Carl Wernicke was the first scientist to describe conducting aphasia. It is manifested in the disruption of verbatim repetition with the relative preservation of expressive speech and understanding of it. Previously, this type of aphasia was associated with white matter pathways and left temporoparietal zones. The authors of the study set their task to prove that the cause of the conduct aphasia is lesions in another part of the brain – in area Spt. This area was discovered in the posterior-most portion of the left planum temporale with the help of functional magnetic resonance imaging (fMRI). Scientists also identified the critical importance of this area for phonological working memory. First, Buchsbaum et al. (2011) hypothesize that area Spt plays an essential role in integrating sensory-motor representations that affect sound sequences’ perception. Second, using 105 fMRI images, they seek to prove that the injuries in the Spt area, rather than in others, are directly related to the conduct aphasia.
Summing up their research, the authors indicate that their hypothesis that conducting aphasia develops as a result of area Spt damage has significant grounds. Area Spt is a sensory-motor area that integrates the vocal tract action system (Buchsbaum et al., 2011). The research results fill several gaps in the problem of studying aphasia, for example, repetition deficit and phonetic paraphasia, retained understanding, and problems with short-term phonological memory. Buchsbaum et al. (2011) also provide similarities and differences with the Wernicke proposal. They argue that their work results significantly expand the possibilities for studying speech processing networks and, in particular, conducting aphasia.
Lesion-definition mapping helped determine the maximum overlap of lesions in patients with aphasia. Examination of MRI images showed active areas when using short-term phonological memory in healthy study participants. They also demonstrated that while understanding and production of speech, the perception of music, actions, similar to the more studied signals, sensory-motor areas occur in the area Spt. Moreover, Spt responds to visual signs accompanying speech, like lips moving. In this case, phonological time memory is an emergent property of such a system. That is, without MRI, it would not have been found that Spt is a sensory-motor area for the speech tract. Applying a map of damages and activity during MRI was also found to be Spt damage and is the cause of aphasia. Thus, studying together fMRI images and lesions form the basis of the study. In the absence of one of them, a connection between the disorder and a certain area of the brain would not have been established.
The conclusions proposed by the authors are partially compatible with Wernicke’s vision of conduction aphasia. In both proposals, scientists use auditory-motor disruption to search for the causes of this disorder. However, the new research significantly expands the context of conducting an aphasia study, as the original vision also focuses on a white matter pathway. Buchsbaum et al. (2011), in turn, are sure that auditory-motor interaction is connected to a cortical network. Moreover, they explain the retained ability to understand the speech when conducting aphasia by the bilateral structure of auditory phonological systems of processing (Buchsbaum et al., 2011). Such results and the hypothesis that auditory-motor integration for all vocal tract actions is similar to other sensory-motor integration systems open up a wider field for studying speech systems.
References
Buchsbaum, B. R., Baldo, J., Okada, K., Berman, K. F., Dronkers, N., D’Esposito, M., & Hickok, G. (2011). Conduction aphasia, sensory-motor integration, and phonological short-term memory–an aggregate analysis of lesion and fMRI data. Brain and language, 119(3), 119-128. Web.