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From the Departments of Neurology (A.V., C.A.P., J.C.M., D.A.K., D.N.I., J.W.G., D.S.R., P.A.C., A.N.), Pathology (C.A.P., P.B.), Neurosciences (J.W.G., A.N.), and Radiology (D.S.R.), Johns Hopkins University School of Medicine; and Departments of Epidemiology (J.C.M., A.N.), Microbiology and Molecular Immunology (D.A.K., D.N.I.), Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD.
Address correspondence and reprint requests to Dr. Avindra Nath, Department of Neurology, Johns Hopkins University, Path 509, 600 N. Wolfe St., Baltimore, MD 21287; e-mail: anath1{at}jhmi.edu
Objective: To describe challenges in diagnosis and management of patients with clinical syndromes of immune reconstitution inflammatory syndrome (IRIS) involving the CNS.
Methods: The authors describe three patients with clinically distinct neurologic manifestations of IRIS with HIV infection who presented as diagnostic and therapeutic challenges.
Results: One patient with cryptococcal meningitis developed acute cerebellitis with mass effect and brainstem compression. Corticosteroid therapy was associated with complete resolution of the cerebellar lesion but the patient developed VZV encephalitis. Another patient with progressive multifocal leukoencephalopathy developed subacute progression of focal neurologic deficits associated with contrast enhancing lesions on brain MRI. This patient had spontaneous resolution of the lesion but was left with residual deficits. One patient developed a progressive dementing syndrome and deterioration over several months resulting in coma during combination antiretroviral therapy. A brain biopsy in this latter patient showed massive infiltration of T lymphocytes predominantly of the CD8 subtype. This patient had a significant improvement with corticosteroids and change in antiretroviral regimen although she was left with residual cognitive impairment.
Conclusions: Immune reconstitution inflammatory syndrome should be suspected in patients who show clinical or radiologic deterioration following initiation of antiretroviral therapy accompanied with improvement in CD4 cell count and viral load. Some patients may respond to a brief course of treatment with corticosteroids.
Commentary, see page 373
Disclosure: The authors report no conflicts of interest.
Received February 13, 2006. Accepted in final form April 19, 2006.
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Neurology 2006 67: 373.
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