Spinal dural arteriovenous fistulas (SDAVFs) are rare vascular malformations in which a dural artery connects abnormally to a medullary vein, producing venous hypertension and progressive myelopathy. The annual incidence is estimated at 5–10 per million, with a strong male predominance (80%) between ages 50–70. We present a unique case of SDAVF in an elderly woman with a proposed novel mechanism related to equestrian activity.

An 81-year-old woman with hypertension and hypothyroidism developed progressive bilateral leg paresthesias evolving into flaccid paralysis, urinary retention, and constipation over three weeks. She had recently taken up horseback riding and denied trauma or back pain. Initial lumbar MRI showed multilevel degenerative changes, and she was discharged with presumed lumbar radiculopathy. Two weeks later, she returned with worsening paraplegia, areflexia, T12–L1 sensory level, and sphincter dysfunction.

Thoracic MRI revealed long-segment T2 cord hyperintensity, expansion, and serpentine flow voids. Angiography confirmed a SDAVF from the right T12 intercostal artery. She underwent Onyx-18 embolization with minimal improvement, followed by T11–L1 laminoplasty and direct ligation with nBCA embolization of a residual extradural component. Postoperatively, she regained partial lower extremity movement but remained Foley-dependent during rehabilitation.

SDAVFs are typically acquired and associated with venous thrombosis, trauma, or prior surgery. This patient lacked these factors; horseback riding may have induced repetitive axial spinal stress contributing to endothelial injury and VEGF-mediated angiogenesis, promoting abnormal arteriovenous communication. The occurrence of SDAVF in an elderly woman without conventional risks, linked to a mechanical lifestyle factor, is extraordinarily rare in published literature. No prior reports have correlated equestrian activity with SDAVF formation, making this a novel etiologic association. This case underscores the diagnostic challenge of SDAVF, often mimicking degenerative spine disease, and highlights the importance of considering vascular etiologies in progressive myelopathy regardless of demographic norms.