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实验性和人类颞叶癫痫中的杏仁核损伤

Amygdala damage in experimental and human temporal lobe epilepsy.

作者信息

Pitkänen A, Tuunanen J, Kälviäinen R, Partanen K, Salmenperä T

机构信息

A.I. Virtanen Institute, University of Kuopio, Finland.

出版信息

Epilepsy Res. 1998 Sep;32(1-2):233-53. doi: 10.1016/s0920-1211(98)00055-2.

Abstract

The amygdala complex is one component of the temporal lobe that may be damaged unilaterally or bilaterally in children and adults with temporal lobe epilepsy (TLE) or following status epilepticus. Most MR (magnetic resonance) imaging studies of epileptic patients have shown that volume reduction of the amygdala ranges from 10-30%. In the human amygdala, neuronal loss and gliosis have been reported in the lateral and basal nuclei. Studies in rats have more specifically identified the amygdaloid regions that are sensitive to status epilepticus-induced neuronal damage. These areas include the medial division of the lateral nucleus, the parvicellular division of the basal nucleus, the accessory basal nucleus, the posterior cortical nucleus, and portions of the anterior cortical and medial nuclei. Otherwise, other amygdala nuclei, such as the magnocellular and intermediate divisions of the basal nucleus and the central nucleus, remain relatively well preserved. Amygdala kindling studies in rats have shown that the density of a subpopulation of GABAergic inhibitory neurons that also contain somatostatin may be reduced even after a low number of generalized seizures. While analyses of histological sections and MR images indicate that in approximately 10% of TLE patients, seizure-induced damage is isolated to the amygdala, more often amygdala damage is combined with damage to the hippocampus and/or other brain areas. Moreover, recent data from rodents and nonhuman primates suggest that structural and functional alterations caused by seizure activity originating in the amygdala are not limited to the amygdala itself, but may also affect other temporal lobe structures. The information gathered so far on damage to the amygdala in epilepsy or after status epilepticus suggests that local alterations in inhibitory circuitries may contribute to a lowered seizure threshold and greater excitability within the amygdala. Furthermore, damage to select nuclei in the amygdala may predict impairment of performance in behavioral tasks that depend on the integrity of the amygdaloid circuits.

摘要

杏仁核复合体是颞叶的一个组成部分,在患有颞叶癫痫(TLE)的儿童和成人中,或在癫痫持续状态后,可能会单侧或双侧受损。大多数对癫痫患者的磁共振成像研究表明,杏仁核体积缩小幅度在10%至30%之间。在人类杏仁核中,已报道外侧核和基底核存在神经元丢失和胶质细胞增生。对大鼠的研究更具体地确定了对癫痫持续状态诱导的神经元损伤敏感的杏仁核区域。这些区域包括外侧核的内侧部、基底核的小细胞部、副基底核、后皮质核以及前皮质核和内侧核的部分区域。否则,其他杏仁核核团,如基底核的大细胞部和中间部以及中央核,仍相对保存完好。对大鼠的杏仁核点燃研究表明,即使在少量全身性发作后,同时含有生长抑素的γ-氨基丁酸能抑制性神经元亚群的密度也可能降低。虽然对组织学切片和磁共振图像的分析表明,在大约10%的TLE患者中,癫痫发作引起的损伤仅局限于杏仁核,但更常见的是杏仁核损伤与海马体和/或其他脑区的损伤同时存在。此外,来自啮齿动物和非人类灵长类动物的最新数据表明,起源于杏仁核的癫痫活动引起的结构和功能改变不仅限于杏仁核本身,还可能影响其他颞叶结构。目前收集到的关于癫痫或癫痫持续状态后杏仁核损伤的信息表明,抑制性回路的局部改变可能导致杏仁核内癫痫阈值降低和兴奋性增加。此外,杏仁核中特定核团的损伤可能预示着依赖杏仁核回路完整性的行为任务表现受损。

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