SELECTIVE LOSS OF NEURONS FROM THE THALAMIC RETICULAR NUCLEUS FOLLOWING SEVERE HUMAN HEAD-INJURY
SELECTIVE LOSS OF NEURONS FROM THE THALAMIC RETICULAR NUCLEUS FOLLOWING SEVERE HUMAN HEAD-INJURY
复制标题
DOI：
10.1089/neu.1993.10.151
复制
发表时间：
1993-06-01
影响因子：
4.2
通讯作者：
ADAMS, JH
中科院分区：
文献类型：
--
作者：
ROSS, DT;GRAHAM, DI;ADAMS, JH
丘脑网状核或丘脑网状核(RT)的GABA能神经元被认为是注意加工系统的重要组成部分。RT中的神经元对红藻氨酸和软骨藻酸中毒、实验性全脑缺血、人类心脏骤停和非人类灵长类动物实验性闭合性头部损伤后的变性非常敏感。本研究旨在探讨重型颅脑损伤后人RT神经元是否发生选择性丢失。对37例脑损伤死亡者的大脑进行了检查，以寻找RT神经元丢失的证据。37例中有36例发现RT病变，占73例网状核中的65例(89%)。在所有年龄组中RT病变的发生率是相似的：14例中13例(92.9%)在儿科(小于或等于16岁)组，33例(89.2%)在青年组(18-45岁)，19/22(86.4%)在老年组(&>45岁)。RT损伤的特点是与额叶皮质、丘脑内侧背侧核(MD)和腹外侧核(VL)相关的核区四分之一至四分之三的神经元丢失。RT神经元的保留与额叶皮质广泛病变的存在高度相关，这表明脑损伤后RT变性需要完整的皮质丘脑投射。提出了一种具有显著兴奋性毒性成分的病理性级联反应。这些抑制性丘脑网状神经元的丧失以及由此导致的丘脑和新皮质神经元功能障碍可能是颅脑损伤后持续存在的某些形式的注意缺陷的基础。
The GABAergic neurons of the thalamic reticular nucleus, or nucleus reticularis thalami (RT), have been implicated as important components in attentional processing systems. Neurons in the RT are exquisitely sensitive to degeneration following kainic and domoic acid toxicity, experimental global ischemia, human cardiac arrest, and experimental closed head injury in nonhuman primates. The present study was performed to establish whether the selective loss of human RT neurons occurred following severe head injury. Brains from 37 human nonsurvivors of head injury were examined for evidence of RT neuronal loss. RT lesions in were found in 36 of 37 cases, representing 65 of 73 (89%) of the reticular nuclei examined. The incidence of RT lesions was similar in all age groups: 13 of 14 cases (92.9%) in the pediatric (less-than-or-equal-to 16 years) group, 33 of 37 (89.2%) in the young adult (18-45 years) group, and 19 of 22 (86.4%) in the older adult (>45 years) group. RT lesions were characterized by loss of one fourth to three fourths of the neurons from the region of the nucleus associated with the frontal cortex and thalamic mediodorsal (MD) and ventrolateral (VL) nuclei. Sparing of RT neurons correlated highly with the presence of extensive frontal cortical lesions, suggesting that an intact corticothalamic projection was necessary for RT degeneration following head injury. A pathologic cascade with a prominent excitotoxic component is proposed. The loss of these inhibitory thalamic reticular neurons and the resultant thalamic and neocortical neuronal dysfunctions may underlie some forms of attentional deficits that persist following head injury.