Acute disseminated encephalomyelitis (ADEM) is an immune mediated inflammatory and demyelinating disorder of central nervous system, which is commonly preceded by an infection 2 days to 4 weeks earlier. Vaccination is less common antecedent factor. The molecular mimicry or autoimmune response toward myelin or other self antigen like myelin oligodendrocyte glycoprotein is proposed to be responsible for disease.

 It principally involve the white matter of the central hemisphere, brainstem, cerebellum, optic nerve & spinal cord. ADEM principally involve children with estimated incidence of 0.4/100000/year aged less than 20 years.

The diagnosis of ADEM requires both multifocal involvement i.e. clinical features could be attributed to more than one central nervous system site or monofocal or encephalopathy. There is no specific biomerkers for diagnosis of ADEM, hence diagnosis made based on the clinical or imaging studies as per following consensus.

Clinical Criteria:  

A first clinical event with a presumed inflammatory or demyelinating cause with acute or subacute onset that affects multifocal areas.

Ø The clinical presentation must be polysymptomatic and must

include encephalopathy.

Encephalopathy is defined as 1 or more of the following:

·        Behavioral change (eg, confusion, excessive irritability)

·        Alteration in consciousness (eg, lethargy, coma)

·        Event should be followed by improvement, either clinically, on MRI, or both but there may be residual deficits

·        No history of a clinical episode with features of a prior demyelinating event             

·        No other etiologies can explain the event.

·        New or fluctuating symptoms, signs, or MRI findings  occurring within 3 months of the inciting acute disseminated encephalomyelitis event are considered to be part of the  acute   event.

Neuroimaging:

Focal or multifocal lesions, predominantly involving white matter, without radiologic evidence of previous destructive white matter changes:

·        Brain MRI, with FLAIR or T2-weighted images, reveals large (1-2cm in size) lesions that are multifocal, hyperintense, and locatedin the supratentorial or infratentorial white matter regions; graymatter, especially basal ganglia and thalamus, is frequently involved

·        In rare cases, brain MR images show a large single lesion (1-2cm), predominantly affecting white matter

·        Spinal cord MRI may show confluent intramedullary lesion(s) with variable enhancement, in addition to abnormal brain.

We performed a randomised control trial on 33 children with ADEM admitted in our hospital and assess the neurological recovery by mRS scale at 1wk, 1month and 3 months interval after completion of treatment with either of the drugs (methylprednisolone and Inravenous immunoglobulin). We also assess neurological deficit, seizure and adverse reaction of the drugs in follow up. Collected data was analysed by Independent samples T- test, Chi- Square test and Mann Whitney test.

There were early recovery observed in patients received IVIg (P=0.019), but at three month follow up, recovery observed between both the groups were comparable. At 1 month follow-up patients received methylprednisolone were more neurologically deficit (P=0.029) as per mRS scale. Incidence of Hyperglycemia was significantly high in patients received methylprednisolone cintravenous immunoglobulin was much costlier than treatment with methylprednisolone (P = <0.001).