Understanding the neural mechanism that supports preserved language processing in aphasia has implications for both basic and applied science. This study examined brain activation associated with correct picture naming in 15 patients with aphasia. We contrasted each patient's activation to the activation observed in a neurologically healthy control group, allowing us to identify regions with unusual activity patterns. The results revealed that increased activation in preserved left hemisphere areas is associated with better naming performance in aphasia. This relationship was linear in nature; progressively less cortical activation was associated with greater severity of anomia. These findings are consistent with others who suggests that residual language function following stroke relies on preserved cortical areas in the left hemisphere.

Most naming treatments in aphasia either assume a phonological or semantic emphasis or a combination thereof. However, it is unclear whether semantic or phonological treatments recruit the same or different cortical areas in chronic aphasia. Employing three persons with aphasia, two of whom were non-fluent, the present study compared changes in neural recruitment associated with phonologic and semantic-based naming treatments. The participants with non-fluent aphasia were able to name more items following both treatment approaches. Although this was not the case for the participant who had fluent aphasia, her naming errors decreased considerably following treatment. Post-treatment fMRI revealed similar changes in neural activity bilaterally in the precuneus among the two non-fluent participants--increased activity was noted in the right entorhinal cortex and posterior thalamus on post-treatment scans for the third participant. These findings imply that cortical areas not traditionally related to language processing may support anomia recovery in some patients with chronic aphasia.

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A praxia of speech (AOS) is a disorder of motor speech planning that can occur after brain damage to the language-dominant hemisphere. Generally, agreed on characteristics of AOS include articulatory imprecision, atypical prosody, frequent errors with consonants when compared with vowels, and distinct from speech production deficits that occur in aphasia and dysarthria, distorted sound additions and substitutions.1,2 The nature of these behaviors differs from that of aphasia, as AOS is neither a linguistic impairment (ie, a problem with the conceptualization of verbal symbols used to communicate thoughts) nor a problem with speech motor execution (ie, dysarthria). Rather, it is a deficit in planning speech motor movements. The study of AOS has been plagued by controversy since its description by Darley in 1968. 4,5 This can be attributed to the fact that the behavioral presentation of AOS is often difficult to distinguish from the speech production deficits that can occur in aphasia and dysarthria, [6][7][8][9] and because the anatomy of brain damage leading to AOS is similar to the pattern of damage leading to aphasia.10,11 A seminal study by Dronkers 12 in 1996 localized AOS to damage to the left insula, specifically the superior precentral gyrus of the insula (SPGI). Twentyfive poststroke patients with chronic AOS had SPGI damage, whereas patients without AOS did not have a lesion in this area. This double dissociation between SPGI damage and AOS has been argued as strong support for the role of the insula in AOS. 6,12,13 However, in the study by Dronkers, 12 none of the patients in the group without AOS were reported to have Broca aphasia or other speech impairment (eg, dysarthria). These patients were classified with Wernicke, anomic, conduction, or unclassifiable/no aphasia. In addition, lesion distribution maps for this group indicate that areas of maximal overlap occurred in posterior perisylvian areas; therefore, it can be argued that the lesion distribution of this group is too different to serve as an adequate comparison. 14 Furthermore, mounting evidence does not support the role of the insula in speech production generally 15 and AOS specifically, as such work has found that AOS can occur in the Background and Purpose-Acquired apraxia of speech (AOS) is a motor speech disorder caused by brain damage. AOS often co-occurs with aphasia, a language disorder in which patients may also demonstrate speech production errors. The overlap of speech production deficits in both disorders has raised questions on whether AOS emerges from a unique pattern of brain damage or as a subelement of the aphasic syndrome. The purpose of this study was to determine whether speech production errors in AOS and aphasia are associated with distinctive patterns of brain injury. Methods-Forty-three patients with history of a single left-hemisphere stroke underwent comprehensive speech and language testing. The AOS Rating Scale was used to rate speech errors specific to AOS versus speech errors that can also be associated with ...