人物专栏 | Andrea Gajardo-Vidal博士、Diego Lorca-Puls博士访谈
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《理论语言学五道口站》（2022年第15期，总第218期）“人物专栏”与大家分享近期Stephen Wilson副教授对Andrea Gajardo-Vidal、Diego Lorca-Puls两位博士的访谈。Stephen Wilson，美国范德堡大学医学中心副教授。Andrea Gajardo-Vidal与Diego Lorca-Puls均为美国加利福尼亚大学神经学博士后研究员。
本期访谈节选自Stephen Wilson副教授于2021年3月与 Andrea Gajardo-Vidal博士及Diego Lorca-Puls博士所做的一期播客。在访谈中，Andrea Gajardo-Vidal、Diego Lorca-Puls两位博士就“Damage to Broca's area does not contribute to long term speech production outcome after stroke”一文回答了与语言产出相关的问题。访谈内容转自网站：https://langneurosci.org/podcast/，由本站成员赵欣宇、雷晨、聂简荻、郭思源、丁子意翻译。
采访人物简介
Andrea Gajardo-Vidal博士（左）
及Diego Lorca-Puls博士（右）
Andrea Gajardo-Vidal与Diego Lorca-Puls均为美国加利福尼亚大学神经学博士后研究员。夫妻二人共同为论文“Damage to Broca's area does not contribute to long term speech production outcome after stroke”的第一作者，该文已于2021年在期刊《大脑》（Brain）上发表。
Brief Introduction of Interviewee
Andrea Gajardo-Vidal and Diego Lorca-Puls are Postdoctoral Scholars in Neurology, University of California, USA. The couple is the first author of the paper “Damage to Broca's area does not contribute to long term speech production outcome after stroke”. The paper was published in the journal Brain in 2021.
采访者简介
Stephen Wilson副教授
Stephen Wilson，美国范德堡大学医学中心副教授。他的研究兴趣主要为语言的神经基础，侧重于大脑的语言处理机制（尤其是不同类型的失语症患者）。
Brief Introduction of Interviewer
Stephen Wilson is an Associate Professor at Vanderbilt University Medical Center, USA. His primary research interests are in the neural basis of language, focusing on language processing mechanisms in the brain (especially in patients with different kinds of aphasia).
访谈内容
01.
Stephen Wilson副教授：在二位的论文“Damage to Broca's area does not contribute to long-term speech production outcome after stroke”中，研究对象是一组脑卒中后失语症（post-stroke aphasia，PSA）患者。在对这些患者进行了病变位置诊断以及语言测试之后，您对特定脑区或神经束的损伤与语言产出的关系进行了探究。关于实验中被试部分，请问被试量是多少？选择被试的标准是什么？他们损伤的部位包括哪些？
Diego Lorca-Puls博士：我们对134名左侧额叶存在损伤的患者进行了研究，他们的病变位置没有扩展到顶叶和颞上关联皮层的后语言区（威尔尼克区，Wernicke's area）。所有患者都是英语母语者、右利手、患脑卒中三个月至十年。是否患有失语症并不是我们选取被试的一项标准，所以研究中有些被试患有失语症，有些则没有。因为这样一来，我们还可以对没有患失语症的脑卒中患者大脑特定区域的损伤与因兴趣缺乏而造成的语言缺陷的相关性进行探究。
02.
Stephen Wilson副教授：您对大脑额叶内脑区的损伤进行了量化研究。请问您选择了哪些脑区？选择它们的理由是什么？您又是如何决定要研究这些脑区的呢？
Andrea Gajardo-Vidal博士：我们专门研究的是大脑的BA44区、BA45区，它们统称为布洛卡区，已经有大量实验数据证实该脑区确实与语言产出相关。还有腹侧前运动皮层，也就是初级运动皮层中与发音器官运动控制相关的部位，双侧中央沟、壳核、额斜束、弓状束前支等区域。其他区域比如辅助运动皮层、弓状束后支，我们没有涉及，因为这些区域与研究问题并不相关。此外，因为Fridriksson及其同事2013年的研究发现下枕额束与持续性语言产出障碍和损伤无明显相关性，我们就排除了下枕额束区域。
03.
