We report the case of a previously healthy 10-year-old boy who developed acute neurological symptoms consistent with SCIWORA during taekwondo training. Notably, this case was characterized by lesions in both the medulla and cervical spinal cord, accompanied by severe autonomic dysfunction.

During the training session, the patient complained of dizziness and headache, prompting staff to move him to the side of the studio for rest. Approximately 20 minutes later, he experienced numbness in both his hands and legs, again accompanied by dizziness. Emergency medical services were summoned. Upon arrival, paramedics found the patient apneic and bradycardic, with a heart rate of approximately 30 bpm. Manual ventilation was initiated with an Ambu bag, and he was transported to the emergency department (ED).

Although the taekwondo training involved forward rolls and handstands, these activities were not performed immediately before symptom onset. According to his mother, the patient had fallen onto a mat 3 days prior, sustaining only a minor facial abrasion. On physical examination in the ED, no external injuries were identified. His past medical history was unremarkable, and there was no family history of stroke.

In the ED, the patient was intubated and placed on mechanical ventilation. Despite regaining consciousness, he exhibited complete motor paralysis (0/5 strength) and sensory loss in all four limbs and remained unable to breathe spontaneously. Laboratory investigations, including vasculitis panels, coagulation studies, and a cardiac workup, yielded unremarkable results. An emergent computed tomography (CT) angiogram and perfusion imaging of the head and neck were also unremarkable.

However, diffusion-weighted imaging (DWI) revealed a focal area of restricted diffusion in the medial medulla (Fig. 1A), corresponding to a very subtle hypointense lesion on the T1-weighted sagittal view (Fig. 1B). Spinal magnetic resonance imaging (MRI) demonstrated subtle T2 hyperintensity along the anterior spinal cord from C2 to C5 (Fig. 2A). Follow-up DWI (Fig. 1C) and limited spinal MRI (Fig. 2B and C) on hospital day 3 showed increased signal intensity with diffuse edema involving both the medulla and cervical spinal cord, as well as ligamentous swelling. Magnetic resonance (MR) angiography did not reveal arterial occlusion or dissection. The patient was admitted to the intensive care unit (ICU) and received high-dose intravenous methylprednisolone (1 g/day) on hospital days 1 and 2, followed by a tapering regimen. A cervical collar was applied for immobilization.

The patient exhibited multiple autonomic disturbances:

(1) Respiratory dysfunction: Persistent respiratory failure required prolonged mechanical ventilation, and a tracheostomy was performed on hospital day 15. The respiratory insufficiency was attributed to diaphragmatic paralysis involving the C3-C5 spinal segments and/or medullary injury.

(2) Thermoregulatory instability: Despite resolution of initial aspiration pneumonia, fevers exceeding 39°C persisted for several weeks. Intravenous antipyretics and external cooling measures were required for nearly a month. Laboratory findings supported the diagnosis of central fever secondary to hypothalamic dysregulation following cervical cord injury [7].

(3) Cardiovascular instability: Sinus bradycardia and hypotension were noted, particularly during nighttime sleep in the first week. Heart rates dropped below 40 bpm without hemodynamic compromise. Cardiology evaluation excluded structural heart disease and arrhythmia, and the findings were attributed to autonomic dysfunction. The patient’s clinical course was closely monitored, with symptoms gradually resolving about 20 days after stroke onset.

(4) Gastrointestinal dysmotility: Persistent vomiting and oral intolerance were suggestive of gastric paresis. Medical management was unsuccessful, and a gastrojejunostomy was performed on hospital day 24 to facilitate enteral feeding.

Bedside rehabilitation was initiated on hospital day 24. By day 50, the patient was transferred to the general ward for continued therapy. Despite some improvement, he remained quadriplegic and ventilator-dependent at the 15-month follow-up. However, he regained the ability to eat orally and communicate using a ventilator-integrated speech system.

