Conduction Aphasia Case Study

Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia. An acquired language disorder, it is characterized by intact auditory comprehension, fluent (yet paraphasic) speech production, but poor speech repetition. They are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as patients show significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce.[1][2] Patients will display frequent errors during spontaneous speech, such as substituting or transposing sounds. They will also be aware of their errors, and will show significant difficulty correcting them.[3] For example: "Clinician: Now, I want you to say some words after me. Say ‘boy’. Patient: Boy. Clinician: Home. Patient: Home. Clinician: Seventy-nine. Patient: Ninety-seven. No … sevinty-sine … siventy-nice…. Clinician: Let’s try another one. Say ‘refrigerator’. Patient: Frigilator … no? how about … frerigilator … no frigaliterlater … aahh! It’s all mixed up!" [4]

Shallice and Warrington (1970) were able to differentiate two variants of this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, afflicting confrontation tasks such as repetition, reading and naming in a similar manner.[5]

Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supra marginal gyrus.[6] The classical explanation for conduction aphasia is that of a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and speech production (Broca's area), due specifically to damage to the arcuate fasciculus, a deep white matter tract. Patients are still able to comprehend speech because the lesion does not disrupt the ventral stream pathway.


Conduction aphasics will show relatively well-preserved auditory comprehension, which may even be completely functional. Spontaneous speech production will be fluent and generally grammatically and syntactically correct. Intonation and articulation will also be preserved. Speech will often contain paraphasic errors: phonemes and syllables will be dropped or transposed (e.g., "snowball" → "snowall", "television" → "vellitision", "ninety-five percent" → "ninety-twenty percent"). The hallmark deficit of this disorder, however, is in repetition. Patients will show a marked inability to repeat words or sentences when prompted by an examiner.[7][8] After saying a sentence to a person with conduction aphasia, he or she will be able to paraphrase the sentence accurately but will not be able to repeat it, possibly because their "motor speech error processing is disrupted by inaccurate forward predictions, or because detected errors are not translated into corrective commands due to damage to the auditory-motor interface".[9][10] When prompted to repeat words, patients will be unable to do so, and produce many paraphasic errors. For example, when prompted with "bagger", a patient may respond with, "gabber".[11] Oral reading can also be poor.[citation needed]

However, patients recognize their paraphasias and errors and will try to correct them, with multiple attempts often necessary for success. This recognition is due to preserved auditory error detection mechanisms.[10] Error sequences frequently fit a pattern of incorrect approximations featuring known morphemes that a) share one or more similarly located phonemes but b) differ in at least one aspect that makes the substituted morpheme(s) semantically distinct. This repetitive effort to approximate the appropriate word or phrase is known as conduite d’approche.[8] For example, when prompted to repeat "Rosenkranz", a German-speaking patient may respond with, "rosenbrau... rosenbrauch... rosengrau... bro... grosenbrau... grossenlau, rosenkranz,... kranz... rosenkranz".[11]

Conduction aphasia is a relatively mild language impairment, and most patients return to day-to-day life.[11][12] Symptoms of conduction aphasia, as with other aphasias, can be transient, lasting only several hours or a few days. As aphasias and other language disorders are frequently due to stroke, their symptoms can change and evolve over time, or simply disappear. This is due to healing in the brain after inflammation or hemorrhage, which leads to decreased local impairment. Furthermore, plastic changes in the brain may lead to the recruitment of new pathways to restore lost function. For example, the right hemisphere speech systems may learn to correct for left-hemisphere damage. However, chronic conduction aphasia is possible, without transformation to other aphasias.[11] These patients show prolonged, profound deficits in repetition, frequent phonemic paraphasias, and conduite d'approche during spontaneous speech.


