1130 - Progressive Myelopathy due to Spinal Dural AVF

Progressive Myelopathy due to Spinal Dural AVF


Case Description:

72-year-old male with history of diabetes and lumbar herniated discs presenting for evaluation for 15-month history of progressive waxing and waning bilateral lower extremity weakness. Weakness was associated with falls and 20-pound wight loss. MRI thoracic spine with spinal cord signal change from T6 to conus with unclear etiology. Had serum NMO/MOG testing which was unremarkable. Repeat MRI thoracic spine showed progression of signal change from T6 to T2. EMG/NCS unremarkable.  MRA thoracic spine demonstrated anterior cord enhancement with vascular abnormalities concerning for spinal dural AVF. Underwent spinal DSA and found to have left L3 dural AVF.


Discussions:
Spinal dural AVFs are the most common type of spinal vascular malformations, typically affecting older males. They represent abnormal connections between a radiculomeningeal artery and a radicular vein, leading to venous hypertension and congestive myelopathy. Presentation is insidious, with progressive motor and sensory deficits, commonly mistaken for lumbar stenosis or peripheral neuropathy, especially in elderly patients with co-morbidities like diabetes.



This case illustrates the diagnostic challenges of spinal dural AVF. Initial imaging findings may be non-specific, and neurological deficits may wax and wane, mimicking other conditions. Notably, spinal cord signal changes on MRI (especially long-segment T2 hyperintensity), in the absence of a clear demyelinating etiology, should prompt vascular imaging.



The patient’s progressive signal changes from T6 to T2, along with anterior cord enhancement and failure to find another cause, were key clues leading to the correct diagnosis. Spinal DSA remains the gold standard for diagnosis.


Conclusions:

This case highlights the importance of considering spinal dural AVF in elderly patients presenting with progressive lower extremity weakness, especially when MRI demonstrates longitudinally extensive T2 hyperintensity and no clear demyelinating or compressive cause. Prompt diagnosis is crucial, as timely intervention (surgical or endovascular) can prevent irreversible spinal cord damage.