Anterior Cord Syndrome

Primary Category

Spine

P-Category

Secondary Category

S-Category

Authors:

Muhammad Ehtesham Javed,
Junaid Kalia MD

Introduction

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Acute spinal cord infarction accounts for 8% of all myelopathies and almost 1% of all strokes.

Anterior cord syndrome is the most common cause of spinal cord infarction.

It is an incomplete cord syndrome that involves infarction of anterior 2/3rd of spinal cord.

Clinical manifestations may vary depending on the portion of the spinal cord affected.

Typical presentation include acute praparesis or quadriparesis depending on the level of spinal cord involved.

Etiology

It results from direct or indirect damage to the ventral spinal cord.

Direct injury arises when the spinal cord is mechanically crushed or compressed.

Indirect injury constitutes the primary etiology, and the resultant tissue damage is secondary to ischemia.

Table 1: Etiological causes of anterior cord syndrome

Etiology	Causes
Iatrogenic	Aortic injury during thoracic and thoracoabdominal aortic aneurysm repair.
Cardiac causes	Cardiac arrest, cardiac emboli, infective endocarditis,
Atherosclerotic disease	Thrombus/emboli that occludes the anterior spinal artery
Thoraco-abdominal aortic disease	Dissection of the aorta causes occlusion of radiculomedullary arteries
Vasculitis	Polyarteritis nodosa, syphilitic arteritis
Degenerative spine disease	Cervical spondylosis or thoracic disc herniation
Vertebral fracture	Anterior cord impingement by a fracture fragment
Fibrocartilaginous embolic myelopathy (idiopathic transverse myelitis)	Migration of nucleus pulposus material into vessels supplying the anterior spinal artery may result in embolic infarction of the spinal cord
Other causes	Hypotensive shock, sickle cell disease, cocaine use, AV malformation, hypercoagulable states, multiple sclerosis

Pathophysiology

The anterior two-thirds of spinal cord includes bilateral anterior horns, lateral horns, spinothalamic tracts, spinocerebellar tracts and corticospinal tracts.

It is supplied by anterior spinal artery, with a few radicular artery contributions.

Ischemia of artery causes symptoms consistent with the dysfunction of these tracts.

Artery of Adamkiwiecz contributes to caudal 2/3rd of anterior spinal artery(T5 to L2), is the most commonly occluded radiculomedullary artery.

Figure 1: Tracts affected by Anterior Cord Syndrome

Shaded area shows tracts affected due to anterior cord syndrome.

Staging

Acute spinal cord injury occurs in two phases.

Initial injury phase results from the initial insult to the cord that takes place within seconds.

Secondary injury phase results from the on-going endogenous triggers that cause tissue destruction.

Secondary phase can be subdivided into immediate (less than 2 hrs), early acute (<48 hrs), and subacute (<2 weeks) phases.

Clinical Manifestations

It results in acute presentation after the insult, with additional decline over a few to several hours.

Symptoms are usually bilateral.

Rarely, unilateral symptoms occur due to occlusion of unilateral sulcal artery, or incomplete collateralization with posterior spinal artery maintaining perfusion to one side of the cord.

Acute clinical findings

Acute back pain at the level of injury.

Bilateral motor deficit immediately below the level of lesion.

Bilateral loss of pain, temperature and crude touch starting two-three dermatomal segments below the level of the lesion.

Autonomic dysfunction with hypotension, bradycardia, and impaired temperature regulation if lateral horns are affected.

Chest pain with ECG changes may be present with C7-T1 spinal cord infarction.

Respiratory failure as a result of high cervical lesion that damages phrenic nerve.

Spinal shock with flaccidity and areflexia occurs early during symptoms onset.

Preservation of proprioception, vibratory sense, fine touch, and two-point discrimination.

Neurogenic shock with hypotension and bradycardia usually with lesions above T6.

Late clinical findings (within days to weeks)

Continued/permanent motor and sensory dysfunction.

Bilateral spastic paralysis with hyperreflexia and Babinski sign.

Neurogenic bladder/bowel and sexual dysfunction.

Radicular or diffuse type of pain can be present.

Figure 2: Affected sensations by Anterior Cord Syndrome

Evaluation

Diagnosis is generally made clinically, with neuroimaging used for confirmation and exclusion of other conditions.

In case of high clinical suspicion with normal initial MRI, a follow-up imaging should be obtained.

Diffusion-weighted images shows characteristic diffusion restriction in the ASA territory.

Sagittal view shows T2 hyperintensities within anterior horns as thin pencil like lesions extending vertically across several spinal levels.

Axial view illustrates hyperintensities as one bright dot within each anterior horn resembling owl’s eyes.

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MRI with axial and sagittal diffusion-weighted imaging is the primary modality of diagnosis.

Figure 3: MR imaging of spinal cord infarction

Legend: (a) T2 weighted sagittal (linearly extending pencil like lesions) (b) T2 weighted axial (owl’s eye sign) (c) T1 weighted sagittal imaging shows hyper-intensity in anterior aspect of C3 to C6/7 level (arrows) with expansion of cord and patch enhancement.

T2 signal abnormalities, even with restricted diffusion, is nonspecific as it can be present in transverse myelitis and intrinsic cord pathologies.

T2 hyperintensities limited to ASA territory or ventral horns (owl’s eyes or snake eyes sign) are more specific.

Absence of owl’s eye sign doesn’t exclude the infarction as it is present in only 4-35% of patients.

MR or CT angiography are adjunctive modalities for further delineation of vascular pathology.

Digital subtraction angiography is necessary if interventional procedure is required.

Lumbar puncture with CSF testing, blood and urine tests along with toxicology screen helps to rule-out other diagnoses or determine the underlying etiology.