Stephen Wilson副教授：接下来我们来讨论一下关于语言测试的问题。在PLORAS（Predicting Language Outcome and Recovery After Stroke）项目中，失语症是如何被评估的？你们倾向于哪种测量方法？
Diego Lorca-Puls博士：PLORAS数据库中收录的患者都要接受失语症综合测试的评估，这项标准化语言测试已经在英国广泛使用。测试中共有27个不同的任务类型来评估综合语言能力，包括命名、复述、阅读和写作。我们把患者在图片口头描述任务中的表现作为检测语言产出能力的行为指标，即患者需要在一分钟内对场景事物进行口头描述。我们决定测试患者是否具有连贯的口语表达能力，而不是单字产出能力，因为连贯口语表达能力更能反映出患者在日常交流中可能出现的问题。而且这项任务的另一个优点是能够有效检测出语言的产出障碍。
04.
Stephen Wilson副教授：我们已经谈及了对患者病变位置及行为结果的测量。您二位之后通过构建统计模型观察哪些脑区的损伤可以预测其对语言产出的影响。那我们接下来就简单聊一下其中的某些模型吧。您拟合了一连串的模型，并做了清晰的描述。从读者的角度来说，我很欣赏这一点。在第一个模型中，您只提及了BA44区和BA45区，您能详细说下有什么发现吗？
Andrea Gajardo-Vidal博士：首先，我们决定单独测量BA45区和BA44区，而不是以整个区域进行测量，构建第一个模型的目的就是测试这一决定是否得到数据的支持。我们在实验中发现，当BA44区受到损伤时，我们可以成功预测到被试在语言产出能力测试中会所取得更低的分数，而当BA45区受损伤时却无法做出这种预测。这一发现也不足为奇，因为之前的研究已经显露出了这种迹象：和BA45区相比，BA44区在语言产出过程中可能起着更重要的作用。由于BA45区（额下回三角部）的损伤对预测语言产出分数的贡献低于BA44区，所以我们将其从其他分析中剔除掉了。上述就是我们第一次实验分析的总结。
05.
Stephen Wilson副教授：所以第一次实验分析主要是为了找出布洛卡区的哪一部分才是您关注的重点。可以看出您基本上对此已经有定论了，如果布洛卡区内有一部分能够预估语言产出能力的缺陷，那很有可能就是额下回岛盖部的BA44区，而不是额下回三角部的BA45区。因此在后续的统计模型中，您基本不用再考虑BA45区，只需要关注BA44区的数据。在我看来，第二个模型可能是最核心的一个模型。您能介绍下第二个模型以及您的发现吗？
Dr. Diego Lorca-Puls：在第二个模型中，我们通过将其余7个兴趣区数据进行回归分析，来证明布洛卡区邻近区域受损的事实。我们还通过增加病变体积，卒中持续时间，卒中患者的年龄以及语义记忆测试所取得的分数，共变出与病变位置或语言产出无关的数据。我们发现，在包括第二个模型在内的所有8个兴趣区中，只有弓状束前支的损伤显著预示了更差的语言产出测试分数。换句话说，当周围区域的损伤得到控制后，BA44区的损伤将不再能预测语言产出能力测试的得分。
06.
Stephen Wilson副教授：如前所述，我认为这篇论文一个最大优点体现在样本量方面。您有着独特的样本量，包括额叶附近不同区域受到损伤的患者样本，这使您有可能将这些相邻区域和神经束的作用进行区分。这并不多见。但是，尽管您有着134名患者的样本规模，却仍然没有区分这些区域，处理方法很大程度上偏向于认为相邻的区域会一起受到损伤。也就是说，如果A区与B区相邻，那么大多数影响A区的病变也会影响到B区。这就在模型中产生了多重共线性，这一问题在论文中得到了解决。您二位是如何面对多重共线性这一挑战的呢？
Diego Lorca-Puls博士：当我们把行为缺陷与脑卒中后的特定病变部位联系起来时，高度的多重共线性可能是我们面临的最大挑战之一。这是因为当一个区域的损伤可以完全从另一个区域的损伤中推测出来时，我们就几乎不可能将它们的影响分离开来。举例来说，如果与X功能相关的A区损伤时，同时出现B区损伤，而B区却与X功能无关，我们就无法知道是哪一个区域导致了观察到的现象。在我们的案例中，我们很幸运能够接触到大量的脑卒中患者，他们的损伤程度或兴趣区各不相同，使得我们有可能将它们的影响分离出来。腹外侧前运动皮层和额斜束这两个区域由于受到高度多重共线性的影响，无法分离，因此，我们通过删除与腹外侧前运动皮层或额斜束高度相关的兴趣区后，重新运行回归统计分析来处理高度多重共线性。值得一提的是，这一操作并没有改变我们的结果，因为弓状束前支的损伤仍然是唯一能预测语言产出测试分数的因素。
07.
