The relationship between verbal and nonverbal auditory signal processing in conduction aphasia: behavioral and anatomical evidence for common decoding mechanisms.

The processing of nonverbal auditory stimuli has not yet been sufficiently investigated in patients with aphasia. On the basis of a duration discrimination task, we examined whether patients with left-sided cerebrovascular lesions were able to perceive time differences in the scale of approximately 150 ms. Further linguistic and memory-related tasks were used to characterize more exactly the relationships in the performances between auditory nonverbal task and selective linguistic or mnemonic disturbances. All examined conduction aphasics showed increased thresholds in the duration discrimination task. The low thresholds on this task were in a strong correlative relation to the reduced performances in repetition and working memory task. This was interpreted as an indication of a pronounced disturbance in integrating auditory verbal information into a long-term window (sampling disturbance) resulting in an additional load of working memory. In order to determine the lesion topography of patients with sampling disturbances, the anatomical and psychophysical data were correlated on the basis of a voxelwise statistical approach. It was found that tissue damage extending through the insula, the posterior superior temporal gyrus, and the supramarginal gyrus causes impairments in sequencing of time-sensitive information.

Phonological, lexical, and semantic errors produced by impairment at the output buffer in a Spanish aphasic patient.

We present a single case of a right-handed female patient, RH, who was categorized as suffering from conduction aphasia. She presented no articulatory problems during spontaneous speech but made a significant number of phonological paraphasias in naming and repetition tasks. The number of errors increased for long words and pseudowords. This pattern of results points to damage in the "Phonological Output Buffer" (POB) as the basis of this disorder. However, this patient did not make mistakes when reading words and pseudowords aloud, even when we introduced a delay between the presentation of the word and its production to test the working memory resources of the phonological buffer. Furthermore, the patient's ability to name objects, repeat words, and write to dictation improved with her degree of familiarity with the items. The damage could be situated at the point where phonemes are selected and ordered to produce words. We posit that the deficits observed in this patient, and the differences encountered between her performance and that of others described in the literature, in particular in reading tasks, can be explained by considering POB damage to be gradual in nature. According to this explanation, the performance of patients with damage to the POB will depend on the amount of information provided by the stimulus (word/nonword), the language particularities (regular/irregular), and the nature of the task demands (repetition, writing, naming, or reading).

Aphasia induced by gliomas growing in the ventrolateral frontal region: assessment with diffusion MR tractography, functional MR imaging and neuropsychology.

INTRODUCTION: Lesions in the ventrolateral region of the dominant frontal lobe have been historically associated with aphasia. Recent imaging results suggest that frontal language regions extend beyond classically defined Broca's area to include the ventral precentral gyrus (VPCG) and the arcuate fasciculus (AF). Frontal gliomas offer a unique opportunity to identify structures that are essential for speech production. The aim of this prospective study was to investigate the correlation between language deficits and lesion location in patients with gliomas. METHODS: Nineteen patients with glioma and 10 healthy subjects were evaluated with diffusion tensor imaging magnetic resonance (MR) tractography, functional MR (verb generation task) and the Aachener Aphasie Test. Patients were divided into two groups according to lesion location with respect to the ventral precentral sulcus: (i) anterior (n=8) with glioma growing in the inferior frontal gyrus (IFG) and underlying white matter; (ii) posterior (n=11) with glioma growing in the VPCG and underlying white matter. Virtual dissection of the AF, frontal intralobar tract, uncinate fasciculus (UF) and inferior frontal occipital fasciculus (IFOF) was performed with a deterministic approach. RESULTS: Seven posterior patients showed aphasia classified as conduction (4), Broca (1), transcortical motor (1) and an isolated deficit of semantic fluency; one anterior patient had transcortical mixed aphasia. All posterior patients had invasion of the VPCG, however only patients with aphasia had also lesion extension to the AF as demonstrated by tractography dissections. All patients with language deficits had high grade glioma. Groups did not differ regarding tumour volume. A functional pars opercularis was identified with functional MR imaging (fMRI) in 17 patients. CONCLUSIONS: Gliomas growing in the left VPCG are much more likely to cause speech deficits than gliomas infiltrating the IFG, including Broca's area. Lesion extension to the AF connecting frontal to parietal and temporal regions is an important mechanism for the appearance of aphasia.

Arcuate fasciculus variability and repetition: the left sometimes can be right.

Repetition ability is a major criterion for classifying aphasic syndromes and its status is helpful in the determination of the involved neural structures. It is widely assumed that repetition deficits correlate with injury to the left perisylvian core including the arcuate fasciculus (AF). However, descriptions of normal repetition despite damage to the AF or impaired repetition without AF involvement cast doubts on its role in repetition. To explain these paradoxes, we analyse two different aphasic syndromes - in which repetition is selectively impaired (conduction aphasia) or spared (transcortical aphasias) - in light of recent neuroimaging findings. We suggest that the AF and other white matter bundles are the anatomical signatures of language repetition and that individual variability in their anatomy and lateralisation may explain negative cases.

