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.

Voice-specific proper name anomia ('phonoanomia') after bilateral temporal hemorrhagic brain lesions.

We describe a patient who developed bilateral temporal lesions due to a haemorrhagic stroke. One year after onset, he showed marked apperceptive prosopagnosia and could not name people from their voices, although he had spared semantic knowledge about people he could not name and could access this knowledge from people's voice. Importantly, the patient was able to retrieve proper name of persons after their description and was able to name sounds and songs; he could also retrieve proper names of monuments, towns and cartoon characters upon visual presentation. No further relevant cognitive impairment was present. This clinical picture represents the auditory counterpart of prosopanomia and could be defined 'phonoanomia'. This case report suggests that naming people from their voice implies specific retrieval processes, and pose specific constraints to theoretical models of person recognition.

Speech and Language Presentations of FTLD-TDP Type B Neuropathology.

Four right-handed patients who presented with an isolated impairment of speech or language had transactive response DNA-binding protein of 43 kDa (TDP-43) type B pathology. Comportment and pyramidal motor function were preserved at presentation. Three of the cases developed axial rigidity and oculomotor findings late in their course with no additional pyramidal or lower motor neuron impairments. However, in all 4 cases, postmortem examination disclosed some degree of upper and lower motor neuron disease (MND) pathology in motor cortex, brainstem, and spinal cord. Although TDP-43 type B pathology is commonly associated with MND and behavioral variant frontotemporal dementia, it is less recognized as a pathologic correlate of primary progressive aphasia and/or apraxia of speech as the presenting syndrome. These cases, taken together, contribute to the growing heterogeneity in clinical presentations associated with TDP pathology. Additionally, 2 cases demonstrated left anterior temporal lobe atrophy but without word comprehension impairments, shedding light on the relevance of the left temporal tip for single-word comprehension.

What Cognitive Neurology Teaches Us about Our Experience of Color.

Color provides valuable information about the environment, yet the exact mechanisms explaining how colors appear to us remain poorly understood. Retinal signals are processed in the visual cortex through high-level mechanisms that link color perception with top-down expectations and knowledge. Here, we review the neuroimaging evidence about color processing in the brain, and how it is affected by acquired brain lesions in humans. Evidence from patients with brain-damage suggests that high-level color processing may be divided into at least three modules: perceptual color experience, color naming, and color knowledge. These modules appear to be functionally independent but richly interconnected, and serve as cortical relays linking sensory and semantic information, with the final goal of directing object-related behavior. We argue that the relations between colors and their objects are key mechanisms to understand high-level color processing.

Selection for sentence generation in the context of severe anomia: A case series of left temporal patients.

INTRODUCTION: Anomia is an impairment of naming: the retrieval of specific lexical items from the mental lexicon. Theoretically, whether anomia reflects a failure of selection at the preverbal "idea" level or at the subsequent linguistic formulation stage remains a topic of debate. We investigated the preverbal mechanism of idea selection for sentence generation, which requires the selection of a proposition from among competing alternatives during message formulation, in patients with severe anomia. METHOD: Patients with lesions to the left temporal lobe (N = 12), presenting with clinically defined anomia, and matched healthy controls (N = 24) completed sentence-level tasks that required the oral generation of a sentence or single word when presented with a word, a word pair, or a sentence. Selection demands were manipulated so that the stimuli activated many competing response options (low constraint) or one dominant or few response options (high constraint). RESULTS: There was no effect of stimuli constraint in the patient group that differed from that in the healthy control group on any of the generation tasks, suggesting that idea-level selection is intact in the patient group. CONCLUSIONS: These findings have implications for theoretical models of spoken language production and for clinical treatments of anomia.

Cognitive consequences of the left-right asymmetry of atrophy in semantic dementia.

