HIVAssociated Myelopathies

Spinal cord involvement associated with HIV-1 infection has diverse causes. As with other neurological disorders associated with HIV-1 infection, different conditions occur with increased prevalence during different stages of HIV-1 infection. Some conditions are related to HIV-1 itself, whereas others are associated with other infectious, neoplastic, vascular, or nutritional and metabolic etiologies (B 12 deficiency).^' , '133' 'is! '135' A self-limiting myelitis at the time of seroconversion and a vacuolar myelopathy that occurs during more advanced HIV-1 disease stages are related to primary HIV-1 infection. y , y Other infectious agents reported include the herpesviruses (VZV, HSV, CMV), HTLV-1, Treponema pallidum, Mycobacterium tuberculosis, and other bacterial pathogens. Compressive lesions may be caused by neoplasms,'! of which lymphoma is most common. Epidural abscesses due to bacteria, fungi, or mycobacteria should also be considered. Intramedullary lesions due to infectious agents have also been described.

Vacuolar myelopathy, the most common myelopathy associated with HIV-1 infection, complicates the clinical course of infection in 5 to 27 percent of patients. It is reported in up to 55 percent of autopsy series and in one recent clinicopathologic series in 47 percent of adult AIDS patients. '39' , y , y^ , y! Myelopathy occurs in the immunosuppressed patient, although it may be the initial presentation of AIDS, but this is not usual. Autopsy cases of vacuolar myelopathy had a high frequency of PCP and MAI infection and a large number of OIs as compared with patients without vacuolar myelopathy. Clinical signs include a progressive paraparesis, sensory ataxia, and sphincter impairment. There is lower extremity hyperreflexia and spasticity with impairment of joint position sense. yj Distal sensory neuropathy may co-exist as may HIV dementia. Pathological findings include a spongy degeneration and intramyelin vacuolation of the dorsal and lateral columns with predominant involvement of the gracile tract. There eventually is macrophage infiltration with evidence of immune activation, cytokine elaboration, and finally necrosis and astrocytosis. The presence of HIV-1, when found, is confined to macrophages. The pathogenesis of vacuolar myelopathy is unclear, and whether or not HIV infection of the spinal cord is important to the pathogenesis is unknown.

In evaluating patients with a myelopathy, human T-cell lymphoma virus (HTLV) infection, abscess, infectious myelitis, and B 12 deficiency should be considered. In appropriate settings, an MRI study may be useful. Cerebrospinal fluid findings in the setting of vacuolar myelopathy are generally nonspecific. Antispasticity agents (baclofen, benzodiazepines) may improve spasms, but typically antiretrovirals agents are not useful.

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