Spinal Cord Infarction

Spinal cord infarction is an ischaemic stroke of the spinal cord, causing acute myelopathy, most often in the territory of the anterior spinal artery. It is uncommon, and accounts for about 1 to 2% of all strokes, with a high rate of permanent disability.

The incidence is about 3 in every 100,000 people each year. It affects all ages, with a mean age of about 55 years, and men and women about equally.

Causes. Aortic disease and surgery (dissection, aneurysm, clamping, endovascular repair), atherosclerosis, profound hypotension, cardiac surgery and arrest, embolism, vasculitis, fibrocartilaginous embolism, sickle cell disease, decompression illness, vertebral artery dissection and spinal vascular procedures. About one third have no cause found.

Course. Maximum deficit within hours; recovery is variable, and about half are unable to walk independently at one year.

Pathophysiology.

Occlusion or hypoperfusion of the spinal arteries (especially the artery of Adamkiewicz, supplying the thoracolumbar cord) leads to infarction of the central grey matter and anterior two thirds of the cord, which is a watershed zone.

The mid-thoracic cord is the most vulnerable because of the sparse segmental supply.

• Sudden severe back or neck pain, then rapid onset of bilateral weakness within minutes to hours.
• Spinal shock with flaccid paralysis and areflexia, then spasticity.
• Loss of pain and temperature sensation caudal to the lesion, with preserved light touch and vibration (dorsal columns spared).
• Urinary retention and bowel dysfunction; autonomic dysreflexia in high lesions.
• Occurs during or after aortic surgery, hypotension, or a Valsalva manoeuvre.

Red flags.

• Cervical lesion with respiratory failure or autonomic instability.
• Fever, spinal tenderness or trauma (infection, compression).
• Progressive weakness over days (inflammatory or compressive).

• MRI of the spine with diffusion weighted imaging: T2 hyperintensity in the anterior horns ("owl's eyes") or pencil like lesions; diffusion changes can be absent in the first 24 hours and MRI should be repeated.
• Exclude compression, haematoma and transverse myelitis; cerebrospinal fluid is usually normal or has mild protein rise.
• MR or CT angiography of the aorta, spine and vertebral arteries.
• ECG, echocardiography, ambulatory rhythm monitoring, lipids, glucose, clotting, thrombophilia and vasculitis tests; sickle cell screening.
• Spinal angiography for suspected vascular malformation.

Differential diagnosis. Transverse myelitis, compressive myelopathy, epidural haematoma or abscess, Guillain-Barré syndrome, neuromyelitis optica spectrum disorder, vascular malformation and acute flaccid myelitis.

• Maintain spinal cord perfusion: avoid hypotension, aim for a mean arterial pressure of at least 85 mmHg for up to 7 days in aortic surgery or spinal ischaemia (use vasopressors as needed), and correct anaemia and hypoxia.
• Cerebrospinal fluid drainage (lumbar drain) to keep pressure at or under 10 mmHg in perioperative aortic ischaemia, by the surgical and anaesthetic team.
• Antiplatelet treatment once haemorrhage is excluded: aspirin 300 mg orally (or rectally if swallowing is impaired) once, then 75 mg daily. Maximum 300 mg daily. Monitor for gastrointestinal bleeding. Avoid in active bleeding, peptic ulcer and aspirin hypersensitivity; use caution in asthma and renal impairment.
• Atorvastatin 80 mg orally once daily at night, aiming for LDL cholesterol under 1.8 mmol/L. Maximum 80 mg daily; limit to 20 mg daily with clarithromycin. Monitor liver function at baseline and 3 months, creatine kinase if muscle symptoms occur, and lipids at 4 to 12 weeks. Avoid in active liver disease and pregnancy; no renal adjustment.
• Treat the cause: aortic repair for dissection, anticoagulation for embolic sources through a specialist, steroids and immunotherapy for vasculitis, hydroxyurea or exchange for sickle cell disease.
• Thromboprophylaxis: enoxaparin 40 mg subcutaneously once daily. Maximum 40 mg daily (20 mg daily when creatinine clearance is under 30 mL/min). Monitor platelets, renal function and bleeding. Avoid in active bleeding.
• Intensive rehabilitation: physiotherapy, bladder and bowel programme, pressure care and spasticity control.
• Intravenous thrombolysis has no established role.

Monitoring. Neurological and blood pressure observation hourly in the first 24 hours; review at 4 to 6 weeks, 3 months and 12 months.

Referral and escalation. Neurology, vascular surgery and spinal injury rehabilitation; intensive care for respiratory involvement.

Special groups. Perioperative patients: strict perfusion targets and drainage. Children: rare, usually from malformation or trauma.