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Signs and symptoms manifested are closely correlated to the portion and extent of spinal cord affected.<ref name=":3" /> Abrupt onset of pain at the back or neck signals the location of ischaemia or hemorrhage at the beginning, which radiates as the damage intensifies.<ref name=":6">{{Cite journal |last=Shaban |first=Amir |last2=Moritani |first2=Toshio |last3=Kasab |first3=Sami Al |last4=Sheharyar |first4=Ali |last5=Limaye |first5=Kaustubh S. |last6=Adams |first6=Harold P. |date=2018-06-01 |title=Spinal Cord Hemorrhage |url=https://www.strokejournal.org/article/S1052-3057(18)30065-X/abstract |journal=Journal of Stroke and Cerebrovascular Diseases |language=English |volume=27 |issue=6 |pages=1435–1446 |doi=10.1016/j.jstrokecerebrovasdis.2018.02.014 |issn=1052-3057 |pmid=29555403}}</ref><ref name=":7">{{Cite journal |last=Vuong |first=Shawn M. |last2=Jeong |first2=William J. |last3=Morales |first3=Humberto |last4=Abruzzo |first4=Todd A. |date=2016-10-01 |title=Vascular Diseases of the Spinal Cord: Infarction, Hemorrhage, and Venous Congestive Myelopathy |url=https://www.sciencedirect.com/science/article/pii/S0887217116300270 |journal=Seminars in Ultrasound, CT and MRI |series=SI: Spinal Cord Imaging, Part 1 |language=en |volume=37 |issue=5 |pages=466–481 |doi=10.1053/j.sult.2016.05.008 |issn=0887-2171}}</ref> Temporary [[paresis]] in limbs may occur days before the onset of spinal ischaemic stroke, though their relationship remains unclear.<ref name=":0" /><ref name=":8">{{Citation |last=Skvortsova |first=Veronika I. |title=Chapter 34 Spinal strokes |date=2008-01-01 |url=https://www.sciencedirect.com/science/article/pii/S0072975208930347 |work=Handbook of Clinical Neurology |volume=93 |pages=683–702 |series=Stroke Part II: Clinical Manifestations and Pathogenesis |publisher=Elsevier |language=en |doi=10.1016/s0072-9752(08)93034-7 |access-date=2022-03-28 |last2=Bahar |first2=Sara Z.}}</ref> While it takes minutes for ischeamic spinal stroke to develop the symptoms, the time could be extended to days and weeks in hemorrhagic spinal stroke.<ref name=":6" /><ref name=":7" /> Infarction in arteries predominates over venous infarction, and the watershed region, which refers thoracic spinal cord, are highly susceptible to ischamic attack.<ref name=":4" /> |
Signs and symptoms manifested are closely correlated to the portion and extent of spinal cord affected.<ref name=":3" /> Abrupt onset of pain at the back or neck signals the location of ischaemia or hemorrhage at the beginning, which radiates as the damage intensifies.<ref name=":6">{{Cite journal |last=Shaban |first=Amir |last2=Moritani |first2=Toshio |last3=Kasab |first3=Sami Al |last4=Sheharyar |first4=Ali |last5=Limaye |first5=Kaustubh S. |last6=Adams |first6=Harold P. |date=2018-06-01 |title=Spinal Cord Hemorrhage |url=https://www.strokejournal.org/article/S1052-3057(18)30065-X/abstract |journal=Journal of Stroke and Cerebrovascular Diseases |language=English |volume=27 |issue=6 |pages=1435–1446 |doi=10.1016/j.jstrokecerebrovasdis.2018.02.014 |issn=1052-3057 |pmid=29555403}}</ref><ref name=":7">{{Cite journal |last=Vuong |first=Shawn M. |last2=Jeong |first2=William J. |last3=Morales |first3=Humberto |last4=Abruzzo |first4=Todd A. |date=2016-10-01 |title=Vascular Diseases of the Spinal Cord: Infarction, Hemorrhage, and Venous Congestive Myelopathy |url=https://www.sciencedirect.com/science/article/pii/S0887217116300270 |journal=Seminars in Ultrasound, CT and MRI |series=SI: Spinal Cord Imaging, Part 1 |language=en |volume=37 |issue=5 |pages=466–481 |doi=10.1053/j.sult.2016.05.008 |issn=0887-2171}}</ref> Temporary [[paresis]] in limbs may occur days before the onset of spinal ischaemic stroke, though their relationship remains unclear.