(See also Spinal Trauma: Immediate care for treatment of spinal trauma.)
Various lesions can compress the spinal cord, causing segmental sensory, motor, reflex, and sphincter deficits. Diagnosis is by MRI. Treatment is directed at relieving compression.
Compression is caused far more commonly by lesions outside the spinal cord (extramedullary) than by lesions within it (intramedullary). Compression may be acute, subacute, or chronic.
Acute compression develops within minutes to hours. It is often due to trauma (eg, vertebral crush fracture with displacement of fracture fragments, acute disk herniation, metastatic tumor, severe bone or ligamentous injury causing hematoma, vertebral subluxation or dislocation). It is occasionally due to abscess and rarely due to spontaneous epidural hematoma. Acute compression may follow subacute and chronic compression, especially if the cause is abscess or tumor.
Subacute compression develops over days to weeks. It is usually caused by a metastatic extramedullary tumor, a subdural or an epidural abscess or hematoma, or a cervical or, rarely, thoracic herniated disk.
Chronic compression develops over months to years. It is commonly caused by bony protrusions into the cervical, thoracic, or lumbar spinal canal (eg, due to osteophytes or spondylosis, especially when the spinal canal is narrow, as occurs in spinal stenosis—see Neck and Back Pain: Lumbar Spinal Stenosis). Compression can be aggravated by a herniated disk and hypertrophy of the ligamentum flavum. Less common causes include arteriovenous malformations and slow-growing extramedullary tumors.
Atlantoaxial subluxation (see Neck and Back Pain: Atlantoaxial Subluxation) and other craniocervical junction abnormalities (see Craniocervical Junction Abnormalities) may cause acute, subacute, or chronic spinal cord compression.
Lesions that compress the spinal cord may also compress nerve roots or, rarely, occlude the spinal cord's blood supply, causing infarction.
Symptoms and Signs
Acute or advanced spinal cord compression causes segmental deficits, paraparesis or quadriparesis, hyporeflexia (when acute) followed by hyperreflexia, extensor plantar responses, loss of sphincter tone (with bowel and bladder dysfunction), and sensory deficits. Subacute or chronic compression may begin with local back pain, often radiating down the distribution of a nerve root (radicular pain), and sometimes hyperreflexia and loss of sensation. Sensory loss may begin in the sacral segments. Complete loss of function may follow suddenly and unpredictably, possibly resulting from secondary spinal cord infarction. Spinal percussion tenderness is prominent if the cause is metastatic carcinoma, abscess, or hematoma.
Intramedullary lesions tend to cause poorly localized burning pain rather than radicular pain and to spare sensation in sacral dermatomes. These lesions usually result in spastic paresis.
Spinal cord compression is suggested by spinal or radicular pain with reflex, motor, or sensory deficits, particularly at a segmental level. MRI is done immediately if available. If MRI is unavailable, CT myelography is done; a small amount of iohexol (a nonionic, low osmolar radiopaque dye) is introduced via a lumbar puncture and allowed to run cranially to check for complete CSF block. If a block is detected, a radiopaque dye is introduced via a cervical puncture to determine the rostral extension of the block. If traumatic bone abnormalities (eg, fracture, dislocation, subluxation) that require immediate spinal immobilization are suspected, plain spinal x-rays can be done. However, CT detects bone abnormalities better.
Treatment is directed at relieving pressure on the cord. Incomplete or very recent complete loss of function may be reversible, but complete loss of function rarely is; thus, for acute compression, diagnosis and treatment must occur immediately.
If compression is due to a tumor, IV dexamethasone 100 mg is given immediately, followed by 25 mg q 6 h and immediate surgery or radiation therapy. Surgery is indicated in the following cases:
Last full review/revision November 2012 by Michael Rubin, MDCM
Content last modified January 2013