Article, Neurology

Backward somersault as a cause of childhood stroke: a case report of isolated middle cerebral artery dissection in an adolescent boy

Case Report

Backward somersault as a cause of childhood stroke: a case report of isolated Middle cerebral artery dissection in an Adolescent boy

Abstract

Arterial dissection is a rare but serious cause of acute childhood stroke. Here, we present the case of a 15-year- old adolescent boy, an art school student, who suddenly experienced left hemi-paralysis after performing repeated backward somersaults, diagnosed as right-sided middle cerebral artery (MCA) hyperacute infarct due to isolated MCA dissection. Middle cerebral artery dissection in childhood is rare, as in our patient; however, pediatricians and emergency physicians should take MCA dissection into consideration in the differential diagnosis when hyperdense MCA sign is detected from unenhanced cranial computed tomography of childhood and/or adolescent stroke, with a special history such as backward somersault as in this case. Besides, unenhanced cranial CT and further imaging studies, including CT angiography and magnetic resonance imaging, provide a crucial role in early diagnosis to design proper treatment of acute childhood stroke in the ED.

Acute cerebral infarction in elderly individuals is usually caused by atherosclerotic lesions. In children, mild trauma or exertion leading to cerebral arterial dissection may be responsible for Ischemic events. Isolated middle cerebral artery dissection (MCAD) has been rarely encountered, occurring particularly in chil- dren. The instances of MCAD probably have been overlooked in the presence of associated cerebral throm- bosis with infarction or hemorrhage. Here we describe the case of a 15-year-old adolescent boy who suddenly developed severe right-sided headache and left hemiplegia after practicing backward somersaults. The initial unen- hanced computed tomography (CT) scan of the brain revealed a hyperdense middle cerebral artery (MCA) sign on the right, and, unpredictably, advanced imaging studies disclosed right MCAD with hyperacute infarct in the striatal territory. Accordingly, even this is an extremely rare case; however, it is very important to distinguish cerebral artery dissection from thromboembolism because

thrombolytic or anticoagulation therapy of a thromboem- bolic episode may be harmful to MCAD.

A 15-year-old adolescent boy, an art school student, suddenly experienced acute right-sided headache and dizzi- ness followed by drowsy consciousness and left-sided weakness after practicing backward somersaults. No head injury was mentioned during this practice. Soon after, he was brought to our ED, where his vital signs were stable in terms of normal blood pressure (106/68 mm Hg), pulse rate (106 beats per minute), respiratory rate (20 beats per minute), and normal body temperature (37.2?C). On physical examina- tion, left-sided facial palsy sparing the ipsilateral orbicularis oculi, left-sided hemiplegia, and presence of ipsilateral Babinski’s sign were noted, indicating a central type of facial palsy. The laboratory tests were unremarkable, except for mild leukocytosis (11, 400 per microliter) and elevated creatine kinase (335 U/L). Unenhanced CT of the brain was performed immediately and showed increased attenuation at the proximal segment of the right MCA (Fig. 1), where focal narrowing was depicted on the CT angiography. Distal branches of the MCA were decreased in number and flow (Fig. 2). Magnetic resonance imaging (MRI) of the brain revealed a hyperAcute ischemic infarct in the posterior limb of the right internal capsule (Fig. 3). magnetic resonance angiography of the circle of Willis depicted similar findings to that on CT imaging performed minutes earlier (Fig. 4). The clinical history and imaging findings indicated dissec- tion of the right MCA at the M1 segment with hyperacute infarct in the striatal territory. We admitted the patient to the pediatric intensive care unit for Antiplatelet therapy. In the following month, the facial palsy ameliorated and the muscle power of the left extremities increased to 4. Only mild disability was left.

Middle cerebral artery dissection is exceptionally unu- sual, especially in young boys. To our knowledge, it has not been reported in the setting of a backward somersault. Unenhanced CT is commonly used for the initial neuroima- ging evaluation in the ED nowadays, because of its widespread availability and rapid acquisition time. Even the hyperdense MCA sign is sometimes false positive in asymptomatic patients with a high hematocrit or calcific atherosclerotic disease; it is usually seen in patients with thromboembolic Arterial occlusion, which results in an increased vessel attenuation value compared to the

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519.e4 Case Report

Fig. 1 Unenhanced CT image of the brain showing increased attenuation at the M1 segment of the right MCA (white arrowhead).

contralateral MCA [1]. However, it has been reported that, in a young patient with Mild head trauma, a hyperdense MCA sign indicates arterial dissection not only as a thromboem- bolic event [2].

Isolated MCAD has rarely been encountered clinically and the most reported cases were verified by autopsy [3,4]. The etiologies, clinical manifestations, natural clinical

Fig. 2 Computed tomography angiography of the brain depicting a narrowing of the right MCA at the M1 segment (black arrow) with decreasED flow and number of distal branches.

Fig. 3 Apparent diffusion map of the brain delineating a 2.4-cm low-signal area in the posterior limb of the right internal capsule, consistent with a hyperacute infarct (arrow).

course, and prognosis of MCAD remain poorly understood [5]. The most common proposed mechanism in the reported cases of MCAD is the impaction of the MCA against the

Fig. 4 Magnetic resonance angiography of the brain showing focal stenosis of the right MCA (white arrowhead) with decreased flow and number of distal branches.

Case Report 519.e5

sphenoid ridge which causes intimal tears and even rupture, after a mild head injury [3,6]. In our case, the patient had

2 clinical features suggestive of an intracranial arterial dissection. One is acute cerebral infarction; the other is severe focal headache contralateral to the side of hemiplegia. Although there was no head trauma according to the statement of the field witness, the unusual exercise of backward somersaults induced an acute decelerating force on the brain leading to the impaction of the MCA against the sphenoid ridge which might have caused the MCAD.

Focal cerebral Ischemic symptoms usually result from thromboembolism. Thrombolytic or anticoagulation therapy is usually recommended in proper clinical condition especially when CT images show hyperdense MCA sign without Intracranial bleeding. However, dissection of the cerebral artery should be considered in a pediatric patient with trauma or exertion history. In MCAD, a fragile vascular wall may be a source of future embolic event. But thrombolytic or anticoagulation therapy may be harmful in patients with MCAD due to the possibility of Hemorrhagic transformation or even dissection process progression [7]. In addition, some patients may develop a subarachnoid hemorrhage. There is still no consensus on the treatment of MCAD so far.

In conclusion, isolated MCAD should be considered in the differential diagnosis of a child with acute flaccid hemiplegia with recent head trauma, exertion, or history of an unusual exercise (ie, backward somersault) and without systemic stroke risk factors. Early investigation by CT and MRI in the ED is of great value to detect MCAD.

Ko-Chiang Hsu MD Department of Emergency Medicine Tri-Service General Hospital National Defense Medical Center

Neihu 114, Taipei, Taiwan, Republic of China

Hung-Wen Kao MD

Department of Radiology Tri-Service General Hospital National Defense Medical Center

Neihu 114, Taipei, Taiwan, Republic of China

Shyi-Jou Chen MD, PhD

Department of Pediatrics Tri-Service General Hospital National Defense Medical Center

Neihu 114, Taipei, Taiwan, Republic of China E-mail address: [email protected]

doi:10.1016/j.ajem.2007.08.028

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