<ref name=":0" /><ref name=":8">{{Citation |last=Skvortsova |first=Veronika I. |title=Chapter 34 Spinal strokes |date=2008-01-01 |url=https://www.sciencedirect.com/science/article/pii/S0072975208930347 |work=Handbook of Clinical Neurology |volume=93 |pages=683–702 |series=Stroke Part II: Clinical Manifestations and Pathogenesis |publisher=Elsevier |language=en |doi=10.1016/s0072-9752(08)93034-7 |access-date=2022-03-28 |last2=Bahar |first2=Sara Z.}}</ref> While it takes minutes for ischeamic spinal stroke to develop the symptoms, the time could be extended to days and weeks in hemorrhagic spinal stroke.<ref name=":6" /><ref name=":7" /> Infarction in arteries predominates over venous infarction, and the watershed region, which refers thoracic spinal cord, are highly susceptible to ischamic attack.<ref name=":4" /> |
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[[File:Kabir Spinal Cord Lesions and Syndromes.jpg|thumb|Symptoms of various types of spinal cord stroke.]] |
[[File:Kabir Spinal Cord Lesions and Syndromes.jpg|thumb|Symptoms of various types of spinal cord stroke.]] |
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''' ''' ''Main article: [[anterior spinal artery syndrome]]'' |
''' ''' ''Main article: [[anterior spinal artery syndrome]]'' |
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A major feature is losing motor function such as reflexes and coordination as a result of compromised [[Anterior corticospinal tract|anterior]] and [[lateral corticospinal tract]], anterior [[grey matter]] and [[spinocerebellar tract]].<ref name=":3" /><ref>{{Citation |last=Rivera |first=V. M. |title=Spinal Stroke |date=2014-01-01 |url=https://www.sciencedirect.com/science/article/pii/B9780123851574004188 |work=Encyclopedia of the Neurological Sciences (Second Edition) |pages=288 |editor-last=Aminoff |editor-first=Michael J. |place=Oxford |publisher=Academic Press |language=en |doi=10.1016/b978-0-12-385157-4.00418-8 |isbn=978-0-12-385158-1 |access-date=2022-03-28 |editor2-last=Daroff |editor2-first=Robert B.}}</ref> There is also a loss in nociception and thermosensation as a result of interrupted [[spinothalamic tract]].<ref name=":3" /> |
A major feature is losing motor function such as reflexes and coordination as a result of compromised [[Anterior corticospinal tract|anterior]] and [[lateral corticospinal tract]], anterior [[grey matter]] and [[spinocerebellar tract]].<ref name=":3" /><ref>{{Citation |last=Rivera |first=V. M. |title=Spinal Stroke |date=2014-01-01 |url=https://www.sciencedirect.com/science/article/pii/B9780123851574004188 |work=Encyclopedia of the Neurological Sciences (Second Edition) |pages=288 |editor-last=Aminoff |editor-first=Michael J. |place=Oxford |publisher=Academic Press |language=en |doi=10.1016/b978-0-12-385157-4.00418-8 |isbn=978-0-12-385158-1 |access-date=2022-03-28 |editor2-last=Daroff |editor2-first=Robert B.}}</ref> There is also a loss in nociception and thermosensation as a result of interrupted [[spinothalamic tract]].<ref name=":3" /> |
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'''Posterior spinal cord''' |
=== '''Posterior spinal cord''' === |
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''' ''' ''Main article: [[Posterior cord syndrome|posterior spinal artery syndrome]]'' |
''' ''' ''Main article: [[Posterior cord syndrome|posterior spinal artery syndrome]]'' |
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Sensory function is undermined heavily mainly, which is associated to [[Dorsal column nuclei|dorsal column]].<ref name=":3" /> Unlike stroke in anterior spinal cord, motor functions are not handicapped.<ref name=":3" /> |
