Dual Vascular Insult of Fibrocartilaginous Embolism and Intercostal Artery Dissection Causing Anterior Spinal Artery Infarction in a 14-Year-Old

Sep 30, 2026

Acute spinal cord infarction (SCI) is a rare, devastating cause of myelopathy in adolescents. A 14-year-old boy developed acute paraplegia about 24 hours after a minor fall with axial loading, presenting as anterior spinal artery (ASA) syndrome with profound lower-limb weakness and dissociated sensory loss. MRI showed anterior cord T2 hyperintensity consistent with ischemia. Aortic angiography demonstrated a concurrent right T10 intercostal artery dissection, supporting post-traumatic ASA infarction from synergistic fibrocartilaginous embolism and intercostal artery dissection. Treatment included neuroprotection, antiplatelet therapy, and intensive rehabilitation, leading to independent, stable gait recovery.

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Review began 11/16/2025 Review ended 11/29/2025 Published 12/10/2025 © Copyright 2025 J et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0. , which permits unrestricted use , distribution , and reproduction in any medium , provided the original author and source are credited. DOI: 10.7759/cureus.98871 Open Access Case Report Dual Vascular Insult of Fibrocartilaginous Embolism and Intercostal Artery Dissection Causing Anterior Spinal Artery Infarction in a 14-Year-Old Sreeraj J 1, Parameswaran Krishnan 1, Anand M 2 1. Neurology, Indo American Hospital, Vaikom, IND 2. Neuroradiology, Indo American Hospital, Vaikom, IND Corresponding author: Sreeraj J, [sreerajjayakumar47@gmail.com](sreerajjayakumar47@gmail.com) Abstract Acute spinal cord infarction (SCI) is a rare and devastating cause of myelopathy in adolescents. We report the case of a 14-year-old boy who developed acute paraplegia approximately 24 hours after a minor fall with axial loading. The clinical picture presented as the anterior spinal artery (ASA) syndrome, characterized by profound lower limb weakness and the pathognomonic finding of dissociated sensory loss (loss of pain and temperature with preserved proprioception) . Magnetic resonance imaging (MRI) confirmed spinal cord ischemia with T2 hyperintensity restricted to the anterior cord. A subsequent aortic angiography revealed a concurrent right T10 intercostal artery dissection, establishing a definitive structural vascular injury. Given the classic clinical presentation (rapid onset, preceding localized pain) highly characteristic of nucleus pulposus fibrocartilaginous embolism (FCE), the final diagnosis was established as post-traumatic ASA territory infarction secondary to synergistic FCE and IC artery dissection. The patient was managed with neuroprotection, antiplatelet therapy directed at the dissection, and intensive rehabilitation. He achieved a remarkable recovery, ultimately regaining an independent and stable gait pattern. This case highlights the complexity of traumatic spinal vasculopathy and the importance of recognizing dual mechanisms of injury. Categories: Neurology, Emergency Medicine, Internal Medicine Keywords: anterior spinal artery infarct, fibrocartilaginous embolism, intercostal artery dissection, pediatric myelopathy, spinal cord ischemia Introduction Acute myelopathy in adolescents presents a significant diagnostic challenge, most commonly arising from underlying inflammatory etiologies. However, vascular etiologies, while rare, must be promptly identified due to their distinct management and prognostic implications [1] . Spinal cord infarction (SCI) results from the occlusion of the anterior spinal artery (ASA), which involves disruption of the motor pathways and pain/temperature sensation [2] . Two distinct and rare post-traumatic vascular mechanisms were involved in this case. The first mechanism, nucleus pulposus fibrocartilaginous embolism (FCE), results from the migration of disc material into theradicular arteries supplying the cord, a mechanism often precipitated by minor trauma or sudden axial loading [3] . This is particularly relevant in the bimodal adolescent age group, during which the disc’s vascular supply is regressing. The resulting embolic occlusion leads to acute ischemia. The second mechanism, intercostal (IC) artery dissection, involves a structural tear in the arterial wall that leads to hematoma formation and subsequent occlusion. If this occurs in a vital feeder vessel, such as the T 10 IC artery (which often gives rise to the artery of Adamkiewicz, or AKA), it mechanically compromises the blood supply to the entire lower spinal cord. This report is significant because it documents the co-existence of a highly suspected FCE (based on clinical picture and exclusion of alternatives) and a confirmed, structural ICarterty dissection (based on angiography), p

FAQs

What condition did the patient develop after the fall?

The patient developed acute paraplegia due to anterior spinal artery territory infarction, presenting as ASA syndrome.

How was the diagnosis of spinal cord ischemia confirmed?

MRI confirmed spinal cord ischemia with T2 hyperintensity restricted to the anterior cord.

What vascular injuries were found that explained the dual mechanism?

Aortic angiography revealed a concurrent right T10 intercostal artery dissection alongside a clinical picture highly characteristic of nucleus pulposus fibrocartilaginous embolism.

Sep 30, 2026

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