Conduction aphasia, sensory-motor integration, and phonological short-term memory - an aggregate analysis of lesion and fMRI data.

Conduction aphasia is a language disorder characterized by frequent speech errors, impaired verbatim repetition, a deficit in phonological short-term memory, and naming difficulties in the presence of otherwise fluent and grammatical speech output. While traditional models of conduction aphasia have typically implicated white matter pathways, recent advances in lesions reconstruction methodology applied to groups of patients have implicated left temporoparietal zones. Parallel work using functional magnetic resonance imaging (fMRI) has pinpointed a region in the posterior most portion of the left planum temporale, area Spt, which is critical for phonological working memory. Here we show that the region of maximal lesion overlap in a sample of 14 patients with conduction aphasia perfectly circumscribes area Spt, as defined in an aggregate fMRI analysis of 105 subjects performing a phonological working memory task. We provide a review of the evidence supporting the idea that Spt is an interface site for the integration of sensory and vocal tract-related motor representations of complex sound sequences, such as speech and music and show how the symptoms of conduction aphasia can be explained by damage to this system.

A review of conduction aphasia.

In this paper, a historical overview of the interpretation of conduction aphasia is initially presented. It is emphasized that the name conduction aphasia was proposed by Wernicke and was interpreted as a disconnection between the temporal and frontal brain language areas; this interpretation was re-taken by Geschwind, attributing the arcuate fasciculus the main role in speech repetition disturbances and resulting in the so-called Wernicke-Geschwind model of language. With the introduction of contemporary neuroimaging techniques, this interpretation of conduction aphasia as a disconnection syndrome due to an impairment of the arcuate fasciculus has been challenged. It has been disclosed that the arcuate fasciculus does not really connect Wernicke's and Broca's areas, but Wernicke's and motor/premotor frontal areas. Furthermore, conduction aphasia can be found in cases of cortical damage without subcortical extension. It is concluded that conduction aphasia remains a controversial topic not only from the theoretic point of view, but also from the understanding of its neurologic foundations.

Diffusion tensor imaging depicting damage to the arcuate fasciculus in patients with conduction aphasia: a study of the Wernicke-Geschwind model.

OBJECTIVES: In contrast with disorders of comprehension and spontaneous expression, conduction aphasia is characterized by poor repetition, which is a hallmark of the syndrome. There are many theories on the repetition impairment of conduction aphasia. The disconnection theory suggests that a damaged in the arcuate fasciculus, which connects Broca's and Wernicke's area, is the cause of conduction aphasia. In this study, we examined the disconnection theory. METHODS: We enrolled ten individuals with conduction aphasia and ten volunteers, and analysed their arcuate fasciculus using diffusion tensor imaging (DTI) and obtained fractional anisotropy (FA) values. Then, the results of the left hemisphere were compared with those of the right hemisphere, and the results of the conduction aphasia cases were compared with those of the volunteers. RESULTS: There were significant differences in the FA values between the left and right hemispheres of volunteers and conduction cases. In volunteers, there was an increase in fiber in the left hemisphere compared with the right hemisphere, whereas there was an increase in fiber in the right hemisphere compared with the left hemisphere in conduction aphasia patients. The results of diffusion tensor tractography suggested that the configuration of the arcuate fasciculus was different between conduction aphasia patients and volunteers, suggesting that there was damage to the arcuate fasciculus of conduction aphasia cases. CONCLUSIONS: The damage seen in the arcuate fasciculus of conduction aphasia cases in this study supports the Wernicke-Geschwind disconnection theory. A disconnection between Broca's area and Wernicke's area is likely to be one mechanism of conduction aphasia repetition impairment.

Density pervades: an analysis of phonological neighbourhood density effects in aphasic speakers with different types of naming impairment.

We investigated the influence of phonological neighbourhood density (PND) on the performance of aphasic speakers whose naming impairments differentially implicate phonological or semantic stages of lexical access. A word comes from a dense phonological neighbourhood if many words sound like it. Limited evidence suggests that higher density facilitates naming in aphasic speakers, as it does in healthy speakers. Using well-controlled stimuli, Experiment 1 confirmed the influence of PND on accuracy and phonological error rates in two aphasic speakers with phonological processing deficits. In Experiments 2 and 3, we extended the investigation to an aphasic speaker who is prone to semantic errors, indicating a semantic deficit and/or a deficit in the mapping from semantics to words. This individual had higher accuracy, and fewer semantic errors, in naming targets from high- than from low-density neighbourhoods. It is argued that the Results provide strong support for interactive approaches to lexical access, where reverberatory feedback between word- and phoneme-level lexical representations not only facilitates phonological level processes but also privileges the selection of a target word over its semantic competitors.

