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There are many different approaches to the rehabilitation of aphasia, a communication disorder that affects a person's understanding and expression of spoken and written language. One approach called “functional communication interventions” aims to enhance communication success as opposed to solely improve linguistic abilities. This approach encompasses many skills (e.g., gesturing) and factors (e.g., access to communication supports) that support sending and receiving messages in “real world” daily activities and environments. Functional communication treatments are highly diverse and not always well described. A framework that may provide structure to the description of functional communication interventions for aphasia is the Rehabilitation Treatment Specification System (RTSS). The RTSS was developed by an interdisciplinary research team to describe interventions across any rehabilitation discipline and in any setting or format. The RTSS uses a common language and a systematic approach to describing treatment and includes three connected elements – a single target, one or more ingredients, and a mechanism of action – that, taken together, attempt to explain how and why a treatment works. While the RTTS has been described previously within the field of speech-language pathology, it has not yet been applied to the field of aphasiology. We applied the RTSS framework to a sample of peer-reviewed studies that represent functional communication treatments, including Promoting Aphasics’ Communicative Effectiveness (PACE), Modified Response Elaboration Training (M-RET), Script Training, Conversation Treatment, and Communication Partner Training. We discuss both the advantages and disadvantages of using the RTSS framework to better understand the important elements of functional communication treatment approaches for aphasia.

Almost 70 years ago, Alexander Luria incorporated semantic aphasia among his aphasia classifications by demonstrating that deficits in linking the logical relationships of words in a sentence could co-occur with non-linguistic disorders of calculation, spatial gnosis and praxis deficits. In line with his comprehensive approach to the assessment of language and other cognitive functions, he argued that deficits in understanding semantically reversible sentences and prepositional phrases, for example, were in line with a single neuropsychological factor of impaired spatial analysis and synthesis, since understanding such grammatical relationships would also draw on their spatial relationships. Critically, Luria demonstrated the neural underpinnings of this syndrome with the critical implication of the cortex of the left temporal-parietal-occipital (TPO) junction. In this study, we report neuropsychological and lesion profiles of 10 new cases of semantic aphasia. Modern neuroimaging techniques provide support for the relevance of the left TPO area for semantic aphasia, but also extend Luria's neuroanatomical model by taking into account white matter pathways. Our findings suggest that tracts with parietal connectivity the arcuate fasciculus (long and posterior segments), the inferior fronto-occipital fasciculus, the inferior longitudinal fasciculus, the superior longitudinal fasciculus II and III, and the corpus callosum are implicated in the linguistic and non-linguistic deficits of patients with semantic aphasia. (C) 2016 Elsevier Ltd. All rights reserved.

• Characterization of mixed cases of aphasia, the most commonly attested in clinical practice.

Comprehension impairments in Wernicke's aphasia are thought to result from a combination of impaired phonological and semantic processes. However, the relationship between these cognitive processes and language comprehension has only been inferred through offline neuropsychological tasks. This study used ERPs to investigate phonological and semantic processing during online single word comprehension. EEG was recorded in a group of Wernicke's aphasia n=8 and control participants n=10 while performing a word-picture verification task. The N400 and Phonological Mapping Negativity/Phonological Mismatch Negativity (PMN) event-related potential components were investigated as an index of semantic and phonological processing, respectively. Individuals with Wernicke's aphasia displayed reduced and inconsistent N400 and PMN effects in comparison to control participants. Reduced N400 effects in the WA group were simulated in the control group by artificially degrading speech perception. Correlation analyses in the Wernicke's aphasia group found that PMN but not N400 amplitude was associated with behavioural word-picture verification performance. The results confirm impairments at both phonological and semantic stages of comprehension in Wernicke's aphasia. However, reduced N400 responses in Wernicke's aphasia are at least partially attributable to earlier phonological processing impairments. The results provide further support for the traditional model of Wernicke's aphasia which claims a causative link between phonological processing and language comprehension impairments.

Primary progressive aphasia is a clinical syndrome caused by a neurodegeneration of areas and neural networks involved in language, usually in the left hemisphere. The term “crossed aphasia” denotes an acquired language dysfunction caused by a lesion in the hemisphere ipsilateral to the dominant hand. A case is presented on a 75-year-old right-handed woman with a logopenic variant of primary progressive aphasia with word-finding difficulties of 2 years onset. The 18F-FDG PET/CT showed right temporoparietal hypometabolism. A functional MRI scan was performed during a verb naming task in order to characterise language lateralisation patterns. A similar activation pattern was observed in both hemispheres, with less activation than expected in bilateral inferior frontal gyrus. These findings support that logopenic variant of primary progressive aphasia should not be considered as a neurodegeneration starting in the left brain hemisphere, but as a syndrome characterised by asymmetric neurodegeneration of brain regions and neural networks involved in language.

Primary progressive aphasia is a clinical syndrome caused by a neurodegeneration of areas and neural networks involved in language, usually in the left hemisphere. The term "crossed aphasia" denotes an acquired language dysfunction caused by a lesion in the hemisphere ipsilateral to the dominant hand. A case is presented on a 75-year-old right-handed woman with a logopenic variant of primary progressive aphasia with word-finding difficulties of 2 years onset. The 18F-FDG PET/CT showed right temporoparietal hypometabolism. A functional MRI scan was performed during a verb naming task in order to characterise language lateralisation patterns. A similar activation pattern was observed in both hemispheres, with less activation than expected in bilateral inferior frontal gyrus. These findings support that logopenic variant of primary progressive aphasia should not be considered as a neurodegeneration starting in the left brain hemisphere, but as a syndrome characterised by asymmetric neurodegeneration of brain regions and neural networks involved in language.