Conduction aphasia is caused by damage to the parietal lobe of the brain, especially in regards to the area associated with the left-hemisphere dominant dorsal stream network.[13][10] The arcuate fasciculus, which connects Broca's area and Wernicke's area (important for speech and language production and comprehension, respectively), is affected.[13] These two areas control speech and language in the brain. The arcuate fasciculus is a thick band of fiber that connects the two areas and carries messages between them. When this area is damaged, the patient experiences damage to the auditory-motor integration system. This results in disruption to the delayed auditory feedback network, causing the individual to have difficulty correcting themselves on speech repetition tasks.[10] Additionally, recent evidence suggests that conduction aphasia can also be caused by lesions in the left superior temporal gyrus and/or the left supramarginal gyrus.[6]

The brain damage causing conduction aphasia is often from a stroke, which can produce both localized and widespread damage. Traumatic brain injury and tumors can also lead to localized lesions, with potential to cause conduction aphasia.[citation needed] Conduction aphasia can also be seen in cases of cortical damage without subcortical extensions.[14]


Traditionally, it has been believed that conduction aphasia was the result of a lesion in the arcuate fasciculus, a deep, white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. It was thought that this bundle transmitted information between Wernicke's area (responsible for language comprehension) and Broca's area (responsible for language production). Wernicke, and later Lichtheim and others, theorized that a disconnect between these two regions caused patients to fail to monitor speech and limited their ability to transfer information between comprehension and production functions, thus leading to paraphasic errors and a deficit in repetition of auditory input. This hypothesis fits well with the Wernicke-Geschwind model of language, which compartmentalizes and localizes speech comprehension and production.[citation needed]

Although the disconnection hypothesis explains many of the conditions associated with conduction aphasia, clinical evidence is lacking, and the Wernicke-Geschwind model has since become obsolete. There have been no known autopsy cases in which conduction aphasia was shown to be the result of a focused arcuate fasciculus lesion.[15] Surveys of conduction aphasics with anatomical confirmation show that in nearly all patients, there was damage to portions of the cortex as well. Furthermore, there are reports of patients with severe disruption of the arcuate fasciculus who show no symptoms of conduction aphasia (although it is plausible that the contralateral hemisphere facilitated repetition in these cases).[16]

Recent research has pointed to a different explanation for conduction aphasia, similar to Wernicke's, which is based on newer models suggesting language is facilitated by "cortically based, anatomically distributed, modular networks."[17] Anderson et al. describe an experiment in which electrical stimulation of the left posterior superior temporal cortex in a human subject induced symptoms consistent with conduction aphasia, indicating that a deep brain disconnection is not necessary.[17] While this study does not completely discredit the disconnection hypothesis, but does point to a system in which transmission of spoken language information involves more than just the arcuate fasciculus. Regardless of the role that the arcuate fasciculus plays in the disorder, the cortical component cannot be denied.[citation needed]


Individuals with conduction aphasia are able to express themselves fairly well, with some word finding and functional comprehension difficulty.[18] Although people with aphasia may be able to express themselves fairly well, they tend to have issues repeating phrases, especially phrases that are long and complex.[18] When asked to repeat something, the patient will be unable to do so without significant difficulty, repeatedly attempting to self-correct (conduite d'approche). When asked a question, however, patients can answer spontaneously and fluently.[citation needed]

Several standardized test batteries exist for diagnosing and classifying aphasias. These tests are capable of identifying conduction aphasia with relative accuracy.[8] The Boston Diagnostic Aphasia Examination (BDAE) and the Western Aphasia Battery (WAB) are two commonly used test batteries for diagnosing conduction aphasia. These examinations involve a set of tests, which include asking patients to name pictures, read printed words, count aloud, and repeat words and non-words (such as shwazel).[citation needed]


Treatment for aphasias is generally individualized, focusing on specific language and communication improvements, and regular exercise with communication tasks. Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery.[19] However, conduction aphasia is a mild aphasia, and conduction aphasics score highly on the WAB at baseline.


In the late 19th century, Paul Broca studied patients with expressive aphasia. These patients had lesions in the anterior perisylvian region (now known as Broca's area), and produced halting and labored speech, lacking in function words and grammar. For example, "clinician: What brought you to the hospital? patient: yes … ah … Monday … ah … Dad … Peter Hogan, and Dad … ah … hospital … and ah … Wednesday … Wednesday … nine o’clock and ah Thursday … ten o’clock … doctors two … two … an doctors and … ah … teeth … yah … and a doctor an girl … and gums, an I." [20] Comprehension is generally preserved, although there can be deficits in interpretation of complex sentences. In an extreme example, one of his patients could only produce a single syllable, "Tan".

