![]() ![]() cerebral abscess), nor does it demonstrate absent signal on DWI as one would expect from a cyst this is due to increase in extracellular water in the region of demyelination T1 C+ (Gd): punctate, ring or arc enhancement ( open ring sign) is often demonstrated along the leading edge of inflammation absence of enhancement does not exclude the diagnosisĭWI: there can be peripherally restricted diffusion the centre of the lesion, although high on T2 and low on T1, does not have increased restriction on DWI (cf. T2: regions of high signal, with surrounding oedema typically situated in subcortical locations the thalami and brainstem can also be involved MRI is far more sensitive than CT and demonstrates lesions characteristic of demyelination: The lesions are usually indistinct regions of low density within the white matter and may demonstrate ring enhancement. The most accepted criteria for differentiation in children are the Callen MS-ADEM criteria 13,14. The spinal cord may show confluent intramedullary lesions with variable enhancement, but these are only seen in approximately one-third of cases 12.ĭespite the clinical and radiological differences mentioned above, it is frequently difficult to differentiate between acute disseminated encephalomyelitis and MS at first presentation. In addition to lesions involving grey matter, antibodies to basal ganglia can also develop, especially in the setting of post-streptococcal pharyngitis, resulting in more diffuse involvement 11,12. Involvement of cerebral cortex, subcortical grey matter - especially the thalami - and the brainstem is not very common, but if present are helpful in distinguishing from multiple sclerosis 4,12. Lesions are usually bilateral but asymmetrical. ![]() Compared to multiple sclerosis, involvement of the callososeptal interface is unusual. MarkersĬerebrospinal fluid may show an increase in myelin basic proteinĪppearances vary from small punctate lesions to tumefactive regions, which have less mass effect than one would expect for their size, distributed in the supratentorial or infratentorial white matter. However, multiple sclerosis typically presents confluent sheets of macrophage infiltration mixed with reactive astrocytes in completely demyelinated regions 9. The pathological hallmark is perivenular inflammation with limited ‘‘sleeves of demyelination", which is also a feature of multiple sclerosis. In approximately half of all confirmed cases, anti-MOG (myelin oligodendrocyte glycoprotein) immunoglobulin G antibodies can be identified (see MOGAD) 12,15. PathologyĪcute disseminated encephalomyelitis is thought to occur from a cross-reactivity in immunity to viral antigens, triggering a subsequent autoimmune attack on the CNS. Unlike multiple sclerosis, symptoms are more systemic rather than focal and include fever, headache, decreased level of consciousness varying from lethargy to coma, seizure, and multifocal neurologic symptoms such as hemiparesis, cranial nerve palsies, and movement disorders behavioural changes like depression, delusions, and psychosis may dominate the symptoms 3. In 10% of cases, relapse within the first three months is encountered 12. Acute disseminated encephalomyelitis is usually a monophasic illness, although, within the episode, individual lesions may be of varying stages of evolution, with different lesions maturing over a number of weeks 4.
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