Conduction Aphasia - Pathophysiology

Pathophysiology

Traditionally, it has been believed that conduction aphasia was the result of a lesion in the arcuate fasciculus, a deep, white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. It was thought that this bundle transmitted information between Wernicke's area (responsible for language comprehension) and Broca's area (responsible for language production). Wernicke, and later Lichtheim and others, theorized that a disconnect between these two regions caused patients to fail to monitor speech and limited their ability to transfer information between comprehension and production functions, thus leading to paraphasic errors and a deficit in repetition of auditory input. This hypothesis fits well with the Wernicke-Geschwind model of language, which compartmentalizes and localizes speech comprehension and production.

Although the disconnection hypothesis explains many of the conditions associated with conduction aphasia, clinical evidence is lacking, and the Wernicke-Geschwind model has since become obsolete. There have been no known autopsy cases in which conduction aphasia was shown to be the result of a focused arcuate fasciculus lesion. Surveys of conduction aphasics with anatomical confirmation show that in nearly all patients, there was damage to portions of the cortex as well. Furthermore, there are reports of patients with severe disruption of the arcuate fasciculus who show no symptoms of conduction aphasia (although it is plausible that the contralateral hemisphere facilitated repetition in these cases).

Recent research has pointed to a different explanation for conduction aphasia, similar to Wernicke's, which is based on newer models suggesting language is facilitated by "cortically based, anatomically distributed, modular networks." Anderson et al. describe an experiment in which electrical stimulation of the left posterior superior temporal cortex in a human subject induced symptoms consistent with conduction aphasia, indicating that a deep brain disconnection is not necessary. While this study does not completely discredit the disconnection hypothesis, but does point to a system in which transmission of spoken language information involves more than just the arcuate fasciculus. Regardless of the role that the arcuate fasciculus plays in the disorder, the cortical component cannot be denied.