Abstract and Keywords
The defining symptoms of transcortical motor aphasia (TCMA) are nonfluent verbal output with relatively preserved repetition. Other symptoms, such as naming difficulties, agrammatic output, or even some paraphasias, may occur, but these are not cardinal symptoms defining TCMA and are not necessary for the diagnosis. The core anatomy involved in TCMA is a lesion of the medial frontal cortex, especially the left presupplementary motor area (pre-SMA) and adjacent Brodmann’s area 32; a lesion of the left posterior inferior frontal cortex, especially pars opercularis and ventral lateral premotor cortex; or a lesion of the pathways between these frontal structures. TCMA occasionally has been reported with a lesion of the left basal ganglia, the left thalamus, or the ascending dopaminergic pathways. From a cognitive standpoint, TCMA can be conceptualized as a disorder of intention, in other words, as a disorder of initiation and continuation of spoken language that is internally motivated. The medial frontal cortex provides the impetus to speak; this impetus to speak is conveyed to lateral frontal structures through frontal–subcortical pathways where it activates various language production mechanisms. The influence of the ascending dopaminergic pathways may occur either through their heavy connections with the pre-SMA region or through their influence on the basal ganglia. The influence of the basal ganglia and thalamus probably occurs through their connections with the medial frontal cortex. Assessments for TCMA should involve a thorough evaluation of conversational or narrative language output and repetition. New treatments are available that attempt to engage right-hemisphere intention mechanisms with left-hand movements and may be effective in TCMA. Although dopamine agonists have also shown some positive effects in increasing verbal output in TCMA, trials have been small, and some caution must be exercised in interpreting these findings.
Keywords: aphasia, intention, adynamic aphasia, transcortical motor aphasia, frontal lobes, nonfluent language, pre-SMA, Broca’s area, frontal–subcortical white matter, thalamus, basal ganglia, ascending dopaminergic pathways
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