Meanwhile, Carl Wernicke described patients with receptive aphasia, who had damage to the left posterior superior temporal lobe, which he named "the area of word images". These patients could speak fluently, but their speech lacked meaning. They had a severe deficit in auditory comprehension. For example, "Clinician: What brings you to the hospital? Patient: Boy, I’m sweating, I’m awful nervous, you know, once in a while I get caught up, I can’t mention the tarripote, a month ago, quite a little, I’ve done a lot well, I impose a lot, while on the other hand, you know what I mean, I have to run around, look it over, trebbin and all that sort of stuff."[21]

The two disorders (expressive and receptive aphasias) thus seemed complementary, and corresponded to two distinct anatomical locations.

Wernicke predicted the existence of conduction aphasia in his landmark 1874 monograph, Der Aphasische Symptomenkompleks: Eine Psychologische Studie auf Anatomischer Basis.[3][17][22] He was the first to distinguish the various aphasias in an anatomical framework, and proposed that a disconnection between the two speech systems (motor and sensory) would lead to a unique condition, distinct from both expressive and receptive aphasias, which he termed Leitungsaphasie. He did not explicitly predict the repetition deficit, but did note that, unlike those with Wernicke's aphasia, conduction aphasics would be able to comprehend speech properly, and intriguingly, would be able to hear and understand their own speech errors, leading to frustration and self-correction.[22][23]

Wernicke was influenced by Theodor Meynert, his mentor, who postulated that aphasias were due to perisylvian lesions. Meynert also distinguished between the posterior and anterior language systems, leading Wernicke to localize the two regions.[17] Wernicke's research into the fiber pathways connecting the posterior and anterior regions lead him to theorize that damage to the fibers under the insula would lead to conduction aphasia. Ludwig Lichtheim expanded on Wernicke's work, although he labeled the disorder commissural aphasia, to distinguish between aphasias tied to processing centers.[24]

Sigmund Freud would argue in 1891 that the old framework was inaccurate; the entire perisylvian area, from the posterior to the anterior regions, were equivalent in facilitating speech function. In 1948 Kurt Goldstein postulated that spoken language was a central phenomenon, as opposed to a differentiated and disparate set of functionally distinct modules. To Freud and Goldstein, conduction aphasia was thus the result of a central, core language breakdown; Goldstein labeled the disorder central aphasia.[17]

Later work and examination of brain structures, however, implicated the arcuate fasciculus, a white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. Norman Geschwind proposed that damage to this bundle caused conduction aphasia; the characteristic deficits in auditory repetition were due to failed transmission of information between the two language centers.[17] Studies showed that conduction aphasics had an intact 'inner voice', which discredited the central deficit model of Freud and Goldstein.[25] The Wernicke-Lichtheim-Geschwind disconnection hypothesis thus became the prevailing explanation for conduction aphasia. However, recent reviews and research have cast doubt on the singular role of the arcuate fasciculus and the model of spoken language in general[citation needed].

See also[edit]


