Spinal cord compression pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Pathophysiology

Anotomy

• The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae.
• At L2 level spinal cord transforms into spinal roots and forms a cone-shaped structure called conus medullaris.
• The cord is protected by the vertebral column, which is mobile and allows for movement of the spine.
• It is enclosed by the dura mater and the vessels supplying it.
• The cord floats in the cerebrospinal fluid which acts as a buffer to movement and early degrees of compression.
• The cord substance contains a gray area centrally and is surrounded by white matter communication tracts, both ascending and descending.

Pathogenesis

• The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling.
• Conditions that interfere, either directly or indirectly, with the blood supply will cause malfunction of the transmission pathway.
• Injury to the spinal cord or nerve roots arises from stretching or from pressure.
• It initiates a cascade of events in the gray matter and white matter, and results in hypoperfusion and eventually hemorrhagic necrosis.
• The extent of necrosis depends on the severity of the trauma, concomitant compression, perfusion pressures and blood flow, and administration of pharmacological agents.
• The tissue responses by gliosis, demyelination, and axonal loss.
• This results in injury to the white matter (myelinated tracts) and the gray matter (cell bodies) in the cord with loss of sensory reflexes (pinprick, joint position sense, vibration, hot/cold, pressure) and motor function.
• Rapid compression will result in the collapse of the venous system, resulting in vasogenic edema.
• Vasogenic edema exacerbates parenchymal pressure and may lead to rapid progression of dysfunction.