Affected people are fully capable of understanding what they are hearing, but fail to encode phonological information for production.

These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, affecting confrontation tasks such as repetition, reading and naming in a similar manner.

Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech.

[10] Recent summaries about the syndrome show similarities between defective speech and writing and their relatively good comprehension.

Individuals with conduction aphasia are able to express themselves fairly well, with some word finding and functional comprehension difficulty.

[11] During an assessment of aphasia, the clinician usually examine the person's verbal fluency, comprehension, repetition, reading, writing, and naming.

Due to their relatively preserved auditory comprehension, conduction aphasics are capable of accurately monitoring, and attempting to correct, their own errors in speech output.

As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear.

[16]Conduction aphasia is caused by damage to the parietal lobe of the brain, especially in regards to the area associated with the left-hemisphere dominant dorsal stream network.

This results in disruption to the delayed auditory feedback network, causing the individual to have difficulty correcting themselves on speech repetition tasks.

Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery.

The main focus for during speech therapy for conduction aphasia person is to strengthen correct word usage and auditory comprehension.

These person 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.

Meanwhile, Carl Wernicke described person with receptive aphasia, who had damage to the left posterior superior temporal lobe, which he named "the area of word images".

Wernicke predicted the existence of conduction aphasia in his landmark 1874 monograph, Der Aphasische Symptomenkompleks: Eine Psychologische Studie auf Anatomischer Basis.

[22][23] Wernicke was influenced by Theodor Meynert, his mentor, who postulated that aphasias were due to perisylvian lesions.

[24] 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.

[21] 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.

[21] Studies showed that conduction aphasics had an intact 'inner voice', which discredited the central deficit model of Freud and Goldstein.

However, recent reviews and research have cast doubt on the singular role of the arcuate fasciculus and the model of spoken language in general.