Semantic dementia (SD) is a condition in which atrophy to the anterior temporal lobes (ATL) produces a selective deterioration of conceptual knowledge. As this atrophy is always bilateral but usually asymmetrical, differences in performance of the two SD subgroups-with left > right (L > R) versus right > left (R > L) atrophy-constitute a major source of evidence regarding the roles of the left and right sides of this region. We explored this issue using large scale case-series methodology, with a pool of 216 observations of neuropsychological data from 72 patients with SD. Anomia was significantly more severe in the L > R subgroup, even when cases from the two subgroups were matched on severity of comprehension deficits. For subgroups matched on the degree of anomia, we show that asymmetry of atrophy also affected both the nature of the naming errors produced, and the degree of a semantic category effect (living things vs artefacts). A comparison across tasks varying in their loading on verbal and visual processing revealed a greater deficit in object naming for L > R cases and in a picture-based semantic association test for R > L cases; this held true whether severity across subgroups was controlled using pairwise matching or statistically via principal components analysis. Importantly, the size of our sample allowed us to demonstrate considerable individual variation within each of the L > R and R > L subgroups, with consequent overlap between them. Our results paint a clear picture of how asymmetry of atrophy affects cognitive performance in SD, and we discuss the results in terms of two mechanisms that could contribute to these differences: variation in the information involved in semantic representations in the left and right ATL, and preferential connectivity between each ATL and other more modality specific intra-hemispheric regions.

Subjective experience of inner speech in aphasia: Preliminary behavioral relationships and neural correlates.

Many individuals with aphasia describe anomia with comments like "I know it but I can't say it." The exact meaning of such phrases is unclear. We hypothesize that at least two discrete experiences exist: the sense of (1) knowing a concept, but failing to find the right word, and (2) saying the correct word internally but not aloud (successful inner speech, sIS). We propose that sIS reflects successful lexical access; subsequent overt anomia indicates post-lexical output deficits. In this pilot study, we probed the subjective experience of anomia in 37 persons with aphasia. Self-reported sIS related to aphasia severity and phonological output deficits. In multivariate lesion-symptom mapping, sIS was associated with dorsal stream lesions, particularly in ventral sensorimotor cortex. These preliminary results suggest that people with aphasia can often provide meaningful insights about their experience of anomia and that reports of sIS relate to specific lesion locations and language deficits.

Common and divergent neural correlates of anomia in amnestic and logopenic presentations of Alzheimer's disease.

The majority of logopenic variant primary progressive aphasia (lv-PPA) cases harbour Alzheimer pathology, suggesting that lv-PPA constitutes an atypical presentation of Alzheimer's disease (AD). However, even if caused by Alzheimer pathology, the clinical manifestations of lv-PPA differ from those observed in the typical or amnestic AD presentation: in lv-PPA, aphasia is the main feature while amnestic AD is characterised by impaired episodic memory. Anomia or impaired naming, however, is present in both AD presentations. Whether these presentations share anatomical and mechanistic processes of anomia has not been fully investigated. Accordingly, we studied naming performance and its relationship with regions of brain atrophy in 23 amnestic AD and 22 lv-PPA cases with presumed underlying Alzheimer pathology. Both AD groups displayed some degree of anomia and impaired word comprehension but these were particularly severe in lv-PPA and accompanied by a range of linguistic deficits, comprising phonological substitutions, superordinate semantic paraphasias and abnormal single-word repetition. Analysis of cortical thickness revealed that anomia was correlated with thinning in left superior temporal gyrus in both groups. In amnestic AD, however, anomia was also associated with thinning in right inferior temporal regions. Single-word comprehension (SWC), by contrast, was associated with cortical thinning involving bilateral fusiform gyri in both groups. These findings suggest that anomia in both amnestic AD and lv-PPA results from the involvement at multiple steps of word processing, in particular, semantic and lexical retrieval; in addition lv-PPA patients display a more marked involvement of phonological processing.

Differences in visual naming performance between patients with temporal lobe epilepsy associated with temporopolar lesions versus hippocampal sclerosis.

OBJECTIVE: Naming difficulties are frequently observed in patients with temporal lobe epilepsy (TLE). Although damage/removal of regions of the anterior temporal neocortex including the temporal pole is considered critical for those difficulties, 1 relevant hypothesis proposes that hippocampal damage also has a role. Our aim was to better understand the specific involvement of temporal pole and hippocampus in visual object naming. METHOD: We assessed 2 types of patients with TLE on a visual confrontation-naming task: patients with hippocampal sclerosis (HS; n = 16) and patients with a lesion on the tip of the temporal pole that spared the hippocampus entirely (n = 18). A common battery of verbal and nonverbal semantic tasks was administered and used as a semantic memory background. Control group were 20 matched healthy participants. RESULTS: Patients with lesions on their temporal poles differed from patients with HS and control group on naming ability, proportion and rate of error type, and influence of concept familiarity. Of note, naming performance was not affected by hippocampal damage. Using a Bayesian model averaging approach, we found that the number of omission errors distinguished patients with temporal pole damage from patients with HS and controls. This differential pattern occurred despite similar impairment on the semantic memory background in both clinical groups. CONCLUSION: Current findings provide evidence that temporal pole damage produces or contributes to naming impairment in TLE, while also suggesting that the hippocampus is not critical for naming. They also highlight the importance of error-type analysis when evaluating visual naming in TLE. (PsycINFO Database Record

Success of Anomia Treatment in Aphasia Is Associated With Preserved Architecture of Global and Left Temporal Lobe Structural Networks.

