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.[1] 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.[1] 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.[1] 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.[2]
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.[1]
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.[3] 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.[4]
^ abcdBrookshire, R. H. (2007). Introduction to Neurogenic Communication Disorders. St. Louis, MO: Mosby.
^Zakariás, Lilla; Keresztes, Attila; Demeter, Gyula; Lukács, Ágnes (2013-12-01). "A specific pattern of executive dysfunctions in transcortical motor aphasia". Aphasiology. 27 (12): 1426–1439. doi:10.1080/02687038.2013.835783. ISSN 0268-7038.
^Gold; et al. (1997). "Adynamic Aphasia: A Transcortical Motor Aphasia with Defective Semantic Strategy Information". Brain and Language. 3 (57): 374–393. doi:10.1006/brln.1997.1750. PMID 9126422. S2CID 24469031.
^PhD, Alfredo Ardila (2010-03-01). "A proposed reinterpretation and reclassification of aphasic syndromes". Aphasiology. 24 (3): 363–394. doi:10.1080/02687030802553704. ISSN 0268-7038.
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