Sandbox spinalcord

Causes

Common causes of acute spinal cord compression include

• Trauma is a leading cause of acute spinal cord compression
• Primary or secondary metastatic spinal tumor
• Vertebral compression fractures due to osteomalacia, osteoporosis, corticosteroid therapy
• Intervertebral disk herniation
• Epidural abscess
• Epidural hematoma

Risk factors

Common risk factors in the development of spinal cord compression include

• Cervical spondylosis
• Atlantoaxial instability
• Congenital conditions (tethered cord)
• Osteoporosis
• Ankylosing spondylitis
• Rheumatoid arthritis of the cervical spine

Less common risk factors

• IV drug abuse
• Immunocompromised

Pathophysiology

Anatomy

• 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.

Pathophysiology

• 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.

Dissemination

Hematogenous spread

Associated conditions

Lesions may develop gradually or acutely and be complete or incomplete. Incomplete lesions often present as distinct syndromes  as follows:

	Sensory dysfunction	Motor dysfunction	Sphincter dysfunction
Central cord syndrome	Sensory loss is very rare	Upper extremity weakness distal muscles are involved more than proximal
Brown-Séquard syndrome	Ipsilateral position and vibration sense loss Contralateral pain and temperature sensation loss	Motor loss ipsilateral to cord lesion
Anterior cord syndrome	Loss of pin and touch sensation Vibration, position sense preserved	Motor loss or weakness below the level of compression
Transverse cord syndrome	Loss of sensation below level of compression	Loss of voluntary motor function below the level of compression	Sphincter control lost
Conus medullaris syndrome	Saddle anesthesia Sensory loss may range from patchy to complete transverse pattern		Sphincter control impaired
Cauda equina syndrome