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Clinicopathologic correlations of HIV-1-associated vacuolar myelopathy

An autopsy-based case-control study

Departments of Neurology (Drs. Dal Pan, Glass, and McArthur), Pathology (Dr. Glass), and Epidemiology (Dr. McArthur), Johns Hopkins University, Baltimore, MD.

To determine the clinical correlates of HIV-1-associated vacuolar myelopathy (VM), we designed a case-control study based on 215 AIDS autopsies in which we examined the spinal cord. We defined a case as an individual dying with AIDS and with VM present at autopsy; we defined a control as an individual dying with AIDS without VM. VM was found in 100 of 215 (46.5%) autopsies, with no apparent temporal trends. A higher number of AIDS-defining illnesses was strongly associated with the likelihood of VM (trend chi-square = 26.52, p < 0.001). Systemic infection with Mycobacterium avium-intracellulare and Pneumocystis carinii pneumonia were each associated with the pathologic findings of VM in both univariate and multivariate models. In the brain, multinucleated giant cells were detected in more cases than in controls (odds ratio = 3.68, 95% CI = 1.73 to 7.47, p < 0.001). The clinical features of HIV-1 dementia were not associated with VM; in contrast, predominantly sensory neuropathy was more common in VM cases than in controls (odds ratio = 5.00, 95% CI = 1.35 to 18.5, p < 0.05). Fifty-six cases with VM had detailed neurologic evaluations, but only 15 (26.8%) had signs and symptoms of myelopathy. The presence of symptomatic myelopathy was related to the pathologic severity: none of 17 cases with grade 1, five of 26 with grade 2, and 10 of 13 with grade 3 had clinical features of myelopathy (trend chi-square = 21.16, p < 0.005). VM is a common neuropathology finding that is frequently unrecognized during life. The association with the number of systemic illnesses, M avium-intracellulare infection, and P carinii pneumonia suggests that the development of VM is related to the severity of immunosuppression.

Address correspondence and reprint requests to Dr. Gerald J. Dal Pan, Department of Neurology, Meyer 6-109, Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21287-7609.

Presented in part at the 45th annual meeting of the American Academy of Neurology, New York, NY, April 1993.

Supported by National Institutes of Health grants NS26643, AI35042, NS01577, and RR00722.

Received October 22, 1993. Accepted in final form May 12, 1994.

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