
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions — written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
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.
- Transverse myelitis is the result of progressive demyelination and axonal loss in addition to gray matter involvement, necrosis and cavitation.
- It is understood that infections may cause transverse myelitis by:
- Direct tissue damage
- Immune-mediated infection-triggered tissue damage
- Multiple sclerosis is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of Multiple sclerosis.
- Acute partial transverse myelitis may be predictive of a subsequent diagnosis of multiple sclerosis in children.
- Invariable histopathological findings of transverse myelitis include:
- Perivascular spread of monocytes
- Focal areas of lymphocytes infiltrating
- Astroglial and microglial activation
- 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:
- Various infectionsin 30% to 60% of the cases:
- Herpesviridae
- Enteroviruses
- Influenza viruses
- Adenoviruses
- Coxsackieviruses
- Enteric cytopathogenic human orphan (ECHO) virus
- Hepatitis A virus
- Lymphocytic choriomeningitis virus (LCMV)
- Mumps virus
- Measles virus
- Rubella virus
- Poliovirus
- Rubeola virus
- Dengue virus
- Russian spring-summer encephalitis virus
- Varicella virus
- Mycoplasma pneumonia bacteria
- Legionella pneumonia bacteria
- Pulmonary tuberculosis
- Borrelia (Lyme disease)
- Listeria
- Bartonella (cat scratch disease)
- Vaccination
- About 30% of pediatric cases are preceded with immunizations within one month of disease onset
Infections can cause transverse myelitis through two main mechanisms:
- Direct tissue damage
- Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect
- This immune response may be caused either by T-cell mediated immune response or by antibody-mediated immune response.
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
- The lesions in acute transverse myelitis are invariably limited to the spinal cord.[1][2]
- There is no involvement of other structures in the central nervous system.[1]
- The spinal cord involvement in patients with transverse myelitis is usually central, uniform and symmetric but in patients with multiple sclerosis it typically affects the spinal cord in a patchy way and the lesions are usually peripheral.
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]
- Transverse myelitis is the result of progressive demyelination and axonal loss in addition to gray matter involvement, necrosis and cavitation.[1]
- It is understood that infections may cause transverse myelitis by: [1]
- Direct tissue damage
- Immune-mediated infection-triggered tissue damage
- Multiple sclerosis is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of Multiple sclerosis.[1]
- Acute partial transverse myelitis may be predictive of a subsequent diagnosis of multiple sclerosis in children.[4]
- Invariable histopathological findings of transverse myelitis include:[1]
- Perivascular spread of monocytes
- Focal areas of lymphocytes infiltrating
- Astroglial and microglial activation
- 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:
- Various infectionsin 30% to 60% of the cases:[1][6][7][8][9][10][11][12][13][14]
- Herpesviridae
- Enteroviruses
- Influenza viruses
- Adenoviruses
- Coxsackieviruses
- Enteric cytopathogenic human orphan (ECHO) virus
- Hepatitis A virus
- Lymphocytic choriomeningitis virus (LCMV)
- Mumps virus
- Measles virus
- Rubella virus
- Poliovirus
- Rubeola virus
- Dengue virus
- Russian spring-summer encephalitis virus
- Varicella virus
- Mycoplasma pneumonia bacteria
- Legionella pneumonia bacteria
- Pulmonary tuberculosis
- Borrelia (Lyme disease)
- Listeria
- Bartonella (cat scratch disease)
- Vaccination[1][15]
- About 30% of pediatric cases are preceded with immunizations within one month of disease onset
Infections can cause transverse myelitis through two main mechanisms:[1][14][16]
- Direct tissue damage
- Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect
- This immune response may be caused either by T-cell mediated immune response or by antibody-mediated immune response.
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]
- Various infections
- Systemic autoimmune diseases like:
Microscopic Pathology
Microscopic Pathology
Findings on microscopic histopathological analysis of transverse myelitis include:[24][25]
References
References
- ↑ 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.
- ↑ Tavasoli A, Tabrizi A (2018). “Acute Transverse Myelitis in Children, Literature Review”. Iran J Child Neurol. 12 (2): 7–16. PMC 5904733. PMID 29696041.
- ↑ 3.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 8.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ ALTROCCHI PH (1963). “ACUTE TRANSVERSE MYELOPATHY”. Arch Neurol. 9: 111–9. doi:10.1001/archneur.1963.00460080021002. PMID 14048158.
- ↑ 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.
- ↑ 14.0 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.
- ↑ 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.
- ↑ 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.
- ↑ Tippett DS, Fishman PS, Panitch HS (1991). “Relapsing transverse myelitis”. Neurology. 41 (5): 703–6. doi:10.1212/wnl.41.5.703. PMID 2027486.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Borchers AT, Gershwin ME (2012). “Transverse myelitis”. Autoimmun Rev. 11 (3): 231–48. doi:10.1016/j.autrev.2011.05.018. PMID 21621005.
- ↑ Tristano AG (2009). “[Autoimmune diseases associated with transverse myelitis. Review]”. Invest Clin. 50 (2): 251–70. PMID 19662820.
- ↑ Cobo Calvo A, Mañé MartÃnez MA, Alentorn-Palau A, Bruna Escuer J, Romero Pinel L, MartÃnez-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.
- ↑ 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.
- ↑ 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.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]
