Spinal cord infarction: Clinical presentation and diagnosis

INTRODUCTION — Spinal cord infarction is a rare but often devastating vascular disorder that may be caused by one of several etiologies. 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 clinical diagnosis and exclude other conditions.

This topic will review the clinical features and diagnosis of acute spinal cord infarction. The etiologies, treatment, prognosis, and chronic complications of spinal cord infarction are discussed separately.

●(See "Spinal cord infarction: Epidemiology and etiologies".)

●(See "Spinal cord infarction: Treatment and prognosis".)

●(See "Chronic complications of spinal cord injury and disease".)

Other causes of myelopathy are also discussed elsewhere. (See "Disorders affecting the spinal cord".)

CLINICAL FEATURES

Presentation — Spinal cord infarction typically presents with acute onset bilateral lower extremity weakness. However, some patients may present with acute weakness in the arms and legs or sensory loss in the limbs; specific symptoms vary according to the location of the injury along the spine and vascular territory involved.

Onset and progression — While the onset of spinal cord infarction may be abrupt, similar to cerebral infarction, a significant proportion of patients 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 of patients [3].

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 [1,4-6].

Triggers — Lifting, Valsalva, or other physical activity occurs at or immediately preceding symptom onset in 25 to 58 percent of cases [3,7]. In one large series of 133 patients with spinal cord infarction, severe back or limb pain was present at symptom onset in 72 percent [3].

Neurologic signs

●Weakness and/or numbness – Bilateral weakness with or without sensory abnormalities is a common feature of many cases of spinal cord infarction because the single anterior spinal artery supplies the bilateral areas of the spinal cord [8]. The severity of motor and sensory impairments can vary widely from complete plegia to minor weakness. The involved cord level can be anywhere along the cord’s length, depending in part on the underlying etiology (table 1).

Paraplegia (of the legs) is most common, but additional weakness of the arms and even respiratory failure may occur with infarction of the cervical spinal cord.

●Pain – Back or neck pain often accompanies spinal cord ischemia and typically occurs at the level of the lesion [1-4,9-13].

●Reflex abnormalities – Muscle stretch reflexes at and below the spinal level of the injury are typically diminished or absent acutely. Within days to weeks, stretch reflexes will become hyperactive below the level of the injury but may remain absent at the level of the injury when injury occurs to anterior horn cell bodies or nerve roots involved in the specific reflex loop [8].

●Autonomic dysfunction – Hemodynamic instability including hypo- or hypertension may occur during the acute setting of spinal cord infarction of the cervical or upper thoracic cord [14]. It is important to recognize that hypotension may be both a cause as well as a manifestation of spinal cord ischemia. (See "Spinal cord infarction: Epidemiology and etiologies", section on 'Systemic hypotension'.)

Acute spinal cord infarction may also cause fever, bladder/bowel dysfunction, or sexual dysfunction [4,15,16]. Chest pain with electrocardiogram (ECG) changes has been reported in a patient with C7 to T1 spinal cord infarction due to autonomic dysfunction [17].

Specific neurologic syndromes — The neurologic presentation of spinal cord infarction is largely defined by the vascular territory involved.

Anterior spinal artery syndrome — The most common clinical presentation of a spinal cord infarction is anterior spinal artery (ASA) syndrome [1,10,18]. Consistent with its functional neuroanatomy, an ASA infarct typically presents as loss of motor function along with loss of pain and temperature sensation, with relative sparing of proprioception and vibratory sense below the level of the lesion (figure 1) [19].

While bilateral presentations are more common, unilateral ASA deficits are frequently reported [1,3,4,9,10,20]. In the hyperacute setting, patients may present with initial isolated proximal leg weakness. 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 [9].

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 (figure 2). 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 syndromes — Uncommon clinical presentations of spinal cord infarction that do not conform to a well-defined arterial distribution may occur in the setting of systemic hypoperfusion, venous infarction, or hemorrhagic infarction. Vascular malformations may cause either hemorrhagic or nonhemorrhagic infarctions. 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 arterial ischemic spinal infarction presents with a more acute onset of symptoms, and hemorrhage is typically associated with an abrupt onset of pain and flaccid paraparesis [15]. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.)

