Spinal cord compression pathophysiology: Difference between revisions
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*The cord floats in the cerebrospinal fluid which acts as a buffer to movement and early degrees of compression. | *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 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. | |||
== References == | == References == | ||
Revision as of 13:37, 13 April 2017
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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]
Overview
Pathophysiology
Anotomy
- 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.
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.
References
- ↑ Bican O, Minagar A, Pruitt AA (2013). "The spinal cord: a review of functional neuroanatomy". Neurol Clin. 31 (1): 1–18. doi:10.1016/j.ncl.2012.09.009. PMID 23186894.
- ↑ Diaz E, Morales H (2016). "Spinal Cord Anatomy and Clinical Syndromes". Semin. Ultrasound CT MR. 37 (5): 360–71. doi:10.1053/j.sult.2016.05.002. PMID 27616310.