Stephen Wilson副教授：如果模型中包含所有区域时，弓状束是唯一能解释额外差异的区域。但我很想知道，如果没有弓状束，这个模型的效果如何。额叶区域的损伤可以解释最终模型中51.5%的方差数据。您有没有构建过一个不包含弓状束的模型？
Diego Lorca-Puls博士：有过。在调整了其他因素之后，受损的弓状束前支占了大约6%的方差。然而，弓状束前支受损的总影响要大得多，约占方差的37%，这非常接近Fridriksson等人的研究报告中对这一白质纤维束受损所解释的40%的方差。我认为同样重要的是将弓状束加入到由病变体积、脑卒中后时间、脑卒中年龄和语义记忆组成的协变量模型中，当然这会导致明显的可决系数（r-squared）的变化。在我们的研究中，其他兴趣区都没有出现这种情况。综上结果表明，弓状束损伤是一个特别有力的预测长期语言产出的因素。
08.
Stephen Wilson副教授：接下来谈到您提及的一种可能性，即弓状束损伤会切断布洛卡区间的联系，进而影响语言产出，但您的多个分析都反对这种可能性。因此，为了保证大家都能理解我们的对话，我们能不能只关注其中一个分析？您是否对患有弓状束损伤及布洛卡区损伤的两组患者分别进行了数据分析？
Andrea Gajardo-Vidal博士：可以说弓状束前支损伤的长期影响可能是由于与布洛卡区的断开造成的。这基本上意味着布洛卡区可能由于弓状束前支的损伤而断开。这才是真正推动行为效应的原因。为了调查这种可能性，我们选择了三组患者，针对于不同的病变部位、病变体积、脑卒中后时间和脑卒中年龄进行研究。第一组包括7名 BA44区受损且弓状束前支相对保留的患者。第二组包括7名弓状束前支受损而BA44区相对保留的患者。第三组包括BA44区和弓状束前支均受损的患者。我们发现，BA44区损伤患者（第一组）的语言产出能力平均在正常范围内，并且明显优于弓状束前支损伤患者（第二组）。因此，从我们的角度来看，这些结果不能用布洛卡区的关联假设来解释。
09.
Stephen Wilson副教授：您反对非关联假设，是吗？我认为这是非常有说服力的论点。您的很多分析都是对弓状束与布洛卡区进行对比。我想知道腹侧前运动皮层是否可以更有效地预测语言产出缺陷。众所周知，刺激导致言语停滞的区域不是布洛卡区。您有没有做过分析来证实腹侧前运动皮层是否有助于预测长期缺陷？
Diego Lorca-Puls博士：的确。在单独分析时，腹侧前运动皮层的损伤是语言产出分数的重要预测指标。然而，一旦控制了对弓状束前支损伤的影响，这种关系就不再具有统计学意义。事实上，在论文中，我们发现超过80%的腹侧前运动皮层损伤对长期语言产出结果可以利用同时发生的弓状束前支损伤来进行解释。这与2014年van Geeman等人的研究结果一致：对浸润腹外侧前运动皮层的肿瘤的部分或完全切除只会导致短暂的语言产出缺陷。
10.
