The pathogenesis of central nervous system manifestations of systemic lupus erythematosus.
The pathogenesis of central nervous system manifestations of systemic lupus erythematosus.
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系统性红斑狼疮中枢神经系统表现的发病机制。
DOI：
10.1002/art.1780250730
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发表时间：
1982
影响因子：
--
通讯作者：
Bluestein,HG
中科院分区：
文献类型：
--
作者：
Zvaifler,NJ;Bluestein,HG
系统性红斑狼疮（SLE）中枢神经系统（CNS）病变的研究尚处于起步阶段。由于缺乏诊断标准，缺乏明确的实验室测试，以及无法在生活中获得脑组织进行研究，这些都阻碍了他们的研究。这种情况类似于三十年前我们对各种形式的狼疮性肾炎的理解。然而，即使在中枢神经系统性红斑狼疮研究的早期阶段，似乎也不可能发现一个单一的发病过程来解释所有的临床特征。因此，局灶性血管事件可能是中风、脑神经病或横贯性脊髓炎的原因，但它们不太可能是器质性精神综合征、脑病、精神病或舞蹈病的原因。此外，认识到这些更弥漫性的脑综合征通常是短暂的或可逆的，似乎不太可能是脑细胞死亡的原因。相反，我们认为这些表现是由于干扰电脉冲或神经递质的过程引起的。对死于SLE的患者的大脑进行尸检，一般仅限于光学显微镜检查。两个最大的研究，虽然相隔十多年，但非常相似（1，Z）。他们发现，在肾脏和SLE的其他全身性病变中非常典型的中小动脉壁的炎性细胞浸润和纤维素样坏死，仅偶尔在脑中观察到。多见于小血管的退行性和增生性改变，与高血压性脑病和血栓性血小板减少性紫癜相似。大脑皮层周围散布着小血管周围的微梗塞和神经胶质增生。受累小动脉增厚
Studies of central nervous system (CNS) disease in systemic lupus erythematosus (SLE) areintheir infancy. They have been hampered by a lack of diagnostic criteria, the absence of definitive laboratory tests, and the inaccessibility of brain tissues for study during life. The situation is analogous to our understanding of lupus nephritis, inits various forms, three decades ago. However, even at this early stage inthestudyof CNS SLE, it seems unlikelythata single pathogenetic process will be found to explain all the clinical features. Thus, focal vascular events may be responsible for strokes, cranial neuropathies, or transverse myelitis, but they are less likely to be the cause of organic mental syndromes, encephalopathic pictures, psychoses, or chorea. Also, in recognition of the fact that these more diffuse cerebral syndromes are often transient or reversible, it seems unlikely that brain cell death is responsible. Rather we would anticipate that these manifestations will result from processes that interfere with electrical impulses or neurotransmitters.Postmortem examination of the brains of patients dying with SLE have, in general, been limited to light microscopy. The two largest studies, although separated by more than ten years, are remarkably similar (1, Z). They found that inflammatory cellinfiltrates and fibrinoid necrosis of the walls of small and medium sized arteries, so typical in the kidney and other systemic lesions of SLE, are only occasionally seen in the brain. More often, there were degenerative and proliferative changes in small vessels, similar to those of hypertensive encephal opathy and thranbotic thrombocytopenic purpura. Scattered about the cerebral cortex were microinfarcts and gliosis around small blood vessels. Affected arterioles showed thickening