Conduction aphasia

            Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia, thought to be caused by a disruption in the fiber pathways connecting Wernicke's and Broca's areas. The arcuate fasciculus has previously been implicated as this fiber bundle, however more recent evidence suggests that the extreme capsule connects Wernicke's and Broca's areas.

             Broca's area and Wernicke's area

Presentation

Patients with conduction aphasia show the following characteristics:

•           speech is fluent

•           comprehension remains good

•           oral reading is poor

•           Major Impairment in repetition

•           many phonemic paraphasias (phone substitution errors)

•           transpositions of sounds within a word ("television" → "velitision") are common.

            To understand the symptoms, recall that Broca's area is associated roughly with expression, Wernicke's area with comprehension.

            With both areas intact but the neural connections between them broken, there is the curious condition where the patient can understand what is being said but cannot repeat it (or repeats it incorrectly). This patient will also end up saying something inappropriate or wrong, realize his/her mistake, but continue making further mistakes while trying to correct it.

Causes

Conduction aphasia is caused by damage in the language-dominant hemisphere (the left hemisphere in most individuals). Basically, the phonological systems involved in speech output are impaired. Lesions in the language centers (and connections between) have been identified as potential inducers for conduction aphasia (and other language disorders, in general). Specifically, patterns of damage in conduction aphasia patients have been observed to cluster in the posterior and inferior temporal lobe, and in the parietal-temporal junction.

The brain damage causing conduction aphasia is often from a stroke, which can produce both localized and widespread damage. Traumatic brain injury and tumors can also lead to localized lesions, with potential to cause conduction aphasia. Conduction aphasia can also be seen in cases of cortical damage without subcortical extensions. 

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.

Diagnosis

Conduction aphasics are capable of normal conversation, so freely conversing is the first opportunity for noticing signs of the disorder. Patients will speak normally, but include occasional paraphasias. When asked to repeat something, the patient will be unable to do so without significant difficulty, repeatedly attempting to self-correct (conduite d'approche). When asked a question, however, patients can answer spontaneously and fluently.

Several standardized test batteries exist for diagnosing and classifying aphasias. These tests are capable of identifying conduction aphasia with relative accuracy. The Boston Diagnostic Aphasia Examination (BDAE) and the Western Aphasia Battery (WAB) are two commonly used test batteries for diagnosing conduction aphasia. These examinations involve a set of tests, which include asking patients to name pictures, read printed words, count aloud, and repeat words and non-words (such as shwazel).

Treatment

Treatment for aphasias is generally individualized, focusing on specific language and communication improvements, and regular exercise with communication tasks. Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery. However, conduction aphasia is a mild aphasia, and conduction aphasics score highly on the WAB at baseline.