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Language impairments caused by stroke (post-stroke aphasia, PSA) and neurodegeneration (primary progressive aphasia, PPA) have overlapping symptomatology, nomenclature and are classically divided into categorical subtypes. Surprisingly, PPA and PSA have rarely been directly compared in detail. Rather, previous studies have compared certain subtypes (e.g. semantic variants) or have focused on a specific cognitive/linguistic task (e.g. reading). This study assessed a large range of linguistic and cognitive tasks across the full spectra of PSA and PPA. We applied varimax-rotated principal component analysis to explore the underlying structure of the variance in the assessment scores. Similar phonological, semantic and fluency-related components were found for PSA and PPA. A combined principal component analysis across the two aetiologies revealed graded intra- and intergroup variations on all four extracted components. Classification analysis was used to test, formally, whether there were any categorical boundaries for any subtypes of PPA or PSA. Semantic dementia formed a true diagnostic category (i.e. within group homogeneity and distinct between-group differences), whereas there was considerable overlap and graded variations within and between other subtypes of PPA and PSA. These results suggest that (i) a multidimensional rather than categorical classification system may be a better conceptualization of aphasia from both causes; and (ii) despite the very different types of pathology, these broad classes of aphasia have considerable features in common.

Impaired social cognition is a core deficit in frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. Social cognitive changes are also common in semantic dementia, with atrophy centred on the anterior temporal lobes. The impairment of social behaviour in FTD has typically been attributed to damage to the orbitofrontal cortex and/or temporal poles and/or the uncinate fasciculus that connects them. However, the relative contributions of each region are unresolved. In this review, we present a unified neurocognitive model of controlled social behaviour that not only explains the observed impairment of social behaviours in FTD, but also assimilates both consistent and potentially contradictory findings from other patient groups, comparative neurology and normative cognitive neuroscience. We propose that impaired social behaviour results from damage to two cognitively- and anatomically-distinct components. The first component is social-semantic knowledge, a part of the general semantic-conceptual system supported by the anterior temporal lobes bilaterally. The second component is social control, supported by the orbitofrontal cortex, medial frontal cortex and ventrolateral frontal cortex, which interacts with social-semantic knowledge to guide and shape social behaviour. [ABSTRACT FROM AUTHOR]

Focal brain damage caused by stroke can result in aphasia and advances in cognitive neuroscience suggest that impairment may be associated with network-level disorder rather than just circumscribed cortical damage. A number of studies have shown meaningful relationships between brain-behaviour using lesions; however only a handful of studies have incorporated in-vivo structural and functional connectivity. Patients with chronic post-stroke aphasia were assessed with structural (N = 68) and functional (N = 39) MRI to assess whether predicting performance can be improved with multiple modalities and if additional variance can be explained compared to lesion models alone. These neural measurements were used to construct models to predict four key language-cognitive factors: 1) phonology, 2) semantics, 3) executive function, and 4) fluency. Our results showed that each factor (except executive ability) could be significantly related to each neural measurement alone; however, structural and functional connectivity models did not explain additional variance above the lesion models. We did find evidence that the structural and functional predictors may be linked to the core lesion sites. First, the predictive functional connectivity features were found to be located within functional resting state networks identified in healthy controls, suggesting that the result might reflect functionally-specific reorganisation (damage to a node within a network can result in disruption to the entire network). Second, predictive structural connectivity features were located within core lesion sites, suggesting that multi-modal information may be redundant in prediction modelling. In addition, we observed that the optimum sparsity within the regularised regression models differed for each behavioural component and across different imaging features, suggesting that future studies should consider optimising hyperparameters related to sparsity per target. Together, the results indicate that the observed network-level disruption was predicted by the lesion alone and does not significantly improve model performance in predicting the profile of language impairment. [ABSTRACT FROM AUTHOR]

