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[Purpose] This study explored health science students' perceptions of motor aphasia and sensory aphasia caused by stroke to provide basic material for the improvement of rehabilitation practitioners' perceptions of aphasia. [Subjects and Methods] The subjects of this study were 642 freshmen and sophomores majoring in health science. Perceptions of aphasia were surveyed on a semantic differential scale using the Anchoring Vignette Method and the difference in perception of the two types of aphasia was analyzed using multi-dimensional scaling. [Results] The analysis revealed that motor aphasia and sensory aphasia have mutually corresponding images. Motor aphasia had high levels of 'quiet', 'passive' 'dumb', 'unstable' and 'gloomy' images, while sensory aphasia had high levels of 'noisy', 'unstable', 'cheerful', 'sensitive', 'fluctuating in emotions', 'active', 'dumb' and 'gloomy' images. [Conclusion] A systematic education is required to be implemented in the future to improve health science students' negative perceptions of the aftereffects of stroke such as aphasia.

Aphasia describes a spectrum of speech impairments due to damage in the language centers of the brain. Insult to the inferior frontal gyrus of the dominant cerebral hemisphere results in Broca’s aphasia - the inability to produce fluent speech. The left cerebral hemisphere has historically been considered the dominant side, a characteristic long presumed to be related to a person’s “handedness”. However, recent studies utilizing fMRI have shown that right hemispheric dominance occurs more frequently than previously proposed and despite a person’s handedness. Here we present a case of a right-handed patient with Broca’s aphasia caused by a right-sided brain tumor. This is significant not only because the occurrence of aphasia in right-handed-individuals with right hemispheric brain damage (so-called “crossed aphasia”) is unusual but also because such findings support dissociation between hemispheric linguistic dominance and handedness.

Purpose Coverbal gesture use, which is affected by the presence and degree of aphasia, can be culturally specific. The purpose of this study was to compare gesture use among Cantonese-speaking individuals: 23 neurologically healthy speakers, 23 speakers with fluent aphasia, and 21 speakers with nonfluent aphasia. Method Multimedia data of discourse samples from these speakers were extracted from the Cantonese AphasiaBank. Gestures were independently annotated on their forms and functions to determine how gesturing rate and distribution of gestures differed across speaker groups. A multiple regression was conducted to determine the most predictive variable(s) for gesture-to-word ratio. Results Although speakers with nonfluent aphasia gestured most frequently, the rate of gesture use in counterparts with fluent aphasia did not differ significantly from controls. Different patterns of gesture functions in the 3 speaker groups revealed that gesture plays a minor role in lexical retrieval whereas its role in enhancing communication dominates among the speakers with aphasia. The percentages of complete sentences and dysfluency strongly predicted the gesturing rate in aphasia. Conclusions The current results supported the sketch model of language–gesture association. The relationship between gesture production and linguistic abilities and clinical implications for gesture-based language intervention for speakers with aphasia are also discussed.

The aim of the study is to assess historical anatomical and functional definitions of Wernicke’s area in light of modern lesion and neuroimaging data. “Wernicke’s area” has become an anatomical label usually applied to the left posterior superior temporal gyrus and adjacent supramarginal gyrus. Recent evidence shows that this region is not critical for speech perception or for word comprehension. Rather, it supports retrieval of phonological forms (mental representations of phoneme sequences), which are used for speech output and short-term memory tasks. Focal damage to this region produces phonemic paraphasia without impairing word comprehension, i.e., conduction aphasia. Neuroimaging studies in recent decades provide evidence for a widely distributed temporal, parietal, and frontal network supporting language comprehension, which does not include the anatomically defined Wernicke area. The term Wernicke’s area, if used at all, should not be used to refer to a zone critical for speech comprehension.

Background/Aims: Although some patients with primary progressive aphasia (PPA) exhibit novel or improved skills after the onset of dementia, these changes have yet to be quantified. Therefore, this study systematically explored and identified the emergence of positive behaviours after dementia onset. Methods: This study included 48 carers of patients with PPA: 12 nonfluent/agrammatic PPA (nfvPPA), 22 semantic variant PPA (svPPA), and 14 logopenic variant PPA (lvPPA). The presence and frequency of positive behaviour changes after dementia onset were established using the Hypersensory and Social/Emotional Scale (HSS). Results: Scores on Sensitivity to Details, Visuospatial Activities, and Music Activities differed significantly among the groups. More specifically, svPPA was associated with increased visuospatial activity, but only in the mild stage of the disease; nfvPPA was associated with increased visuospatial activity and decreased music activity, while lvPPA exhibited the reverse profile. Conclusions: The results demonstrate that subsets of PPA patients show novel or increased positive behaviours following dementia onset, and differences among subtypes may be helpful for improving diagnostic accuracy. Additionally, harnessing these skills may improve the quality of life of both patients and carers.

The purpose of this study was to analyze the question: how do people with aphasia experience the world? Three questions are approached: (1) how is behavior controlled in aphasia, considering that a normal linguistic control is no longer available; (2) what is the pattern of intellectual abilities in aphasia; and (3) what do aphasia patients' self-report regarding the experience of living without language. In aphasia, behavior can no longer be controlled through the "second signal system" and only the first signal system remains. Available information suggests that sometimes no verbal abilities may be affected in aphasia. However, an important variability is observed: whereas, in some patients, evident nonverbal defects are found; in other patients, performance verbal abilities are within normal limits. Several self-reports of recovered aphasic patients explain the experience of living without language. Considering that language represents the major instrument of cognition, in aphasia, surrounding information is evidently interpreted in a partially different way and cognitive strategies are reorganized, resulting in an idiosyncratic cognitive world.

