Spinal Cord Infarction: Causes, Symptoms, and Risks

Spinal cord infarction is a rare but serious condition caused by an interruption of blood supply to the spinal cord, leading to tissue damage and neurological impairment. While less common than strokes affecting the brain, it can result in significant disability, including paralysis or sensory loss. Recognizing this condition early is critical for timely intervention and management.

Mechanisms Of Blood Flow Interruption

The spinal cord relies on a complex vascular network, with the anterior spinal artery supplying approximately two-thirds of its blood flow and the paired posterior spinal arteries covering the remaining third. Disruptions to circulation can arise from various pathological processes, leading to ischemic injury. Atherosclerosis, where plaque buildup narrows the aorta or spinal arteries, is a common cause, particularly in older adults and individuals with cardiovascular disease. Even without complete occlusion, reduced blood supply can trigger infarction.

Embolic events also contribute to spinal cord ischemia. Emboli from cardiac sources, such as atrial fibrillation or valvular disease, may travel through the arterial system and obstruct spinal vessels. Surgical procedures involving the aorta, like aneurysm repair or dissection management, increase risk due to dislodged atheromatous debris or intraoperative vascular manipulation. In some cases, paradoxical embolism through a patent foramen ovale further complicates the condition.

Systemic hypotension is another major factor, particularly in watershed areas of the spinal cord vulnerable to perfusion fluctuations. Prolonged low blood pressure from cardiac arrest, septic shock, or excessive antihypertensive therapy can deprive the spinal cord of oxygen and nutrients. This risk is heightened in perioperative settings, where anesthesia-induced hypotension can worsen preexisting vascular insufficiency. Autonomic dysfunction in neurodegenerative diseases may also impair blood pressure regulation, increasing susceptibility to ischemic damage.

Vascular malformations, including arteriovenous fistulas and malformations, can disrupt spinal cord perfusion. These abnormal connections create high-flow shunts that divert blood from surrounding tissues, leading to chronic ischemia. Over time, increased venous pressure further compromises circulation, causing progressive neurological deterioration. Early imaging is crucial for identifying and treating these lesions.

Common Symptoms And Neurological Deficits

The clinical presentation varies depending on the affected vascular territory, with anterior spinal artery syndrome being the most common. Symptoms typically appear abruptly, reflecting sudden blood supply deprivation. Acute flaccid paralysis, often affecting both lower extremities, results from corticospinal tract involvement. Loss of pain and temperature sensation below the infarction level occurs due to spinothalamic pathway disruption, while proprioception and vibratory sense remain intact unless the posterior spinal arteries are involved.

Autonomic dysfunction frequently accompanies spinal cord infarction, particularly when the thoracic region is affected. Neurogenic bladder and bowel dysfunction lead to urinary retention or incontinence and impaired defecation control. Orthostatic hypotension can cause dizziness and syncope, while sexual dysfunction reflects autonomic fiber disruption. These issues complicate rehabilitation, requiring a multidisciplinary approach.

Pain is another common symptom, often described as burning or aching at the infarction site. Some individuals experience a tight, band-like sensation around the torso, known as girdle pain, corresponding to the dermatomal level of injury. In cases preceded by transient ischemic attacks, patients may recall brief, reversible neurological symptoms, offering diagnostic clues.

Typical Medical Evaluation Approaches

Diagnosing spinal cord infarction requires a thorough assessment integrating clinical presentation, imaging studies, and exclusion of alternative conditions. The abrupt onset of neurological deficits necessitates differentiation from other acute myelopathies, such as transverse myelitis or compressive lesions. A detailed neurological examination helps localize the injury and determine vascular involvement. Sensory level changes, flaccid paralysis, and autonomic dysfunction raise suspicion, especially in patients with vascular risk factors or recent surgery.

Magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) is the preferred diagnostic tool. While conventional MRI may reveal cord swelling or T2 hyperintensity, DWI detects restricted diffusion in ischemic tissue. A characteristic “owl’s eye” pattern, indicating bilateral anterior horn involvement, is often seen in anterior spinal artery infarction. If early imaging is inconclusive, repeat scans may be necessary. Contrast-enhanced MR angiography can identify vascular abnormalities, such as aortic dissection or arterial stenosis.

Laboratory tests support diagnosis by ruling out mimicking conditions. Inflammatory markers help assess for vasculitis, while cerebrospinal fluid analysis can distinguish ischemic injury from infectious or autoimmune causes. Elevated protein levels with a normal white blood cell count are common but nonspecific. Coagulation studies and cardiac workups may identify embolic sources, especially in younger patients without traditional atherosclerotic risk factors.

Risk Factors

Vascular disease significantly increases the risk of spinal cord infarction. Atherosclerosis and hypertension contribute to arterial narrowing and reduced perfusion, while chronic hypertension accelerates endothelial dysfunction, increasing susceptibility to ischemic events. Diabetes exacerbates risk by promoting microvascular damage and systemic inflammation, impairing normal blood flow regulation. Individuals with longstanding metabolic disorders often experience silent vascular disease progression, making them vulnerable to sudden ischemic insults.

Cardiac pathology also plays a major role, particularly in patients with atrial fibrillation or valvular disease, where embolic events are a concern. Irregular heart rhythms facilitate clot formation, which can dislodge and obstruct spinal vessels. Patients with prosthetic heart valves or recent myocardial infarctions face higher risk due to altered hemodynamics and increased thrombotic activity. Anticoagulation therapy mitigates risk, but subtherapeutic dosing or noncompliance can leave individuals vulnerable.

Variation In Clinical Presentations

Symptoms differ based on the severity, location, and extent of ischemic damage. Some patients experience immediate and profound motor and sensory loss, while others have a more gradual progression over hours or days. This variability complicates early diagnosis, particularly when initial symptoms are mild or transient. Some individuals report brief episodes of limb weakness or numbness before sustained deterioration, resembling transient ischemic attacks seen in cerebral strokes.

The level of infarction dictates specific impairments. Cervical involvement, though less common, can be devastating, leading to quadriplegia and respiratory compromise if upper segments are affected. Thoracic infarctions often result in paraparesis with pronounced bowel and bladder dysfunction, while lumbar involvement may present with lower motor neuron signs such as flaccid paralysis or areflexia. Some patients retain partial motor function but experience severe sensory disturbances, including dysesthesia or allodynia. Given this broad spectrum of clinical manifestations, a high index of suspicion is essential for timely recognition and intervention.