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Transient Resolved Neurologic Symptoms

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A case of pediatric stroke after flipping on a trampoline

Strokes are rare in children but require a high index of suspicion given high levels of morbidity and mortality. We present the case of a healthy seven-year-old male who presented with transient neurologic deficit. Four hours later, he was noted to have right sided facial droop and extremity weakness.

Case:

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A seven-year-old male, with no past medical history, was enroute to the ED with altered mental status after playing on a trampoline.  A trauma activation was initiated, and EMS reported an Initial GCS of 3, quickly improving to an 8 and then 13.

In the ED he had age-appropriate vital signs, without fever, tachycardia, or hypertension and appeared well with normal mentation, GCS of 15. His exam showed no evidence of external trauma. On neurologic exam, he was moving all four extremities spontaneously and equally and there was no evidence of facial asymmetry. He had no tenderness or step off noted on palpation of his cervical, thoracic, and lumbar spine. He had no evidence of anterior neck trauma.

After his mother arrived, she provided additional information that he was playing unwitnessed on the trampoline doing flips.  She recounted that he came inside complaining of right eye pain and that his face appeared abnormal, with a right-sided facial droop. She denied any known head injury or fall off the trampoline. She additionally observed that he seemed to be having some difficulty walking and was not speaking normally. She reports that shortly after coming inside, he became unresponsive, and she contacted EMS.

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A CT head/brain without contrast was obtained given the history and initial concern for possible trauma. It showed no evidence of acute intracranial abnormality. Cervical spine x-rays showed no evidence of acute fracture or subluxation. Given the history, the decision was made to admit him to our trauma service for close monitoring overnight.

Four hours after initial presentation, the trauma team was called to his bedside given new onset of a right sided facial droop. His neurologic examination at that time revealed right sided facial paralysis of both the upper and lower face. His sensation was intact, and he had symmetric palate elevation and tongue was midline. His strength was decreased, 4/5, in the right upper extremity in both grip strength and elbow flexion with notable drift against gravity when extended and 4/5 in the lower extremity at the hip and knee.

He had full strength in the left upper extremity and lower extremity. He was noted to have a normal gait and appropriate reflexes at the bilateral knees and ankles. His sensation to light touch was appropriate throughout his upper and lower extremities. He was able to answer questions but with decreased fluency and had frequent slurred or unintelligible words.

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Neurology was consulted and he was given an NIH stroke scale of 7.[1]  CTA of the head and neck was obtained, which showed dissection of the left internal carotid artery with an associated filling defect of the left distal internal carotid artery and middle carotid artery. He was transferred to the PICU for treatment with systemic tPA.

The tPA was administered 0.09mg/kg push over 5 minutes, followed by an additional 0.81mg/kg dose, given over 60 minutes. The patient did have intermittent episodes of somnolence and agitation with headache during tPA administration, so the dose was held and then resumed after a CT scan showed no evidence of hemorrhage.

The morning following tPA administration, the patient had an MRI/MRA of the brain and neck was obtained as well as echocardiogram and EKG to rule out cardiac source of embolus. Laboratory evaluation for hypercoagulability screening was also obtained.

MRI/MRA showed infarction of the left basal ganglia and internal limb capsule with additional scattered small infarcts within the left MCA territory as well as persistent luminal irregularity and narrowing of the left internal carotid artery terminus and proximal M1 segment, consistent with an arterial dissection.

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Echocardiogram revealed no evidence of thrombus or intracardiac mass, no atrial shunt or evidence of depressed function. A cerebral angiogram was obtained, which showed a left M1 proximal dissection flap with occlusion of the left M2 superior division. 24 hours after tPA administration, the patient was started on 81 mg aspirin daily with plans for at least a three-month course. Thrombophilia work up done was notably negative.

During his hospitalization, he had gradual return of function. He was assessed by the inpatient rehabilitation service while admitted with plans to continue physical therapy, occupational therapy, and speech therapy after discharge. He spent five days admitted to the hospital.

