Spinal cord blood supply

Why anaesthetists care (clinical links)

• Spinal cord perfusion depends on the balance between inflow and outflow pressures; ischaemia can occur with hypotension, raised CSF pressure, or interruption of segmental feeders.
  • SCPP ≈ MAP − max(CSF pressure, venous pressure).
  • Practical: maintain MAP; avoid high intrathoracic/venous pressures; consider CSF drainage in selected aortic surgery pathways.
• Anterior spinal artery territory (motor pathways) is more vulnerable than posterior territory; anterior cord syndrome is a key pattern to recognise.
  • Motor weakness/paralysis + loss of pain/temperature below lesion; dorsal column modalities (vibration/proprioception) relatively spared.
• High-risk settings: thoracoabdominal aortic aneurysm repair, aortic cross-clamping, prolonged hypotension, severe anaemia/hypoxia, spinal deformity surgery, epidural haematoma/abscess, vasculitis/embolism.
• Neuraxial anaesthesia: sympathectomy reduces MAP; if severe/prolonged, can reduce SCPP (especially in patients with compromised segmental supply).
  • Management principle: treat hypotension early (vasopressors + fluids as appropriate) and avoid sustained low MAP in vulnerable patients.

Applied anatomy patterns that map to blood supply

• Central cord (sulcal arteries from ASA) supplies anterior horns and adjacent white matter; infarction can cause motor deficits and segmental LMN signs.
• Peripheral cord (pial plexus/vasocorona) supplies outer white matter; watershed risk between central and peripheral territories.

Core arterial anatomy (high-yield)

• Longitudinal arteries: 1 anterior spinal artery (ASA) + 2 posterior spinal arteries (PSA).
  • ASA runs in anterior median fissure; PSAs run posterolaterally near dorsal root entry zones.
• Territories: ASA supplies anterior ~2/3 of cord; PSAs supply posterior ~1/3.
  • ASA: anterior horns, corticospinal tracts, spinothalamic tracts, intermediolateral cell columns (sympathetic outflow T1–L2).
  • PSA: dorsal columns (vibration, proprioception), dorsal horns (variable).
• Reinforcement by segmental medullary (radiculomedullary) arteries from vertebral, deep/ascending cervical, posterior intercostal, lumbar, and sacral arteries.
  • Not every segment has a large feeder; supply is discontinuous with a few dominant radiculomedullary arteries.
• Artery of Adamkiewicz (great anterior segmental medullary artery): dominant feeder to ASA for lower thoracic/lumbar enlargement.
  • Most commonly arises from a left posterior intercostal artery between T9–T12 (range ~T5–L2).
  • Clinical: interruption during aortic surgery can cause anterior spinal artery syndrome and paraplegia.
• Pial arterial network (vasocorona) encircles cord and connects ASA and PSAs; gives penetrating branches to peripheral cord.

Venous drainage (often examined)

• Intrinsic venous network drains to longitudinal anterior and posterior spinal veins, then via radicular veins to epidural venous plexus (Batson plexus).
• Epidural venous plexus is valveless; venous pressure can rise with increased intrathoracic/abdominal pressure and can reduce SCPP.
  • Examples: high PEEP, coughing/straining, pneumoperitoneum, IVC obstruction, raised CVP.

Physiology of spinal cord perfusion

• Perfusion pressure concept: SCPP ≈ MAP − max(CSF pressure, venous pressure).
  • Spinal canal is a closed compartment: raised CSF pressure (e.g., oedema/haematoma) can critically reduce perfusion even with normal MAP.
• Autoregulation exists but is less robust than cerebral circulation and can be impaired by ischaemia, inflammation, anaemia, and extremes of PaCO2.
  • Hypercapnia tends to vasodilate spinal cord vessels; hypocapnia tends to vasoconstrict (directionally similar to brain), but clinical impact is less predictable.
• Watershed vulnerability: mid-thoracic cord (classically ~T4–T8) has fewer large segmental feeders and is prone to ischaemia during systemic hypoperfusion.

Clinical syndromes and localisation

• Anterior spinal artery syndrome: bilateral motor weakness + loss of pain/temperature; dorsal column function preserved; may have autonomic dysfunction (e.g., hypotension, bladder/bowel).
• Posterior spinal artery infarction: loss of vibration/proprioception, sensory ataxia; motor relatively preserved.
• Central cord (sulcal artery) infarcts can produce segmental LMN weakness and dissociated sensory loss depending on level/extent.

Aortic surgery and spinal cord protection (principles)

• Mechanisms of injury: interruption of segmental feeders (incl. Adamkiewicz), embolism, prolonged hypotension, raised CSF pressure, reperfusion injury.
• Protection strategies (conceptual): maintain MAP/SCPP, limit cross-clamp time, reimplant key intercostals when appropriate, CSF drainage to lower CSF pressure, avoid anaemia/hypoxia, normothermia or controlled hypothermia depending on protocol, neuromonitoring (MEPs/SSEPs).
  • MEPs are more sensitive to anterior cord (motor) ischaemia than SSEPs (dorsal column).