Many dementia subtypes have more shared signs and symptoms than defining ones. We shall review eight cases with four overlapping syndromes and demonstrate how to distinguish the cases. These include focal cortical presentations of Alzheimer’s Disease(AD) (Posterior Cortical Atrophy and Corticobasal Syndrome), fluent aphasia (Semantic Dementia and Logopenic Aphasia), late-onset slowly progressive dementia (Hippocampal Sclerosis and Limbic Predominant AD) and rapidly progressive dementia (Creutzfeldt-Jakob Disease and Limbic Encephalitis). Recognizing the different syndromes described in this paper can help the clinician improve their diagnostic skills leading to improved patient outcomes by early and accurate diagnosis, prompt treatment, appropriate counseling and guidance.

This study examined patterns of acquired dyslexia in Serbian aphasic speakers, comparing profiles of groups with Broca’s versus Wernicke’s aphasia. The study also looked at the relationship of reading and auditory comprehension and between reading comprehension and reading aloud in these groups. Participants were 20 people with Broca’s and 20 with Wernicke’s aphasia. They were asked to read aloud and to understand written material from the Serbian adaptation of the Boston Diagnostic Aphasia Examination. A Serbian Word Reading Aloud Test was also used. The people with Broca’s aphasia achieved better results in reading aloud and in reading comprehension than those with Wernicke’s aphasia. Those with Wernicke’s aphasia showed significantly more semantic errors than those with Broca’s aphasia who had significantly more morphological and phonological errors. From the data we inferred that lesion sites accorded with previous work on networks associated with Broca’s and Wernicke’s aphasia and with a posterior-anterior axis for reading processes centred on (left) parietal-temporal-frontal lobes.

Chronic aphasia is a common consequence of a left-hemisphere stroke. Since the early insights by Broca and Wernicke, studying the relationship between the loci of cortical damage and patterns of language impairment has been one of the concerns of aphasiology. We utilized multivariate classification in a cross-validation framework to predict the type of chronic aphasia from the spatial pattern of brain damage. Our sample consisted of 98 patients with five types of aphasia (Broca's, Wernicke's, global, conduction, and anomic), classified based on scores on the Western Aphasia Battery (WAB). Binary lesion maps were obtained from structural MRI scans (obtained at least 6 months poststroke, and within 2 days of behavioural assessment); after spatial normalization, the lesions were parcellated into a disjoint set of brain areas. The proportion of damage to the brain areas was used to classify patients' aphasia type. To create this parcellation, we relied on five brain atlases; our classifier (support vector machine - SVM) could differentiate between different kinds of aphasia using any of the five parcellations. In our sample, the best classification accuracy was obtained when using a novel parcellation that combined two previously published brain atlases, with the first atlas providing the segmentation of grey matter, and the second atlas used to segment the white matter. For each aphasia type, we computed the relative importance of different brain areas for distinguishing it from other aphasia types; our findings were consistent with previously published reports of lesion locations implicated in different types of aphasia. Overall, our results revealed that automated multivariate classification could distinguish between aphasia types based on damage to atlas-defined brain areas.

Frontal dynamic aphasia is characterised by a profound reduction in spontaneous speech despite well-preserved naming, repetition and comprehension. Since Luria (1966, 1970) designated this term, two main forms of dynamic aphasia have been identified: one, a language-specific selection deficit at the level of word/sentence generation, associated with left inferior frontal lesions; and two, a domain-general impairment in generating multiple responses or connected speech, associated with more extensive bilateral frontal and/or frontostriatal damage. Both forms of dynamic aphasia have been interpreted as arising due to disturbances in early prelinguistic conceptual preparation mechanisms that are critical for language production. We investigate language-specific and domain-general accounts of dynamic aphasia and address two issues: one, whether deficits in multiple conceptual preparation mechanisms can co-occur; and two, the contribution of broader cognitive processes such as energization, the ability to initiate and sustain response generation over time, to language generation failure. Thus, we report patient WAL who presented with frontal dynamic aphasia in the context of progressive supranuclear palsy (PSP). WAL was given a series of experimental tests that showed that his dynamic aphasia was not underpinned by a language-specific deficit in selection or in microplanning. By contrast, WAL presented with a domain-general deficit in fluent sequencing of novel thoughts. The latter replicated the pattern documented in a previous PSP patient (Robinson, et al., 2006); however, unique to WAL, generating novel thoughts was impaired but there was no evidence of a sequencing deficit because perseveration was absent. Thus, WAL is the first unequivocal case to show a distinction between novel thought generation and subsequent fluent sequencing. Moreover, WAL's generation deficit encompassed verbal and non-verbal responses, showing a similar (but more profoundly reduced) pattern of performance to frontal patients with an energization deficit. In addition to impaired generation of novel thoughts, WAL presented with a concurrent strategy generation deficit, both falling within the second form of dynamic aphasia comprised of domain-general conceptual preparation mechanisms. Thus, within this second form of dynamic aphasia, concurrent deficits can co-occur. Overall, WAL presented with the second form of dynamic aphasia and was impaired in the generation of novel thoughts and internally-generated strategies, in the context of PSP and bilateral frontostriatal damage.

The consensus criteria for the diagnosis and classification of primary progressive aphasia (PPA) have served as an important tool in studying this group of disorders. However, a large proportion of patients remain unclassifiable whilst others simultaneously meet criteria for multiple subtypes. We prospectively evaluated a large cohort of patients with degenerative aphasia and/or apraxia of speech using multidisciplinary clinical assessments and multimodal imaging. Blinded diagnoses were made using operational definitions with important differences compared to the consensus criteria. Of the 130 included patients, 40 were diagnosed with progressive apraxia of speech (PAOS), 12 with progressive agrammatic aphasia, 9 with semantic dementia, 52 with logopenic progressive aphasia, and 4 with progressive fluent aphasia, while 13 were unclassified. The PAOS and progressive fluent aphasia groups were least impaired. Performance on repetition and sentence comprehension was especially poor in the logopenic group. The semantic and progressive fluent aphasia groups had prominent anomia, but only semantic subjects had loss of word meaning and object knowledge. Distinct patterns of grey matter loss and white matter changes were found in all groups compared to controls. PAOS subjects had bilateral frontal grey matter loss, including the premotor and supplementary motor areas, and bilateral frontal white matter involvement. The agrammatic group had more widespread, predominantly left sided grey matter loss and white matter abnormalities. Semantic subjects had bitemporal grey matter loss and white matter changes, including the uncinate and inferior occipitofrontal fasciculi, whereas progressive fluent subjects only had left sided temporal involvement. Logopenic subjects had diffuse and bilateral grey matter loss and diffusion tensor abnormalities, maximal in the posterior temporal region. A diagnosis of logopenic aphasia was strongly associated with being amyloid positive, (46/52 positive). Our findings support consideration of an alternative way of identifying and categorizing subtypes of degenerative speech and language disorders.

