Acute polyradiculopathies in HIV-infected patients

Abstract

We studied 17 consecutive cases of acute polyradiculopathy (PR) diagnosed in HIV-infected patients to investigate the possible causes of this syndrome in our milieu. Sixteen patients presented with lumbosacral PR and one patient had predominantly cervical PR. Electrophysiological study showed a predominantly motor axonal neuropathy in all patients examined. Six patients had a laboratory-confirmed aetiology for the PR: cytomegalovirus (CMV) was isolated from cerebrospinal fluid (CSF) in three cases, meningeal lymphomatosis was diagnosed by CSF cytology in two cases, and one patient had cryptococcal meningitis. Another patient was thought to have acute axonal polyradiculoneuritis associated with HIV infection. CMV and Mycobacterium tuberculosis were the probable agents in four and three patients, respectively. Finally, in three patients a cause could not be foscarnet were effective in the treatment of definite or probable CMV PR. The present study confirms that acute lumbosacral PR in HIV-infected patients must be considered a syndrome with different causes. CMV and M. tuberculosis infections were the most frequent causative agents in our series (41% and 18% of the cases, respectively). Early empirical therapy is often necessary as definite diagnosis may be delayed or never achieved. Our experience suggests that, at least in our milieu, anti-tuberculous drugs should be considered in some cases together with ganciclovir or foscarnet in the empirical therapy for PR in HIV-infected patients.

Rhesus Cytomegalovirus (Macacine Herpesvirus 3)–Associated Facial Neuritis in Simian Immunodeficiency Virus–Infected Rhesus Macaques (Macaca mulatta)

“…Whether the discrepancy between HCMV and RhCMV tropism to Schwann cells represents a deviation in the pathogenesis of the two related viruses requires further investigation. 9 Although it is not known whether RhCMV in facial nerves arises from local reservoirs of latent virus or is spread to the facial nerves from distant tissues, the pattern of histologic damage in the cases presented in this study suggests that RhCMV-infected macrophages and infiltrating neutrophils initially invade into the nerves from the adjacent interstitial tissues and results in inflammation-driven nerve damage to the axons, myelin, and Schwann cells. This sequential mode of infection explains the progressive loss of nerve architecture.…”

“…HIV, HSV, and HCMV have been implicated in the pathogenesis of the nerve lesions. 7,9 HCMV and RhCMV are ubiquitous viral infections of humans and nonhuman primates, respectively, that target a broad range of host cells and causes extensive lesions. In the absence of immunosuppression, infection is limited by cellular immune response that controls viral replication and results in viral latency within the infected host.…”

HIV neuropathy: Insights in the pathology of HIV peripheral nerve disease

“…Opportunistic infections such as CMV and VZV may involve the PNS, mostly in the intermediate and late stages of AIDS. Progressive polyradiculopathies are frequently associated with CMV infection, mostly in the very late stages of AIDS when the CD 4 count is below 50 cells/mm 3 ( Anders and Goebel, 1999 ; Baudrimont and Moulignier, 1997 ; Corral et al, 1997 ; Grafe and Wiley, 1989 ; Kim and Hollander, 1993 ; Lipkin et al, 1987 ; Said et al, 1991 ). VZV infection of the PNS manifests itself mostly as a sensory ganglionitis and myeloradiculitis often characterized by sensory symptoms and pain ( Brown et al, 1988 ; Henin et al, 1995 ; Lipkin et al, 1987 ; Oh et al, 1999 ).…”

Viral Infections of the Human Nervous System

“…EDX typically show evidence for lumbosacral radiculopathy, though features of concomitant HIV-PN are common (Corral et al 1997;So and Olney 1994). CSF reveals a polymorphonuclear pleocytosis (average cell count of 500-600/mL) with elevated protein and decreased glucose, although may be normal (Kim and Hollander 1993;Corral et al 1997;Anders and Goebel 1998;So and Olney 1994;Miller et al 1996).…”

“…CSF reveals a polymorphonuclear pleocytosis (average cell count of 500-600/mL) with elevated protein and decreased glucose, although may be normal (Kim and Hollander 1993;Corral et al 1997;Anders and Goebel 1998;So and Olney 1994;Miller et al 1996). CMV PCR is both sensitive and specific.…”