Resting state correlates of picture description informativeness in left vs. right hemisphere chronic stroke.

Introduction: Despite a growing emphasis on discourse processing in clinical neuroscience, relatively little is known about the neurobiology of discourse production impairments. Individuals with a history of left or right hemisphere stroke can exhibit difficulty with communicating meaningful discourse content, which implies both cerebral hemispheres play a role in this skill. However, the extent to which successful production of discourse content relies on network connections within domain-specific vs. domain-general networks in either hemisphere is unknown. Methods: In this study, 45 individuals with a history of either left or right hemisphere stroke completed resting state fMRI and the Cookie Theft picture description task. Results: Participants did not differ in the total number of content units or the percentage of interpretative content units they produced. Stroke survivors with left hemisphere damage produced significantly fewer content units per second than individuals with right hemisphere stroke. Intrinsic connectivity of the left language network was significantly weaker in the left compared to the right hemisphere stroke group for specific connections. Greater efficiency of communication of picture scene content was associated with stronger left but weaker right frontotemporal connectivity of the language network in patients with a history of left hemisphere (but not right hemisphere) stroke. No significant relationships were found between picture description measures and connectivity of the dorsal attention, default mode, or salience networks or with connections between language and other network regions. Discussion: These findings add to prior behavioral studies of picture description skills in stroke survivors and provide insight into the role of the language network vs. other intrinsic networks during discourse production.

Corticocerebellar White Matter Integrity Is Related to Naming Outcome in Post-Stroke Aphasia.

Studies have shown that the integrity of white matter tracts connecting different regions in the left cerebral hemisphere is important for aphasia recovery after stroke. However, the impact of the underlying structural connection between the cortex and the cerebellum in post-stroke aphasia is poorly understood. We studied the microstructural integrity of the cerebellum and the corticocerebellar connections and their role in picture naming. Fifty-six patients with left cerebral infarcts (sparing the cerebellum) underwent diffusion tensor imaging (DTI) and Boston Naming Test. We compared the fractional anisotropy (FA) and mean diffusivity (MD) values of the right and the left cerebellum (lobular gray and white matter structures) and cerebellocortical connections. Recursive feature elimination and Spearman correlation analyses were performed to evaluate the relationship between naming performance and the corticocerebellar connections. We found that the right, relative to left, cerebellar structures and their connections with the left cerebrum showed lower FA and higher MD values, both reflecting lower microstructural integrity. This trend was not observed in the healthy controls. Higher MD values of the right major cerebellar outflow tract were associated with poorer picture naming performance. Our study provides the first DTI data demonstrating the critical importance of ascending and descending corticocerebellar connections for naming outcomes after stroke.

Resting-State Connectivity in Acute and Subacute Poststroke Aphasia: A Functional Near-Infrared Spectroscopy Pilot Study.

Background: Understanding how brain function and language skills change during early (acute and subacute) stroke phases is critical for maximizing patient recovery, yet functional neuroimaging studies of early aphasia are scarce. In this pilot study, we used functional near-infrared spectroscopy (fNIRS) to investigate how resting-state functional connectivity (rs-FC) in early aphasia differs from neurologically healthy adults and is related to language deficits. Materials and Methods: Twenty individuals with aphasia (12 acute and 8 subacute phase) and 15 healthy controls underwent rs-fNIRS imaging with a 46-channel montage centered over bilateral perisylvian language areas. FC was computed using a prewhitening, autoregressive Pearson correlation routine applied to preprocessed oxyhemoglobin (HbO) data. Connections were classified as left intra-, right intra-, or interhemispheric. We then compared rs-FC between groups by connection type and examined Spearman correlations between rs-FC averages and language measures within patients. Results: Participants in the acute phase had significantly reduced global rs-FC across all HbO-based connections compared to healthy controls. No significant differences were found in rs-FC between controls and patients in the subacute phase. Controlling for days since stroke, stronger right intra- and interhemispheric rs-FC was related to milder aphasia across all patients. Exploratory correlations revealed that relationships between language measures and rs-FC differed between acute and subacute patient groups. Conclusion: This study provides preliminary evidence that fNIRS-based rs-FC measures may be a viable metric to index the early impacts of stroke in people with aphasia.

Digital 3D Brain MRI Arterial Territories Atlas.