Specific clinical syndromes that may occur with spinal cord infarction include [1,10,21,22]:

●Brown-Sequard (hemicord) syndrome – ipsilateral weakness and loss of vibration/proprioception and contralateral loss of pain/temperature sensation

●Full transverse lesions – bilateral weakness and loss of sensation, similar to symptoms found in cord transection

●Central cord syndrome – bilateral weakness, rostrally greater than caudally, and loss of pain/temperature sensation in dermatome at level of the lesion

The anatomy and clinical features of spinal syndromes are discussed in greater detail separately. (See "Anatomy and localization of spinal cord disorders".)

Additionally, we have observed cases of spinal cord infarction presenting with 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 [10].

DIFFERENTIAL DIAGNOSIS — While there are many potential causes of myelopathy, only a few are characterized by an abrupt symptom onset typical of spinal cord infarction. These conditions are typically discriminated by neuroimaging or other diagnostic testing. In addition, symptoms that extend beyond the distribution of either the anterior or posterior spinal artery suggest a cause other than spinal cord infarction.

●Extraaxial compressive conditions of the spine – Compressive myelopathy results from extraaxial lesions adjacent to the spinal cord. These conditions include:

•Neoplasm (eg, meningioma, lymphoma, leptomeningeal metastasis) (see "Spinal cord tumors", section on 'Intradural extramedullary tumors' and "Spinal cord tumors", section on 'Extradural primary tumors')

•Extramedullary inflammation (eg, sarcoidosis) (see "Neurologic sarcoidosis")

•Epidural or subdural spinal hematoma (see "Disorders affecting the spinal cord", section on 'Spinal epidural hematoma')

•Epidural spinal abscess (see "Spinal epidural abscess")

•Cervical or thoracic intervertebral disc herniation (see "Cervical spondylotic myelopathy")

Extraaxial compression conditions typically cause pain and point tenderness along with myelopathic symptoms. Specific conditions may be identified by clinical circumstances. As examples, 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. Some patients with an epidural abscess may also present with systemic symptoms such as fever.

While these lesions typically develop over time, the clinical presentation can be fairly abrupt and mimic spinal cord infarction. Suspected compressive lesions typically mandate urgent neuroimaging to identify findings that may require urgent surgical decompression.

●Inflammatory or infiltrative spinal conditions – Spinal intramedullary pathologies that may mimic spinal cord infarction include inflammatory and neoplastic conditions:

•Transverse myelitis (see "Transverse myelitis: Etiology, clinical features, and diagnosis")

•Infectious myelitis (eg, Lyme encephalomyelitis) (see "Nervous system Lyme disease", section on 'Lyme encephalomyelitis')

•Intramedullary neoplasm (eg, ependymoma, astrocytoma) (see "Spinal cord tumors", section on 'Intramedullary tumors')

•Intramedullary granulomatous inflammation (eg, sarcoidosis) (see "Neurologic sarcoidosis")

Inflammatory conditions such as transverse myelitis are more typically associated with a slower onset of myelopathic symptoms, typically over hours and days, but symptoms can sometimes develop acutely. Rapid onset of paralysis from transverse myelitis has been reported to occur in as short a period as 10 minutes [23,24].

Clinical history may help to identify these conditions. For example, a history of tick bite may suggest Lyme disease, and a recent vaccination or viral illness may suggest infectious or transverse myelitis. Insidious onset and progressive symptoms may suggest neoplasm.

Spinal magnetic resonance imaging (MRI) is required to identify neoplasm, and the presence of contrast enhancement may also help discriminate sarcoidosis or transverse myelitis. Additional diagnostic studies (lumbar puncture, brain imaging) may also be required. Diagnostic features that favor transverse myelitis over infarction include MRI lesions that extend beyond a vascular territory, gadolinium enhancement, and cerebrospinal fluid (CSF) findings of pleocytosis or elevated immunoglobulin G (IgG) levels [25].