Artikulu honen helburua da neurozientzia kognitiboaren ikuspegitik defi- nitzea afasia zer den eta afasiologia zertan datzan. Horrez gain, afasia hizkuntza ezberdinetan aztertzearen ezinbestekotasuna erakustea du xedea, burmuinaren eta hizkuntzaren arteko eraginak hobeki ulertzeko. Gaixo agramatikoen aditz-prozesamenduaren azterketa hartzen dut adibidetzat. Bukatzeko, etorkizunari begira, euskal afasiologiari eta afasiadun eleaniztunen azterketari buruzko ikerketa-lerro batzuk aipatzen ditut.

Background and Objectives: aphasia is common consequence of stroke. Most people with aphasia in the acute phase show some degree of spontaneous recovery, most of which occurs during the first two to three months. Neuro-linguistic mechanisms of recovery in aphasia remain a lot unknown still, but considerably depends to the amount of change plasticity in brain of patients after stroke. The aim of this article is review of the role of Neuroplasticity types in aphasia recovery and its influencing factors: a systematic review of literatureMethods: this study is a review of all articles listed in PubMed database from January 1990 to September, 2016 that were identified using the keywords Neuroplasticity and aphasia (in titles) and language.Results: Three types of changes in the activity of the nervous system after a stroke, is closely linked with aphasia recovery: 1. Reactivation of damaged areas of the left hemisphere or activities it`s surrounding in language tasks 2. Acquisition or manifest of the ability to process language in the nondominant right Hemisphere 3. The wrong activity of nondominant right hemisphere that can prevent language improvement.Discussion and Conclusion: Most of studies have shown involvement of surrounding areas in the left hemisphere lesion in language improvement, others reported employment of the right hemisphere regions and some others have known useful the involvement of both hemispheres in language improvement. It is difficult, aphasia improvement prediction due to the interaction of various factors. The most promising results aphasia treatment for the reorganization of the brain, caused by speech therapy that lead to quick improvements considerably.

Introduction: The neuropharmacology of aphasia is an area of cognitive neuroscience. In this article we review what is known about these domain, especially with regard to treating aphasia with drugs. Neurotransmitters can improve language function in certain patients with aphasia. We discuss which neurotransmitters work for which language functions in which patients.Method: PubMed and Science databases were searched to identify studies investigated effects of drugs on language function in aphasia in peer-reviewed journals between 2000 and 2015. Results: Studies show that Catecholamines seem especially promising for nonfluent aphasias. Dopamine agonists, in particular bromocriptine, improve verbal fluency in transcortical motor aphasia. Norepinephrine affects prefrontal functions and seems to relieve symptoms of depression and improve overall recovery of function, including language, following stroke. Amphetamines potentiate norepinephrine to promote general recovery, and have been shown to improve language performance in some patients with nonfluent aphasia.Conclusion: studies have been looking at the possibility of manipulating brain chemistry for functional gain in patients with aphasia, but, to date, no overwhelming evidence has emerged to support routine use of drugs as either a complementary or alternative treatment for aphasia. Studies have been largely anecdotal with small numbers of patients and varying types of aphasia. Improvements due to spontaneous recovery have been difficult to separate from treatment benefits.

Numerous studies over the span of more than a decade have shown that noninvasive brain stimulation techniques, namely transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS), can facilitate language recovery for patients who have suffered from aphasia due to stroke. While stroke is the most common etiology of aphasia, neurodegenerative causes of language impairment—collectively termed primary progressive aphasia (PPA)—are increasingly being recognized as important clinical phenotypes in dementia. Very limited data now suggest that noninvasive brain stimulation may have some benefit in treating PPAs. However, before applying the same approaches to patients with PPA as have previously been pursued in patients with post-stroke aphasia, it will be important for investigators to consider key similarities and differences between these aphasia etiologies that is likely to inform successful approaches to stimulation. While both post-stroke aphasia and the PPAs have clear overlaps in their clinical phenomenology, the mechanisms of injury and theorized neuroplastic changes associated with the two etiologies are notably different. Importantly, theories of plasticity in post-stroke aphasia are largely predicated on the notion that regions of the brain that had previously been uninvolved in language processing may take on new compensatory roles. PPAs, however, are characterized by slow distributed degeneration of cellular units within the language system; compensatory recruitment of brain regions to subserve language is not currently understood to be an important aspect of the condition. This review will survey differences in the mechanisms of language representation between the two etiologies of aphasia and evaluate properties that may define and limit the success of different neuromodulation approaches for these two disorders.

After World War II, the centre of gravity in aphasiology research shifted from Europe to North America [1]. In this period, interest in the German and French localist theories waned to virtual non-existence in clinical practice. The localist view was replaced by ideas with a more holistic character. A factor that likely contributed to this transition was the many war casualties, whose complex disturbances and potential for recovery were not very well explained by the contemporary language theories. These observations triggered basic research on aphasia, as well as efforts to rehabilitate patients [2]. Somehow, then, interest renewed to a point where localism again became the dominant clinical view that it remains today.

An acquired disorder of language is known as aphasia (or dysphasia). Symptoms can include impairments of object naming, word finding, syntax, and comprehension. Some patients have a sparse, labored output; others have unusually voluminous but uninformative speech. The nature of the aphasia varies from patient to patient and reflects the principal lesion site within a distributed left-hemisphere language network. Aphasia can start suddenly when caused by cerebrovascular accidents or progresses relentlessly when caused by neurodegeneration. A neurodegenerative disease that selectively impairs language is known as primary progressive aphasia.