The locus and extent of brain damage in the event of vascular insult can be quantitatively established quickly and easily with vascular atlases. Although highly anticipated by clinicians and clinical researchers, no digital MRI arterial atlas is readily available for automated data analyses. We created a digital arterial territory atlas based on lesion distributions in 1,298 patients with acute stroke. The lesions were manually traced in the diffusion-weighted MRIs, binary stroke masks were mapped to a common space, probability maps of lesions were generated and the boundaries for each arterial territory was defined based on the ratio between probabilistic maps. The atlas contains the definition of four major supra- and infra-tentorial arterial territories: Anterior, Middle, Posterior Cerebral Arteries and Vertebro-Basilar, and sub-territories (thalamoperforating, lenticulostriate, basilar and cerebellar arterial territories), in two hierarchical levels. This study provides the first publicly-available, digital, 3D deformable atlas of arterial brain territories, which may serve as a valuable resource for large-scale, reproducible processing and analysis of brain MRIs of patients with stroke and other conditions.

Association of Regional Atrophy With Naming Decline in Primary Progressive Aphasia.

BACKGROUND AND OBJECTIVES: Primary progressive aphasia (PPA) is a neurodegenerative condition that predominantly impairs language. Most investigations of how focal atrophy affects language consider 1 time point compared with healthy controls. However, true atrophy quantification requires comparing individual brains over time. In this observational cohort study, we identified areas where focal atrophy was associated with contemporaneous decline in naming in the same individuals. METHODS: Cross-sectional analyses-related Boston Naming Test (BNT) performance and volume in 22 regions of interests (ROIs) at each time point using Least Absolute Shrinkage and Selection Operator (LASSO) regression. Longitudinal analysis evaluated changes in BNT performance and change in volume in the same ROIs. RESULTS: Participants (N = 62; 50% female; mean age = 66.8 ± 7.4 years) with PPA completed the BNT and MRI twice (mean = 343.9 ± 209.0 days apart). In cross-sectional left inferior frontal gyrus pars opercularis, superior temporal pole, middle temporal gyrus, and inferior temporal gyrus were identified as critical for naming at all time points. Longitudinal analysis revealed that increasing atrophy in the left supramarginal gyrus and middle temporal pole predicted greater naming decline, as did female sex and longer intervals between time points. DISCUSSION: Although cross-sectional analyses identified classic language areas that were consistently related to poor performance at multiple time points, it was not increasing atrophy in these areas that lead to further decline: longitudinal analysis of each person's atrophy over time instead identified nearby but distinct regions where increased atrophy was related to decreasing performance. The results demonstrate that directly examining atrophy (in each individual) over time furthers understanding of decline in PPA and reveal the importance of left supramarginal gyrus and middle temporal pole in maintaining naming when areas normally critical for language degenerate. The novel results provide insight into how the underlying disease progresses to result in the clinical decline in naming, the deficit most common among all 3 PPA variants.

The contribution of white matter pathology, hypoperfusion, lesion load, and stroke recurrence to language deficits following acute subcortical left hemisphere stroke.

Aphasia, the loss of language ability following damage to the brain, is among the most disabling and common consequences of stroke. Subcortical stroke, occurring in the basal ganglia, thalamus, and/or deep white matter can result in aphasia, often characterized by word fluency, motor speech output, or sentence generation impairments. The link between greater lesion volume and acute aphasia is well documented, but the independent contributions of lesion location, cortical hypoperfusion, prior stroke, and white matter degeneration (leukoaraiosis) remain unclear, particularly in subcortical aphasia. Thus, we aimed to disentangle the contributions of each factor on language impairments in left hemisphere acute subcortical stroke survivors. Eighty patients with acute ischemic left hemisphere subcortical stroke (less than 10 days post-onset) participated. We manually traced acute lesions on diffusion-weighted scans and prior lesions on T2-weighted scans. Leukoaraiosis was rated on T2-weighted scans using the Fazekas et al. (1987) scale. Fluid-attenuated inversion recovery (FLAIR) scans were evaluated for hyperintense vessels in each vascular territory, providing an indirect measure of hypoperfusion in lieu of perfusion-weighted imaging. We found that language performance was negatively correlated with acute/total lesion volumes and greater damage to substructures of the deep white matter and basal ganglia. We conducted a LASSO regression that included all variables for which we found significant univariate relationships to language performance, plus nuisance regressors. Only total lesion volume was a significant predictor of global language impairment severity. Further examination of three participants with severe language impairments suggests that their deficits result from impairment in domain-general, rather than linguistic, processes. Given the variability in language deficits and imaging markers associated with such deficits, it seems likely that subcortical aphasia is a heterogeneous clinical syndrome with distinct causes across individuals.

