SPINAL CORD INFARCTION: CLINICAL PRESENTATION AND

DIAGNOSIS
Authors
Michael Mullen, MD
Michael L McGarvey, MD
Section Editor
Scott E Kasner, MD
Deputy Editor
Janet L Wilterdink, MD

Disclosures

Last literature review version 19.3: Fri Sep 30 00:00:00 GMT

2011 | This topic last updated: Wed Oct 19 00:00:00 GMT
2011 (More)

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: Vascular anatomy and

etiologies" and "Spinal cord infarction: Prognosis and

treatment" and "Chronic complications of spinal cord

injury" and "Disorders affecting the spinal cord" and "Anatomy and

localization of spinal cord disorders".)

CLINICAL PRESENTATION — As with cerebral infarction, the onset of

spinal cord infarction is typically abrupt [1,2]. In a few cases, symptoms

1
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 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 [1-7].

Anterior spinal artery syndrome — The most common clinical

presentation of a spinal cord infarction is anterior spinal artery (ASA)

syndrome [1,5,8]. 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 [9]. 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

[4,10,11]. 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 [1,3-5,12]. This occurs either because of

2
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 [3].

Posterior spinal artery syndrome — Posterior spinal artery (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 [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 [1,5]. (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

comprise one-third of patients [5].

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 [1,4,13].

3
Venous infarction of the spinal cord has been described, usually in

association with spinal vascular malformations. These infarcts may be

either hemorrhagic or non-hemorrhagic. In non-hemorrhagic venous

infarcts, venous hypertension decreases the arterial-venous pressure

gradient leading to decreased perfusion. Non-hemorrhagic venous

infarction typically present with a gradual onset of progressive neurologic

decline, whereas hemorrhage is associated with the sudden onset of pain

and flaccid paraparesis [10]. (See "Disorders affecting the spinal cord",

section on 'Vascular malformations'.)

DIFFERENTIAL DIAGNOSIS — While there are many potential causes

of myelopathy, only a few present in an abrupt presentation.

(See "Disorders affecting the spinal cord".)

 Compressive myelopathy from neoplasm, epidural or subdural

hematoma, or abscess is the most important category of diagnosis

to exclude, as these often require urgent surgical decompression.

While these lesions typically develop over time, the clinical

presentation can be fairly abrupt and mimic spinal cord infarction.

This diagnostic consideration mandates urgent neuroimaging in all

patients presenting with spinal cord infarction. (See "Disorders

affecting the spinal cord", section on 'Neoplasms' and "Clinical

features and diagnosis of neoplastic epidural spinal cord

compression, including cauda equina syndrome" and "Epidural

abscess".)

4
 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 [14,15]. A history of recent

vaccination or viral illness may suggest this diagnosis, but these are

often absent. Symptoms isolated to the anterior spinal artery

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 MRI lesions

that extend beyond a vascular territory, gadolinium enhancement,

and cerebrospinal fluid findings of pleocytosis or elevated IgG levels

[16]. (See "Disorders affecting the spinal cord", section on

'Transverse myelitis'.)

 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 (see 'Clinical

presentation' above) [17]. 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,

5
 differentiating these diagnoses requires diagnostic tests (magnetic

resonance imaging, electromyography) and the passage of time to

allow upper motor neuron signs to emerge. (See "Clinical features

and diagnosis of Guillain-Barré syndrome in adults".)

 In the postoperative setting, the differential diagnosis of paraplegia

includes an epidural hematoma, 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 [18].

 In patients with acute dissection or rupture of the descending aorta,

paraplegia may result from impaired perfusion of the brain and

lower extremities, as well as from spinal ischemia. It is also possible

for all three of these phenomena to occur simultaneously.

DIAGNOSIS

Spinal MRI — Magnetic resonance imaging (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 images (figure 1). The sensitivity of standard MRI is

6
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 [1,4,5,10,19]. 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 [6]. A finding of

restricted diffusion on diffusion weighted images (DWI-MRI) appears to be

significantly more sensitive than standard T2 images, but the limited

number of case reports preclude a numerical estimate of its sensitivity

[20-23].

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. When these findings are restricted to a vascular

territory, they are more specific, but not perfectly so. 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

[24]. However, this is found in only 4 to 35 percent of patients, and its

absence does not exclude spinal cord infarction [1,5,7].

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 [7].

7
  Spinal cord vascular malformations also have distinct patterns of

abnormalities that may be seen on MRI [25]. (See "Disorders

affecting the spinal cord", section on 'Vascular malformations'.)

 In one case series, vertebral body infarction was highly associated

with aortic disease pathology [7].

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 CT, and MRI. While an uncommon

cause of spinal cord infarction, aortic dissection can lead to serious

adverse sequelae if unrecognized. Therefore, this should be

considered and specifically excluded in high-risk patients. Such

patients will include 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 probably also include 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 manifestations and diagnosis of aortic dissection".)