Cognitive dysfunction frequently occurs in aphasic patients and primarily compromises linguistic skills. However, patients suffering from severe aphasia show heterogeneous performance in basic cognition. Our aim was to characterize the cognitive profiles of patients with severe aphasia and to determine whether they also differ as to residual linguistic abilities. We examined 189 patients with severe aphasia with standard language tests and with the CoBaGA (Cognitive Test Battery for Global Aphasia), a battery of nonverbal tests that assesses a wide range of cognitive domains such as attention, executive functions, intelligence, memory, visual-auditory recognition, and visual-spatial abilities. Twenty patients were also followed longitudinally in order to assess their improvement in cognitive skills after speech therapy. Three different subgroups of patients with different types and severity of cognitive impairment were evidenced. Subgroups differed as to residual linguistic skills, in particular comprehension and reading-writing abilities. Attention, reasoning, and executive functions improved after language rehabilitation. This study highlights the importance of an extensive evaluation of cognitive functions in patients with severe aphasia.

Wernicke proposed that knowledge of the outside world was conceptualized and that the necessary information that makes up these concepts is stored in many different and interconnected areas of the brain. He clearly made a distinction between knowledge of a word itself (i.e. the sound or pronunciation of it) and knowledge of its meaning or ‘concept’. Since the era of the diagram makers (see also Chap. 4), there has been a discussion of how concepts are anatomically represented in the brain. Several of the earlier researchers truly considered a ‘centre’ for conceptual knowledge, similar to the anatomical centres for motor or speech functions. Some, for example, Mills, even believed that this concept centre was identical to the naming centre [1]. Most others, like Wernicke or Lichtheim, considered the concept centre more of a theoretical construct with a largely heuristic purpose, at least not something with a strict anatomical definition. To them, the true meaning of words and sentences emerged as the result of the complex interplay (association) between many different areas.

The master´s thesis is focused on aphasia as a speech disorder. Aphasia is an element of research in many fields of study. The aim of this thesis is to interpret academic background and conclusions. Aphasiology, linguistics, speech therapy, neurology, neurolinguistics, psycholinguistics, cognitive psychology and cognitive neuropsychology are interested in aphasia. At the beginning of this thesis we can read about aphasia, its causes, classifications and diagnostics. Other chapters summarize conclusions of mentioned disciplines.

Background: Semantic priming in individuals with anomic aphasia has never been the primary focus of an investigation. To date, one study investigated the effects of semantic priming in individuals with fluent aphasia (including anomic aphasia), revealing an inconsistency in semantic priming in the anomic group. Parallels from Broca’s aphasia and Wernicke’s aphasia literature may be drawn. However, due to the heterogeneity of anomic aphasia, a focused investigation was necessary.Aims: Semantic priming effects were investigated using a cross-modal pairwise paradigm. It was hypothesised that participants with anomic aphasia would demonstrate priming patterns at a stimulus onset asynchrony (SOA) of 500 ms with slower overall reaction times (RTs) than the control participants. It was further hypothesised that the participants with anomic aphasia might show less inhibition effects than the control participants.Methods & Procedures: Participants with anomic aphasia (n = 11) and healthy control participants (n = ...

Background: Individuals with agrammatic aphasia (IWAs) have problems with grammatical decoding of tense inflection. However, these difficulties depend on the time frame that the tense refers to. Verb morphology with reference to the past is more difficult than with reference to the non-past, because a link needs to be made to the past event in discourse, as captured in the PAst Discourse Linking Hypothesis (PADILIH; Bastiaanse, R., Bamyaci, E., Hsu, C., Lee, J., Yarbay Duman, T., Thompson, C. K., 2011. Time reference in agrammatic aphasia: A cross-linguistic study. J. Neurolinguist. 24, 652-673). With respect to reference to the (non-discourse-linked) future, data so far indicate that IWAs experience less difficulties as compared to past time reference (Bastiaanse, R., Bamyaci, E., Hsu, C., Lee, J., Yarbay Duman, T., Thompson, C. K., 2011. Time reference in agrammatic aphasia: A cross-linguistic study. J. Neurolinguist. 24, 652-673), supporting the assumptions of the PADILIH. Previous online studies of time reference in aphasia used methods such as reaction times analysis (e.g., Faroqi-Shah, Y., Dickey, M. W., 2009. On-line processing of tense and temporality in agrammatic aphasia. Brain Lang. 108, 97-111). So far, no such study used eye-tracking, even though this technique can bring additional insights (Burchert, F., Hanne, S., Vasishth, S., 2013. Sentence comprehension disorders in aphasia: the concept of chance performance revisited. Aphasiology 27, 112-125, doi:10.1080/02687038.2012.730603).Aims: This study investigated (1) whether processing of future and past time reference inflection differs between non-brain-damaged individuals (NBDs) and IWAs, and (2) underlying mechanisms of time reference comprehension failure by IWAs.Methods and procedures: A visual-world experiment combining sentence picture matching and eye-tracking was administered to 12 NBDs and 6 IWAs, all native speakers of German. Participants heard German sentences with periphrastic future ('will+V') or periphrastic past ('has+ V-d') verb forms while they were presented with corresponding pictures on a computer screen.Results and discussion: NBDs scored at ceiling and significantly higher than the IWAs. IWAs had below-ceiling performance on the future condition, and both participant groups were faster to respond to the past than to the future condition. These differences are attributed to a pre-existing preference to look at a past picture, which has to be overcome. Eye movement patterns suggest that both groups interpret future time reference similarly, while IWAs show a delay relative to NBDs in interpreting past time reference inflection. The eye tracking results support the PADILIH, because processing reference to the past in discourse syntax requires additional resources and thus, is problematic and delayed for people with aphasia. (C) 2014 Elsevier Ltd. All rights reserved.

Background: Experimental studies of short-term memory and working memory (WM) in aphasia fail to discriminate cognitive impairments of different aphasia types—non-fluent, Broca-type aphasia and fluent, Wernicke-type aphasia. However, based on the varying fundamental features of these two aphasia syndromes, the potentially different underlying mechanisms of impairment and scant preliminary evidence of varying cognitive deficits, a differential relationship between cognitive function and language processing in these two groups can be predicted.Aims: The current study investigates the hypothesis concerning the differential impact of cognitive impairments in individuals with fluent versus non-fluent aphasia types.Methods & Procedures: Participants with fluent (n = 19) and non-fluent (n = 16) aphasia and participants without brain damage (n = 36) were presented with an eye-tracking WM task. Additionally, individuals with aphasia completed two language comprehension tasks.Outcomes & Results: Results revealed si...

