Pediatric miliary tuberculosis presenting with stroke: contribution to the paper “Tuberculosis of the central nervous system in children”

Abstract

Dear Editor: We wish to thank Dr. Muzumbar and his coauthors for their recent article and his valued comments about neurological involvement of tuberculosis. Reading with interest his manuscript, we would like to report a case of disseminated tuberculosis disease presenting with extended stroke [1]. We believe that it represents a critical issue because tuberculous meningitis (TBM) is a destructive entity with high mortality [2, 3]. Neurological sequelae occur up to 80% in resourcepoor setting and 60% in developed countries [2, 4]. Hydrocephalus, cerebrovascular complications, and tuberculoma are some indicators of poor outcome [1]. In order to update this article, providing a more comprehensive overview of the diagnosis and treatment of stroke in tuberculosis, we suggest that additional references are considered. As such, we report a Moroccan infant without relevant family background and uneventful pregnancy. She presented repeated respiratory tract infections since 7 months. Progressive macrocephaly and ventriculomegaly since 2 months of age (cranial computed tomography (CT) was done at 7 months) and mother revealed failure to thrive beginning at 8 months. Close contacts were not sick. Immunizations were up to date not including BCG. At 10 months, she was referred to our hospital with a first episode consisting of generalized tonic seizures controlled with levetiracetam. Her parents reported fever to 102.2 °F, night sweats, and cough over the last week. On physical examination, her modified Glasgow coma scale (GCS) score was 15/15. She had a bulging fontanelle, left hemiparesis without other neurological deficits. She presented tachypnea, subcostal retraction, and hypoventilation with hypoxemia. She had inguinal lymphadenopathies without splenomegaly or hepatomegaly. Cranial CT (Fig. 1) showed a new right large fronto-parietal area of subacute hypointensity, suggesting ischemic injury. Focal ischemic infarct was observed in the right temporal territory and caudate nucleus. MRI showed a right stroke involving frontal and parietal lobes, coincident with severe leptomeningitis in medial cranial fossa that occludes the flow of medial cerebral artery. Nodular enhancement images in posterior fossa identified as tuberculomas were demonstrated, as well as ventriculomegaly previously reported (Fig. 1). According to the Modified Medical Research Council (MMRC) score, her clinical stage was II. CSF documented normal protein and glucose with lymphocytic pleocytosis (25 cells/μl). Chest Xray showed miliary mottling tuberculosis and right middle lobe consolidation (Fig. 2). Purified protein derivative test was 0 mm at 72 h. Interferon gamma release assay was positive. Mycobacterium tuberculosis polymerase chain reaction (GeneXpert MTB) from CFS and gastric aspirates was positive. HIV was negative. Her isolates were pansusceptible to the first line anti-TB drugs. According to the World Health Organization, she received standard 4-drug regimen for 2 months followed by rifampicin and isoniazid during 10 months. She was also treated with aspirin and dexamethasone (0.6 mg/kg/day) IV during 48 h and subsequently prednisone orally (2 mg/kg/day) for 6 weeks tapered gradually. Ventricular drainage was unnecessary. A source case was not identified. She recovered well on pulmonary tuberculosis after treatment. Seizures did not present recurrence. At 22 months, she started to perform unsteady gait. However, we identified signs of cerebral palsy with severe left hemiparesis and marked spasticity. She did not present other deficits. TBM includes a broad spectrum of central nervous system (CNS) complications. Hydrocephalus appears in about 80% of TBM cases [1, 3, 4]. Springer et al. reviewed a rate of cerebral infarction as a complication in up to 13 to 53% of patients [5]. Predominant basal exudate, close to the circle of * María Isabel Sánchez-Códez [email protected]