Conduction Aphasia

Conduction aphasia is a language disorder characterized by selective defect of oral repetition of words or sentences in the presence of relative preservation of auditory comprehension.

From: The Neurology of Conciousness (Second Edition) , 2016

Aphasia and Aphasic Syndromes

Joseph Jankovic Medico , in Bradley and Daroff'southward Neurology in Clinical Exercise , 2022

Conduction Aphasia

Conduction aphasia is a theoretically important syndrome that can be remembered by its hitting deficit of repetition. Most patients accept relatively fluent spontaneous speech merely brand literal paraphasic errors and hesitate ofttimes for self-correction. Naming may be impaired, but auditory comprehension is preserved. Repetition may be disturbed to seemingly ridiculous extremes, such that a patient who can express himself or herself at a sentence level and embrace conversation may be unable to repeat even single words. Ane such patient could non echo the word "boy" but said "I like girls better." Reading and writing are somewhat variable, but reading aloud may share some of the same difficulty as repeating. Associated deficits include hemianopia in some patients; right-sided sensory loss may exist present, but correct hemiparesis is unremarkably mild or absent. Some patients accept limb apraxia, creating a misimpression that comprehension is impaired. Bedside examination findings in conduction aphasia are summarized inTable 13.iv.

The lesions of conduction aphasia ordinarily involve either the superior temporal or the inferior parietal regions. Benson and associates suggested that patients with limb apraxia take parietal lesions, whereas those without apraxia have temporal lesions (Benson et al., 1973). Conduction aphasia may stand for a phase of recovery in patients with Wernicke aphasia in whom the harm to the superior temporal gyrus is not consummate.

Conduction aphasia has been advanced every bit a classical disconnection syndrome. Wernicke originally postulated that a lesion disconnecting the Wernicke and Broca areas would produce this syndrome; Geschwind later pointed to the arcuate fasciculus, a white matter tract traveling from the deep temporal lobe, around the sylvian crack to the frontal lobe, equally the site of disconnection. Anatomical interest of the arcuate fasciculus is present in almost, if not all, cases of conduction aphasia, but some doubt has been raised well-nigh the importance of the arcuate fasciculus to conduction aphasia or even to repetition (Bernal and Ardila, 2009). In cases of conduction aphasia, in that location is unremarkably also cortical involvement of the supramarginal gyrus or temporal lobe. The supramarginal gyrus appears to exist involved in auditory immediate memory and in phoneme perception related to word meaning, as well as phoneme generation (Hickok and Poeppel, 2000). Lesions in this area are associated with conduction aphasia and phonemic paraphasic errors. Others have pointed out that lesions of the arcuate fasciculus do non e'er produce conduction aphasia. Some other theory of conduction aphasia has involved a defect in auditory verbal brusk-term (or what near neurologists would telephone call immediate) memory.

Speech and Language

Margaret M. Swanberg , ... Jeffrey L. Cummings , in Textbook of Clinical Neurology (Tertiary Edition), 2007

CONDUCTION APHASIA

Conduction aphasia occurs in up to 15% of admissions of patients with aphasia in some reports. 37,39 The defining feature of conduction aphasia is the repetition difficulty (Video 96, Conduction Aphasia). Conduction aphasia may be "Wernicke‐similar" or "Broca‐like." When of the sometime variety, verbal output is fluent and paraphasic, but the amount of output is less than in Wernicke's aphasia.. In the latter, articulation is excellent, and comprehension of spoken linguistic communication is intact; however, fluency may be diminished. In dissimilarity, the repetition of numbers or the naming of colors may be contaminated with phonemic paraphasias. Confrontational naming is likewise disturbed, mainly considering of paraphasic errors. Reading out loud may be similarly compromised; in dissimilarity, reading silently for comprehension is intact. The ability to write is invariably disturbed to some extent. Most often, syllables and letters are substituted or misspelled or misplaced. Oft, conduction aphasia is not diagnosed at the onset just develops in the recovery phase from Wernicke's aphasia. With further improvement, patients remain anomic.

The neurological exam oftentimes shows no abnormalities, but variable motor or sensory findings and ideomotor apraxia may exist present. A pseudothalamic pain syndrome may develop in the recovery phase. Visual fields may testify variable deficits reflecting involvement of unlike sites neighboring the locus of pathology underlying conduction aphasia. xiii

The site of pathology in conduction aphasia involves the left hemisphere arcuate fasciculus, well-nigh often deep to the supramarginal gyrus. This may produce a separation of the sensory and motor language areas, every bit originally suggested past Wernicke. 40, 41 The discovery of a trifurcatin of fibers in the arcuate fasciculus may account for the different presentation of conduction aphasia. Lesions in the inductive segment disrupt connections between the frontal lobe (i.e., Broca's area) and the parietal lobe, whereas lesions in the posterior segments would disconnect Wernicke'southward area from the parietal region. This could account for reports of conduction aphasia described with lesions outside the classical arcuate fasciculus region, notably in the left supramarginal gyrus and left temporal gyrus. 37,39 The most common cause of conduction aphasia is occlusion of a portion of the angular branch of the middle cognitive artery.

