Two children, ages 2 years and 2 months, presenting with acute hemiparesis and focal seizures as the initial manifestations of human immunodeficiency virus (HIV) infection are reported from Ramathibodi Hospital, Mahidol University, Bangkok, Thailand. CT in the 2-year-old with hemiparesis showed acute infarction of the right thalamus and internal capsule, and old infarction with bilateral basal ganglia calcification and cerebral atrophy. MRI revealed narrowing of the right middle cerebral artery. The 2-month-old infant with a one week history of multiple focal seizures and impaired consciousness was jaundiced, and the CT revealed hemorrhagic infarction of the right cerebral hemisphere, with acute intraparenchymal bleeding. MRI showed narrowing and irregularity of the right middle cerebral and internal carotid arteries. HIV infection was documented only after the onset of acute neurologic manifestations. Neither coagulopathy nor other cause of stroke was identified. Tests for opportunistic infections were negative. [1]
My colleague, Dr Leon Epstein, Head of the Division of Neurology, Children’s Memorial Hospital, Chicago, has written extensively on the neurologic manifestations of HIV infection in children [2], (and other subsequent publications). A progressive encephalopathy is reported most commonly. In his experience, seizures are not a prominent symptom of HIV infection, and opportunistic infections, including measles, must be excluded as possible alternative causes of neurologic manifestations.
In a study reviewed in Ped Neur Briefs (June 1998; 12:44), Cooper ER et al. report encephalopathy in 21% of 128 HIV-perinatally infected children, with a mortality of 41%. Failure to gain weight predated the onset of encephalopathy in infected infants. A high viral load during infancy, failure to thrive, and early signs of hepatomegaly and lymphadenopathy are risk factors for HIV encephalopathy. The 2-month-old infant in the Bangkok study had a low birth weight and hepato-splenomegaly, while the 2-year-old was reported to have a normal development up to the onset of stroke.