Conduction Aphasia - History

History

In the late 19th century, Paul Broca studied patients with expressive aphasia. These patients had lesions in the anterior perisylvian region (now known as Broca's area), and produced halting and labored speech, lacking in function words and grammar. Comprehension is generally preserved, although there can be deficits in interpretation of complex sentences. In an extreme example, one of his patients could only produce a single syllable, "Tan".

Meanwhile, Carl Wernicke described patients with receptive aphasia, who had damage to the left posterior superior temporal lobe, which he named "the area of word images". These patients could speak fluently, but their speech lacked meaning. They had a severe deficit in auditory comprehension. The two disorders (expressive and receptive aphasias) thus seemed complementary, and corresponded to two distinct anatomical locations.

Wernicke predicted the existence of conduction aphasia in his landmark 1874 monograph, Der Aphasische Symptomenkompleks: Eine Psychologische Studie auf Anatomischer Basis. He was the first to distinguish the various aphasias in an anatomical framework, and proposed that a disconnection between the two speech systems (motor and sensory) would lead to a unique condition, distinct from both expressive and receptive aphasias, which he termed Leitungsaphasie. He did not explicitly predict the repetition deficit, but did note that, unlike those with Wernicke's aphasia, conduction aphasics would be able to comprehend speech properly, and intriguingly, would be able to hear and understand their own speech errors, leading to frustration and self-correction.

Wernicke was influenced by Theodor Meynert, his mentor, who postulated that aphasias were due to perisylvian lesions. Meynert also distinguished between the posterior and anterior language systems, leading Wernicke to localize the two regions. Wernicke's research into the fiber pathways connecting the posterior and anterior regions lead him to theorize that damage to the fibers under the insula would lead to conduction aphasia. Ludwig Lichtheim expanded on Wernicke's work, although he labeled the disorder commissural aphasia, to distinguish between aphasias tied to processing centers.

Sigmund Freud would argue in 1891 that the old framework was inaccurate; the entire perisylvian area, from the posterior to the anterior regions, were equivalent in facilitating speech function. In 1948 Kurt Goldstein postulated that spoken language was a central phenomenon, as opposed to a differentiated and disparate set of functionally distinct modules. To Freud and Goldstein, conduction aphasia was thus the result of a central, core language breakdown; Goldstein labeled the disorder central aphasia.

Later work and examination of brain structures, however, implicated the arcuate fasciculus, a white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. Norman Geschwind proposed that damage to this bundle caused conduction aphasia; the characteristic deficits in auditory repetition were due to failed transmission of information between the two language centers. Studies showed that conduction aphasics had an intact 'inner voice', which descredited the central deficit model of Freud and Goldstein. The Wernicke-Lichtheim-Geschwind disconnection hypothesis thus became the prevailing explanation for conduction aphasia. However, recent reviews and research have cast doubt on the singular role of the arcuate fasciculus and the model of spoken language in general.