I commend Simpson and Tagliati [1] for their excellent review of the neurologic manifestations of human immunodeficiency virus (HIV) infection. I emphasize that cerebrovascular disease is not uncommon in HIV infection. It is estimated that 0.5% to 7% of HIV-infected patients develop cerebrovascular disease [2], a rate higher than that for the younger age group in the general population. Postmortem studies have shown abnormalities in higher proportions, of which thrombosis secondary to cerebral vasculitis appears to be the most common. The hyperviscosity syndrome and dehydration could lead to cerebral thrombosis in some patients. Hemorrhage may occur secondary to thrombocytopenia, but embolic events seem to be confined to intravenous drug users.

Toxoplasma infection is considered to be the most common cause of focal cerebral lesions. Because most cases are caused by reactivation of previously acquired endogenous infection in countries where the background seroprevalence of toxoplasma infection is low, the incidence of toxoplasma infection will also be lower.

During my experience working in two centers in the south (Portsmouth) and southwest (Bournemouth) of the United Kingdom (where the seroprevalence of toxoplasma infection in our HIV clinic attendees is less than 5%) I have seen and treated more cases in which cerebrovascular disease was the cause of focal neurologic signs than cases caused by toxoplasma infection. All patients with cerebrovascular disease were white homosexual men younger than 40 years of age. None had any precipitating cardiovascular disease. All had the acquired immunodeficiency syndrome and CD4 counts less than 0.10 x 10⁹/L. Presentations varied but were similar to those in patients without HIV infection. However, the prognosis was poor in HIV-infected patients. Cerebrovascular disease should therefore be considered in the differential diagnosis of focal neurologic lesions in HIV-infected patients.