Listening to Yourself and Watching Your Tongue: Distinct Abilities and Brain Regions for Monitoring Semantic and Phonological Speech Errors.

Despite the many mistakes we make while speaking, people can effectively communicate because we monitor our speech errors. However, the cognitive abilities and brain structures that support speech error monitoring are unclear. There may be different abilities and brain regions that support monitoring phonological speech errors versus monitoring semantic speech errors. We investigated speech, language, and cognitive control abilities that relate to detecting phonological and semantic speech errors in 41 individuals with aphasia who underwent detailed cognitive testing. Then, we used support vector regression lesion symptom mapping to identify brain regions supporting detection of phonological versus semantic errors in a group of 76 individuals with aphasia. The results revealed that motor speech deficits as well as lesions to the ventral motor cortex were related to reduced detection of phonological errors relative to semantic errors. Detection of semantic errors selectively related to auditory word comprehension deficits. Across all error types, poor cognitive control related to reduced detection. We conclude that monitoring of phonological and semantic errors relies on distinct cognitive abilities and brain regions. Furthermore, we identified cognitive control as a shared cognitive basis for monitoring all types of speech errors. These findings refine and expand our understanding of the neurocognitive basis of speech error monitoring.

Do People With Apraxia of Speech and Aphasia Improve or Worsen Across Repeated Sequential Word Trials?

PURPOSE: During motor speech examinations for suspected apraxia of speech (AOS), clients are routinely asked to repeat words several times sequentially. The purpose of this study was to understand the task in terms of the relationship among consecutive attempts. We asked to what extent phonemic accuracy changes across trials and whether the change is predicted by AOS diagnosis and sound production severity. METHOD: One hundred thirty-three participants were assigned to four diagnostic groups based on quantitative metrics (aphasia plus AOS, aphasia-only, and aphasia with two borderline speech profiles). Each participant produced four multisyllabic words 5 times consecutively. These productions were audio-recorded and transcribed phonetically and then summarized as the proportion of target phonemes that was produced accurately. Nonparametric statistics were used to analyze percent change in accuracy from the first to the last production based on diagnostic group and a broad measure of speech sound accuracy. RESULTS: Accuracy on the repeated words deteriorated across trials for all groups, showing reduced accuracy from the first to the last repetition for 62% of participants. Although diagnostic groups differed on the broad measure of speech sound accuracy, severity classification based on this measure did not determine degree of deterioration on the repeated words task. DISCUSSION: Responding to a request to say multisyllabic words 5 times sequentially is challenging for people with aphasia with and without AOS, and as such, performance is prone to errors even with mild impairment. For most, the task does not encourage self-correction. Instead, it promotes errors, regardless of diagnosis, and is, therefore, useful for screening purposes.

Structural disconnection of the posterior medial frontal cortex reduces speech error monitoring.

Optimal performance in any task relies on the ability to detect and correct errors. The anterior cingulate cortex and the broader posterior medial frontal cortex (pMFC) are active during error processing. However, it is unclear whether damage to the pMFC impairs error monitoring. We hypothesized that successful error monitoring critically relies on connections between the pMFC and broader cortical networks involved in executive functions and the task being monitored. We tested this hypothesis in the context of speech error monitoring in people with post-stroke aphasia. Diffusion weighted images were collected in 51 adults with chronic left-hemisphere stroke and 37 age-matched control participants. Whole-brain connectomes were derived using constrained spherical deconvolution and anatomically-constrained probabilistic tractography. Support vector regressions identified white matter connections in which lost integrity in stroke survivors related to reduced error detection during confrontation naming. Lesioned connections to the bilateral pMFC were related to reduce error monitoring, including many connections to regions associated with speech production and executive function. We conclude that connections to the pMFC support error monitoring. Error monitoring in speech production is supported by the structural connectivity between the pMFC and regions involved in speech production, comprehension, and executive function. Interactions between pMFC and other task-relevant processors may similarly be critical for error monitoring in other task contexts.

