Spinal stenosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
Overview
Spinal stenosis is the narrowing of the vertebral canal tube. This narrowing produces neurovascular compression that may lead to pain and other neurology manifestations of spinal stenosis. Radiographic changes associated with stenosis are very common with aging. Although symptoms may arise from narrowing of the spinal canal, not all patients with narrowing develop symptoms. 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 stenosis may result from any condition that narrows the spinal canal and compresses nerve roots. The most common cause of spinal stenosis is degenerative joint disease. 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. 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 compression, and blood flow. 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
Spinal stenosis is the narrowing of the vertebral canal tube. This narrowing produces neurovascular compression that may lead to pain and other neurology manifestations of spinal stenosis. Radiographic changes associated with stenosis are very common with aging. Although symptoms may arise from narrowing of the spinal canal, not all patients with narrowing develop symptoms.
Anatomy
- 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 stenosis may result from any condition that narrows the spinal canal and compresses nerve roots.
- The most common cause of spinal stenosis is degenerative joint disease.
- 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.
- 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 compression, and blood flow.
- 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.
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.