ILLUSTRATIVE CASE

Vertebral Artery Dissection Causing Stroke After Trampoline Use Courtney S. Casserly, MD,* Rodrick K. Lim, MD, FRCPC,† and Asuri Narayan Prasad, MBBS, MD, FRCPE, FRCPC† Objectives: The aim of this study was to report a case of a 4-year-old boy who had been playing on the trampoline and presented to the emergency department (ED) with vomiting and ataxia, and had a vertebral artery dissection with subsequent posterior circulation infarcts. Methods: This study is a chart review. Results: The patient presented to the emergency department with a 4-day history of vomiting and gait unsteadiness. A computed tomography scan of his head revealed multiple left cerebellar infarcts. Subsequent magnetic resonance imaging/magnetic resonance angiogram of his head and neck demonstrated multiple infarcts involving the left cerebellum, bilateral thalami, and left occipital lobe. A computed tomography angiogram confirmed the presence of a left vertebral artery dissection. Conclusions: Vertebral artery dissection is a relatively common cause of stroke in the pediatric age group. Trampoline use has been associated with significant risk of injury to the head and neck. Patients who are small and/or young are most at risk. In this case, minor trauma secondary to trampoline use could be a possible mechanism for vertebral artery dissection and subsequent strokes. The association in this case warrants careful consideration because trampoline use could pose a significant risk to pediatric users. Key Words: stroke, pediatric stroke, vertebral artery dissection, trampoline (Pediatr Emer Care 2015;31: 771–773)

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n unwell child with vomiting is a common reason for presentation to the emergency department. In this scenario, a comprehensive history and neurological examination revealed truncal ataxia. We report the case of a child who presented to the pediatric emergency department (ED) with vomiting, truncal ataxia, and recent history of trampoline use. In this case, imaging was clearly indicated and identified an unexpected diagnosis.

CASE A 4-year-old boy presented to the pediatric ED with complaints of gait unsteadiness for 4 days. On day 1, he vomited repeatedly and had taken to bed. His family had assumed that he had the flu. He stayed in bed for an entire weekend, and the vomiting persisted. On day 3, his mother suggested that he get out of bed and go to school. When he attempted this, he was unsteady on his feet and was stumbling around “as if he was drunk.” He denied vertigo, tinnitus, or hearing loss. His mother was concerned and brought him to the ED. On direct questioning, he did report having a low-grade holocephalic headache that had been present for the last 3 weeks. There was no history of fever, and he had no sick contacts. There was no neck pain and no known history of head or neck trauma. However, his family had just purchased a full-size From the *University of Western Ontario; and †Children's Hospital at London Health Sciences Centre, Western University, London, Ontario, Canada. Disclosure: The authors declare no conflict of interest. Reprints: Courtney S. Casserly, MD, c/o Lisa Baker-Spiller, Department of Neurological Sciences, Schulich School of Medicine and Dentistry, University Hospital, 339 Windermere Rd, London, Ontario, N6A 5A5 Canada (e‐mail: [email protected]). Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0749-5161

trampoline, and he and his older siblings, ages 17 and 20 years, had engaged in play on it on 2 occasions over the preceding 2 days. He was the product of a normal pregnancy and delivery, was developmentally normal, and had no personal or family history of a neurological disorder, hypercoagulable state, or connective tissue disorder. On examination on admission, he was alert and appropriate. On general inspection, the patient was not dysmorphic and had a normal upper segment to lower segment ratio. His blood pressure was 130/56 mm Hg, and his heart rate was 88 beats per minute and regular; he was afebrile and had 99% oxygen saturation on room air. He had a normal fundoscopic examination with no evidence of papilledema. Cranial nerve examination was unremarkable. He had no nystagmus. He had full visual fields to confrontation testing. He had full strength in the upper and lower extremities. Reflexes were 2/2 and symmetrical at the biceps, triceps, brachioradialis, knees, and ankles, and plantar responses were down-going bilaterally. Appendicular coordination was intact (finger-to-nose, heelto-shin), although slightly slower on the left as compared with right. His gait was remarkable for a slightly wide base of support, and without support, he fell twice to the left hand side. There was no evidence of excessive joint laxity and no visual, dental, skeletal, dermatological, or cardiac abnormalities. The patient had a computed tomography head scan that demonstrated multiple small hypodensities in the left cerebellar hemisphere (Fig. 1A). The patient then had a magnetic resonance imaging (MRI)/magnetic resonance angiogram of the head and neck, which demonstrated multiple foci of diffusion restriction on MRI diffusion-weighted imaging within the posterior circulation including the left cerebellum, left brachium pontis, thalami, and the right medial occipital lobe (Fig. 1B). Magnetic resonance imaging dissection sequences (fat-saturated images) demonstrated high signal within the left vertebral artery, which could represent a dissection. A computed tomography angiogram of the head was then performed, which confirmed an abnormality of the left vertebral artery at the C1 to C2 level (Fig. 1C). There was a filling defect within the lumen of the vessel as well as vessel wall thickening. This abnormality was diagnosed as a dissection with luminal thrombus. The patient also had a transthoracic echocardiogram, which was unremarkable. Over the next several days, his gait improved significantly, and he was ambulating without any assistance. His nausea and vomiting also resolved. He was started on therapeutic anticoagulation with enoxaparin for a planned duration of 3 months, with a plan to follow-up with the pediatric hematology service. He was discharged home on day 3 after admission with no clear deficits on neurological examination. To date, formal visual field testing has not been carried out.

