Transverse myelitis pathophysiology: Difference between revisions
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A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis. | |||
A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.<ref name="pmid22379456" /> | |||
[18, 22, 50]. | [18, 22, 50]. | ||
In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated. [4, 51]. | In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated.<ref name="pmid22379456" /> [4, 51]. | ||
Revision as of 17:23, 16 April 2020
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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
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, and Bartonella (cat scratch disease).
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]
[18, 22, 50].
In the spinal fluid of patients with transverse myelitis, Interleukin 6 (IL-6) levels were also markedly elevated.[1] [4, 51].
IL-6 is secreted by astrocytes and microglia and binds to oligodendroglia and axons. High levels of IL-6 can cause direct tissue injury and indirect damage by inducing nitric oxide synthetase in microglia. Interestingly, Interferon-beta (IFN-β), a medication used to treat MS, was found to induce IL-6 [52]. IL-6 has probably a bell-shaped effect where at certain levels could cause damage and at different levels can induce repair [51, 53, 54].
One study that was conducted in Japan found that several patients with TM have much higher serum IgE levels than MS patients or controls pointing towards the immune-mediated process as well [55]. Concordant with these findings, tissue biopsies of two patients with TM and elevated total and specific serum IgE disclosed the presence of antibody deposition within the spinal cord and perivascular infiltration with eosinophils that could induce tissue damage [56].
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
Conditions associated with [disease name] include:
- Various infections
- [Condition 2]
- [Condition 3]
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
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 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.
- ↑ 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.
- ↑ 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.