Conduction Aphasia

Characterization of Conduction Aphasia

Conduction aphasia, first identified in 1874 by Carl Wernicke, is an acquired disorder of language, typically caused by stroke, that is characterized by frequent phonemic paraphasias (sound-based speech errors) with attempts at self-correction, impaired verbatim repetition, naming difficulties, but otherwise fluent and grammatical speech output. Auditory comprehension is relatively spared. The deficits in conduction aphasia are exacerbated with increasing phonological load such as when the task involves multisyllabic words, phrases, and/or reduced semantic content. The three major symptoms all point to a deficit at the phonemic level of processing. The paraphasias tend to be phonemic level errors [Page 182](sound based errors such as strool for stool or cokie for cookie), the repetition deficit appears to reflect dysfunction of phonological short-term memory (ability to immediately recall a list of words, numbers, or nonsense words), and the naming deficit is both aided by phonemic cueing (providing the first sound) and characterized by tip-of-the-tongue states, that sense of knowing the word or name one is looking for but failing to access it, which has been linked to failures to access phonological information during naming. Thus, while conduction aphasia is commonly referred to as a disorder of “repetition,” it is clear that the syndrome is not restricted to this one behavior. Instead, the disorder appears to involve a phonemic level of processing that is appreciable not only in repetition but also in other production-related tasks. Crucially, the phonemic level deficit does not substantially affect receptive functions as auditory comprehension is typically well preserved in conduction aphasia. Consistent with this, it has been observed that conduction aphasics often get the gist of sentences that they fail to repeat. For example, one patient, when asked to repeat the phrase, The pastry cook was elated, responded with Something about a happy baker.

The Classical Interpretation

Classically, conduction aphasia was thought to result from damage to a white matter bundle, the arcuate fasciculus, which resulted in a disconnection of the two major speech centers, Wernicke's and Broca's area. This is no longer a viable model, however, because damage to the arcuate fasciculus is not associated with conduction aphasia, and because cortical stimulation of the left posterior temporal lobe is sufficient to cause the symptoms of conduction aphasia. Recent evidence suggests instead that conduction aphasia is caused by damage to the left posterior superior temporal gyrus and/or the left supramarginal gyrus, that is, a location centered around the left planum temporale/parietal operculum (see Figure 1).

Figure 1 Three-dimensional rendering of a human brain, left hemisphere

Conduction Aphasia as a Short-Term Memory Deficit

Modern theorists have suggested that the repetition deficit in conduction aphasia results from a disruption of phonological short-term memory. On this view, the phonological trace fades too quickly in conduction aphasics to allow for accurate verbatim repetition of speech, whereas comprehension is spared because access to semantic representations is less dependent on phonological working memory. Consistent with this view is the observation that conduction aphasics can be impaired on tests of phonological short-term memory and often get the gist of a sentence without retaining a memory for the specific words used. This clearly explains one aspect of the symptom cluster in conduction aphasia but does not alone explain the other phonological-level symptoms of conduction aphasia such as the naming deficit and phonemic paraphasias. It is possible that the short-term memory deficit and the other phonological symptoms stem from damage to different neural subsystems that happen to be damaged in conduction aphasia.

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