White matter microstructural integrity pre- and post-treatment in individuals with chronic post-stroke aphasia.

While previous studies have found that white matter damage relates to impairment severity in individuals with aphasia, further study is required to understand the relationship between white matter integrity and treatment response. In this study, 34 individuals with chronic post-stroke aphasia underwent behavioral testing and structural magnetic resonance imaging at two timepoints. Thirty participants within this sample completed typicality-based semantic feature treatment for anomia. Tractography of bi-hemispheric white matter tracts was completed via Automated Fiber Quantification. Associations between microstructural integrity metrics and behavioral measures were evaluated at the tract level and in nodes along the tract. Diffusion measures of the left inferior longitudinal, superior longitudinal, and arcuate fasciculi were related to aphasia severity and diffusion measures of the left inferior longitudinal fasciculus were related to naming and treatment response. This study also found preliminary evidence of left inferior longitudinal fasciculus microstructural changes following treatment.

Neural regions underlying object and action naming: Complementary evidence from acute stroke and primary progressive aphasia.

Background: Naming impairment is commonly noted in individuals with aphasia. However, object naming receives more attention than action naming. Furthermore, most studies include participants with aphasia due to only one aetiology, commonly stroke. We developed a new assessment, the Hopkins Action Naming Assessment (HANA), to evaluate action naming impairments. Aims: Our aims were to show that the HANA is a useful tool that can (1) identify action naming impairments and (2) be used to investigate the neural substrates underlying naming. We paired the HANA with the Boston Naming Test (BNT) to compare action and object naming. We considered participants with aphasia due to primary progressive aphasia (PPA) or acute left hemisphere stroke to provide a more comprehensive picture of brain-behaviour relationships critical for naming. Behaviourally, we hypothesised that there would be a double dissociation between object and action naming performance. Neuroanatomically, we hypothesised that different neural substrates would be implicated in object vs. action naming and that different lesion-deficit associations would be identified in participants with PPA vs. acute stroke. Methods & Procedures: Participants (N=138 with PPA, N=37 with acute stroke) completed the BNT and HANA. Behavioural performance was compared. A subset of participants (N=31 with PPA, N=37 with acute stroke) provided neuroimaging data. The whole brain was automatically segmented into regions of interest (ROIs). For participants with PPA, the image variables were the ROI volumes, normalised by the brain volume. For participants with acute stroke, the image variables were the percentage of each ROI affected by the lesion. The relationship between ROIs likely to be involved in naming performance was modelled with LASSO regression. Outcomes & Results: Behavioural results showed a double dissociation in performance: in each group, some participants displayed intact performance relative to healthy controls on actions but not objects and/or significantly better performance on actions than objects, while others showed the opposite pattern. These results support the need to assess both objects and actions when evaluating naming deficits. Neuroimaging results identified different regions associated with object vs. action naming, implicating overlapping but distinct networks of regions. Furthermore, results differed for participants with PPA vs. acute stroke, indicating that critical information may be missed when only one aetiology is considered. Conclusions: Overall, the study provides a more comprehensive picture of the neural bases of naming, underscoring the importance of assessing both objects and actions and considering different aetiologies of damage. It demonstrates the utility of the HANA.

Dysfunctional Tissue Correlates of Unrelated Naming Errors in Acute Left Hemisphere Stroke.

Most naming error lesion-symptom mapping (LSM) studies have focused on semantic and/or phonological errors. Anomic individuals also produce unrelated word errors, which may be linked to semantic or modality-independent lexical deficits. To investigate the neural underpinnings of rarely-studied unrelated errors, we conducted LSM analyses in 100 individuals hospitalized with a left hemisphere stroke who completed imaging protocols and language assessments. We used least absolute shrinkage and selection operator regression to capture relationships between naming errors and dysfunctional brain tissue metrics (regional damage or hypoperfusion in vascular territories) in two groups: participants with and without impaired single-word auditory comprehension. Hypoperfusion-particularly within the parietal lobe-was an important error predictor, especially for the unimpaired group. In both groups, higher unrelated error proportions were associated with primarily ventral stream damage, the language route critical for processing meaning. Nonetheless, brain metrics implicated in unrelated errors were distinct from semantic error correlates.

