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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] Its preventive measures include decreasing the risk factors and maintaining enough spinal cord perfusion pressure during and after the operation. Radiologists always apply different MRI protocols for the diagnosis of both ischaemic and haemorrhagic spinal stroke.[7][8] Treatment for spinal cord stroke is mainly determined by the symptoms and the causes of the disease. For ischaemic spinal stroke patients, antiplatelet and corticosteroids might be used to reduce the risk of blood clot. For haemorrhagic spinal stroke patients, rapid surgical decompression is applied to minimize neurological injuries.[9] Patients may spend years for significant recovery after the spinal cord stroke.[3]

Signs and symptoms[edit]

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.[9][10] Temporary paresis in limbs may occur days before the onset of spinal ischaemic stroke, though their relationship remains unclear.[1][11] 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.[9][10] Infarction in arteries predominates over venous infarction, and the watershed region, which refers thoracic spinal cord here, are highly susceptible to ischaemic attack.[5] 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]

Symptoms of various types of spinal cord stroke.

Anterior spinal cord[edit]

       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][13] There is also a loss in nociception and thermosensation as a result of interrupted spinothalamic tract.[4]

Posterior spinal cord[edit]

       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[edit]

       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][14]

Brown-Séquard syndrome[edit]

       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[edit]

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.[11]

Causes[edit]

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]

Artery of Adamkiewicz is supplied by posterior intercostal artery, and drains into anterior spinal artery.

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][9] 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][11]

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.[9] Correlation between anticoagulating drugs and hemorrhagic stroke is present.[9]

It should be noted causes of spinal stroke are often not clearly defined in clinical setting.[3]

Mechanism[edit]

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.[15] 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.[15][16] 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.[16] 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.[16] Such excitotoxicity is closely associated with the eventual neuronal cell death and loss of tract function.[16]

Prevention[edit]

Risk factors[edit]

Modifiable risk factors that contribute to the common strokes such as hypertension and heart disease, are found less commonly in the formation of spinal cord stroke.[3] On the other hand, diabetes mellitus, peripheral artery disease, smoking and cholesterol are associated more with such disease.[3] Prevention and treatment of these modifiable risk factors could reduce the likelihood of spinal cord stroke.

Intraoperative strategy[edit]

As the high difficulty for the detection during operation, somatosensory evoked potential monitoring or motor evoked potential monitoring is necessary to early detect the spinal cord ischaemia in anesthetized patients for quick intervention.[12][17] Cerebrospinal fluid drainage is always used to decrease intraspinal pressure and increase blood flow to the spinal cord to avoid hypotension, thus reducing the risk of spinal cord ischaemia.[17]

Postoperative strategy[edit]

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]The aims of postoperative management are to maintain enough spinal cord perfusion pressure, and make serial neurologic assessments to detect the disease. Similar to the intraoperative strategy, increasing the spinal cord perfusion as an immediate intervention may increase the chance of successful treatment.[18] Neurological examination should be conducted after anesthesia to test the motor function of the low extremity of patients. By using this method to detect whether patients have spinal cord ischaemia, doctors could decide whether rapid treatment should be provided.[12]

Diagnosis[edit]

Owl-eyes sign exhibits bilaterally symmetric circular to ovoid foci of T2-weighted signals in anterior horn cells.

Spinal stroke could be easily misdiagnosed because of its rarity.[10] The doctor will first assess the clinical symptoms of the patient, such as paralysis, sensory loss and urinary and bowel dysfunction, to determine whether it is possible for the spinal stroke. After that, different MRI imaging protocols will be used, including axial and sagittal T1 and T2-weighted sequences and diffusion-weighted imaging (DWI).

Ischemic spinal cord stroke[edit]

As the non-contrast CT and spine CT angiography are ineffective in imaging modalities, doctors use MRI to confirm the diagnosis. MRI findings, including pencillike hyperintensities on T2-weighted sagittal images and “owl’s eyes” or “snake eyes” sign on T2 axial images, indicating the infarction is predominately in the watershed area of the gray matter of ventral horn (ASA infarct).[10] Also, posterior paramedian triangular hyperintensity in T2 hyperintensity indicates PSA infarct. On a T1 sequence, we may also observe a cord expansion and a decreased signal.[19] However, traditional MRI may show no abnormality especially for those patients in the acute phase.[8] DWI is very sensitive for early detection of spinal cord infarction and shows a typical high signal intensity.[20]

Hemorrhagic spinal cord stroke[edit]

On axial imaging at the level of the denticulate ligaments, the inverted Mercedes-Benz sign denotes the form taken on by a spinal subdural hematoma.