  1. ^Conduction Aphasia. (n.d.). Retrieved from
  2. ^Carlson, Neil R.; Heth, C. Donald (2007). Psychology the science of behaviour (4th ed.). Pearson Education Inc. ISBN 0-205-64524-0. 
  3. ^ abGazzaniga, Michael S.; Ivry, Richard B.; Mangun, George R. (2002). Cognitive neuroscience: the biology of the mind. New York: W. W. Norton. p. 389. ISBN 0-393-97777-3. 
  4. ^Robert H. Brookshire. An Introduction to Neurogenic Communication Disorders, 6e. volume. Mosby Year Book, St. Louis, 2003.
  5. ^Sidiropoulos, Kyriakos; De Bleser, Ria; Ackermann, Hermann; Preilowski, Bruno (2008). "Pre-lexical disorders in repetition conduction aphasia". Neuropsychologia. 46 (14): 3225–38. doi:10.1016/j.neuropsychologia.2008.07.026. PMID 18761023. 
  6. ^ abTippett, Donna C; Hillis, Argye E (2016). "Vascular Aphasia Syndromes". In Hickok, Gregory; Small, Steven L. Neurobiology of Language. pp. 913–22. doi:10.1016/B978-0-12-407794-2.00073-0. ISBN 978-0-12-407794-2. 
  7. ^Damasio, Hanna; Damasio, Antonio R (1980). "The Anatomical Basis of Conduction Aphasia". Brain. 103 (2): 337–50. doi:10.1093/brain/103.2.337. PMID 7397481. 
  8. ^ abcKohn, Susan E. (1992). Conduction aphasia. Hillsdale, N.J: L. Erlbaum. pp. 40–42. ISBN 0-8058-0681-4. 
  9. ^Manasco, Hunter (2017). "The Aphasias". Introduction to Neurogenic Communication Disorders. pp. 93–44. ISBN 978-1-284-10072-3. 
  10. ^ abcdBehroozmand, Roozbeh; Phillip, Lorelei; Johari, Karim; Bonilha, Leonardo; Rorden, Chris; Hickok, Gregory; Fridriksson, Julius (2018). "Sensorimotor impairment of speech auditory feedback processing in aphasia". NeuroImage. 165: 102–11. doi:10.1016/j.neuroimage.2017.10.014. 
  11. ^ abcdBartha, Lisa; Benke, Thomas (2003). "Acute conduction aphasia: An analysis of 20 cases". Brain and Language. 85 (1): 93–108. doi:10.1016/S0093-934X(02)00502-3. PMID 12681350. 
  12. ^Benson, D. Frank; Sheremata, W. A; Bouchard, R; Segarra, J. M; Price, D; Geschwind, N (1973). "Conduction Aphasia". Archives of Neurology. 28 (5): 339–46. doi:10.1001/archneur.1973.00490230075011. PMID 4696016. 
  13. ^ abManasco, M. Hunter (2014). Introduction to Neurogenic Communication Disorders. Jones & Bartlett Learning. [page needed]
  14. ^Ardila, Alfredo (2010). "A Review of Conduction Aphasia". Current Neurology and Neuroscience Reports. 10 (6): 499–503. doi:10.1007/s11910-010-0142-2. PMID 20711691. 
  15. ^Tanabe, H; Sawada, T; Inoue, N; Ogawa, M; Kuriyama, Y; Shiraishi, J (1987). "Conduction aphasia and arcuate fasciculus". Acta Neurologica Scandinavica. 76 (6): 422–7. doi:10.1111/j.1600-0404.1987.tb03597.x. PMID 3434200. 
  16. ^Shuren, Jeffrey E; Schefft, Bruce K; Yeh, Hwa-Shain; Privitera, Michael D; Cahill, William T; Houston, Wes (1995). "Repetition and the arcuate fasciculus". Journal of Neurology. 242 (9): 596–8. doi:10.1007/BF00868813. PMID 8551322. 
  17. ^ abcdefAnderson, J.M; Gilmore, R; Roper, S; Crosson, B; Bauer, R.M; Nadeau, S; Beversdorf, D.Q; Cibula, J; Rogish, M; Kortencamp, S; Hughes, J.D; Gonzalez Rothi, L.J; Heilman, K.M (1999). "Conduction Aphasia and the Arcuate Fasciculus: A Reexamination of the Wernicke–Geschwind Model". Brain and Language. 70 (1): 1–12. doi:10.1006/brln.1999.2135. PMID 10534369. 
  18. ^ ab"Conduction Aphasia". Retrieved 2015-11-13. 
  19. ^Bakheit, A.M.O; Shaw, S; Carrington, S; Griffiths, S (2016). "The rate and extent of improvement with therapy from the different types of aphasia in the first year after stroke". Clinical Rehabilitation. 21 (10): 941–9. doi:10.1177/0269215507078452. PMID 17981853. 
  20. ^Howard, H. (2017, October 7). Cerebral cortex. Retrieved from
  21. ^Howard, H. (2017, October 7). Cerebral cortex. Retrieved from
  22. ^ abKohn, Susan E. (1992). Conduction aphasia. Hillsdale, N.J: L. Erlbaum. pp. 25–26. ISBN 0-8058-0681-4. 
  23. ^Köhler, Kerstin; Bartels, Claudius; Herrmann, Manfred; Dittmann, Jürgen; Wallesch, Claus-W (1998). "Conduction aphasia—11 classic cases". Aphasiology. 12 (10): 865–84. doi:10.1080/02687039808249456. 
  24. ^Kohn, Susan E. (1992). Conduction aphasia. Hillsdale, N.J: L. Erlbaum. pp. 28–29. ISBN 0-8058-0681-4. 
  25. ^Feinberg, T. E; Rothi, L. J. G; Heilman, K. M (1986). "'Inner Speech' in Conduction Aphasia". Archives of Neurology. 43 (6): 591–3. doi:10.1001/archneur.1986.00520060053017. PMID 3718287. 

