Spinal cord compression pathophysiology: Difference between revisions
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*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=== | ===Pathogenesis=== | ||
*The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling. | *The spinal cord and nerve roots depend on a constant blood supply to perform axonal signaling.<ref name="pmid24406153">{{cite journal |vauthors=Pekny M, Wilhelmsson U, Pekna M |title=The dual role of astrocyte activation and reactive gliosis |journal=Neurosci. Lett. |volume=565 |issue= |pages=30–8 |year=2014 |pmid=24406153 |doi=10.1016/j.neulet.2013.12.071 |url=}}</ref><ref name="pmid23250681">{{cite journal |vauthors=Vilar-González S, Pérez-Rozos A, Torres-Campa JM, Mateos V |title=[Spinal cord compression: a multidisciplinary approach to a real neuro-oncological emergency] |language=Spanish; Castilian |journal=Rev Neurol |volume=56 |issue=1 |pages=43–52 |year=2013 |pmid=23250681 |doi= |url=}}</ref><ref name="pmid16194459">{{cite journal |vauthors=Schmidt MH, Klimo P, Vrionis FD |title=Metastatic spinal cord compression |journal=J Natl Compr Canc Netw |volume=3 |issue=5 |pages=711–9 |year=2005 |pmid=16194459 |doi= |url=}}</ref> | ||
*Conditions that interfere, either directly or indirectly, with the blood supply will cause malfunction of the transmission pathway. | *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 material or ischemia | *Injury to the spinal cord or nerve roots arises from direct trauma, compression by bone fragments, hematoma, or disk material or ischemia | ||
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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.[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 disk material 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, 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.
- ↑ Pekny M, Wilhelmsson U, Pekna M (2014). "The dual role of astrocyte activation and reactive gliosis". Neurosci. Lett. 565: 30–8. doi:10.1016/j.neulet.2013.12.071. PMID 24406153.
- ↑ Vilar-González S, Pérez-Rozos A, Torres-Campa JM, Mateos V (2013). "[Spinal cord compression: a multidisciplinary approach to a real neuro-oncological emergency]". Rev Neurol (in Spanish; Castilian). 56 (1): 43–52. PMID 23250681.
- ↑ Schmidt MH, Klimo P, Vrionis FD (2005). "Metastatic spinal cord compression". J Natl Compr Canc Netw. 3 (5): 711–9. PMID 16194459.