Grand Rounds

Continued Neurological Damage in HIV Infected Despite Antiretroviral Therapy


Ira Shah, Drishti Tolani
Pediatric HIV Clinic, Department of Pediatrics, B.J.Wadia Hospital for Children, Mumbai, India

Address for Correspondence: Dr Ira Shah, 1/B Saguna, 271/B St Francis Road, Vile Parle (W), Mumbai 400056, India.


Clinical Problem:
A 13 years old HIV infected boy on ART since 6 years of age presented with progressive increase of involuntary movements of left side of body with increased tone in Sept 2011. He was diagnosed to have left sided dystonia due to infarct in right lentiform nucleus & left cerebellar cortex in April 2004 due to positive antiphospholipid syndrome. (1) At that time he was diagnosed to be HIV infected and was started on Zidovudine (AZT), Lamivudine (3TC) and Nevirapine (NVP) along with aspirin and carbamazepine. His dystonia improved and in 2007 due to epistaxis, his aspirin was omitted. He continued to do well on ART till Feb 2010 when he had CMV retinitis. (2) At that time HIV viral load was undetectable and CD¬4 count was 920 cells/cumm. He was treated with valganciclovir to which his vision improved. His MRI brain in Feb 2010 showed thinning and atrophy of left cerebellar peduncle and left cerebellar hemisphere of unknown etiology. He continued to remain well till July 2011 when parents noticed increased falls due to increase in involuntary movements of left side of body. In Sept 2011, cerebrospinal fluid (CSF) was tested for cytomegalovirus (CMV), Herpes simplex virus (HSV), Epstein barr virus (EBV), HIV proviral DNA and Toxoplasma PCR which were all negative. A repeat MRI was done in Nov 2011 which showed hyper intensities in bilateral cerebellar hemispheres more marked on left side of unknown etiology and right putaminal area of gliosis suggestive of old insult. (Fig 1) His MR angiogram was normal. Subsequently, he became bedridden in Dec 2011 and was hospitalized. His CSF Measles and mumps antibodies were negative. His antiphospholipid antibody (APLA) and anti cardiolipin antibodies were also negative. A brain biopsy from right frontal lobe did not show any viral inclusion bodies. EEG showed generalized slowing. He was continued on ART but he succumbed to his illness.

Why did the child have continued neurological damage inspite of ART?


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