Sandbox spinalcord

Causes

Common causes of acute spinal cord compression include trauma, tumor, epidural abscess, and epidural hematoma.

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.

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.
Intracellular calcium is increased and reperfusion injury takes place which plays a key role in cellular injury.
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.