tracts which may be responsible for this presentation. Posterior circulation strokes can be missed about 9–14% of the time, possibly due to atypical presentations. We believe that presenting this case can help to improve the current available literature on this topic.

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