Two types of phonological reading impairment in stroke aphasia.

Alexia is common in the context of aphasia. It is widely agreed that damage to phonological and semantic systems not specific to reading causes co-morbid alexia and aphasia. Studies of alexia to date have only examined phonology and semantics as singular processes or axes of impairment, typically in the context of stereotyped alexia syndromes. However, phonology, in particular, is known to rely on subprocesses, including sensory-phonological processing, motor-phonological processing, and sensory-motor integration. Moreover, many people with stroke aphasia demonstrate mild or mixed patterns of reading impairment that do not fit neatly with one syndrome. This cross-sectional study tested whether the hallmark symptom of phonological reading impairment, the lexicality effect, emerges from damage to a specific subprocess of phonology in stroke patients not selected for alexia syndromes. Participants were 30 subjects with left-hemispheric stroke and 37 age- and education-matched controls. A logistic mixed-effects model tested whether post-stroke impairments in sensory phonology, motor phonology, or sensory-motor integration modulated the effect of item lexicality on patient accuracy in reading aloud. Support vector regression voxel-based lesion-symptom mapping localized brain regions necessary for reading and non-orthographic phonological processing. Additionally, a novel support vector regression structural connectome-symptom mapping method identified the contribution of both lesioned and spared but disconnected, brain regions to reading accuracy and non-orthographic phonological processing. Specifically, we derived whole-brain structural connectomes using constrained spherical deconvolution-based probabilistic tractography and identified lesioned connections based on comparisons between patients and controls. Logistic mixed-effects regression revealed that only greater motor-phonological impairment related to lower accuracy reading aloud pseudowords versus words. Impaired sensory-motor integration was related to lower overall accuracy in reading aloud. No relationship was identified between sensory-phonological impairment and reading accuracy. Voxel-based and structural connectome lesion-symptom mapping revealed that lesioned and disconnected left ventral precentral gyrus related to both greater motor-phonological impairment and lower sublexical reading accuracy. In contrast, lesioned and disconnected left temporoparietal cortex is related to both impaired sensory-motor integration and reduced overall reading accuracy. These results clarify that at least two dissociable phonological processes contribute to the pattern of reading impairment in aphasia. First, impaired sensory-motor integration, caused by lesions disrupting the left temporoparietal cortex and its structural connections, non-selectively reduces accuracy in reading aloud. Second, impaired motor-phonological processing, caused at least partially by lesions disrupting left ventral premotor cortex and structural connections, selectively reduces sublexical reading accuracy. These results motivate a revised cognitive model of reading aloud that incorporates a sensory-motor phonological circuit.

Domains of Health-Related Quality of Life Are Associated With Specific Deficits and Lesion Locations in Chronic Aphasia.

BACKGROUND: Health-related quality of life (HRQL) in stroke survivors is related to numerous factors, but more research is needed to delineate factors related to HRQL in people with aphasia. OBJECTIVE: To examine the relationship between HRQL and demographic factors, impairment-based measures, and lesion characteristics in chronic aphasia. METHODS: A total of 41 left-hemisphere stroke survivors with aphasia underwent cognitive testing and magnetic resonance imaging. To address relationships with demographic and impairment-based measures, test scores were entered into a principal component analysis (PCA) and multiple linear regression was performed for overall and domain (physical, communication, psychosocial) scores of the Stroke and Aphasia Quality of Life Scale (SAQOL-39g). Independent variables included factor scores from the PCA, motricity, lesion volume, depressed mood, and demographic variables. To address relationships with lesion location, multivariate support vector regression lesion-symptom mapping (SVR-LSM) was used to localize lesions associated with SAQOL-39g scores. RESULTS: The PCA yielded 3 factors, which were labeled Language Production, Nonlinguistic Cognition, and Language Comprehension. Multiple linear regression revealed that depression symptoms predicted lower SAQOL-39g average and domain scores. Lower motricity scores predicted lower SAQOL-39g average and physical scores, and lower Language Production factor scores predicted lower communication scores. SVR-LSM demonstrated that basal ganglia lesions were associated with lower physical scores, and inferior frontal lesions were associated with lower psychosocial scores. CONCLUSIONS: HRQL in chronic left-hemisphere stroke survivors with aphasia relates to lesion location, depression symptoms, and impairment-based measures. This information may help identify individuals at risk for specific aspects of low HRQL and facilitate targeted interventions to improve well-being.