At the time of discharge, his speech was noted to be fluent and while he was still noted to have some facial asymmetry at rest, there was improvement in facial motor function on the right. He was noted to continue to favor his left side with decreased spontaneous movement on the right but strength in his right upper and lower extremity had improved, although still decreased when compared to the left.  At follow up with Neurology three months later, he is doing well, and they recommend ongoing aspirin therapy until the next appointment in three months.

Discussion:

Spontaneous cranio-cervical dissection (CCAD) occurs with no known history of trauma or after minor trauma. Minor trauma is thought to include sports, chiropractic manipulation, and trampoline use. [2]

Most children with CCAD present with symptoms of an acute stroke or transient ischemic attack.[2] Spontaneous CCADs mostly present with non-specific symptoms including headache, vomiting, dizziness, and neck pain. [2]

This patient did not present with all the classical features of CCAD, however he did present with transient symptoms of eye pain, ataxia, aphasia and altered mental status at home that had resolved upon arrival to the emergency department. He did have some of the classic historical elements including elusive injury from trampoline play with reports of flipping on the trampoline. As his symptoms returned a few hours later several of them were classic for left MCA stroke involving the M1 segment, namely: aphasia and facial>arm>leg weakness.

Neurologically well appearing children presenting with historical transient resolved symptoms after mild trauma are a diagnostic and management conundrum. This differential has high morbidity including cervical artery dissection, stroke, and death. What should be done with these puzzling pediatric presentations: prolonged observation or admission with frequent neurological checks, consultation, and what imaging if any? What should be the duration or timing of these events?

While most cases of CCAD are considered spontaneous, minor trauma in a variety of sports is thought to play a role. In one study, sports were self-reported in approximately 6% of patients with cervical artery dissection, compared to 0.8% of those with ischemic stroke not attributed to cervical artery dissection.[3]

In one review of 115 case reports and case series that identified 190 patients with cervical artery dissection related to a sports injury, 44 different types of sports (basketball, vigorous exercise, trampoline use) [4,5] were thought to have a temporal relationship to injury. [4] The most commonly described sports included scuba diving, running/jogging, and golf. [4] In these cases, 48% of patients had symptoms that started during or soon after the activity; however, the remainder of symptoms were noted to be delayed with an average time of four days and up to 14 days. [4, 5] This was thought to be related to the time to full occlusion of the affected vessel4. Observational data suggest that cervical artery dissection can be caused by minor mechanical triggers, forgotten trauma and other minor triggers.

Literature review demonstrates history of either major or minor trauma in most children with CCAD, which is higher than reported numbers in adults5. The remainder are typically considered spontaneous dissections, likely because minor trauma is not reported or thought to be significant to the patient6. One proposed mechanism is hyperextension, hyperflexion, and rotation of the neck6, which is a possible mechanism in our patient given the fact that he had been doing flips.

Despite neurologic symptoms at home, our patient was asymptomatic on presentation.  Later he developed findings concerning for stroke. On initial presentation, vessel imaging was not obtained given his normal neurologic exam and a normal non-contrast head CT was reported after his initial evaluation in the trauma bay. Three hours later, CT angiography was obtained after stroke symptoms developed revealing a left carotid artery dissection.

Clear recommendations for when vessel imaging should be obtained is lacking in the pediatric population. Studies have shown that strict use of adult blunt cerebrovascular injury screening criteria, Denver and Memphis criteria (table 1), will likely lead to unnecessary imaging. [7] In one study by Mallicote, application of the Denver and Memphis criteria to their trauma patients retrospectively showed that 332 patients out of a total of 2,795 trauma patients would have met criteria for imaging with only 1 positive study (0.3%). [7] In the same paper, a retrospective chart review of pediatric trauma patients in the National Trauma Database (778,542 patients screened from 2007-2014), showed that strict utilization of the Denver criteria would have led to negative CTA in 97.4% of patients. [7]

