A 12-year-old male child was admitted to our hospital with complaints of severe headache, vertigo, rash, cough, and recurrent episodes of vomiting. Two weeks before he had fever and was hospitalized in another center with an initial diagnosis of Typhoid fever (Widal positive) and was treated with antibiotics. At admission, patient was febrile, oriented, and conscious. Neurological examination and fundus showed normal results. No signs of meningeal irritation were found. Hematological examination revealed Total Leukocyte Count (TLC) of 5,200/mul with thrombocytopenia (1.1 lakh/mm3). Liver function tests and coagulation profile were deranged. Subsequently, the patient's neurological status deteriorated, and he suffered a single episode of seizure and developed nystagmus. Magnetic Resonance Imaging (MRI) was done, and it revealed a diffusely swollen left cerebellar hemisphere without a well-defined mass, appearing hypointense on T1-weighted images, hyperintense on T2-weighted images [Figure 1], and Fluid-Attenuated Inversion Recovery (FLAIR)- weighted images. There was a significant mass effect over the fourth ventricle and the brainstem with ascending transtentorial herniation and hydrocephalous. No evidence of diffusion restriction was seen. Possibility of hemicerebellitis was considered. The patient was started on antibiotics, acyclovir, and high-dose steroids; also, External Ventricular Drain (EVD) was placed. Cultures and neutrophilic virus antibodies, as well as Polymerase Chain Reaction (PCR) for Herpes and Tuberculosis were negative in the cerebrospinal fluid (ventricular) and blood. Malarial serology was negative. Follow-up contrast-enhanced CT done after a week of initial MRI showed ill-defined non-enhancing hypodense area in the left cerebellar hemisphere with resolution of mass effect. Neurological status gradually improved and repeat contrast-enhanced MRI performed three weeks after admission revealed a decrease in the swelling and mass effect of the left cerebellar hemisphere, without significant atrophy [Figure 2]. Signal abnormalities were much less severe and mild pial enhancement was noted in post-contrast images [Figure 3]. Few linear areas of T1 hyperintensity showing blooming on Gradient Recalled Echo (GRE) images were seen in the affected cerebellum as well as in the contralateral cerebellar hemisphere [Figure 4]. The patient completely recovered and was discharged 4 weeks after admission.