7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Spinal cord infarction: Clinical presentation and diagnosis : Michael T Mullen, MD, Michael L McGarvey, MD : Scott E Kasner, MD, Glenn A Tung, MD, FACR : Richard P Goddeau, Jr, DO, FAHA All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Sep 03, 2021. INTRODUCTION 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: Epidemiology 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".) CLINICAL PRESENTATION Onset and precipitating factors While the onset of spinal cord infarction may be abrupt, similar to cerebral infarction, a significant proportion experience a decline over a few to several hours [1,2]. In one case series of 133 patients with spinal cord infarction, the time from symptom onset to nadir deficit was more than four hours in 44 percent of patients, and greater than 12 hours in 23 percent [3]. In this same cohort, lifting, Valsalva, or other physical activity was described at or preceding symptom onset in 25 percent of cases. Most patients (72 percent) had severe back or limb pain at symptom onset. https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 1/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Neurologic syndromes 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 [1-9]. Anterior spinal artery syndrome The most common clinical presentation of a spinal cord infarction is anterior spinal artery (ASA) syndrome [1,6,10]. 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 [11]. 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 [5,12,13]. Chest pain with electrocardiogram (ECG) changes has been reported in a patient with C7 to T1 spinal cord infarction [14]. 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 [1,3-6,15]. This occurs either because of occlusion of a unilateral sulcal artery, or because incomplete collateralization with the posterior spinal artery (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 [4]. Posterior spinal artery syndrome PSA infarction produces loss of proprioception and vibratory sense below the level of the injury and total anesthesia at the level of the injury. Weakness has been described, but is typically mild and transient. Unilateral involvement is more common, but bilateral presentations have been described ( image 1) [1]. Other presentations Atypical presentations of spinal cord infarction that do not fit a well- defined vascular distribution include Brown-Sequard syndrome, full transverse lesions similar to that found in cord transection, and central cord syndrome [1,6] (see "Anatomy and localization of spinal cord disorders"). Additionally, we have observed cases of lower extremity weakness (unilateral and bilateral) without sensory loss. The etiology for this is unknown but likely relates to incomplete collateralization from the complex network of anastomosis that make up the spinal vascular supply. Among case series, these atypical, seemingly nonvascular syndromes compose one-third of patients [6]. https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 2/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Transient symptoms lasting a few minutes to several hours, so-called spinal transient ischemic attacks (TIAs), have also been described in a variety of clinical settings, but these are unusual [1,5,16,17]. Venous infarction of the spinal cord has been described, usually in association with spinal vascular malformations. These infarcts may be either hemorrhagic or nonhemorrhagic. In nonhemorrhagic venous infarcts, venous hypertension decreases the arterial-venous pressure gradient leading to decreased perfusion ( image 2). Nonhemorrhagic venous infarction typically presents with a gradual onset of progressive neurologic decline, whereas hemorrhage is associated with the sudden onset of pain and flaccid paraparesis [12]. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.) DIFFERENTIAL DIAGNOSIS While there are many potential causes of myelopathy, only a few are characterized by an abrupt symptom onset. (See "Disorders affecting the spinal cord".) Compressive myelopathy from neoplasm, epidural or subdural hematoma, or abscess are important diagnostic considerations and typically mandate urgent neuroimaging to identify findings that may require urgent surgical decompression. While these lesions typically develop over time, the clinical presentation can be fairly abrupt and mimic spinal cord infarction. (See "Disorders affecting the spinal cord", section on 'Neoplasms' and "Clinical features and diagnosis of neoplastic epidural spinal cord compression" and "Spinal epidural abscess".) Transverse myelitis is more typically associated with an evolution of myelopathic symptoms over hours and days, but these can develop in as short a period as 10 minutes [18,19]. A history of recent vaccination or viral illness may suggest this diagnosis, but these are often absent. Symptoms isolated to the anterior spinal artery (ASA) territory suggest infarction over inflammation, but this is not definitive. Other diagnostic studies (lumbar puncture, brain imaging) may be required. Because individual clinical and diagnostic features are not sensitive or specific for either diagnosis, clinicians must consider the preponderance of the evidence when determining the more likely diagnosis. Clinical and diagnostic features that favor transverse myelitis over infarction include progression of symptoms over at least a few hours, symptoms and magnetic resonance imaging (MRI) lesions that extend beyond a vascular territory, gadolinium enhancement, and cerebrospinal fluid (CSF) findings