Abstract

To the Editors: Brain abscess is a rare disease with variable incidence between 1% and 8% of all intracranial space occupying lesions of which only 25% reported in children.1,2 Cerebellum is not a common site for brain abscess. Shachor-Meyouhas et al2 reported 28 children with brain abscess and none of them were described to have a cerebellar abscess. It carries high morbidity and mortality rate if not treated adequately.1 Here we report a 2-year-old previously healthy male managed for a cerebellar abscess. He presented to us with acute progressive ataxia and axial hypotonia for 6 days preceded by a history of on-and-off fever for 4 months before his presentation. Pyrexia of unknown origin work-up was unrevealing. He received a course of oral antibiotics for 2 weeks for presumed chest infection and the fever disappeared few weeks before his presentation with ataxia. He had no other associated neurological or infectious symptoms. His immunization was up-to-date including Haemophilus influenzae type b (Hib) vaccine that he received at 2, 4 and 6 months of age. Physical examination showed axial hypotonia, axial ataxia and dysmetria on both sides. The remaining of neurological examination was unremarkable. Dental, ear, nose and throat examination was normal. His brain magnetic resonance imaging showed a ring-enhancing lesion measuring 2.6 × 2.5 cm suggestive of cerebellar abscess with surrounding edema compressing the fourth ventricle and aqueduct resulting in mild hydrocephalus (Fig. 1). He had no leukocytosis at presentation but his C-reactive protein was 275 mg/L.FIGURE 1.: MRI brain at the initial presentation: Axial T2-weighted images show dilation of the lateral and third ventricles (A) and a large collection centered mainly in the vermis (B) with adjacent edema. Diffusion-weighted image and ADC map (C and D, respectively) show significant diffusion restriction in the collection. Contrast-enhanced axial T1 image (E) and sagittal reformat (F) demonstrate thick peripheral enhancement of the collection with effacement of the CSF spaces. MRI indicates magnetic resonance imaging.He underwent abscess drainage through posterior fossa craniotomy. Influenzae type b grew from the drained pus. The patient received 6 weeks intravenous antibiotics and he was back to his baseline by the end of the treatment course and the repeated neuroimaging showed no localized collection or diffusion restriction. Investigations to look for risk factors included immunodeficiency work-up and echocardiogram were reported to be normal. We could not identify any risk factors in our patient and the route of infection was unclear. About 80%–90% of patients who were found to have central nervous system (CNS) abscess were reported to have risk factors that predispose them for this presentation.1,3 These factors may include ear, sinus, or dental infections or procedures, neurosurgical procedures and head trauma.1 The chronic risk factors may include congenital heart defects, arteriovenous fistulas and immunosuppressive states.1 We grew Haemophilus influenzae type-B (HiB) from our patient, which is an unusual organism in a fully immunized child. Immune work-up did not reveal any evidence of primary immunodeficiency to explain this infection. Since the introduction of the universal Hib immunization, there has been a significant drop in severe Hib invasive disease among children <5 years of age. The estimated number of cases of invasive Hib infections among children <5 years old has dropped from >8 million to 340,000 cases and number of deaths from >300,000 to <30,000 worldwide between 2000 and 2015.4,5 In conclusion, one should have a low index of suspicion for CNS abscesses in a child presenting with neurological deficit even in the absence of fever at the time of presentation. Once abscess identified, thorough examination is warranted to look for any risk factors for the CNS-abscesses.

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