Transcortical motor aphasia (TMoA), also known as commissural dysphasia or white matter dysphasia, results from damage in the anterior superior frontal lobe of the language-dominant hemisphere. This damage is typically due to cerebrovascular accident (CVA). TMoA is generally characterized by reduced speech output, which is a result of dysfunction of the affected region of the brain. The left hemisphere is usually responsible for performing language functions, although left-handed individuals have been shown to perform language functions using either their left or right hemisphere depending on the individual. The anterior frontal lobes of the language-dominant hemisphere are essential for initiating and maintaining speech. Because of this, individuals with TMoA often present with difficulty in speech maintenance and initiation. Damage in the watershed region does not directly harm the areas of the brain involved in language production or comprehension; instead, the damage isolates these areas from the rest of the brain. If there is damage to the frontal lobe, executive functions related to language use are often affected. Executive functions relevant to language include activating language responses, controlling syntax (grammar), and narrative discourse. Difficulties in these areas can lead to supplementary deficits involving difficulties forming complex sentences, choosing which words to use appropriately, and initiating speech in conversation. The extent and location of the brain damage will impact the degree and variety of language functioning characteristics (i.e. damage deep to the frontal lobe and/or damage across multiple regions will greatly impair language). Right hemiparesis, or right-sided paralysis, may coincide with TMoA if the lesion in the anterior frontal lobe is large enough and extends into the posterior frontal lobe. There are some other forms of aphasia that relate to TMoA. For instance, adynamic aphasia is a form of TMoA that is characterized by sparse speech. This occurs as a result of executive functioning in the frontal lobe. Another form of aphasia related to TMoA is dynamic aphasia. Patients with this form of aphasia may present with a contiguity disorder in which they have difficulty combining linguistic elements. For dynamic aphasia, this is most apparent when the patient is asked to sequence at the sentence level whereas for other aphasias contiguity disorder can be seen at the phoneme or word level.
Symptoms and signs TMoA is classified as a non-fluent aphasia that is characterized by a significantly reduced output of speech, but good auditory comprehension. Auditory comprehension skills remain intact because the arcuate fasciculus and Wernicke's area are not impaired. Individuals with TMoA also exhibit good repetition skills and can repeat long, complex phrases effortlessly and without error. However, spontaneous speech often presents with paraphasias (a wide category of speech errors that are caused by aphasia). Regardless of any relative communication strengths, individuals with TMoA are typically poor conversational partners. Due to damage in the anterior superior frontal lobe, people with TMoA have deficits in initiation and maintenance of conversations, which results in reduced speech output. A person with TMoA may seldom produce utterances and typically remain silent. The utterances that they do produce are typically only one to two words long. However, in more structured and predictable interactions, individuals with TMoA tend to respond more fluently and promptly. In addition, these individuals are characterized by their attentiveness and cooperation and are often described as being task-oriented.
Causes Neurological imaging has shown that TMoA is typically caused by an infarct of the anterior superior frontal lobe in the perisylvian area of the left, or language-dominant, hemisphere. The anterior superior frontal lobe is known as the prefrontal cortex which is responsible for the initiation and ideation of verbal speech. The damage leaves the major language networks, Broca's and Wernicke’s areas and the arcuate fasiculus, unaffected. Brain injury can result from a stroke caused by left anterior cerebral artery (ACA) occlusion, brain tumors, traumatic brain injury (TBI), or progressive neurological disorders.
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