Further reading[edit]

  • Hickok, Gregory; Buchsbaum, Bradley; Humphries, Colin; Muftuler, Tugan (2003). "Auditory–Motor Interaction Revealed by fMRI: Speech, Music, and Working Memory in Area Spt". Journal of Cognitive Neuroscience. 15 (5): 673–82. doi:10.1162/089892903322307393. PMID 12965041. 
  • Hickok, Gregory; Poeppel, David (2004). "Dorsal and ventral streams: A framework for understanding aspects of the functional anatomy of language". Cognition. 92 (1–2): 67–99. doi:10.1016/j.cognition.2003.10.011. PMID 15037127. 
  • Baldo, J; Klostermann, E; Dronkers, N (2008). "It's either a cook or a baker: Patients with conduction aphasia get the gist but lose the trace". Brain and Language. 105 (2): 134–40. doi:10.1016/j.bandl.2007.12.007. PMID 18243294. 
  • Carlson, Neil R.; Heth, C. Donald (2007). Psychology the science of behaviour (4th ed.). Pearson Education Inc. ISBN 0-205-64524-0. 
  • Sidiropoulos, Kyriakos; Ackermann, Hermann; Wannke, Michael; Hertrich, Ingo (2010). "Temporal processing capabilities in repetition conduction aphasia". Brain and Cognition. 73 (3): 194–202. doi:10.1016/j.bandc.2010.05.003. PMID 20621742. 

External links[edit]


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.

arcuate fasciculus, conduction aphasia, language repetition, tractography, vocal imitation


Conduction aphasia, initially described by Wernicke in 1874, is usually defined as a language disturbance characterized by relatively fluent spontaneous speech, good comprehension, but poor repetition associated with abundant phonological (literal) paraphasias (e.g. Goldstein, 1948; Kertesz, 1979, 1985; Benson, 1988; Kohn, 1992; Benson and Ardila, 1994, 1996; Bartha and Benke, 2003). Patients with conduction aphasia may also have: (i) impairments in naming (from literal paraphasic contamination to total inability to produce the appropriate word); (ii) reading disturbances (comprehension is much better than reading aloud); (iii) writing disturbances (from mild spelling difficulties to profound agraphia); (iv) ideomotor apraxia (buccofacial and limb); and (v) elementary neurological abnormalities (some right hemiparesis and cortical sensory loss) (Benson et al., 1973). Language comprehension (auditory and reading) is only mildly impaired. Paraphasias are mainly due to phoneme substitutions and deletions, and they usually result in switches in phoneme manner and place of articulation (Ardila, 1992). Patients with phonological paraphasias due to posterior cortical lesions are usually unaware of their mistakes; in contrast, patients with conduction aphasia are aware of their paraphasic errors. The attempt to correct these errors results in the so-called conduit d’approche (successive attempts to self-correct their mispronunciations). Luria (1976) assumed that paraphasias in this type of aphasia are articulatory based (that is, errors in the articulatory patterns of the phoneme productions). Based on these differences, some authors have even considered conduction aphasia to be rather a segmental ideomotor apraxia (e.g. Brown, 1972, 1975; Luria 1976, 1980; Ardila and Rosselli, 1990). It is noteworthy that the recovery in conduction aphasia is usually good, and sometimes complete (Kertesz and McCabe, 1977).

