New Case 7 yr old Female child , well immunized, developed fever with cough 3 weeks ago which was controlled by supportive measures and got resolved by 4 days.Following that the child was active and asymptomatic for the next 4 days.Later on while child was sleeping the mother noted to have deviation of angle of mouth to left side and was consulted in the hospital and was admitted for 14 days.During the hospital days she developed weakness of the limbs, difficulty in walking with difficulty in swallowing.During the hospital stay no bowel or bladder symptoms, no alteration in sensorium, no seizures, no blurring of vision Child was given antibiotics ceftriaxone, discharge on 28th April and suggested to consult higher centre for furtger management. On exam fully concious, slurring of speech ,normal optic fundi and pupils. left LMN facial weakness .Gaze evoked nystagmus on horizontal gaze, bilateral cerebellar signs with gait ataxia Diagnosis
Thanks Curofy and all Doctors who tried to answer the case . Child is under pediatric neurologist. Started Albendazole with steroid on the day of admission .ELISA for NCC - ve. CSF ROUTIEN INCONCLUSIVE .GENE EXPERT + ve. 1week albendazole with steroid, deteriorated the level of conciousness. Started ATT. Child is better.Still in the hospital. MRI report: Numerous well defind subcentimetric lesions in gray white matter junction of bilateral cerebral hemisphere , and in the cerebellar hemisphere, in the brain stem, capsuloganglionic areas which shows central hypointensity with peripheral hyperintense rim on T2/ FLAIR images and show ring enhancement on post contrast images.The lesion in RT high frontal lobe appear conglomerate.Linear and nodular enhancing areas noted in bilateral superior cerebellar folia, bilateral parietal, frontal and Rt occipital lobe, temporal lobe sulci. Patchy areas of diffusion restriction noted in bilateral superior cerebellum - likely leptomeningitis. Imp : The spectrum of findings suggest possibility of solid caseating tuberculosis.Cebteal hypointense T2 signals favours Tuberculoma.No eccentric muscle nodule, no varying stages of neurocercosis, no adjacent muscle involvement - unfavourable diagnosis of Neurocysticercosis. Leptomeninges involvement favours tuberculou etiology
Thanks Curofy and all Doctors who tried to answer the case . Child is under pediatric neurologist. Started Albendazole with steroid on the day of admission .ELISA for NCC - ve. CSF ROUTIEN INCONCLUSIVE .GENE EXPERT + ve. 1week albendazole with steroid, deteriorated the level of conciousness. Started ATT. Child is better.Still in the hospital. MRI report: Numerous well defind subcentimetric lesions in gray white matter junction of bilateral cerebral hemisphere , and in the cerebellar hemisphere, in the brain stem, capsuloganglionic areas which shows central hypointensity with peripheral hyperintense rim on T2/ FLAIR images and show ring enhancement on post contrast images.The lesion in RT high frontal lobe appear conglomerate.Linear and nodular enhancing areas noted in bilateral superior cerebellar folia, bilateral parietal, frontal and Rt occipital lobe, temporal lobe sulci. Patchy areas of diffusion restriction noted in bilateral superior cerebellum - likely leptomeningitis. Imp : The spectrum of findings suggest possibility of solid caseating tuberculosis.Cebteal hypointense T2 signals favours Tuberculoma.No eccentric muscle nodule, no varying stages of neurocercosis, no adjacent muscle involvement - unfavourable diagnosis of Neurocysticercosis. Leptomeninges involvement favours tuberculou etiology
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No change in consciousness n begavior of the child. ...so encephlitis n adem are out.....looks like gb syndrome
Disseminated neurocysticercosis / tuberculomata with infarcts.
GBSyndrome.. Multiple tuberculoma seen. Rule out T. B. Do Lumber punctureand CSF examination. Review report.
Neurocysticercosis spread in brain dexa1mg per kg body wt per day then tapper
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