Spinal Arteriovenous Malformation (AVM)
Abnormal spinal cord blood vessel tangle causing ischemia or hemorrhage
ICD-10: Q28.2 · systemic condition
A spinal arteriovenous malformation (AVM) is an abnormal tangle of blood vessels — arteries connected directly to veins without the normal intervening capillary bed — located on or within the spinal cord or its surrounding structures. The abnormal shunting of high-pressure arterial blood into the low-pressure venous system causes venous hypertension, spinal cord ischemia, and in some cases hemorrhage (hematomyelia or subarachnoid hemorrhage), leading to progressive or sudden neurological deterioration. Spinal AVMs are classified by angioarchitecture. Type I dural arteriovenous fistulas (AVF) — the most common type in adults — are abnormal connections between a radicular artery and an epidural vein on the dura mater, causing slowly progressive myelopathy from venous congestion. Type II and III intramedullary AVMs are located within the cord parenchyma and carry higher hemorrhage risk. Type IV perimedullary fistulas connect spinal arteries directly to perimedullary veins without a nidus. Diagnosis requires spinal MRI showing edema or flow voids, followed by spinal angiography to define the exact fistula anatomy. Treatment is either endovascular embolization or microsurgical disconnection depending on lesion type and accessibility.
Anatomy & Pathology
Normal spinal cord circulation flows from spinal arteries through a fine capillary bed and drains into spinal veins. In an AVM, arteries connect directly to veins at high pressure, creating engorged, tortuous vessels that compress adjacent cord tissue and deprive it of oxygenated blood. The thoracic and thoracolumbar cord are the most common sites.
Symptoms
- Slowly progressive weakness and sensory loss in the legs (Type I AVF pattern)
- Sudden onset of back or neck pain with acute paraplegia from hemorrhage
- Neurogenic claudication worsened by exercise (venous engorgement pattern)
- Bladder and bowel dysfunction as cord dysfunction advances
- Back pain that may precede neurological deficits by months to years
- Asymmetric leg weakness and patchy sensory changes
- Worsening symptoms with Valsalva or physical exertion (venous hypertension sign)
Causes & Risk Factors
- Congenital vascular malformation of the spinal cord or dura (Type II, III AVMs)
- Acquired dural arteriovenous fistula formation from venous hypertension or prior thrombosis (Type I)
- Associated hereditary conditions: Osler-Weber-Rendu (HHT), Klippel-Trenaunay syndrome
- Spontaneous formation without identifiable predisposing cause in most adult Type I cases
Treatment Options
Conservative
- Observation with serial MRI for incidentally discovered, asymptomatic small AVMs without hemorrhage risk features
- Antiplatelet therapy to reduce thrombotic risk in select cases (adjunct only)
- Rehabilitation therapy to maintain function while awaiting or following definitive treatment
Surgical
- Endovascular embolization with Onyx or NBCA glue — first-line for Type I dural AVF and accessible Type II AVMs
- Microsurgical disconnection of the fistula or resection of intramedullary nidus — for lesions not amenable to embolization or after failed embolization
- Combined embolization followed by surgical resection for large complex intramedullary AVMs
When to see a spine specialist
Seek emergency care for sudden back or neck pain accompanied by leg weakness, sensory loss, or loss of bladder or bowel control — these suggest spinal AVM hemorrhage. Gradual progressive leg weakness without trauma, particularly in a younger adult, should prompt urgent MRI evaluation. Diagnosis is frequently delayed due to misattribution to disc disease.
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Search spine specialists →Frequently Asked Questions
What is the difference between a spinal AVM and a spinal dural AVF?
A spinal dural arteriovenous fistula (Type I) is an acquired connection between a meningeal artery and an epidural vein on the dura, causing venous hypertension and slow cord injury without a true malformation nidus. A spinal AVM (Types II–III) is a congenital tangle of abnormal vessels — the nidus — located within the cord parenchyma, carrying a higher spontaneous hemorrhage risk. Type I dural AVF is far more common in adults; intramedullary AVMs more often present in younger patients.
Can a spinal AVM be completely cured?
Type I dural AVFs are highly curable. Surgical disconnection of the fistula achieves durable cure in over 95% of cases. Endovascular embolization alone has a higher recurrence rate (~25–40%) unless the fistula point is completely occluded. Intramedullary AVMs are more complex; complete cure depends on whether the nidus can be fully resected or embolized without unacceptable cord injury risk. Partial treatment reduces hemorrhage risk but may not fully halt neurological progression.
Does neurological function recover after treatment of a spinal AVM?
Recovery depends on duration and severity of injury before treatment. Patients treated early with minimal preoperative deficits often experience significant neurological improvement after venous hypertension is relieved. Those with longstanding cord injury from chronic venous congestion typically stabilize (stop deteriorating) but recover less fully. Recovery after hemorrhage is variable and depends on the extent of cord damage at the time of bleeding.