Basal ganglia lesions and the theory of fronto-subcortical loops: Neuropsychological findings in two patients with left caudate lesions
Basal ganglia lesions and the theory of fronto-subcortical loops: Neuropsychological findings in two patients with left caudate lesions
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DOI：
10.1076/neur.9.1.70.14374
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发表时间：
2003-01-01
期刊：
影响因子：
0.8
通讯作者：
Auer, A
中科院分区：
文献类型：
--
作者：
Benke, T;Delazer, M;Auer, A
基底神经节病变相关行为障碍的患病率很高。然而，认知功能障碍的确切模式及其与基底神经节病变的关系很少通过详细的神经心理学和病变研究进行研究。此外，已经提出了与观察到的认知缺陷相关的不同机制;在这些机制中，额叶皮层下回路的假设（亚历山大等人，1986）已经对特定的纹状体-额叶回路的损伤与所导致的行为障碍之间的关系做出了预测，其有待临床证实。我们提出了一项研究的两名受试者谁遭受了MRI记录局灶性左基底节血肿。这两个病人不同，他们的病变;在一个病人（PJ）的尾状核大部分被破坏，而在其他（AS）主要是苍白球和壳核病变和尾状核只遭受轻微的损害。在急性期，两种情况下的行为和神经心理异常相似，主要包括精神丧失、执行和注意力功能受损以及严重的遗忘综合征。几个月后，AS的许多功能都恢复了，而PJ的能力仍然存在很大的缺陷。根据这些数据和以前的案例研究得出了几个结论。左侧尾状核病变会引起明显且持久的行为和神经心理障碍，主要包括驱动力、执行控制、注意力和记忆力。尾状核头部的病变程度是综合征严重程度和预后的关键因素，而壳核和苍白球的损伤对认知功能的影响则不那么重要。行为改变的一个子集，其中包括精神障碍、注意力和额叶执行功能障碍，可以很好地归因于基底神经节水平的前扣带回回路和背外侧-额叶回路的病变。其他损伤，最重要的是突出的遗忘综合征，更难以解释的理由，这一假设，并可能与其他病理机制。
Basal ganglia lesions have a high prevalence for associated behavioural impairments. However, the exact pattern of cognitive impairments and its relationship to individual basal ganglia lesion have rarely been investigated by means of a detailed neuropsychological and lesion study. Furthermore, different mechanisms have been proposed as relevant for the observed cognitive deficits; among these, the hypothesis of fronto-subcortical loops (Alexander et al., 1986) has made predictions regarding the relationship between the damage of particular striato-frontal circuits and the resulting behavioural impairment which await clinical confirmation. We present a study of two subjects who suffered a MRI-documented focal left basal ganglia hematoma. The two patients differed in their lesions; in one patient (PJ) large parts of the caudate nucleus were destroyed whereas in the other (AS) mainly the pallidum and putamen were lesioned and the caudate suffered only minor damage. In the acute phase, the behavioural and neuropsychological abnormalities were similar in both cases and included mainly abulia, an impairment of executive and attentional functions, and a severe amnestic syndrome. After several months many functions were restored in AS, whereas PJ's abilities remained largely defective. Based on these data and on previous case studies several conclusions are drawn. Left caudate lesions induce marked and long-lasting behavioural and neuropsychological impairments comprising predominantly drive, executive control, attention, and memory. The extent of lesion in the head of the caudate nucleus is the critical factor regarding the severity and the outcome of the syndrome, whereas damage to the putamen and pallidum is less crucial for cognitive functions. A subset of behavioural alterations, among them abulia, attentional and frontal-executive dysfunctions, can well be attributed to lesions of the anterior cingulate circuit and the dorsolateral-frontal circuit at the basal ganglia level. Other impairments, most importantly the prominent amnestic syndrome, are more difficult to interpret on the grounds of this hypothesis and may be related to other pathomechanisms.