Spinal cord vascular syndromes are uncommon but distinctive — and often missed. The cord’s blood supply is anatomically vulnerable, with watersheds, end zones, and a critical reliance on the artery of Adamkiewicz for the lower thoracic and lumbar segments. Vascular cord lesions can produce anterior cord, posterior cord, or central cord syndromes; they can also produce subtle long-term syndromes (dural arteriovenous fistula). This page covers the vascular anatomy of the cord and the syndromes that arise when it is compromised.

Vascular Anatomy of the Cord

Arterial Supply

The cord is supplied by:

  • Anterior spinal artery: a single midline vessel running along the anterior surface of the cord from foramen magnum to conus. Formed at the foramen magnum by branches from each vertebral artery. Supplies the anterior two-thirds of the cord through penetrating sulcal arteries.
  • Two posterior spinal arteries: paired vessels along the posterolateral surface of the cord. Supply the posterior third (dorsal columns and posterior horns).
  • Radicular arteries: segmental contributions from the aorta and its branches enter through the intervertebral foramina with the nerve roots. Most are small and supply only the roots and meninges. A few are large enough to reach and reinforce the anterior or posterior spinal arteries — these are called radiculomedullary arteries.
  • Artery of Adamkiewicz (arteria radicularis magna): the largest radiculomedullary artery, supplying the lower thoracic and lumbar cord. Usually arises from a left intercostal or lumbar artery between T8 and L1 (most often around T9-T12). Critical: this single artery supplies the cord region from mid-thoracic to conus. Its compromise produces a devastating anterior cord syndrome.

Watershed Zones

Two important watersheds:

  • Mid-thoracic watershed (T4-T8 approximately): between the cervical anterior spinal supply from vertebrals and the lower supply from artery of Adamkiewicz. Most vulnerable to global hypoperfusion or aortic disease.
  • Internal watershed: between the central (penetrating sulcal) and peripheral (radicular) circulation.

Venous Drainage

The cord drains via radicular veins to the epidural venous plexus and onward to systemic veins. Venous hypertension from a dural arteriovenous fistula causes one of the most important treatable cord syndromes.

Spinal Cord Infarction

Anterior Spinal Artery Infarct

Affects the anterior two-thirds of the cord — corticospinal tracts, anterior horns, and spinothalamic tracts. Dorsal columns are spared.

Clinical features:

  • Abrupt onset of paraplegia or quadriplegia (depending on level) with weakness from corticospinal tract involvement.
  • Loss of pain and temperature below the level (spinothalamic).
  • Preservation of vibration and proprioception (dorsal columns spared) — a key distinguishing feature.
  • Bladder retention.
  • Often preceded by severe back pain at the level of infarction.
  • Sometimes a prodrome of “spinal TIA” — transient leg weakness or sensory change.

Causes:

  • Aortic disease: aortic dissection, aneurysm, aortic surgery (especially repair of thoracoabdominal aneurysm), trauma. The artery of Adamkiewicz is at risk.
  • Severe hypotension or cardiac arrest.
  • Atherosclerotic disease.
  • Embolic (cardiac, paradoxical, septic).
  • Vasculitis (rare).
  • Fibrocartilaginous embolism (disc material): rare but classical — sudden onset cord ischemia after minor trauma.
  • Hypercoagulable states (rare cause).
  • Cocaine, methamphetamine.
  • Decompression sickness.

Imaging: MRI cord with diffusion. Acute infarction shows restricted diffusion. Cord swelling, T2 hyperintensity in a “pencil-like” central distribution on sagittal images and the anterior horn or anterior cord on axial.

Treatment: supportive. No proven thrombolysis or thrombectomy protocols (unlike brain stroke). Treat the underlying cause. CSF drainage during high-risk aortic surgery reduces risk. Antiplatelet therapy and treatment of vascular risk factors.

Posterior Spinal Artery Infarct

Less common than anterior. Affects the posterior third of the cord — dorsal columns and posterior horns. Produces loss of vibration and proprioception with preserved motor and pain-temperature. Often patchy because of the bilateral paired posterior arteries.

Central Cord Infarction

Can occur with selective infarction of the penetrating sulcal arteries — produces a central cord pattern with cape distribution. Rare; more often the differential of a central cord syndrome includes syringomyelia and intramedullary tumor.