DISCUSSION Stroke is rare in children, with an estimated incidence of 2.5 to 3.1 cases per 100,000 per year.1 However, although cervical artery dissection accounts for an estimated 2% of stroke in adults, it accounts for more than 20% of stroke in the pediatric population.1–3

Pediatric Emergency Care • Volume 31, Number 11, November 2015

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FIGURE 1. A, Computed tomography head scan showing multiple small hypodensities in the left cerebellar hemisphere. B, Magnetic resonance imaging (MRI) and angiogram of the head and neck, showing multiple foci of diffusion restriction within the posterior circulation. C, Computed tomography angiogram of the head confirming an abnormality of the left vertebral artery at the C1 to C2 level.

Dissections occur in the vertebral arteries because the interosseous portion has limited mobility within the transverse process of the cervical vertebrae. Abrupt hyperextension and rotation caused by minimal trauma can tear the vessel wall. Most vertebral artery dissections occur at the level of C1 to C2, where there is rotation of atlantoaxial joint and minimal bony protection present as compared with the lower cervical column.1 A thrombus forms at the site of the dissection, leading to downstream artery-to-artery embolism or complete vessel occlusion.4 These dissections may occur secondary to trauma or may be “spontaneous.” In the pediatric literature, a history of trauma, minor or major, is reported in approximately 50% to 68% of children with vertebral artery dissection.5,6 This figure is somewhat smaller in adults, where the incidence of trauma resulting in dissection is estimated at closer to 25% to 50%.3,7,8 Trauma can be very minor, such as coughing or sneezing.9 In the remaining spontaneous cases, an underlying genetic or structural abnormality, such as a connective tissue disease, is identified in less than 1% to 5% of patients.10 It remains unclear whether in these “idiopathic cases,” a history of minor trauma may exist. In the case of a pediatric spontaneous dissection, is it impossible that the insult is so minor that it is forgotten or goes unnoticed?1 Are young children unable to accurately report the insult? When flexion/extension cervical spine x-rays were performed on 10 pediatric patients with spontaneous vertebral artery dissections, 8 were found to have subluxation at C2/ C3 at extremes of physiological motion.5 This may represent an

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underlying mechanical or musculoskeletal laxity that predisposes some pediatric patients to develop a dissection secondary to minor trauma. It remains unclear whether this type of cervical ligamentous laxity is more common in children. Thrombosis of the vertebral artery, or artery-to-downstream artery embolism, can lead to stroke. The classic Wallenberg or lateral medullary syndrome may be seen (crossed sensory findings, Horner syndrome, dysarthria, vertigo). This syndrome is uncommonly reported in children.8 However, in both adults and children, infarcts from vertebral artery dissection with subsequent infarction can present with any combination of vertigo, nausea and vomiting, dysarthria, dysphagia, hiccups, hemiparesis, ataxia, and seizure.8,11 Although most adults with vertebral artery dissection will present with pain, pain is a less common presenting feature in pediatric patients (headache 50%, neck pain

Vertebral Artery Dissection Causing Stroke After Trampoline Use.

The aim of this study was to report a case of a 4-year-old boy who had been playing on the trampoline and presented to the emergency department (ED) w...
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