Stephen Wilson副教授：在您的讨论中，您总结到，“我们并不是在反驳布洛卡区在正常大脑中的语言产出中所起的作用，而是对“布洛卡区受损会导致脑卒中后的长期语言产出障碍”提出了挑战。所以如果您认为布洛卡区确实在正常的语言产出中发挥了作用，那么它的损伤为什么没有带来长期的影响呢？
Diego Lorca-Puls博士：我们的研究结果表明，布洛卡区对语言产出并不像通常认为的那样重要，布洛卡区受损不会影响脑卒中后的长期语言产出结果。然而，许多研究表明，在正常大脑中，布洛卡区确实在语言产出过程中发挥着作用。这与我们的结论存在明显矛盾，其原因可能在于恢复效果的不同。换言之，相比于弓状束前支受损的情况，布洛卡区受损后的恢复潜力可能大得多，这一点也得到了越来越多研究的证实。例如，2016年Herbert等人在期刊《大脑》（Brain）上发表文章，基于脑肿瘤患者术中测绘的结果表明，大脑皮质受损后代偿功能程度普遍较高，脑白质受损后则较低。但是，脑卒中和脑肿瘤并不是同一回事。因此，对于布洛卡区或弓状束前支相对局灶性损伤的脑卒中患者语言产出的恢复情况，未来还需要继续进行跟踪研究。
11.
Stephen Wilson副教授：您曾反对弓状束受损会使之与布洛卡区产生断连这一观点。在您看来，弓状束前支损伤是如何对语言产出造成长期影响的呢？
Andrea Gajardo-Vidal博士：是这样的，我们已经说过为什么它与布洛卡区的断连不能从逻辑上解释我们的结果。然而，弓状束前支受损对语言产出的持久影响可能是参与语言产出的额下皮质、顶叶皮层下区以及下颞皮质中多个区域之间快速功能整合的结果。换句话说，我认为弓状束前支受损可能会破坏语言产出网络的重要部分，从而导致语言产出障碍。这就是我的观点。
12.
Stephen Wilson副教授：您能告诉我们您的研究结果是如何与以往的研究相衔接，又是如何使其进一步得到扩展的吗？
Diego Lorca-Puls博士：我们的研究确实受到了以往研究的启发和激励。以您所说的为例，Fridriksson等人已经强调过弓状束前支对于语言产出的重要性，依据是在脑卒中患者的白质纤维束损伤与语言产出不流利有关。我们有能力在更大的脑卒中患者样本中复证并扩展这些发现。另一方面，我们所做研究的独特之处在于，我们关注的是在相对局灶性左额叶卒中的情况下，布洛卡区受损的影响。我们通过对一小群损伤部位不同的患者进行事后比较，检验了布洛卡区的连接假设。我们还提供了证据，以证明布洛卡区的损伤对语言产出没有长期的影响，这比仅仅表明缺乏显著的关联要有意义得多。最后，我们发现在后额叶皮层下区不同部位的损伤对语言产出的影响中，70%以上可以用弓状束前支的损伤来解释，这也与保罗·布洛卡的两个历史病例中的损伤部位一致，两人都同时发生了弓状束前支损伤。
English Version
01.
Prof. Stephen Wilson: Your paper (Damage to Broca's area does not contribute to long-term speech production outcome after stroke，2021) involves a group of patients with chronic post-stroke aphasia. They all had their lesions mapped, and they have language evaluations, like you said. What you're going to do is look for relationships between damage to specific regions and tracts, and language outcomes. So let's kind of go through and talk about the different pieces of the puzzle, starting with the patients. So can you guys tell me how many patients are included in the study? What kind of inclusion criteria and lesion locations did you have for your patient sample?
Dr. Diego Lorca-Puls: We studied 134 stroke patients with left frontal lesions that didn't extend into posterior speech production areas in lateral inferior parietal and superior temporal association cortices. All patients were right-handed, native speakers of English, between three months and ten years after stroke. And importantly, the presence of aphasia wasn't part of the inclusion criteria. So some of the patients did have aphasia, while others didn't. And this is because patients without aphasia allow us to investigate how consistently damage to a specific part of the brain is associated with a deficit of interest.
02.
Prof. Stephen Wilson: What you did is quantifying damage to a set of brain regions within the frontal lobe. Can you tell me which brain regions you included and why? And which ones you didn't include and why? How did you decide on your set of brain regions to quantify?
