PDF(Pubmed)
Abstract：
UNASSIGNED: Limbic encephalitis is an increasingly recognized cause of medial temporal lobe epilepsy (mTLE) and associated cognitive deficits, potentially resulting in hippocampal sclerosis (HS). For several reasons, these patients usually do not undergo epilepsy surgery. Thus, histopathologic examinations in surgical specimens of clearly diagnosed limbic encephalitis are scarce. The purpose of this study was a detailed histopathologic analysis of surgical tissue alterations, including neurodegenerative markers, in patients with limbic encephalitis undergoing epilepsy surgery.
UNASSIGNED: We investigated the surgical specimens of six patients operated on with mTLE related to limbic encephalitis (among them four patients were with GAD65 and one with Ma1/2 antibodies), and compared the findings to a control group with six patients matched according to age at the time of surgery without limbic encephalitis and without early inciting events.
UNASSIGNED: Histopathologic analysis in the group with limbic encephalitis revealed HS in four patients, while three of them also displayed signs of an active inflammatory reaction with lymphocytes. In one of the patients with GAD65-encephalitis who was suffering from a late-onset mTLE and a long disease course, neurodegenerative protein markers (β-amyloid and hyperphosphorylated tau) were found coexisting with inflammatory reactions and HS. Investigations in the control group did not reveal any inflammatory reaction or neurodegenerative marker.
UNASSIGNED: Our findings suggest a possible link between long-lasting immune reactions in the medial temporal lobe, HS, and further toward the development of neurodegenerative diseases. Presently, however, a causal relationship between these entities cannot yet be established. Furthermore, our results suggest that an immunological etiology should always be considered in late onset (> 18 years) mTLE, also in cases of long disease duration and the presence of HS.
UNASSIGNED: We investigated the surgical specimens of six patients operated on with mTLE related to limbic encephalitis (among them four patients were with GAD65 and one with Ma1/2 antibodies), and compared the findings to a control group with six patients matched according to age at the time of surgery without limbic encephalitis and without early inciting events.
UNASSIGNED: Histopathologic analysis in the group with limbic encephalitis revealed HS in four patients, while three of them also displayed signs of an active inflammatory reaction with lymphocytes. In one of the patients with GAD65-encephalitis who was suffering from a late-onset mTLE and a long disease course, neurodegenerative protein markers (β-amyloid and hyperphosphorylated tau) were found coexisting with inflammatory reactions and HS. Investigations in the control group did not reveal any inflammatory reaction or neurodegenerative marker.
UNASSIGNED: Our findings suggest a possible link between long-lasting immune reactions in the medial temporal lobe, HS, and further toward the development of neurodegenerative diseases. Presently, however, a causal relationship between these entities cannot yet be established. Furthermore, our results suggest that an immunological etiology should always be considered in late onset (> 18 years) mTLE, also in cases of long disease duration and the presence of HS.
摘要：
未经证实：边缘叶脑炎是颞叶内侧癫痫（mTLE）和相关认知缺陷的日益公认的原因，可能导致海马硬化（HS）。出于几个原因,这些患者通常不接受癫痫手术。因此，在明确诊断的边缘叶脑炎的手术标本中，组织病理学检查很少。这项研究的目的是对手术组织改变进行详细的组织病理学分析，包括神经退行性标记物,接受癫痫手术的边缘叶脑炎患者。
UNASSIGNED：我们调查了6例与边缘叶脑炎相关的mTLE患者的手术标本（其中4例患者为GAD65，1例患者为Ma1/2抗体），并将结果与对照组进行了比较，对照组为6例患者，根据手术时的年龄相匹配，无边缘叶脑炎且无早期煽动事件。
UNASSIGNED：边缘叶脑炎组的组织病理学分析显示4例患者出现HS，而其中三个还显示出淋巴细胞活跃的炎症反应。在患有GAD65脑炎的患者中，有一名患有晚发性mTLE和病程较长的患者，发现神经退行性蛋白标志物(β-淀粉样蛋白和高磷酸化tau)与炎症反应和HS共存。对照组的研究未发现任何炎症反应或神经变性标志物。
未经证实：我们的研究结果表明，颞叶内侧持续的免疫反应之间可能存在联系，HS,并进一步发展神经退行性疾病。目前,然而,这些实体之间的因果关系尚无法确定。此外，我们的结果表明，在晚期（>18岁）的mTLE中，应始终考虑免疫学病因，在疾病持续时间长和存在HS的情况下也是如此。
UNASSIGNED：我们调查了6例与边缘叶脑炎相关的mTLE患者的手术标本（其中4例患者为GAD65，1例患者为Ma1/2抗体），并将结果与对照组进行了比较，对照组为6例患者，根据手术时的年龄相匹配，无边缘叶脑炎且无早期煽动事件。
UNASSIGNED：边缘叶脑炎组的组织病理学分析显示4例患者出现HS，而其中三个还显示出淋巴细胞活跃的炎症反应。在患有GAD65脑炎的患者中，有一名患有晚发性mTLE和病程较长的患者，发现神经退行性蛋白标志物(β-淀粉样蛋白和高磷酸化tau)与炎症反应和HS共存。对照组的研究未发现任何炎症反应或神经变性标志物。
未经证实：我们的研究结果表明，颞叶内侧持续的免疫反应之间可能存在联系，HS,并进一步发展神经退行性疾病。目前,然而,这些实体之间的因果关系尚无法确定。此外，我们的结果表明，在晚期（>18岁）的mTLE中，应始终考虑免疫学病因，在疾病持续时间长和存在HS的情况下也是如此。