For decades, category-specific semantic impairment--i.e., better comprehension of items from one semantic category than another--has been the driving force behind many claims about the organisation of conceptual knowledge in the brain. Double dissociations between patients with category-specific disorders are widely interpreted as showing that different conceptual domains are necessarily supported by functionally independent systems. We show that, to the contrary, even strong or classical dissociations can also arise from individual differences in premorbid expertise. We examined two patients with global and progressive semantic degradation who, unusually, had known areas of premorbid expertise. Patient 1, a former automotive worker, showed selective preservation of car knowledge, whereas Patient 2, a former botanist, showed selective preservation of information about plants. In non-expert domains, these patients showed the typical pattern: i.e., an inability to differentiate between highly similar concepts (e.g., rose and daisy), but retention of broader distinctions (e.g., between rose and cat). Parallel distributed processing (PDP) models of semantic cognition show that expertise in a particular domain increases the differentiation of specific-level concepts, such that the semantic distance between these items resembles non-expert basic-level distinctions. We propose that these structural changes interact with global semantic degradation, particularly when expert knowledge is acquired early and when exposure to expert concepts continues during disease progression. Therefore, category-specific semantic impairment can arise from at least two distinct mechanisms: damage to representations that are critical for a particular category (e.g., knowledge of hand shape and action for the category "tools") and differences in premorbid experience. (Contains 12 figures and 2 tables.)

The key question of how the brain codes the meaning of words and pictures is the focus of vigorous debate. Is there a "semantic hub" in the temporal poles where these different inputs converge to form amodal conceptual representations? Alternatively, are there distinct neural circuits that underpin our comprehension of pictures and words? Understanding words might be primarily left-lateralised, linked to other language areas, while semantic representation of pictures may be more bilateral. To elucidate this debate, we used offline, low-frequency, repetitive transcranial magnetic stimulation (rTMS) to disrupt neural processing temporarily in the left or right temporal poles. During the induced refractory period, participants made judgements of semantic association for verbal and pictorial stimuli. The efficiency of semantic processing was reduced by rTMS, yet a perceptual task of comparable difficulty was unaffected. rTMS applied to the left or right temporal poles disrupted semantic processing for words and pictures to the same degree, while rTMS delivered at a control site had no impact. The results confirm that both temporal poles form a critical substrate within the neural network that supports conceptual knowledge, regardless of modality. (Contains 4 figures.)

Focal brain lesions are assumed to produce language deficits by two basic mechanisms: local cortical dysfunction at the lesion site, and remote cortical dysfunction due to disruption of the transfer and integration of information between connected brain regions. However, functional imaging studies investigating language outcome after aphasic stroke have tended to focus only on the role of local cortical function. In this positron emission tomography functional imaging study, we explored relationships between language comprehension performance after aphasic stroke and the functional connectivity of a key speech-processing region in left anterolateral superior temporal cortex. We compared the organization of left anterolateral superior temporal cortex functional connections during narrative speech comprehension in normal subjects with left anterolateral superior temporal cortex connectivity in a group of chronic aphasic stroke patients. We then evaluated the language deficits associated with altered left anterolateral superior temporal cortex connectivity in aphasic stroke. During normal narrative speech comprehension, left anterolateral superior temporal cortex displayed positive functional connections with left anterior basal temporal cortex, left inferior frontal gyrus and homotopic cortex in right anterolateral superior temporal cortex. As a group, aphasic patients demonstrated a selective disruption of the normal functional connection between left and right anterolateral superior temporal cortices. We observed that deficits in auditory single word and sentence comprehension correlated both with the degree of disruption of left-right anterolateral superior temporal cortical connectivity and with local activation in the anterolateral superior temporal cortex. Subgroup analysis revealed that aphasic patients with preserved positive intertemporal connectivity displayed better receptive language function; these patients also showed greater than normal left inferior frontal gyrus activity, suggesting a possible "top-down" compensatory mechanism. These results demonstrate that functional connectivity between anterolateral superior temporal cortex and right anterior superior temporal cortex is a marker of receptive language outcome after aphasic stroke, and illustrate that language system organization after focal brain lesions may be marked by complex signatures of altered local and pathway-level function.