of pleocytosis or elevated immunoglobulin G (IgG) levels [20]. (See "Disorders affecting the spinal cord", section on 'Transverse myelitis'.) https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 3/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Acute polyneuropathy (eg, Guillain-Barr syndrome [GBS]) can be confused with acute myelopathy because both are associated with flaccidity and loss of reflexes in the acute stage [21] (see 'Clinical presentation' above). Contributing to potential diagnostic confusion is that back pain is a common feature in both GBS and acute spinal cord infarction. A history of ascending symptoms over time suggests GBS, while a sensory level and impaired bladder function suggest spinal cord infarction. In some cases, differentiating these diagnoses requires diagnostic tests (MRI, electromyography) and the passage of time to allow upper motor neuron signs to emerge. (See "Guillain-Barr syndrome in adults: Pathogenesis, clinical features, and diagnosis".) Epidural hematoma is an important cause of acute paraplegia in the postoperative setting, especially if the patient has had either a lumbar drain or epidural anesthesia. Although epidural hematoma usually has a more subacute presentation with evolution over time, this presentation may be obscured in the perioperative period [22]. Aortic dissection or rupture may cause paraplegia from impaired perfusion of the brain and lower extremities, as well as from spinal ischemia. It is also possible for all these mechanisms to occur simultaneously. DIAGNOSIS The diagnosis of spinal cord infarction is made in the setting of a compatible clinical syndrome: rapidly developing myelopathic deficits in the absence of another identifiable etiology by history, examination, magnetic resonance imaging (MRI), or other testing (when indicated) [3]. Spinal MRI MRI is required in the diagnosis of spinal cord infarction. Perhaps its most important role is to rule out the alternative diagnosis of compressive myelopathy. MRI can also provide confirmatory evidence of spinal cord infarction and may provide information as to the underlying etiology. In most cases, this test should be performed urgently, although it may be deferred if the patient requires urgent aortic surgery or another life-saving intervention. MRI changes associated with spinal cord ischemia include hyperintensities on T2-weighted and short-tau inversion recovery images( image 3 and image 1 and image 2 and image 4). The sensitivity of standard MRI is limited, particularly in the first several hours. The percentage of patients with T2 changes on MRI scan in published reports ranges from 45 to 73 percent depending in part on the scan's timing [1,3,5,6,12,23,24]. If clinical suspicion is high and the initial MRI is normal, follow-up imaging should be obtained. However, a significant minority of patients (14 percent in one series) will also have normal follow-up MRI scans [7,24]. A finding of restricted diffusion on diffusion-weighted images (DWI-MRI) appears to be significantly more https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 4/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate sensitive than standard T2 images ( image 5) [25-29]. While the limited number of case reports precludes a definitive estimate of its sensitivity, in one series of 19 patients with spinal cord infarction, restricted diffusion was found in all patients [29]. A finding of T2 signal abnormality, even with restricted diffusion, is not specific for ischemia and can be seen in transverse myelitis and other intrinsic cord pathologies. The finding of T2- hyperintense signal restricted to a spinal vascular territory or the ventral horns ("owl's eyes" or "snake eyes" sign) is more specific for spinal cord infarction ( image 1 and image 2 and image 4). A finding of vertebral body infarction adjacent to a cord signal abnormality on MRI is a specific indicator of ischemia and a useful confirmatory sign if present [30]. However, this is found in only 4 to 35 percent of patients, and its absence does not exclude spinal cord infarction [1,3,6,8]. MRI may also help define the underlying etiology: Intervertebral disc disease at the level of infarction may suggest possible fibrocartilaginous embolism. Spondylotic disease may suggest a possible bony compression mechanism, particularly if the onset of symptoms is associated with activity involving twisting or torquing of the spine [8]. Spinal cord vascular malformations also have distinct patterns of abnormalities that may be seen on MRI [31]. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.) In one case series, vertebral body infarction was highly associated with aortic disease pathology [8]. Other tests Further testing is not always necessary. As an example, in the setting of paraplegia after aortic surgery, a patient with typical spine MRI findings will likely not require further testing. However, depending on the clinical presentation, other tests should be ordered to further exclude alternative diagnoses (see 'Differential diagnosis' above) and to identify an underlying etiology ( table 1). Aortic dissection can be identified by multiplane transesophageal echocardiography (TEE), chest computed tomography (CT), and MRI. Descending aortic dissection is a known cause of spinal cord infarction; it can lead to morbidity if unrecognized. Therefore, this should be considered and specifically excluded in all at-risk patients including those who present with prominent pain, abnormal distal pulses, known aortic aneurysm, and/or an underlying collagen