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Cortical Syndromes

Edward J. Fly Dr., FACP, FIDSA , in Cecil Essentials of Medicine , 2022

Aphasia

Aphasia ordysphasia refers to a loss or harm of linguistic communication function every bit a issue of damage to the specific linguistic communication centers of the dominant hemisphere. It is singled-out from dysarthria, which is a disturbance in the articulation of speech. The master types of aphasia are summarized inTable 109.ii.

Clinical assessment for aphasia requires testing of fluency, comprehension, repetition, naming, reading, adding, and writing.Anomia refers to difficulty in the naming of objects. Patients mayhave difficulty with the correct identification of common items such as a watch, oftentimes using a word that either sounds like the intended word ("a spotch"—a literal paraphasic error) or a word with a broadly like meaning ("a clock"—a semantic paraphasic error. There are two broad types of aphasia depending on the anatomic site of the lesion: anterior (Broca) aphasia and posterior (Wernicke) aphasia.

Broca aphasia is characterized past a severe disruption in the fluency of speech communication, with profound impairments of expression in both speech and writing. Comprehension may exist mildly affected. The language disturbance is near invariably accompanied by contralateral face up and arm weakness as a result of the proximity of the motor homunculus to the Broca speech area in the inferior frontal lobe.

Wernicke aphasia is characterized by an inability to embrace spoken or written language. Afflicted patients speak fluently, but the content is meaningless. The lesion is located in the posterior superior temporal surface area and may be associated with a homonymous hemianopic visual field deficit.

Conduction aphasia is characterized by normal comprehension and fluent speech but a striking inability to repeat a phrase. The responsible lesion lies in the arcuate fasciculus connecting the Broca and Wernicke areas.Global aphasia results from large lesions of the frontal lobe; all aspects of language are afflicted. Lesions of the language areas of the nondominant hemisphere event indysprosody. For example, patients with lesions in the junior frontal lobe of the nondominant hemisphere, analogous to the Broca area, speak with a monotonous voice, losing the ability to add together emotional cadence to their speech. Similarly, lesions affecting the nondominant Wernicke area result in patients declining to selection up on the emotional inflexions (such as anger) of what is said to them.

Writing is almost invariably affected in patients with disturbances of language (Fig. 109.3). An exception to this occurs in the syndrome ofalexia without agraphia, which results from a lesion in the ascendant occipital lobe and splenium of the corpus callosum (unremarkably caused by infarction in the territory of the posterior cognitive artery). The patient's linguistic communication center is "disconnected" from the contralateral (unaffected) visual cortex. Such patients tin can write a sentence merely are unable to read what they have written.

Vascular Aphasia Syndromes

Donna C. Tippett , Argye East. Hillis , in Neurobiology of Language, 2016

73.2.iv Conduction Aphasia

Conduction aphasia is usually defined as a linguistic communication impairment characterized past relatively fluent, although paraphasic, spontaneous spoken communication, intact auditory comprehension, and disproportionately impaired speech communication repetition. Secondary features include reading impairments, variable writing difficulties, and ideomotor apraxia ( Benson et al., 1973). Individuals with conduction aphasia display well-articulated responses that are phonemically similar to target words and repetitive cocky-corrections resulting in increasingly closer approximations to targets. This miracle is termed "conduit d'approache" (Goodglass, 1992). Traditionally, conduction aphasia is thought to be caused by a lesion in the arcuate fasciculus, a white matter tract that runs between Broca's and Wernicke's areas, and thus is considered a disconnection syndrome considering a lesion in the arcuate fasciculus is assumed to interrupt advice between the sensory and motor modules of the classically defined speech-language system (Geschwind, 1965). This hypothesis has been challenged. More recent evidence shows that conduction aphasia is not the result of impairment only to the arcuate fasciculus. Although impairment to the arcuate fasciculus is reported exist present in the setting of conduction aphasia in some gimmicky accounts (Geldmacher, Quigg, & Elias, 2007; Yamada et al., 2007; Zhang et al., 2010), information technology is not reported in others. In fact, cortical lesions lone may produce conduction aphasia (Anderson et al., 1999; Quigg, Geldmacher, & Elias, 2006), indicating that damage to the arcuate fasciculus is not a prerequisite condition for conduction aphasia. Furthermore, lesions of the arcuate fasciculus do not e'er cause conduction aphasia (Epstein-Peterson, Vasconcellos-Faria, Mori, Hillis, & Tsapkini, 2012; Selnes, van Zijl, Barker, Hillis, & Mori, 2002). Substantial anatomical show suggests that conduction aphasia is caused by damage to the left superior temporal gyrus and/or the left supramarginal gyrus (Axer, von Keyserlingk, Berks, & von Keyserlingk, 2001; Baldo & Dronkers, 2006) due to occlusion of a co-operative of the inferior division of the left MCA.