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

Background Aphasia is an important stroke sequel that impacts negatively on the HQoL of stroke patients. Although a number of stroke patients with aphasia will have good functional recovery, many are left with language deficits. Method Papers were identified through PubMed and MEDLINE search, with keywords such as: ‘stroke', ‘aphasia', ‘post-stroke aphasia', ‘factors that predict aphasia recovery', ‘aphasia outcomes' and ‘aphasia prognosis'. Results The most important factors that determine recovery are the lesion location and size, aphasia type and severity and to some extent the nature of early haemodynamic response, and treatment received. Anagraphic factors like gender, age, handedness and education have not been found to be robust predictors of recovery. Conclusions Predicting post-stroke aphasia recovery is difficult, because of the interplay between lesion, anagraphic, and treatment-related factors, in addition to the role of neuroplasticity.

The logopenic variant of primary progressive aphasia is a syndrome with neuropsychological and linguistic specificities, including phonological loop impairment for which diagnosis is currently mainly based on the exclusion of the two other variants, semantic and nonfluent/agrammatic primary progressive aphasia. The syndrome may be underdiagnosed due (1) to mild language difficulties during the early stages of the disease or (2) to being mistaken for mild cognitive impairment or Alzheimer's disease when the evaluation of episodic memory is based on verbal material and (3) finally, it is not uncommon that the disorders are attributed to psychiatric co-morbidities such as, for example, anxiety. Moreover, compared to other variants of primary progressive aphasia, brain abnormalities are different. The left temporoparietal junction is initially affected. Neuropathology and biomarkers (cerebrospinal fluid, molecular amyloid nuclear imaging) frequently reveal Alzheimer's disease. Consequently this variant of primary progressive aphasia does not fall under the traditional concept of frontotemporal lobar degeneration. These distinctive features highlight the utility of correct diagnosis, classification, and use of biomarkers to show the neuropathological processes underlying logopenic primary progressive aphasia. The logopenic variant of primary progressive aphasia is a specific form of Alzheimer's disease frequently presenting a rapid decline; specific linguistic therapies are needed. Further investigation of this syndrome is needed to refine screening, improve diagnostic criteria and better understand the epidemiology and the biological mechanisms involved.

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.

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

Phonation is a fundamental feature of human communication. Control of phonation in the context of speech-language disturbances has traditionally been considered a characteristic of lesions to subcortical structures and pathways. Evidence suggests however, that cortical lesions may also implicate phonation. We carried out acoustic and perceptual analyses of the phonation of /a/ in 60 males with aphasia (20 Wernicke’s, 20 Broca’s, 20 subcortical aphasia) and 20 males matched in age with no neurological or speech-language disturbances. All groups with aphasia were significantly more impaired on the majority of acoustic and perceptual measures as compared with the control speakers. Within the subjects with aphasia, subjects with subcortical aphasia were more impaired on most measures compared to subjects with Broca’s aphasia, and they, in turn, more impaired than those with Wernicke’s aphasia. Lesions in regions involved in sound production–perception result in dysfunction of the entire neurocognitive system of articulation–phonological language processing.

Objective and background Linguistic function is one of vulnerable aspects of traumatic brain injury (TBI) which may have destructive effects on patients' communicative activities and daily life, years following trauma. This paper attempts to answer the controversy whether surgery affects increase and decrease of linguistic impairment or not. Materials and methods Two hundred forty-one TBI patients aged 18–65 with abnormal CT findings and at least 20 minute post-trauma amnesia (PTA), who were conscious at discharge, participated in this study. Based on operative intervention, the samples were divided into two groups: operative and nonoperative. Cognitive and aphasic deficits were inspected formally and pragmatic disorder was informally appraised at discharge. Results The groups had no significant differences in aphasia incidence and language pragmatic impairment, though they were significantly distinctive in aphasia subcategories and cognitive deficit after trauma. Fluent aphasia was more common in both groups alike. In aphasia subcategories, however, transcortical sensory aphasia (TSA) in operative and anomia in nonoperative group were the most prevalent. Several variables appeared strikingly related to higher aphasia in operative groups as follows: moderate to severe injury, 18–35 and over 50 years of age, more than 1 week PTA, intracranial surgery of multiple lesions in left or bilateral hemisphere fronto-temporal cortex plus post-trauma cognitive and pragmatic impairments, and diffuse axonal injuries. Discussion Almost certainly, meaningful drop of cognitive function post surgery roots back in significant loss of initial consciousness level. Related factors to postoperative aphasia suggest taking policies through surgery intervention. Discerning the indispensable contributions of neurosurgeons, neurolinguists, and neuroscientists, results inspire more clinical future studies.

