Spinal cord infarction: Clinical presentation and diagnosis
- Michael T Mullen, MD
Michael T Mullen, MD
- Assistant Professor of Neurology
- University of Pennsylvania School of Medicine
- Michael L McGarvey, MD
Michael L McGarvey, MD
- Associate Professor of Neurology
- University of Pennsylvania School of Medicine
Spinal cord infarction is a rare but often devastating disorder caused by a wide array of pathologic states. Patients typically present with acute paraparesis or quadriparesis, depending on the level of the spinal cord involved. The diagnosis is generally made clinically, with neuroimaging to confirm the diagnosis and exclude other conditions.
This topic discusses the clinical features and diagnosis of spinal cord infarction. The vascular anatomy of the spinal cord, and the etiologies, prognosis, treatment, and chronic complications of spinal cord infarction are discussed separately. Other causes of myelopathy are also discussed separately. (See "Spinal cord infarction: Vascular anatomy and etiologies" and "Spinal cord infarction: Prognosis and treatment" and "Chronic complications of spinal cord injury and disease" and "Disorders affecting the spinal cord" and "Anatomy and localization of spinal cord disorders".)
As with cerebral infarction, the onset of spinal cord infarction is typically abrupt [1,2]. In a few cases, symptoms progress over several minutes or even a few hours. The neurologic presentation of spinal cord infarction is largely defined by the vascular territory involved. The severity of the impairments can vary widely, from paraplegia to minor weakness. The involved cord level can be anywhere along the cord's length, depending in part on the underlying etiology. Back or neck pain often accompanies spinal cord ischemia, and has been reported in as many as 70 percent of patients, typically occurring at the level of the lesion [1-8].
Anterior spinal artery syndrome — The most common clinical presentation of a spinal cord infarction is anterior spinal artery (ASA) syndrome [1,5,9]. Consistent with its functional neuroanatomy, an ASA infarct typically presents as loss of motor function and pain/temperature sensation, with relative sparing of proprioception and vibratory sense below the level of the lesion . The acute stages are characterized by flaccidity and loss of deep tendon reflexes; spasticity and hyperreflexia develop over ensuing days and weeks. Autonomic dysfunction may be present and can manifest as hypotension (either orthostatic or frank hypotension), sexual dysfunction, and/or bowel and bladder dysfunction [4,11,12]. Chest pain with ECG changes has been reported in a patient with C7 to T1 spinal cord infarction . In the acute evaluation of patients, it is important to recognize that hypotension may be both a cause as well as a manifestation of spinal cord ischemia. If the lesion is in the rostral cervical cord, respiration is compromised.
While bilateral presentations are more common, unilateral ASA deficits are frequently reported [1,3-5,14]. This occurs either because of occlusion of a unilateral sulcal artery, or because incomplete collateralization with the PSA maintains perfusion on one side of the cord. Very rostral ASA infarctions produce sensory loss in all modalities because of involvement of the medial lemniscus in the medulla .To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
- Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006; 63:1113.
- Cheng MY, Lyu RK, Chang YJ, et al. Spinal cord infarction in Chinese patients. Clinical features, risk factors, imaging and prognosis. Cerebrovasc Dis 2008; 26:502.
- Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases and review of the literature. Medicine (Baltimore) 1989; 68:282.
- Cheshire WP, Santos CC, Massey EW, Howard JF Jr. Spinal cord infarction: etiology and outcome. Neurology 1996; 47:321.
- Nedeltchev K, Loher TJ, Stepper F, et al. Long-term outcome of acute spinal cord ischemia syndrome. Stroke 2004; 35:560.
- Masson C, Pruvo JP, Meder JF, et al. Spinal cord infarction: clinical and magnetic resonance imaging findings and short term outcome. J Neurol Neurosurg Psychiatry 2004; 75:1431.
- Cheng MY, Lyu RK, Chang YJ, 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; 256:1418.
