Spinal cord compression pathophysiology

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

The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae. 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 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 direct trauma, compression by bone fragments, hematoma, or disk herniation or ischemia. 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.^[1][2]

• The spinal cord extends from the foramen magnum down to the level of the first and second lumbar vertebrae.^[1][2]
• 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.

• The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling.^[3][4][5]
• 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 direct trauma, compression by bone fragments, hematoma, or disc herniation or ischemia.
• It initiates a cascade of events in the gray matter and white matter and results in hypoperfusion.
• The following results in autonomic dysfunction leading to neurogenic shock ( triad of hypotension, bradycardia and peripheral vasodilation) and eventually hemorrhagic necrosis.
• The extent of necrosis depends on the severity of the trauma, concomitant compression, and blood flow.
• 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.

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