Re-examining the brain regions crucial for orchestrating speech articulation
Re-examining the brain regions crucial for orchestrating speech articulation
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DOI：
10.1093/brain/awh172
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发表时间：
2004-07-01
期刊：
影响因子：
14.5
通讯作者：
Maurer, K
中科院分区：
文献类型：
--
作者：
Hillis, AE;Work, M;Maurer, K
一种定位大脑功能的传统方法是识别具有特定缺陷的个体的共同脑损伤区域。这种“损伤重叠”方法的基本原理很简单：如果个体不能再执行该功能，那么大多数这些个体的大脑受损区域必须负责该功能。然而，相互关联，即病变引起缺陷的概率，往往不被评估。在这项研究中，我们通过重新检查大脑中对协调言语表达至关重要的区域，说明了这种方法的潜在弱点。一项特别优雅且被广泛引用的损伤重叠研究发现，患有“言语失用”（一种言语运动规划和编程障碍）的慢性中风患者，脑岛中央前回的上部（在脑岛前部）是共同的损伤区域。其他人已经证实，言语失用症患者通常有前脑岛损伤。然而，这种可靠的关联可能反映了脑岛在大脑中动脉闭塞或狭窄后的损伤脆弱性（这可以独立导致言语失用和许多其他缺陷）。为了评估这种可能性，我们以三种独特的方式检查了语言失用症与脑岛之间的关系：(i)我们通过检查两个连续系列的急性左半球非腔隙性中风患者的言语清晰度和高级mri，确定了损伤导致缺陷的概率，以及缺陷与病变相关；（ii）我们研究了中风发作时的患者，以便在小中风患者的缺陷消失之前确定缺陷；（三）我们确定了功能失调的脑组织区域，以及结构损伤。使用这种方法，我们发现语言失用症与左岛、前岛或岛中央前回上尖的病变之间没有关联。相反，在有或没有岛叶病变的患者中，言语失用症与左侧额下后回的结构损伤或低血流量有关。这些结果说明了病变重叠研究的潜在局限性，并说明了识别大脑行为关系的另一种方法。
A traditional method of localizing brain functions has been to identify shared areas of brain damage in individuals who have a particular deficit. The rationale of this 'lesion overlap' approach is straightforward: if the individuals can no longer perform the function, the area of brain damaged in most of these individuals must have been responsible for that function. However, the reciprocal association, i.e. the probability of the lesion causing the deficit, is often not evaluated. In this study, we illustrate potential weaknesses of this approach, by re-examining regions of the brain essential for orchestrating speech articulation. A particularly elegant and widely cited lesion overlap study identified the superior part of the precentral gyrus of the insula (in the anterior insula) as the shared area of damage in chronic stroke patients with 'apraxia of speech', a disorder of motor planning and programming of speech. Others have confirmed that patients with apraxia of speech commonly have damage to the anterior insula. However, this reliable association might reflect the vulnerability of the insula to damage following occlusion or narrowing of the middle cerebral artery (which can independently cause apraxia of speech and many other deficits). To evaluate this possibility, we examined the relationship between apraxia of speech and the insula in three unique ways: (i) we determined the probability of the lesion causing the deficit, as well as the deficit being associated with the lesion, by examining speech articulation and advanced MRIs in two consecutive series of patients with acute left hemisphere, non-lacunar stroke, 40 with and 40 without insular damage; (ii) we studied patients at stroke onset to identify the deficit before it resolved in cases of small stroke; and (iii) we identified regions of dysfunctional brain tissue, as well as structural damage. Using this approach, we found no association between apraxia of speech and lesions of the left insula, anterior insula or superior tip of the precentral gyrus of the insula. Instead, in patients with and without insular lesions, apraxia of speech was associated with structural damage or low blood flow in left posterior inferior frontal gyrus. These results illustrate a potential limitation of lesion overlap studies, and illustrate an alternative method for identifying brain-behaviour relationships.