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Quick Consult: Symptoms Seizure, Extremity Weakness

Wiler, Jennifer L. MD, MBA

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doi: 10.1097/01.EEM.0000436454.92245.fd

    A 30-year-old man with a history of epilepsy presents with seizure. Bystanders said he hit his head on a door frame, and then had two or three minutes of generalized tonic-clonic seizure activity. Initially, he was post-ictal, but this resolved.

    The patient complained in the ED of progressive upper extremity weakness. He had no known illicit drug or alcohol use. His past surgical history was significant for anterior cervical discectomy and fusion at C4-5.

    This is what his CT scan showed. What diagnosis concerns you, and how would you make it? See p. 27.


    Diagnosis: Anterior Cord Syndrome

    Anterior cord syndrome is the most common form of spinal cord “stroke.” (J Emerg Med 2010;38[5]:e49.) Spinal cord infarctions are rare, however, and responsible for less than one percent of all strokes. (Arch Neurol 2006;63[8]:1113.) This condition occurs when the vascular supply to the anterior two-thirds of the spinal cord is compromised, resulting in death to neural cells. The anterior portion of the spinal cord is singularly supplied by the anterior spinal artery. The anterior spinal artery is created by the union of the two descending vertebral arteries (superiorly, starting at the foramen magnum) and feeders from the aorta (inferiorly). The posterior spinal artery, on the other hand, has collateral circulatory inputs that make ischemic injury much rarer.

    The etiology of anterior cord syndrome includes trauma, conditions that can cause aortic insufficiency (transaction, dissection, atherosclerosis [Br J Neurosurg 2011;25(6):666]), malignancy, acute disk herniation, kyphoscoliosis, conditions that result in microscopic ischemia (polycythemia, sickle cell disease, vasculitis, hypercoaguable states [Rev Neurol 2009;48(1):52]), vasospasm (cocaine), or decompression sickness. (Neurology 1996;47[2]:321; J Clin Anesth 2004;16[6]:440.) Hyperreflexive injuries cause relative ischemia from stretching, dissection, or transection of the anterior spinal artery, but the most common, accounting for nearly 45 percent of all spinal cord infractions, is iatrogenic from low-flow intra-operative states. (Neurology 2012;78:114.)

    Like any acute vascular compromising condition, symptoms typically develop quickly, usually within an hour of cord injury. Patients exhibit weakness or flaccid paralysis in the extremities (legs greater than arms) that is often accompanied by painful myelopathy and sensory anesthesia to pain and temperature. Vascular compromise of the anterior spinal artery is characterized by loss of motor function (corticospinal tract) below the level of injury (carried by the anterolateral fibers), and loss of pain and temperature sensations (carried by the spinothalamic tract). Sensations carried by the dorsal/posterior columns (fine touch, vibration, and proprioception) are intact. Patients also may demonstrate urinary retention, bowel incontinence related to anal sphincter tone flaccidity, paralytic ileus, and areflexia depending on the level of the lesion.

    MRI is the diagnostic study of choice for spinal cord infarction, and can detect the magnitude and location of the damage within minutes of symptomatic onset. (Neurology 2003;61[11]:1622; J Clin Neurosci 2013;20[4]:565.) MRI also has the advantage of allowing visualization of ligaments, paravertebral soft tissue, and intervertebral discs, and can detect epidural hematoma. (Neuroradiology 2006;48[4]:223.)

    Treating anterior cord syndrome depends on the etiology of the condition and the location of the lesion. (J Neurosurg Anesthesiol 2003;15[3]:215.) Patients with high cervical spine lesions may have respiratory paralysis and require intubation. Hypotension may occur from loss of sympathetic vascular tone or injury-related hemorrhage. Standard critical care resuscitation should be followed in these cases. Patients with suspected spinal cord injury should have precautions including cervical spine immobilization performed (if injury suspected at the cervical spine level). Treatment includes resection of any inciting lesions and stabilization of the vertebral column at the level of the lesion when necessary. Spinal decompression with a laminectomy may be required at times. Adjuvant intravenous steroid treatment is no longer recommended. (Neurosurgery 2013;72[Suppl 2]:93.)

    The prognosis for anterior cord syndrome is the worst of all the cord syndromes. Only 10-15 percent of patients demonstrate some functional recovery; lack of sacral sensation to pain and temperature 24 hours after symptom onset indicate poor prognosis. (Wheeless' Textbook of Orthopedics; The overall mortality rate is as high as 20 percent. (J Emerg Med 2010;38[5]:e49.) The National Spinal Cord Injury Statistical Center reported that patients with tetraplegia (bilateral arms and legs paralyzed) have some high complication rates: 60.3 percent developed pneumonia and 52.8 percent developed pressure ulcers. The center also said 16.4 percent developed deep vein thrombosis, 5.2 percent developed a pulmonary embolism, and 2.2 percent developed a postoperative wound infection. (

    This patient went on to develop paraplegia and urine retention during hospitalization. He was noted on CT to have a C3 spinous process fracture (photo previous page) and the anterior cervical discectomy and fusion plate C4-5. The MRI of his cervical spine demonstrated moderate canal stenosis at C3-4 with moderate cord contusion from C2-3 to 4-5. Prevertebral edema and interspinous edema suggest hyperflex and hyperextend injury. Moderate disc extrusion at L4-5 was seen, with moderate spinal canal narrowing (photo this page). The patient was transferred on hospital day 11 to an acute rehabilitation hospital that specializes in neurologic injuries.

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