Background: Little is known about the linguistic, structural and functional recovery on which the production of aphasic recurring utterances (RUs) is based.Methods & Procedures: Retrospective database analysis was performed to study the prevalence of RUs among aphasia patients. Language features and recovery were examined in patients with RUs, who were matched with aphasic controls with similar demographic and clinical characteristics.Outcomes & Results: Of the 147 aphasia patients admitted to a rehabilitation unit, between 2008 and 2012, 12.92% exhibited some form of RU. When we examined the prevalence among those with global aphasia, it increased to 24.6%. Each patient displayed the stereotypy, with some meaningful modulation or intonation with communicative intent. Although there was some recovery (particularly in comprehension), language of all patients remained severely impaired. Patients with RU scored considerably less than the control group in aphasia quotient (U = 209.00; p =.000), in naming task (U = 174.0; p =.002) and in word repetition (U = 196.0; p =.000). But there were no significant differences between the two groups on a comprehension task (t = -.75 (1,28); p =.261) and Token test scores (U = 321.1; p =.130).Conclusions: Our data support the notion that RUs do not represent an absence of language abilities. Language characteristics and recovery pattern were discussed in terms of cognitive processes and neuroplasticity. The social impact of RUs is also highlighted.

It is debated how language and praxis are co-represented in the left hemisphere (LH). As voxel-based lesion-symptom mapping in LH stroke patients with aphasia and/or apraxia may contribute to this debate, we here investigated the relationship between language and praxis deficits at the behavioral and lesion levels in 50 sub-acute stroke patients. We hypothesized that language and (meaningful) action are linked via semantic processing in Broca's region. Behaviorally, half of the patients suffered from co-morbid aphasia and apraxia. While 24% (n = 12) of all patients exhibited aphasia without apraxia, apraxia without aphasia was rare (n = 2, 4%). Left inferior frontal, insular, inferior parietal, and superior temporal lesions were specifically associated with deficits in naming, reading, writing, or auditory comprehension. In contrast, lesions affecting the left inferior frontal gyrus, premotor cortex, and the central region as well as the inferior parietal lobe were associated with apraxic deficits (i.e., pantomime, imitation of meaningful and meaningless gestures). Thus, contrary to the predictions of the embodied cognition theory, lesions to sensorimotor and premotor areas were associated with the severity of praxis but not language deficits. Lesions of Brodmann area (BA) 44 led to combined apraxic and aphasic deficits. Data suggest that BA 44 acts as an interface between language and (meaningful) action thereby supporting parcellation schemes (based on connectivity and receptor mapping) which revealed a BA 44 sub-area involved in semantic processing.

This review provides a summary and appraisal commentary on the treatment review by Woolf, C., Panton, A., Rosen, S., Best, W., & Marshall, J. (2014). Therapy for auditory processing impairment in aphasia: An evaluation of two approaches. Aphasiology, 28, 1481–1505.Source of funding and disclosure of interests: Funded by The Stroke Association Award Number 40251. No conflicts of interest were reported.

The goal of this article is to outline the utility of both language and non-language testing in making a diagnosis of logopenic, nonfluent/agrammatic, and semantic variant primary progressive aphasias PPA as well as delineate important behavioral and speech features that can be detected via clinical observation. We review speech/language presentations, non-language cognitive domains, and behavioral manifestations associated with each disorder. Patients with logopenic variant PPA evidence non-language cognitive impairments that include acalculia, phonological working memory deficits, and mild/variable difficulties with memory and visuospatial functions. In contrast, patients with nonfluent/agrammatic variant PPA display non-language impairments in executive functions, and show relative preservation of memory and visuospatial functions. Finally, semantic variant patients display behavioral changes in social comportment as well as non-language difficulties with category fluency and arithmetic facts; they display relative preservation, if not enhancement, of visuospatial functions. In summary, broad neural networks that support both language and non-language functions are affected in PPA syndromes, thus a comprehensive assessment of additional neuropsychological domains may aid in solidifying and subtyping PPA diagnoses.

Neuroimaging is a standard part of a primary progressive aphasia (PPA) diagnostic work-up and an important component of research investigating changes in the speech-language network in patients with PPA. In this paper, structural neuroimaging, including computed tomography (CT), magnetic resonance imaging (MRI), and diffusion tensor imaging (DTI), as well as functional neuroimaging, including single photon emission computed tomography (SPECT), positron emission tomography (PET), and functional MRI (fMRI), are discussed. Neuroimaging, in conjunction with meticulous clinical and neuropsychological evaluation, can increase diagnostic certainty for PPA subtyping and identification of underlying pathology, which is important for justification of potential pharmacological treatments, such as cholinesterase inhibitors. MRI and, more recently, DTI, have expanded our knowledge of structural brain changes in PPA, including gray matter abnormalities as well as alterations in neuronal tracts. SPECT and PET provide information regarding brain regional blood perfusion (SPECT) or metabolism (PET). Recently, thanks to PET ligands that bind to amyloid protein, it has become possible to diagnose or rule out Alzheimer pathology as a cause for PPA and tau imaging may be forthcoming. Finally, fMRI provides a unique window into brain-behavior relations for language as well as reorganization of the language network in disease. fMRI has also been used to gauge the effects of therapeutic interventions, including language treatment, and can be used for implementation of neuromodulatory mediations, such as repetitive transcranial magnetic stimulation (TMS).