The role of the arcuate fasciculus in conduction aphasia.

In aphasia literature, it has been considered that a speech repetition defect represents the main constituent of conduction aphasia. Conduction aphasia has frequently been interpreted as a language impairment due to lesions of the arcuate fasciculus (AF) that disconnect receptive language areas from expressive ones. Modern neuroradiological studies suggest that the AF connects posterior receptive areas with premotor/motor areas, and not with Broca's area. Some clinical and neurophysiological findings challenge the role of the AF in language transferring. Unusual cases of inter-hemispheric dissociation of language lateralization (e.g. Broca's area in the left, and Wernicke's area in the right hemisphere) have been reported without evident repetition defects; electrocortical studies have found that the AF not only transmits information from temporal to frontal areas, but also in the opposite direction; transferring of speech information from the temporal to the frontal lobe utilizes two different streams and conduction aphasia can be found in cases of cortical damage without subcortical extension. Taken altogether, these findings may suggest that the AF is not required for repetition although could have a subsidiary role in it. A new language network model is proposed, emphasizing that the AF connects posterior brain areas with Broca's area via a relay station in the premotor/motor areas.

It's either a cook or a baker: patients with conduction aphasia get the gist but lose the trace.

Patients with conduction aphasia have been characterized as having a short-term memory deficit that leads to relative difficulty on span and repetition tasks. It has also been observed that these same patients often get the gist of what is said to them, even if they are unable to repeat the information verbatim. To study this phenomenon experimentally, patients with conduction aphasia and left hemisphere-injured controls were tested on a repetition recognition task that required them to listen to a sentence and immediately point to one of three sentences that matched it. On some trials, the distractor sentences contained substituted words that were semantically-related to the target, and on other trials, the distractor sentences contained semantically-distinct words. Patients with conduction aphasia and controls performed well on the latter condition, when distractors were semantically-distinct. However, when the distractor sentences were semantically-related, the patients with conduction aphasia were impaired at identifying the target sentence, suggesting that these patients could not rely on the verbatim trace. To further understand these results, we also tested elderly controls on the same task, except that a delay was introduced between study and test. Like the patients with conduction aphasia, the elderly controls were worse at identifying target sentences when there were semantically-related distractors. Taken together, these results suggest that patients with conduction aphasia rely on non-phonologic cues, such as lexical-semantics, to support their short-term memory, just as normal participants must do in long-term memory tasks when the phonological trace is no longer present.

The rises and falls of disconnection syndromes.

In a brain composed of localized but connected specialized areas, disconnection leads to dysfunction. This simple formulation underlay a range of 19th century neurological disorders, referred to collectively as disconnection syndromes. Although disconnectionism fell out of favour with the move against localized brain theories in the early 20th century, in 1965, an American neurologist brought disconnection to the fore once more in a paper entitled, 'Disconnexion syndromes in animals and man'. In what was to become the manifesto of behavioural neurology, Norman Geschwind outlined a pure disconnectionist framework which revolutionized both clinical neurology and the neurosciences in general. For him, disconnection syndromes were higher function deficits that resulted from white matter lesions or lesions of the association cortices, the latter acting as relay stations between primary motor, sensory and limbic areas. From a clinical perspective, the work reawakened interest in single case studies by providing a useful framework for correlating lesion locations with clinical deficits. In the neurosciences, it helped develop contemporary distributed network and connectionist theories of brain function. Geschwind's general disconnectionist paradigm ruled clinical neurology for 20 years but in the late 1980s, with the re-emergence of specialized functional roles for association cortex, the orbit of its remit began to diminish and it became incorporated into more general models of higher dysfunction. By the 1990s, textbooks of neurology were devoting only a few pages to classical disconnection theory. Today, new techniques to study connections in the living human brain allow us, for the first time, to test the classical formulation directly and broaden it beyond disconnections to include disorders of hyperconnectivity. In this review, on the 40th anniversary of Geschwind's publication, we describe the changing fortunes of disconnection theory and adapt the general framework that evolved from it to encompass the entire spectrum of higher function disorders in neurology and psychiatry.

Conduction aphasia and the arcuate fasciculus: A reexamination of the Wernicke-Geschwind model.

Wernicke, and later Geschwind, posited that the critical lesion in conduction aphasia is in the dominant hemisphere's arcuate fasciculus. This white matter pathway was thought to connect the anterior language production areas with the posterior language areas that contain auditory memories of words (a phonological lexicon). Alternatively, conduction aphasia might be induced by cortical dysfunction, which impairs the phonological output lexicon. We observed an epileptic patient who, during cortical stimulation of her posterior superior temporal gyrus, demonstrated frequent phonemic paraphasias, decreased repetition of words, and yet had intact semantic knowledge, a pattern consistent with conduction aphasia. These findings suggest that cortical dysfunction alone may induce conduction aphasia.