Dr. Andrea Gajardo-Vidal: We exclusively select brain regions that had been previously associated with the speech production by a large body of evidence. These were BA 44, BA 45, which are together known as Broca's area. The ventral lateral premotor cortex, the parts of the primary motor cortex that are implicated in the motor control of articulators. Both parts of the superior part of the central sulcus of the insula, the putamen, the frontal aslant tract, the anterior arcuate fasciculus. And finally, the uncinate fasciculus. So there were other regions such as the supplementary motor cortex, posterior parts of the arcuate fasciculus that we didn't include because they didn't overlap with the patient's issues. So in the case of the inferior frontal occipital fasciculus, we excluded it because a previous study led by Fridriksson and colleagues from 2013, did not find a significant relationship between persistent speech production impairments and damage to this particular white matter tract.
03.
Prof. Stephen Wilson: Let’s now talk about the language assessment. How does aphasia get assessed in the PLORAS project, and what outcome measure that you guys decide to focus on?
Dr. Diego Lorca-Puls: All patients recruited to the PLORAS database are assessed with the Comprehensive Aphasia Test, which is a standardized language battery widely used in the UK. It comprises 27 different tasks that evaluate a wide range of language abilities, including naming, repetition, reading and writing. Our behavioral index of speech production abilities, was the spoken picture description task from the comprehensive aphasia test, where the patient is prompted to describe verbally what is happening in a scene for one minute. We decided to use connected speech production rather than single word production as our outcome measure because it is more likely to capture the difficulties that a patient might experience in everyday communication. And one of the advantages that this task is particularly sensitive to is speech production difficulties.
04.
Prof. Stephen Wilson: Now we have kind of described the regions that you quantify damage in and the behavioral outcome measure. You then constructed statistical models to see in which regions would damage predict speech production outcomes. So let's kind of talk about some of those models. So you can fit a sequence of models. I think in the paper, you describe them all really nicely and clearly. So I appreciated that as a reader. In the first model, you had only BA 44 and BA 45. What did you find in that model?
Dr. Andrea Gajardo-Vidal: So, let me start by saying that the aim of this first model was to test whether our decision to investigate BA 45 and BA 44 individually rather than a single area was supported by the data. So that was the aim of model one, our first model. Here, we found that damage to BA 44, but not BA 45, significantly predicted worse speech production scores, which is not entirely surprising, because previous work has shown that BA 44 probably plays a more active role in speech production than BA 45. So, since damage to BA 45, pars triangularis, did not make a unique contribution to the prediction of speech production scores above and beyond that of BA 44, we excluded it from other analyses. So that is a summary of our first analysis.
05.
Prof. Stephen Wilson: So the first analysis is primarily aimed at figuring out which part of Broca's area you should be focused on. And you've basically found that if any part of Broca's area was going to be predictive of the speech production deficits, and it's going to be pars opercularis, BA 44, rather than the pars triangularis, BA 45. And then in your subsequent models, you basically don't really look at BA45 anymore, you're focusing on 44. Okay, so to my mind, model 2 in your paper was probably the most central one. Can you tell me about model 2 and what you found in that model?
Dr. Diego Lorca-Puls: So in model 2, we accounted for the fact of damage to regions neighboring Broca's area, by entering the seven remaining regions of interest into the regression. We also covaried out variance unrelated to lesion site or speech production by adding lesion volume, time post-stroke, age at the stroke, and semantic memory scores. And we found that across all eight regions of interest including model two, only damage to the anterior arcuate fasciculus, significantly predicted worse speech production scores. In other words, damage to BA44, no longer predicted speech production scores when damage to surrounding regions was controlled for.
06.
Prof. Stephen Wilson: I think one of the great strengths of this paper, like we talked about earlier, is the sample size, right. You have this unique sample size of patients with damage to different adjacent frontal regions, that kind of gives you the potential to parcellate out the contributions of these neighboring regions and tracts. Few of us have ever had that opportunity before. But even though you have this very large sample size with 134 patients, you still have pretty strong patterns of adjacent regions tending to be damaged together. So if something's next to you know, that if region A is next to region B, most lesions that affect region A are going to affect region B. And that creates multicollinearity in the model, which you guys address in the paper. So can you tell me about how you go about addressing the multicollinearity challenge?