Conroy PJ, Snell C, Sage KE, Lambon Ralph MA. Using phonemic cueing of spontaneous naming to predict item responsiveness to therapy for anomia in aphasia. Background Anomia refers to difficulties retrieving words and is 1 of the most common symptoms of aphasia and hence often the target of therapy. The principal aim of the present study was to explore, for the first time, whether it is possible to predict the responsiveness of individual words to naming therapy from the psycholinguistic properties of those words and from the length of the phonemic cue required to name them. The relationship between this form of cueing and the outcome of naming therapy is of particular interest given that cueing is an established research and clinical tool within aphasiology, and is commonly used to probe naming performance. Method By amalgamating data from 3 previous studies, we were able to analyze data from 22 participants with chronic aphasia, yielding cueing and therapy data for 1080 target words. Cross-session changes in cueing and naming accuracy were collated for 298 target words. Results The results demonstrated that items which were accurately named after therapy (both at 1wk and 5wk later) required a significantly shorter phonemic cue to prompt correct naming in assessments prior to therapy. Imageability was a significant predictor of the required cue level, whereas word age of acquisition and word frequency were not. Highly imageable words required less cueing and were more likely to be accurately named posttherapy. A novel analysis of cross-session accuracy revealed that, even though the required cue length reduced across the first 6 of 10 therapy sessions, the relationship between the required cue length and final posttherapy accuracy was present throughout therapy. Discussion The findings are discussed in the context of their clinical implications for intervention, specifically for therapies that focus on accurate production of specific word targets. Themes for future related research are also considered.

In 1908 on June 11th, on July 9th and 23rd, three symposiums devoted to aphasia were organized in Paris by Charcot's successor: Fulgence Raymond. This extraordinary Society of Neurology meeting was justified by an antagonism between Jules Dejerine and Pierre Marie about Broca's aphasia. Cases of loss of speech secondary to a lesion in the left cerebral hemisphere had been already reported by Littre in 1828, Dax in 1836 and Lordat in 1843. On April 18 1861, Paul Broca, a surgeon, reported the observation of a patient named Leborgne whose death took place in his unit. He had lost the ability to speak twenty years ago. Broca blamed this “aphemia” on the progressive softening of a frontal circumvolution (probably the third one), which he labeled as the language center in the brain. For Wernicke (1874), Broca's aphasia became the prototype for motor cortical aphasias. One hundred pages in The Neurological Journal, signed by M. Klippel, Head of the Society and Francois Moutier's thesis are the irreplaceable sources for this event. During the first meeting, a list of questions was disclosed. What was the debate's stake? In 1906, Pierre Marie published an article entitled “Revision about the Aphasia issue: the third frontal left circumvolution is not playing any specific role in the language function”. In 1892, he had written that Dejerine “was performing science as well as others were playing the lottery”, which almost caused an authentic fight. For Pierre Marie, Broca's aphasia was only adding up Wernicke's aphasia and anarthria to which he assigned a precise localization, “his quadrilateral space” encompassing basal ganglia and internal capsule ( Figure 1 ). On the contrary, Jules Dejerine was keeping to Broca's classical conception. The meeting on June 11th opened with this issue: are motor and sensory aphasias clinically different from one another? Dejerine showed than in sensory aphasia, verbal blindness and verbal deafness are a lot more intense than in motor aphasia in which they are either missing or less marked, to which Pierre Marie answered that these were only nuances and that there is only one type of aphasia. Andre Thomas, a Dejerine's student, proved the opposite, comparing the two entities seriatim. It came to total aphasia. For Dejerine, it was the association between a sensory aphasia and a motor one. For Pierre Marie, all the aphasias are total. Dejerine criticized the term “anarthria” which evokes neurological dysarthria. The patient affected with motor aphasia presents a reduced ability to speak but is able to utter some words without any difficulty to articulate and is able to sing. Dupre agreed. This led to the issue of pure motor aphasia. Then, Pierre Marie introduced the interesting concept of “inner language”, abolished in all types of aphasia and preserved in pure anarthria, which has to be distinguished from aphasia. The second confrontation was devoted to anatomy. F. Raymond attended it along with his Head Clinician Georges Guillain and Francois Moutier. Where are the limits of “Pierre Marie quadrilateral space”? Jules Dejerine regretted that a mere horizontal brain section did not take into account the volume under scrutiny's dorsal and ventral limits. Madame Dejerine enquired about the structures found there and asked (without obtaining any answer) which one of these was causing “anarthria”. She proved brilliantly that “the body and the foot of the third frontal circumvolution are situated backwards from this anterior limit and that going from this, the F3 foot and cap are part of the quadrilateral space in which they occupy the upper, anterior and external part”… hypothesis which is perfectly attested by “a vertical-transversal view but escapes from the too low view presented by P. Marie”. Brissaud agreed. For Dejerine, a lesion within the quadrangle is able to cause aphasia only if it affects the anterior, upper and external parts of the area, thus sectioning the nervous fibers issued from the anterior area devoted to language skills (that is to say F3 foot and cap). F. Moutier, called by P. Marie, reported data from six observations of common Broca's aphasia without any lesion within F3. Dejerine retorted that lesions could be present within the radiant crown and white matter, containing projection or association fibers from the frontal cortex. Then Pierre Marie asked Dejerine if, in his opinion, the term Broca's aphasia implied necessarily cortical lesions, “a complete mistake”? Mrs Dejerine repeated that Broca's aphasia was resulting from cortical lesions within F3 and from lesions in the frontal cortex's axons devoted to projection and association. P. Marie asked for convincing observations supporting this theory. Dejerine supported the Lelong's case published by Broca in 1861. Marie considered it as a case involving “a poor elderly man aged 84 and affected with senile dementia (!) and in whom aphasia was no more present than obvious cortical lesions except for senile atrophy”. The very detailed report published by Broca (which is reported in the book written by Philippe Mond-Broca) contradicts P. Marie's fantasy; actually, it was a Broca's aphasia of sudden onset and without dementia. Jules Dejerine then reported five typical observations of cases. A long discussion followed between Andre Thomas and Moutier. In his thesis, are reported 20 cases of Broca's aphasia, studied by serial sections without the frontal cortex being affected and three cases of patients suffering from left cortical lesion of F3 without aphasia. M. Dejerine studied these cases in detail again and found lacks in anamneses studies. During the last meeting, the role played by the lentiform nucleus and insula in language remained an unsettled question. Georges Guillain quoted Mills and Spiller who are assigning to the lentiform nucleus a role in phonation. Then was tackled the issue of aphasia as a fundamental disorder. P. Marie stated that it was an intelligence disturbance; finally, he raised his voice against the individualization of defined language areas along with a defined centre for words images supported by Wernicke. Klippel concluded: “We are all agreeing about the necessity of revising some of the issues, relating to aphasia”. These three days, initiated by Fulgence Raymond, showed pathological anatomy limits and opened a new neuro-linguistic pathway with Theophile Alajouanine.