Dissociable language and executive control deficits and recovery in post-stroke aphasia: An exploratory observational and case series study.

A growing body of evidence indicates many, but not all, individuals with post-stroke aphasia experience executive dysfunction. Relationships between language and executive function skills are often reported in the literature, but the degree of interdependence between these abilities remains largely unanswered. Therefore, in this study, we investigated the extent to which language and executive control deficits dissociated in 1) acute stroke and 2) longitudinal aphasia recovery. Twenty-three individuals admitted to Johns Hopkins Hospital with a new left hemisphere stroke completed the Western Aphasia Battery-Revised (WAB-R), several additional language measures (of naming, semantics, spontaneous speech, and oral reading), and three non-linguistic cognitive tasks from the NIH Toolbox (i.e., Pattern Comparison Processing Speed Test, Flanker Inhibitory Control and Attention Test, and Dimensional Change Card Sort Test). Two participants with aphasia (PWA) with temporoparietal lesions, one of whom (PWA1) had greater temporal but less frontal and superior parietal damage than the other (PWA2), also completed testing at subacute (three months post-onset) and early chronic (six months post-onset) time points. In aim 1, principal component analysis on the acute test data (excluding the WAB-R) revealed language and non-linguistic executive control tasks largely loaded onto separate components. Both components were significant predictors of acute aphasia severity per the WAB-R Aphasia Quotient (AQ). Crucially, executive dysfunction explained an additional 17% of the variance in AQ beyond the explanatory power of language impairments alone. In aim 2, both case patients exhibited language and executive control deficits at the acute post-stroke stage. A dissociation was observed in longitudinal recovery of these patients. By the early chronic time point, PWA1 exhibited improved (but persistent) deficits in several language domains and recovered executive control. In contrast, PWA2 demonstrated mostly recovered language but persistent executive dysfunction. Greater damage to language and attention networks in these respective patients may explain the observed behavioral patterns. These results demonstrate that language and executive control can dissociate (at least to a degree), but both contribute to early post-stroke presentation of aphasia and likely influence longitudinal aphasia recovery.

Transcranial Direct Current Stimulation Paired With Verb Network Strengthening Treatment Improves Verb Naming in Primary Progressive Aphasia: A Case Series.

PURPOSE: There are few evidence-based treatments for language deficits in primary progressive aphasia (PPA). PPA treatments are often adopted from the poststroke aphasia literature. The poststroke aphasia literature has shown promising results using Verb Network Strengthening Treatment (VNeST), a behavioral therapy that focuses on improving naming by producing verbs and their arguments in phrases and sentences. Emerging research in poststroke aphasia and PPA has shown promising results pairing behavioral language therapy with transcranial direct current stimulation (tDCS). METHOD: This study used a double-blind, within-subjects, sham-controlled crossover design to study the effect of anodal tDCS applied to left inferior frontal gyrus (IFG) plus VNeST versus VNeST plus sham stimulation in two individuals with nonfluent variant PPA and one individual with logopenic variant PPA. Participants received two phases of treatment, each with 15 1-hr sessions of VNeST. One phase paired VNeST with tDCS stimulation, and one with sham. For each phase, language testing was conducted at baseline, and at 1 week and 8 weeks posttreatment conclusion. For each participant, treatment efficacy was evaluated for each treatment phase by comparing the mean change in accuracy between baseline and the follow-up time points for naming trained verbs (primary outcome measure), untrained verbs, and nouns on the Object and Action Naming Battery. Mean change from baseline was also directly compared between tDCS and sham phases at each time point. RESULTS: Results revealed a different pattern of outcomes for each of the participants. A tDCS advantage was not found for trained verbs for any participant. Two participants with nonfluent variant PPA had a tDCS advantage for generalization to naming of untrained verbs, which was apparent at 1 week and 8 weeks posttreatment. One participant with nonfluent variant also showed evidence of generalization to sentence production in the tDCS phase. CONCLUSION: VNeST plus anodal tDCS stimulation of left IFG shows promising results for improving naming in PPA.

