Transcortical motor aphasia

Transcortical motor aphasia (TMoA), also known as commissural dysphasia and white matter dysphasia, results from damage, typically due to cerebrovascular accident (CVA), in the anterior superior frontal lobe of the language-dominant hemisphere. The left hemisphere usually performs language functions, although left-handed individuals have been shown to perform language functions with both their right and left hemispheres. Damage in the watershed region does not directly damage the areas of the brain involved in language production or comprehension; instead, the damage isolates these areas from the rest of the brain.[1] Due to damage in areas of the frontal lobe, executive functions related to language use are often affected in individuals with TMoA. Relevant executive functions include activating language responses and controlling syntax (grammar) and narrative discourse, which can lead to difficulties forming complex sentences, choosing which words to use appropriately, and initiating speech in conversation.[2] The extent of brain damage will impact how much language functioning is impaired (i.e. damage deep to the frontal lobe and/or damage across multiple regions will greatly impair language). Right hemiparesis, which is right-sided paralysis, may occur along with TMoA if the lesion in the anterior frontal lobe is large enough and extends into the posterior frontal lobe.[1] There are also other forms of aphasias that are a result of TMoA. Adynamic aphasia is one example; it is a form of TMoA characterized by sparse speech. Adynamic aphasia has normal spontaneous speech due to the fact that when new concepts are introduced by external stimuli, spontaneous speech improves. This is a result of executive functioning in the frontal lobe.[3]

Characteristics

TMoA is a type of non-fluent aphasia with a lower occurrence than Broca’s aphasia. TMoA often resembles Broca’s but with preserved repetition.[4] A person with TMoA may be echolalic and can repeat long complex phrases effortlessly.[5] People with TMoA generally have good auditory comprehension since the arcuate fasciculus and Wernicke's area are not impaired. However, they have a reduced speech output due to damage in the left anterior superior frontal lobe.[4] A person with TMoA has difficulty producing spontaneous speech and their utterances are usually one to two words long. When they do speak, their speech is well articulated although sparse.[5] Initiation is also a problem due to damage in the prefrontal cortex. For instance, someone with TMoA might not be able to answer open-ended questions but would be able to answer yes/no questions.[6]

Causes

TMoA is caused by damage in the anterior superior frontal lobe of the language-dominant hemisphere, which is typically the left hemisphere.[1] Such damage is most commonly a result of a stroke, but other causes include brain tumors, traumatic brain injury and progressive neurological disorders.[7] The anterior frontal lobes are responsible for initiation and maintenance of purposeful activity. In regards to TMoA, damage to the anterior frontal lobes affects the purposeful activity of speech output, impacting one’s ability to communicate verbally.[1]

Diagnosis

The signs and symptoms of transcortical motor aphasia are typically recognized first by a neurologist after a stroke or a type of brain injury.[8] If TMoA is suspected, the neurologist will refer the individual to a speech-language pathologist (SLP) to complete a comprehensive evaluation of the patient. A comprehensive evaluation most often includes the use of standardized and/or nonstandardized tests to evaluate the individual's overall communication and language skills.[8] These tests will look for the patient's ability to speak, listen, read, write, understand and use their language, as well as the ability to swallow.[1] During the evaluation, the SLP will determine the individual's strengths and deficits in communication and the impact of the deficits on the person's quality of life.[8] This comprehensive evaluation will help professionals to determine the proper diagnosis for the individual. The key characteristic for the diagnosis of TMoA is the patient's ability to repeat.[9] The ability to easily repeat speech is a leading factor when differentiating TMoA from other diagnoses of aphasia.[5][9] Likely, when an individual's repetition is spared after a stroke or brain injury, a professional will diagnose the patient with transcortical motor aphasia.

Treatment

Individuals with TMoA experience difficulties with fluency of speech, but generally have good repetition and auditory comprehension. There are specific therapy tasks that are beneficial for individuals with TMoA based on their language abilities.[10] In general, speech-language pathologists can use information processing tasks to help restore expressive communicative abilities for individuals with TMoA. Types of intervention strategies include naming objects, describing object functions, and answering yes/no questions about materials. Speech-language pathologists can provide scaffolding techniques for individuals with TMoA to help them formulate sentences and engage in conversational turn-taking.[11]

More specifically, reduced syntax therapy has helped patients overcome their non-fluent speech and agrammatism that often occurs as a result of TMoA. Because agrammatism inhibits the patient's ability to form grammatically correct sentences,[12] this type of treatment involves reducing these agrammatic deficits and teaching the patient to use linguistic structures that simplify the message that want to convey. Reduced syntax therapy helps the patient's language production to be more productive and efficient.[12]

From a neuroscience perspective, research has found that a dopamine agonist, bromocriptine, has provided positive outcomes during intervention for non-fluent types of aphasia, such as TMoA or adynamic aphasia.[13] Studies have found that bromocriptine increased neural networks to assist with the initiation of speech in individuals who possess non-fluent characteristics of speech.[14] With regard to intensity and duration of treatment, studies reported maximum recovery when intense weekly therapy (approximately 8 hours per week) was delivered over a 2–3 month period.[15]

