Human immunodeficiency virus type 1-related transient neurological deficits.

PURPOSE: To characterize human immunodeficiency virus type 1 (HIV-1)-related transient neurological deficit (TND).

DESIGN

A 3-year prospective study based at a tertiary referral center.

METHODS

Patients with TND in the absence of an opportunistic infection, neoplasm, neurosyphilis, or seizure were recruited and further investigated. The frequency of hospital admission for these patients was compared with those who were HIV-1 seronegative and with those who were admitted for HIV-1-related thromboembolic events.

RESULTS

Twenty-seven patients were identified: mean age of 39 +/- 9 years; CD4+ cell count of 130 +/- 80/microL. Seven patients had no history of an AIDS-defining illness. Hemiparesis and hemisensory disturbance occurred in 23 patients (85%); 15 had preexisting ADC, 7 stage 1 and 8 stage 2; 3 developed ADC after 18 months. Thirteen patients had multiple attacks and 5 had more than 20; 2 patients developed a cerebral infarct. No cause for the TND was identified in 8 patients (30%). Anticardiolipin antibodies were found in 70% and low protein S levels in 53% which was significantly more often than in a neurologically normal group with similarly advanced HIV-1 disease. The frequency of admission was 0.8% whereas the frequency for similar TND in HIV-1-seronegative patients was 0.4% and the frequency for HIV-1-related thromboembolic events was 0.9%.

CONCLUSIONS

Transient neurological deficits occur in advanced HIV-1 disease and are often associated with ADC, elevated concentrations of anticardiolipin antibodies, and low protein S levels. Future studies will need to define the precise role of these associations in the pathogenesis of HIV-1-related TND.