Neural correlates of syntactic comprehension: A longitudinal study.

Broca's area is frequently implicated in sentence comprehension but its specific role is debated. Most lesion studies have investigated deficits at the chronic stage. We aimed (1) to use acute imaging to predict which left hemisphere stroke patients will recover sentence comprehension; and (2) to better understand the role of Broca's area in sentence comprehension by investigating acute deficits prior to functional reorganization. We assessed comprehension of canonical and noncanonical sentences in 15 patients with left hemisphere stroke at acute and chronic stages. LASSO regression was used to conduct lesion symptom mapping analyses. Patients with more severe word-level comprehension deficits and a greater proportion of damage to supramarginal gyrus and superior longitudinal fasciculus were likely to experience acute deficits prior to functional reorganization. Broca's area was only implicated in chronic deficits. We propose that when temporoparietal regions are damaged, intact Broca's area can support syntactic processing after functional reorganization occurs.

The role of disrupted functional connectivity in aphasia.

Language is one of the most complex and specialized higher cognitive processes. Brain damage to the distributed, primarily left-lateralized language network can result in aphasia, a neurologic disorder characterized by receptive and/or expressive deficits in spoken and/or written language. Most often, aphasia is the consequence of stroke-termed poststroke aphasia (PSA)-yet, aphasia can also manifest due to neurodegenerative disease, specifically, a disorder called primary progressive aphasia (PPA). In recent years, functional connectivity neuroimaging studies have provided emerging evidence supporting theories regarding the relationships between language impairments, structural brain damage, and functional network properties in these two disorders. This chapter reviews the current evidence for the "network phenotype of stroke injury" hypothesis (Siegel et al., 2016) as it pertains to PSA and the "network degeneration hypothesis" (Seeley et al., 2009) as it pertains to PPA. Methodologic considerations for functional connectivity studies, limitations of the current functional connectivity literature in aphasia, and future directions are also discussed.

Executive control deficits and lesion correlates in acute left hemisphere stroke survivors with and without aphasia.

In contrast to the traditional definition of the disorder, many individuals with aphasia exhibit non-linguistic cognitive impairments, including executive control deficits. Classic lesion studies cite frontal lobe damage in executive dysfunction, but more recent lesion symptom-mapping studies in chronic aphasia present mixed results. In this study, we compared executive control abilities of acute stroke survivors with and without aphasia and investigated lesion correlates of linguistic and non-linguistic cognitive tasks. Twenty-nine participants with acute left hemisphere stroke resulting in aphasia (n = 14) or no aphasia (n = 15) completed clinical MRI and testing, including three NIH Toolbox Cognition Batteries (Pattern Comparison Processing Speed, Flanker Inhibitory Control and Attention, and Dimensional Change Card Sort Tests) and the Boston Naming Test. We compared performance between groups using Wilcoxon rank sum tests. We used Least Absolute Shrinkage and Selection Operator Regression to identify neural markers (percent regional damage, hypoperfusion within vascular territories, and total lesion volume) of executive control deficits and anomia. Group performance was comparable on the Pattern Comparison Processing Speed Test, but people with aphasia had poorer standard scores, lower accuracy, and slower response times on the Dimensional Change Card Sort Test than people without aphasia. Damage to extrasylvian regions (dorsolateral prefrontal cortex, intraparietal sulcus) was related to executive control deficits, whereas language network damage (to inferior frontal and superior and posterior middle temporal gyri) was linked to naming impairments. These results suggest people with aphasia can exhibit comorbid executive control impairments linked to damage outside classic language network areas.

Abnormally weak functional connections get stronger in chronic stroke patients who benefit from naming therapy.

Language recovery in aphasia is likely supported by a network of brain regions, but few studies have investigated treatment-related changes in functional connectivity while controlling for the absence of treatment. We examined functional connectivity in a 38-region picture-naming network in 30 patients with chronic aphasia who did or did not receive naming therapy. Compared to healthy controls, patients had abnormally low connectivity in a subset of connections from the naming network. Linear mixed models showed that the connectivity of abnormal connections increased significantly in patients who benefited from therapy, but not in those who did not benefit from or receive therapy. Changes in responders were specific to abnormal connections and did not extend to the larger network. Thus, successful naming therapy was associated with increased connectivity in connections that were abnormal prior to treatment. The potential to strengthen such connections may be a prerequisite for a successful treatment response.

