Spinal Cord Infarction Clinical Presentation
- Author: Thomas F Scott, MD; Chief Editor: Helmi L Lutsep, MD more...
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), 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. A guide to determine the spinal cord level is below.
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.
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.
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.
Weakness and sensory loss (for all primary sensory modalities) are found at the spinal cord segmental levels of the spinal cord infarct.
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]
Cheshire WP, Santos CC, Massey EW, Howard JF Jr. Spinal cord infarction: etiology and outcome. Neurology. 1996 Aug. 47(2):321-30. [Medline].
Salvador de la Barrera S, Barca-Buyo A, Montoto-Marques A. Spinal cord infarction: prognosis and recovery in a series of 36 patients. Spinal Cord. 2001 Oct. 39(10):520-5. [Medline].
Combarros O, Vadillo A, Gutierrez-Perez R. Cervical spinal cord infarction simulating myocardial infarction. Eur Neurol. 2002. 47(3):185-6. [Medline].
Weber P, Vogel T, Bitterling H, Utzschneider S, von Schulze Pellengahr C, Birkenmaier C. Spinal cord infarction after operative stabilisation of the thoracic spine in a patient with tuberculous spondylodiscitis and sickle cell trait. Spine. 2009 Apr 15. 34(8):E294-7. [Medline].
Joseph G, Santosh C, Marimuthu R. Spinal cord infarction due to a self-inflicted needle stick injury. Spinal Cord. 2004 Nov. 42(11):655-8. [Medline].
Hogan EL, Romanul FC. Spinal cord infarction occurring during insertion of aortic graft. Neurology. 1966 Jan. 16(1):67-74. [Medline].
Ross RT. Spinal cord infarction in disease and surgery of the aorta. Can J Neurol Sci. 1985 Nov. 12(4):289-95. [Medline].
Faivre A, Bonnel S, Leyral G, Gisserot O, Alla P, Valance J. [Essential thrombocythemia presenting as spinal cord infarction.]. Presse Med. 2009 Apr 22. [Medline].
Lyders EM, Morris PP. A Case of Spinal Cord Infarction Following Lumbar Transforaminal Epidural Steroid Injection: MR Imaging and Angiographic Findings. AJNR Am J Neuroradiol. 2009 Apr 15. [Medline].
Zhang J, Huan Y, Qian Y. Multishot diffusion-weighted imaging features in spinal cord infarction. J Spinal Disord Tech. 2005 Jun. 18(3):277-82. [Medline].
Vijayan N, Peacock JH. Spinal cord infarction during use of zolmitriptan: a case report. Headache. 2000 Jan. 40(1):57-60. [Medline].
Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases and review of the literature. Medicine (Baltimore). 1989 Sep. 68(5):282-92. [Medline].
Satran R. Spinal cord infarction. Stroke. 1988 Apr. 19(4):529-32. [Medline].
Lee SH, Kim SB, Choi SG, Lim YJ. Paraplegia due to Spinal Cord Infarction After Lifting Heavy Objects. J Korean Neurosurg Soc. 2008 Feb. 43(2):114-6. [Medline]. [Full Text].
Tosi L, Rigoli G, Beltramello A. Fibrocartilaginous embolism of the spinal cord: a clinical and pathogenetic reconsideration. J Neurol Neurosurg Psychiatry. 1996 Jan. 60(1):55-60. [Medline]. [Full Text].
Weidauer S, Nichtweiss M, Lanfermann H. Spinal cord infarction: MR imaging and clinical features in 16 cases. Neuroradiology. 2002 Oct. 44(10):851-7. [Medline].
Luo CB, Chang FC, Teng MM. Magnetic resonance imaging as a guide in the diagnosis and follow-up of spinal cord infarction. J Chin Med Assoc. 2003 Feb. 66(2):89-95. [Medline].
KÃ¼ker W, Weller M, Klose U. Diffusion-weighted MRI of spinal cord infarction--high resolution imaging and time course of diffusion abnormality. J Neurol. 2004 Jul. 251(7):818-24. [Medline].
Shinoyama M, Takahashi T, Shimizu H. Spinal cord infarction demonstrated by diffusion-weighted magnetic resonance imaging. J Clin Neurosci. 2005 May. 12(4):466-8. [Medline].
Thomas T, Branson HM, Verhey LH, Shroff M, Stephens D, Magalhaes S, et al. The Demographic, Clinical, and Magnetic Resonance Imaging (MRI) Featuresof Transverse Myelitis in Children. J Child Neurol. 2012;27:11-21. 1. 27:11-21. [Full Text].
Robertson CE, Brown RD Jr, Wijdicks EF, Rabinstein AA. Recovery after spinal cord infarcts: Long-term outcome in 115 patients. Neurology. 2012 Jan 10. 78(2):114-21. [Medline].
Castro-Moure F, Kupsky W, Goshgarian HG. Pathophysiological classification of human spinal cord ischemia. J Spinal Cord Med. 1997 Jan. 20(1):74-87. [Medline].
Cheng MY, Lyu RK, Chang YJ, Chen CM, Chen ST, Wai YY, et al. Concomitant spinal cord and vertebral body infarction is highly associated with aortic pathology: a clinical and magnetic resonance imaging study. J Neurol. 2009 Apr 28. [Medline].
Cheshire WP Jr. Spinal cord infarction mimicking angina pectoris. Mayo Clin Proc. 2000 Nov. 75(11):1197-9. [Medline].
Cunningham JN. Spinal cord ischemia. Semin Thorac Cardiovasc Surg. 1973. 10:3-5.
Di Chiro G, Herdt JR. Angiographic demonstration of spinal cord arterial occlusion in postradiation myelomalacia. Radiology. 1973 Feb. 106(2):317-9. [Medline].
Garland H, Greenberg J, Harriman DG. Infarction of the spinal cord. Brain. 1966 Dec. 89(4):645-62. [Medline].
Gass A, Back T, Behrens S, Maras A. MRI of spinal cord infarction. Neurology. 2000 Jun 13. 54(11):2195. [Medline].
Hogan EL, Dale AJD. Disorders of the spinal cord. In: Clinical Medicine. Vol 10. 1982:1-36.
Laguna J, Cravioto H. Spinal cord infarction secondary to occlusion of the anterior spinal artery. Arch Neurol. 1973 Feb. 28(2):134-6. [Medline].
Leite I, Monteiro L. Spinal cord infarction. Neurology. 1997 May. 48(5):1478. [Medline].
Wheeler HB, O'Donnell JA, Anderson FA. Bedside screening for venous thrombosis using occlusive impedance phlebography. Angiology. 1975 Feb. 26(2):199-210. [Medline].
Young G, Krohn KA, Packer RJ. Prothrombin G20210A mutation in a child with spinal cord infarction. J Pediatr. 1999 Jun. 134(6):777-9. [Medline].