Aberrations of inner speech have been linked to psychotic symptoms such as thought insertion and auditory verbal hallucinations. These symptoms may reflect failures of prediction and source monitoring. Normally, efference copies of speech motor commands are sent to auditory cortices and suppressed, helping distinguish self-generated from external input. If suppression malfunctions, predicted auditory input may become perceptually salient. Further, if self-monitoring or error detection-related regions are also impaired (e.g., anterior cingulate cortex, ACC), inner speech may be misattributed as external. We tested this proposal using neuroimaging meta-analyses, examining how the brain systems in overt and inner speech production in neurotypical participants overlap with findings from psychosis spectrum participants performing a range of tasks. They showed increased activity in motor-related regions associated with inner speech (e.g., ventral premotor cortices) and decreased grey matter in bilateral auditory cortices and ACC, in regions specific to overt speech. Coactivation-based network analyses revealed that these ventral premotor and auditory regions form distinct, inversely coupled audiomotor networks. Classification suggests the ventral premotor network supports 'higher-level' language processing, while the audiomotor network supports 'lower-level' speech and self-referential processing. Overall, results accord with the proposal that psychotic symptoms like auditory verbal hallucinations derive from phenotypic hyperactivation in inner speech-related regions that yield affectively salient efference copy signals that are insufficiently suppressed and monitored as self-produced. In line with a hierarchical predictive-processing account, disruption of a distributed recurrent system distorts self-awareness and conscious experience.

Object naming is widely used for assessing aphasia. We provide the first quantitative analysis of how well: (A) impaired spoken object naming (anomia) detects auditory repetition and/or speech comprehension impairments and (B) intact naming rules these impairments out. Participants were 382 stroke survivors (1 month to 34 years post-stroke) with impaired naming, repetition and/or comprehension, but intact object recognition. We assessed: (1) Incidence of anomia within the full sample; (2) its positive predictive value (PPV), i.e., the proportion of patients with anomia who had impaired repetition and/or comprehension; (3) its sensitivity to other impairments, i.e., the proportion of patients with impaired repetition or comprehension who had anomia; and (4) how object naming, word repetition, sentence repetition, word comprehension and sentence comprehension compared in their incidence, PPV and sensitivity, when each was treated as the reference task. Incidence, PPV and Sensitivity of anomia were 66%, 90% and 63% across sample; 93%, 100% and 93% for the most severely aphasic patients and 50%, 86% and 46% for the remaining patients. These metrics were not higher for object naming than sentence comprehension, sentence repetition and word repetition; but word comprehension showed markedly lower incidence and sensitivity. Although anomia may be the most salient symptom of aphasia in everyday conversation, our findings (i) challenge assumptions that object naming is a superior test of aphasia, (ii) show that the presence of anomia was insensitive to 37% of patients with repetition and comprehension impairments and (iii) highlight how PPV and sensitivity within an aphasic sample are influenced by impairment severity, task dependency, measurement variability and inter-patient differences.

Functional imaging and clinical cases implicate the left thalamus in object naming, yet the prevalence of naming impairment after focal thalamic damage is low with variable impact and often rapid resolution. This suggests that compensatory mechanisms, within or beyond the thalamus, may support recovery. We hypothesized that thalamic damage would (a) not cause chronic anomia if other naming-related regions remain intact but (b) exacerbate anomia when co-occurring with damage to non-thalamic naming regions. To test these hypotheses, we retrospectively assessed naming ability in 550 left hemisphere chronic stroke survivors (52% with anomia). Lesion sites included focal thalamic lesions (n = 14), combined thalamic and non-thalamic lesions (n = 271), and lesions sparing the thalamus (n = 265). Whole-brain lesion-symptom mapping (LSM), using multivariate support vector regression, identified brain regions where damage was significantly related to naming ability. Contributions of different thalamic subregions to naming were assessed using ridge regression. Focal thalamic lesions were not associated with chronic anomia. LSM identified two naming-related clusters: a temporoparietal region of interest (ROI-TP) and a subcortical-insular region of interest (ROI-SC) including the lateral thalamus. However, lesion load in the lateral thalamus did not independently contribute to naming performance when controlling for damage to other parts of the ROI-SC, nor did any thalamic nuclei show additive effects beyond the ROI-TP and the non-thalamic ROI-SC. These findings suggest that thalamic damage in the dominant hemisphere does not cause long-term anomia in chronic stroke. Future research therefore needs longitudinal designs to track the trajectory of transient thalamic effects from the acute to chronic phases and to investigate whether naming impairments after thalamic lesions are (a) lesion specific but context dependent, emerging under increased cognitive load, or (b) attributable to non-lesion-site-dependent post-stroke factors such as fatigue.