Effects of age and left hemisphere lesions on audiovisual integration of speech.

Neuroimaging studies have implicated left temporal lobe regions in audiovisual integration of speech and inferior parietal regions in temporal binding of incoming signals. However, it remains unclear which regions are necessary for audiovisual integration, especially when the auditory and visual signals are offset in time. Aging also influences integration, but the nature of this influence is unresolved. We used a McGurk task to test audiovisual integration and sensitivity to the timing of audiovisual signals in two older adult groups: left hemisphere stroke survivors and controls. We observed a positive relationship between age and audiovisual speech integration in both groups, and an interaction indicating that lesions reduce sensitivity to timing offsets between signals. Lesion-symptom mapping demonstrated that damage to the left supramarginal gyrus and planum temporale reduces temporal acuity in audiovisual speech perception. This suggests that a process mediated by these structures identifies asynchronous audiovisual signals that should not be integrated.

Brain structures and cognitive abilities important for the self-monitoring of speech errors.

The brain structures and cognitive abilities necessary for successful monitoring of one's own speech errors remain unknown. We aimed to inform self-monitoring models by examining the neural and behavioral correlates of phonological and semantic error detection in individuals with post-stroke aphasia. First, we determined whether detection related to other abilities proposed to contribute to monitoring according to various theories, including naming ability, fluency, word-level auditory comprehension, sentence-level auditory comprehension, and executive function. Regression analyses revealed that fluency and executive scores were independent predictors of phonological error detection, while a measure of word-level comprehension related to semantic error detection. Next, we used multivariate lesion-symptom mapping to determine lesion locations associated with reduced error detection. Reduced overall error detection related to damage to a region of frontal white matter extending into dorsolateral prefrontal cortex (DLPFC). Detection of phonological errors related to damage to the same areas, but the lesion-behavior association was stronger, suggesting the localization for overall error detection was driven primarily by phonological error detection. These findings demonstrate that monitoring of different error types relies on distinct cognitive functions, and provide causal evidence for the importance of frontal white matter tracts and DLPFC for self-monitoring of speech.

Dissociable Mechanisms of Verbal Working Memory Revealed through Multivariate Lesion Mapping.

Two maintenance mechanisms with separate neural systems have been suggested for verbal working memory: articulatory-rehearsal and non-articulatory maintenance. Although lesion data would be key to understanding the essential neural substrates of these systems, there is little evidence from lesion studies that the two proposed mechanisms crucially rely on different neuroanatomical substrates. We examined 39 healthy adults and 71 individuals with chronic left-hemisphere stroke to determine if verbal working memory tasks with varying demands would rely on dissociable brain structures. Multivariate lesion-symptom mapping was used to identify the brain regions involved in each task, controlling for spatial working memory scores. Maintenance of verbal information relied on distinct brain regions depending on task demands: sensorimotor cortex under higher demands and superior temporal gyrus (STG) under lower demands. Inferior parietal cortex and posterior STG were involved under both low and high demands. These results suggest that maintenance of auditory information preferentially relies on auditory-phonological storage in the STG via a nonarticulatory maintenance when demands are low. Under higher demands, sensorimotor regions are crucial for the articulatory rehearsal process, which reduces the reliance on STG for maintenance. Lesions to either of these regions impair maintenance of verbal information preferentially under the appropriate task conditions.

Localization of Phonological and Semantic Contributions to Reading.

