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Spinal cord compression
Last reviewed: 04.07.2025
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Various causes lead to compression of the spinal cord, causing segmental sensory and motor deficits, changes in reflexes and sphincter dysfunction.
The diagnosis of the disease is confirmed by MRI.
Treatment is aimed at eliminating compression.
Causes spinal cord compression
In most cases, the source of compression is located outside the spinal cord (extramedullary), less often - within the spinal cord (intramedullary). Compression can be acute, subacute and chronic.
Acute spinal cord compression develops within a few hours. It usually occurs with trauma (vertebral compression fracture with displacement of bone fragments, significant bone or ligament damage with hematoma development, subluxation or dislocation of vertebrae) or accompanies spontaneous epidural hematoma. Acute compression can develop after subacute or chronic compression, especially if the cause is an abscess or tumor.
Subacute spinal cord compression develops over days or weeks. Common causes include: metastatic extramedullary tumor, subdural or epidural abscess or hematoma, cervical or (less commonly) thoracic disc rupture.
Chronic spinal cord compression develops over months or years. Causes: bone or cartilage protrusion into the spinal canal at the cervical, thoracic or lumbar level (e.g. osteophytes or spondylosis, especially in the setting of a congenitally narrow spinal canal, more often at the lumbar level), arteriovenous malformations, intramedullary and slowly growing extramedullary tumors.
Subluxation of the atlantoaxial joint or other abnormalities of the craniocervical junction can cause acute, subacute, or chronic spinal cord compression.
Formations that compress the spinal cord can have the same effect on the nerve roots or, in rare cases, disrupt the blood supply to the spinal cord, leading to an infarction.
[ Symptoms spinal cord compression
Acute or subacute spinal cord compression causes segmental deficit, paraparesis or tetraparesis, hyperreflexia, extensor plantar reflexes, loss of sphincter tone (dysfunction of the pelvic organs) with loss of sensitivity. Subacute and chronic compression may debut with local back pain, often radiating to the innervation zone of the nerve root (radicular pain), or with hyperreflexia and loss of sensitivity. Initially, sensitivity may be lost in the sacral segments. Sudden complete loss of function is possible with spinal cord infarction. With metastasis, abscess or hematoma, percussion of the spinous processes is painful.
Intramedullary formations often cause a difficult to localize burning sensation rather than radicular pain, sensitivity is preserved, and spastic paresis develops.
Diagnostics spinal cord compression
Spinal cord compression involves spinal or radicular pain with motor, sensory and reflex deficits, especially at the segmental level. If MRI is not possible, CT myelography is performed.
A non-ionic low-osmolar radioactive preparation is administered via lumbar puncture, which, moving cranially, contrasts the lower level of the complete spinal canal block. The radioactive preparation is then introduced from above via cervical puncture, and the rostral level of the block is determined. Spinal radiography is useful for the rapid detection of bone pathology (fracture, dislocation, subluxation) in trauma.
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Treatment spinal cord compression
Treatment is aimed at reducing the pressure on the spinal cord. Partial and recent complete loss of function may be reversible (complete loss is rare). Therefore, in acute compression, diagnosis and treatment are urgent.
If the compression is due to a tumor, dexamethasone 100 mg intravenously is administered immediately, then 25 mg every 6 hours, and surgery or radiation therapy is started immediately. If, despite conservative treatment, the neurological deficit increases, surgery is indicated. Surgery is also indicated in cases where a biopsy is necessary, the spine is unstable, the tumor recurs after radiation therapy, and if an abscess, subdural or epidural hematoma is suspected.