Sensory function is undermined heavily mainly, which is associated to [[Dorsal column nuclei|dorsal column]].<ref name=":3" /> Unlike stroke in anterior spinal cord, motor functions are not handicapped.<ref name=":3" /> |
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'''Central spinal cord''' |
=== '''Central spinal cord''' === |
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''' ''' ''Main article: [[Central cord syndrome|central spinal cord syndrome]]'' |
''' ''' ''Main article: [[Central cord syndrome|central spinal cord syndrome]]'' |
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Impairment of motor function in the upper body is considerably more severe than that of lower body, which is related to hyperextension of corticospinal tracts and spinocerebellar tract in cervical spinal cord, accompanied by dysfunction in urinary bladder and sensational loss at a varying degree.<ref name=":3" /><ref>{{Cite journal |last=Brooks |first=Nathaniel P. |date=2017-01-01 |title=Central Cord Syndrome |url=https://www.sciencedirect.com/science/article/pii/S1042368016300456 |journal=Neurosurgery Clinics of North America |series=Adult and Pediatric Spine Trauma |language=en |volume=28 |issue=1 |pages=41–47 |doi=10.1016/j.nec.2016.08.002 |issn=1042-3680}}</ref> |
Impairment of motor function in the upper body is considerably more severe than that of lower body, which is related to hyperextension of corticospinal tracts and spinocerebellar tract in cervical spinal cord, accompanied by dysfunction in urinary bladder and sensational loss at a varying degree.<ref name=":3" /><ref>{{Cite journal |last=Brooks |first=Nathaniel P. |date=2017-01-01 |title=Central Cord Syndrome |url=https://www.sciencedirect.com/science/article/pii/S1042368016300456 |journal=Neurosurgery Clinics of North America |series=Adult and Pediatric Spine Trauma |language=en |volume=28 |issue=1 |pages=41–47 |doi=10.1016/j.nec.2016.08.002 |issn=1042-3680}}</ref> |
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'''Brown-Séquard syndrome''' |
=== '''Brown-Séquard syndrome''' === |
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''' ''' ''Main article: [[Brown-Séquard syndrome]]'' |
''' ''' ''Main article: [[Brown-Séquard syndrome]]'' |
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Brown-Séquard syndrome is only the subtype that affect the spinal cord unilaterally, either anteriorly, posteriorly, or both.<ref name=":1" /> Ipsilateral loss of vibration, fine touch, location perception and fine movement control, as well as contralateral loss of axial muscles and movement coordination are found.<ref name=":3" /> |
Brown-Séquard syndrome is only the subtype that affect the spinal cord unilaterally, either anteriorly, posteriorly, or both.<ref name=":1" /> Ipsilateral loss of vibration, fine touch, location perception and fine movement control, as well as contralateral loss of axial muscles and movement coordination are found.<ref name=":3" /> |
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'''Transverse''' |
=== '''Transverse''' === |
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Necrosis of spinal cells at the complete transverse level is the most severe form of spinal cord stroke, presented clinically as lower [[paraplegia]] or [[quadriplegia]], sensory loss below the lesion, urinary incontinence, and disturbances in autonomous nervous system and hormonal system.<ref name=":8" /> |
Necrosis of spinal cells at the complete transverse level is the most severe form of spinal cord stroke, presented clinically as lower [[paraplegia]] or [[quadriplegia]], sensory loss below the lesion, urinary incontinence, and disturbances in autonomous nervous system and hormonal system.<ref name=":8" /> |
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Revision as of 01:43, 28 March 2022