BACKGROUND AND OBJECTIVE: Targeted speech therapy can lead to substantial naming improvement in some subjects with anomia following dominant-hemisphere stroke. We investigated whether treatment-induced improvement in naming is associated with poststroke preservation of structural neural network architecture. METHODS: Twenty-four patients with poststroke chronic aphasia underwent 30 hours of speech therapy over a 2-week period and were assessed at baseline and after therapy. Whole brain maps of neural architecture were constructed from pretreatment diffusion tensor magnetic resonance imaging to derive measures of global brain network architecture (network small-worldness) and regional network influence (nodal betweenness centrality). Their relationship with naming recovery was evaluated with multiple linear regressions. RESULTS: Treatment-induced improvement in correct naming was associated with poststroke preservation of global network small worldness and of betweenness centrality in temporal lobe cortical regions. Together with baseline aphasia severity, these measures explained 78% of the variability in treatment response. CONCLUSIONS: Preservation of global and left temporal structural connectivity broadly explains the variability in treatment-related naming improvement in aphasia. These findings corroborate and expand on previous classical lesion-symptom mapping studies by elucidating some of the mechanisms by which brain damage may relate to treated aphasia recovery. Favorable naming outcomes may result from the intact connections between spared cortical areas that are functionally responsive to treatment.

Is the logopenic-variant of primary progressive aphasia a unitary disorder?

Logopenic progressive aphasia is one of the clinical presentations of primary progressive aphasia and formally defined by the co-occurrence of impaired naming and sentence repetition. Impaired naming is attributed to failure of lexical retrieval, which is a multi-staged process subserved by anatomically segregated brain regions. By dissecting the neurocognitive processes involved in impaired naming, we aimed to disentangle the clinical and neuroanatomical heterogeneity of this syndrome. Twenty-one individuals (66.7% females, age range 53-83 years) who fulfilled diagnostic criteria for logopenic variant and had at least two clinical and language assessments, 1 year apart, were recruited and matched for age, sex distribution and level of education with a healthy control sample (n = 18). All participants underwent a structural brain scan at the first visit and surface-wise statistical analysis using Freesurfer. Seventeen participants with logopenic variant underwent amyloid imaging, with 14 demonstrating high amyloid retention. Based on their performance on single-word comprehension, repetition and confrontation naming, three subgroups of logopenic cases with distinctive linguistic profiles and distribution of atrophy were identified. The first subgroup (n = 10) demonstrated pure anomia and left-sided atrophy in the posterior inferior parietal lobule and lateral temporal cortex. The second subgroup (n = 6), presented additional mild deficits in single-word comprehension, and also exhibited bilateral thinning of the fusiform gyri. The third subgroup (n = 5) showed additional impaired single-word repetition, and cortical thinning focused on the left superior temporal gyrus. The subgroups differed in the proportion of cases with high amyloid retention and in the rate of decline of naming performance over time, suggesting that neurodegeneration spreads differentially throughout regions subserving word processing. In line with previous reports, these results confirm the extensive damage to the language network and, in part, explain the clinical heterogeneity observed across logopenic cases.

Proper name anomia with preserved lexical and semantic knowledge after left anterior temporal lesion: a two-way convergence defect.

This article describes the case of a patient who, following herpes simplex encephalitis (HSE), retained the ability to access rich conceptual semantic information for familiar people whom he was no longer able to name. Moreover, this patient presented the very rare combination of name production and name comprehension deficits for different categories of proper names (persons and acronyms). Indeed, besides his difficulty to retrieve proper names, SL presented a severe deficit in understanding and identifying them. However, he was still able to recognize proper names on familiarity decision, demonstrating that name forms themselves were intact. We interpret SL's deficit as a rare form of two-way lexico-semantic disconnection, in which intact lexical knowledge is disconnected from semantic knowledge and face units. We suggest that this disconnection reflects the role of the left anterior temporal lobe in binding together different types of knowledge and supports the classical convergence-zones framework (e.g., Damasio, 1989) rather than the amodal semantic hub theory (e.g., Patterson, Nestor, & Rogers, 2007).

