eMedicine Specialties > Neurology > Neurological Emergencies

Spinal Cord Infarction

Author: Edward Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
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Updated: Mar 29, 2006

Introduction

Background

Occlusive vascular lesions affecting the spinal cord (spinal stroke) are diagnostic challenges. As is the case for the more common cerebrovascular accident affecting cerebral circulation, an acute onset and a requirement to exclude hemorrhage are paramount concerns. The circulation to the spinal cord has unique features related to the elongated and multimeric anatomy of the cord that affect both mechanism and clinical presentation (see Images 1-3).

Pathophysiology

The anterior spinal artery is a single long anastomotic channel that lies at the mouth of the anterior central sulcus and supplies the circulation to the anterior two thirds of the spinal cord (see Image 3). It gives origin to sulcal arteries that take an arching course to one or the other anterior gray horns. The posterior spinal arteries are smaller paired arteries lying just medial to the dorsal roots. The arterial supply of the spinal cord arises from the aorta and at its cephalad and caudal ends from tributaries of the subclavian and iliac arteries. Eight to ten unpaired anterior medullary arteries are branches of the larger afferent aorta and vertebral and iliac arteries. The largest anterior medullary artery, the great anterior medullary artery of Adamkiewicz, which is susceptible to occlusion with neurologic deficit, is located at the lumbar enlargement, usually at L2 on the left side (but may be at any point from T8 to L2).

Frequency

United States

Spinal cord infarction is not common, but only fragmentary or indirect data are available on incidence or prevalence. A large study showed that only 9 of 3784 autopsies revealed spinal cord infarction, with a rate of occurrence of 0.23% at death. Conversely, if spinal stroke is approximately 1.2% of strokes, an overall annual incidence of 12 in 100,000 can be estimated.

International

International incidence is similar to that in the United States. Recent reports that describe patients developing spinal cord infarction in an increasing number of situations and pathologies would influence this because procedures ranging from major surgery to injections for epidural anesthesia, infections and especially meningitis, and medications (eg, zolmitriptan for migraine) vary in different countries.

Mortality/Morbidity

The risk to life and its quality from spinal cord infarction is substantial because of the disability, which can be severe, with paraplegia, risk of pulmonary emboli, and risk of infection (eg, bladder, lungs, decubiti). However, no epidemiologic studies are available because of the relatively small number of patients affected.

Published series of reports of spinal cord infarction are relatively small ranging up to 36-44 patients. They find a mortality in the vicinity of 20-25% of patients admitted to hospital with spinal cord infarction (Cheshire, 1996; de la Barrera, 2001).

Race

No relationship to race is reported.

Sex

No relationship to sex is reported.

Age

No relationship to age is reported. However, the reported series do have a median age of 52 years.

Clinical

History

Spinal cord infarction is marked by an acute onset, often heralded by sudden and severe spinal (back) pain, which may radiate caudad. This is associated with bilateral weakness, paresthesias, and sensory loss. Loss of sphincter control with hesitancy and inability to void or defecate becomes evident within a few hours.

• The spinal cord stroke, either ischemic or hemorrhagic, has an acute and often apoplectic onset evolving over minutes. This is emphasized because many of the confounding diagnoses, including acute transverse myelopathy, viral myelitis, Guillain-Barré syndrome, and mass lesions in the spinal canal, develop over 24-72 hours with an acute but discernibly slower evolution than the vascular lesions. Recent reports emphasize the occasional confusion of this diagnosis with angina pectoris or acute myocardial infarction (Chesire, 2000; Gross, 2001; Combarros, 2002).
• Neurologic deficit may occur without pain, but most (>80%) spinal infarcts are painful. This is an interesting and unexplained difference from cerebral infarction, which is usually not painful. However, it should be mentioned that closer scrutiny of this association in recent years has found a higher proportion of patients without pain (de la Barrera, 2002). In addition, the mimic of coronary ischemia is because of the occurrence of chest pain, which may be severe.
• Uncomplicated spinal cord infarction is most commonly thoracic (with peak at T8 in the series reported by Cheshire [1996]), and presents as acute paraparesis or paraplegia, numbness of the legs, and inability to void.
• The syndrome depends on the level of the cord lesion and may vary from mild or moderate and even reversible leg weakness to quadriplegia (see Image 4).
• Fever is a warning ("red flag"); heed this warning by considering infectious origins of a spinal cord syndrome, particularly acute bacterial meningitis, and focal extramedullary spinal lesions (eg, epidural and subdural abscess, granuloma) and viral myelitis due to herpes simplex, varicella-zoster, and other viruses.
• Many reports exist, and theses are usually of single or a few cases of spinal cord infarction occurring in context of and classed as complications of surgical procedures in which hypotension and prolonged positioning (eg, seated neurosurgical approaches, hyperlordosis) may be prominent factors. Also, injections for foraminal nerve block, for epidural anesthesia, or even self-injection by the addict seeking an intravenous access (Joseph, 2004) have been reported in association with and probably causative of spinal cord infarction.

Physical

Neurologic dysfunction usually (ie, in approximately 95% of reported cases) stems from a lesion located in the anterior two thirds (or in the central "watershed") of the spinal cord and spares vibration and position sense perception, which are carried by the posterior columns and are relatively spared. See Image 2 for sensory pathways in the spinal cord and Image 3 for vascular anatomy of the spinal cord in the axial plane.

• In the acute stage (usually for several days),"spinal shock" with flaccid muscle tone and areflexia, including absent Babinski reflexes, is observed commonly.
• The classic presentation is a sensory pattern distal to the lesion, superficial pain and temperature discrimination are lost bilaterally with preservation of light touch, vibration, and position sense. See Image 4 for clinical determination of spinal level.
• Weakness and sensory loss (for all primary sensory modalities) are found at the spinal cord segmental levels of the spinal cord infarct.

Causes

Classifying the causes of spinal cord infarction according to the location of the vascular pathology is convenient and systematic. The pathology may involve the aorta or an intervening arterial feeder (eg, thoracic, intercostal, or cervical branch from subclavian or vertebral artery), or the radicular artery may affect the anterior spinal artery and intrinsic arterial vessels within the spinal cord. Spinal venous pathology may produce spinal infarction, although this is clinically rare.

• Involvement of intrinsic cord vessels has been reported with arteritis, both in systemic lupus erythematosus and granulomatous arteritis, and from emboli of atheroma or even from compression by or emboli of intervertebral disk fragments.
• Anterior spinal artery occlusion has been reported with arteritis, including that associated with syphilis and diabetes mellitus; after trauma; spontaneously or without recognized cause; and as a complication of spinal angiography, cervical spondylosis, spinal adhesive arachnoiditis, administration of intrathecal phenol, and spinal anesthesia.
• Aortic disease has produced spinal infarction in a variety of situations including dissecting aneurysm; aortic surgery, especially with aortic cross-clamping above the renal artery (below that level anastomotic flow via the artery of Adamkiewicz usually provides protective circulation); aortography; atherosclerotic embolization; and aortic thrombosis.
• Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy; circulatory failure as a result of cardiac arrest or prolonged hypotension; and vascular steal in the presence of an arteriovenous malformation, or vascular compression by tumors in the spinal canal, vertebral fracture, or a herniated intervertebral disk. In 2000, Vijayan and Peacock reported a spinal cord infarct that occurred after treatment of a migraine headache with zolmitriptan.

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