In recent years there has been an increase in research describing the behavioral characteristics and underlying pathology of primary progressive aphasia (PPA). One of the earliest and most prominent features of PPA, particularly for the logopenic and semantic variants, is anomia, and this is often the symptom that prompts individuals with PPA to seek treatment. However, speech-language pathologists who encounter individuals with PPA on their clinical caseloads often have questions about how best to manage progressive language decline in these patients. A small body of literature suggests that treatment for anomia in PPA is indeed warranted, and that item-specific improvement can be expected for a majority of individuals receiving treatment. Although generalization and maintenance of treatment gains are variable in the face of progressive decline, there are some emerging themes as to treatment approaches and patient characteristics that may promote more generalized and relatively durable treatment outcomes. Ultimately, treatment that engages residual semantic, phonologic and orthographic skills, using both strategic training and stimulation, may be appropriate for PPA patients with mild-moderate anomia.

When Norman Geschwind (1926-1984) attended medical school in the 1940s, his psychiatry professors taught as if behavior were unrelated to neuropathology. The focus of neurology remained the diagnosis and treatment of aphasias and epilepsies, while cognitive impairments and developmental disorders were classified as functional (psychological) disorders. Geschwind was troubled by the fact that many of the patients he saw with neurological deficits also presented with behavioral (developmental) disorders. Geschwind's generation also had been taught that aphasias resulted from global rather than localized or focal neurological lesions. These holists, including the prepsychoanalytic Sigmund Freud, targeted the work of aphasiologist Carl Wernicke as an exemplar of the flaws of the localizationist hypothesis. Reading Wernicke in the original, Geschwind discovered a complex and multilayered explanation for aphasias that implicated lesions located in association pathways that, when extensive, resulted in behavioral disorders. Geschwind also reread the works of the holists, discovering that, while their rhetoric rejected Wernicke, their explanations of aphasias actually reinforced Wernicke's hypothesis. Building on his reading of these historical documents and his clinical experiences, Geschwind urged the resurrection of Wernicke's disconnection syndromes that Geschwind labeled as Behavioral Neurology.

The current study describes aphasia in a deaf user of Indian Sign Language (ISL). One congenitally deaf adult with LHD was evaluated for signs of aphasia. The tools used were Aphasia Diagnostic Battery in Indian Sign Language (ADB in ISL), Magnetic Resonance Imaging (MRI) investigation, linguistic, and neurobehavioral profile. The results of all investigative procedures revealed signs and symptoms consistent with non-fluent aphasia specifically Broca’s aphasia. The data from ISL in brain damaged individual further emphasize the role of left hemisphere in sign language processing.

Despite being perhaps the most studied form of aphasia, the critical lesion location for Broca's aphasia has long been debated, and in chronic patients, cortical damage often extends far beyond Broca's area. In a group of 70 patients, we examined brain damage associated with Broca's aphasia using voxel-wise lesion-symptom mapping (VLSM). We found that damage to the posterior portion of Broca's area, the pars opercularis, is associated with Broca's aphasia. However, several individuals with other aphasic patterns had considerable damage to pars opercularis, suggesting that involvement of this region is not sufficient to cause Broca's aphasia. When examining only individuals with pars opercularis damage, we found that patients with Broca's aphasia had greater damage in the left superior temporal gyrus (STG; roughly Wernicke's area) than those with other aphasia types. Using discriminant function analysis and logistic regression, based on proportional damage to the pars opercularis and Wernicke's area, to predict whether individuals had Broca's or another types of aphasia, over 95% were classified correctly. Our findings suggest that persons with Broca's aphasia have damage to both Broca's and Wernicke's areas, a conclusion that is incongruent with classical neuropsychology, which has rarely considered the effects of damage to both areas.

This review provides a summary and appraisal commentary on the assessment review by Wilshire, C. E., Lukkien, C. C., and Burmester, B. R. (2014). The sentence production test for aphasia. Aphasiology, 28(6), 658–691.

This review provides a summary and appraisal commentary on the treatment review by Hurkmans, J., de Brujin Boonstra, A. M., Jonkers, R., Bastiaanse, R., Arendzen, H., & Reinders-Messelink, H. A. (2012). Music in the treatment of neurological language and speech disorders: A systematic review. Aphasiology, 26, 1–19.Source of funding and declaration of interests: Not reported.

Despite accruing evidence for relative preservation of episodic memory in the semantic variant of primary progressive aphasia (previously semantic dementia), the neural basis for this remains unclear, particularly in light of their well-established hippocampal involvement. We recently investigated the Papez network of memory structures across pathological subtypes of behavioural variant frontotemporal dementia and demonstrated severe degeneration of all relay nodes, with the anterior thalamus in particular emerging as crucial for intact episodic memory. The present study investigated the status of key components of Papez circuit (hippocampus, mammillary bodies, anterior thalamus, cingulate cortex) and anterior temporal cortex using volumetric and quantitative cell counting methods in pathologically-confirmed cases with semantic variant of primary progressive aphasia (n = 8; 61-83 years; three males), behavioural variant frontotemporal dementia with TDP pathology (n = 9; 53-82 years; six males) and healthy controls (n = 8, 50-86 years; four males). Behavioural variant frontotemporal dementia cases with TDP pathology were selected because of the association between the semantic variant of primary progressive aphasia and TDP pathology. Our findings revealed that the semantic variant of primary progressive aphasia and behavioural variant frontotemporal dementia show similar degrees of anterior thalamic atrophy. The mammillary bodies and hippocampal body and tail were preserved in the semantic variant of primary progressive aphasia but were significantly atrophic in behavioural variant frontotemporal dementia. Importantly, atrophy in the anterior thalamus and mild progressive atrophy in the body of the hippocampus emerged as the main memory circuit regions correlated with increasing dementia severity in the semantic variant of primary progressive aphasia. Quantitation of neuronal populations in the cingulate cortices confirmed the selective loss of anterior cingulate von Economo neurons in behavioural variant frontotemporal dementia. We also show that by end-stage these neurons selectively degenerate in the semantic variant of primary progressive aphasia with preservation of neurons in the posterior cingulate cortex. Overall, our findings demonstrate for the first time, severe atrophy, although not necessarily neuronal loss, across all relay nodes of Papez circuit with the exception of the mammillary bodies and hippocampal body and tail in the semantic variant of primary progressive aphasia. Despite the longer disease course in the semantic variant of primary progressive aphasia compared with behavioural variant frontotemporal dementia, we suggest here that the neural preservation of crucial memory relays (hippocampal→mammillary bodies and posterior cingulate→hippocampus) likely reflects the conservation of specific episodic memory components observed in most patients with semantic variant of primary progressive aphasia.

