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or a loss of those previously attained. With effective antiretroviral therapy PHE has become an
infrequent and reversible complication of HIV infection. However, PHE may relapse if viral
control is lost. Though children on antiretroviral therapy may show significant improvement,
they show higher rates of residual neurologic, cognitive, and scholastic impairments compared
with children who never had PHE.[1051]
There are three major patterns of encephalopathy in children, which is the counterpart of
AIDS dementia complex, or human immunodeficiency virus-associated dementia (HIVD) in
adults: (1) subacute progressive - patients at first develop normally but then social, language,
and motor skills are lost, and microcephaly may be present; (2) plateau progressive - patients
initially develop at a normal pace but then decline in their rate of developmental progress with
little or no further acquisition of skills, and microcephaly may be present; (3) static
encephalopathy - children are late to acquire motor and language skills, are cognitively impaired,
and acquire skills slowly; radiographic scans are normal.[746]
Neuropathologic findings distinctive to pediatric HIV infection include acquired
microcephaly. In such cases there is no gross or microscopic malformation, only decreased brain
weight accompanied by cortical atrophy and ventriculomegaly. Gliosis is seen microscopically.
Other frequent histologic findings include calcification in vascular walls of basal ganglia and
deep cerebral white matter, and these changes are often progressive with age. As in adult AIDS
cases, multinucleated giant cells are often present. Children with encephalopathy often have
corticospinal tract degeneration from myelin loss, while the vacuolar myelopathy seen in spinal
cords of adults is uncommon. An anoxic-ischemic encephalopathy with neuronal necrosis in
cerebral cortex, hippocampus, and basal ganglia may be seen in association with systemic
hypoxemia from cardiovascular disease. Although non-Hodgkin lymphoma can be seen in
pediatric AIDS patients with focal CNS lesions, opportunistic infections such as toxoplasmosis,
cryptococcosis, cytomegalovirus, and progressive multifocal leukoencephalopathy are
uncommon in pediatric AIDS, as contrasted with adult AIDS cases.[1052,1053]

ORAL LESIONS.—Children manifest many of the same oral lesions, such as oral
candidiasis, as to adults with HIV infection. The use of antiretroviral therapy has reduced the
prevalence of most oral diseases in the pediatric age range. However, oral warts have increased
in frequency, likely related to immune reconstitution. Salivary gland enlargement, often the first
manifestation of HIV illness, remains more common in children than adults. Xerostomia may or
may not be present. Benign lymphoepithelial lesions are the most commonly diagnosed parotid
condition.[1054]

NEOPLASIA.-- Neoplasms are seen less frequently in cases of pediatric AIDS than in
adult cases. About 2.5% will develop a malignant neoplasm. The most frequent neoplasm of
HIV-infected children is high-grade non-Hodgkin lymphoma (NHL). A third of NHL's in
children are of the intermediate (Burkitt) type and a fourth are seen to occur in the brain.[1055]
Clinical findings seen at presentation with NHL’s in pediatric AIDS include fever, weight loss,
jaundice, hepatosplenomegaly, abdominal distension, anemia, and neurologic abnormalities.
Most patients are at stage III or IV on presentation. In children, NHL’s are more likely to occur
in boys who are Caucasians and who are older. Brain lymphomas tend to occur late in the course
of AIDS. In addition to NHL’s, mucosa-associated lymphoid tissue (MALT) lesions have been
seen in association with pediatric HIV infection.[573]