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Aphasia, Alexia, and Agraphia

1000.H. Purdy , in Encyclopedia of Mental Wellness (2d Edition), 2016

Conduction aphasia

Conduction aphasia is some other fluent aphasia with speech that contains numerous phonemic paraphasias, and repetition is poor. It differs from Wernicke's aphasia in that the individuals take relatively skillful comprehension. They are very aware of their exact errors and will oft try to self-correct their mistakes. Conduction aphasia is considered a 'disconnection syndrome' caused by a lesion in the arcuate fasciculus, a packet of nervus fibers connects Wernicke's and Broca's areas. However, impairment to the arcuate fasciculus is not a prerequisite of conduction aphasia. Most available anatomical evidence suggests that this item aphasia is most often caused by damage to the left superior temporal gyrus and/or the left inferior parietal lobe and posterior arcuate fasciculus ( Buchsbaum et al., 2011; Fridriksson et al., 2010).

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Disorders of Higher Cortical Function

Anna Berti , ... Marco Neppi-Modona , in Neurobiology of Brain Disorders, 2015

Conduction Aphasia

Conduction aphasia shares with Broca and Wernicke aphasias the inability to echo sentences, a defective assembly of phonemes, and an impaired naming power, but information technology differs from them in the relatively preserved spoken language production and auditory comprehension. In classical descriptions (Wernicke's model 6 and Lichtheim's model 4 ), conduction aphasia was uniquely ascribed to lesions of the arcuate fasciculus, a white matter pathway connecting the Wernicke and Broca areas. It is now known that, although the subcortical projections linking temporal, parietal, and frontal cortices are often damaged in patients affected past this kind of linguistic communication trouble there is no evidence that a pure white matter disconnection can cause conduction aphasia. In addition, the involvement of the left inferior parietal lobe (BA   xl), the left primary auditory cortices (BA   41 and 42), and the insula seems to be necessary to cause the symptoms.

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Language Disorders: Aphasia

H.A. Whitaker , in Encyclopedia of Gerontology (Second Edition), 2007

Conduction Aphasia

Conduction aphasia has also been chosen central aphasia, disorganized execution of the encoding plan related to disturbed auditory feedback, repetition aphasia, and afferent motor aphasia. The primary role of language that is afflicted is the repetition of voice communication, whereas comprehension and production tend to be much less impaired. Conduction aphasic patients frequently endeavor to correct their repetition errors, implying a better preserved comprehension. The repetition errors may be at the level of individual sounds or words; repetition may exhibit an agrammatic character. The oral communication of the patient with conduction aphasia is more often like that seen in Wernicke'south aphasia only sometimes is similar that seen in Broca's aphasia. In addition to the repetition arrears, patients with conduction aphasia are often afflicted with anomia; literal paraphasias (commutation of sounds) may intrude in both spontaneous speaking and in attempts to repeat what is heard. Within single words or very short phrases, articulatory fluency may be good, simply patients with conduction aphasia typically display phonemic (or literal) paraphasias, a substitution of sounds. Although within-phrase syntactic patterns tend to exist normal, many conduction aphasic patients have difficulty with sentences containing pronouns and grammatical role words, also equally polysyllabic words. Other characteristics that may be establish include difficulties in writing, showing some forms of agraphia and ideomotor apraxia. Writing ability usually parallels spoken communication output, showing deficits in spelling and alphabetic character omissions or substitutions. As is the case for Broca'south aphasia, conduction aphasic patients are typically aware of their spoken communication and language deficits.

The lesions leading to conduction aphasia tend to be located in and around the supramarginal gyrus and the arcuate fasciculus; the latter pathway connects the temporal lobe to the frontal lobe. Other lesions are along the edge of the Sylvian scissure, extending to the subjacent white affair.