Spinal cord stroke, also known as spinal stroke, is a rare type of stroke with compromised blood flow to any region of spinal cord owing to occlusion or bleeding, leading to irreversible neuronal death.[1] It can be classified into two types, ischaemia and hemorrhage, in which the former accounts for 86% of all spinal stroke cases, a pattern similar to cerebral stroke.[2][3] Either arisen spontaneously from aortic illnesses or postoperatively, the disease deprives patients of motor and/or sensory function.[4][5] Infarction usually occurs in regions perfused by anterior spinal artery, which spans the anterior two-third of spinal cord.[6]
Signs and symptoms
Signs and symptoms manifested are closely correlated to the portion and extent of spinal cord affected.[4] Abrupt onset of pain at the back or neck signals the location of ischaemia or hemorrhage at the beginning, which radiates as the damage intensifies.[7][8] Temporary paresis in limbs may occur days before the onset of spinal ischaemic stroke, though their relationship remains unclear.[1][9] While it takes minutes for ischeamic spinal stroke to develop the symptoms, the time could be extended to days and weeks in hemorrhagic spinal stroke.[7][8] Infarction in arteries predominates over venous infarction, and the watershed region, which refers thoracic spinal cord, are highly susceptible to ischamic attack.[5]
Anterior spinal cord
Main article: anterior spinal artery syndrome
A major feature is losing motor function such as reflexes and coordination as a result of compromised anterior and lateral corticospinal tract, anterior grey matter and spinocerebellar tract.[4][10] There is also a loss in nociception and thermosensation as a result of interrupted spinothalamic tract.[4]
Posterior spinal cord
Main article: posterior spinal artery syndrome
Sensory function is undermined heavily mainly, which is associated to dorsal column.[4] Unlike stroke in anterior spinal cord, motor functions are not handicapped.[4]
Central spinal cord
Main article: central spinal cord syndrome
Impairment of motor function in the upper body is considerably more severe than that of lower body, which is related to hyperextension of corticospinal tracts and spinocerebellar tract in cervical spinal cord, accompanied by dysfunction in urinary bladder and sensational loss at a varying degree.[4][11]
Brown-Séquard syndrome
Main article: Brown-Séquard syndrome
Brown-Séquard syndrome is only the subtype that affect the spinal cord unilaterally, either anteriorly, posteriorly, or both.[2] Ipsilateral loss of vibration, fine touch, location perception and fine movement control, as well as contralateral loss of axial muscles and movement coordination are found.[4]
Transverse
Necrosis of spinal cells at the complete transverse level is the most severe form of spinal cord stroke, presented clinically as lower paraplegia or quadriplegia, sensory loss below the lesion, urinary incontinence, and disturbances in autonomous nervous system and hormonal system.[9]
Causes and risk factors
Diseases in aorta are recognized as the most widely seen contributor of spontaneous spinal cord ischaemia, represented by rupturing of thoracic aortic aneurysm, arterial occlusion by aortic intima separated from endothelial wall of aortic dissection, and aortic coarctation.[5] Embolism, meningeal inflammation at spinal cord, global ischaemia and abusing nicotinic drugs are also identified to factors.[2]
