Aphasia can be defined as an acquired deficit in language processing due to dysfunction in specific areas of the brain. The classic aphasias (Broca's, Wernicke's and Global) are representative of impairment in the very epicenters of language areas, thus inducing signs and symptoms that affect all levels of linguistic processing: phonological, syntactical, lexical, and semantic. However, there is a group of aphasias in which the lesion site spares the classic language areas, thus inducing more subtle signs and symptoms, and leading to a combination of linguistic symptoms mixed with those arising from other cognitive functions also affected by the same lesion. That is the case with the so called “transcortical aphasias” and “conduction aphasia”. Transcortical aphasias are classified as motor, sensory, and mixed. In transcortical motor aphasia (TCMA), the medial and the dorsolateral frontal lobes are compromised, interrupting the connections between these two systems and language areas; TCMA patients have impairment performance on tasks demanding speech generation (diminished fluency, impairment in narrative, and in the production of grammatically complex sentences), and a reduction in the motivation to engage in communication. In transcortical sensory aphasia (TCSA) there is a disorder in semantic processing, manifesting as comprehension and naming impairment, which indicates a disconnection between posterior language areas and semantic memory. In mixed transcortical aphasia (MTA) there is a combination of signs and symptoms of both TCMA and TCSA in varying degrees. Conduction aphasia, in which the core symptom is repetition deficit, represents a primary failure of the phonological loop.
Keywords: Aphasia, focal lesions, conduction aphasia, transcortical aphasias
