Dr.R.R.Singh

HIV infection is on the rise. With the advent of antiretroviral therapy, better general care of patients, general awareness of the disease and better control of opportunistic infection at all levels, children are surviving longer. This infection has acquired a model of chronic disease. With multisystem affection and especially infections at sanctuary sites (e.g. brain) this infection has acquired a totally new dimension and has prompted many research work and specially scope for future development of treatment and prevention of the disease.

The neurotropism of this viral infection and persistence of HIV in astrocyte and glial cell has definite implication in this age group. Children are in developmental stage hence HIV infection compounded with social factors and neurological manifestation plays a complex role in developmental delay and psychosocial failure to thrive.

First pediatric patient with HIV positive infection was diagnosed in 1982. HIV has a selective tropism for the immune system and nervous system. CNS involvement is due to either direct or indirect effect of HIV on CNS. Pathologically HIV infection affects deep white matter, grey matter, predominantly involving the macrophages and multi nucleate giant cells and occasionally within endothelial cells. CNS involvement is common and results in neurological disease that is characteristically slow and progressive.

The The most common neurological presentation in the pediatric population with AIDS is that of encephalopathy. The clinical picture of HIV encephalopathy is of

1. Cognitive defect.
2. Motor deficit.
3. Behavioral changes

Encephalopathy is of 2 types:

1. Progressive encephalopathy
2. Static encephalopathy
   
   

It is based on rapidity of progression. Progressive encephalopathy is characterized by delayed development, loss of milestones, pyramidal signs, extrapyramidal signs, microcephaly and cerebral calcification.

• Slow steady progressive encephalopathy is characterized by developmental abnormalities, delay in acquisition of language and motor milestones, cognitive affection, motor affection. (Development continues at a very slow rate leading to impairment. DQ and IQ ranged from low average to borderline to retarded range but relatively stable over time.)
  
  
• Rapidly progressive encephalopathy is characterized deterioration of play, decreased vocalization, loss of previously acquired milestones, loss of social and adaptive milestones, progressive motor dysfunction, change of gait, inability to stand without support, progressive pyramidal signs, bulbar and pseudobulbar palsy, movement disorder, progressive quadriparesis, cerebellar involvement. Characteristic facial feature are wide-eyed expression, Mask like face, Paucity of spontaneous facial expression, Reduced eye blinking, apathetic look and loss of interest in surrounding.

It is characterized by hyperreflexia, clumsiness, mild spastic gait, axial hypotonia and delayed head control. Most children have indolent course. Cognitive impairment becomes evident as the rate of mental development progressively declines. Overtime although child may gain further cognitive skills, language and social adaptive skills, the rate of acquisition of these skills are slow. Rapidly progressive course or improvement can follow indolent course.

HIV encephalopathy in pediatric population shows a bimodal evolution. The first hump occurs in infancy where the second one occurs later in the childhood. The true evolution of pediatric HIV related CNS disease is probably trimodal with third hump occurring in late childhood and preadolescence. Some patient develops CNS disease in the absence of major AIDS defining illness or severe immune deficiency.

It can therefore be anticipated that an increasing number of asymptomatic or mildly symptomatic HIV infected school aged children will develop signs of HIV related CNS disease before or concomitant with the onset of systemic signs.

Treatment of child both psychiatrically and medically is crucial with the knowledge that the signs and symptoms may reflect functional or acquired etiology but in either case they may lead to progression of the underlying HIV infection. There are some soft markers which will mark the onset neurological invovement. Pschyomotor retardation is one of the earliest marker or say predictor of subtle neurological involvement. Other cognitive parameters which needs to be exvaluated are temporal sequencing defect, verbal based skills. Performance based skills are also reduced. Our observation suggested that even a child with normal IQ (VIQ and PIQ ) there were some constructs of cognition which was affected.

These subtle behavioural changes needs attention as they can become more disruptive as they grow. Psychological assessment and intervention are equally important as much as anti retrovial therapy.

Last updated: 1-05-2005

Singh RR. HIV and Brain. Pediatric Oncall [serial online] 2005 [cited 2005 May 1];2. Available from:
http://www.pediatriconcall.com/fordoctor/viewersChoice/HivBrain.asp