Although less common than in the late stages of HIV-1 infection, the nervous system may also be afflicted earlier, indeed as early as the stage of primary infection and seroconversion. Thus, individual reports have described examples of focal or diffuse encephalopathy, ataxia, myelopathy, and meningitis presenting within the context of HIV-1 seroconversion. These conditions appear to evolve acutely or subacutely, to pursue a monophasic course, and to be followed by good recovery. Peripheral nervous system disorders, including mononeuropathy involving cranial or segmental nerves, brachial plexopathy, and polyneuropathy, have also been reported during this phase. At times these peripheral and central nervous system (CNS) disorders occur together.

Subsequently, during the “clinically latent” phase of infection, several neurologic conditions have been reported. Among these is the Guillain-Barre syndrome and its more protracted counterpart, chronic idiopathic demyelinating polyneuropathy (CIDP), both of which are clinically indistinguishable from demyelinating polyneuropathies affecting non-HIV-1-infected individuals, except for higher cerebrospinal fluid (CSF) cell counts and perhaps a poorer prognosis.

Response to treatment with corticosteroids, plasma exchange, and intravenous immunoglobulin has been noted, supporting an autoimmune pathogenesis. Because of the potential hazards of corticosteroids, plasma exchange and immunoglobulin are the preferred therapies. Isolated cases of a multiple sclerosis-like demyelinating CNS disease have also been reported in this stage of HIV-1 infection, but this appears to be rare.

An additional important aspect of HIV-1 infection, with both diagnostic and pathogenetic implications, is the early development of CSF abnormalities, which relate to early asymptomatic HIV-1 infection of the CNS soon after initial systemic infection. Prospective studies have reported that the majority of asymptomatic HIV-1-infected individuals exhibit mild CSF changes, including elevations in the cell count and protein and immunoglobulin levels as well as evidence of local “intra-blood-brain barrier” synthesis of anti-HIV-1 antibody. Additionally, in a substantial number of asymptomatic patients HIV-1 can be detected in the CSF using nucleic acid amplification techniques. These findings have not been shown to have an adverse prognostic significance for the subject; indeed, it is clear that patients with such abnormalities can continue to function without symptoms or signs of neurologic impairment. These “background” abnormalities may confound CSF analysis.