Conduction Aphasia and the Arcuate Fasciculus: A Reexamination of the Wernicke–Geschwind Model

Brain and Language 70, 1–12 (1999) Article ID brln.1999.2135, available online at http://www.idealibrary.com on

Conduction Aphasia and the Arcuate Fasciculus: A Reexamination of the Wernicke–Geschwind Model J. M. Anderson,*,† R. Gilmore,* S. Roper,‡ B. Crosson,*,§ R. M. Bauer,§ S. Nadeau,* D. Q. Beversdorf,* J. Cibula,储 M. Rogish III,§ S. Kortencamp,§ J. D. Hughes,* L. J. Gonzalez Rothi,*,†,§ and K. M. Heilman*,§ *Department of Neurology, †Department of Communication Sciences and Disorders, ‡Department of Neurosurgery, and §Department of Clinical and Health Psychology, University of Florida, Gainesville; and 储 Department of Neurology, University of Kentucky 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.  1999 Academic Press

Key Words: conduction aphasia; cortical stimulation; arcuate fasciculus.

After Paul Broca (1865) described patients with nonfluent aphasia from anterior perisylvian lesions, Karl Wernicke (1874) reported patients who were fluent but made frequent paraphasic speech errors and were impaired at naming, auditory comprehension, and repetition. Wernicke’s patients had lesions in the posterior portion of the superior temporal lobe of the left hemisphere. Wernicke posited that whereas the anterior perisylvian area, described by Broca, is important for the production of speech sounds or phonemes, the region of the cortex in the posterior portion of the superior temporal lobe This work was supported in part by the Research Service of the Gainesville, Florida, V.A. Medical Center. Address correspondence and reprint requests to Jeffrey M. Anderson, Research Department No. 151, V.A. Medical Center, 1601 S.W. Archer Road, Gainesville, FL 32608-1197. E-mail: [email protected] 1 0093-934X/99 $30.00 Copyright  1999 by Academic Press All rights of reproduction in any form reserved.

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FIG. 1. Wernicke’s (1874) classic diagram of the main pathways involved in language comprehension, production, and repetition. In this diagram a1 represents the center for acoustic imagery (Wernicke’s area) and b, the center for motor images concerned with speed production (Broca’s area) and b, the center for motor images concerned with speech production (Broca’s area). Wernicke hypothesized that lesions in the a1 –b pathway would cause conduction aphasia. T, temporal lobe; O, occipital lobe; F, frontal lobe; S, Sylvian fissure; a, acoustic nerve; b1, efferent pathways involved in speech production.

contained the memories of how words sound. Wernicke labeled this posterior temporal region ‘‘the area of word images.’’ Both Wernicke and later Lichtheim (1884) posited that a disconnection of this ‘‘area of word images’’ from the anterior regions important in motor programming of speech sounds would produce a fluent speech disorder with good comprehension, yet with impaired spontaneous speech, naming, and repetition (Fig. 1). Because the disorder was thought to be caused by a failure of information carried from the ‘‘area of word images’’ to the anterior speech production areas Wernicke (1874) termed it Leitungsaphasia, or conduction aphasia. Lichtheim (1885) preferred to term it commissural aphasia to make a distinction between aphasia due to damage to centers (Broca’s and Wernicke’s) versus interruptions of commissural pathways between centers (conduction aphasia and transcortical aphasias). Wernicke was influenced by the famous neuroanatomist Theodor Meynert, who had been his mentor. Meynert had suggested that aphasia could be attributed to perisylvian lesions (Meynert, 1884; Sachs, 1934; Henderson, 1992b). This was based on Meynert’s (1884) exploration of temporal lobe pathways and his conclusion that whereas regions of cortex anterior to the Rolandic sulcus are primarily motoric, posterior regions are primarily sensory in function. Meynert (1884) introduced Wernicke to the idea of cortical centers, which Wernicke went on to substantiate in greater detail. Wernicke’s own explorations of fiber pathways in the temporal lobe of postmortem brains revealed connections between the anterior and the posterior perislyian re-

