A 6-year-old child presents with acute-onset altered consciousness, fever, and left hemiparesis 3 weeks after measles infection. MRI brain shows the finding marked **A** in the diagram—multifocal subcortical white-matter T2 hyperintensities that are bilateral but asymmetric, involving the basal ganglia and thalami as well. All lesions appear to be of the same age. Which of the following best describes the pathophysiological mechanism underlying these MRI findings in this clinical context?
A. Molecular mimicry leading to perivenular demyelination and immune-mediated inflammation of CNS myelin
B. Viral direct invasion and lytic destruction of oligodendrocytes with secondary demyelination
C. Chronic progressive demyelination with accumulation of lesions of different ages over months
D. Vasculitic occlusion of small penetrating arteries causing ischaemic white-matter infarction
Explanation
Why "Molecular mimicry leading to perivenular demyelination and immune-mediated inflammation of CNS myelin" is right
The clinical presentation (acute encephalopathy, fever, hemiparesis 3 weeks post-measles) and the MRI pattern marked A (bilateral asymmetric subcortical white-matter T2 hyperintensities with grey-matter involvement, all lesions of the same age) are pathognomonic for Acute Disseminated Encephalomyelitis (ADEM). Per Nelson Textbook of Pediatrics and IPMSSG 2013 criteria, ADEM is a monophasic immune-mediated demyelinating disorder in which molecular mimicry—cross-reactivity between the viral antigen and CNS myelin epitopes—triggers perivenular demyelination and inflammation. This mechanism directly explains the acute multifocal white-matter lesions seen on MRI.
Why each distractor is wrong
Viral direct invasion and lytic destruction of oligodendrocytes: ADEM is not caused by direct viral invasion of the CNS; it is an immune-mediated post-infectious phenomenon. The virus triggers the immune response but does not directly destroy oligodendrocytes. This mechanism describes viral encephalitis, not ADEM.
Chronic progressive demyelination with accumulation of lesions of different ages over months: This describes Multiple Sclerosis (MS), not ADEM. ADEM is monophasic with lesions all of the same age; MS is relapsing-remitting with lesions of differing ages and Dawson fingers on MRI.
Vasculitic occlusion of small penetrating arteries causing ischaemic white-matter infarction: This describes vasculitic stroke or CADASIL, not ADEM. ADEM lesions are demyelinating (perivenular inflammation), not ischaemic, and do not follow arterial territories.
High-YieldNEET PG
ADEM = monophasic, post-infectious/post-vaccination, molecular mimicry-driven perivenular demyelination with grey-matter involvement (thalami/basal ganglia); MS = relapsing, periventricular Dawson fingers, lesions of different ages, no encephalopathy required.
Nelson Textbook of Pediatrics, 22nd ed; IPMSSG criteria 2013
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