Within the connectionist triangle model of reading aloud, interaction between semantic and phonological representations occurs for all words but is particularly important for correct pronunciation of lower frequency exception words. This framework therefore predicts that (a) semantic dementia, which compromises semantic knowledge, should be accompanied by surface dyslexia, a frequency-modulated deficit in exception word reading, and (b) there should be a significant relationship between the severity of semantic degradation and the severity of surface dyslexia. The authors evaluated these claims with reference to 100 observations of reading data from 51 cases of semantic dementia. Surface dyslexia was rampant, and a simple composite semantic measure accounted for half of the variance in low-frequency exception word reading. Although in 3 cases initial testing revealed a moderate semantic impairment but normal exception word reading, all of these became surface dyslexic as their semantic knowledge deteriorated further. The connectionist account attributes such cases to premorbid individual variation in semantic reliance for accurate exception word reading. These results provide a striking demonstration of the association between semantic dementia and surface dyslexia, a phenomenon that the authors have dubbed SD-squared.

Semantic dementia patients make numerous phoneme migration errors in their immediate serial recall of poorly comprehended words. In this study, similar errors were induced in the word recall of healthy participants by presenting unpredictable mixed lists of words and nonwords. This technique revealed that lexicality, word frequency, imageability, and the ratio of words to nonwords all influence the stability of the phonological trace. These factors affected phoneme migrations and phoneme identity errors for both the words themselves and the nonwords they were presented with. Therefore, lexical/semantic knowledge encourages the phonological segments of familiar words to emerge together in immediate serial recall. In the absence of such knowledge, the elements of a particular item are more likely to recombine with the phonemes of other list items. These findings demonstrate the importance of lexical and semantic binding in verbal short-term memory.

Presents evidence that although patients with semantic deficits can sometimes show good performance on tests or object decisions, this pattern applies when nonsee-objects do not respect the regularities of the domain. Patients with semantic dementia viewed line drawings of a real and chimeric animals side-by-side and were asked to decide which was real. Object-decision scores were highly correlated with other pictorial and verbal assessments of conceptual knowledge. (Author/VWL)

These features could result in a more global recovery pattern reflecting the impact of generalized recovery mechanisms acting systemically across multiple neurocognitive components. Given the urgent and pressing need to understand language recovery mechanisms in post-stroke aphasia, we were delighted in the interest taken by Walker and Hickok[1] in our recent exploration. [Extracted from the article]

The logopenic variant of primary progressive aphasia is characterized by early deficits in language production and phonological short-term memory, attributed to left-lateralized temporoparietal, inferior parietal and posterior temporal neurodegeneration. Despite patients primarily complaining of language difficulties, emerging evidence points to performance deficits in non-linguistic domains. Temporoparietal cortex, and functional brain networks anchored to this region, are implicated as putative neural substrates of non-linguistic cognitive deficits in logopenic variant primary progressive aphasia, suggesting that degeneration of a shared set of brain regions may result in co-occurring linguistic and non-linguistic dysfunction early in the disease course. Here, we provide a Review aimed at broadening the understanding of logopenic variant primary progressive aphasia beyond the lens of an exclusive language disorder. By considering behavioural and neuroimaging research on non-linguistic dysfunction in logopenic variant primary progressive aphasia, we propose that a significant portion of multidimensional cognitive features can be explained by degeneration of temporal/inferior parietal cortices and connected regions. Drawing on insights from normative cognitive neuroscience, we propose that these regions underpin a combination of domain-general and domain-selective cognitive processes, whose disruption results in multifaceted cognitive deficits including aphasia. This account explains the common emergence of linguistic and non-linguistic cognitive difficulties in logopenic variant primary progressive aphasia, and predicts phenotypic diversification associated with progression of pathology in posterior neocortex. [ABSTRACT FROM AUTHOR]