The possibility of several mechanisms, each of which is capable of giving rise to deficient repetition has led to the postulation of two different forms of conduction aphasia, described earlier as efferent/afferent (Kertesz, 1979, 1985); reproduction/repetition (e.g. Shallice and Warrington, 1977; Caplan et al., 1986); supra and infrasylvian (Axer et al., 2001); or simply parietal and temporal (e.g. Bartha and Benke, 2003). The efferent-reproduction type involves the phonemic organization and representation of words and is correlated with parietal and insular damage, whereas the afferent-repetition conduction aphasia involves short-term memory defects, and affects the repetition of large strings of material (e.g. Caramazza et al., 1981); this second subtype of conduction aphasia has been described more frequently with lesions of the temporal lobe (Hickok et al., 2000). In this article, we will exclusively refer to the first type of conduction aphasia, i.e. suprasylvian or parietal (Luria's afferent motor aphasia).

Since the time of Wernicke (1874), the aetiology of conduction aphasia has been attributed to a disconnection between the superior temporal gyrus (‘the centre of the acoustic image’) and the inferior frontal gyrus (‘the centre of motor image’). Wernicke's view was backed up by Geschwind in the 1960s, who put it in terms of modern anatomical nomenclature, attributing the arcuate fasciculus (AF) the main role in the speech repetition problem. Nonetheless, most patients diagnosed with conduction aphasia do have some anomia, and reading difficulties, etc. and hence, usually conduction aphasia is not a pure repetition disorder.

In addition to the disconnection hypothesis, conduction aphasia has also been explained by verbal memory defects, and as a form of segmental ideomotor apraxia. It is important to underline that many features of conduction aphasia relate more to a cortical deficit than a pure disconnection mechanism, as pointed out by different authors (e.g. Levine and Calvanio, 1982). Brown (1975) emphasized that conduction aphasia is not seen in pure white matter disorders such as multiple sclerosis, as would be expected if disconnection were the principal problem, thereby suggesting a cortical involvement. Likewise, putaminal haemorrhages rarely cause conduction aphasia, in spite of the fact that they often disrupt the AF (Hier, 1977). Goldstein (1948) used the name ‘central aphasia’ to refer to conduction aphasia, implying a cortical rather than a white matter anomaly. He supposed that conduction aphasia may be explained as a disturbance in inner speech, ‘the central phenomenon of instrumentalities of speech’. However, Feinberg et al. (1986) tested this hypothesis in five conduction aphasia patients and found that the inner speech explanation may have been correct for only a subgroup of conduction aphasics. Boller and Marcie (1978) proposed a possible disturbance in auditory feedback in conduction aphasia. They describe the case of a 63-year-old man with conduction aphasia who, after being exposed to Delayed Auditory Feedback, spoke faster and with fewer errors than controls and patients with other types of aphasia (Boller et al., 1978; Boller and Marcie, 1978). They felt that this paradoxical decreased Delayed Auditory Feedback effect in conduction aphasia only makes sense if the system that supports auditory–motor interaction is disrupted in that syndrome.

The great deal of confusion brought by the term ‘conduction aphasia’ arises from the attempts to harmonize the heterogeneous presentation of lesions, and hence the clinical findings, with a well-defined small structure such as the AF, that is located in an area where critical language functions exist. According to semantics, ‘conduction’ should mean only a white matter problem. However, many authors (e.g. Levine and Calvanio, 1982) have described cortical lesions with repetition problems a key symptom of disconnection. Geschwind (1965) proposed that disconnection syndromes could also arise from lesions of the association cortex. Hence, it could raise the question: is conduction aphasia a topographic diagnosis (implying the AF) or is it a syndromatic diagnosis? If conduction aphasia is instead a syndromatic diagnosis, many cases can be accommodated under the same umbrella even with cortical lesions. In those cases, anomia, agraphia and other language problems could be found, depending on the extension of the cortical lesion. If it were just a subcortical disconnection, we would expect a more limited clinical picture, probably with only phonological defects, correlating with findings of functional AF disruption produced by intra-operative electrical stimulation (Mandonet et al., 2007).

