Simpson D M, Olney R K
Department of Neurology, Mount Sinai Medical Center, New York, New York.
Neurol Clin. 1992 Aug;10(3):685-711.
In the 1990s, HIV has replaced syphilis as the "great masquerader." Virtually every level of the neuraxis may be affected in a patient with HIV infection. The superimposition of multiple levels of neuropathology further complicate the bedside neurologic diagnosis of an AIDS patient. This article has reviewed the variety of forms of peripheral neuropathy that may be associated with HIV infection and its treatment. Distal symmetrical polyneuropathy may be produced in patients with HIV infection by neurotoxic drugs (e.g., vincristine, INH, ddC, or ddI) or by vitamin B12 deficiency or may develop in the later stages of HIV infection without identifiable cause. GBS and CIDP occur with increased frequency in early HIV infection owing to presumed autoimmunity, and these IDPs respond to plasmapheresis or prednisone, similar to HIV-seronegative patients. A limited distribution of mononeuropathy simplex or multiplex occurs in patients with CD4 counts greater than 200; the neuropathy will usually spontaneously improve in these patients. Widespread mononeuropathy multiplex may occur in patients with AIDS and CD4 counts less than 50 and is then usually caused by CMV infections; those neuropathies are usually progressive unless antiviral treatment is given. Progressive polyradiculopathy usually occurs in patients with AIDS and low CD4 counts. If the cerebrospinal fluid has a polymorphonuclear pleocytosis, CMV infection is almost always present, and progression is expected unless ganciclovir therapy is promptly started. Finally, mild autonomic neuropathy is commonly present in HIV-infected patients. Protocols for the evaluation and therapy of cranial and peripheral neuropathies are presented (Figs. 6 and 7). It is unfortunate but likely that increasing numbers of "neuro-AIDS" patients will be encountered, not only in urban medical centers but also in general community practice. The pace at which research in the field of HIV research has proceeded is unprecedented. It is, therefore, important that neurologists stay at the forefront of investigation and clinical care of these complex disorders.
在20世纪90年代,人类免疫缺陷病毒(HIV)已取代梅毒成为“伪装大师”。HIV感染患者的神经轴几乎每个层面都可能受到影响。多种神经病理学层面的叠加进一步使艾滋病患者的床边神经学诊断复杂化。本文回顾了可能与HIV感染及其治疗相关的各种周围神经病变形式。HIV感染患者的远端对称性多发性神经病可能由神经毒性药物(如长春新碱、异烟肼、双脱氧胞苷或双脱氧肌苷)或维生素B12缺乏引起,也可能在HIV感染后期无明确原因地出现。由于推测存在自身免疫,格林-巴利综合征(GBS)和慢性炎症性脱髓鞘性多发性神经病(CIDP)在早期HIV感染中出现的频率增加,并且这些炎性脱髓鞘性多发性神经病对血浆置换或泼尼松有反应,这与HIV血清阴性患者相似。单纯性或多发性单神经病分布有限见于CD4细胞计数大于200的患者;这些患者的神经病变通常会自发改善。广泛的多发性单神经病可能发生在艾滋病且CD4细胞计数小于50的患者中,通常由巨细胞病毒(CMV)感染引起;除非给予抗病毒治疗,这些神经病变通常会进展。进行性多发性神经根病通常发生在艾滋病且CD4细胞计数低的患者中。如果脑脊液有多形核白细胞增多,几乎总是存在CMV感染,除非立即开始更昔洛韦治疗,否则病情预计会进展。最后,轻度自主神经病变在HIV感染患者中很常见。本文还介绍了评估和治疗颅神经和周围神经病变的方案(图6和图7)。不幸的是,不仅在城市医疗中心,而且在普通社区医疗实践中,可能会遇到越来越多的 “神经艾滋病” 患者。HIV研究领域的研究进展速度是前所未有的。因此,神经科医生站在这些复杂疾病调查和临床护理的前沿很重要。