Explicit Training to Improve Affective Prosody Recognition in Adults with Acute Right Hemisphere Stroke.

Difficulty recognizing affective prosody (receptive aprosodia) can occur following right hemisphere damage (RHD). Not all individuals spontaneously recover their ability to recognize affective prosody, warranting behavioral intervention. However, there is a dearth of evidence-based receptive aprosodia treatment research in this clinical population. The purpose of the current study was to investigate an explicit training protocol targeting affective prosody recognition in adults with RHD and receptive aprosodia. Eighteen adults with receptive aprosodia due to acute RHD completed affective prosody recognition before and after a short training session that targeted proposed underlying perceptual and conceptual processes. Behavioral impairment and lesion characteristics were investigated as possible influences on training effectiveness. Affective prosody recognition improved following training, and recognition accuracy was higher for pseudo- vs. real-word sentences. Perceptual deficits were associated with the most posterior infarcts, conceptual deficits were associated with frontal infarcts, and a combination of perceptual-conceptual deficits were related to temporoparietal and subcortical infarcts. Several right hemisphere ventral stream regions and pathways along with frontal and parietal hypoperfusion predicted training effectiveness. Explicit acoustic-prosodic-emotion training improves affective prosody recognition, but it may not be appropriate for everyone. Factors such as linguistic context and lesion location should be considered when planning prosody training.

Characterizing subtypes and neural correlates of receptive aprosodia in acute right hemisphere stroke.

INTRODUCTION: Speakers naturally produce prosodic variations depending on their emotional state. Receptive prosody has several processing stages. We aimed to conduct lesion-symptom mapping to determine whether damage (core infarct or hypoperfusion) to specific brain areas was associated with receptive aprosodia or with impairment at different processing stages in individuals with acute right hemisphere stroke. We also aimed to determine whether different subtypes of receptive aprosodia exist that are characterized by distinctive behavioral performance patterns. METHODS: Twenty patients with receptive aprosodia following right hemisphere ischemic stroke were enrolled within five days of stroke; clinical imaging was acquired. Participants completed tests of receptive emotional prosody, and tests of each stage of prosodic processing (Stage 1: acoustic analysis; Stage 2: analyzing abstract representations of acoustic characteristics that convey emotion; Stage 3: semantic processing). Emotional facial recognition was also assessed. LASSO regression was used to identify predictors of performance on each behavioral task. Predictors entered into each model included 14 right hemisphere regions, hypoperfusion in four vascular territories as measured using FLAIR hyperintense vessel ratings, lesion volume, age, and education. A k-medoid cluster analysis was used to identify different subtypes of receptive aprosodia based on performance on the behavioral tasks. RESULTS: Impaired receptive emotional prosody and impaired emotional facial expression recognition were both predicted by greater percent damage to the caudate. The k-medoid cluster analysis identified three different subtypes of aprosodia. One group was primarily impaired on Stage 1 processing and primarily had frontotemporal lesions. The second group had a domain-general emotion recognition impairment and maximal lesion overlap in subcortical areas. Finally, the third group was characterized by a Stage 2 processing deficit and had lesion overlap in posterior regions. CONCLUSIONS: Subcortical structures, particularly the caudate, play an important role in emotional prosody comprehension. Receptive aprosodia can result from impairments at different processing stages.

Stroke Recurrence and Its Relationship With Language Abilities.