Introduction:This study investigates how chronological age at stroke onset affects post-stroke language abilities and recovery. Using cross-sectional and retrospective data, we investigated (A) which language tasks are sensitive to age; (B) whether any age-related effects are modified by factors such as lesion size, initial severity and education and (C) whether age influences recovery from aphasia. Methods:Language abilities were assessed in 749 participants using (i) the Comprehensive Aphasia Test (CAT) at a single time point and (ii) self-reported measures of speaking, understanding, reading and writing ability both at 1 week and 1 year post-stroke. The outcomes investigated, using multiple linear regression, were (1) CAT language scores and (2) self-reported recovery scores at 1 year post-stroke. Lesion size, initial severity, sex, handedness, pre-stroke education and time post-stroke were controlled. Bayesian statistics assessed the strength of evidence for observed effects. Results:(A) Irrespective of lesion or symptom severity, older age at stroke onset was associated with worse performance across multiple language domains, including overall language ability, nonword and word repetition, semantic and letter fluency, object naming and comprehension of spoken and written words and sentences. Effect sizes were strongest for nonword repetition (β = -0.258) and weakest for written word comprehension (β = -0.061). (B) The disadvantage of older age was heightened in participants with the largest lesions and most severe initial aphasia, but (C) there was no evidence that older age hindered language recovery in any subgroup. Conclusion:Older age at stroke onset significantly worsened language outcomes, highlighting the sensitivity of aphasia assessments to age-related differences in post-stroke language abilities. This disadvantage was greatest in participants with both large lesions and severe initial symptoms. Considering age when interpreting assessment scores would optimise diagnosis and prognostic accuracy.

This study examines whether auditory cortex anatomy reflects multilingual experience, specifically individuals’ phonological repertoire. Using data from over 200 participants exposed to 1–7 languages across 36 languages, we analyzed the role of language experience and typological distances between languages they spoke in shaping neural signatures of multilingualism. Our findings reveal a negative relationship between the thickness of the left and right second transverse temporal gyrus (TTG) and participants’ degree of multilingualism. Models incorporating phoneme-level information in the language experience index explained the most variance in TTG thickness, suggesting that a more extensive and more phonologically diverse language experience is associated with thinner cortices in the second TTG. This pattern, consistent across two datasets, supports the idea of experience-driven pruning and neural efficiency. Our findings indicate that experience with typologically distant languages appear to impact the brain differently than those with similar languages. Moreover, they suggest that early auditory regions seem to represent phoneme-level cross-linguistic information, contrary to the most established models of language processing in the brain, which suggest that phonological processing happens in more lateral posterior superior temporal gyrus (STG) and superior temporal sulcus (STS).

Background:A greater amount of education is known to positively impact language skills in neurotypical populations, but its influence on language outcomes and recovery after stroke remains unclear. Aims:This study of 749 stroke survivors, with and without aphasia, investigated (A) which aphasia assessment tasks benefitted most from more pre-stroke education; and whether the effect of education (B) differs for aphasic and non-aphasic participants or other stroke and non-stroke-related variables, and/or (C) facilitates recovery from post-stroke aphasia. Methods:Participants ranged from one month to 42 years post-stroke. They were assessed using (i) the Comprehensive Aphasia Test (CAT), and (ii) self-report questionnaires that measured speech production, comprehension, reading, and writing at one week and one year post-stroke. Multiple regression analyses investigated the effect of education amount, and its interaction with other variables, on language outcomes and recovery. Bayesian statistics assessed the strength of the evidence for any observed effects. Many variables including lesion size, age at stroke, and initial severity were controlled for. Results:(A) More years of formal education were associated with better overall language skills, with significant, albeit small effects found for semantic and letter fluency (β = 0.123 and 0.166) and spoken picture description, specifically, the number of words produced (β = 0.085) and grammatical well-formedness (β = 0.087). (B) The benefit of more pre-stroke education was mostly additive with the effects of other variables including initial aphasia severity and left hemisphere lesion size, but was reduced in older participants who had large lesions with severe initial symptoms. Finally, (C) no significant effect of education on language recovery was observed. Conclusion:More pre-stroke formal education is associated with higher post-stroke language scores on a wide range of tasks for both aphasic and non-aphasic participants, but, in participants with large lesions that cause severe aphasia, this advantage diminishes with age. These results suggest a generic benefit of education on language test performance rather than a specific role of pre-stroke education in aiding language outcomes and recovery. An individual's educational background should therefore be considered when interpreting assessment scores.

