Acute disseminated encephalomyelitis diagnostic study of choice
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]
Overview
Diagnostic study of choice
MRI is the best method for further evaluation after an initial suspicion of ADEM. MRI brain with gadolinium enhancement is indicated in stable patients whereas, MRI of the dorsal and cervical spinal cord can determine the extent of inflammation in symptoms and signs suggestive of myelopathy[1].
Lesion features
- T2-weighted and fluid-attenuated inversion recovery sequences typically demonstrate multifocal, hyperintense lesions, which vary from small, round/oval foci to flocculent, "cotton-ball"lesions with fuzzy margins[2]
- It can involve both white matter (WM) and gray matter(GM), involvement of the former being typically bilateral and asymmetric[2]
- Abnormalities are found in the subcortical and central WM, cortical GM-WM junction and deep GM of brainstem, cerebellar thalami and basal ganglia[2].
- Pre-contrast T1-weighted images show a weak hypointensity only when the lesions are large in size[3].
- Post-contrast T1-weighted images reveal enhancing lesions in 30-100% of patients in varying patterns (incomplete ring or arch enhancement along the edge of inflammation, nodular, gyral or spotty enhancement)[4]
- Tumefactive lesions with horse-shoe shaped enhancement and cranial nerve involvement is common. However, the absence of enhancement does not exclude the diagnosis of ADEM[5].
MRI patterns[4]
- ADEM with small lesions (<5mm)
- ADEM with large, confluent, asymmetric, WM lesions
- ADEM with symmetric, bithalamic involvement
- ADEM with acute, hemorrhagic encephalomyelitis
Evolution of lesions
- Despite the absence of specific criteria, especially for children[6], follow up MRI scans at intervals no lesser than six months help establish or confirm the diagnosis of ADEM. The lesions should resolve or remain unchanged[7].
- Persistent hypointense WM lesions are infrequent in ADEM[8].
References
- ↑ Callen DJ, Shroff MM, Branson HM, Li DK, Lotze T, Stephens D; et al. (2009). "Role of MRI in the differentiation of ADEM from MS in children". Neurology. 72 (11): 968–73. doi:10.1212/01.wnl.0000338630.20412.45. PMID 19038851.
- ↑ 2.0 2.1 2.2 Atzori M, Battistella PA, Perini P, Calabrese M, Fontanin M, Laverda AM; et al. (2009). "Clinical and diagnostic aspects of multiple sclerosis and acute monophasic encephalomyelitis in pediatric patients: a single centre prospective study". Mult Scler. 15 (3): 363–70. doi:10.1177/1352458508098562. PMID 18987105.
- ↑ Rossi A (2008). "Imaging of acute disseminated encephalomyelitis". Neuroimaging Clin N Am. 18 (1): 149–61, ix. doi:10.1016/j.nic.2007.12.007. PMID 18319160.
- ↑ 4.0 4.1 Tenembaum S, Chitnis T, Ness J, Hahn JS, International Pediatric MS Study Group (2007). "Acute disseminated encephalomyelitis". Neurology. 68 (16 Suppl 2): S23–36. doi:10.1212/01.wnl.0000259404.51352.7f. PMID 17438235.
- ↑ Tenembaum S, Chamoles N, Fejerman N (2002). "Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients". Neurology. 59 (8): 1224–31. doi:10.1212/wnl.59.8.1224. PMID 12391351.
- ↑ Mikaeloff Y, Adamsbaum C, Husson B, Vallée L, Ponsot G, Confavreux C; et al. (2004). "MRI prognostic factors for relapse after acute CNS inflammatory demyelination in childhood". Brain. 127 (Pt 9): 1942–7. doi:10.1093/brain/awh218. PMID 15289266.
- ↑ Kesselring J, Miller DH, Robb SA, Kendall BE, Moseley IF, Kingsley D; et al. (1990). "Acute disseminated encephalomyelitis. MRI findings and the distinction from multiple sclerosis". Brain. 113 ( Pt 2): 291–302. doi:10.1093/brain/113.2.291. PMID 2328406.
- ↑ Krupp LB, Tardieu M, Amato MP, Banwell B, Chitnis T, Dale RC; et al. (2013). "International Pediatric Multiple Sclerosis Study Group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions". Mult Scler. 19 (10): 1261–7. doi:10.1177/1352458513484547. PMID 23572237.