If infections are suspected, serological tests for borreliosis, Lyme, syphilis, HIV, human T-cell lymphotropic virus, and herpes virus are necessary.

Screening for antinuclear and antineutrophil cytoplasmic antibodies if suspicion of vasculitis.

Suspicion of aortic dissection requires transesophageal echocardiography (TEE), chest CT/MRI.

Echocardiography can be performed to look for the source of embolism.

Treatment

Current treatment is mainly supportive.

Symptomatic improvement and prevention of complications is the main focus of management.

Prompt treatment of the treatable underlying cause is the most important prognostic factor.

Treatment follows the guidelines for cerebral ischemia, atherosclerotic vascular disease, and acute traumatic spinal cord injury.

High cervical and thoracic cord infarct requires ICU admission with close monitoring of vitals and neurological signs.

Figure 4: Management algorithm of Anterior cord syndrome

General Medical Care

Management involves addressing of underlying cause, anticoagulation, antiplatelet and thromboprophylaxis therapy.

Protect airways and maintain blood pressure support.

Mechanical ventilation if phrenic nerve is involved in high cervical lesions

Indwelling urinary catheter for neurogenic urinary retention, that is replaced by intermittent catheterization after 3-4 days.

Treatment and prevention of hypertension and diabetes mellitus.

Intravenous fluids, phenylephrine, norepinephrine and high-dose dopamine can be used for neurogenic hypotension.

Hypertension can be managed by Labetalol, esmolol, and nicardipine.

Body temperature maintenance in cervical cord infarcts, due to lack of vasomotor control and inability to sweat below the lesion.

Subcutaneous LMW heparin or fixed, low-dose unfractionated heparin can be given within the first 72 hours to reduce the risk of thromboembolic events.

Prophylactic proton pump inhibitor to prevent GIT stress ulcers, especially in cervical cord infarct.

Frequent side to side turning every 2-3 ours along with use of special mattress to avoid pressure sores.

Specific Treatment

There are no specific therapies proven to reverse or limit the ischemic spinal cord injury.

Intravenous thrombolysis within 4.5 hours of symptom onset, for atherosclerotic/embolic cause is still investigational.

24-hour infusion of high-dose steroids can be offered to adult patients within first 8 hours, especially if there is a doubt in infarction and demyelinating spinal cord lesion.

Immunosuppression therapy, if vasculitis is the underlying cause of infarct.

Surgical Management

Early surgical decompression can be offered to adults.

Surgery within 24 hours may reduce length of ICU stay and post-injury medical complications.

Aortic dissection and vascular malformations require surgical repair.

Rehabilitation care

Offered when patient is medically stable and can tolerate required rehabilitation intensity.

Physical, occupational, and psychological therapy are needed for better outcome.

Limitations in mobility and activities of daily living, bladder, bowel and sexual dysfunction should be addressed.

Body weight–supported treadmill and overground walking for ambulation training.

Psychosocial support to achieve increase independence, quality of life, and better prognosis.

Use of necessary adaptive equipment to optimize functional independence.

Functional electrical therapy to improve hand and upper extremity function.

Complications

Neurogenic Hypotension due to involvement of lateral horn’s sympathetic neuronal cell bodies.

Respiratory failure in high cervical infarctions due to involvement of the phrenic nerve.

Bradycardia, due to high cervical lesion, requires treatment with atropine or electrical pacing.

Motor impairment, prolonged immobilization can lead to DVT or pulmonary embolism.

Neurogenic bowel/bladder and sexual dysfunction due to autonomic impairment.

Pressure ulcers, chronic pain, GIT stress ulcers and spasticity are other common complications.

Increase risk for fractures and osteoporosis because of immobility.

Infections (urinary tract infections, pneumonia, bacteremia), electrolyte imbalances, renal failure and depression are also reported.

Differential Diagnosis

It is rare and often misdiagnosed disease.

Compressive myelopathy from neoplasm, epidural/subdural hematoma or abscess are important differentials, requiring urgent neuroimaging and surgical decompression.

Transverse myelitis has similar symptoms but gradual onset over hours and days, usually with the recent history of recent viral illness or vaccination.

Multiple sclerosis has similar MRI findings but has cranial and ocular symptoms.

Venous congestive myelopathy may present similarly but imaging shows enlarged pial veins with central and peripheral white matter changes.

Spinal cord neoplasms may present similarly but with slower symptom onset.

Spinal cord AV malformations, disk herniation,, central and dorsal cord syndrome should also be ruled-out.

Prevention

Many etiologies causing anterior cord syndrome result from preventable disease processes.

Primary disease prevention includes smoking cessation, healthy lifestyle, exercise and proper nutrition habits.

Secondary prevention through lifestyle guidance and management of risk factors.

Antiplatelet therapy for secondary prevention in patients with atherosclerotic risk factors or underlying comorbid atherosclerotic vascular disease.

Control of risk factors prevent reoccurrence and continued functional decline.

During aortic surgery, CSF drainage and incremental increases in arterial pressure by IV fluids/vasopressor decreases the risk of infarction.

Prognosis

The overall mortality rate for spinal cord infarction is between 9-23%

The majority of deaths occur shortly after the initial injury.

Aortic dissection/rupture and high cervical lesions have a higher mortality rate.

Severe symptoms in high spinal lesions.

Poor prognosis if severe presenting symptoms and lack of significant improvement in the first 24 hours.

Female sex and old age are associated with poor prognosis.

Varying degree of functional, motor and sensory dysfunction remains even after treatment.

Some patients can regain full walking ability in less severe cases.

Functional improvements can slowly develop over several years.

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Crucial prognostic factors are initial symptoms severity and amount of improvement in first 24 hours.

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