Proper name anomia after right-hemispheric lesion: a case study.

This study describes the case of CH, a 68-year-old left-handed woman who suffered a right temporo-parieto-occipital infarct in the territory of the middle cerebral artery and who exhibits severe proper name anomia. During the acute stage, CH was diagnosed with severe amnestic aphasia (Aachen Aphasia Test). Her lesion mirrors those of left hemisphere impairing the processing proper names, without an aphasic language disorder in general. Seven weeks later, language improved to a mild amnestic aphasia that currently does not interfere with her daily life. However, the use of proper names in both the visual and auditory modalities was still impaired and showed no improvement after 6 months of speech therapy. While not being able to name family members or familiar persons, she was, however, still able to describe the persons' backgrounds along with some additional semantic information. Furthermore, in a simple semantic design test, CH was selectively impaired in correctly classifying proper names into their respective word classes. Conversely, she was able to correctly name and classify other word categories (e.g., common nouns). In the subsequent study, we assessed the modalities "auditory comprehension," "picture naming," and "reading comprehension" and classified her responses in the categories "correctly named," "correctly classified," "correctly described attributes" (e.g., occupation) and "falsely named." The results were compared with those of an age-matched healthy control group. In the visual task, CH correctly named 80% of the visualized objects, 3% of the familiar persons and 15% of the familiar city views.

Proper name anomia in poststroke aphasics: evidence from a multiple-case study.

We aimed to characterize difficulties in famous face naming in three poststroke aphasic patients with a lesion limited to the left mid-posterior temporal language regions, sparing the anterior temporal lobe. The patients did not present semantic deficits specific to known people. Nonetheless, they showed difficulties naming famous buildings in addition to famous faces, but they were comparable to healthy controls in generating proper names. Our results support the critical role of the mid-posterior temporal language regions in the lexical retrieval of proper names, namely from pictorial stimuli, in absence of semantic impairments.

Changes in white matter connectivity following therapy for anomia post stroke.

BACKGROUND: The majority of studies investigating the neural mechanisms underlying treatment-induced recovery in aphasia have focused on the cortical regions associated with language processing. However, the integrity of the white matter connecting these regions may also be crucial to understanding treatment mechanisms. OBJECTIVE: This study investigated the integrity of the arcuate fasciculus (AF) and uncinate fasciculus (UF) before and after treatment for anomia in people with aphasia. METHOD: Eight people with aphasia received 12 treatment sessions to improve naming; alternating between phonologically-based and semantic-based tasks, with high angular resolution diffusion imaging conducted pre and post treatment. The mean generalized fractional anisotropy (GFA), a measure of fiber integrity, and number of fibers in the AF and UF were compared pre and post treatment, as well as with a group of 14 healthy older controls. RESULTS: Pre treatment, participants with aphasia had significantly fewer fibers and lower mean GFA in the left AF compared with controls. Post treatment, mean GFA increased in the left AF to be statistically equivalent to controls. Additionally, mean GFA in the left AF pre and post treatment positively correlated with maintenance of the phonologically based treatment. No differences were found in the right AF, or the UF in either hemisphere, between participants with aphasia and controls, and no changes were observed in these tracts following treatment. CONCLUSIONS: Anomia treatments may improve the integrity of the white matter connecting cortical language regions. These preliminary results add to the understanding of the mechanisms underlying treatment outcomes in people with aphasia post stroke.

The involvement of the thalamus in semantic retrieval: a clinical group study.

There is increasing attention about the role of the thalamus in high cognitive functions, including memory. Although the bulk of the evidence refers to episodic memory, it was recently proposed that the mediodorsal (MD) and the centromedian-parafascicular (CM-Pf) nuclei of the thalamus may process general operations supporting memory performance, not only episodic memory. This perspective agrees with other recent fMRI findings on semantic retrieval in healthy participants. It can therefore be hypothesized that lesions to the MD and the CM-Pf impair semantic retrieval. In this study, 10 patients with focal ischemic lesions in the medial thalamus and 10 healthy controls matched for age, education, and verbal IQ performed a verbal semantic retrieval task. Patients were assigned to a target clinical group and a control clinical group based on lesion localization. Patients did not suffer from aphasia and performed in the range of controls in a categorization and a semantic association task. However, target patients performed poorer than healthy controls on semantic retrieval. The deficit was not because of higher distractibility but of an increased rate of false recall and, in some patients, of a considerably increased rate of misses. The latter deficit yielded a striking difference between the target and the control clinical groups and is consistent with anomia. Follow-up high-resolution structural scanning session in a subsample of patients revealed that lesions in the CM-Pf and MD were primarily associated with semantic retrieval deficits. We conclude that integrity of the MD and the CM-Pf is required for semantic retrieval, possibly because of their role in the activation of phonological representations.

