Chronic temporal lobe epilepsy: a neurodevelopmental or progressively dementing disease?
Chronic temporal lobe epilepsy: a neurodevelopmental or progressively dementing disease?
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DOI：
10.1093/brain/awp182
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发表时间：
2009-10-01
期刊：
影响因子：
14.5
通讯作者：
Elger, C. E.
中科院分区：
文献类型：
--
作者：
Helmstaedter, C.;Elger, C. E.
在慢性颞叶癫痫(TLE)患者中观察到的记忆障碍在多大程度上归因于大脑对慢性癫痫的“初始打击”？我们对1156例慢性TLE患者(年龄范围6-68岁，平均癫痫发作14+/-11岁)和1000名健康对照组(年龄范围6-80岁)的言语学习和记忆的年龄相关倒退进行了横断面比较，并检验了年龄倒退偏离(即缓慢上升、加速下降)将揭示癫痫干扰认知发展的关键阶段的假设。患者是在波恩大学癫痫系招募的，历时20年。健康受试者来自Verbaler Lern-und Merkfahigkeitstest的最新标准人群，这是雷伊听觉言语学习测试的德国挂件。年龄回归的显著差异表明，患者在儿童时期，特别是青春期，未能建立足够的学习和记忆表现。患者(大约16-17岁)比对照组(大约23-24岁)更早出现学习高峰(即交叉进入衰退)。随着年龄的增长，患者和对照组的表现下降是平行的，但由于两组之间最初的距离，患者比对照组更早达到非常差的表现水平。左侧和右侧TLEs患者在言语记忆方面的表现比对照组差。此外，左侧TLE患者的表现比右侧TLE患者差。然而，偏侧差异仅在青少年和成人患者中明显，而在儿童和老年患者中不明显(或较少)。与年龄无关，海马体硬化症与其他病理疾病相比表现较差。结果表明，在慢性TLE患者中，发育障碍加上认知障碍与智力老化的负面交互作用，而不是逐渐痴呆的下降。在童年时期，尤其是在青春期之后的十年里，出现了建立间歇性记忆缺陷的关键阶段。这增加了日后过早患上痴呆症的风险，即使在没有加速下降的情况下也是如此。左侧TLE的物质特异性言语记忆障碍是成熟大脑的一个特征，似乎在较年长的时候消失。研究结果表明，应更多地关注癫痫发作的时间及之后的时间。早期控制癫痫是为了在较小的年龄就抵消发育障碍和损害。
To what degree does the so-called 'initial hit' of the brain versus chronic epilepsy contribute towards the memory impairment observed in chronic temporal lobe epilepsy (TLE) patients ? We examined cross-sectional comparisons of age-related regressions of verbal learning and memory in 1156 patients with chronic TLE (age range 6-68 years, mean epilepsy onset 14 +/- 11 years) versus 1000 healthy control subjects (age range 6-80 years) and tested the hypothesis that deviations of age regressions (i.e. slowed rise, accelerated decline) will reveal critical phases during which epilepsy interferes with cognitive development. Patients were recruited over a 20-year period at the Department of Epileptology, University of Bonn. Healthy subjects were drawn from an updated normative population of the Verbaler Lern- und Merkfahigkeitstest, the German pendant to the Rey Auditory Verbal learning Test. A significant divergence of age regressions indicates that patients fail to build up adequate learning and memory performance during childhood and particularly during adolescence. The learning peak (i.e. crossover into decline) is seen earlier in patients (at about the age of 16-17 years) than for controls (at about the age of 23-24 years). Decline in performance with ageing in patients and controls runs in parallel, but due to the initial distance between the groups, patients reach very poor performance levels much earlier than controls. Patients with left and right TLEs performed worse in verbal memory than controls. In addition, patients with left TLE performed worse than those with right TLE. However, laterality differences were evident only in adolescent and adult patients, and not (or less so) in children and older patients. Independent of age, hippocampal sclerosis was associated with poorer performance than other pathologies. The results indicate developmental hindrance plus a negative interaction of cognitive impairment with mental ageing, rather than a progressively dementing decline in chronic TLE patients. During childhood, and even more so during the decade following puberty, the critical phases for establishing episodic memory deficits appear. This increases the risk of premature 'dementia' later on, even in the absence of an accelerated decline. Material specific verbal memory impairment in left TLE is a characteristic of the mature brain and seems to disappear at an older age. The findings suggest that increased attention is to be paid to the time of epilepsy onset and thereafter. Early control of epilepsy is demanded to counteract developmental hindrance and damage at a younger age.