Few studies have directly compared the clinical and anatomical characteristics of patients with progressive aphasia to those of patients with aphasia caused by stroke. In the current study we examined fluent forms of aphasia in these two groups, specifically semantic dementia (SD) and persisting Wernicke's aphasia (WA) due to stroke. We compared 10 patients with SD to 10 age- and education-matched patients with WA in three language domains: language comprehension (single words and sentences), spontaneous speech and visual semantics. Neuroanatomical involvement was analyzed using disease-specific image analysis techniques: voxel-based morphometry (VBM) for patients with SD and overlays of lesion digitized lesion reconstructions in patients with WA. Patients with SD and WA were both impaired on tasks that involved visual semantics, but patients with SD were less impaired in spontaneous speech and sentence comprehension. The anatomical findings showed that different regions were most affected in the two disorders: the left anterior temporal lobe in SD and the left posterior middle temporal gyrus in chronic WA. This study highlights that the two syndromes classically associated with language comprehension deficits in aphasia due to stroke and neurodegenerative disease are clinically distinct, most likely due to distinct distributions of damage in the temporal lobe.

Introduction The objective of this study is to determine which cognitive processes underlying spelling are most affected in the three variants of primary progressive aphasia (PPA): Logopenic variant primary progressive aphasia (lvPPA), Semantic variant primary progressive aphasia (svPPA), and Nonfluent variant primary progressive aphasia (nfvPPA). Methods 23 PPA patients were administered The Johns Hopkins Dysgraphia Battery to assess spelling. Subtests evaluate for effects of word frequency, concreteness, word length, grammatical word class, lexicality (words vs pseudowords), and “regularity” by controlling for the other variables. Significant effects of each variable were identified with chi square tests. Responses on all spelling to dictation tests were scored by error type. 16 of the 23 subjects also had a high resolution MRI brain scan to identify areas of atrophy. Results We identified 4 patterns of spelling that could be explained by damage to one or more cognitive processes underlying spelling. Nine patients (3 unclassifiable, 4 with lvPPA, 2 with svPPA) had dysgraphia explicable by impaired access to lexical representations, with reliance on sublexical phonology-to-orthography conversion (POC). Two patients (with nfvPPA) showed dysgraphia explicable by impaired access to lexical representations and complete disruption of sublexical POC. Seven patients (4 with lvPPA, 1 with svPPA, 2 unclassifiable) showed dysgraphia explicable by impaired access to lexical-semantic representations and/or lexical representations with partially spared sublexical POC mechanisms. Five patients (1 with nfvPPA, 2 with svPPA, 1 with lvPPA, and 1 unclassifiable) showed dysgraphia explicable by impairment of the graphemic buffer. Conclusions Any cognitive process underlying spelling can be affected in PPA. Predominance of phonologically plausible errors, more accurate spelling of regular words than irregular words, and more accurate spelling of pseudowords than words (indicating spared POC mechanisms) may indicate a low probability of progression to nfvPPA.

Broca's aphasia is the most challenging communication deficit in stroke. Left inferior frontal gyrus (IFG), a key region of the mirror-neuron system, gets lesioned in Broca's aphasia. Mirror therapy (MT), a form of action-observation, may trigger the mirror neurons. The aim of this study was to report a case of poststroke subject with Broca's aphasia, who exhibited an inadvertent and significant improvement in speech after MT for the paretic upper limb. The 20-month old stroke patient underwent MT through goal-directed tasks. He received a total absence of spontaneous speech, writing, and naming. After 45 sessions of task-based MT for the upper limb, he showed tremendous recovery in expressive communication. He had fluent and comprehensive communication; however, with a low pitch and minor pronunciation errors. He showed a substantial change (from 18/100 to 79/100) on the Communicative Effective Index, particularly, on items such as expressing emotions, one-to-one conversation, naming, and spontaneous conversation.

Simmons-Mackie N, Raymer A, Armstrong E, Holland A, Cherney LR. Communication partner training in aphasia: a systematic review. Objectives To describe the effects of communication partner training on persons with aphasia and their communication partners. Specifically the systematic review addressed 3 clinical questions regarding the impact of partner training on language, communication activity and participation, psychosocial adjustment, and quality of life for adults with aphasia and their communication partners. Data Sources Twenty-three terms were used to search 12 electronic databases (eg, PubMed, CINAHL, PsychINFO, PsychArticles, CSA Linguistics and Language Behavior Abstracts, Social Sciences Citation Index [Web of Science], SUMSearch, TRIP, EMBASE, REHABDATA, National Library for Health, Cochrane Database of Systematic Reviews) and the journal "Aphasiology." References from all relevant articles were hand-searched. Study Selection Two reviewers independently applied inclusion criteria to select potential relevant articles from the titles and abstracts of references retrieved by the literature search. The full text of the remaining articles was reviewed by a 5-member panel, resulting in a corpus of 31 studies that met the final inclusion criteria. Data Extraction Two independent reviewers extracted the descriptive data related to the participants, the intervention, the outcome measures, and the results. Data Synthesis The 5-member review team by consensus classified the studies using the American Academy of Neurology system for classification of evidence (2004). Conclusions Evidence shows that communication partner training is effective in improving communication activities and/or participation of the communication partner and is probably effective in improving communication activities and/or participation of persons with chronic aphasia when they are interacting with trained communication partners. There is insufficient evidence to make recommendations related to the impact of partner training on persons with acute aphasia or the impact of training on language impairment, psychosocial adjustment, or quality of life for either the person with aphasia or the communication partner.