●Acute polyneuropathies – Acute polyneuropathy (eg, Guillain-Barré syndrome [GBS]) can be confused with acute myelopathy because both are associated with flaccidity and loss of reflexes in the acute stage [26] (see 'Clinical features' 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 progressive symptoms (over several days) 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/or the passage of time to allow spasticity or hyperreflexia associated with infarction to emerge. (See "Guillain-Barré syndrome in adults: Pathogenesis, clinical features, and diagnosis".)

Less common peripheral neuropathies that may mimic spinal cord infarction include toxic neuropathies (eg, arsenic poisoning, n-hexane exposure) and tick paralysis. These conditions may be identified by a history of exposure to the causal agent. In addition, toxic neuropathies typically present with prominent paresthesias and pain and symptoms not restricted to a spinal vascular territory. Tick paralysis typically presents with progressive gait impairment and weakness along with sensory impairment. (See "Arsenic exposure and chronic poisoning", section on 'Neurologic' and "Common occupational chemical exposures: General approach and management of selected exposures", section on 'N-hexane, methyl-n-butyl ketone' and "Tick paralysis".)

●Brainstem or cerebral conditions – Cerebral conditions may rarely present with isolated bilateral lower extremity symptoms that mimic spinal cord infarction. These conditions include:

•Cerebral infarction (see "Overview of the evaluation of stroke", section on 'Neurologic examination')

•Intracranial hemorrhage (eg, subdural hematoma, subarachnoid hemorrhage, intracerebral hemorrhage) (see "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis" and "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis")

•Tumor (eg, parafalcine meningioma) (see "Overview of the clinical features and diagnosis of brain tumors in adults")

Midline mass lesions (eg, neoplasm, hemorrhage) of the cerebral hemispheres may cause neurologic impairment of bilateral corticospinal tracts. Ischemic stroke involving the bilateral anterior cerebral arteries may also produce isolated lower extremity symptoms. Additional neurologic symptoms are typically present with these cerebral conditions. These include cortical symptoms (eg, aphasia, apraxia) and cranial nerve dysfunction (eg, dysarthria, diplopia). Brain imaging, typically MRI, is used to identify cerebral mimics of spinal cord infarction.

●Aortic dissection – 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 these mechanisms to occur simultaneously. (See "Clinical features and diagnosis of acute aortic dissection".)

DIAGNOSTIC EVALUATION — The diagnosis of spinal cord infarction should be suspected in patients with an abrupt onset of neurologic deficits that localize to the spinal cord (eg, paraplegia). The diagnosis is made in patients when a compatible clinical syndrome and diagnostic testing including neuroimaging of the spine both support the diagnosis and exclude another identifiable etiologies [3].

Neuroimaging — Neuroimaging is required for the diagnosis of spinal cord infarction. For most patients, we perform spinal MRI to exclude alternative causes and to confirm the diagnosis. For selected patients with acute presentations highly suggestive of spinal cord infarct who are hemodynamically unstable or otherwise unable to undergo MRI, we perform spinal computed tomography (CT) to exclude alternative causes.

Spinal site of imaging is typically directed to localizing symptoms when present, but whole spine imaging may be warranted when lesion location is uncertain or initial testing is nondiagnostic. As examples, cervical imaging may be performed for patients with sensorimotor symptoms in both arms and legs. Thoracic imaging (that includes the conus medullaris) may be performed for patients with midback pain and neurologic signs and symptoms restricted to the lower extremities. However, cervical imaging may be warranted if thoracic imaging is normal to evaluate for a more rostral lesion.

Spinal MRI — MRI is the preferred imaging modality to exclude compressive causes of myelopathic symptoms and can also provide confirmatory evidence of spinal cord infarction. It may also help to identify 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.

For patients with suspected spinal cord infarction, spinal MRI should be performed with gadolinium contrast.

●Findings in spinal cord infarction – MRI changes associated with spinal cord ischemia include (image 3 and image 1 and image 2 and image 4):

•Focal spinal cord swelling

•Hyperintensity on T2-weighted and short-tau inversion recovery (STIR) images

•Restricted diffusion on diffusion-weighted images (DWI)

•Enhancement on postcontrast images

A finding of restricted diffusion on DWI appears to be significantly more sensitive than standard T2 images (image 5) [27-31]. 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 [31].