It is noteworthy that language repetition defects are observed not only in conduction aphasia, but also in other aphasia syndromes, particularly in Broca's and Wernicke's aphasia. Involved mechanisms, however, are different. Language repetition deficits in Broca's aphasia are the result of the speech apraxia and agrammatism associated with this syndrome; phonetic deviations and phonological paraphasias (particularly phoneme omissions) are observed during repetition tasks; furthermore, repetition is agrammatical and patients tend to omit grammatical elements in repetition tests (Li and Williams, 1990; Ardila and Rosselli, 1992; Benson and Ardila, 1996; Martin, 2001). In Wernicke's aphasia, severe and frequently persistent repetition deficits can result from two sources: (i) associated phoneme discrimination defects disturbing the ability for recognition of spoken language; and (ii) verbal memory defects impairing the repetition of long strings of information. The significance of these verbal memory defects and repetition difficulties has lead to the proposal that temporal damage is sometimes associated with a conduction type of aphasia (Shallice and Warrington, 1977; Kertesz, 1979, 1985; Caramazza et al., 1981; Caplan et al., 1986; Hickok et al., 2000; Axer et al., 2001; Bartha and Benke, 2003).

Modern neuroimaging techniques have renewed the interest of the neuroscience community in understanding brain connectivity, due to its ability to depict the distinct white matter tracts of the brain. Magnetic Resonance Imaging (MRI) techniques, such as Diffusion Tensor Imaging, and computer-based post-processing that allow complex mathematical data analysis, have made fibre tracking possible. In recent years, an increasing number of publications have appeared in medical journals reviewing the anatomy of the association tracts and their particular features, asymmetries and variations (e.g. Xia et al., 2005; Catani and Thiebaut de Schotten, 2008; Mori et al., 2002). Undoubtedly, one of the tracts that has received most attention is the AF due to its potential implication on speech and language brain organization (Catani and Mesulam, 2008). The AF is a brain association tract composed of arched fibres (hence its name) that supposedly connects the Wernicke's and Broca's areas (Fig. 1). The AF is the main part of a larger tract located lateral to the corticospinal tract, termed the superior longitudinal fasciculus. Four different types of connecting fibres have been recently proposed to be included in the superior longitudinal fasciculus (Makris et al., 2005). All of them have a frontal terminus in the posterior part of the frontal lobe, but they differ in their origin: the superior horizontal bundle originating in the parietal lobe; two more bundles in the angular and supramarginal gyri and the inferior portion consisting of long arched fibres originating in the ipsilateral superior and middle temporal gyri. Most authors publishing information on the AF (e.g. Duffau, 2008; Catani and Thiebaut de Schotten, 2008) refer to two major anterior–posterior connections of the superior longitudinal fasciculus: (i) the horizontal bundle (parieto-opercular); and (ii) its (inferior) arched part, i.e. the AF that constitutes by far the bulk of the track. Even though the AF is just a component of the superior longitudinal fasciculus, their names are often interchanged. For example, in the atlas of single tracts presented by Catani and Thiebaut de Schotten (2008), the authors include an image of the superior longitudinal fasciculus as the AF (Fig. 11 of their work).

Figure 1

The superior longitudinal fasciculus. Diffusion Tensor Imaging-fibre tractography of the superior longitudinal fasciculus of both sides, over an axial T1 MRI-cut at the level of the temporal lobe. Left lateral view. Tracts are directional colour coded for better tracking. Blue colour indicates top–down; green indicates anterior–posterior and red indicates right to left directions. Reversed directions are encoded within the same colours. White arrow = parieto-frontal fibres (dorsal part of the superior longitudinal fasciculus); black arrow = AF. Within the circle, the opercular endpoint is depicted. Notice the asymmetry of the fibres for more prominent left AF. (Images courtesy of Miami Children's Hospital, Department of Radiology).

