Farrell M A, Droogan O, Secor D L, Poukens V, Quinn B, Vinters H V
Department of Pathology (Neuropathology), Beaumont Hospital, Dublin, Ireland.
Acta Neuropathol. 1995;89(4):313-21. doi: 10.1007/BF00309624.
Chronic encephalitis has been recognized as a cause of epilepsy since the work of Rasmussen et al. in the late 1950s. Despite this, few immunohistochemical studies of the affected brain tissue have been attempted. We have studied specimens of brain tissue from seven patients with this condition who underwent therapeutic multilobar cortical resection or hemispherectomy. Immunohistochemical studies were carried out using antibodies to glial fibrillary acidic protein (GFAP), proliferating cell nuclear antigen (PCNA, PC10), T lymphocytes (UCHL-1), B lymphocytes (L26), macrophages and microglia (HAM-56), and major histocompatibility complex molecules (LN3 and beta 2-microglobulin). Additionally, the results of preliminary immunohistochemical and ultrastructural investigation of possible immune complex deposition in blood vessel walls of affected brain tissue are presented. The pattern of GFAP immunoreactivity suggested a patchy and/or laminar disease process in most patients. GFAP immunoreactive cells were especially prominent around microvessels in some cases, suggesting an abnormality and perivascular collections of inflammatory cells, seen to a variable extent in all cases, contained abundant cells immunolabelled with UCHL-1, LN3 and beta 2-microglobulin. L26-labelled B lymphocytes were extremely sparse. Anti-PCNA frequently labelled microvascular endothelial cells, rare pericytes and occasional cells with microglial/macrophage morphology. The data suggest that chronic encephalitis found in patients with epilepsy results from patchy but widespread parenchymal brain injury, in the course of which cells of both microglial and lymphocyte series accumulate or proliferate within brain.(ABSTRACT TRUNCATED AT 250 WORDS)
自20世纪50年代末拉斯穆森等人开展研究以来,慢性脑炎一直被认为是癫痫的病因之一。尽管如此,针对受影响脑组织的免疫组化研究却鲜有尝试。我们研究了7例患有这种疾病并接受了治疗性多叶皮质切除术或大脑半球切除术患者的脑组织标本。使用针对胶质纤维酸性蛋白(GFAP)、增殖细胞核抗原(PCNA,PC10)、T淋巴细胞(UCHL-1)、B淋巴细胞(L26)、巨噬细胞和小胶质细胞(HAM-56)以及主要组织相容性复合体分子(LN3和β2-微球蛋白)的抗体进行免疫组化研究。此外,还展示了对受影响脑组织血管壁中可能的免疫复合物沉积进行初步免疫组化和超微结构研究的结果。GFAP免疫反应模式表明,大多数患者存在斑片状和/或层状疾病过程。在某些情况下,GFAP免疫反应性细胞在微血管周围尤为突出,提示存在异常以及血管周围炎症细胞聚集,在所有病例中均不同程度地可见,其中含有大量用UCHL-1、LN3和β2-微球蛋白免疫标记的细胞。L26标记的B淋巴细胞极为稀少。抗PCNA经常标记微血管内皮细胞、罕见的周细胞以及偶尔具有小胶质细胞/巨噬细胞形态的细胞。数据表明,癫痫患者中发现的慢性脑炎是由斑片状但广泛的脑实质损伤引起的,在此过程中,小胶质细胞和淋巴细胞系列的细胞在脑内积聚或增殖。(摘要截选至250词)