In most cases, aphasia is caused by strokes involving the left hemisphere, with more extensive damage typically being associated with more severe aphasia. The classical model of aphasia commonly adhered to in the Western world is the Wernicke-Lichtheim model. The model has been in existence for over a century, and classification of aphasic symptomatology continues to rely on it. However, far more detailed models of speech and language localization in the brain have been formulated. In this regard, the dual stream model of cortical brain organization proposed by Hickok and Poeppel is particularly influential. Their model describes two processing routes, a dorsal stream and a ventral stream, that roughly support speech production and speech comprehension, respectively, in normal subjects. Despite the strong influence of the dual stream model in current neuropsychological research, there has been relatively limited focus on explaining aphasic symptoms in the context of this model. Given that the dual stream model represents a more nuanced picture of cortical speech and language organization, cortical damage that causes aphasic impairment should map clearly onto the dual processing streams. Here, we present a follow-up study to our previous work that used lesion data to reveal the anatomical boundaries of the dorsal and ventral streams supporting speech and language processing. Specifically, by emphasizing clinical measures, we examine the effect of cortical damage and disconnection involving the dorsal and ventral streams on aphasic impairment. The results reveal that measures of motor speech impairment mostly involve damage to the dorsal stream, whereas measures of impaired speech comprehension are more strongly associated with ventral stream involvement. Equally important, many clinical tests that target behaviours such as naming, speech repetition, or grammatical processing rely on interactions between the two streams. This latter finding explains why patients with seemingly disparate lesion locations often experience similar impairments on given subtests. Namely, these individuals' cortical damage, although dissimilar, affects a broad cortical network that plays a role in carrying out a given speech or language task. The current data suggest this is a more accurate characterization than ascribing specific lesion locations as responsible for specific language deficits.awx363media15705668782001.

Several dual route models of human speech processing have been proposed suggesting a large-scale anatomical division between cortical regions that support motor-phonological aspects vs. lexical-semantic aspects of speech processing. However, to date, there is no complete agreement on what areas subserve each route or the nature of interactions across these routes that enables human speech processing. Relying on an extensive behavioral and neuroimaging assessment of a large sample of stroke survivors, we used a data-driven approach using principal components analysis of lesionsymptom mapping to identify brain regions crucial for performance on clusters of behavioral tasks without a priori separation into task types. Distinct anatomical boundaries were revealed between a dorsal frontoparietal stream and a ventral temporal-frontal stream associated with separate components. Collapsing over the tasks primarily supported by these streams, we characterize the dorsal stream as a form-to-articulation pathway and the ventral stream as a form-to-meaning pathway. This characterization of the division in the data reflects both the overlap between tasks supported by the two streams as well as the observation that there is a bias for phonological production tasks supported by the dorsal stream and lexical-semantic comprehension tasks supported by the ventral stream. As such, our findings show a division between two processing routes that underlie human speech processing and provide an empirical foundation for studying potential computational differences that distinguish between the two routes.aphasia | speech production | speech comprehension | voxel-based lesionsymptom mapping | speech processing U nderstanding how and where in the brain speech processing occurs has been the focus of concerted scientific endeavor for over one and a half centuries. The most influential model of the neuroanatomical basis of speech processing was proposed by Wernicke (1) and later refined by Lichtheim (2)-the WernickeLichtheim (W-L) model. The W-L model includes two separate routes from a posterior auditory comprehension center to an anterior motor speech production center: a direct route that enables speech repetition and an indirect route via ideation that mediates comprehension and propositional speech. More recently, dual route processing has been recognized as a central principle in the functional organization of the brain. Ungerleider and Mishkin (3) proposed that visual perception in primates is supported by a ventral "what" stream (involving an occipital-temporal lobe route) and a dorsal "where" stream [or later, a "how" stream mediated by an occipital-parietal route (4)]. Similarly, in the auditory domain (5), Rauschecker and Tian (6) proposed a "dual stream" model to account for the identification of what was being heard and from where the sound originated (5, 6). This model, mostly derived from nonhuman primate data, distinguishes between an anterior/ ventral route ("what" stream) involving connections from the left posterior superio...