Dr. Diego Lorca-Puls: So high multicollinearity is probably one of the biggest challenges we face when relating behavioral deficits to specific lesion sites after stroke. And this is because when damage to one region can almost perfectly be predicted from damage to another region, disassociating their effects becomes virtually impossible. So for example, if damage to region A, which is associated with function X, very frequently co-occurs with damage to region B, which is not associated with function X, we won't be able to know which of these regions is driving the observed behavioral effects. Or even worse, we might wrongly conclude that both regions contribute to function X. In our case, we were fortunate enough to have access to a large number of stroke patients who differed in the degree of damage or regions of interest, making it possible for us to dissociate their effects except for the ventral lateral premotor cortex, and the frontal aslant tract, which were affected by high multicollinearity. In these cases, we dealt with high multicollinearity by rerunning the regression after removing the regions of interest with which the ventral lateral premotor cortex or frontal aslant tract were highly correlated. Importantly, this didn't change our results because damage to the anterior arcuate fasciculus continued to be the only significant predictor of speech production scores.
07.
Prof. Stephen Wilson: It's really neat that the arcuate fasciculus is the only region that can explain additional variance once everything else is included in the model. But I'm interested in knowing how well the model would do without the arcuate. So in your final model, you basically explained 51.5% of the variance, which is quite a lot. Half of the variance is explained by damage to these frontal regions, in combination. Did you ever run a model that didn't include the arcuate and get a sense of how much you could explain without the arcuate?
Dr. Diego Lorca-Puls: Um, yeah. So the unique effect of damaging anterior arcuate fasciculus accounts for around 6% of the variance. This is after adjusting for everything else. However, the total effect of damage to the anterior arcuate fasciculus is much larger, accounting for around 37% of the variance, which is very close to the 40% of variance explained by damage to this white matter tract reported in the Fridriksson et al study. Yeah, and I think it's also important to mention that adding the arcuate fasciculus to a covariate-only model comprising lesion volume, time post-stroke, age of stroke, and semantic memory, of course, leads to a significant r-squared change. This isn't the case for any of the other regions of interest examined in our study. Taken together, our results suggest that damage to the anterior arcuate fasciculus is a particularly robust predictor of long-term speech production.
08.
Prof. Stephen Wilson: So you next address the possibility that arcuate fasciculus damage might impact language by disconnecting Broca's area. You argue against this interpretation. You've got several analyses agreeing against that interpretation. So just for the sake of keeping our conversation intelligible to our listeners, can we focus on just one of those analyses? Can you tell us about the analysis where you derive from two groups of patients that had lesions to either one or the other of these regions, either to the arcuate alone or to Broca's area alone?
Dr. Andrea Gajardo-Vidal: So it could be argued that long-lasting effects of damage to the anterior arcuate fasciculus might be explained by a disconnection of Broca's area. So this basically means that Broca's area might disconnect as a result of damage to the anterior arcuate fasciculus. And this is what really drives the behavioural effect. So to investigate this possibility, we selected three groups of patients. So with different lesion sites, who were for lesion volume, time post-stroke, and age at the stroke. So the first group comprises seven patients with damage to BA 44, and relative sparing of the anterior arcuate fasciculus. The second group comprised seven patients with damage to the anterior arcuate fasciculus, and relatively sparing of BA 44. And the third group comprised of patients with damage to both BA 44 and the anterior arcuate fasciculus. And we found that the speech production ability of patients with damage to BA 44 (group one), were on average, within the normal range and significantly better than those patients with damage to the anterior arcuate fasciculus, those from group two. So these results cannot be explained by Broca's area, this connection hypothesis, from our point of view.
09.
Prof. Stephen Wilson: You argue against that disconnection hypothesis? I think it's a pretty compelling argument. So many of your analyses kind of play off the arcuate fasciculus versus Broca's area. I wonder if like a stronger candidate for a cortical predictor of speech production deficits might have been ventral premotor cortex. As you guys know, this is the area where stimulation actually leads to speech arrest as opposed to Broca's area. Did you do any analyses where you looked at whether ventral premotor cortex might contribute to predicting long-term deficits?