Research into acquired child aphasia can provide useful evidence about the neural mechanisms involved in recovery from aphasia because the functional plasticity of the brain is greater in children than in adults. To investigate the neural correlates underlying functional recovery from acquired child aphasia, we followed a 9-year-old boy with aphasia for 2–16 months after traumatic head injury. The patient's language ability was assessed four times by the Standard Language Test of Aphasia (SLTA). Regional cerebral blood flow (rCBF) was also measured four times with 99mTc-ECD and a fully automated quantitative image analysis system. The patient showed substantial improvement of language during this period. Although overall rCBF fluctuated throughout the 1st–4th measurements, there was a significant relative dominance of rCBF in the left cerebral hemisphere compared with the right hemisphere throughout the four measurements, especially in the paracentral and temporo-parietal regions. These findings may suggest that the left cerebral hemisphere rather than the right hemisphere plays a major role in the early recovery from child aphasia.

We report the case of a woman with primary progressive aphasia (PPA) presenting with conduction aphasia. Neurological findings showed bilateral finger tremor and signe de poignet fige in her right hand. Memory, orientation, and activities of daily living were well preserved. Linguistic examination showed severe impairment in repetition, fluent spontaneous speech with phonemic paraphasia, and relatively well preserved comprehension. Limb-kinetic apraxia and parkinsonism were not observed during the course of her illness. T1-weighted magnetic resonance imaging revealed severe atrophy of the left temporal lobe and dilatation of the left Sylvian fissure. Neuropathological findings demonstrated the most severe atrophy in the left superior temporal gyrus and Gallyas–Braak-positive or phosphorylated tau-immunoreactive cytoskeletal structures, which were consistent with corticobasal degeneration (CBD). We speculate that the progressive conduction aphasia of our patient might have been caused by left temporal lobe impairment. We suggest that progressive conduction aphasia may be a feature of CBD presenting with PPA.

In addition to the seminal lesion studies of aphasiology, the development of functional neuroimaging has allowed a better understanding of the neural foundations of language. However, despite a substantial improvement in the knowledge of the cortical networks organization, the underlying subcortical association circuits have received less attention. Recent advances in fiber tracking using diffusion tensor imaging, combined with personal studies using intraoperative electrostimulation, which temporarily inactivates restricted regions during brain surgery, have enabled to map language pathways in humans with spatiotemporal resolution unmatched by other techniques. On the basis of these new insights, my purpose is to revisit the anatomo-functional connectivity of language. First, I discuss the role of the white bundles thought to be essential for language, with special emphasis regarding the structure-function relationships pertaining to the distinct subcomponents of language. Second, I propose an integrative view of connectivity, that considers language as the final product of the well-synchronized functioning of parallel distributed cortico-subcortical networks.

Most naming treatments in aphasia either assume a phonological or semantic emphasis or a combination thereof. However, it is unclear whether semantic or phonological treatments recruit the same or different cortical areas in chronic aphasia. Employing three persons with aphasia, two of whom were non-fluent, the present study compared changes in neural recruitment associated with phonologic and semantic based naming treatments. The participants with non-fluent aphasia were able to name more items following both treatment approaches. Although this was not the case for the participant who had fluent aphasia, her naming errors decreased considerably following treatment. Post-treatment fMRI revealed similar changes in neural activity bilaterally in the precuneus among the two non-fluent participants – increased activity was noted in the right entorhinal cortex and posterior thalamus on post treatment scans for the third participant. These findings imply that cortical areas not traditionally related to language processing may support anomia recovery in some patients with chronic aphasia.

S.E. Henschen (1847-1930) was the author of a significant 8 volume textbook on diseases of the brain, Klinische und anatomische Betrage zur Pathologie des Gehirns . This work has not been available to English readers. An outline is presented of the contents of each volume. Details are given of the work on aphasia. An extended pre´cis of the arguments regarding sensory and motor aphasia is the focus of the paper with reference made to contemporaneous authors.

Ullman and colleagues should be congratulated for an energetic assault on some of the core issues in neurolinguistics. This work attempts to detect an impact of productivity differences in morphology upon fluency differences in aphasia. This basic goal is well-motivated empirically and should eventually succeed. However, I believe that the links currently being proposed between language and the brain are not well structured conceptually. If these conceptual problems can be successfully addressed, then this work could make a contribution. Without these clarifications, I believe that the current formulation represents a conceptual step backward. The idea that word formation involves both productive and non-productive processes is an old one, dating back to Panini and the Greeks. This contrast has served as a cornerstone of diachronic morphology for nearly two centuries. In developmental psycholinguistics, the decision to analyze words as based on rote or rule crops up at virtually every stage in the analysis of emerging grammars (MacWhinney, 1978). From the viewpoint of neurology and aphasiology, the contrast between fluent and non-fluent aphasia is also fundamental. The traditional interpretation of this contrast has been one that focuses on the role of anterior areas in motor processing and posterior areas in sensory processing. In the 1970s, evidence that nonfluent aphasics also had disabilities in comprehending complex syntax (Zurif, Caramazza, & Myerson, 1972) led researchers to challenge this analysis. Following Jakobson (1955), neurolinguistics began to imagine that frontal areas might control grammatical processing, whereas posterior areas control lexical insertion. The dual-route analysis of Ullman and colleagues represents an attempt to advance the Jakobsonian view

Functional imaging studies with nonfluent aphasia patients have observed "over-activation" in right (R) language homologues. This may represent a maladaptive strategy; suppression may result in language improvement. We applied slow, 1 Hz repetitive transcranial magnetic stimulation (rTMS) to an anterior portion of R Broca's homologue daily, for 10 days in four aphasia patients who were 5-11 years poststroke. Significant improvement was observed in picture naming at 2 months post-rTMS, with lasting benefit at 8 months in three patients. This preliminary, open trial suggests that rTMS may provide a novel treatment approach for aphasia by possibly modulating the distributed, bi-hemispheric language network.