disorder (Marfan syndrome). A low threshold for this diagnosis should also include https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 5/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate older adults with vascular risk factors in whom the underlying cause of spinal cord infarction is not immediately known. In patients with hemodynamic instability, this evaluation will take priority over spine imaging. (See "Clinical features and diagnosis of acute aortic dissection".) Vascular imaging, either CT angiography or magnetic resonance angiography, should be performed to exclude a vertebral artery dissection in a patient with a rostral cervical cord infarction. A gadolinium-enhanced MRI of the brain may be helpful to exclude multiple sclerosis if the clinical presentation is consistent with transverse myelitis. Echocardiography can be performed to look for a source of embolism. A lumbar puncture and cerebrospinal fluid (CSF) analysis should be performed in younger patients to look for signs of infection or inflammatory diseases. CSF testing should include cell count, protein, glucose, Gram stain and culture, cytology/flow cytometry, oligoclonal bands, as well as tests for syphilis, Lyme, herpes, varicella, and cytomegalovirus. Serum tests for syphilis, Lyme, HIV, enterovirus, coxsackie A and B, adenovirus, and Epstein-Barr virus may be of value. CSF analysis in spinal cord infarction is typically normal, but there can be pleocytosis (rarely more than 100 white blood cell count [WBC]) and an elevated protein (usually less than 119 mg/dL) [3-5,7,24]. Blood tests to evaluate a possible hypercoagulable condition should be performed when the cause of spinal cord infarction is obscure, particularly in younger patients and those without vascular risk factors. Urine or blood toxicology screen should exclude cocaine and other drugs of abuse. Rheumatologic tests are likely of low yield if there are no other suggestive clinical features, but these tests (sedimentation rate, antinuclear antibody, antineutrophil cytoplasmic antibodies, and SSA/B antibodies) could be considered. Initial vascular imaging with contrast-enhanced MR- or CT-angiography should be performed when there is either clinical concern for a vascular malformation, dural arteriovenous fistula, or suspicious findings on MRI (eg, evidence of venous infarction or enlarged venous collateral vessels surrounding a cord with abnormal T2- or STIR- hyperintense signal) ( image 2). Digital subtraction angiography (DSA) is performed with abnormal noninvasive vascular imaging to further characterize lesions. In addition, DSA is performed in patients with https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 6/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate normal noninvasive vascular imaging when clinical suspicion for a vascular malformation is high. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.) SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".) SUMMARY AND RECOMMENDATIONS Spinal cord infarction is a rare condition caused by a wide array of pathologic conditions. Clinical presentation Most patients with spinal cord infarction present with acute neurologic deficits attributable to the anterior spinal artery (ASA) territory. However, one- third of patients may have less typical presentations including posterior spinal artery (PSA), central cord, and complete cord transection syndromes. (See 'Clinical presentation' above.) Differential diagnosis Acute spinal cord infarction must be distinguished from lesions compressing the spinal cord. Transverse myelitis and acute demyelinating polyneuropathy are other important diagnostic considerations, depending on the clinical setting. (See 'Differential diagnosis' above.) Diagnosis The diagnosis of spinal cord infarction is made in the setting of a compatible clinical syndrome: rapidly developing myelopathic deficits in the absence of another identifiable etiology by history, examination, magnetic resonance imaging (MRI), or other testing. (See 'Diagnosis' above.) MRI of the spine is performed to exclude a compressive myelopathy, as well as to provide evidence supporting the diagnosis of infarction. Spine MRI findings have imperfect sensitivity and specificity for ischemia. However, diffusion-weighted images (DWI-MRI) improve the sensitivity of MRI to detect acute spinal ischemia. (See 'Spinal MRI' above.) Additional testing Other tests are used to further exclude alternative diagnoses and to identify an underlying etiology ( table 1). The choice of tests is tailored to the clinical situation and may include echocardiography, brain imaging, vascular imaging, and laboratory tests to identify for a hypercoagulable condition. (See 'Other tests' above.) https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 7/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Use of UpToDate is subject to the Terms of Use. REFERENCES 1. 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. 2. 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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. 9. 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. 10. Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. Spinal cord infarction: MR imaging and clinical features in 16 cases. Neuroradiology 2002; 44:851. 11. Foo D, Rossier AB. Anterior spinal artery syndrome and its natural history. Paraplegia 1983; 21:1. 12. Mohr JP, Benavente O, Barnett HJ. Spinal Cord Ischemia. In: Stroke Pathophysiology, Diagno sis, and Management, Barnett HJ, Mohr JP, Stein BM, Yatsu FM (Eds), Churchill Livingstone, P hiladelphia 1998. p.423. 