Aortic surgeries contribute to most iatrogenic spinal cord ischaemia, although its percentage is much lower than that of spontaneous type.[5] Thoracic endovascular aortic repair (TEVAR) was carried out to introduce a stent graft in order to treat thoracoabdominal aortic aneurysm, a condition of enlarged aorta with weakened vascular wall, as well as traumas and atherosclerosis.[12] Segmental medullary arteries, notably the artery of Adamkiewicz, could be excluded from circulation after blockage of intercostal arteries by the device, which directly branches from descending aorta.[12] During open repair, blood flow within aorta is halted by clamping to facilitate the sewing of interposition graft.[10] The reduced blood flow to anterior and posterior radicular artery triggers spinal stroke.[12] Cases of spinal stroke following operations like aortography, spinal anesthesia and lumbar spine surgery are reported.[5]
Abnormalities in blood vessels including arteriovenous malformations, arteriovenous fistulas and cavernomas are preferably presented as ischaemia and occasionally hemorrhage, of which dural AV fistulas account for most cases.[2][6][7] The direct fusion between arteries and veins increases blood pressure in radiculomedullary vein and coronal venous plexus, which is an important factor of venous congestive myelopathy and infarction.[6]
Prolonged compression on the blood network by vertebral diseases such as cervical spondylosis and protruded intervertebral disks can be attributed to acute ischaemia in spinal cord, yet the correlation is uncertain.[3][9]
Trauma, which generally originates from terminal vascular network, is the most common cause of spinal cord hemorrhage for all four subtypes, namely haematomyelia, subarachnoid hemorrhage, subdural hemorrhage and epidural hemorrhage.[4]
It should be noted causes of spinal stroke are often not clearly defined in clinical setting.[3]
Patients with a male gender, younger age, lower body mass index, hypertension, diabetes mellitus, renal insufficiency and chronic obstructive pulmonary disease are predisposed to more severe spinal cord stroke.[3][12] Probability of postoperative spinal cord stroke is linked to both aneurysm extent, particularly extent II (descending aorta at full length) and length of graft.[12]
Mechanism
The pathophysiology of spinal stroke is similar to its counterpart in brain. Decreasing blood flow hampers oxygen and glucose delivery to neurones, causing a huge decline in ATP production and failure of calcium pump.[13] The rising intracellular calcium level activates a series of enzymes like phospholipase A2 (PLA2), COX-2, calcineurin, calpain, mitogen-activated protein kinase, nitric oxide synthase, matrix metalloproteinases (MMPs) to produce proinflammatory and proapoptotic chemicals.[13][14] PGE2 from PLA2, nitric oxide and MMPs enhance vascular permeability and immune cells infiltration that amplify inflammation.[14] Calcineurin dephosphorylates BAD and activates caspase-3.[14] Meanwhile, glutamate is released to extracellular space and binds to its excitatory receptors, further exacerbating calcium influx and a cascade of events involving mitochondrial, cell membrane damage, and production of free radicals.[14] Such excitotoxicity is closely associated with the eventual neuronal cell death and loss of tract function.[14]
References
- ^ a b Leys, D.; Pruvo, J.-P. (May 2021). "Spinal infarcts". Revue Neurologique. 177 (5): 459–468. doi:10.1016/j.neurol.2020.12.002.
- ^ a b c d Bhole, R.; Caplan, L. R. (2017-01-01), Caplan, Louis R.; Biller, José; Leary, Megan C.; Lo, Eng H. (eds.), "Chapter 89 - Spinal Cord Strokes", Primer on Cerebrovascular Diseases (Second Edition), San Diego: Academic Press, pp. 433–438, doi:10.1016/b978-0-12-803058-5.00089-8, ISBN 978-0-12-803058-5, retrieved 2022-03-28
- ^ a b c d Romi, Fredrik; Naess, Halvor (2016). "Spinal Cord Infarction in Clinical Neurology: A Review of Characteristics and Long-Term Prognosis in Comparison to Cerebral Infarction". European Neurology. 76 (3–4): 95–98. doi:10.1159/000446700. ISSN 0014-3022. PMID 27487411.
