Brain regions essential for word comprehension: Drawing inferences from patients

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A core aim of modern neuroscience is to identify the anatomical cortical networks underlying specific cognitive functions. It is widely agreed that although functional neuroimaging has provided substantial insights into networks engaged in particular cognitive tasks, these studies reveal areas where activity is correlated with task performance, but not necessarily critical for that task.1 Lesion–deficit association studies provide a complementary methodology, revealing areas essential for the task. The assumption is that if an individual has impairment of a particular function following brain damage, the lesioned region must have been necessary for that function. However, the opposite inference—if there is damage to a particular area, and the individual does not have impairment in a function, that area must not be necessary for that function—does not necessarily follow. This latter assumption will be false when (1) other brain regions have assumed the function of the damaged area (eg, in the course of recovery after stroke, or over time in the presence of slow‐growing tumors3 or chronic brain disease4) or (2) damage to the critical area is insufficient to cause a detectable impairment due to residual function of surviving portions—the so‐called partial‐injury problem.5
Here we examine the strength of evidence, and conclusions that can be drawn, from lesion–deficit association studies, illustrating with studies of auditory word comprehension in stroke. We chose spoken word comprehension because this topic has recently engendered controversy. Whereas many previous studies from autopsy,6 direct cortical stimulation,7 and stroke have indicated that superior temporal gyrus posterior to the temporal pole (pSTG) is necessary for auditory word comprehension, a recent study of primary progressive aphasia (PPA) shed doubt on this conclusion.8 The investigators found that 7 of 72 patients with PPA had peak cortical thinning in left temporoparietal cortex, but relatively intact word comprehension. Although at a group level, areas of cortical thinning associated with word comprehension error rate included parts of pSTG, results were interpreted as evidence against classical thinking that Wernicke's area (defined as pSTG, middle temporal gyrus, and inferior parietal cortex) is critical for auditory word comprehension.
The article by Mesulam and colleagues illustrates that studies of neurodegenerative disorders may complement studies of patients with acute lesions and chronic lesions to help understand brain function.8 Their study emphasized the role of areas beyond the usual bounds of Wernicke's area in word comprehension. Although this information is important for identifying the entire network of brain regions that support word comprehension, consideration of focal lesion studies is also necessary to put these findings into context.
Here we focus on lesion studies that have evaluated areas critical for auditory word comprehension, and touch on areas critical for sentence comprehension. Both entail numerous cognitive functions (Table), and each function likely relies on a complex cortical–subcortical network. We cannot review all areas involved in all of these functions underlying comprehension. For example, a vast literature is devoted to the neural representation of semantics, showing broadly distributed areas including the bilateral anterior and inferior temporal cortex represent object semantics.9 To elucidate our points, we review studies of acute and chronic stroke patients that have evaluated the role of pSTG in auditory comprehension. We propose that lesion studies can use a variety of approaches to evaluate associations between deficits and tissue damage or dysfunction, but should rely on positive (rather than null) results. Furthermore, the strongest evidence is obtained when results from a variety of approaches converge on the same conclusions.
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