Purpose Many factors influence poststroke language recovery, yet little is known about the influence of previous stroke(s) on language after left hemisphere stroke. In this prospective longitudinal study, we investigated the role of prior stroke on language abilities following an acute left hemisphere ischemic stroke, while controlling for demographic and stroke-related factors, and examined if earlier stroke impacted language recovery at a chronic time point. Method Participants (n = 122) with acute left hemisphere ischemic stroke completed language evaluation and clinical neuroimaging. They were divided into two groups: single stroke (SS; n = 79) or recurrent stroke (RS; n = 43). A subset of participants (n = 31) completed chronic-stage re-evaluation. Factors studied included age, education, diabetes and hypertension diagnoses, lesion volume and broad location, group status, aphasia prevalence, and language scores. Results Groups did not differ in language performance across time points. The only significant group differences were that participants with RS were older, had smaller acute lesions, and were less educated. Stroke group membership (SS vs. RS) was not associated with language performance at either time point. In patients with prior stroke, large acute lesion volumes were associated with acute language performance, whereas both large acute and chronic volumes influenced recovery. Conclusions History of prior stroke in itself may not significantly influence language impairment after an additional acute left hemisphere stroke, unless it contributes substantially to the total volume of infarcted brain tissue. Chronic and acute lesion volumes should be accounted for in studies investigating poststroke language performance and recovery. Supplemental Material https://doi.org/10.23641/asha.14669715.

Thalamic Nuclei and Thalamocortical Pathways After Left Hemispheric Stroke and Their Association with Picture Naming.

Background: Previous studies utilized lesion-centric approaches to study the role of the thalamus in language. In this study, we tested the hypotheses that non-lesioned dorsomedial and ventral anterior nuclei (DMVAC) and pulvinar lateral posterior nuclei complexes (PLC) of the thalamus and their projections to the left hemisphere show secondary effects of the strokes, and that their microstructural integrity is closely related to language-related functions. Methods: Subjects with language impairments after a left-hemispheric cortical and/or subcortical, early stroke (n = 31, ≤6 months) or late stroke (n = 30, ≥12 months) sparing thalamus underwent the Boston Naming Test (BNT) and diffusion tensor imaging (DTI). The tissue integrity of DMVAC, PLC, and their cortical projections was quantified with DTI. The right-left asymmetry profiles of these structures were evaluated in relation to the time since stroke. The association between microstructural integrity and BNT score was investigated in relation to stroke chronicity with partial correlation analyses adjusted for confounds. Results: In both early stroke and late stroke groups, left-sided tracts showed significantly higher mean diffusivities (MDs), which were likely due to Wallerian degeneration. Higher MD values of the cortical projections from the left PLC (r = -0.5, p = 0.005) and DMVAC (r = -0.53, p = 0.002) were correlated with lower BNT score in the late stroke but not early stroke group. Conclusion: Nonlesioned thalamic nuclei and thalamocortical pathways show rightward lateralization of the microstructural integrity after a left hemispheric stroke, and this pattern is associated with poorer naming. Impact statement To the best of our knowledge, our study is the first diffusion tensor imaging study suggesting that the thalamic nuclei and pathways of the left hemisphere spared by direct ischemic insult undergo secondary degeneration over time that is associated with poorer picture naming. Our study may pave the way for targeted interventions such as invasive or noninvasive brain stimulation techniques that engage these spared pathways to prevent secondary degeneration and lead to better outcomes in poststroke aphasia.

Naming errors and dysfunctional tissue metrics predict language recovery after acute left hemisphere stroke.

Language recovery following acute left hemisphere (LH) stroke is notoriously difficult to predict. Global language measures (e.g., overall aphasia severity) and gross lesion metrics (e.g., size) provide incomplete recovery predictions. In this study, we test the hypothesis that the types of naming errors patients produce, combined with dysfunctional brain tissue metrics, can provide additional insight into recovery following acute LH stroke. One hundred forty-eight individuals who were hospitalized with a new LH stroke completed clinical neuroimaging and assessments of naming and global language skills. A subset of participants again completed language testing at subacute, early (5-7 months post-stroke), and late (≥11 months post-stroke) chronic phases. At each time point, we coded naming errors into four types (semantic, phonological, mixed and unrelated) and determined error type totals and proportions. Dysfunctional tissue measures included the percentage of damage to language network regions and hypoperfusion in vascular territories. A higher proportion of semantic errors was associated with better acute naming, but higher proportions of other error types was related to poorer accuracy. Naming and global language skills significantly improved over time , but naming error profiles did not change. Fewer acute unrelated errors and less damage to left angular gyrus resulted in optimal naming and language recovery by the final testing time point, yet patients with more acute errors and damage to left middle temporal gyrus demonstrated the greatest increases in language over time. These results illustrate that naming error profiles, particularly unrelated errors, add power to predictions of language recovery after stroke.