The neurological findings in 41 HIV-seropositive children are described from the Departments of Paediatric Neurology and Hematology and Oncology, Zentrum der Kinderheilkunde, Goethe Universitat, Frankfurt, Germany. 23 children were symptomatic. HIV encephalopathy was manifested by acquired microcephaly, developmental regression and progressive motor deterioration. Progressive pyramidal signs, ankle clonus and generalized muscle weakness were documented for 6 children, 4 had extrapyramidal and cerebellar symptoms, and 5 infants of drug-addicted HIV infected mothers had seizures during the neonatal period. Behavioral changes consisting of aggression, anxiety and depression were noted in 5 children. Autistic behavior combined with deterioration in play and loss of language skills developed in one child. 4 patients had recurrent headaches which disappeared in 3 cases after treatment with azidothymidine (AZT). 8 children treated with immunoglobulin therapy (IVIG) and 7 treated with IVIG and AZT have not deteriorated neurologically since therapy began. [1]

COMMENT. The differentiation of static and progressive encephalopathy is sometimes difficult. The majority of HIV infected children have developmental delay and deficits in cognitive functions, language and motor skills. Seizures are an uncommon feature and usually an isolated event associated with fever or opportunistic CNS infection. Opportunistic CNS infections are uncommon with childhood HIV infection. Isolated cases of cerebrovascular involvement including intracranial hemorrhage and ischemic infarctions have occurred among children with immune thrombocytopenia or arteritis. Acute hemiplegia secondary to a large infarct is described in a 16-month-old infant with congenially acquired HIV infection [2]. School achievement and tasks requiring motor speed, attention and concentration were impaired at 4-8 years of age in 15 HIV-1 seropositive children infected through neonatal blood transfusion. [3]

CT scans may demonstrate enlarged CSF spaces and bilateral symmetrical calcification of the basal ganglia and frontal white matter 17-61% [4]. Wiley C A et al. report neocortical damage during HIV infection in an autopsy study of adults [5]. Wizdicks E F M et al. report a fatal disseminated hemorrhagic toxoplasmotic encephalopathy as the initial manifestation of AIDS in a 28 year-old woman. [6]