Background: Current research in theoretical linguistics, experimental psychology, and clinical aphasiology suggests that adjective training may facilitate unique aspects of language production and functional communication in persons with aphasia. Although considerable research has been devoted to treatments targeting nouns and verbs, there has been relatively little treatment research directed towards adjectives.Aims: The goal of this study was to further investigate the viability of adjective training in aphasia by applying an integrated treatment approach targeting adjective production in the context of single word, sentence, and discourse levels of communication. Specific objectives were to quantify baseline adjective production, acquisition of target structures, and treatment generalisation effects.Method: A single-participant multiple-baseline design was used to evaluate treatment effects in three individuals with nonfluent chronic aphasia. A battery of experimental measures and standardised tests wa...

Objective The aim of this follow-up study is to describe the clinical and neuroradiological findings in an exceptional case presenting a marked discrepancy between oral and written language impairment. Methods In this 22-year-old right-handed patient in-depth neurolinguistic investigations were, conducted 5, 15 and 27 weeks after head trauma inducing a left frontotemporoparietal traumatic brain lesion. Oral as well as written communication is qualitatively analyzed. Results Initially, the aphasia profile was primarily characterized by a striking dissociation between oral and written output. In the acute phase, neurolinguistic findings were consistent with phonological jargon aphasia selectively affecting oral output. By contrast, no fluent aphasia symptoms were found in written output. The patient wrote slowly and intelligibly but written output was distorted by agrammatism. As such, typical fluent aphasia symptoms marked oral output, while nonfluent aphasia symptoms characterized written output. During longitudinal follow-up the dissociation between oral and written output resolved. Phonological errors and self-corrections in speech indicated an evolution to conduction aphasia. Conclusions The exceptional aphasia profile of this patient at 5 weeks posttrauma consists of a unique typological combination of typical fluent, Wernicke-like symptoms confined to oral output and typical nonfluent, Broca-like symptoms in writing. This case study shows the existence of a layered semantic system and an autonomic orthographic lexicon. Follow-up results revealed the impact of a controller system, by means of which the patient could sidestep disturbed phonology at the expense of communicative content.

Background: The syndrome of conduction aphasia is an umbrella term to label clinically heterogeneous language disorders that all include a deficit of repetition due to impaired immediate memory or, in some patients, impaired speech production. The present article reviews the currently available literature on conduction aphasia. It covers aspects of the history of conduction aphasia as a fascicular disconnection syndrome and the objections to this view and discusses the proposed subtypes of this syndrome and the underlying cortical and white matter lesions.Aims: The primary objectives of this article are to critically review the influence of historical concepts on recent approaches to optimise existing theoretical synergies. In addition, the article seeks to advance our understanding of the first steps of verbal auditory processing in individuals with normal and impaired language skills.Main Contribution: We present first indications for an involvement of the left hemisphere in both short- and long-term in...

Background: Primary progressive aphasia (PPA) with its three variants is a progressive neurodegenerative dementia in which language impairment is the first and most dominant symptom. Traditionally, speech-language pathologists who deliver therapy to adults with acquired neurogenic language disorders shy away from treatment of progressive aphasia as there is no promise of lasting effects and only limited data regarding treatment efficacy.Aims: This paper comprises the most current review of the literature focused on treatment of naming impairments in PPA, and aims to encourage and assist clinicians in selecting intervention approaches for individuals with PPA. It highlights current trends and challenges in delivering successful therapy for naming deficits in PPA.Main Contribution: We reviewed papers that reported different forms of naming therapy for patients with PPA, which included interventions that, although not always aimed directly at anomic deficits, brought about improvement in naming. Immediate ga...

Fifty-eight autopsies of patients with primary progressive aphasia are reported. Twenty-three of these were previously described (Mesulam et al., 2008) but had their neuropathological diagnoses updated to fit current criteria. Thirty-five of the cases are new. Their clinical classification was guided as closely as possible by the 2011 consensus guidelines (Gorno-Tempini et al., 2011). Tissue diagnoses included Alzheimer's disease in 45% and frontotemporal lobar degeneration (FTLD) in the others, with an approximately equal split between TAR DNA binding protein 43 proteinopathies and tauopathies. The most common and distinctive feature for all pathologies associated with primary progressive aphasia was the asymmetric prominence of atrophy, neuronal loss, and disease-specific proteinopathy in the language-dominant (mostly left) hemisphere. The Alzheimer's disease pathology in primary progressive aphasia displayed multiple atypical features. Males tended to predominate, the neurofibrillary pathology was more intense in the language-dominant hemisphere, the Braak pattern of hippocampo-entorhinal prominence was tilted in favour of the neocortex, and the APOE e4 allele was not a risk factor. Mean onset age was under 65 in the FTLD as well as Alzheimer's disease groups. The FTLD-TAR DNA binding protein 43 group had the youngest onset and fastest progression whereas the Alzheimer's disease and FTLD-tau groups did not differ from each other in either onset age or progression rate. Each cellular pathology type had a preferred but not invariant clinical presentation. The most common aphasic manifestation was of the logopenic type for Alzheimer pathology and of the agrammatic type for FTLD-tau. The progressive supranuclear palsy subtype of FTLD-tau consistently caused prominent speech abnormality together with agrammatism whereas FTLD-TAR DNA binding protein 43 of type C consistently led to semantic primary progressive aphasia. The presence of agrammatism made Alzheimer's disease pathology very unlikely whereas the presence of a logopenic aphasia or word comprehension impairment made FTLD-tau unlikely. The association of logopenic primary progressive aphasia with Alzheimer's disease pathology was much more modest than has been implied by results of in vivo amyloid imaging studies. Individual features of the aphasia, such as agrammatism and comprehension impairment, were as informative of underlying pathology as more laborious subtype diagnoses. At the single patient level, no clinical pattern was pathognomonic of a specific neuropathology type, highlighting the critical role of biomarkers for diagnosing the underlying disease. During clinical subtyping, some patients were unclassifiable by the 2011 guidelines whereas others simultaneously fit two subtypes. Revisions of criteria for logopenic primary progressive aphasia are proposed to address these challenges.