I consider 2 interlinked connections between Judy Kroll's research and my own work. Both concern the nature of language control in speakers of more than 1 language. My first connection is with her pioneering revised hierarchical model (Kroll & Stewart, 1994). This model raised questions about the organization of the bilingual lexicon, the pathways to word production, and the nature of changes with language proficiency in a second language. For me, the model raised questions about the nature of the language control processes involved. My second connection is to Judy Kroll's advocacy of the importance of identifying and researching the consequences of variety in the language experience of bilinguals. My work aims to unpack the language control processes that support such variety. Importantly, as Judy Kroll has recently advocated, it is vital to place the lived experience of bilinguals center- stage in our research inquiries. This shift requires an increase in multidisciplinary collaboration and epitomizes her continued research leadership.

We investigated which parts of the cerebellum are involved in formulating and articulating sentences using (i) a sentence production task that involved describing simple events in pictures; (ii) an auditory sentence repetition task involving the same sentence articulation but not sentence formulation; and (iii) an auditory sentence-to-picture matching task that involved the same pictorial events and no overt articulation. Activation for each of these tasks was compared to the equivalent word processing tasks: noun production, verb production, auditory noun repetition, and auditory noun-to-picture matching. We associate activation in bilateral cerebellum lobule VIIb with sequencing words into sentences because it increased for sentence production compared to all other conditions and was also activated by word production compared to word matching. We associate a paravermal part of right cerebellar lobule VIIIb with overt motor execution of speech, because activation was higher during (i) production and repetition of sentences compared to the corresponding noun conditions and (ii) noun and verb production compared to all matching tasks, with no activation relative to fixation during any silent (nonspeaking) matching task. We associate activation within right cerebellar Crus II with covert articulatory activity because it activated for (i) all speech production more than matching tasks and (ii) sentences compared to nouns during silent (nonspeaking) matching as well as sentence production and sentence repetition. Our study serendipitously segregated, for the first time, three distinct functional roles for the cerebellum in generic speech production, and it demonstrated how sentence production enhanced the demands on these cerebellar regions.

We tell one another stories of our lives. Sharing subjective experience is part of what it means to be an embodied, languaging being. In order to explore this aspect of our nature we need to relate our phenomenal experience to its neural bases as we talk. I describe a three-step procedure to do so as a person recounts a personal story. The first step characterizes their subjective experience. I describe two complementary ways to do so. The second step infers the attentional and attributional processes that compose that experience. I suppose that telling a personal story is a form of reliving it. The process of mental simulation involved recruits other attributional processes and is itself nested under one that sustains attention to the goal of telling the story. The third step identifies these processes with their possible neural bases expressed through the language network. I take the mapping from the phenomenal to the neural to be the neurophenomenal space and offer a visualization of it. I illustrate the procedure using the hypothetical example of a bilingual speaker who tells of a recent experience walking in a new city.

Functional imaging studies of neurotypical adults report activation in the left putamen during speech production. The current study asked how stroke survivors with left putamen damage are able to produce correct spoken responses during a range of speech production tasks. Using functional magnetic resonance imaging, activation during correct speech production responses was assessed in 5 stroke patients with circumscribed left dorsal striatal lesions, 66 stroke patient controls who did not have focal left dorsal striatal lesions, and 54 neurotypical adults. As a group, patients with left dorsal striatal damage (our patients of interest) showed higher activation than neurotypical controls in the left superior parietal cortex during successful speech production. This effect was not specific to patients with left dorsal striatal lesions as we observed enhanced activation in the same region in some patient controls and also in more error-prone neurotypical participants. Our results strongly suggest that enhanced left superior parietal activation supports speech production in diverse challenging circumstances, including those caused by stroke damage. They add to a growing body of literature indicating how upregulation within undamaged parts of the neural systems already recruited by neurotypical adults contributes to recovery after stroke.

