Anterior cord syndrome (ACS) is an incomplete cord syndrome affecting the anterior ⅔ of the spinal cord while sparing the dorsal columns, resulting in loss of motor and sensory function below the level of injury.
- Estimated incidence: 3.1 per 100,000
- 2.7% of traumatic spinal cord injuries
- The most common pattern of spinal cord infarction
- Occlusion of the anterior spinal artery (ASA) and ischemia to the area the ASA supplies:
- Iatrogenic (most common): cross-clamping of the aorta during thoracic and abdominal aortic aneurysm repair
- Severe hypotension
- Atherothrombotic disease
- Cocaine (rare)
- Direct injury/trauma:
- Crush injury
- Acute spinal disc herniation
- Burst fracture
- Gunshot or knife injury
- Spinal canal mass:
- Benign or malignant tumor
- Radiation myelopathy
Anterior cord syndrome starts with occlusion of the blood supply or injury to the vertebral column. The syndrome is infrequently due to spinal cord tumors.
Mechanisms of injury
- ASA occlusion:
- Blood flow through the ASA is interrupted → spinal cord tissue ischemia and infarction from the level of interruption of flow downwards →
- Infarction of the corticospinal and spinothalamic pathways → ACS
- Vertebral/burst fractures:
- Force coming from above or below the vertebral body (depending on the injury) →
- Nucleus pulposus of the intervertebral disk is forced into the vertebral body → shatters outward (burst) fracture → spinal cord injury related to the force and direction of the traumatic event
- Posteriorly displaced fracture fragments → ACS
- Anatomy: Motor nuclei of the spinal cord are contained within the ventral horn. →
- Interneurons mediate information from other descending tracts (pyramidal and extrapyramidal motor systems). →
- Synapse on the alpha and gamma motor neurons →
- Leave the ventral horn via the ventral nerve root →
- Injury to the ventral horn/anterior spinal cord → damage to:
- Corticospinal tract (CST) → motor paralysis and absent reflexes
- Spinothalamic tract (STT) → bilateral loss of pain and temperature sensation
- Descending autonomic tracts → loss of bladder control
- Tactile, position, and vibratory sensation are normal (dorsal columns intact).
- With acute spinal cord injury:
- Secondary injury due to spinal cord edema may manifest as neurologic deterioration over the 1st 8–12 hours.
- Maximal 3–6 days after the injury
- Recedes approximately 9 days after the injury
- Gradually replaced by central hemorrhagic necrosis
Clinical Presentation and Diagnosis
Understanding the structures affected by an anterior cord lesion is key to correlating clinical signs and symptoms.
- May report the acute onset of neurologic symptoms or trauma
- Individuals with acute cervical spondylotic myelopathy and a history of mild or no previous deficits: neurologic emergency
- May arrive at the emergency department as a result of trauma and unable to give a history
- May present with symptoms in the hospital after aortic surgery
Physical exam findings:
- Almost always bilateral
- Motor deficit: paralysis below the level of lesion
- Sensory deficit: loss of pain and temperature sensation
- Preserved (posterior columns are spared): position, vibration sense, and light touch
- Autonomic dysfunction: urinary incontinence
- X-ray of the spine: to evaluate fracture
- Preferred imaging modality
- Sagittal view: thin, “pencil-like” hyperintensities on T2 within the anterior horns
- Axial view: hyperintense bilaterally symmetric circular to ovoid foci in the anterior horns of the spinal cord resembling “owl eyes” (also known as “snake-eyes sign” or “fried-eggs sign”)
- Lab tests:
- If indicated, CBC and blood cultures to check for infection
- Erythrocyte sedimentation rate (ESR) and CRP to evaluate for inflammatory etiology
- Coagulation tests for a potential hypercoagulable state
- CSF lumbar puncture may be needed to rule out infection.
Management and Prognosis
Management is directed at relieving symptoms and preserving motor function.
Acute emergency care
- Medications (dependent on the cause of ACS):
- Outcomes improve with high-dose IV steroids within 8 hours of the injury.
- Infuse IV bolus of methylprednisolone for the 1st 23 hours.
- Thrombolysis can be considered in atherothrombotic or embolic causes.
- Immunosuppression therapy in vasculitis and other autoimmune causes
- Bladder catheterization for neurogenic bladder
- Laminectomy for spinal decompression if indicated
- Prevention of ACS during surgical procedures:
- Protocols to avoid spinal cord ischemia during aortic surgery
- Avoiding prolonged clamp times and IV vasopressors
Long-term care via rehabilitation
- Extensive physical therapy aimed at:
- Preserving strength and range of motion
- Stretching to relieve spasticity
- Occupational therapy: to help retain functional abilities with self-care
Complications of spinal cord injury
- Respiratory failure (above C3–C5): loss of phrenic nerve function → paralysis of the diaphragm (may require long-term ventilator care)
- Autonomic dysreflexia (above T6): lack of a coordinated autonomic response with heart rate and blood pressure in spinal injuries
- Urinary incontinence
- Complications of immobility:
- Deep vein thrombosis (DVT)
- GI stress ulcers
- Pressure ulcers
- Chronic pain
- ACS: the worst prognosis of all spinal cord syndromes
- Recovery of function is poor:
- Most deaths occur immediately after injury.
- Few individuals recover the ability to walk.
- Improvement may continue in the years following injury.
- Women and older individuals: ↑ risk of worse outcomes
- Central cord syndrome: a neurological syndrome caused by an injury to the center of the spinal cord, which affects the spinothalamic and corticospinal tracts. Central cord syndrome is often caused by trauma in individuals with cervical spondylosis. Clinical manifestations are motor deficits (affects upper limbs more than lower limbs), variable sensory deficits below the level of injury, and bladder dysfunction. Diagnosis is made by exam and MRI. Management can be medical or surgical depending on the severity of the injury.
- Posterior cord syndrome: an incomplete cord syndrome characterized by loss of vibration and sense of position below the level of injury. As a very rare condition, the status of posterior cord syndrome as a separate clinical entity is still under debate in the literature and may overlap with central cord syndrome. Diagnosis is made clinically and with neuroimaging. Management includes steroids, medication for spasticity, and/or surgery for the repair of vertebral fractures.
- Brown-Séquard syndrome: hemisection of the spinal cord secondary to injury. Brown-Séquard syndrome is most commonly from a penetrating trauma (e.g., knife or bullet injury), but other etiologies include tumors, disc herniation, demyelination, and infarction. Clinical presentation includes weakness and paralysis of 1 side of the body and sensory loss on the opposite side. Diagnosis is with neurological exam and MRI. Management includes early treatment with high-dose steroids; additional treatment is symptomatic and supportive.
- Multiple sclerosis: a chronic inflammatory autoimmune disease leading to demyelination of the CNS. The etiology of multiple sclerosis is uncertain, but both genetic and environmental factors are believed to play a role. Diagnosis is by MRI and CSF examination. Management involves corticosteroids for acute exacerbations and disease-modifying agents to reduce exacerbations/slow the progression of the disease.
- Spinal disc herniation (also known as herniated nucleus pulposus): the expulsion of the nucleus pulposus through a perforation in the annulus fibrosus of the intervertebral disc. Most commonly caused by degenerative disc disease, spinal disc herniation is an important pain syndrome with the potential for neurologic impairment. Diagnosis is by clinical exam and MRI. Management can be conservative with medications and physical therapy. Surgery is indicated for intractable pain or myelopathy.
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