Background: Based upon the profile linguistic and speech deficits, the current International Criteria for diagnosis and classification of primary progressive aphasia (PPA) suggest the distinction of semantic, nonfluent/agrammatic and logopenic variants, each of which is commonly associated with specific pathology and distribution of brain atrophy. Although the vast majority of cases fit in this tripartite schema, some cases remain unclassifiable because of the presence of overlapping deficits, or conversely, because of the presence of isolated deficits.Aims: In this review, we describe relevant clinical features that characterise each variant and discuss emerging issues derived from the application of the International Criteria.Main Contribution: Based on a hierarchical approach that comprises the evaluation of single-word comprehension, motor speech disorder, agrammatism and sentence repetition, we propose a heuristic solution aimed to reduce the number of cases with ambiguous identification and thereby ...

(2018). Report from ROMA: an update on the development of a core outcome set for aphasia research. Aphasiology: Vol. 32, International Aphasia Rehabilitation Conference (IARC) September 2018, pp. 241-242.

Two case histories are presented to describe the clinical and neuropsychological characteristics of semantic dementia – one of the main clinical forms of frontotemporal degeneration – with predominant involvement of the anterior parts of the temporal lobes of the right and left hemispheres. Disturbances to semantic speech structure were found when the left hemisphere was involved, along with a predominance of prosopagnosia and behavioral impairments when the right hemisphere showed predominant involvement.

Background: Recent studies imply that executive functions (EF) are closely related to our ability to comprehend and produce language. A number of findings suggest that functional communication and language recovery in aphasia depend not only on intact language abilities but on EF as well. Some patients with transcortical motor aphasia (TMA) show language deficits only in tasks in which conflicting representations must be resolved by executive processes. In line with these results, others have proposed that TMA should be referred to as “dysexecutive aphasia”. EF in aphasia have mostly been studied using neuropsychological tests, therefore there is a need for systematic experimental investigations of these skills.Aims: 1. To investigate EF in TMA, and to test whether executive dysfunctions are specific to TMA. 2. To experimentally measure different components of EF: updating working memory representations and inhibition of prepotent responses.Methods & Procedures: Five individuals with TMA, five patients wi...

International audience; Within primary progressive aphasia the logopenic variant remains less understood than the two other main variants, namely semantic and non-fluent progressive aphasia. This may be because of the relatively small number of explored patients and because of the lack of investigations with a comprehensive three-level characterization of cognitive, brain localization and biological aspects. The aim of the present study was to decipher the logopenic variant through a multimodal approach with a large cohort of 19 patients (age 66.5 ± 8.7 years, symptom duration 3.2 ± 0.6 years) using detailed cognitive and linguistic assessments, magnetic resonance imaging and perfusion single-photon emission computed tomography as well as cerebrospinal fluid biomarkers screening for Alzheimer pathology. The linguistic assessment unveiled that language dysfunction is not limited to the typical feature of word finding and verbal working memory impairments but that it extends into the language system affecting to some degree syntactic production, phonological encoding and semantic representations. Perfusion tomography revealed damage of the temporal-parietal junction with a peak of significance in the superior temporal gyrus (Brodmann area 42), and of some less significant prefrontal areas (Brodmann areas 8, 9 and 46), whereas hippocampal cortices were unaffected. Magnetic resonance imaging, which was visually assessed in a larger group of 54 patients with logopenic, non-fluent, semantic variants as well as with posterior cortical atrophy, confirmed that the logopenic variant demonstrates predominant atrophy of left temporal-parietal junction, but that this atrophy pattern has a relatively poor sensitivity and specificity for clinical diagnosis. Finally, the biomarker study revealed that two-thirds of the logopenic patients demonstrated a profile indicative of Alzheimer pathology whereas one-third had a non-Alzheimer profile. Splitting the two groups showed that logopenic aphasia due to probable Alzheimer pathology is a more aggressive variant characterized by more extensive language/cognitive disorders affecting, in addition to lexical processes and verbal working memory, also phoneme sequencing, semantic processing and ideomotor praxis. Concordantly, logopenic aphasia due to probable Alzheimer pathology demonstrated more extensive brain hypoperfusion involving larger regions throughout the inferior parietal, the posterior-superior and the middle temporal cortex. These findings allow for unfolding logopenic aphasia into two subvariants differing by disease severity, lesion nature and lesion distribution, which has important implications for diagnosis, patient management and for potential future trials with anti-Alzheimer drugs. The present data therefore provide novel insight into the cognition and brain damage of logopenic patients while unveiling the existence of distinct diseases constituting a 'logopenic aphasia complex'.

