Paediatric AIDS dementia in India. Lancet 2004; 364: 1460

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Case Report. A hint from the past

Binu V , S Subramanian, Dhanya Mohan, Ankamma Rao, Kurien

[The Lancet. Volume 364, Number 9443 16 October 2004]

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Lancet 2004; 364: 1460

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Departments of Medicine

Unit 2 (B V MD, S Subramanian MD, D Mohan MBBS, K MD) and

Radiodiagnosis (A Rao DNB), Christian Medical College, Vellore, Tamil

Nadu 632004, India

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Correspondence to: Dr Binu V binuvalsanjohn@...

A 13-year-old boy was admitted in January, 2004, with a 4-year history

of recurrent fever and cough, and progressive neurological symptoms.

He was diagnosed elsewhere to have lower respiratory infections, and

treated with oral antibiotics. His mother reported progressive

cognitive decline with inability to concentrate and worsening

scholastic performance over the past year. 6 months previously, he had

developed weakness of the right lower limb, followed by weakness of

the left lower limb and trunk, and was bed-ridden for the past 2

months. There was no upper limb or bulbar involvement. Sensory and

autonomic symptoms were absent. On examination we found that he had

mild hepatomegaly, with no splenomegaly, and coarse crackles in both

lung fields. He also had a deficit in recent memory, and bilateral

pyramidal signs, but normal sensory and cerebellar function. His Mini

Mental State Examination Score was 10/30.

MRI of the brain showed diffuse hyperintensity involving the central

white matter and corpus callosum, with no mass effect, and diffuse

cerebral atrophy on T2 FLAIR axial images (figure). MRI of the spinal

cord was normal. An electroencephalogram showed abnormal bitemporal

waves. We did a lumbar puncture; cerebrospinal fluid (CSF) analysis

showed 3 lymphocytes, protein 5•5 mg/L (normal 2-4), and glucose 2•7

mmol/L. Thoracic CT showed multilobar cylindrical bronchiectasis. We

made a working diagnosis of delayed-onset leucodystrophy and

attributed his recurrent respiratory infections to pre-existent

bronchiectasis.

Figure: T2 FLAIR axial MRI showing cerebral atrophy and diffuse

hyper-intensity involving the central white matter and corpus

callosum, with no mass effect

During his hospital stay, the boy's cognitive function declined even

further, so we searched for alternative diagnoses. On further

questioning we learned that his father had died of tuberculosis 7

years previously, at the age of 36. We reconsidered the child's

symptoms in the context of his father's early death, and added HIV

infection to our differential diagnosis. Serum assays showed

antibodies to HIV-1. The boy's CD4 count was 122 cells per µL by flow

cytometry and plasma HIV viral load was 4973 copies per mL. His

mother, who was asymptomatic, was subsequently found to be

HIV-positive. We did bacterial, mycobacterial, and fungal cultures of

CSF, and PCR for M tuberculosis, JC virus, and cytomegalovirus, but

were unable to find evidence of an opportunistic infection. We made a

diagnosis of AIDS dementia and started zidovudine, lamivudine, and

nevirapine, and co-trimoxazole prophylaxis. The boy developed

leucopenia, so we changed zidovudine to stavudine. His cognitive

function improved, and when he was discharged in March, 2004, he was

capable of sitting up with support. In July, 2004 his mother reported

that he had developed weakness of his left upper limb; however, he had

had no subsequent respiratory infections, had gained weight, and there

was further improvement in cognitive function.

We had difficulty diagnosing AIDS dementia in the absence of known HIV

infection or AIDS-defining illness in the child or his parents.

Clinical signs of paediatric AIDS dementia include cortical atrophy,

pyramidal signs, pseudobulbar palsy, and psychosis.1 In developing

countries, where neonatal screening programmes were recently

introduced and not universally available, AIDS dementia should be

considered in any child with progressive neurological deterioration.2

Because perinatally-infected, untreated children may progress to AIDS

faster than adults,3 an AIDS-defining illness in a child may be the

first indication of HIV in the family.

We thanks Priya Abraham MD, Department of Virology, Christian Medical

College, Vellore, for arranging the Polymerase Chain Reaction for JC

virus to be done in a laboratory in the UK.

References

1 Criteria for the medical care of children and adolescents with HIV

infection. Neurologic complications in HIV-infected children and

adolescents. http://www.hivguidelines.org/public_html/

center/clinical-guidelines/ped_adolescent_hiv_guidelines/

ped_neuro/ped-neuro.htm (accessed April 18th, 2004).

2 Vardhaman S, Udgirkar VS, Tullu MS, et al. Neurological

manifestations of HIV Infection. Indian Pediatrics 2003; 40: 230-34.

[PubMed]

3 Gray L, Newell ML, Thorne C, et al. European Collaborative Study.

Fluctuations in symptoms in human immunodeficiency virus-infected

children: the first 10 years of life. Pediatrics 2001; 108: 116-22.

[PubMed]