R Teggi1, N Ceserani, F Lira Luce, A Lazzarin, M Bussi. 1. Department of ENT, Istitudo di Ricovero e Cura a Carattere Scientifico San Raffaele Hospital, Vita-Salute University, Milan, Italy. teggi.roberto@hsr.it
Abstract
OBJECTIVE: To investigate vestibular function in human immunodeficiency virus positive subjects. METHODS: We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness. RESULTS: Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects. CONCLUSIONS: In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).
OBJECTIVE: To investigate vestibular function in human immunodeficiency virus positive subjects. METHODS: We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness. RESULTS: Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects. CONCLUSIONS: In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).
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