Background: Despite the clinical importance of assessing the efficiency and accuracy of fluency in terms of content words production during connected speech, assessments based on discourse tasks are very time-consuming and thus not clinically feasible. Aims: (1) Examine the relationship between single-word naming and word retrieval during discourse production. (2) Investigate the relationship between word retrieval and content word fluency derived from a simple versus naturalistic discourse tasks. (3) Develop and validate an efficient and accurate index of content word fluency that is clinically viable. Methods: Two discourse tasks (simple picture description and naturalistic storytelling narrative) were collected from 46 participants with post-stroke aphasia, and 20 age/education matched neuro-typical controls. Each discourse sample was fully transcribed and quantitative analysis was applied to each sample to measure word retrieval and content word fluency. Three single-word naming tasks were also administered to each participant with aphasia. Results: Correlational analyses between single-word naming and word retrieval in connected speech revealed weak/moderate relationships. Conversely, strong correlations were found between measures derived from simple picture description against naturalistic storytelling discourse tasks. Moreover, we derived a novel, transcription-less index of content word fluency from the discourse samples of an independent group (neuro-typical controls), and then we validated this index across two discourse tasks in the tested group (persons with aphasia). Correlation and regression analyses revealed extremely strong relationships between participants' (neuro-typical controls and persons with aphasia) scores on the novel index and measures of content word fluency derived from the formal transcription and quantitative analyses of discourse samples, indicating high accuracy and validity of the new index. Conclusions: Simple picture description rather than picture naming provides a better estimate of word retrieval in naturalistic connected speech. The novel developed index is transcription-less and can be implemented online to provide an accurate and efficient measure of content word fluency. Thus, it is viable during clinical practice for assessment purposes, and possibly as an outcome measure to monitor therapy effectiveness, which can also be used in randomised clinical trials. [ABSTRACT FROM AUTHOR]

The connectionist triangle model of reading aloud proposes that semantic activation of phonology is particularly important for correct pronunciation of low-frequency exception words. Our consideration of this issue (Woollams, Lambon Ralph, Plant, & Patterson, 2007) reported computational simulations demonstrating that reduction and disruption of this semantic activation resulted in the marked deficit in low-frequency exception word reading that is characteristic of surface dyslexia. We then presented 100 observations of reading aloud from 51 patients with semantic dementia (SD) demonstrating a universal decline into surface dyslexia, a phenomenon we termed 'SD-squared.' Coltheart, Tree, and Saunders (2010) have more recently provided a simulation of the SD-squared data within the dual route cascaded (DRC) model, achieved by varying the amount of damage to components of the lexical and nonlexical pathways. Although they suggested that these simulations provide a closer fit to the SD patients' reading data than our own, we demonstrate here that this is not the case. Moreover, we argue that the connectionist triangle model account has substantially greater explanatory and predictive power than the DRC account. Keywords: surface dyslexia, semantic memory, reading aloud, frequency, regularity DOI: 10.1037/a0017641

Semantic short-term memory (STM) patients have a reduced ability to retain semantic information over brief delays but perform well on other semantic tasks; this pattern suggests damage to a dedicated buffer for semantic information. Alternatively, these difficulties may arise from mild disruption to domain-general semantic processes that have their greatest impact on demanding STM tasks. In this study, mild semantic processing impairments were demonstrated in 2 semantic STM patients. They performed well on untimed semantic tasks but were deficient in accuracy and reaction times on speeded tasks. Demanding semantic production tasks were also affected. These patients were compared with a case series of individuals with semantic aphasia whose multimodal semantic difficulties stemmed from poor cognitive control. STM and semantic performance were more impaired in this group, but there were qualitative similarities to the semantic STM patients. The difference between the 2 patient types may be a matter of degree. In semantic aphasia, severe disruption to semantic control leads to global semantic impairments, whereas in semantic STM milder disruption might impact mainly on STM tests because of the high control demands of these tasks. Keywords: short-term memory, stroke aphasia, semantic control