Anatomy of aphasia revisited

Abstract

In most cases, aphasia is caused by strokes involving the left hemisphere, with more extensive damage typically being associated with more severe aphasia. The classical model of aphasia commonly adhered to in the Western world is the Wernicke-Lichtheim model. The model has been in existence for over a century, and classification of aphasic symptomatology continues to rely on it. However, far more detailed models of speech and language localization in the brain have been formulated. In this regard, the dual stream model of cortical brain organization proposed by Hickok and Poeppel is particularly influential. Their model describes two processing routes, a dorsal stream and a ventral stream, that roughly support speech production and speech comprehension, respectively, in normal subjects. Despite the strong influence of the dual stream model in current neuropsychological research, there has been relatively limited focus on explaining aphasic symptoms in the context of this model. Given that the dual stream model represents a more nuanced picture of cortical speech and language organization, cortical damage that causes aphasic impairment should map clearly onto the dual processing streams. Here, we present a follow-up study to our previous work that used lesion data to reveal the anatomical boundaries of the dorsal and ventral streams supporting speech and language processing. Specifically, by emphasizing clinical measures, we examine the effect of cortical damage and disconnection involving the dorsal and ventral streams on aphasic impairment. The results reveal that measures of motor speech impairment mostly involve damage to the dorsal stream, whereas measures of impaired speech comprehension are more strongly associated with ventral stream involvement. Equally important, many clinical tests that target behaviours such as naming, speech repetition, or grammatical processing rely on interactions between the two streams. This latter finding explains why patients with seemingly disparate lesion locations often experience similar impairments on given subtests. Namely, these individuals' cortical damage, although dissimilar, affects a broad cortical network that plays a role in carrying out a given speech or language task. The current data suggest this is a more accurate characterization than ascribing specific lesion locations as responsible for specific language deficits.5705668782001awx363media15705668782001.

Figure 1

Univariate RLSM (red-yellow) and CLSM (blue-green) results for each of the speech and language tests. For CLSM, both colour intensity and link thickness denote how strongly damage to a given link predicts speech or language test performance. AQ = aphasia quotient; AOS = apraxia of speech; N.S. = non-significant.

Figure 2

Multivariate RLSM (blue-green) and CLSM (red-yellow) results for each of the speech and language tests. Note that the colour scales represent amount of variance (R²) explained by each region of interest or link. AQ = aphasia quotient; AOS = apraxia of speech.

Figure 3

Univariate and multivariate analyses of RLSM and CLSM data derived from the PCA analysis of speech comprehension and speech production tests/tasks. The top panel shows results from component 1 and the bottom panel shows component 2. The left images show univariate results whereas the right images show multivariate results. Note that the scales form the univariate (Z-scores) and multivariate (R²) analyses are different.