Spinal Cord Hemorrhage

  • Hematomyelia: hemorrhage into the cord substance. Often from vascular malformation, trauma, anticoagulation. Produces acute cord syndrome corresponding to the level and the cross-section affected.
  • Epidural hematoma: hemorrhage in the epidural space, often spontaneous in anticoagulated patients or after spinal procedures (epidural anesthesia, lumbar puncture). Compresses the cord. Acute back pain followed by progressive cord syndrome — surgical emergency.
  • Subdural hematoma: rare; similar presentation.
  • Subarachnoid hemorrhage: rare in the cord; usually from vascular malformation or tumor.

Vascular Malformations

Dural Arteriovenous Fistula (Spinal Dural AV Fistula)

The most common spinal vascular malformation in adults. An abnormal connection between a radicular artery and a radicular vein at a single dural site. The fistula raises venous pressure throughout the cord venous system, leading to chronic cord ischemia and progressive myelopathy. Most often in older men, lower thoracic location.

Clinical features:

  • Slowly progressive lower extremity weakness, sensory disturbance, bladder dysfunction.
  • Sometimes stepwise worsening or worsening with exercise (vascular steal phenomenon).
  • Easy to mistake for cervical spondylotic myelopathy, transverse myelitis, MS, or normal-pressure hydrocephalus.
  • Often misdiagnosed for months to years before correct diagnosis.

Imaging: MRI shows central cord T2 hyperintensity (cord edema) with prominent flow voids on the cord surface. Diagnosis confirmed by spinal angiography. Treatment is embolization or surgical disconnection of the fistula. Early treatment improves outcome.

Spinal Arteriovenous Malformation (AVM)

Less common than dural AVF. True parenchymal AVM in the cord, with arterial-to-venous shunt through a nidus. Presents at younger age, often with hemorrhage or progressive myelopathy. Treatment is more complex and may require embolization, microsurgery, or stereotactic radiosurgery.

Cavernous Malformation

Intramedullary cavernoma. Can be sporadic or familial (multiple). Can cause recurrent hemorrhage or slowly progressive myelopathy from low-flow vascular pathology. MRI shows characteristic appearance with hemosiderin rim (“popcorn” pattern). Surgical resection considered for symptomatic lesions.

Spinal Aneurysm

Rare. Can rupture into the cord (hematomyelia) or subarachnoid space.

Surfer’s Myelopathy

An unusual cord ischemic syndrome described in novice surfers after prolonged hyperextension of the spine while learning to surf. The pathophysiology is thought to be infarction in the lower thoracic to lumbar cord from hyperextension-related compromise of the artery of Adamkiewicz. Acute back pain, leg weakness, sensory loss, urinary retention. MRI shows cord T2 hyperintensity in the relevant segments. Outcome variable.

Distinguishing Vascular Cord Syndromes from Other Causes of Acute Myelopathy

Feature Anterior spinal artery infarct Transverse myelitis Epidural compression Dural AVF
Onset Sudden (seconds to minutes) Hours to days Subacute (days to weeks), can be sudden in pathologic fracture Insidious (months to years)
Pain Severe back pain at level Mild pain or none Often severe local back pain Minimal pain
Cord pattern Anterior 2/3 (motor + pain-temp loss, vibration spared) Typically central/posterior, variable Cord compression — sensory level, weakness below, often complete cross-section Central cord edema, progressive
Imaging T2 cord hyperintensity, restricted diffusion acutely, “pencil” pattern Cord T2 hyperintensity, length variable, may enhance Extrinsic mass compressing cord T2 hyperintensity + flow voids on cord surface
CSF Often normal Pleocytosis, elevated protein Often normal unless mass-related Often normal or mildly elevated protein
Treatment Supportive, treat underlying cause Steroids, plasma exchange Surgical decompression Embolization or surgery

Approach to the Patient with Acute Myelopathy

  1. Establish the sensory and motor level.
  2. Distinguish anterior vs posterior vs full cord syndrome (test vibration vs pain-temperature dissociation).
  3. Note tempo: hyperacute (vascular), acute-subacute (inflammatory, infectious), chronic (compressive, dural AVF).
  4. Look for triggers: recent aortic surgery, trauma, anticoagulation, history of fistula, AVM, vasculitis.
  5. Urgent MRI cord with gadolinium and diffusion.
  6. CSF analysis if inflammatory cord disease in differential.
  7. Specialized vascular imaging (MR angiography of cord, CT angiography of aorta, conventional spinal angiography) if vascular cause suspected and not seen on standard MRI.
  8. Treatment based on diagnosis: steroids for inflammatory; reversal of anticoagulation + surgical decompression for hematoma; embolization for dural AVF; supportive for infarct.

