What are the American Stroke Association (ASA) guidelines for managing an acute anterior spinal artery infarction in an adult presenting with sudden loss of motor function and pain sensation below the lesion?

ASA Guidelines for Anterior Spinal Artery Infarction Syndrome

The American Stroke Association does not have specific published guidelines for anterior spinal artery infarction syndrome. The available ASA/AHA guidelines focus exclusively on cerebral ischemic stroke, not spinal cord infarction 1. Management must therefore be extrapolated from general acute ischemic stroke principles and limited case reports.

Critical Recognition

Anterior spinal artery syndrome presents with acute bilateral motor deficits below the lesion level, loss of pain and temperature sensation (spinothalamic tract), but preserved proprioception and vibratory sensation (posterior columns). 2, 3, 4 The classic presentation includes sudden severe back or neck pain followed by rapidly progressive paraplegia or quadriplegia depending on the level of infarction 2, 5.

Diagnostic Approach

Immediate Imaging

• Obtain urgent MRI of the spine with diffusion-weighted imaging (DWI) to confirm spinal cord infarction. 2, 5, 4 Look for restricted diffusion in the anterior spinal cord territory with characteristic "owl's eyes" or "snake eyes" appearance on axial images 5.
• T2-weighted sequences show hyperintense signal in the anterior two-thirds of the cord 5, 4.
• Perform spinal angiography if considering intra-arterial intervention, which can demonstrate anterior spinal artery cutoff. 2

Exclude Mimics

• Rule out compressive myelopathy (epidural abscess, hematoma, tumor) which requires urgent surgical decompression 5.
• Assess for vertebral artery dissection or occlusion with MRA/CTA of the neck 1, 4.

Treatment Options (Based on Limited Evidence)

Medical Management (Most Common Approach)

Supportive care remains the standard approach, as no randomized trials exist for spinal cord infarction treatment. 1

• Maintain mean arterial pressure (MAP) >85-90 mmHg for at least 72 hours to optimize spinal cord perfusion through collaterals. This is extrapolated from traumatic spinal cord injury protocols, though not specifically validated in ischemic spinal stroke 5.
• Administer antiplatelet therapy (aspirin 325 mg) after excluding hemorrhagic transformation, similar to cerebral stroke protocols. 1, 6
• Consider anticoagulation with low molecular weight heparin (enoxaparin) if fibrocartilaginous embolism or vertebral artery dissection is suspected. 5 One pediatric case showed near-complete recovery with early enoxaparin and corticosteroids 5.
• High-dose corticosteroids (methylprednisolone) may be considered within 12 hours, though evidence is extrapolated from traumatic spinal cord injury and remains controversial. 5

Experimental Interventional Approach

Intra-arterial thrombolysis has been reported in isolated case reports but is NOT guideline-recommended. 2 One case demonstrated successful treatment with direct anterior spinal artery catheterization and administration of tissue plasminogen activator (t-PA) combined with verapamil and eptifibatide within hours of symptom onset 2. However:

• This requires immediate availability of neurointerventional expertise 2.
• The anterior spinal artery is technically challenging to catheterize 2.
• No safety or efficacy data exist beyond single case reports 2.
• IV thrombolysis (alteplase) has NOT been studied for spinal cord infarction and cannot be recommended based on cerebral stroke guidelines alone. 1, 6

Critical Pitfalls

Do NOT delay diagnosis by assuming symptoms are from peripheral nerve or muscle pathology. The acute onset of bilateral motor deficits with dissociated sensory loss (loss of pain/temperature with preserved proprioception) is pathognomonic for anterior spinal artery syndrome 2, 3, 4.

Do NOT aggressively lower blood pressure. Unlike cerebral stroke where permissive hypertension has limits, spinal cord perfusion may be even more dependent on systemic pressure due to limited collateral circulation 5.

Do NOT assume poor prognosis universally. While many patients have permanent deficits 3, 7, early aggressive treatment in select cases has resulted in near-complete recovery 5.

Secondary Prevention

• Investigate underlying etiology: fibrocartilaginous embolism (history of trauma or unusual physical activity) 5, aortic pathology (dissection, atherosclerosis), vertebral artery disease 1, 4, cardiac embolism, or vasculitis 3.
• Initiate appropriate secondary prevention based on etiology: antiplatelet therapy for atherosclerotic disease 1, anticoagulation for cardiac sources or arterial dissection 1.
• Aggressive risk factor modification including statin therapy, blood pressure control, and diabetes management as per cerebral stroke guidelines 1, 8.

Rehabilitation

Early mobilization and intensive rehabilitation are critical, as neurological recovery can continue for months. 5, 4 Multidisciplinary team involvement including physical therapy, occupational therapy, and bladder/bowel management is essential 6, 8.