Imaging findings should be correlated to clinical features because a T2 signal abnormality of the spine with associated restricted diffusion can be seen in transverse myelitis and other intrinsic cord pathologies. The findings of T2-hyperintensity or restricted diffusion restricted to a spinal vascular territory or the ventral horns ("owl's eyes" or "snake eyes" sign) is more specific for spinal cord infarction. A finding of vertebral body infarction adjacent to a cord signal abnormality on MRI is a useful confirmatory sign if present [32]. However, this is found in only 4 to 35 percent of patients, and its absence does not exclude spinal cord infarction [1,3,10,12].

The sensitivity of spinal MRI is limited for spinal cord infarction, particularly in the first several hours. The percentage of patients with T2 changes on MRI ranges from 45 to 73 percent depending in part on the interval to imaging [1,3,4,10,15,33,34]. The sensitivity of MRI for infarction may be highest approximately 72 hours after injury [35]. 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 due to the small size of the suspected spinal lesion, high volume of white matter in the spinal cord, and other spine-related bony imaging artifacts [11,34,36].

●MRI findings suggestive of underlying cause – Spinal MRI may show other supportive findings adjacent to the spinal cord. These findings, when present, can support the diagnosis of spinal cord infarction and may also help identify the underlying etiology.

•Intervertebral disc disease at the level of infarction may suggest possible fibrocartilaginous embolism [37].

•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 [12].

•Spinal cord vascular malformations may be seen as prominent flow voids in subarachnoid or paraspinal spaces (image 2) [38].

•Vertebral body infarction may suggest aortic disease pathology [12].

Spinal CT — CT of the spine with contrast may be performed to support the clinical diagnosis of spinal cord infarction when suspicion for spinal cord infarct is high (eg, acute onset of paraplegia following aortic surgery) and for unstable patients with acute presentations and those otherwise with a contraindication to MRI. Spinal CT is used to exclude extraaxial compressive causes of myelopathy such as hematoma, abscess, or neoplasm. However, the sensitivity of spinal CT for spinal cord infarction is low. In addition, spinal CT has limited utility to identify other inflammatory spinal conditions such as transverse myelitis.

Spinal MRI may be performed as a follow-up imaging study to confirm the diagnosis after resolution of unstable conditions. Additional testing is also typically performed to support the diagnosis of spinal cord infarction for patients unable to undergo spinal MRI. (See 'Additional diagnostic testing for selected patients' below.)

Additional diagnostic testing for selected patients — We perform additional testing to confirm the clinical diagnosis for patients with atypical clinical features and those with normal or otherwise nondiagnostic initial imaging findings. Clinical features atypical for spinal cord infarction include:

●Progression in symptoms >12 hours from onset

●Neurologic deficits that extend beyond specific neurologic spinal syndrome (see 'Specific neurologic syndromes' above)

●Neurologic deficits suggestive of peripheral nerve pathology (eg, persisting areflexia, presences of ataxia, bowel/bladder dysfunction)

●History of or exposure to infectious, toxic, or other systemic cause (eg, tick bite, fever, recent viral infection)

For other patients with typical clinical features and spinal MRI findings suggestive of spinal infarction, further testing may be unnecessary. As an example, in the setting of paraplegia after aortic surgery, a patient with typical spine MRI findings will likely not require further testing.

Additional testing varies by clinical presentation and alternative diagnostic considerations (see 'Differential diagnosis' above), but may include:

●CSF analysis – A lumbar puncture and cerebrospinal fluid (CSF) analysis should be performed to assess for infection or inflammatory diseases. CSF testing typically includes:

•Routine studies: cell count, protein, and glucose

•Gram stain and culture

•Cytology/flow cytometry

•Inflammatory markers: oligoclonal bands, IgG index

•Assays for syphilis, Lyme, herpes, varicella, and cytomegalovirus

CSF analysis in spinal cord infarction is typically normal, but a mild to moderate pleocytosis may be present (rarely more than 100 white blood cell count [WBC]), and an elevated protein may also be seen (usually less than 119 mg/dL) [3,4,9,11,34].