Primary progressive aphasia (PPA) is a progressive neurodegenerative disorder characterized by the deterioration of language functions. The Han language bears some unique features from the Latin languages; however, the features of PPA in the Han language-speaking population are not well understood. In this study, we performed a 3-year follow-up on a Han language-speaking PPA patient with corresponding changes in magnetic resonance imaging (MRI). During the early stage, linguistic analysis revealed several symptoms including difficulty with auditory comprehension, right-left disorientation, reading disorders, and agraphia, specifically the execution of serial oral instructions. This Chinese PPA patient presented with a reading disorder, but his word comprehension ability remained intact. There are two different possible modalities of incorrect writing in this case. The patient also presented with noun-verb double dissociation. The early-stage MRI showed atrophy of the left frontal lobe, which was most severe in the inferior frontal gyrus. Three years later, the patient was found to have progressive atrophy in the parietal, frontal, and temporal lobes, among which the frontal lobe remained the most severely affected region. The brain imaging of the Chinese-speaking PPA patient showed changes similar to those of a Latin language-speaking PPA patient. The prominent change was asymmetrical atrophy in the frontal and temporal lobes. This is the first report of noun-verb double dissociation existing in a Chinese-language speaking PPA patient. The dissociation may be related to an impaired function of the inferior frontal gyrus, which is likely associated with verb-naming in Chinese-speaking people. Several unique features were observed in this case, including impairment in writing ability.

The aim of this paper was to show the role of Augusta Dejerine-Klumpke in a concept of a cerebral localization of language, built on lesion studies of patients with aphasia or language deficits and comparative data in the outgoing 19th century. Augusta Dejerine-Klumpke, an American Medical Doctor living in Paris, tried to uncover the morphological basis of language and aphasia in her husband's laboratory, by using the most sophisticated methods available at her time including secondary (Wallerian) degeneration and serial sectioning. Her anatomical concept of the lesions involved in Broca's aphasia was very precise and might have been a reason for her conflict with more holistic researchers, such as Pierre Marie. Augusta Dejerine-Klumpke contributed actively and substantially to a concept of language and aphasia which was explicitly stated as shared contribution by her husband Joseph Jules Dejerine. Their so-called localizationistic concept in fact limited the importance of circumscribed cortical lesions to Broca's area, emphasized the role of subcortical structures in the genesis of aphasia, and remained accurate in certain ways with our current understanding of language as a complex functional system based on different interconnecting brain regions.

A great number of studies in aphasiology have reported devoicing of voiced consonants in patients who have particular difficulty with the phonetic processing of speech. Recently, other studies have made attempts to account for these difficulties not only in negative terms of ‘deficit’ but also, positively, as a palliative strategy which patients would resort to in order to compensate, at least partly, for their deficit. The aim of this chapter is to contribute to the ongoing debate about devoicing phenomena in aphasia. We carried out a multiple-case study in which we acoustically analysed consonants distinguished by the voiced–voiceless contrast in order to determine, for each patient: (a) the nature of their deficit: whether it is phonological (pre-motor level of speech processing) or phonetic (motor level); and (b) the existence of possible palliative strategies. Results obtained from anarthria and Broca’s aphasia speech output indicate that the subjects differ in a statistically significant way ( p

Primary progressive aphasia (PPA) is a clinical syndrome diagnosed when three core criteria are met. First, there should be a language impairment (i.e., aphasia) that interferes with the usage or comprehension of words. Second, the neurological work-up should determine that the disease is neurodegenerative, and therefore progressive. Third, the aphasia should arise in relative isolation, without equivalent deficits of comportment or episodic memory. The language impairment can be fluent or non-fluent and may or may not interfere with word comprehension. Memory for recent events is preserved although memory scores obtained in verbally mediated tests may be abnormal. Minor changes in personality and behavior may be present but are not the leading factors that bring the patient to medical attention or that limit daily living activities. This distinctive clinical pattern is most conspicuous in the initial stages of the disease, and reflects a relatively selective atrophy of the language network, usually located in the left hemisphere. There are different clinical variants of PPA, each with a characteristic pattern of atrophy. The underlying neuropathological diseases are heterogeneous and can include Alzheimer's disease as well as frontotemporal lobar degeneration. The clinician's task is to recognize PPA and differentiate it from other neurodegenerative phenotypes, use biomarkers to surmise the nature of the underlying neuropathology, and institute the most fitting multimodal interventions. RESUMO. A afasia progressiva primária (APP) é uma síndrome clínica diagnosticada quando três critérios centrais são preenchidos. Inicialmente deve haver comprometimento da linguagem (afasia) que interfere com o uso ou a compreensão das palavras. Em segundo lugar, os métodos diagnósticos devem determinar que a doença é neurodegenerativa e, portanto, progressiva. Por último, a afasia deve emergir de forma relativamente isolada, sem alterações equivalentes de comportamento ou memória episódica. O comprometimento da linguagem pode ser de tipo fluente ou não fluente, e pode ou não interferir com a compreensão de palavras. A memória para eventos recentes está preservada, embora escores de memória em testes verbais possam ser anormais. Alterações discretas de personalidade e comportamento podem estar presentes, mas não são os fatores que levam o paciente ao atendimento médico ou que o limitam em suas atividades de vida diária. Este padrão distinto é mais evidente nas fases iniciais da doença e reflete a atrofia relativamente seletiva da rede de linguagem, geralmente localizada no hemisfério cerebral esquerdo. Há diferentes variantes clínicas da APP, cada uma com padrão de atrofia característico. Os substratos neuropatológicos são heterogêneos e podem incluir a doença de Alzheimer e a degeneração lobar frontotemporal. A tarefa do clínico é reconhecer a APP e diferenciá-la de outros fenótipos neurodegenerativos, utilizar biomarcadores para inferir a natureza da neuropatologia subjacente e instituir as intervenções multimodais cabíveis.