In this chapter, we discuss a hierarchical model of bilingual language control and attentional/control states during conversations. Conversations necessitate a close interchange between language control and understanding other’s state of mind. Here we explore another fundamental aspect of language use that requires different attentional states: in their speech acts, speakers talk about different topics. Using a hierarchical control framework, we describe the attentional control demands of the various interactional contexts and the attentional states induced by different types of topics nested within the sustained attentional demand to the conversation. We also consider aspects of neural networks involved in language use, specifically the involvement of frontal-subcortical regions during utterance planning and production. Lastly, we discuss future directions of research methods needed to explore bilingual control processes during conversation. Through this exploration into everyday conversations in different interactional contexts, we conclude that the mind/brain can be in several co-occurring and dissociable attentional/control states: ones induced through specific content and others induced by language control processes.

Both classic and contemporary models of auditory word repetition involve at least four left hemisphere regions: primary auditory cortex for processing sounds; pSTS (within Wernicke’s area) for processing auditory images of speech; pOp (within Broca’s area) for processing motor images of speech; and primary motor cortex for overt speech articulation. Previous functional-MRI (fMRI) studies confirm that auditory repetition activates these regions, in addition to many others. Crucially, however, contemporary models do not specify how regions interact and drive each other during auditory repetition. Here, we used dynamic causal modelling, to test the functional interplay among the four core brain regions during single auditory word and pseudoword repetition. Our analysis is grounded in the principle of degeneracy—i.e., many-to-one structure-function relationships—where multiple neural pathways can execute the same function. Contrary to expectation, we found that, for both word and pseudoword repetition, (i) the effective connectivity between pSTS and pOp was predominantly bidirectional and inhibitory; (ii) activity in the motor cortex could be driven by either pSTS or pOp; and (iii) the latter varied both within and between individuals. These results suggest that different neural pathways can support auditory speech repetition. This degeneracy may explain resilience to functional loss after brain damage.

Using fMRI, we investigated how right temporal lobe gliomas affecting the posterior superior temporal sulcus alter neural processing observed during speech perception and production tasks. Behavioural language testing showed that three pre-operative neurosurgical patients with grade 2, grade 3 or grade 4 tumours had the same pattern of mild language impairment in the domains of object naming and written word comprehension. When matching heard words for semantic relatedness (a speech perception task), these patients showed under-activation in the tumour infiltrated right superior temporal lobe compared to 61 neurotypical participants and 16 patients with tumours that preserved the right postero-superior temporal lobe, with enhanced activation within the (tumour-free) contralateral left superior temporal lobe. In contrast, when correctly naming objects (a speech production task), the patients with right postero-superior temporal lobe tumours showed higher activation than both control groups in the same right postero-superior temporal lobe region that was under-activated during auditory semantic matching. The task dependent pattern of under-activation during the auditory speech task and over-activation during object naming was also observed in eight stroke patients with right hemisphere infarcts that affected the right postero-superior temporal lobe compared to eight stroke patients with right hemisphere infarcts that spared it. These task-specific and site-specific cross-pathology effects highlight the importance of the right temporal lobe for language processing and motivate further study of how right temporal lobe tumours affect language performance and neural reorganisation. These findings may have important implications for surgical management of these patients, as knowledge of the regions showing functional reorganisation may help to avoid their inadvertent damage during neurosurgery.

Establishing whether speech and language therapy after stroke has beneficial effects on speaking ability is challenging because of the need to control for multiple non-therapy factors known to influence recovery. We investigated how speaking ability at three time points post-stroke differed in patients who received varying amounts of clinical therapy in the first month post-stroke. In contrast to prior studies, we factored out variance from: initial severity of speaking impairment, amount of later therapy, and left and right hemisphere lesion size and site. We found that speaking ability at one month post-stroke was significantly better in patients who received early therapy (n = 79), versus those who did not (n = 64), and the number of hours of early therapy was positively related to recovery at one year post-stroke. We offer two non-mutually exclusive interpretations of these data: (1) patients may benefit from the early provision of self-management strategies; (2) therapy is more likely to be provided to patients who have a better chance of recovery (e.g., poor physical and/or mental health may impact suitability for therapy and chance of recovery). Both interpretations have implications for future studies aiming to predict individual patients' speech outcomes after stroke, and their response to therapy.