●Laboratory testing – Blood tests to assess for infectious or inflammatory conditions include:

•Erythrocyte sedimentation rate and C-reactive protein

•Syphilis, Lyme disease, varicella, HIV (human immunodeficiency virus)

•Aquaporin-4 and myelin oligodendrocyte glycoprotein antibodies

•Angiotensin-converting enzyme, vitamin B12 level, copper level

●Brain imaging – A gadolinium-enhanced MRI of the brain may be helpful to exclude midline cerebral causes of lower extremity symptoms such as a parafalcine meningioma, tumor, or hemorrhage. In addition, brain MRI may help identify multiple sclerosis or related inflammatory conditions as causes to the spinal symptoms such as when the clinical presentation is consistent with transverse myelitis.

●Repeat spinal MRI – Patients with normal results on an initial spinal MRI performed in the acute setting may warrant repeat follow-up imaging 48 to 72 hours after symptom onset to increase diagnostic yield. MRI evidence of spinal cord infarction on diffusion-weighted imaging may be apparent within three hours after the onset of clinical symptoms in some patients (image 5) [39-42]. However, abnormal cord signal may not be apparent for up to two days after the onset of symptoms [39-41]. (See 'Spinal MRI' above.)

Testing for underlying cause — For patients with an uncertain cause to spinal cord infarction, further testing is performed to identify an underlying etiology (table 2). Specific testing varies by risk factors and individual clinical features. (See "Spinal cord infarction: Epidemiology and etiologies", section on 'Etiologies'.)

●Aortic dissection – Aortic imaging is warranted for all at-risk patients with spinal cord infarction who present with additional features suggestive of aortic dissection including:

•Hemodynamic instability

•Prominent chest/back/lower extremity pain

•Abnormal distal pulses

•Associated acute myocardial infarction

•History of aortic aneurysm

•Presence of an underlying collagen disorder (eg, Marfan syndrome)

In patients with hemodynamic instability, aortic evaluation will take priority over spine imaging. A low threshold for this diagnosis should also include older adults with vascular risk factors in whom the underlying cause of spinal cord infarction is not immediately known. (See "Clinical features and diagnosis of acute aortic dissection".)

Aortic dissection can be identified by transesophageal echocardiography (TEE), CT angiography of the chest/abdomen, or magnetic resonance angiography of the chest/abdomen. (See "Clinical features and diagnosis of acute aortic dissection".)

●Vertebral dissection – Vascular imaging should be performed for patients with a rostral cervical cord infarction. Options include either CT angiography or magnetic resonance angiography of the head and neck. Additional imaging with brain MRI may be warranted if dissection extends intracranially or if additional brainstem symptoms (eg, dysarthria, ataxia, diplopia) are present. (See "Cerebral and cervical artery dissection: Clinical features and diagnosis".)

●Vascular malformation – Spinal vascular imaging is warranted for patients with spinal cord infarction when spinal MRI shows a venous infarction or features suggestive of a vascular malformation such as enlarged venous collateral vessels surrounding a cord with abnormal T2- or STIR-hyperintense signal (image 2).

Options for initial spinal vascular imaging include either CT angiography or magnetic resonance angiography of the spine. Digital subtraction angiography (DSA) is performed when noninvasive vascular imaging is nondiagnostic and to further characterize lesions in preparation for treatment. In addition, DSA is performed in patients with normal noninvasive vascular imaging when clinical suspicion for a vascular malformation is high, such as those who present with a stepwise, progressive myelopathy. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.)

●Other causes of ischemic stroke – Cardiac and laboratory testing may be warranted for patients with an uncertain underlying cause to evaluate for embolic, hypercoagulable, or other conditions. Testing may include:

•Transthoracic echocardiography

•Cardiac rhythm monitoring (for subclinical atrial fibrillation)

•Laboratory testing for hypercoagulable conditions

•Urine and blood toxicology screening tests

The evaluation for underlying causes of ischemic stroke is discussed in greater detail separately. (See "Overview of the evaluation of stroke".)