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The Nature of Conduction Aphasia: A Study of Anatomic and Clinical Features and of Underlying Mechanisms

Eugene Green , Davis H. Howes , in Studies in Neurolinguistics, Volume three, 1977

IDENTIFYING THE DISORDER

The Syndrome

Conduction aphasia is an acquired disorder of language, attributable to focal lesions in the posterior area of the dominant cortical hemisphere which impair the ability of patients to express themselves in well formed utterances ( Hécaen, 1972). Contempo summaries (Brown, 1972; Benson, Sheremata, Bouchard, Segarra, Price, & Geschwind, 1973) that describe the syndrome of conduction aphasia emphasize a contrast between the defective speech and writing of patients and their relatively skilful comprehension. The spontaneous speech of a conduction aphasic is fluent, yet it is circumlocutory and inadequately structured. Not only is the syntax of utterances defective, but patients have difficulty in finding words appropriate to a context and in pronouncing words accurately. Similarly, defects of structure and gross misspelling characterize their spontaneous writing or writing to dictation (though copied work is often good). Failures in naming, reading aloud, and repeating are quite evident. Performances in naming tasks typically demonstrate an impaired ability to detect words for presented objects, for body parts, and for colors. Oral reading is probable to be laborious and attended by the aforementioned errors that occur in spontaneous speech. Above all, the difficulty in repetition is remarkable. Despite self-criticism and repeated trials, patients characteristically fail to provide a suitable lucifer for the examiner'southward model. In short, all forms of expression (except in such tasks equally counting off numbers, the days of the week, or the months of the yr) are severely impaired in conduction aphasia.

On the other hand, patients comprehend oral and written textile satisfactorily. They read silently with understanding, deport on normal conversations, and respond accordingly to everyday questions and commands. The features of conduction aphasia distinguish information technology clearly from other aphasic disorders. Broca's aphasia, for case, is likewise a disorder in which comprehension remains largely intact, whereas spoken communication output is dysarthric and agrammatic. Only different the conduction aphasic, the spoken language of the Broca's aphasic is not at all fluent; his spontaneous speech is, in fact, worse than his repetition. In Wernicke's or sensory aphasia, there is fluent speech and poor repetition, but at that place is also a gross defect of comprehension that contrasts sharply with the conduction aphasic'south intact power to understand. Finally, conduction aphasia differs in its features from anomic aphasia, inasmuch every bit the anomic aphasic not merely has good auditory comprehension, speaks fluently, but mostly repeats without error. Dubois, Hecaen, Angelergues, de Chatelier, & Marcie (1964) emphasize, too, that the spoken communication of the anomic aphasic contains none of the audio substitutions normally found in the conduction aphasic's utterances. Detailed accounts of the contrasts betwixt conduction aphasia and other aphasias appear in Goldstein (1948) and Brownish (1972).

Unresolved Problems

To identify conduction aphasia and to contrast its symptoms with those of other aphasic disorders is not to say, however, that it is recognized everywhere as a distinctive grade of linguistic arrears. The showtime analysis of conduction aphasia, fabricated by Wernicke in 1874, met with the resistance of such contemporaries as Freud (1891), and even recent authors still feel the need to urge that it exist recognized as ane of the chief aphasic syndromes (Hécaen, Dell, & Roger, 1955;Geschwind, 1965). Benson et al. (1973) annotation that cases of conduction aphasia are frequent enough, and that they can be identified, for example, in five% to 10% of new admissions to the aphasia ward of the Boston Veterans Administration Hospital. Yet the reluctance to recognize conduction aphasia as a well divers syndrome is due not and then much to its relative infrequency as to a persistent uncertainty both most the anatomic lesions which underlie it and the nature and function of the mechanisms it disturbs. Luria (1966) asserts that conduction aphasia is a disorder "that has non received anatomical confirmation." Kinsbourne (1972) discusses some possible relations between focal lesions and the difficulties conduction aphasics have in repeating, yet he concludes that his findings "practise non rely for their validity on whatever detail neuroanatomic hypothesis." And even studies similar that of Benson et al.(1973), which suggest that in that location is a close correlation between focal lesions and the features of the syndrome, neglect to demonstrate convincingly why it is that the same pattern of linguistic disorder should result from damage to dissimilar, though neighboring, areas of the posterior, dominant hemisphere of the cortex.

Moreover, from the pattern of linguistic disorder in conduction aphasia it is not immediately articulate which mechanisms of oral communication suffer impairment. The features of the syndrome–good comprehension, fluent only poorly structured spontaneous speech, dumb naming, severely disturbed repetition–bespeak a disturbance primarily in some machinery of speech output. Simply the nature of such mechanism and its components are by no ways clearly understood; it is, indeed, inappreciably surprising, as Goodglass and Blumstein (1973) annotation, that analyses of conduction aphasia are probable to yield interpretations "totally different" from one another.

