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

## TL;DR

A 14-year-old boy suffered spinal cord infarction due to a rare combination of fibrocartilaginous embolism and artery dissection after a minor fall.

## Contribution

This case highlights a dual vascular mechanism causing spinal infarction in adolescents, emphasizing the need for comprehensive diagnosis.

## Key findings

- Acute paraplegia occurred 24 hours after a minor fall with axial loading in a 14-year-old.
- MRI and angiography confirmed ischemia and intercostal artery dissection as contributing factors.
- The patient recovered significantly with neuroprotection, antiplatelet therapy, and rehabilitation.

## 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.