Dr. Diego Lorca-Puls: Indeed. Damage to the ventral lateral premotor cortex is a significant predictor of speech production scores when analyzed in isolation. However, as soon as the effect of damage to anterior arcuate fasciculus is controlled for, this relationship stops being statistically significant. In fact, in the paper, we showed that more than 80% of the contribution of damage to the ventral lateral premotor cortex to long-term speech production outcome can be explained by co-occurring damage to the anterior arcuate fasciculus. This is consistent with the findings from van Geeman et al. reported in 2014, where the partial resection, the partial or complete resection, actually, of tumors infiltrating the ventral lateral premotor cortex only resulted in transient speech production deficits.
10.
Prof. Stephen Wilson: You conclude, in your discussion, you say, I'm going to quote, “we are not refuting the role that Broca's area has been shown to play in speech production in the undamaged brain. But we are challenging the long-held assumption that damage to Broca's area contributes to long term speech production impairments after stroke”. So if you think that Broca’s area does play a role in normal speech production, then how can it be that damaging it doesn't have a long-term effect?
Dr. Diego Lorca-Puls: Our findings indicate that Broca's area is not as critical for speech production, as commonly thought, because we have shown that damage to Broca's area doesn't contribute to long-term speech production outcome after a stroke. However, many studies of the undamaged brain have shown that Broca's area does play a role in speech production. This apparent discrepancy might be explained by the effect of recovery. In other words, it might be the case that the recovery potential is much greater after damage to Broca's area than the anterior arcuate fasciculus, as an increasing number of studies have started to show. For example, the results reported by Herbert et al. in Brain in 2016, based on intraoperative mapping in patients with brain tumors, suggest that the degree of functional compensation is generally high after cortical damage, and low after white matter damage. However, strokes and tumors are not the same things. So future longitudinal studies are needed to investigate the speech production recovery in the stroke patients with relatively focal damage to Broca's area, or anterior arcuate fasciculus.
11.
Prof. Stephen Wilson: You've kind of argued against the effect of the arcuate fasciculus as being a disconnection of Broca's area. How do you think the damage to the anterior arcuate fasciculus exerts its long-term effect on speech production?
Dr. Andrea Gajardo-Vidal: Yeah, so we have already stated why its disconnection of Broca's area cannot logically explain our results. It is possible, however, that the long-lasting effect of damage to the anterior arcuate fasciculus on speech production might be the consequence of this rapid functional integration among the multiple regions in inferior frontal, inferior parietal, and inferior temporal cortices that are involved in speech production. So in other words, I would say that damage to anterior arcuate fasciculus might disrupt a substantial part of the speech production network, thereby resulting in speech production impairments. So that's my view about it.
12.
Prof. Stephen Wilson: Do you want to talk about how your findings sort of converge with this prior work as well as how you extend it?
Dr. Diego Lorca-Puls: So, our study was certainly informed and motivated by previous work. For example, the importance of the anterior arcuate fasciculus, as you have said, for a speech production had already been highlighted by Fridriksson et al. who showed the damage to this white matter tract was associated with nonfluent speech production in chronic stroke patients. We were able able to replicate and extend these findings in a much larger sample with stroke patients. On the other hand, some unique aspects of our study is that we focus on the effect of damage to Broca's area in the context of relatively focal left frontal strokes. We tested Broca's area, this connection hypothesis, by conducting post-hoc group comparisons on a small group of patients with different lesion sites. We also provided evidence for the absence of a long-lasting effect of damage to Broca's area on speech production, which is much more informative than just showing a lack of significant association. And finally, we showed that more than 70% of the influence of damage to different parts of the posterior inferior frontal cortex on speech production can be explained by conquering damage to the anterior arcuate fasciculus, which is consistent with the lesion sites of Paul Broca's two historic cases, both of whom had co-ocurring damage to the anterior arcuate fasciculus.
Reference
Gajardo-Vidal A, Lorca-Puls DL, Team P, Warner H, Pshdary B, Crinion JT, Leff AP, Hope TMH, Geva S, Seghier ML, Green DW, Bowman H, Price CJ. Damage to Broca’s area does not contribute to long-term speech production outcome after stroke. Brain 2021; doi: 10.1093/brain/awaa460. [doi]
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编辑：闫玉萌 赵欣宇 雷晨
排版：闫玉萌 赵欣宇 雷晨
审校：李芳芳 田英慧
英文编审责任人：赵欣宇