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Aphasia: Sudden and Progressive☆

M.-1000. Mesulam , in Reference Module in Neuroscience and Biobehavioral Psychology, 2017

Conduction Aphasia

In conduction aphasia, speech output is fluent only paraphasic, comprehension of speech is intact, and repetition is severely impaired. Naming and writing are also dumb. Reading aloud is impaired, simply reading comprehension is preserved. The lesion sites spare Broca's and Wernicke's areas just may induce a functional disconnection between the two such that neural word representations formed in Wernicke'south area and adjacent regions cannot exist transmitted to Broca's area for assembly into respective articulatory patterns. Occasionally, a Wernicke'south area lesion gives rise to a transient Wernicke's aphasia that rapidly resolves into a conduction aphasia. The paraphasic output in conduction aphasia interferes with the ability to limited meaning, but this arrears is not nearly as severe as the one displayed by patients with Wernicke's aphasia.

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Linguistic communication: Aphasia

N.F. Dronkers , J.V. Baldo , in Encyclopedia of Neuroscience, 2009

Conduction Aphasia

Conduction aphasia was offset described by Wernicke to characterize patients with relatively preserved comprehension and paraphasic oral communication. Later, Wernicke added to the list of deficits a disorder of repetition. Clinically, patients with conduction aphasia present with fluent oral communication and relatively good comprehension, but their speech is somewhat paraphasic and their power to repeat is greatly reduced. Reading and writing, also equally naming, are besides affected to a moderate degree. A clinical sample of such a patient's fluent spoken output describing the picnic scene follows:

I come across a agglomeration of people. At that place'south a tree and a car and a business firm and h2o and the pier. Guy'due south fishing, and a couple o' guys that are saying how-do-you-do to the sail'southward person. And a guy washing something next to a/hail/of sand and grass. A flag – is that a flag? And the wind and the pole and some more than grass.

Despite such relatively fluent speech, patients with conduction aphasia exhibit significantly impaired repetition. Patients may get the gist or general meaning of what is said (as evidenced by their relatively skillful comprehension), but they are dumb at repeating textile verbatim. For case, in an endeavour to repeat the sentence 'The pastry cook was elated,' one patient responded "Something most a happy baker." This phenomenon suggests that patients with conduction aphasia are relying on a nonverbatim, semantic route since the phonological trace is no longer available. Dependence on this semantic road is besides revealed by the fact that repetition is severely affected for nonsense words (e.thou., 'meppen'). Such words have no meaning and thus cannot give ascension to a paraphrase or synonym, let alone reproduction of the same discussion.

Although controversial, some researchers divide patients with conduction aphasia into two groups – reproduction and repetition conduction aphasia. These two groups reflect different parts of the complex repetition process. Repetition conduction aphasics are idea to primarily accept a problem at the level of holding a retention trace – in other words, a deficit in exact working memory. Reproduction conduction aphasics are thought to have their primary trouble with the processing and product of phonological information. Researchers who maintain this division acknowledge that some patients diagnosed with conduction aphasia fall into both groups.

Paraphasic errors in patients with conduction aphasia may have the form of phonemic substitutions (e.g., 'free' for 'tree') or semantic substitutions (e.k., 'male parent' for 'brother'). However, they are more likely (than patients with Wernicke's aphasia) to effort to right their errors. For instance, a patient with conduction aphasia was asked to proper noun a line drawing of a cactus and responded by saying "gaktus, no, gaksus, gackone, no, cackus, little screwed upwards in that location, cack, cactus! cactus!"

Traditional models of aphasia originally suggested that conduction aphasia should arise from lesions to the arcuate fasciculus, the white matter tract connecting Wernicke'southward and Broca's areas. Despite the fact that no data exist to support this model, most textbooks in psychology and neuroscience perpetuate this notion. Instead, patients with conduction aphasia most normally have lesions centered in left posterior neocortex, most notably in inferior parietal cortex, not the arcuate fasciculus. Figure 3 shows a lesion overlay map of thirteen patients with chronic conduction aphasia. Every bit can be seen, the region of common overlap is centered in inferior parietal cortex. This region has been suggested to be disquisitional for exact working retention, which is consistent with the pattern of repetition deficits observed in this patient group.

Figure3. Average lesion map of thirteen stroke patients with chronic conduction aphasia, showing a region of common overlap in the inferior parietal cortex.

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