This case underscores the importance of considering SCIWORA in pediatric patients presenting with sudden-onset myelopathy, particularly following sports-related activities or minor trauma. A key challenge in this case was the initial diagnosis. A medullary lesion was clearly visible on brain DWI, while the spinal lesion was subtle, resulting in an initial working diagnosis of medullary infarction. The presence of a focal medullary lesion on DWI strongly suggested a primary vascular event, such as infarction from vertebral artery dissection, which can occur after minor cervical trauma. However, dedicated CT and MR angiography of the head and neck revealed no evidence of arterial occlusion or dissection. Follow-up MRI on hospital day 3 revealed pronounced spinal cord edema and ligamentous swelling, findings more consistent with SCIWORA. It is important to recognize that spinal cord and ligamentous abnormalities may not be evident on early imaging and can become apparent only on delayed studies [8]. While brainstem involvement in SCIWORA is rare, it is plausible that a single traumatic mechanism—such as a severe hyperextension or flexion-distraction injury—could cause both ligamentous and spinal cord injury as well as transient vertebral artery compression or vasospasm, resulting in ischemic injury to the medulla. We therefore propose that the entire clinical and radiologic picture is best explained by a single SCIWORA event with a rare but devastating extension to the brainstem, rather than by dual pathology.

In this patient, the extensive lesion involving both the medulla and high cervical spinal cord led to severe, multi-system autonomic dysfunction. While some degree of autonomic disturbance is expected in high cervical injuries, the constellation of severe and prolonged respiratory, thermoregulatory, cardiovascular, and gastrointestinal dysfunction observed here is rarely reported in the SCIWORA literature. Previous reports have described issues such as central fever or cardiovascular instability following cervical cord injury, but few have documented simultaneous and persistent failure of multiple autonomic domains as seen in our patient [9,10]. This case underscores the profound impact that combined medullary and high cervical cord injury can have on central autonomic control networks. The severe autonomic symptoms persisted for several weeks and required extended ICU management.

High-dose intravenous methylprednisolone was administered during the acute phase. The use of high-dose steroids in acute spinal cord injury remains controversial and lacks support from high-level evidence, especially in the pediatric population [11]. Given the absence of robust pediatric data, the decision to use methylprednisolone in this case was based on the severity of the neurological deficit, with the intention of providing possible neuroprotective benefits in a devastating clinical scenario.

Despite this therapy, the patient experienced an unfavorable outcome. This observation is consistent with existing literature, which indicates that the initial neurological status and the extent of spinal cord involvement on MRI are the most reliable predictors of prognosis [12]. On presentation, the patient had quadriplegia, complete sensory loss, and respiratory failure. Follow-up MRI demonstrated a distinct lesion extending from the medulla to the C5 level, both of which are considered markers of poor prognosis.

Although the myelopathy occurred during a taekwondo session, the absence of an immediately preceding traumatic event may have influenced the emergency physician’s decision to consult a pediatric neurologist rather than a spine specialist. Given the underlying cervical cord pathology, early involvement of a spine specialist may have been more appropriate.

While SCIWORA is more commonly seen in the pediatric population, pediatric neurologists are not spinal cord specialists and may have limited experience with this condition. As a result, diagnosis and appropriate early management can be delayed. To facilitate prompt and effective care, adherence to a clear diagnostic algorithm is essential. Ideally, MRI should be performed within 24 hours of injury to assess for parenchymal cord lesions, ligamentous injury, or epidural hematomas. If the initial MRI is negative but clinical suspicion remains high, a repeat scan within 72 hours to 7 days is recommended, as edema and other abnormalities may be delayed in their appearance [12].

Management of SCIWORA is primarily conservative, relying on strict spinal immobilization with a rigid cervical collar to prevent secondary injury. Surgical intervention should be considered in cases of clear ligamentous instability, persistent spinal cord compression, or progressive neurological deterioration despite conservative management [12]. Pediatric neurologists should maintain a high index of suspicion for SCIWORA, even in the absence of radiologic abnormalities on initial imaging. A thorough understanding of the clinical presentation and the ability to manage serious complications—particularly respiratory failure and autonomic instability—are crucial. Early recognition and interdisciplinary collaboration, including timely consultation with spine specialists, are critical to improving outcomes in these children.

This study was approved by the Institutional Review Board of International St. Mary's Hospital, Catholic Kwandong University College of Medicine (approval number: IS24RISI0034).