Covert reading of letters in a case of global alexia.

This study describes the case of a global alexic patient with a severe reading deficit affecting words, letters and Arabic numbers, following a left posterior lesion. The patient (VA) could not match spoken letters to their graphic form. A preserved ability to recognize shape and canonical orientation of letters indicates intact access to the representation of letters and numbers as visual objects. A relatively preserved ability to match lowercase to uppercase letters suggests partially spared access to abstract letter identities independently of their visual forms. The patient was also unable to match spoken letters and numbers to their visual form, indicating that she could not access the graphemic representations of letters from their phonological representations. This pattern of performance suggests that the link between graphemic and phonological representations is disrupted in this patient. We hypothesize that VA' residual reading abilities are supported by the right hemisphere.

Semantic interference during object naming in agrammatic and logopenic primary progressive aphasia (PPA).

This study examined the time course of object naming in 21 individuals with primary progressive aphasia (PPA) (8 agrammatic (PPA-G); 13 logopenic (PPA-L)) and healthy age-matched speakers (n=17) using a semantic interference paradigm with related and unrelated interfering stimuli presented at stimulus onset asynchronies (SOAs) of -1000, -500, -100 and 0 ms. Results showed semantic interference (SI) (i.e. significantly slower RTs in related compared to unrelated conditions) for all groups at -500, -100 and 0 ms, indicating timely spreading activation to semantic competitors. However, both PPA groups showed a greater magnitude of SI than normal across SOAs. The PPA-L group and six PPA-G participants also evinced SI at -1000 ms, suggesting an abnormal time course of semantic interference resolution, and concomitant left hemisphere cortical atrophy in brain regions associated with semantic processing. These subtle semantic mapping impairments in non-semantic variants of PPA may contribute to the anomia of these patients.

Naming with proper names: the left temporal pole theory.

Existing empirical data on proper names processing are critically reviewed in trying to understand which tasks may involve the left temporal pole, which proper name related functions are supported by this structure and eventually offer some speculations about why these functions might have developed in this location in the course of human evolution. While clinical group studies support the idea that proper name processing takes place in the left temporal pole, single case studies of selective proper name anomia or sparing, as well as neuroimaging studies, suggest the involvement of a larger neural network. Within this network, an important role may be played by the ventro-medial prefrontal cortex, including areas critical in social interaction. The differentiation in the brain of proper name processing from common names processing could in part be due to social pressure, favouring a neural system able to more efficiently and unambiguously sustain designating categories or designating individual entities. The activation of the left temporal pole in proper name processing is shown to increase with age. Longer social interaction may thus contribute to convey proper names processing toward areas closer to those supporting social cognition.

Preservation and modulation of specific left hemisphere regions is vital for treated recovery from anomia in stroke.

The location and extent of brain changes that support recovery in chronic stroke is probably related to the structural integrity of the remaining cortex. However, little is known about the specifics of this relationship and how it influences treatment outcome in chronic stroke. To examine this issue, the current study examined frank brain damage and changes in cortical activation as predictors of language-treatment outcome in patients with chronic aphasia caused by stroke. Twenty-six patients received multiple MRI sessions before and after 30 h of aphasia treatment targeting anomia, an impairment in the ability to name common objects. Improved naming was associated with increased brain activation in the anterior and posterior regions of the left hemisphere, whereas damage to the posterior portion of the left middle temporal lobe and the temporal-occipital junction had a particularly negative effect on treatment outcome. Specifically, patients whose brain damage included regions commonly associated with lexical retrieval and phonological processing (e.g., Brodmann's areas 37 and 39) were less likely to show treatment-related improvement in correct naming compared with cases where the same areas were intact. These findings suggest that brain changes associated with improved naming ability in chronic aphasia rely on preservation and recruitment of eloquent cortex in the left hemisphere. In general, it seems likely that a similar relationship between cortical preservation and recruitment may also pertain to recovery from other functional impairments in chronic stroke.