Reading involves the rapid extraction of sound and meaning from print through a cooperative division of labor between phonological and lexical-semantic processes. Whereas lesion studies of patients with stereotyped acquired reading deficits contributed to the notion of a dissociation between phonological and lexical-semantic reading, the neuroanatomical basis for effects of lexicality (word vs pseudoword), orthographic regularity (regular vs irregular spelling-sound correspondences), and concreteness (concrete vs abstract meaning) on reading is underspecified, particularly outside the context of strong behavioral dissociations. Support vector regression lesion-symptom mapping (LSM) of 73 left hemisphere stroke survivors (male and female human subjects) not preselected for stereotyped dissociations revealed the differential contributions of specific cortical regions to reading pseudowords (ventral precentral gyrus), regular words (planum temporale, supramarginal gyrus, ventral precentral and postcentral gyrus, and insula), and concrete words (pars orbitalis and pars triangularis). Consistent with the primary systems view of reading being parasitic on language-general circuitry, our multivariate LSM analyses revealed that phonological decoding depends on perisylvian areas subserving sound-motor integration and that semantic effects on reading depend on frontal cortex subserving control over concrete semantic representations that aid phonological access from print. As the first study to localize the differential cortical contributions to reading pseudowords, regular words, and concrete words in stroke survivors with variable reading abilities, our results provide important information on the neurobiological basis of reading and highlight the insights attainable through multivariate, process-based approaches to alexia.SIGNIFICANCE STATEMENT Whereas fMRI evidence for neuroanatomical dissociations between phonological and lexical-semantic reading is abundant, evidence from modern lesion studies establishing the differential contributions of specific brain regions to specific reading processes is lacking. Our application of multivariate lesion-symptom mapping revealed that effects of lexicality, orthographic regularity, and concreteness on reading differentially depend on areas subserving auditory-motor integration and semantic control. Phonological decoding of print relies on a dorsal perisylvian network supporting auditory and articulatory representations, with unfamiliar words relying especially on articulatory mapping. In tandem with this dorsal decoding system, anterior inferior frontal gyrus may coordinate control over concrete semantic representations that support mapping of print to sound, which is a novel potential mechanism for semantic influences on reading.

Behavioral Effects of Chronic Gray and White Matter Stroke Lesions in a Functionally Defined Connectome for Naming.

BACKGROUND: In functional magnetic resonance imaging studies, picture naming engages widely distributed brain regions in the parietal, frontal, and temporal cortices. However, it remains unknown whether those activated areas, along with white matter pathways between them, are actually crucial for naming. OBJECTIVE: We aimed to identify nodes and pathways implicated in naming in healthy older adults and test the impact of lesions to the connectome on naming ability. METHODS: We first identified 24 cortical nodes activated by a naming task and reconstructed anatomical connections between these nodes using probabilistic tractography in healthy adults. We then used structural scans and fractional anisotropy (FA) maps in 45 patients with left hemisphere stroke to assess the relationships of node and pathway integrity to naming, phonology, and nonverbal semantic ability. RESULTS: We found that mean FA values in 13 left hemisphere white matter tracts within the dorsal and ventral streams and 1 interhemispheric tract significantly related to naming scores after controlling for lesion size and demographic factors. In contrast, lesion loads in the cortical nodes were not related to naming performance after controlling for the same variables. Among the identified tracts, the integrity of 4 left hemisphere ventral stream tracts related to nonverbal semantic processing and 1 left hemisphere dorsal stream tract related to phonological processing. CONCLUSIONS: Our findings reveal white matter structures vital for naming and its subprocesses. These findings demonstrate the value of multimodal methods that integrate functional imaging, structural connectivity, and lesion data to understand relationships between brain networks and behavior.

White Matter Correlates of Auditory Comprehension Outcomes in Chronic Post-Stroke Aphasia.