To identify the hematoma in the spinal cord, MRI with and without gadolinium enhancement is the preferred choice.[9] CT is also used to identify the hemorrhage and provide evidence for pathological analysis. Complete spinal MRI with MR angiography is used when patients with subarachnoid hemorrhage without the intracranial etiology.[21] As the evaluation of the need for intradural interrogation is important, it is necessary to differentiate between subdural and epidural hematomas. Based on the location of the hematoma, use both axial and sagittal images of MRI to identify the boundary between hematoma and fat.[7] An inverted Mercedes-Benz sign shows the spinal subdural hematoma on the axial image.[22]

Treatment[edit]

Given the rarity and heterogeneity of spinal cord stroke, symptomatic treatment of associated complications is applied, which is based on patients' own circumstances.

Ischaemic spinal cord stroke[edit]

Although some literature suggest that thrombolysis could be the treatment for ischaemic spinal stroke, the associated risks are unknown due to the scarce data.[23] If the cause is global hypoperfusion, maintaining enough blood pressure to maintain adequate spinal perfusion is needed.[19] Also, anticoagulation and antiplatelet agents have been prescribed to prevent vascular occlusion or embolism.[8] Corticosteroids are prescribed in situations of vasculitis or aortitis.[19]

Haemorrhagic spinal cord stroke[edit]

Surgical decompression[edit]

The goal of treatment in an acute situation is to relieve pressure on the spinal cord. To limit neurological injury, surgical decompression should be undertaken as soon as possible.[24] Several case studies show a substantial link between the time from bleeding to surgical decompression and neurological outcome, with the greatest results coming from individuals who had surgery within 12 hours after symptom onset.[25]

Administration of large dose corticosteroids[edit]

While waiting for surgery, high-dose corticosteroids were administered in the acute phase. It could reduce oedema and secondary cord compression.[26]

Reversal of anticoagulation[edit]

As anticoagulation treatment with warfarin or heparin has been linked to spontaneous hematomyelia, reversal anticoagulation is used to reduce the risk of bleeding by using suitable antidotes. Protamine is used to reverse heparin and low molecular-weight heparin. Vitamin K is a reversal agent for warfarin.[27]

Prognosis[edit]

It is possible that spinal cord ischaemia patients have a full recovery. Although the mortality rate after spinal cord ischaemia is relatively high (23%), 58% of the survivors were ambulating with or without gait assistance at their final follow-up appointment. Patients with total paraplegia and sensory loss at nadir can, however, progress significantly over months to years.[28]

References[edit]