- ^ a b c d e f g h i Massicotte, Eric M.; Tator, Charles (2012), Vincent, Jean-Louis; Hall, Jesse B. (eds.), "Spinal Cord Injury Syndromes", Encyclopedia of Intensive Care Medicine, Berlin, Heidelberg: Springer, pp. 2101–2104, doi:10.1007/978-3-642-00418-6_363, ISBN 978-3-642-00418-6, retrieved 2022-03-28
- ^ a b c d e Takayama, Hiroo; Patel, Virendra I.; Willey, Joshua Z. (2022), "Stroke and Other Vascular Syndromes of the Spinal Cord", Stroke, Elsevier, pp. 466–474.e3, doi:10.1016/b978-0-323-69424-7.00031-4, ISBN 978-0-323-69424-7, retrieved 2022-03-28
- ^ a b c Tang, Yang (2020), Tang, Yang (ed.), "Spinal Vascular Diseases", Atlas of Emergency Neurovascular Imaging, Cham: Springer International Publishing, pp. 143–151, doi:10.1007/978-3-030-43654-4_11, ISBN 978-3-030-43654-4, retrieved 2022-03-28
- ^ a b c Shaban, Amir; Moritani, Toshio; Kasab, Sami Al; Sheharyar, Ali; Limaye, Kaustubh S.; Adams, Harold P. (2018-06-01). "Spinal Cord Hemorrhage". Journal of Stroke and Cerebrovascular Diseases. 27 (6): 1435–1446. doi:10.1016/j.jstrokecerebrovasdis.2018.02.014. ISSN 1052-3057. PMID 29555403.
- ^ a b Vuong, Shawn M.; Jeong, William J.; Morales, Humberto; Abruzzo, Todd A. (2016-10-01). "Vascular Diseases of the Spinal Cord: Infarction, Hemorrhage, and Venous Congestive Myelopathy". Seminars in Ultrasound, CT and MRI. SI: Spinal Cord Imaging, Part 1. 37 (5): 466–481. doi:10.1053/j.sult.2016.05.008. ISSN 0887-2171.
- ^ a b c Skvortsova, Veronika I.; Bahar, Sara Z. (2008-01-01), "Chapter 34 Spinal strokes", Handbook of Clinical Neurology, Stroke Part II: Clinical Manifestations and Pathogenesis, vol. 93, Elsevier, pp. 683–702, doi:10.1016/s0072-9752(08)93034-7, retrieved 2022-03-28
- ^ Rivera, V. M. (2014-01-01), Aminoff, Michael J.; Daroff, Robert B. (eds.), "Spinal Stroke", Encyclopedia of the Neurological Sciences (Second Edition), Oxford: Academic Press, p. 288, doi:10.1016/b978-0-12-385157-4.00418-8, ISBN 978-0-12-385158-1, retrieved 2022-03-28
- ^ Brooks, Nathaniel P. (2017-01-01). "Central Cord Syndrome". Neurosurgery Clinics of North America. Adult and Pediatric Spine Trauma. 28 (1): 41–47. doi:10.1016/j.nec.2016.08.002. ISSN 1042-3680.
- ^ a b c d e Cheung, Albert T.; López, Jaime R. (2021), Cheng, Davy C.H.; Martin, Janet; David, Tirone (eds.), "Spinal Cord Ischemia Monitoring and Protection", Evidence-Based Practice in Perioperative Cardiac Anesthesia and Surgery, Cham: Springer International Publishing, pp. 323–343, doi:10.1007/978-3-030-47887-2_28, ISBN 978-3-030-47887-2, retrieved 2022-03-28
- ^ a b Farooqui, Akhlaq A. (2010), Farooqui, Akhlaq A. (ed.), "Neurochemical Aspects of Ischemic Injury", Neurochemical Aspects of Neurotraumatic and Neurodegenerative Diseases, New York, NY: Springer, pp. 27–65, doi:10.1007/978-1-4419-6652-0_2, ISBN 978-1-4419-6652-0, retrieved 2022-03-28
- ^ a b c d Farooqui, Akhlaq A. (2010), Farooqui, Akhlaq A. (ed.), "Neurochemical Aspects of Spinal Cord Injury", Neurochemical Aspects of Neurotraumatic and Neurodegenerative Diseases, New York, NY: Springer, pp. 107–149, doi:10.1007/978-1-4419-6652-0_4, ISBN 978-1-4419-6652-0, retrieved 2022-03-28