Neuroimaging studies have shown that speech comprehension involves a number of widely distributed regions within the frontal and temporal lobes. We aimed to examine the differential contributions of white matter connectivity to auditory word and sentence comprehension in chronic post-stroke aphasia. Structural and diffusion MRI data were acquired on 40 patients with chronic post-stroke aphasia. A battery of auditory word and sentence comprehension tests were administered to all the patients. Tract-based spatial statistics were used to identify areas in which white matter integrity related to specific comprehension deficits. Relevant tracts were reconstructed using probabilistic tractography in healthy older participants, and the mean values of fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) of the entire tracts were examined in relation to comprehension scores. Anterior temporal white matter integrity loss and involvement of the uncinate fasciculus related to word-level comprehension deficits (RFA = 0.408, P = 0.012; RMD = -0.429, P = 0.008; RAD = -0.424, P = 0.009; RRD = -0.439, P = 0.007). Posterior temporal white matter integrity loss and involvement of the inferior longitudinal fasciculus related to sentence-level comprehension deficits (RFA = 0.382, P = 0.02; RMD = -0.461, P = 0.004; RAD = -0.457, P = 0.004; RRD = -0.453, P = 0.005). Loss of white matter integrity in the inferior fronto-occipital fasciculus related to both word- and sentence-level comprehension (word-level scores: RFA = 0.41, P = 0.012; RMD = -0.447, P = 0.006; RAD = -0.489, P = 0.002; RRD = -0.432, P = 0.008; sentence-level scores: RFA = 0.409, P = 0.012; RMD = -0.413, P = 0.011; RAD = -0.408, P = 0.012; RRD = -0.413, P = 0.011). Lesion overlap, but not white matter integrity, in the arcuate fasciculus related to sentence-level comprehension deficits. These findings suggest that word-level comprehension outcomes in chronic post-stroke aphasia rely primarily on anterior temporal lobe pathways, whereas sentence-level comprehension relies on more widespread pathways including the posterior temporal lobe.

Mapping Common Aphasia Assessments to Underlying Cognitive Processes and Their Neural Substrates.

BACKGROUND: Understanding the relationships between clinical tests, the processes they measure, and the brain networks underlying them, is critical in order for clinicians to move beyond aphasia syndrome classification toward specification of individual language process impairments. OBJECTIVE: To understand the cognitive, language, and neuroanatomical factors underlying scores of commonly used aphasia tests. METHODS: Twenty-five behavioral tests were administered to a group of 38 chronic left hemisphere stroke survivors and a high-resolution magnetic resonance image was obtained. Test scores were entered into a principal components analysis to extract the latent variables (factors) measured by the tests. Multivariate lesion-symptom mapping was used to localize lesions associated with the factor scores. RESULTS: The principal components analysis yielded 4 dissociable factors, which we labeled Word Finding/Fluency, Comprehension, Phonology/Working Memory Capacity, and Executive Function. While many tests loaded onto the factors in predictable ways, some relied heavily on factors not commonly associated with the tests. Lesion symptom mapping demonstrated discrete brain structures associated with each factor, including frontal, temporal, and parietal areas extending beyond the classical language network. Specific functions mapped onto brain anatomy largely in correspondence with modern neural models of language processing. CONCLUSIONS: An extensive clinical aphasia assessment identifies 4 independent language functions, relying on discrete parts of the left middle cerebral artery territory. A better understanding of the processes underlying cognitive tests and the link between lesion and behavior may lead to improved aphasia diagnosis, and may yield treatments better targeted to an individual's specific pattern of deficits and preserved abilities.

Right Hemisphere Remapping of Naming Functions Depends on Lesion Size and Location in Poststroke Aphasia.

The study of language network plasticity following left hemisphere stroke is foundational to the understanding of aphasia recovery and neural plasticity in general. Damage in different language nodes may influence whether local plasticity is possible and whether right hemisphere recruitment is beneficial. However, the relationships of both lesion size and location to patterns of remapping are poorly understood. In the context of a picture naming fMRI task, we tested whether lesion size and location relate to activity in surviving left hemisphere language nodes, as well as homotopic activity in the right hemisphere during covert name retrieval and overt name production. We found that lesion size was positively associated with greater right hemisphere activity during both phases of naming, a pattern that has frequently been suggested but has not previously been clearly demonstrated. During overt naming, lesions in the inferior frontal gyrus led to deactivation of contralateral frontal areas, while lesions in motor cortex led to increased right motor cortex activity. Furthermore, increased right motor activity related to better naming performance only when left motor cortex was lesioned, suggesting compensatory takeover of speech or language function by the homotopic node. These findings demonstrate that reorganization of language function, and the degree to which reorganization facilitates aphasia recovery, is dependent on the size and site of the lesion.

