# Spinal Cord Infarction Presenting as Cauda Equina Syndrome With Concurrent Pulmonary Embolism: A Case Report

## TL;DR

A rare case where spinal cord infarction mimicked cauda equina syndrome and occurred alongside pulmonary embolism is reported, highlighting diagnostic challenges and management considerations.

## Contribution

The paper presents a novel clinical case linking spinal cord infarction, cauda equina syndrome, and pulmonary embolism with antiphospholipid antibodies.

## Key findings

- Spinal cord infarction can mimic cauda equina syndrome on initial MRI, leading to delayed diagnosis.
- Concurrent pulmonary embolism and antiphospholipid antibody positivity suggest a prothrombotic state.
- Early repeat MRI and assessment of thromboembolic risk factors are critical for timely management.

## Abstract

Spinal cord infarction is rare and can be difficult to recognize early in emergency settings, especially when it mimics cauda equina syndrome (CES) with concurrent pulmonary embolism (PE). CES typically results from compression of lumbosacral roots, presenting with lower limb sensory changes or weakness and bladder dysfunction, whereas spinal cord ischaemia can present with overlapping features that delay diagnosis.

A 58-year-old woman presented with acute back pain, saddle numbness, urinary retention, and asymmetric leg weakness consistent with suspected CES. Initial lumbar MRI showed degenerative changes without compressive pathology. Within 48 hours, neurological status worsened to flaccid paraplegia with sphincter dysfunction. Repeat MRI demonstrated T2/STIR (short tau inversion recovery) signal from the conus to approximately T12, consistent with spinal cord infarction. Concurrently, she developed chest pain and hypoxia. CT pulmonary angiogram (CTPA) identified a saddle embolus in the main trunk of the pulmonary artery, and therapeutic anticoagulation was initiated. Workup revealed antiphospholipid antibody positivity. She was using oral hormone replacement therapy and a GLP-1 agent for obesity, constituting a prothrombotic context, although a direct arterial embolic source was not confirmed.

This case underscores three points: maintain a vascular differential for CES phenotypes with non-compressive MRI, consider early repeat MRI when symptoms evolve, and assess for systemic thromboembolism and prothrombotic risk factors to guide urgent management and follow-up.