Spinal cord compression pathophysiology
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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
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 material 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.
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.