  1. ^ 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.
  2. ^ 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
  3. ^ a b c d e f g 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.
  4. ^ a b c d e f g h 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
  5. ^ 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
  6. ^ 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
  7. ^ a b Hausmann, O.; Kirsch, E.; Radü, E.; Mindermann, Th.; Gratzl, O. (2001-03-01). "Coagulopathy Induced Spinal Intradural Extramedullary Haematoma: Report of Three Cases and Review of the Literature". Acta Neurochirurgica. 143 (2): 135–140. doi:10.1007/s007010170118. ISSN 0942-0940.
  8. ^ a b c Zalewski, Nicholas L.; Rabinstein, Alejandro A.; Krecke, Karl N.; Brown, Robert D., Jr; Wijdicks, Eelco F. M.; Weinshenker, Brian G.; Kaufmann, Timothy J.; Morris, Jonathan M.; Aksamit, Allen J.; Bartleson, J. D.; Lanzino, Giuseppe (2019-01-01). "Characteristics of Spontaneous Spinal Cord Infarction and Proposed Diagnostic Criteria". JAMA Neurology. 76 (1): 56–63. doi:10.1001/jamaneurol.2018.2734. ISSN 2168-6149. PMC 6440254. PMID 30264146.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: multiple names: authors list (link)
  9. ^ a b c d e f g 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.
  10. ^ a b c d 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.
  11. ^ 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
  12. ^ a b c d e f g 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
  13. ^ 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
  14. ^ 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.
  15. ^ 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
  16. ^ 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
  17. ^ a b Epstein, NancyE (2018). "Cerebrospinal fluid drains reduce risk of spinal cord injury for thoracic/thoracoabdominal aneurysm surgery: A review". Surgical Neurology International. 9 (1): 48. doi:10.4103/sni.sni_433_17. ISSN 2152-7806. PMC 5843969. PMID 29541489.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  18. ^ Keith, Charles J.; Passman, Marc A.; Carignan, Martin J.; Parmar, Gaurav M.; Nagre, Shardul B.; Patterson, Mark A.; Taylor, Steven M.; Jordan, William D. (January 2012). "Protocol implementation of selective postoperative lumbar spinal drainage after thoracic aortic endograft". Journal of Vascular Surgery. 55 (1): 1–8. doi:10.1016/j.jvs.2011.07.086.
  19. ^ a b c Yadav, Nishtha; Pendharkar, Hima; Kulkarni, Girish Baburao (October 2018). "Spinal Cord Infarction: Clinical and Radiological Features". Journal of Stroke and Cerebrovascular Diseases. 27 (10): 2810–2821. doi:10.1016/j.jstrokecerebrovasdis.2018.06.008.
  20. ^ Weidauer, Stefan; Nichtweiß, Michael; Hattingen, Elke; Berkefeld, Joachim (March 2015). "Spinal cord ischemia: aetiology, clinical syndromes and imaging features". Neuroradiology. 57 (3): 241–257. doi:10.1007/s00234-014-1464-6. ISSN 0028-3940.
  21. ^ Lawton, Michael T.; Vates, G. Edward (2017-07-20). Solomon, Caren G. (ed.). "Subarachnoid Hemorrhage". New England Journal of Medicine. 377 (3): 257–266. doi:10.1056/NEJMcp1605827. ISSN 0028-4793.
  22. ^ Kobayashi, Kazuyoshi; Imagama, Shiro; Ando, Kei; Nishida, Yoshihiro; Ishiguro, Naoki (November 2017). "Acute non-traumatic idiopathic spinal subdural hematoma: radiographic findings and surgical results with a literature review". European Spine Journal. 26 (11): 2739–2743. doi:10.1007/s00586-017-5013-y. ISSN 0940-6719.
  23. ^ Lee, K.; Strozyk, D.; Rahman, C.; Lee, L.K.; Fernandes, E.M.; Claassen, J.; Badjatia, N.; Mayer, S.A.; Pile-Spellman, J. (2010). "Acute Spinal Cord Ischemia: Treatment with Intravenous and Intra-Arterial Thrombolysis, Hyperbaric Oxygen and Hypothermia". Cerebrovascular Diseases. 29 (1): 95–98. doi:10.1159/000259618. ISSN 1421-9786.
  24. ^ Akpınar, Aykut; Celik, Bahattin; Canbek, Ihsan; Karavelioğlu, Ergun (2016). "Acute Paraplegia due to Thoracic Hematomyelia". Case Reports in Neurological Medicine. 2016: 1–3. doi:10.1155/2016/3138917. ISSN 2090-6668. PMC 4960333. PMID 27478663.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  25. ^ Lawton, Michael T.; Porter, Randall W.; Heiserman, Joseph E.; Jacobowitz, Ronald; Sonntag, Volker K. H.; Dickman, Curtis A. (July 1995). "Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome". Journal of Neurosurgery. 83 (1): 1–7. doi:10.3171/jns.1995.83.1.0001. ISSN 0022-3085.
  26. ^ Bracken, Michael B (2012-01-18). Cochrane Injuries Group (ed.). "Steroids for acute spinal cord injury". Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD001046.pub2. PMC 6513405. PMID 22258943.{{cite journal}}: CS1 maint: PMC format (link)
  27. ^ Frontera, Jennifer A.; Lewin III, John J.; Rabinstein, Alejandro A.; Aisiku, Imo P.; Alexandrov, Anne W.; Cook, Aaron M.; del Zoppo, Gregory J.; Kumar, Monisha A.; Peerschke, Ellinor I. B.; Stiefel, Michael F.; Teitelbaum, Jeanne S (February 2016). "Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for Healthcare Professionals from the Neurocritical Care Society and Society of Critical Care Medicine". Neurocritical Care. 24 (1): 6–46. doi:10.1007/s12028-015-0222-x. ISSN 1541-6933.
  28. ^ Robertson, C. E.; Brown, R. D.; Wijdicks, E. F. M.; Rabinstein, A. A. (2012-01-10). "Recovery after spinal cord infarcts: Long-term outcome in 115 patients". Neurology. 78 (2): 114–121. doi:10.1212/WNL.0b013e31823efc93. ISSN 0028-3878.
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