The common mechanism in the patient with a potentially reversible condition is the presence of a mass lesion that has reached a critical size. Because the spinal cord lies within the bony spinal canal, an obstructive extradural or intradural extramedullary process causes compression of the cord and its vessels. If treatment is initiated before severe damage to spinal cord tissue causes total paraplegia, useful recovery is possible.
The acute onset of back pain in any patient, and particularly in a patient with cancer, should alert the physician to the potential for an impending spinal disaster. Often, however, the patient is not seen until further symptoms have developed.
PREDISPOSING CAUSES
Metastatic Deposits. The most common cause of an acute spinal cord syndrome, particularly in patients in the middle to late decades of life, is epidural spinal cord compression from metastatic cancer. Most patients have a known preexisting malignancy, but a spinal metastatic lesion may be the first indication of a primary tumor elsewhere, and particularly of prostate, breast, or lung cancer; other common causes are non–Hodgkin lymphoma and plasmacytoma or multiple myeloma (see Plate 2-21). Patients have leg weakness and an impaired gait and frequently complain also of ascending numbness and paresthesias. A spinal sensory level may be present but may be one to several levels below that where the cord is compressed. A “saddle” sensory loss may be present with cauda equina lesions. Depending on the site of spinal involvement, muscle stretch reflexes may be exaggerated if the spinal cord is compressed or lost with cauda equina lesions. Bladder and bowel involvement occur later, most often with urinary retention. Magnetic resonance imaging (MRI) of the entire spine is mandatory; computed tomography (CT) myelography provides similar and sometimes complementary information.
Infarction. Occlusion of the anterior spinal artery affects the anterior two thirds of the spinal cord (see Plates 2-18 and 2-20). Spinal cord infarction is usually precipitous. The clinical findings include paraparesis or paraplegia in combination with dissociated sensory loss, that is, loss of pain and temperature sensation, with preservation of position and vibration sense. During the acute stage, tone is flaccid and muscle stretch reflexes are lost; spasticity and hyperreflexia develop subsequently. Sphincter control is lost. Back pain, often at a segmental level, may be present.
Although in many cases spinal cord infarction may be idiopathic, in other instances it relates to aortic dissection that compromises the artery of Adamkiewicz (major anterior radiculomedullary artery), emboli from aortic atheroma, profound hypotension, or various types of arteritis. It may also occur as a complication of cardiac or aortic surgery.
Spinal MRI or CT myelography is indicated to exclude other (compressive) lesions, including spontaneous epidural hematoma. The MRI may also confirm that infarction of the spinal cord has occurred. Spinal angiography may help to confirm the diagnosis. Aortic dissection must be excluded. Treatment is based on the underlying pathology. The prognosis for recovery of useful function is poor.
Epidural Abscess. This lesion has a fairly characteristic clinical setting (see Plate 2-20). The vast majority of patients are febrile, and most are acutely ill, sometimes becoming disoriented but always complaining of severe back and nerve root pain. Examination demonstrates exquisite tenderness on percussion over the affected spinal process and signs of spinal cord impairment. Weakness, sensory changes, and bladder or bowel dysfunction, occur with progression. If the abscess remains untreated, paralysis develops and may not be reversible.
There is often an apparent predisposing source of infection; staphylococci and gram-negative bacilli are the predominant causative organisms. Risk factors include epidural catheter placement (e.g., for anesthesia), spinal surgery, paraspinal injections, impaired immunity, alcoholism, diabetes mellitus, and intravenous drug use.

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