Pierelli F, Garrubba C, Tilia G, Parisi L, Fattapposta F, Pozzessere G, Soldati G, Stanzione P, D'Offizi G, Mezzaroma I
Istituto di Clinica delle Malattie Nervose e Mentali, Università La Sapienza, Roma, Italia.
Acta Neurol Scand. 1996 Apr;93(4):266-71. doi: 10.1111/j.1600-0404.1996.tb00519.x.
Multimodal evoked potentials (PRVEP, BAEP, mSEP) were recorded in 56 HIV-1 seropositive outpatients free from opportunistic CNS pathologies and/or overt HIV-1 encephalopathy. EPs were altered in 17 of 39 (43.6%) seropositive subjects without AIDS (group A) and in 13 of 17 (76.5%) patients with AIDS (group B). A high incidence of subclinical alterations (30.8%) were found in group A patients. Significant BAEP (I-III, III-V, I-V) interpeak latency and mSEP (N9-N13, N9-N20) conduction time prolongations were found in group A and B patients. PRVEP P100 was significantly prolonged only in group B. An inverse relationship between BAEP interpeak latencies and CD4 count was found. Our findings support the hypothesis of an important role of immunodepression in the development of neurophysiologic abnormalities, together with a preferential involvement of acoustic pathways, in the course of HIV-1 infection.
对56例无机会性中枢神经系统病变和/或明显的HIV-1脑病的HIV-1血清阳性门诊患者进行了多模式诱发电位（PRVEP、BAEP、mSEP）记录。在39例无艾滋病的血清阳性受试者（A组）中有17例（43.6%）诱发电位发生改变，在17例艾滋病患者（B组）中有13例（76.5%）诱发电位发生改变。在A组患者中发现亚临床改变的发生率很高（30.8%）。在A组和B组患者中均发现BAEP（I-III、III-V、I-V）峰间潜伏期和mSEP（N9-N13、N9-N20）传导时间显著延长。仅在B组中PRVEP P100显著延长。发现BAEP峰间潜伏期与CD4计数呈负相关。我们的研究结果支持这样的假说，即在HIV-1感染过程中，免疫抑制在神经生理异常的发生发展中起重要作用，同时听觉通路优先受累。