Six participants with chronic aphasia secondary to first-ever ischemic stroke within the middle cerebral artery (MCA) distribution of the left hemisphere and six neurologically intact controls of similar age were given a running recognition memory task for words while the magnetic flux normal to the scalp surface was measured with a whole-head neuromagnetometer. This task had been previously shown to be valid for the localization and lateralization of brain activity specific to receptive language function. As expected, patients exhibited relatively decreased activation in areas known to be involved in receptive language function, including superior temporal gyrus (STG) in the left hemisphere, as well as increased activation of areas outside of the left STG that might potentially support language function. Decreased activation within left STG was associated with a reduction in receptive language in patients, as was increased activation outside of left STG. Results support hypotheses suggesting that peri-lesional areas outside premorbid language areas may assume receptive language function after aphasia secondary to stroke, but that better recovery occurs when putative premorbid language areas are able to normalize.

Crossed aphasia is a phenomenon in which an individual sustains a lesion in the right hemisphere (typically non-language dominant), but who exhibits an aphasic syndrome. The authors present a case study of an individual with crossed aphasia (CA) in an attempt to provide anecdotal information for four questions posed by : (a). Is CA a reversal of the normal cerebral hemisphere pattern of language function? (b). Does the presence of aphasia following a right cerebral hemisphere lesion indicate that typical right hemisphere functions (e.g., visual perception) are intact? (c). How may the aphasia's presentation differ from typical left hemisphere aphasias? And (d). is the pattern of improvement following CA similar to that of typical left hemisphere aphasias? We longitudinally examined the communicative-cognitive performance of an adult man with crossed aphasia of the Wernicke's type following a cerebrovascular accident. A 21-week follow-up evaluation indicated improvements in his language functioning from our initial evaluation, but he continued to exhibit a classic, moderately severe Wernicke's aphasia.

In contrast to the estimated low incidence of crossed aphasia in dextral adults (among 1%), crossed aphasia in children has been considered a common finding for almost a century. However, reviewing the literature on crossed aphasia in dextrals (CAD) and its related topics from 1975 onward, we encountered only 5 children in a corpus of 180 cases (2.7%). Critical analysis rendered three of the reported cases ambiguous and hence not suitable to draw potentially relevant conclusions. In this review, the neurobehavioral manifestations of the two representative childhood CAD cases are analyzed and compared with adult CAD and acquired childhood aphasia (ACA). In the light of our findings, which support the position of innate cerebral specialization for language, the long-standing controversy as to whether lateralized hemispheric specialization for language is innate or develops progressively during maturation is briefly discussed.

Few systematic descriptions of aphasia characteristics are available about the Spanish language. Three different language aspects are examined in this paper: phonology, aphasic substitutions (paraphasias), and morphosyntax. It has been observed that phonological errors in Spanish speaking aphasies more frequently involve vowels than consonants. It is proposed that this is related to the salience of vowels observed in Spanish. Phonological paraphasias are about 10 times more frequent than verbal paraphasias in conduction aphasia. In Broca's aphasia, they are only five times more frequent, whereas in Wernicke's aphasia the number of phonemic and verbal paraphasias is roughly the same. It is difficult to know how well this distribution fits in other languages, due to the absence of cross-linguistic comparisons. Agrammatism in Spanish has certain distinguishing characteristics, particularly due to the significant flexibility of the word order in the sentence and the use of some preposition to distinguish the object from the subject. Certain aspects of Spanish grammar are relatively resistant in cases of brain pathology, such as the subject-verb concordance. Some relatively unusual types of sentences, such as passive sentences, are significantly impaired in cases of agrammatism. Obviously, those grammatical aspects that are stronger (i.e., more crucial to distinguish the agent and the patient, such as the use of the preposition “a”) are also better preserved in cases of Broca's aphasia associated with agrammatism. It is concluded that, despite similarities with aphasia described in other Indo-European languages, certain aphasia features can be considered characteristic of the Spanish language.

The purpose of this paper is to examine the linguistic problems of aphasic speakers of Finnish. The focus is on Broca's and Wernicke's aphasia. First, we present an overview of the special characteristics of the grammar of Finnish. Secondly, there is a discussion of previous studies on aphasic speakers of Finnish. Thirdly, we present an analysis of our data from conversation and picture description task by speakers with Broca's and Wernicke's aphasia. The analysis focuses on case marking, subject-verb agreement, word order and the expression of tense in the speech of Finnish aphasics. As a whole, many linguistic features are preserved both in Broca's and Wernicke's aphasia. Even the neologistic words in Wernicke's aphasia are appropriately inflected. However, our findings suggest that aphasic errors are not always systematic and furthermore, they may be context-dependent. For example, Broca's aphasics produced case marking and agreement patterns in some contexts correctly, whereas in some other contexts they were produced erroneously. The word order patterns were similar to those found in conversational discourse in general. However, it is sometimes impossible to give a definitive analysis of the word order or structure of a given grammatical construction. This is due to the fact that sentence structure is sometimes badly distorted both in Broca's and Wernicke's aphasic cases because of difficulty in finding lexical content words. We conclude with a comparison of our findings with previous studies of Finnish aphasics, proposing some methodological implications for further studies.