Recently, two different white matter regions that support speech fluency have been identified: the aslant tract and the anterior segment of the arcuate fasciculus (ASAF). The role of the ASAF was demonstrated in patients with post-stroke aphasia, while the role of the aslant tract shown in primary progressive aphasia. Regional white matter integrity appears to be crucial for speech production; however, the degree that each region exerts an independent influence on speech fluency is unclear. Furthermore, it is not yet defined if damage to both white matter regions influences speech in the context of the same neural mechanism (stroke-induced aphasia). This study assessed the relationship between speech fluency and quantitative integrity of the aslant region and the ASAF. It also explored the relationship between speech fluency and other white matter regions underlying classic cortical language areas such as the uncinate fasciculus and the inferior longitudinal fasciculus (ILF). Damage to these regions, except the ILF, was associated with speech fluency, suggesting synergistic association of these regions with speech fluency in post-stroke aphasia. These observations support the theory that speech fluency requires the complex, orchestrated activity between a network of pre-motor, secondary, and tertiary associative cortices, supported in turn by regional white matter integrity.

Agrammatism in aphasia is not a homogeneous syndrome, but a characterization of a nonuniform set of language behaviors in which grammatical markers and complex syntactic structures are omitted, simplified, or misinterpreted. In a sample of 71 left-hemisphere stroke survivors, syntactic processing was quantified with the Northwestern Assessment of Verbs and Sentences (NAVS). Classification analyses were used to assess the relation between NAVS performance and morphosyntactically reduced speech in picture descriptions. Voxel-based and connectivity-based lesion-symptom mapping were applied to investigate neural correlates of impaired syntactic processing. Despite a nonrandom correspondence between NAVS performance and morphosyntactic production deficits, there was variation in individual patterns of syntactic processing. Morphosyntactically reduced production was predicted by lesions to left-hemisphere inferior frontal cortex. Impaired verb argument structure production was predicted by damage to left-hemisphere posterior superior temporal and angular gyrus, as well as to a ventral pathway between temporal and frontal cortex. Damage to this pathway was also predictive of impaired sentence comprehension and production, particularly of noncanonical sentences. Although agrammatic speech production is primarily predicted by lesions to inferior frontal cortex, other aspects of syntactic processing rely rather on regional integrity in temporoparietal cortex and the ventral stream.

Individuals with the val/val BDNF genotype are more likely to benefit from A-tDCS during aphasia treatment.

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 ...

A number of brain regions have been implicated in articulation, but their precise computations remain debated. Using functional magnetic resonance imaging, we examine the degree of functional specificity of articulation-responsive brain regions to constrain hypotheses about their contributions to speech production. We find that articulation-responsive regions (1) are sensitive to articulatory complexity, but (2) are largely nonoverlapping with nearby domain-general regions that support diverse goal-directed behaviors. Furthermore, premotor articulation regions show selectivity for speech production over some related tasks (respiration control), but not others (nonspeech oral-motor [NSO] movements). This overlap between speech and nonspeech movements concords with electrocorticographic evidence that these regions encode articulators and their states, and with patient evidence whereby articulatory deficits are often accompanied by oral-motor deficits. In contrast, the superior temporal regions show strong selectivity for articulation relative to nonspeech movements, suggesting that these regions play a specific role in speech planning/production. Finally, articulation-responsive portions of posterior inferior frontal gyrus show some selectivity for articulation, in line with the hypothesis that this region prepares an articulatory code that is passed to the premotor cortex. Taken together, these results inform the architecture of the human articulation system.

Lesion load in left pSTG and SLF/AF at onset predicts later naming performance. Although based on a small number of patients, our preliminary results suggest outcome might be modulated by SSRIs, but these associations need to be confirmed in a larger randomized controlled trial. Ann Neurol 2018;83:612-622.