Figure 1

The superior longitudinal fasciculus. Diffusion Tensor Imaging-fibre tractography of the superior longitudinal fasciculus of both sides, over an axial T1 MRI-cut at the level of the temporal lobe. Left lateral view. Tracts are directional colour coded for better tracking. Blue colour indicates top–down; green indicates anterior–posterior and red indicates right to left directions. Reversed directions are encoded within the same colours. White arrow = parieto-frontal fibres (dorsal part of the superior longitudinal fasciculus); black arrow = AF. Within the circle, the opercular endpoint is depicted. Notice the asymmetry of the fibres for more prominent left AF. (Images courtesy of Miami Children's Hospital, Department of Radiology).

Role of the AF in conduction aphasia

As previously mentioned, conduction aphasia has been classically explained as a disconnection syndrome between Wernicke's and Broca's areas (e.g. Wernicke, 1874; Geschwind, 1965; Damasio and Damasio, 1980) due to a lesion affecting the AF. It is noteworthy that one major problem of the cases reported with AF lesions is that they are usually due to infarcts and tumours, and therefore they are not limited within the AF boundaries. Infarcts and tumours usually affect directly and indirectly other adjacent bundles, and also the cortex, including the temporal, parietal and insular cortices. Indeed, it is extremely unlikely to find a case of conduction aphasia with a lesion limited just to the AF. So far, the majority of cases describing clinical findings associated with AF lesions are in reality findings in cases in which the AF was damaged the most amongst other white and grey matter structures. Actually, Wernicke (1874) described the very first case of conduction aphasia in a patient with an insular lesion. Certainly, the AF is often reported to be involved in conduction aphasia (e.g. Tanabe et al., 1987; Geldmacher et al., 2007; Yamada et al., 2007), but cortical lesions alone without subcortical extension may also produce conduction aphasia (Anderson et al., 1999; Quigg et al., 2006); furthermore, patients with lesions of the AF may retain the ability to repeat (Shuren et al., 1995; Kreisler et al., 2000). Consequently, the AF does not seem to be crucial for repetition.

Taking these particularities into account, it is difficult to be completely certain of the AF's specific role in conduction aphasia. The question that a disconnected Broca's area can explain repetition problems in the absence of any other major language abnormalities remains unsettled. But the fact that conduction aphasia has been mostly characterized by language repetition problems makes it worthy to ascertain the neurophysiology of vocal repetition in both animals and humans.

What supports vocal repetition?

To account for vocal repetition, at least two neural subsystems should be assumed: one for vocalization, i.e. for the programming, production and control of vocal sounds; and the other for transferring phonological cues decoded in the auditory areas towards areas of motor programming, representation and execution. The former relates to the brainstem (vocal nuclei) network; the latter to the AF or another similar connecting pathway (Ghazanfar and Rendall, 2008). This mechanical interplay between phonological schemes and motor sequences; however, is not necessarily linked to meaning extraction or semantic awareness. One can repeat a foreign language word or even entire sentences without knowing their meaning. Furthermore, repetition of phonemes and words is not exclusively a human ability either. For example, some birds can repeat human speech (e.g. parrots, macaws, cockatoos), but presumably they do not make sense of it. This observation implies that repetition should not be necessarily regarded as language ability but rather as speech ability. Consequently, conduction ‘aphasia’ may, strictly speaking, be interpreted as a speech disturbance rather than as a language disturbance; and therefore not as an aphasia, or at least not as a ‘primary aphasia’ (Ardila, 2009).

It can be conjectured that any vocal repetition system (human or animal) also needs a subsystem to carry information from auditory receptive areas to executive areas. Here is the point where the AF or any similar bundle may play a crucial role.

Unfortunately, the AF has not been investigated in talking birds. Monkeys, and in general mammals, without a vocal repetition ability, do not have an AF (Schmahmann et al., 2007

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