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. 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. 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. 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. of the left, or language-dominant, hemisphere. The damage leaves the major language networks, Broca's and Wernicke’s areas and the arcuate fasiculus, unaffected.

Diagnosis

TMoA is diagnosed by the referring physician and speech-language pathologist (SLP). The overall sign of TMoA is nonfluent, reduced, fragmentary echoic, and perseverative speech with frequent hesitations and pauses. The hallmark sign of TMoA is intact repetition in the presence of these signs and symptoms. In general for individuals with TMoA, treatment should capitalize on their strong auditory comprehension and repetition skills and address the individual's reduced speech output and difficulty initiating and maintaining a conversation. Based on the specific needs of the patient, SLPs can provide a variety of treatment activities.

To improve word retrieval and initiation difficulties, clinicians may use confrontation naming in which the patient is asked to name various objects and pictures. Depending on the severity, they may also use sentence completion tasks in which the clinician says sentences with the final word(s) missing and expects the patient to fill in the blank.

To increase speech output, the clinician may provide a set of pictures and prompt the patient to describe or elaborate on the events pictured. The clinician can also provide spoken or written words and prompt the patient to use the words in a sentence.

To improve conversational skills, SLPs may engage the patient in structured conversations in which supports are provided to help the patient take appropriate conversational turns, maintain the topic of conversation, and formulate appropriate sentences. Clinicians often need to provide pragmatic guidelines so that the patient's responses go beyond the clinician's request and so the clinician does not do the majority of the talking.

In order to improve the patient's abilities to functionally communicate in their natural settings, the SLP will provide strategies and techniques to enhance their success in communicative settings (i.e. supplementing speech with nonverbal communication).

Additionally, they may train the patient's communication partners to support the conversational abilities of the patient by facilitating the use of preserved cognitive and social functions. Research supports the use of various partner training programs such as Supported Conversation for Adults with Aphasia from the Aphasia Institute. In this program, the focus is put on acknowledging the patient's competence and helping them to reveal that competence. Strategies include saying “I know you know” when appropriate, using gestures to supplement messages, limiting background noise, and given sufficient time for response.

From a neuroscience perspective, research has found that a dopamine agonist, bromocriptine, taken by mouth, has provided positive outcomes during intervention for non-fluent types of aphasia, such as TMoA or adynamic aphasia. Studies have found that bromocriptine increased neural networks which assist with the initiation of speech in individuals who possess non-fluent characteristics of speech.

In order to capitalize on neuroplasticity for treatment of all types of aphasia, timing, intensity, duration, and repetition of treatment should be taken into consideration. Research has found that aphasia treatment initiated during the earlier acute post-injury phase is more effective compared to treatment initiated in the chronic phase. With regard to intensity and duration of treatment, studies reported maximum recovery occurred with intense weekly therapy (approximately 8 hours per week) was delivered over a 2–3 month period. Other research shows that distributed therapy may be more beneficial than high intensity therapy. More research is needed to determine which is best, but it may be found that the ideal duration and intensity of therapy is variable depending on the patient and their needs.

Prognosis

In relation to other types of aphasia, TMoA occurs less frequently, so there is less information on its prognosis. This suggests a positive long-term prognosis for patients with TMoA. However, this might not be the case for all patients and more research is needed in order to solidify these findings. Another study found that prognosis of TMoA is affected by lesion size. Smaller lesions typically cause delays in speech initiation; whereas, larger lesions lead to more profound language abnormalities and difficulty with abstract language abilities. Intensity, duration and timing of treatment all need to be taken in to consideration when choosing a course of treatment and determining a prognosis. In general, greater intensity leads to greater improvement. For duration, longer-term treatment produces more permanent changes. As for timing, beginning treatment too early may be difficult for the system which has not recovered enough to do intensive therapy, but beginning too late may result missing the window of the opportunity in which the most change can occur.

See also

  • Transcortical sensory aphasia

References

<br>

<!-- Categories below -->