Spinal cord 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
Pathophysiology
Physiology
Spinal cord 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. The compression Although symptoms may arise from narrowing of the spinal canal, not all patients with narrowing develop symptoms. The reason why some patients develop symptomatic stenosis and others do not is still unknown. Therefore, the term lumbar spinal stenosis refers not to the pathoanatomic finding of spinal canal narrowing, but rather to a clinical syndrome of lower extremity pain caused by mechanical compression on the neural elements or their blood supply.
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 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 disc herniation 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, 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.
- 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.
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.