Clinical Cases — Recognizing the Pattern

Case 1: 70-year-old man develops sudden onset back pain followed within minutes by paraplegia and urinary retention during routine activity. Vibration and proprioception are preserved; pain-temperature is lost below T10. → Anterior spinal artery infarct, likely at the artery of Adamkiewicz territory. Image with MRI and CT angiography of the aorta. Look for aortic dissection.

Case 2: 60-year-old man has 2 years of slowly progressive leg weakness and sensory disturbance, worse with prolonged standing or exertion. Urinary urgency over the past year. Cord MRI shows T2 hyperintensity in the lower thoracic cord with prominent flow voids on the cord surface. → Spinal dural AV fistula. Refer for spinal angiography and treatment.

Case 3: 35-year-old woman on apixaban for a recent DVT presents with severe acute mid-back pain followed by rapid progressive lower extremity weakness over six hours. → Epidural hematoma. Reverse anticoagulation and urgent surgical decompression.

Case 4: 25-year-old surfer presents with acute lower back pain and lower extremity weakness after a hyperextension event while paddling out. MRI shows T2 hyperintensity in the lower thoracic cord. → Surfer’s myelopathy.

🔍 Did You Know?

The artery of Adamkiewicz — the great anterior radicular artery supplying the lower thoracic and lumbar cord — is anatomically eccentric in ways that surprise clinicians. In about three-quarters of people, it arises from a left-sided intercostal or lumbar artery between T8 and L1 — most often around T10-T12. In the other quarter, it arises from elsewhere — sometimes higher (T5-T8), sometimes lower, sometimes from the right. This variability is critical in thoracoabdominal aortic surgery: the surgeon must preserve the segmental artery that feeds the artery of Adamkiewicz, or risk cord infarction. Preoperative CT or MR angiography is increasingly used to identify the level. Aortic surgery for thoracoabdominal aneurysm carries a 5-15% risk of paraplegia historically, much reduced by CSF drainage, MAP support, and selective intercostal artery preservation. The artery’s name commemorates Albert Wojciech Adamkiewicz, the Polish anatomist who described it in 1882. Two centuries later, the artery and its location remain one of the most clinically consequential pieces of cord vascular anatomy.

Pitfalls and Pearls

  • Anterior spinal artery infarct spares vibration and proprioception — distinguishes from compressive myelopathy.
  • Sudden onset back pain + paraplegia + pain-temperature loss with preserved vibration = anterior cord infarct.
  • Artery of Adamkiewicz is the critical supply for lower thoracic / lumbar cord. Most often left-sided, between T8 and L1.
  • Spinal dural AV fistula is the great masquerader — slowly progressive myelopathy, often misdiagnosed. Look for cord edema + flow voids on MRI in older men with progressive paraparesis.
  • Spinal epidural hematoma in an anticoagulated patient or after spinal procedure → surgical emergency. Reverse anticoagulation, decompress.
  • Aortic dissection or thoracoabdominal aortic surgery are high-risk settings for cord infarct.
  • Cardiac arrest can produce cord infarction in the watershed (T4-T8) along with cerebral anoxic injury — the so-called “watershed myelopathy.”
  • Acute back pain at the level is common with anterior spinal artery infarct.
  • Cavernous malformations of the cord can produce recurrent hemorrhage and progressive myelopathy. MRI shows hemosiderin rim.
  • Spinal angiography is the gold standard for dural AVF and parenchymal AVM diagnosis.
  • CSF drainage during high-risk aortic surgery reduces paraplegia risk.
  • Surfer’s myelopathy: hyperextension-related cord ischemia in novice surfers.

References

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