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Transverse myelitis pathophysiology

Introduction

Overview

Overview

  • In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of neural cells within the spinal cord.
  • Other histopathological findings of transverse myelitis include:
    • Infiltration of CD4+ and CD8+ T-lymphocytes
    • Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

Infections can cause transverse myelitis through two main mechanisms:

  1. Direct tissue damage
  2. Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.

In the spinal fluid of patients with transverse myelitis, Interleukin 6 (IL-6) levels were also markedly elevated.

Pathophysiology

Pathophysiology

Physiology

Pathogenesis

  • In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of neural cells within the spinal cord.[3]
  • Other histopathological findings of transverse myelitis include:[1][5]
    • Infiltration of CD4+ and CD8+ T-lymphocytes
    • Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

Infections can cause transverse myelitis through two main mechanisms:[1][14][16]

  1. Direct tissue damage
  2. Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.[1][17][18][19]

In the spinal fluid of patients with transverse myelitis, Interleukin 6 (IL-6) levels were also markedly elevated.[1][8][20]

Associated Conditions

Associated Conditions

Conditions associated with transverse myelitis include:[21][22][1][3][23]

Microscopic Pathology

Microscopic Pathology

Findings on microscopic histopathological analysis of transverse myelitis include:[24][25]

References

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 Awad A, Stüve O (2011). “Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices”. Curr Neuropharmacol. 9 (3): 417–28. doi:10.2174/157015911796557948. PMC 3151596. PMID 22379456.
  2. ↑ Tavasoli A, Tabrizi A (2018). “Acute Transverse Myelitis in Children, Literature Review”. Iran J Child Neurol. 12 (2): 7–16. PMC 5904733. PMID 29696041.
  3. ↑ 3.0 3.1 Kerr DA, Ayetey H (2002). “Immunopathogenesis of acute transverse myelitis”. Curr Opin Neurol. 15 (3): 339–47. doi:10.1097/00019052-200206000-00019. PMID 12045735.
  4. ↑ Meyer P, Leboucq N, Molinari N, Roubertie A, Carneiro M, Walther-Louvier U; et al. (2014). “Partial acute transverse myelitis is a predictor of multiple sclerosis in children”. Mult Scler. 20 (11): 1485–93. doi:10.1177/1352458514526943. PMID 24619933.
  5. ↑ Moulignier A, Lescure FX, Savatovsky J, Campa P (2014). “CD8 transverse myelitis in a patient with HIV-1 infection”. BMJ Case Rep. 2014. doi:10.1136/bcr-2013-201073. PMC 3918629. PMID 24503658.
  6. ↑ Jeffery DR, Mandler RN, Davis LE (1993). “Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events”. Arch Neurol. 50 (5): 532–5. doi:10.1001/archneur.1993.00540050074019. PMID 8489410.
  7. ↑ Christensen PB, Wermuth L, Hinge HH, Bømers K (1990). “Clinical course and long-term prognosis of acute transverse myelopathy”. Acta Neurol Scand. 81 (5): 431–5. doi:10.1111/j.1600-0404.1990.tb00990.x. PMID 2375246.
  8. ↑ 8.0 8.1 Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA (2004). “Transverse Myelitis: pathogenesis, diagnosis and treatment”. Front Biosci. 9: 1483–99. doi:10.2741/1351. PMID 14977560.
  9. ↑ PAINE RS, BYERS RK (1953). “Transverse myelopathy in childhood”. AMA Am J Dis Child. 85 (2): 151–63. doi:10.1001/archpedi.1953.02050070160004. PMID 13007166.
  10. ↑ Ropper AH, Poskanzer DC (1978). “The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms”. Ann Neurol. 4 (1): 51–9. doi:10.1002/ana.410040110. PMID 697326.
  11. ↑ Knebusch M, Strassburg HM, Reiners K (1998). “Acute transverse myelitis in childhood: nine cases and review of the literature”. Dev Med Child Neurol. 40 (9): 631–9. doi:10.1111/j.1469-8749.1998.tb15430.x. PMID 9766742.
  12. ↑ ALTROCCHI PH (1963). “ACUTE TRANSVERSE MYELOPATHY”. Arch Neurol. 9: 111–9. doi:10.1001/archneur.1963.00460080021002. PMID 14048158.
  13. ↑ Lerer RJ, Kalavsky SM (1973). “Central nervous system disease associated with Mycoplasma pneumoniae infection: report of five cases and review of the literature”. Pediatrics. 52 (5): 658–68. PMID 4598176.
  14. ↑ 14.0 14.1 Salgado CD, Weisse ME (2000). “Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient”. Clin Infect Dis. 31 (2): 609–11. doi:10.1086/313986. PMID 10987731.
  15. ↑ Agmon-Levin N, Kivity S, Szyper-Kravitz M, Shoenfeld Y (2009). “Transverse myelitis and vaccines: a multi-analysis”. Lupus. 18 (13): 1198–204. doi:10.1177/0961203309345730. PMID 19880568.
  16. ↑ Giobbia M, Carniato A, Scotton PG, Marchiori GC, Vaglia A (1999). “Cytomegalovirus-associated transverse myelitis in a non-immunocompromised patient”. Infection. 27 (3): 228–30. doi:10.1007/bf02561538. PMID 10378139.
  17. ↑ Tippett DS, Fishman PS, Panitch HS (1991). “Relapsing transverse myelitis”. Neurology. 41 (5): 703–6. doi:10.1212/wnl.41.5.703. PMID 2027486.
  18. ↑ Pandit L, Rao S (1996). “Recurrent myelitis”. J Neurol Neurosurg Psychiatry. 60 (3): 336–8. doi:10.1136/jnnp.60.3.336. PMC 1073861. PMID 8609515.
  19. ↑ Bashir K, Whitaker JN (2000). “Importance of paraclinical and CSF studies in the diagnosis of MS in patients presenting with partial cervical transverse myelopathy and negative cranial MRI”. Mult Scler. 6 (5): 312–6. doi:10.1177/135245850000600503. PMID 11064439.
  20. ↑ Kaplin AI, Deshpande DM, Scott E, Krishnan C, Carmen JS, Shats I; et al. (2005). “IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis”. J Clin Invest. 115 (10): 2731–41. doi:10.1172/JCI25141. PMC 1224298. PMID 16184194.
  21. ↑ Borchers AT, Gershwin ME (2012). “Transverse myelitis”. Autoimmun Rev. 11 (3): 231–48. doi:10.1016/j.autrev.2011.05.018. PMID 21621005.
  22. ↑ Tristano AG (2009). “[Autoimmune diseases associated with transverse myelitis. Review]”. Invest Clin. 50 (2): 251–70. PMID 19662820.
  23. ↑ Cobo Calvo A, Mañé Martínez MA, Alentorn-Palau A, Bruna Escuer J, Romero Pinel L, Martínez-Yélamos S (2013). “Idiopathic acute transverse myelitis: outcome and conversion to multiple sclerosis in a large series”. BMC Neurol. 13: 135. doi:10.1186/1471-2377-13-135. PMC 3856522. PMID 24090445.
  24. ↑ Krishnan C, Kaplin AI, Pardo CA, Kerr DA, Keswani SC (2006). “Demyelinating disorders: update on transverse myelitis”. Curr Neurol Neurosci Rep. 6 (3): 236–43. doi:10.1007/s11910-006-0011-1. PMID 16635433.
  25. ↑ Mirich DR, Kucharczyk W, Keller MA, Deck J (1991). “Subacute necrotizing myelopathy: MR imaging in four pathologically proved cases”. AJNR Am J Neuroradiol. 12 (6): 1077–83. PMID 1763730.

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