Hillis Argye E, Work Melissa, Barker Peter B, Jacobs Michael A, Breese Elisabeth L, Maurer Kristin
Department of Neurology, Meyer 5-185, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287, USA.
Brain. 2004 Jul;127(Pt 7):1479-87. doi: 10.1093/brain/awh172. Epub 2004 Apr 16.
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.
一种传统的脑功能定位方法是在患有特定缺陷的个体中识别脑损伤的共同区域。这种“病变重叠”方法的基本原理很简单：如果个体无法再执行该功能，那么这些个体中大多数人脑部受损的区域一定是负责该功能的区域。然而，这种相互关联，即病变导致缺陷的概率，往往没有得到评估。在本研究中，我们通过重新审视协调言语发音所必需的脑区，来说明这种方法的潜在弱点。一项特别精妙且被广泛引用的病变重叠研究，将脑岛中央前回的上部（位于前脑岛）确定为患有“言语失用症”（一种言语运动计划和编程障碍）的慢性中风患者的共同损伤区域。其他人也证实，言语失用症患者通常脑岛前部会受损。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易受损伤的特性（大脑中动脉闭塞或狭窄可独立导致言语失用症和许多其他缺陷）。为了评估这种可能性，我们通过三种独特的方式研究了言语失用症与脑岛之间的关系：（i）我们通过检查两组连续的急性左半球非腔隙性中风患者（40例有脑岛损伤，40例无脑岛损伤）的言语发音和高级磁共振成像，确定病变导致缺陷的概率以及缺陷与病变的关联；（ii）我们在中风发作时研究患者，以在小中风病例中在缺陷消失之前识别出该缺陷；（iii）我们识别出功能失调的脑组织区域以及结构损伤。使用这种方法，我们发现言语失用症与左脑岛、前脑岛或脑岛中央前回上尖端的病变之间没有关联。相反，在有和无脑岛病变的患者中，言语失用症与左后下额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一个潜在局限性，并展示了一种识别脑与行为关系的替代方法。
