Gray F, Lescs M C
Service d'Anatomie Pathologique et de Médecine Légale, Neuropathologie, Hôpital Raymond Poincaré, Garches, France.
Eur J Med. 1993 Feb;2(2):89-96.
True demyelination, or at least a leukoencephalopathy with predominant involvement of myelin, may occur in many neurological complications of human immunodeficiency virus (HIV)-infection, resulting from various mechanisms which are not all well understood. These include lesions directly related to infection of the nervous tissue by HIV, opportunistic infections and lymphomas secondary to the cell-mediated immunodeficiency, and changes due to other general or systemic complications of acquired immunodeficiency syndrome (AIDS). HIV-induced pathology of the nervous system includes HIV-specific disease, due to direct infection of the nervous system by the virus. This is characterized by the presence of distinctive multinucleated giant cells and white matter changes, HIV encephalitis and HIV leukoencephalopathy, which may overlap in one third of cases. The pathogenesis of myelin destruction is unclear. Direct infection of neurons or glial cells has never been demonstrated. Indirect immunopathologic, toxic, metabolic, or vascular mechanisms secondary to infection of monocytes/macrophages are more likely. Less specific HIV-associated central nervous system (CNS) pathology including vacuolar myelopathy, and vacuolar leukoencephalopathy are characterized by numerous vacuolar myelin swellings in spinal or cerebral white matter. The exact aetiopathological relationship of these changes to HIV infection is uncertain. It seems likely that factors other than, or additional to, HIV infection play a role in their causation. Apart from these changes which usually occur at the late stages of the disease, acute perivenous inflammatory leukoencephalopathy, presenting either as acute haemorrhagic leukoencephalopathy, acute demyelinating perivenous encephalitis, or acute multiple sclerosis-like leukoencephalopathy revealing HIV-infection occur in rare cases.(ABSTRACT TRUNCATED AT 250 WORDS)
真正的脱髓鞘,或至少是一种以髓鞘为主受累的白质脑病,可能发生于人类免疫缺陷病毒(HIV)感染的许多神经并发症中,其由多种尚未完全明了的机制所致。这些机制包括与HIV直接感染神经组织相关的病变、继发于细胞介导免疫缺陷的机会性感染和淋巴瘤,以及获得性免疫缺陷综合征(AIDS)其他全身或系统性并发症所导致的改变。HIV引起的神经系统病变包括因病毒直接感染神经系统所致的HIV特异性疾病。其特征为存在独特的多核巨细胞和白质改变、HIV脑炎和HIV白质脑病,在三分之一的病例中二者可能重叠。髓鞘破坏的发病机制尚不清楚。从未证实神经元或神经胶质细胞会被直接感染。更有可能的是继发于单核细胞/巨噬细胞感染的间接免疫病理、毒性、代谢或血管机制。特异性较低的与HIV相关的中枢神经系统(CNS)病变包括空泡性脊髓病和空泡性白质脑病,其特征是脊髓或脑白质中出现大量空泡性髓鞘肿胀。这些改变与HIV感染的确切病因病理关系尚不确定。似乎除了HIV感染之外,其他因素或额外因素在其病因中也起作用。除了这些通常发生在疾病晚期的改变外,急性静脉周围炎性白质脑病,表现为急性出血性白质脑病、急性脱髓鞘静脉周围脑炎或提示HIV感染的急性多发性硬化样白质脑病,在罕见情况下会出现。(摘要截选至250词)