Prognosis

In relation to other types of aphasia, TMoA occurs less frequently, so there is less information on prognosis. In a study involving eight patients with border zone lesions, initially after the stroke all patients presented with transcortical mixed aphasia. Three of these patients made a complete recovery within a few days post-stroke. For three other patients with more anterior lesions, their aphasia transitioned to TMoA. All participants in the study regained full language abilities within 18 months following their stroke.[16] This suggests long term prognosis for patients with TMoA is positive, however; more studies need to be completed in order to solidify these findings.

Other factors need to be considered when determining prognosis for a patient with TMoA. One factor includes location and site of lesion. Since the lesion that results in TMoA occurs in the watershed area and does not directly involve the areas of the brain responsible for general language abilities, prognosis for these patients is good. Other factors that determine a patient’s prognosis include age, education prior to the stroke, gender, motivation, and support.[17]

See also

References

  1. 1 2 3 4 5 Brookshire, R. H. (2007). Introduction to Neurogenic Communication Disorders. St. Louis, MO: Mosby.
  2. ↑ 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. ISSN 0268-7038. doi:10.1080/02687038.2013.835783.
  3. ↑ 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.
  4. 1 2 Manasco, M. Hunter. Introduction to Neurogenic Communication Disorders. Jones & Bartlett Learning. ISBN 9781449652449.
  5. 1 2 3 "Transcortical motor aphasia".
  6. ↑ Goodglass, Harold; Kaplan, Edith (1983). The Assessment of Aphasia and Related Disorders. Lea & Febiger.
  7. ↑ American Speech-Language-Hearing Association. "Aphasia". Retrieved 2015. Check date values in: |access-date= (help)
  8. 1 2 3 "Aphasia: Assessment". American-Speech-Language-Hearing Association. 2015. Retrieved 2015. Check date values in: |access-date= (help)
  9. 1 2 Rogalsky, Corianne; Poppa, Tasha; Chen, Kuan-Hua; Anderson, Steven W.; Damasio, Hanna; Love, Tracy; Hickok, Gregory (2015). "Speech repetition as a window on the neurobiology of auditory-motor integration for speech: A voxel-based lesion symptom mapping study". Neuropsychologia. 71: 18–27. PMC 4417364 Freely accessible. PMID 25777496. doi:10.1016/j.neuropsychologia.2015.03.012.
  10. ↑ Cicerone KD, Langenbahn DM, Braden C, et al. (2011). "Evidence-based cognitive rehabilitation: Updated review of the literature from 2003 through 2008". Archives of Physical Medicine and Rehabilitation. 92 (4): 519–530. PMID 21440699. doi:10.1016/j.apmr.2010.11.015.
  11. ↑ Shigaki CL, Frey SH, Barrett AM (2014). "Rehabilitation of poststroke cognition". Medscape. 34 (5): 496–503.
  12. 1 2 Ruiter MB, Kolk HH, Rietveld TC (2010). "Speaking in ellipses: the effect of a compensatory style of speech on functional communication in chronic agrammatism". Neuropsychological Rehabilitation. 20 (3): 423–58. PMID 20155573. doi:10.1080/09602010903399287.
  13. ↑ Pulvemüller F, Bethier ML (2008). "Aphasia therapy on a neuroscience basis". Aphasiology. 22 (6): 563–599. PMC 2557073 Freely accessible. PMID 18923644. doi:10.1080/02687030701612213.
  14. ↑ Berthier ML, Starkstein SE, Leiguarda R, Ruiz A, Mayberg HS, Wagner H, et al. (1991). "Transcortical aphasia: Importance of the nonspeech dominant hemisphere in language repetition". Brain. 114 (3): 1409–1427. doi:10.1093/brain/114.3.1409.
  15. ↑ Bhogal SK, Teasell R, Speechley M (2003). "Stroke: Intensity of aphasia therapy, impact on recovery". Stroke. 34 (4): 987–993. doi:10.1161/01.STR.0000062343.64383.D0.
  16. ↑ Flamand-Roze, C.; Cauquil-Michon, C.; Roze, E.; Souillard-Scemama, R.; Maintigneux, L.; Ducreux, D.; Adams, D.; Denier, C. (2011-12-01). "Aphasia in border-zone infarcts has a specific initial pattern and good long-term prognosis". European Journal of Neurology. 18 (12): 1397–1401. ISSN 1468-1331. PMID 21554494. doi:10.1111/j.1468-1331.2011.03422.x.
  17. ↑ Thompson, Cynthia (2000). "Neuroplasticity: Evidence from aphasia". J Commun Disord. 33 (4): 357–366. PMC 3086401 Freely accessible. PMID 11001162.


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