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Spinal Cord Infarction Clinical Presentation

  • Author: Thomas F Scott, MD; Chief Editor: Helmi L Lutsep, MD  more...
 
Updated: Aug 11, 2015
 

History

Spinal cord infarction is usually 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. Reports emphasize the occasional confusion of this diagnosis with angina pectoris or acute myocardial infarction.[3, 4]

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. The mimic of coronary ischemia is seen 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),[1] and presents as acute paraparesis or paraplegia, numbness of the legs, and inability to void.[4]

The syndrome depends on the level of the cord lesion and may vary from mild or moderate and even reversible leg weakness to quadriplegia. A guide to determine the spinal cord level is below.

Guide to clinical determination of the segmental s Guide to clinical determination of the segmental spinal cord level.

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 these 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, aortic surgeries, injections for foraminal nerve block for epidural anesthesia, or even self-injection by the addict seeking an intravenous access[4, 5, 6, 7, 8, 9] have been reported in association with and probably causative of spinal cord infarction.

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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. The images below depict sensory pathways in the spinal cord and vascular anatomy of the spinal cord in the axial plane.

Simplified representation of course of major senso Simplified representation of course of major sensory pathways in the spinal cord. Decussation of the spinothalamic tracts occurs within one or two segments of their entry.
Pattern of arterial supply to spinal cord and (lef Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.

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 relative preservation of light touch, vibration, and position sense. The image below provides a guide for clinical determination of spinal level.

Guide to clinical determination of the segmental s Guide to clinical determination of the segmental spinal cord level.

Weakness and sensory loss (for all primary sensory modalities) are found at the spinal cord segmental levels of the spinal cord infarct.

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Causes

Identifying the cause of spinal cord infarction according to clues related to the location of the vascular pathology is generally attempted. 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 as a manifestation of degenerative arteriosclerosis (with typical risk factors, most notably age related), but infarction of the spinal cord remains rare in this high risk group relative to infarction of other organs, due to the rich anastamotic network of the spinal cord.  Equally rare, but with demographics tilted towards a younger group on average, is infarction with arteritis, both in systemic lupus erythematosus and granulomatous arteritis.   Varicella zoster virus is known to induce arteritis and can rrsult in the same acute process.
  • Emboli consisting of intervertebral disk fragments have been reported to enter and occlude arteries supplying the spinal cord, not only in humans, but in other large vertabrate animals..
  • 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, and treatment of migraine headache with zolmitriptan. [10, 11, 12, 13, 14, 15]
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Contributor Information and Disclosures
Author

Thomas F Scott, MD Professor, Program Director, Department of Neurology, Drexel University College of Medicine; Director, Allegheny MS Treatment Center

Thomas F Scott, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society Advisory Board, Allegheny Chapter

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Additional Contributors

Norman C Reynolds, Jr, MD Neurologist, Veterans Affairs Medical Center of Milwaukee; Clinical Professor, Medical College of Wisconsin

Norman C Reynolds, Jr, MD is a member of the following medical societies: American Academy of Neurology, Association of Military Surgeons of the US, International Parkinson and Movement Disorder Society, Sigma Xi, Society for Neuroscience

Disclosure: Nothing to disclose.

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Transverse section of spinal cord showing location of main pathways. The lamination of fibers in posterior columns and in lateral spinothalamic and lateral corticospinal tracts is indicated (C, cervical; T, thoracic; L, lumbar; S, sacral).
Simplified representation of course of major sensory pathways in the spinal cord. Decussation of the spinothalamic tracts occurs within one or two segments of their entry.
Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.
Guide to clinical determination of the segmental spinal cord level.
Transverse section of spinal cord at T12-L1 showing infarction of central cord. The patient became paraplegic following resection of a ruptured abdominal aortic aneurysm. During surgery, prolonged occlusion of the abdominal aorta and great anterior radicular artery was necessary.
 
 
 
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