13. Cheung AT, Weiss SJ, McGarvey ML, et al. Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction. 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In: Resonance Imaging of the Brain and Spine, 2nd ed, https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 9/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Atlas SW (Ed), Lippincott, Philadelphia 2006. p.1387. Topic 1117 Version 17.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 10/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate GRAPHICS Spinal cord infarction in the distribution of the posterior spinal artery Sagittal T2-weighted MRI image (A) shows hyperintensity in dorsal thoracic spinal cord (arrow). Axial turbo spin-echo T2-weighted MRI images (B, C) show hyperintensities consistent with infarction in the distribution of the posterior spinal arteries (arrowheads). Courtesy of Glenn A Tung, MD. Graphic 132591 Version 1.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 11/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Venous infarction of the spinal cord from a spinal AVF Sagittal T2-weighted MRI image (A) shows hyperintensity in the lower half of the thoracic spinal cord (arrows). Axial turbo spin-echo T2-weighted MRI images (B, C, D) shows hyperintensity in greater than half of the spinal cord in a pattern atypical for arterial infarction (smaller arrowhead) as well as linear hypodensities in the subarachnoid space consistent with small vessels (short arrows). Spinal angiogram (E) shows catheter (thick arrow), spinal dural AVF (dashed arrow), and dilated intradural veins (larger arrowheads). AVF: arteriovenous fistula; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD. Graphic 132592 Version 1.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 12/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate MRI findings in spinal cord ischemia Magnetic resonance images (MRI) of the thoracolumbar spine demonstrating spinal cord infarction in a patient with paraplegia after thoracoabdominal aneurysm repair. T2 weighted sagittal imaging through the center of the spinal cord (left panel) showed central infarction extending from the high thoracic level into the lumbar segments. T2 weighted axial images of the spinal cord at the thoracic level demonstrated central infraction (right panel). Courtesy of Michael L McGarvy, MD and Michael Mullen, MD. Graphic 72280 Version 4.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 13/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Spinal cord infarction in the distribution of the anterior spinal artery Sagittal STIR MRI image (A) shows hyperintensity in lower cervical and upper thoracic cord (arrows). Axial turbo spin-echo T2-weighted images (B, C) show hyperintensities in the ventral horns of the central gray matter ("owl's eyes sign") consistent with acute cervicothoracic cord infarction (arrowheads). STIR: short tau inversion recovery; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD. Graphic 132593 Version 1.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 14/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate MRI sequences showing acute spinal cord infarction Sagittal MRI images showing contrast enhancement (arrow) on post-contrast T1-weighted image (A) and reduced diffusivity (arrowheads) on DWI image (B) and ADC map image (C). MRI: magnetic resonance imaging; DWI: diffusion-weighted imaging; ADC: apparent diffusion coefficient. Courtesy of Glenn A Tung, MD. Graphic 132595 Version 1.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 15/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Causes of spinal cord infarction Aorta disease, procedures Infection Aortic surgery Bacterial meningitis Thoracic endovascular aortic repair (TEVAR) Syphilis Aortic dissection Mucormycosis Traumatic rupture of the aorta Hematologic disease Aortic thrombosis Hypercoagulable conditions Aortic aneurysm Sickle cell anemia Coarctation of the aorta Non-aortic surgeries Aortography Spine disease Systemic hypoperfusion Spine surgery Cardiac arrest Cervical spondylosis Systemic bleeding Fibrocartilaginous embolism Cardiogenic embolism Epidural steroid injections Atrial myxoma Miscellaneous Mitral valve disease Cocaine abuse Patent foramen ovale Vertebral artery dissection Bacterial endocarditis Spinal vascular malformation Cardiac catheterization Decompression sickness Vasculitis Systemic lupus erythematosus Polyarteritis nodosa Behcet syndrome Giant cell arteritis Graphic 57862 Version 7.0 https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 16/17 7/5/23, 11:59 AM Spinal cord infarction: Clinical presentation and diagnosis - UpToDate Contributor Disclosures Michael T Mullen, MD Grant/Research/Clinical Trial Support: NINDS [Asymptomatic carotid disease]. All of the relevant financial relationships listed have been mitigated. Michael L McGarvey, MD No relevant financial relationship(s) with ineligible companies to disclose. Scott E Kasner, MD Grant/Research/Clinical Trial Support: Bayer [Stroke]; Bristol Meyers Squibb [Stroke]; Medtronic [Stroke]; WL Gore and Associates [Stroke]. Consultant/Advisory Boards: Abbvie [Stroke]; AstraZeneca [Stroke]; BMS [Stroke]; Diamedica [Stroke]; Medtronic [Stroke]. All of the relevant financial relationships listed have been mitigated. Glenn A Tung, MD, FACR No relevant financial relationship(s) with ineligible companies to disclose. Richard P Goddeau, Jr, DO, FAHA No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/spinal-cord-infarction-clinical-presentation-and-diagnosis/print 17/17