Functional activation independently contributes to naming ability and relates to lesion site in post-stroke aphasia.

Language network reorganization in aphasia may depend on the degree of damage in critical language areas, making it difficult to determine how reorganization impacts performance. Prior studies on remapping of function in aphasia have not accounted for the location of the lesion relative to critical language areas. They rectified this problem by using a multimodal approach, combining multivariate lesion-symptom mapping and fMRI in chronic aphasia to understand the independent contributions to naming performance of the lesion and the activity in both hemispheres. Activity was examined during two stages of naming: covert retrieval, and overt articulation. Regions of interest were drawn based on over- and under-activation, and in areas where activity had a bivariate relationship with naming. Regressions then tested whether activation of these regions predicted naming ability, while controlling for lesion size and damage in critical left hemisphere naming areas, as determined by lesion-symptom mapping. Engagement of the right superior temporal sulcus (STS) and disengagement of the left dorsal pars opercularis (dPOp) during overt naming was associated with better than predicted naming performance. Lesions in the left STS prevented right STS engagement and resulted in persistent left dPOp activation. In summary, changes in activity during overt articulation independently relate to naming outcomes, controlling for stroke severity. Successful remapping relates to network disruptions that depend on the location of the lesion in the left hemisphere. Hum Brain Mapp 38:2051-2066, 2017. © 2017 Wiley Periodicals, Inc.

Depression Symptoms in Chronic Left Hemisphere Stroke Are Related to Dorsolateral Prefrontal Cortex Damage.

Damage to the brain's mood regulation systems may contribute to poststroke depression. This study examines relationships between depression symptoms and psychosocial factors and then uses multivariate lesion-symptom mapping to localize depression symptoms in people with chronic left hemisphere stroke. Depression symptoms relate inversely to education and directly to physical disability. Damage in the left dorsolateral prefrontal cortex is associated with greater depression symptoms. These results demonstrate a neurological contribution to depression symptoms in chronic left hemisphere stroke and provide evidence of convergent biological mechanisms for poststroke depression symptoms and major depression with regard to left dorsolateral prefrontal cortex dysfunction.

Right hemisphere grey matter structure and language outcomes in chronic left hemisphere stroke.

The neural mechanisms underlying recovery of language after left hemisphere stroke remain elusive. Although older evidence suggested that right hemisphere language homologues compensate for damage in left hemisphere language areas, the current prevailing theory suggests that right hemisphere engagement is ineffective or even maladaptive. Using a novel combination of support vector regression-based lesion-symptom mapping and voxel-based morphometry, we aimed to determine whether local grey matter volume in the right hemisphere independently contributes to aphasia outcomes after chronic left hemisphere stroke. Thirty-two left hemisphere stroke survivors with aphasia underwent language assessment with the Western Aphasia Battery-Revised and tests of other cognitive domains. High-resolution T1-weighted images were obtained in aphasia patients and 30 demographically matched healthy controls. Support vector regression-based multivariate lesion-symptom mapping was used to identify critical language areas in the left hemisphere and then to quantify each stroke survivor's lesion burden in these areas. After controlling for these direct effects of the stroke on language, voxel-based morphometry was then used to determine whether local grey matter volumes in the right hemisphere explained additional variance in language outcomes. In brain areas in which grey matter volumes related to language outcomes, we then compared grey matter volumes in patients and healthy controls to assess post-stroke plasticity. Lesion-symptom mapping showed that specific left hemisphere regions related to different language abilities. After controlling for lesion burden in these areas, lesion size, and demographic factors, grey matter volumes in parts of the right temporoparietal cortex positively related to spontaneous speech, naming, and repetition scores. Examining whether domain general cognitive functions might explain these relationships, partial correlations demonstrated that grey matter volumes in these clusters related to verbal working memory capacity, but not other cognitive functions. Further, grey matter volumes in these areas were greater in stroke survivors than healthy control subjects. To confirm this result, 10 chronic left hemisphere stroke survivors with no history of aphasia were identified. Grey matter volumes in right temporoparietal clusters were greater in stroke survivors with aphasia compared to those without history of aphasia. These findings suggest that the grey matter structure of right hemisphere posterior dorsal stream language homologues independently contributes to language production abilities in chronic left hemisphere stroke, and that these areas may undergo hypertrophy after a stroke causing aphasia.