Kurt Goldstein is regarded as one of the major proponents of the holistic movement at the beginning of the 20th century. He rejected the strong localization hypothesis in the field of aphasiology and attempted to link language disturbances to an underlying general intellectual impairment. Goldstein‘s criticism was based on his subtle symptomatology, his organismic biology, and his philosophical reflections. In his concept of abstract attitude Goldstein searched for a general psychological function that might explain a variety of aphasic symptoms. Abstract attitude bridges the gap between cognitive and linguistic structures. According to Goldstein, it is the basis for words to have a meaning, to be employed in a categorical sense. Since amnesic aphasics are confined to a concrete attitude, their words have lost their representational function. Although Goldstein‘s concept of abstract attitude is no longer used in scientific discourse, it is analyzed for its heuristic value. It led Goldstein to questions about the relation between cognition and language and to fragments of a semantic theory.

Well-documented cases of crossed (transcortical sensory) aphasia, especially those with longitudinal evaluation, are rare. We report a case of crossed transcortical sensory aphasia following watershed infarcts in the right hemisphere, from the moment of the accident until 15 months afterward. The aphasia type, and the course of recovery, is a “mirror” representation of that seen in cases of uncrossed aphasia. Unfortunately, the data do not permit strong conclusions regarding the lateralization of language in association with praxis and visuospatial abilities. This underlines the need for more well-documented (case) studies to come to a better understanding of the mechanisms through which lateralization occurs.

We report a case of a woman with primary progressive aphasia (PPA) who presented with conduction aphasia. A 60-year-old, right-handed, Japanese female suffering from progressive aphasia had difficulty in repeating words and phrases. She displayed phonemic paraphasias but had preserved comprehension and had no cognitive or behavior disorder for more than 6 years after the onset of the condition. She was able to continue to work successfully and to perform all her normal daily activities. T1-weighted magnetic resonance imaging revealed minute dilatation of the left inferior horn and sulci in the left hemisphere, and positron emission tomography revealed mild hypometabolism in the left supramarginal gyrus and its surrounding areas. Therefore, she was diagnosed as suffering from PPA presenting as conduction aphasia. We believe that the progressive conduction aphasia of the patient belongs to one of the fluent forms of PPA, and the ability to continue normal work along with the clinical portrayal of preserved memory and cognition skills may be features of a form of PPA presenting as conduction aphasia.

A decision tree and decimal rating scales were used for psychotherapy with a patient with post-stroke subcortical motor aphasia. These two methods used in combination were highly efficient in obtaining information about the patient's mood and issues of concern. The patient was able to report on changing levels of anxiety and depression. He was able to relate his emotional state to environmental or personal factors. Values as low as 1 and as high as 10 for anxiety and depression were reported by the patient during the course of 25 psychotherapy sessions. A Pearson correlation indicated that anxiety and depression varied independently.

A case of crossed aphasia is presented in a strongly right-handed 77-year-old white female without history of familial sinistrality or prior neurological illness. She developed a right middle cerebral artery infarction documented by CT and accompanied by obvious clinical signs of a conduction aphasia with some resolution but continuing obvious language defect after 9 weeks in rehabilitation. Comprehensive neuropsychological and aphasia testing suggested anomalous lateralization of phonologic-output aspects of language, emotional prosody, motor planning and body schema modules with usual lateralization of lexical-semantic aspects of language and visuo-spatial functions. Experimental validation of the uncrossed lexical-semantic aspects of language using tachistoscope methods found support for the Alexander-Annett theory that different aspects of language can be dissociated in their lateralization. The subject had difficulty identifying a semantic associate of a picture presented to the left visual field (7 errors out of 10) relative to right visual field presentation (2 errors out of 10). Bilateral free naming errors (6 and 5 errors in the left and right visual fields, respectively) occurred consistent with the aphasic presentation, suggesting phonologic-output dysfunction from the right cerebral vascular accident. Implications of the results for aphasia classification are discussed.

In order to study the functional anatomy of hemispheric dominance for language comprehension we compared the patterns of activations and deactivations with PET and H(2)15O during a story-listening task in two groups of normal volunteers selected on the basis of their handedness. The reference task was a silent rest. The results showed asymmetrical temporal activations favoring the left hemisphere in right handers (RH) together with Broca's area and medial frontal activations. A rightward lateralization of deactivations located in the parietal and inferior temporal gyrus was also observed. In left handers (LH) the temporal activations were more symmetrical as were the parietal and inferior frontal deactivations. Broca's area and medial frontal gyrus activations were present in LH. The direct comparison of RH and LH activations revealed larger activations in the left superior temporal, in particular in the left planum temporale and temporal pole of RH, while LH activated an additional right middle temporal region. Individual analysis of LH differences images superimposed on individual MRI planes demonstrated an important variability of functional dominance, with two LH leftward lateralized, two symmetrical, and one showing a rightward lateralization of temporal activations. There was no relationship between functional dominance and handedness scores. These results are in accordance with data from aphasiology that suggest a greater participation of the right hemisphere in language processing in LH. In addition, the presence of bilateral deactivations of the dorsal route could support the assumption that LH ambilaterality concerns, in addition to language, other cognitive functions such as visuospatial processing.

Stuttering secondary to nervous system damage (neurogenic stuttering) has been considered not to have any localizing significance. Recently, it has been suggested, though, that stuttering due to damage of the supplementary motor region might yet represent a specific constellation of dysfluencies. Ackermann et al. 1996 Aphasiology 10, 409–417, put forward the suggestion that in stuttering associated with supplementary motor region involvement dysfluencies are restricted to word-initial position and are absent during sentence repetition and reading aloud. We present a case to the contrary in this article.

The literature on aphasia with subcortical lesions is reviewed. Lesions of thalamic relay nuclei linked to the cortical language areas are related to paraphasic aphasia. The data with white matter lesions is less consistent. A number of reports describe propositional aphasia with lesions of the frontostriatal pathways, transcortical motor aphasia with lesions in the area of the knee of the internal capsule and paraphasic aphasia with lesions of the anterior limb of the internal capsule. Only few studies have found aphasia with lesions of the basal ganglia proper. In general, subcortical aphasias are transient. Models of the participation of the subcortical nuclei in language functions have to consider recent developments in our understanding of their organization and function.