Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J, et al. for detailed evaluation. Examination revealed no focal deficits and repeat imaging [Physique 2] revealed decrease in lesion size and resolution of enhancement, without any additional lesion. She had a history of recurrent seizures (right focal to bilateral tonic clonic) at 6 years of age for which she was evaluated and found to have normal brain imaging and was treated with sodium valproate. Subsequently, she was seizure-free and the drug was discontinued 1 year ago. However, she had seizure recurrence (left focal Rabbit polyclonal to ADNP to bilateral tonic clonic), 1 month prior to symptom onset Tamoxifen and was controlled with oxcarbazepine. Her cerebrospinal fluid (CSF) examination was acellular, Tamoxifen with a protein and glucose content of 20.9 mg/dl and 56.9 mg/dl (corresponding random blood sugar-91 mg/dl), respectively. CSF oligoclonal bands, Venereal Disease Research Laboratory (VDRL), gene Xpert for tuberculosis, India Ink staining, and Cryptococcal antigen testing were all unfavorable. Serum aquaporin-4 antibody Tamoxifen was unfavorable but serum MOG antibody by cell-based assay was positive. She was continued on oral steroids and azathioprine followed by gradual taper with no relapses. Open in a separate window Physique 1 Axial T1-WI (a) shows focal area of hypointensity (arrow in A) in left precentral cortical region, which is usually hyperintense (arrows in b and c) on T2-WI (b) and FLAIR images (c). On follow-up imaging, axial T2-WI (d) and FLAIR (e, f) images show multifocal hyperintense lesions in bilateral dentate nuclei and adjacent white matter (Right side left, arrows in d, e, and g), left middle cerebellar peduncles, right anterolateral pons (arrowheads in d, e, and g), left posterior thalamus (arrowhead in f and h), and both occipital lobes (arrows in f and H). On contrast administration, axial T1-WIs (g and h) shows patchy enhancement within these lesions Open in a separate window Figure 2 Axial T2-W (a and b) and coronal FLAIR (c) images show areas of hyperintensities in bilateral frontal lobes (arrowheads in b and c) and left thalamus (arrow in b and c). No diffusion restriction is seen in diffusion trace images (c) and ADC maps (d). No enhancement is seen following gadolinium administration in T1-WI (g). Sagittal T2 (g) images show no focal lesions in the spinal cord Case 2: A 13-year-old boy presented with recurrent episodes of focal neurological deficits associated with fever since the past 7 years. He had two episodes of pure motor paraparesis with stiffness of limbs, and one episode of horizontal binocular diplopia, all of which were exquisitely responsive to corticosteroids. He also had history of febrile seizures (semiology: generalized tonic clonic) at the age of 5 years (imaging: Not done) and one episode of febrile status epilepticus 6 months later, which required ventilator assistance and treatment in the hospital for 10 days. His current complaints were acute onset progressive difficulty in walking associated with difficulty gripping objects. Examination revealed grade 1 + spasticity in all 4 limbs (modified Ashworth scale), power of bilateral 4/5 and 5/5 Tamoxifen in the lower and upper limbs (modified research council) respectively, and a handgrip of 80%. Sensory examination was normal and deep tendon reflexes were brisk with bilateral extensor plantar. His previous and follow up MRI brain and the last MRI spine images are provided in Figures ?Figures3,3, ?,4,4, and ?and5,5, respectively. Possibilities of.