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

●Clinical presentation – Patients with spinal cord infarction typically present with acute onset paraparesis or quadriparesis depending on the level of the spinal cord involved. In the acute setting, patients may also have back pain and hemodynamic instability (eg, hypotension, hypertension). Muscle stretch reflexes may be absent below the level of the lesion acutely but eventually become hyperactive. (See 'Neurologic signs' above.)

Most patients with spinal cord infarction present specific neurologic syndromes that correlate with the neurovascular anatomy of the spine. (See 'Specific neurologic syndromes' above.)

•The most common syndrome is an infarction of the anterior spinal artery (ASA). ASA infarct typically presents as loss of motor function along with loss of pain and temperature sensation, with relative sparing of proprioception and vibratory sense below the level of the lesion (figure 1).

•The posterior spinal artery infarction that produces loss of proprioception and vibratory sense below the level of the injury and total anesthesia at the level of the injury (figure 2).

•Other spinal cord infarctions syndromes include a full transverse infarction that produces bilateral weakness and loss of sensation and central cord syndrome that presents with bilateral weakness, rostrally greater than caudally, and loss of pain/temperature sensation in dermatome at the level of the lesion.

●Differential diagnosis – Acute spinal cord infarction must be distinguished from other conditions that may cause an abrupt onset of myelopathic symptoms. These conditions include (see 'Differential diagnosis' above):

•Extraaxial compressive lesions such as spinal epidural abscess or intervertebral disc herniation

•Inflammatory or infiltrative spinal conditions such as transverse myelitis or intramedullary spinal ependymoma

•Acute polyneuropathies such as Guillain-Barré syndrome (GBS)

•Cerebral midline conditions such as parafalcine meningioma or ischemic stroke

●Diagnosis and evaluation – The diagnosis of spinal cord infarction is made in patients when a compatible clinical syndrome and diagnostic testing including neuroimaging of the spine both support the diagnosis and exclude another identifiable etiologies. (See 'Diagnostic evaluation' above.)

•Spinal imaging – Neuroimaging is required for the diagnosis of spinal cord infarction. Initial imaging is typically directed to localizing symptoms (eg, thoracic imaging for paraplegia and cervical imaging for quadriplegia), but whole spine imaging may be warranted when lesion location is uncertain or initial testing is nondiagnostic. (See 'Neuroimaging' above.)

For most patients, we perform spinal MRI to exclude alternative causes and to confirm the diagnosis. For selected patients with acute presentations highly suggestive of spinal cord infarct who are hemodynamically unstable or otherwise unable to undergo MRI, we perform spinal CT to exclude alternative causes.

-Spinal MRI – MRI is the preferred imaging modality to exclude compressive causes of myelopathic symptoms and can also provide confirmatory evidence of spinal cord infarction. It may also help to identify the underlying etiology. MRI changes associated with spinal cord ischemia include focal spinal cord swelling, hyperintensity on T2-weighted and short-tau inversion recovery (STIR) images, restricted diffusion on diffusion-weighted images (DWI), and enhancement on postcontrast images (image 3 and image 1 and image 2 and image 4 and image 5). (See 'Spinal MRI' above.)

-Spinal CT – Spinal CT is used for unstable patients with acute presentations to exclude extraaxial compressive causes of myelopathy such as hematoma, abscess, or neoplasm. However, the sensitivity of spinal CT for spinal cord infarction is low. (See 'Spinal CT' above.)

•Additional testing for selected patients – We perform additional testing for patients with atypical clinical features and those with normal or otherwise nondiagnostic initial imaging findings. Additional testing varies by clinical presentation and alternative diagnostic considerations but may include lumbar puncture for cerebrospinal fluid (CSF) analysis, laboratory testing, brain MRI, and/or repeat spinal MRI. (See 'Additional diagnostic testing for selected patients' above.)

•Evaluation for underlying causes – For patients with an uncertain cause to spinal cord infarction, further testing is performed to identify an underlying etiology (table 2). Specific testing varies by risk factors and individual clinical features. (See 'Testing for underlying cause' above.)