Journal of the neurological sciences · 1998
Progressive peripheral and central sensory tract lesion in HIV-infected patients evidenced by evoked potentials (a three-year follow-up study).
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Husstedt I W, Evers S, Reichelt D, Sprinz A, Riedasch M, Grotemeyer K H
Аннотация
OBJECTIVE: To investigate progression of peripheral and central sensory tract lesion and its correlation to immunological deterioration.
METHODS: Clinical and neurophysiological investigation (evoked potentials of the median and tibial nerve) and immunological parameters (CD4-cells, beta 2-microglobuline) were followed up in 160 patients (24 females, 136 males, HIV infection for 2.7 +/- 2.3 years, mv +/- 1 sd) up to four times over approximately 3 years regardless of disease stage and evidence of neurological symptoms. Recordings were done using needle electrodes over the Th12 and C7 spinous process and from the scalp (10/20 system) in the conventional manner. Statistical analysis was performed intraindividually and in comparison to normal laboratory values (n = 96).
RESULTS: All parameters deteriorated during the follow-up period. Statistical analysis showed significant differences between probands and patients for evoked potentials, but also a significant deterioration for evoked potentials after three years at the end of the follow-up study. A significant correlation between progressive impairment of evoked potentials and laboratory data was found.
CONCLUSION: HIV infection induces a progressive lesion of the ascending sensory tracts. The results indicate a peripheral neuropathy as well as a progressive lesion of the ascending central sensory tracts. Pathogenesis of polyneuropathy and of central sensory tract lesion is up to now conjectural. Laboratory investigations indicate a clear-cut correlation between immunological alterations induced by HIV infection and its neurologic manifestation on ascending sensory tracts.
METHODS: Clinical and neurophysiological investigation (evoked potentials of the median and tibial nerve) and immunological parameters (CD4-cells, beta 2-microglobuline) were followed up in 160 patients (24 females, 136 males, HIV infection for 2.7 +/- 2.3 years, mv +/- 1 sd) up to four times over approximately 3 years regardless of disease stage and evidence of neurological symptoms. Recordings were done using needle electrodes over the Th12 and C7 spinous process and from the scalp (10/20 system) in the conventional manner. Statistical analysis was performed intraindividually and in comparison to normal laboratory values (n = 96).
RESULTS: All parameters deteriorated during the follow-up period. Statistical analysis showed significant differences between probands and patients for evoked potentials, but also a significant deterioration for evoked potentials after three years at the end of the follow-up study. A significant correlation between progressive impairment of evoked potentials and laboratory data was found.
CONCLUSION: HIV infection induces a progressive lesion of the ascending sensory tracts. The results indicate a peripheral neuropathy as well as a progressive lesion of the ascending central sensory tracts. Pathogenesis of polyneuropathy and of central sensory tract lesion is up to now conjectural. Laboratory investigations indicate a clear-cut correlation between immunological alterations induced by HIV infection and its neurologic manifestation on ascending sensory tracts.