In the same paper, they reviewed 2,136 patients found to have a blunt cerebrovascular injury (BCVI) to assess for injury patterns which might be associated with BCVI7.  They propose that imaging (CTA or four-vessel cerebral angiography) of the cerebrovascular vessels should be obtained in patients with skull base fracture, cervical spine fractures, cervical spine fracture with cervical cord injury, traumatic jugular venous injury, and cranial nerve injury. They recommend that these injuries should be considered part of the new screening criteria for BCVI7. We agree with Mallicote et al. that a multi-institutional study evaluating these risk factors as part of a screening criteria should help determine their specificity in detecting the true incidence of BCVI and effect on patient outcomes.

It is essential for providers to not dismiss transient neurological symptoms with minor pediatric trauma, without thoughtful consideration. We believe these scenarios warrant emergent consultation with neurology to determine management and disposition. Although, the literature is lacking at the time of this writing it is likely that a certain percentage will warrant specialized imaging and or prolonged observation. Further research and analysis of the above screening criteria for blunt pediatric cerebrovascular injury will guide future management.

References

  1. National Institute of Neurological Disorders and Stroke (U.S.). NIH Stroke Scale. National Institute of Neurological Disorders and Stroke. Revised October 1, 2003. Accessed July 27, 2022. https://www.stroke.nih.gov/documents/NIH_Stroke_Scale_508C.pdf
  1. Stence NV, Fenton LZ, Goldenberg NA, Armstrong-Wells J, Bernard TJ. Craniocervical arterial dissection in children: diagnosis and treatment. Curr Treat Options Neurol. 2011;13(6):636-648. Doi:10.1007/s11940-011-0149-2
  1. Engelter ST, Traenka C, Grond-Ginsbach C, et al. Cervical Artery Dissection and Sports. Front Neurol. 2021;12:663830. Published 2021 May 31. Doi:10.3389/fneur.2021.663830
  1. Schlemm L, Nolte CH, Engelter ST, Endres M, Ebinger M. Cervical artery dissection after sports – An analytical evaluation of 190 published cases. Eur Stroke J. 2017;2(4):335-345. Doi:10.1177/2396987317720544
  1. Casserly CS, Lim RK, Prasad AN. Vertebral Artery Dissection Causing Stroke After Trampoline Use. Pediatr Emerg Care. 2015;31(11):771-773. Doi:10.1097/PEC.0000000000000388
  1. Alboudi AM, Sarathchandran P, Geblawi SS. Delayed presentation of neck arteries dissection, caused by water slide activity. BMJ Case Rep. 2018;11(1):e226333. Published 2018 Dec 13. Doi:10.1136/bcr-2018-226333
  2. Mallicote MU, Isani MA, Golden J, Ford HR, Upperman JS, Gayer CP. Screening for blunt cerebrovascular injuries in pediatric trauma patients. J Pediatr Surg. 2019;54(9):1861-1865. Doi:10.1016/j.jpedsurg.2019.04.014
ABOUT THE AUTHORS

Jennifer L. Hemberg, MD is an assistant professor at Michigan State University, division of Pediatric Emergency Medicine at Helen Devos Children's Hospital in Grand Rapids, Michigan.

Matthew Steimle, DO, FAAP, is an Assistant Professor of Pediatric, University of Utah, division of Pediatric Emergency Medicine, University of Utah and is the Emergency Ultrasound Director.

2 Comments

  1. Interesting that there are “no comments,” given that I had posted comments, complete with scientific resource links. Censorship is never right folks! (and btw, it was not an anti-vac comment; just data to consider).

  2. Interesting case. Pediatric NIH of 71? I assume typo. Curious if consult was made to IR or facility capable of Mechanical Thrombectomy as the CTA sounds like there was LVO. Very little literature on LVO in Carotid dissection but there are some positive outcomes.

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