8
 Vascular imaging, either CT angiography or MR 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 WBC)

and an elevated protein (usually less than 119 mg/dl) [3,4,6].

 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. (See "Evaluation of the patient with established venous

thrombosis", section on 'Screening for inherited thrombophilia'.)

Urine or blood toxicology screen should exclude cocaine and other

9
 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.

 A dedicated spinal angiogram is indicated when a vascular

malformation is considered a possible etiology. In general, this is

performed when the spine MRI has suspicious findings or when a

patient presents with recurrent events. It may also be reasonable to

consider this test in patients without recurrent events when the

clinical suspicion for a vascular malformation is high. Despite the

invasive nature of spinal angiography, observational studies suggest

that in experienced hands, the complications are infrequent (1 to 2

percent) and do not involve significant morbidity [26].

(See "Disorders affecting the spinal cord", section on 'Vascular

malformations'.)

SUMMARY AND RECOMMENDATIONS — Spinal cord infarction is a rare

condition caused by a wide array of pathologic conditions.

 Most patients with spinal cord infarction present with acute

neurologic deficits attributable to the anterior spinal artery territory.

However, one-third of patients may have less typical presentations

including posterior spinal artery, central cord, and complete cord

transection syndromes. (See 'Clinical presentation' above.)

10
  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.)

 All patients with spinal cord infarction should have a spine MRI to

exclude a compressive myelopathy, as well as to provide further

evidence supporting the diagnosis of infarction. Diffusion weighted

images improve the sensitivity of MRI for acute ischemia; however,

spine MRI findings have imperfect sensitivity and specificity for

ischemia. (See 'Spinal MRI' above.)

 Other tests can further exclude alternative diagnoses and identify

the etiology. The choice of tests is tailored to the clinical situation.

Clinicians should have a low threshold for excluding aortic

dissection. (See 'Other tests' above.)

Use of UpToDate is subject to the Subscription and License Agreement.

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. 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.
3. Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases
and review of the literature. Medicine (Baltimore) 1989; 68:282.
4. Cheshire WP, Santos CC, Massey EW, Howard JF Jr. Spinal cord
infarction: etiology and outcome. Neurology 1996; 47:321.
5. Nedeltchev K, Loher TJ, Stepper F, et al. Long-term outcome of
acute spinal cord ischemia syndrome. Stroke 2004; 35:560.
6. 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.
7. Cheng MY, Lyu RK, Chang YJ, et al. Concomitant spinal cord and
vertebral body infarction is highly associated with aortic pathology:

11
 a clinical and magnetic resonance imaging study. J Neurol 2009;
256:1418.
8. Weidauer S, Nichtweiss M, Lanfermann H, Zanella FE. Spinal cord
infarction: MR imaging and clinical features in 16 cases.
Neuroradiology 2002; 44:851.
9. Foo D, Rossier AB. Anterior spinal artery syndrome and its natural
history. Paraplegia 1983; 21:1.
10. 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.
11. 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.
12. STEEGMANN AT. Syndrome of the anterior spinal artery. Neurology
1952; 2:15.
13. Hussain MS, Shuaib A, Siddiqi ZA. Spinal cord transient ischemic
attacks: a possible role for abciximab. Neurology 2005; 64:761.
14. Transverse Myelitis Consortium Working Group. Proposed diagnostic
criteria and nosology of acute transverse myelitis. Neurology 2002;
59:499.
15. Wilmshurst JM, Walker MC, Pohl KR. Rapid onset transverse myelitis
in adolescence: implications for pathogenesis and prognosis. Arch
Dis Child 1999; 80:137.
16. Nance JR, Golomb MR. Ischemic spinal cord infarction in children
without vertebral fracture. Pediatr Neurol 2007; 36:209.
17. Hui AC, Wong KS, Fu M, Kay R. Ischaemic myelopathy presenting as
Guillain-Barré syndrome. Int J Clin Pract 2000; 54:340.
18. 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.
19. 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.
20. Thurnher MM, Bammer R. Diffusion-weighted MR imaging (DWI) in
spinal cord ischemia. Neuroradiology 2006; 48:795.
21. Beslow LA, Ichord RN, Zimmerman RA, et al. Role of diffusion MRI
in diagnosis of spinal cord infarction in children. Neuropediatrics
2008; 39:188.
22. 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.
23. Shinoyama M, Takahashi T, Shimizu H, et al. Spinal cord infarction
demonstrated by diffusion-weighted magnetic resonance imaging. J
Clin Neurosci 2005; 12:466.

12
24. 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.
25. Hurst RW. Spinal vascular disorders. In: Resonance Imaging of the
Brain and Spine, 2nd, Atlas SW (Ed), Lippincott, Philadelphia 2006.
p.1387.
26. Chen J, Gailloud P. Safety of spinal angiography: Complication rate
analysis in 302 diagnostic angiograms. Neurology 2011; 77:1235.

***

13