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Acute disseminated encephalomyelitis risk factors
Introduction
Overview
Overview
The risk factors for ADEM include:
- Infections (most common)
- Vaccinations
- Genetic predisposition
Risk Factors
Risk Factors
Infections
- The pathogens remain mostly unknown[1].
- The prodromal phase is characterised by flu-like symptoms (56-61%) and non-specific upper respiratory or gastrointestinal manifestations. The latent period varies from 4 to 41 days[2].
- Viral exanthems usually precede the onset of pediatric ADEM[3].
- The most common associated pathogens are viruses namely, Epstein-Barr, measles, mumps, rubella and coxsackie B[4]. Bacteria like Borrelia burgdorferi, Legionella and Mycoplasma are infrequently reported[5][6].
Vaccinations
- Immunisation is the precipitating factor for less than 5% of ADEM cases[7].
- The most frequent occurrences are with measles, mumps and rubella vaccines[8].
- The latent period varies from 2 to 30 days[8].
Genetic susceptibility
- An association between ADEM and HLA-DR genes has been elucidated in a recent study[9].
- Patients with congenital adrenal hyperplasia or acquired adrenal insufficiency have been reported to suffer from sequelae of encephalopathy with white matter lesions[10].
References
References
- ↑ Hung KL, Liao HT, Tsai ML (2001). “The spectrum of postinfectious encephalomyelitis”. Brain Dev. 23 (1): 42–5. doi:10.1016/s0387-7604(00)00197-2. PMID 11226729.
- ↑ Berzero G, Cortese A, Ravaglia S, Marchioni E (2016). “Diagnosis and therapy of acute disseminated encephalomyelitis and its variants”. Expert Rev Neurother. 16 (1): 83–101. doi:10.1586/14737175.2015.1126510. PMID 26620160.
- ↑ Berzero G, Cortese A, Ravaglia S, Marchioni E (2016). “Diagnosis and therapy of acute disseminated encephalomyelitis and its variants”. Expert Rev Neurother. 16 (1): 83–101. doi:10.1586/14737175.2015.1126510. PMID 26620160.
- ↑ Berzero G, Cortese A, Ravaglia S, Marchioni E (2016). “Diagnosis and therapy of acute disseminated encephalomyelitis and its variants”. Expert Rev Neurother. 16 (1): 83–101. doi:10.1586/14737175.2015.1126510. PMID 26620160.
- ↑ Menge T, Hemmer B, Nessler S, Wiendl H, Neuhaus O, Hartung HP; et al. (2005). “Acute disseminated encephalomyelitis: an update”. Arch Neurol. 62 (11): 1673–80. doi:10.1001/archneur.62.11.1673. PMID 16286539.
- ↑ Esposito S, Di Pietro GM, Madini B, Mastrolia MV, Rigante D (2015). “A spectrum of inflammation and demyelination in acute disseminated encephalomyelitis (ADEM) of children”. Autoimmun Rev. 14 (10): 923–9. doi:10.1016/j.autrev.2015.06.002. PMC 7105213 Check
|pmc=value (help). PMID 26079482. - ↑ Esposito S, Di Pietro GM, Madini B, Mastrolia MV, Rigante D (2015). “A spectrum of inflammation and demyelination in acute disseminated encephalomyelitis (ADEM) of children”. Autoimmun Rev. 14 (10): 923–9. doi:10.1016/j.autrev.2015.06.002. PMC 7105213 Check
|pmc=value (help). PMID 26079482. - ↑ 8.0 8.1 Huynh W, Cordato DJ, Kehdi E, Masters LT, Dedousis C (2008). “Post-vaccination encephalomyelitis: literature review and illustrative case”. J Clin Neurosci. 15 (12): 1315–22. doi:10.1016/j.jocn.2008.05.002. PMC 7125578 Check
|pmc=value (help). PMID 18976924. - ↑ Imbesi D, Calabrò RS, Gervasi G, Casella C, Vita G, Musolino R (2012). “Does HLA Class II haplotype play a role in adult acute disseminated encephalomyelitis? Preliminary findings from a Southern Italy hospital-based study”. Arch Ital Biol. 150 (1): 1–4. doi:10.4449/aib.v150i1.1384. PMID 22786832.
- ↑ Bergamaschi R, Livieri C, Uggetti C, Candeloro E, Egitto MG, Pichiecchio A; et al. (2006). “Brain white matter impairment in congenital adrenal hyperplasia”. Arch Neurol. 63 (3): 413–6. doi:10.1001/archneur.63.3.413. PMID 16540460.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]