Multiple Oral Re-reading treatment for alexia: The parts may be greater than the whole.

This study examines the reasons for the success of Multiple Oral Re-reading (MOR; Moyer, 1979), a non-invasive, easily administered alexia treatment that has been reported in the literature and is currently in clinical use. The treatment consists of reading text passages aloud multiple times a day. Findings that MOR improves reading speed on practised as well as novel text have been inconsistent, making MOR's role in the rehabilitation of alexia unclear. We hypothesised that MOR's treatment mechanism works through repetition of high frequency words (i.e., bottom-up processing). We designed and controlled our text passages to test the hypothesis that participants would not improve on all novel text but would improve on text that includes a critical mass of the words contained in the passages they were re-reading. We further hypothesised that the improvement would be at the level of their specific alexic deficit. We tested four participants with phonological alexia and two with pure alexia during 8 weeks of MOR treatment. Contrary to the conclusions of previous studies, our results indicate that improvements in top-down processing cannot explain generalisation in MOR and that much of the improvement in reading is through repetition of the practised words. However, most patients also showed improvement when specific phrases were re-used in novel passages, indicating that practice of difficult words in context may be crucial to reading improvement.

Reading, writing, and their disorders.

Reading and writing are complex forms of communication. Disorders of these abilities reflect this complexity. Although distinct syndromes do exist, it is more common to see these disorders in the context of related dysfunction. For example, alexia and agraphia commonly occur together. Not only do they occur together, but frequently, although not exclusively, a patient with both has similar patterns of performance in each modality. Reading, the transformation of written symbols into spoken output, is intimately related to visual input and speech. Disorders of these abilities are commonly reflected in alexia. Writing, the transformation of oral input (writing to dictation) or conceptual thought into written symbols, is interconnected with speech and motor function. Again, disorders of these abilities are commonly reflected in agraphia. Understanding alexia and agraphia allows insight into multiple realms of left hemispheric dysfunction and provides significant clinical insight into patients with left hemispheric lesions.

A patient with phonologic alexia can learn to read "much" from "mud pies".

People with phonologic alexia often have difficulty reading functors and verbs, in addition to pseudowords. Friedman et al. [Friedman, R. B., Sample, D. M, & Lott, S. N. (2002). The role of level of representation in the use of paired associate learning for rehabilitation of alexia. Neuropsychologia, 40, 223-234] reported a successful treatment for phonologic alexia that paired problematic functors and verbs with easily read relays that were homophonous nouns (e.g. "be" paired with "bee"). The current study evaluates the efficacy of pairing problematic grammatical words with relays that share initial phonemes, but vary in the relationship of their final phonemes. Results showed that reading of target grammatical words improved to criterion level (90% accuracy over two consecutive probes) in all experimental conditions with shared phonology, but remained far below criterion level in control conditions. There was a significant correlation between degree of phonologic relatedness and error rate. Maintenance of the treatment effect was poor as assessed by traditional measurement, however a dramatic savings during relearning was demonstrated during a subsequent treatment phase. The finding that reading can be re-organized by pairing target words not only with homophones, but with other phonologically related relays, suggests that this approach could be applied to a wide corpus of words and, therefore, potentially be of great use clinically. We suggest, within a connectionist account, that the treatment effect results from relays priming the initial phonologic units of the targets.