- Hsu CY, Cheng CY, Lee JD, et al. Clinical features and outcomes of spinal cord infarction following vertebral artery dissection: a systematic review of the literature. Neurol Res 2013; 35:676.
- Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. Spinal cord infarction: MR imaging and clinical features in 16 cases. Neuroradiology 2002; 44:851.
- Foo D, Rossier AB. Anterior spinal artery syndrome and its natural history. Paraplegia 1983; 21:1.
- Mohr JP, Benavente O, Barnett HJ. Spinal Cord Ischemia. In: Stroke Pathophysiology, Diagnosis, and Management, Barnett HJ, Mohr JP, Stein BM, Yatsu FM (Eds), Churchill Livingstone, Philadelphia 1998. p.423.
- Cheung AT, Weiss SJ, McGarvey ML, et al. Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction. Ann Thorac Surg 2002; 74:413.
- Nakae Y, Johkura K, Kudo Y, Kuroiwa Y. Spinal cord infarction with cervical angina. J Neurol Sci 2013; 324:195.
- STEEGMANN AT. Syndrome of the anterior spinal artery. Neurology 1952; 2:15.
- Hussain MS, Shuaib A, Siddiqi ZA. Spinal cord transient ischemic attacks: a possible role for abciximab. Neurology 2005; 64:761.
- Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and nosology of acute transverse myelitis. Neurology 2002; 59:499.
- Wilmshurst JM, Walker MC, Pohl KR. Rapid onset transverse myelitis in adolescence: implications for pathogenesis and prognosis. Arch Dis Child 1999; 80:137.
- Nance JR, Golomb MR. Ischemic spinal cord infarction in children without vertebral fracture. Pediatr Neurol 2007; 36:209.
- Hui AC, Wong KS, Fu M, Kay R. Ischaemic myelopathy presenting as Guillain-Barré syndrome. Int J Clin Pract 2000; 54:340.
- SreeHarsha CK, Rajasekaran S, Dhanasekararaja P. Spontaneous complete recovery of paraplegia caused by epidural hematoma complicating epidural anesthesia: a case report and review of literature. Spinal Cord 2006; 44:514.
- Salvador de la Barrera S, Barca-Buyo A, Montoto-Marqués A, et al. Spinal cord infarction: prognosis and recovery in a series of 36 patients. Spinal Cord 2001; 39:520.
- Robertson CE, Brown RD Jr, Wijdicks EF, Rabinstein AA. Recovery after spinal cord infarcts: long-term outcome in 115 patients. Neurology 2012; 78:114.
- Thurnher MM, Bammer R. Diffusion-weighted MR imaging (DWI) in spinal cord ischemia. Neuroradiology 2006; 48:795.
- Beslow LA, Ichord RN, Zimmerman RA, et al. Role of diffusion MRI in diagnosis of spinal cord infarction in children. Neuropediatrics 2008; 39:188.
- Küker W, Weller M, Klose U, et al. Diffusion-weighted MRI of spinal cord infarction--high resolution imaging and time course of diffusion abnormality. J Neurol 2004; 251:818.
- Shinoyama M, Takahashi T, Shimizu H, et al. Spinal cord infarction demonstrated by diffusion-weighted magnetic resonance imaging. J Clin Neurosci 2005; 12:466.
- Nogueira RG, Ferreira R, Grant PE, et al. Restricted diffusion in spinal cord infarction demonstrated by magnetic resonance line scan diffusion imaging. Stroke 2012; 43:532.
- Faig J, Busse O, Salbeck R. Vertebral body infarction as a confirmatory sign of spinal cord ischemic stroke: report of three cases and review of the literature. Stroke 1998; 29:239.
- Hurst RW. Spinal vascular disorders. In: Resonance Imaging of the Brain and Spine, 2nd, Atlas SW (Ed), Lippincott, Philadelphia 2006. p.1387.
- Chen J, Gailloud P. Safety of spinal angiography: complication rate analysis in 302 diagnostic angiograms. Neurology 2011; 77:1235.