Background: Inflammatory complications have been observed in HIV-infected patients (pts) following HAART and partial recovery of the immune system, and termed as immune restoration disease (IRD). We investigated the occurrence of IRD interesting in the central nervous system (CNS).

Methods: We retrospectively reviewed 290 cases of HIV-related CNS complications observed of HIV infection in the period 1998–2002. CNS-IRD was defined in the presence of magnetic resonance imaging (MRI) lesions consistent with inflammation, not explained by other causes after careful clinical, radiological, and cerebrospinal fluid examination, in concomitantce with CD4 increase and viral load (VL) decrease induced by anti-HIV drugs.

PatientsResults: Eight (8) pts (2.8%) were identified fulfilling our criteria, presenting were identified fullfilling our criteria with vasculitis-like lesions (A), white matter lesions (B) or ring-enhanced parenchymal lesions (C)). A. Four (4) pts showed focal neurological signs and vasculitis- like brain lesions a median of 5.5 months (mos) (range 2–7 months) after start of HAARTthe beginning of HAART. Brain biopsy, performed in 1 patient, showed a In one patient the diagnosisperivascular infiltrate. Median CD4+ increased from 28 cells/mmc µl (6–44) at baseline to 183 (70–360) at onset of eventCNS-IRD. Median VL decreased from 133,000 copiesp/mL (16,000–340,000) to 11,000 (< 80–40,000). Two patients were treated with corticosteroid; clinicalClinical and MRI condition picture improved spontaneously in all after a median of 5 mos (3–5). B. White matter lesions were observed in 3 neurologically asymptomatic pts after a median of 6 mos (6–9) from after the beginning of HAART. No patient had concomitant neurological signs. Two (2) patients had CNS toxoplasmosis before starting therapy. Median CD4 at baseline was 198 (9–340) at baseline and 354 (192–423) at IRD onset. Median VL was 47,000 (34,000–750,000) at baseline and became undetectable in all. the patients MRI lesions improved spontaneously in 2 pts after 3 mos. C. One (1) pt showed multiple small ring-enhanced parenchymal brain lesions ten 10 mos after beginning of HAART with no neurological signs. She had a  had had a diagnosis ofprimary CNS lymphoma 2 mos before and CNS cryptococcosis two months before 3 mos after HAART, respectively and received whole brain radiation; meningeal cryptococcosis developed after 3 month. CD4 was 13 at baseline and 587 at the time of theonset of parenchymal new lesions. VL declined from 520,000 to undetectable. Lesions began to improve spontaneously after two 2 mos.

Conclusions: CNS inflammatory lesions of probable inflammatory nature may develop in association with HAART-induced immune restoration. Presentation may differ, but prognosis seems goodathogenesis may differ. Since theseThese pictures were not always associated with neurological symptoms or signs, so they might occur more frequently than currently recognized and should be considered in the differential diagnosis of HIV-related CNS complications.