These terms refer to disorders of language that result not from lesions of the cortical language areas themselves but from an apparent interruption of association pathways joining the primary receptive (sensory, auditory, and visual) areas to the language areas. Included also in this category are aphasias from lesions that separate the more strictly receptive parts of the language mechanism itself from the purely motor ones (conduction aphasia; see the following text) and to lesions that isolate the perisylvian language areas, separating them from the other parts of the cerebral cortex (transcortical aphasias).
The anatomic basis for most of these so-called disconnection syndromes is only partly defined. The theoretical concept is an interesting one and emphasizes the importance of afferent, intercortical, and efferent connections of the language mechanisms. However, the locale of the lesion that causes loss of a language function does not localize the language function itself, a warning enunciated long ago by Hughlings Jackson. Nevertheless, the language disorders described below occur with sufficient regularity and clinical uniformity to be almost as useful as the more common types of aphasia in localization and in revealing the complexity of language functions.
As indicated earlier, Wernicke theorized that certain clinical symptoms would follow a lesion that effectively separated the auditory and motor language areas without directly damaging either of them. Since then a number of well-studied cases have been described that conform to his proposed model of Leitungsaphasie (conduction aphasia), which is the name he gave it. The characteristic feature is severely impaired repetition of spoken language; the defect applies to both single words and nonwords. The second essential feature is reduced but still relatively preserved comprehension in comparison to Wernicke aphasia. In other respects, the features of conduction aphasia resemble those of a mild Wernicke aphasia. They share fluency and paraphasias in self-initiated speech, in repeating what is heard, and in reading aloud; writing is also similarly impaired. Dysarthria and dysprosody are usually lacking. Speech output is normal or somewhat reduced. As mentioned, comprehension is by no means perfect, but compared with one who has Wernicke aphasia, the patient with conduction aphasia has relatively little difficulty in understanding words that are heard or seen and is aware of his deficit.
The lesion in the few autopsied cases has been located in the cortex and subcortical white matter in the upper bank of the left sylvian fissure, usually involving the supramarginal gyrus and occasionally the most posterior part of the superior temporal region. The reason for classifying this aphasia as a disconnection syndrome according to Damasio and Geschwind is that the Wernicke and Broca areas are spared, and the critical structure involved is the connection between them—the arcuate fasciculus. This fiber tract streams out of the temporal lobe, proceeding somewhat posteriorly, around the posterior end of the sylvian fissure; there it joins the superior longitudinal fasciculus, deep in the anteroinferior parietal region, and proceeds forward, deep to the suprasylvian operculum, to the motor association cortex, including the Broca and Exner areas (see Fig. 23-1). However, in most of the reported cases, including those described by the Damasios, the left auditory complex, insula, and supramarginal gyrus were also involved. In any case, the usual cause of conduction aphasia is an embolic occlusion of the ascending parietal or posterior temporal branch of the middle cerebral artery, but other forms of vascular disease, particularly small subcortical hemorrhage, neoplasm, or trauma in this region produce the same syndrome.
Transcortical Aphasias (Preservation of Repetition)