Many diseases affect the spinal cord by mechanical compression, which often presents stereotypically and can be treated effectively if detected early.
Acute compression is usually traumatic, producing signs of segmental damage at the level of compression usually combined with corticospinal tract dysfunction (eg, hyperreflexia, Babinski's sign, weakness) and sensory deficits below the level of compression (see Spinal Cord Injury, below).
Subacute compression is usually caused by an extramedullary neoplasm (see Spinal Cord Neoplasms in Ch. 177), a subdural or epidural abscess or hematoma (see below), or a cervical (or rarely thoracic) disk rupture. Patients present with local spinal pain, often with a radicular distribution, and reflex changes due to corticospinal tract dysfunction. Weakness (often proximal) of the legs, sensory loss, and, finally, loss of sphincter control follow. Segmental motor or sensory loss in the arms is common with cervical lesions. Pain and mild weakness may last hours to days, but the transition to total loss of function caudal to the lesion may take only minutes or less if vascular compromise to or transection of the cord develops.
Chronic compression may be caused by bony or cartilaginous protrusions into the cervical, thoracic, or lumbar spinal canal (eg, from osteophytes or spondylosis, especially in patients with a congenitally narrow spinal canal--see Cervical Spondylosis in Ch. 183) or by slow-growing extramedullary or intramedullary neoplasms. The course of chronic compression is substantially slower than that of subacute compression; serious symptoms may take months or years to develop. Pain may be less intense, motor and sensory abnormalities may evolve concurrently, and spasticity develops in the lower limbs. Segmental neurologic impairment in the arms usually accompanies cervical lesions.
Diagnosis and Treatment
Initially, diagnosis is based on symptoms and clinical signs: spine tenderness (percussion tenderness is especially prominent with metastatic carcinoma, vertebral infection, or spinal or epidural abscess), paraparesis, sensory deficits of the limbs or trunk, and corticospinal reflex changes. Spinal x-rays are rarely diagnostic. MRI is usually diagnostic, showing bony erosion, severe hypertrophic changes, collapse, fracture, or subluxation at the level of the lesion. If MRI is unavailable, CT or myelography of the appropriate level may be used to confirm cord compression and fully define the level and extent of the lesion.
Treatment depends on the underlying disorder. For management of acute injuries and of disorders causing chronic compression, see the chapters referred to above.
Prompt intervention in subacute compression is essential. If treated before weakness becomes marked, many patients recover full neurologic function; once paraplegia or autonomic deficits have occurred, few do well. For metastatic lesions, high-dose corticosteroids (oral or IV dexamethasone) should be given promptly, and if the tissue type is known to be radiosensitive, immediate radiation therapy may be effective. If radiation therapy is unavailable or if neurologic signs worsen despite medical therapy, surgical decompression should be performed unless the patient is not a surgical candidate. Surgery is also indicated when a biopsy is needed, when the spine is unstable, when tumors have recurred after radiation therapy, or when compressing subdural or epidural hematoma or any abscess is present. After surgery for epidural metastases, patients should generally receive radiation therapy.