Conversation is a major site for our use of language. Each conversation elicits a distinct subjective experience: a specific and dynamic phenomenal field, and it is this field that controls our communicative actions. We cannot hope to understand the neural bases of conversation without relating these to the phenomenal field. We need a neurophenomenology of the bilingual speaker. I propose and illustrate an approach involving path diagrams together with retrospective experience sampling to capture the richness of the phenomenal field as a speaker talks through an issue of concern, and relate this process to large-scale attentional networks. The proposal offers a general approach to developing a neurophenomenology of the bilingual speaker and listener.

Broca's area in the posterior half of the left inferior frontal gyrus has long been thought to be critical for speech production. The current view is that long-term speech production outcome in patients with Broca's area damage is best explained by the combination of damage to Broca's area and neighbouring regions including the underlying white matter, which was also damaged in Paul Broca's two historic cases. Here, we dissociate the effect of damage to Broca's area from the effect of damage to surrounding areas by studying long-term speech production outcome in 134 stroke survivors with relatively circumscribed left frontal lobe lesions that spared posterior speech production areas in lateral inferior parietal and superior temporal association cortices. Collectively, these patients had varying degrees of damage to one or more of nine atlas-based grey or white matter regions: Brodmann areas 44 and 45 (together known as Broca's area), ventral premotor cortex, primary motor cortex, insula, putamen, the anterior segment of the arcuate fasciculus, uncinate fasciculus and frontal aslant tract. Spoken picture description scores from the Comprehensive Aphasia Test were used as the outcome measure. Multiple regression analyses allowed us to tease apart the contribution of other variables influencing speech production abilities such as total lesion volume and time post-stroke. We found that, in our sample of patients with left frontal damage, long-term speech production impairments (lasting beyond 3 months post-stroke) were solely predicted by the degree of damage to white matter, directly above the insula, in the vicinity of the anterior part of the arcuate fasciculus, with no contribution from the degree of damage to Broca's area (as confirmed with Bayesian statistics). The effect of white matter damage cannot be explained by a disconnection of Broca's area, because speech production scores were worse after damage to the anterior arcuate fasciculus with relative sparing of Broca's area than after damage to Broca's area with relative sparing of the anterior arcuate fasciculus. Our findings provide evidence for three novel conclusions: (i) Broca's area damage does not contribute to long-term speech production outcome after left frontal lobe strokes; (ii) persistent speech production impairments after damage to the anterior arcuate fasciculus cannot be explained by a disconnection of Broca's area; and (iii) the prior association between persistent speech production impairments and Broca's area damage can be explained by co-occurring white matter damage, above the insula, in the vicinity of the anterior part of the arcuate fasciculus.

Functional imaging studies of neurologically intact adults have demonstrated that the right posterior cerebellum is activated during verb generation, semantic processing, sentence processing, and verbal fluency. Studies of patients with cerebellar damage converge to show that the cerebellum supports sentence processing and verbal fluency. However, to date there are no patient studies that investigated the specific importance of the right posterior cerebellum in language processing, because: (i) case studies presented patients with lesions affecting the anterior cerebellum (with or without damage to the posterior cerebellum), and (ii) group studies combined patients with lesions to different cerebellar regions, without specifically reporting the effects of right posterior cerebellar damage. Here we investigated whether damage to the right posterior cerebellum is critical for sentence processing and verbal fluency in four patients with focal stroke damage to different parts of the right posterior cerebellum (all involving Crus II, and lobules VII and VIII). We examined detailed lesion location by going beyond common anatomical definitions of cerebellar anatomy (i.e., according to lobules or vascular territory), and employed a recently proposed functional parcellation of the cerebellum. All four patients experienced language difficulties that persisted for at least a month after stroke but three performed in the normal range within a year. In contrast, one patient with more damage to lobule IX than the other patients had profound long-lasting impairments in the comprehension and repetition of sentences, and the production of spoken sentences during picture description. Spoken and written word comprehension and visual recognition memory were also impaired, however, verbal fluency was within the normal range, together with object naming, visual perception and verbal short-term memory. This is the first study to show that focal damage to the right posterior cerebellum leads to language difficulties after stroke; and that processing impairments persisted in the case with most damage to lobule IX. We discuss these results in relation to current theories of cerebellar contribution to language processing. Overall, our study highlights the need for longitudinal studies of language function in patients with focal damage to different cerebellar regions, with functional imaging to understand the mechanisms that support recovery.