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gions that he believed had functional significance (Henderson, 1992a). As noted by Bastian (1887) it was Meynert’s initial suggestion that a disruption to the fibers deep to the insula would lead to aphasia. Wernicke (1874) suggested that disruption of the fibers deep to the insula induced conduction aphasia, although subsequently, in 1910, he renounced this view. Although the Lichtheim–Wernicke model provided an explanation of the aphasic syndromes and was therefore a major milestone, many researchers questioned the distinctness of speech–language centers and the concept that aphasic disorders could be explained by either destruction or disconnection of these centers. For example, Freud (1891) argued that the Lichtheim– Wernicke framework, which differentiated between centers and commissural pathways, was a false dichotomy. Rather, he argued that the entire perisylvian region including the posterior and anterior regions was equivalent in the mediation of speech. The posterior and anterior syndromes were therefore disruptions of sensory input or motor output from this integrated perisylvian region. In contrast to the localizationist models of Wernicke and Lichtheim, the German neurologist Goldstein along with Marmor reported a case of conduction aphasia in 1938 and argued that this syndrome was not due solely to a failure of a transmission of information between posterior and anterior language centers but rather that a central deficit at the core of the language system had occurred (Goldstein, 1948). Goldstein relabeled this disorder central aphasia and argued that a disintegration of inner speech had occurred: ‘‘. . . the inner structure is loosened or even broken up. The parts of which the word consists do not occur immediately in the right sequence. The first part of the word may be produced correctly but then disorder takes place’’ (p. 99). Goldstein (1948) also noted that this ‘‘paraphasic destruction of the words,’’ or in modern terms this phonologic disintegration characteristic of conduction aphasia, is often followed by multiple attempts at self repair or conduite d’approche. The posterior portion of the superior temporal lobe is connected to the anterior perisylvian area (Petrides & Pandya, 1988) by a white matter bundle called the arcuate fasciculus. As part of his comprehensive disconnection model of language dysfunction, Geschwind (1965) posited that a lesion of this pathway was responsible for conduction aphasia (Fig. 2). He hypothesized that deficits in repetition occurred because the main transmission route between these two well developed, functionally autonomous, posterior and anterior language modules had been disrupted (Benson, et al. 1973; Geschwind, 1974). Support for this disconnection model versus the central deficit models of Freud and Goldstein comes from the Feinberg, Rothi, and Heilman (1986) study where, using a homophone test, these investigators demonstrated that inner speech was intact. Although the Wernicke–Lichtheim–Geschwind disconnection hypothesis

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FIG. 2. Geschwind’s (1970) diagram in which he depicts the pathway involved in conduction aphasia, ‘‘Despite the good comprehension of spoken language there is a gross defect in repetition. The lesion for this disorder typically lies in the lower parietal lobe, and is so placed as to disconnect Wernicke’s area from Broca’s area. . . . The disorder in repetition exhibits some remarkable linguistic features which are not yet explained. B, Broca’s area; W (open circles), Wernicke’s area; A (closed circles), arcuate fasciculus, which connects Wernicke’s to Broca’s area.’’ Reprinted (abstracted/excerpted) with permission from Science (Nov. 27th, Vol. 170, pp. 941, 942). Copyright 1970 American Association for the Advancement of Science.

could account for many of the signs associated with conduction aphasia, there has never been an autopsy documented case of conduction aphasia occurring secondary to a focal arcuate fasciculus lesion (Tanabe et al. 1987). Whereas many patients with conduction aphasia have dominant inferior parietal lesions that extend deep to the arcuate fasciculus, most of these patient’s lesions also involve the overlying cortex. For example, Green and Howes (1978) reviewed 25 cases of conduction aphasia that had anatomical confirmation and all of these cases had involvement of the posterior perisylvian cortex, involving either the posterior portion of the superior temporal gyrus, the supramarginal gyrus or angular gyrus, or portions of the insula. Also, a number of patients have been reported that have demonstrated a deficit in repetition, yet had lesions that had spared the arcuate fasciculus (Damasio & Damasio, 1980; Brown & Wilson, 1973; Green & Howes, 1978; Hecaen, Mazars, Ramier, Goldblum, & Merienne, 1971; Henderson, Oken, & Aleander, 1981; Hoeft, 1957; Kleist, 1962; Liepmann & Pappenheim, 1914; Mendez, & Benson, 1985; Yarnell, 1981). More recently, Shuren et al. (1995) described a patient with left-hemispheric language dominance documented by cortical stimulation, who did not demonstrate a deficit in repetition even after a tumor resection which included his left anterior arcuate fasciculus

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and the inferior two-thirds of his superior longitudinal fasciculus. However, it remains possible that repetition in this patient was mediated by the right hemisphere. A third explanation of conduction aphasia, which is similar to Wernicke’s explanation but is based on recent cognitive neuropsychological models, suggests that spoken language is mediated by cortically based, anatomically distributed, modular networks. A modern equivalent of Wernicke’s ‘‘area of word images’’ is the phonologic lexicon, which is a store of learned phonological representations for familiar words that is thought to have both input and output components. The phonological input lexicon is posited to be involved in recognizing the sound pattern of words, and the phonological output lexicon is important for planning the production of spoken words. Based on this model conduction aphasia may be explained as a deficit of the phonological output lexicon (Caramazza, Basili, Koller, Berndt 1981; McCarthy & Warrington, 1984; Kohn & Smith, 1991; Kohn, 1984, 1992). Dysfunction of this output lexicon accounts not only for deficits in repetition, but also for the phonemic paraphasic errors that are so prevalent in this disorder. Lesion studies (Caplan, 1987), functional imaging (Demonet et al., 1992), and electrical stimulation studies (Ojemann, 1983) have provided converging support for Wernicke’s localization of the phonological lexicon. Whereas lesions of posterior perisylvian cortex may also damage subcortical white matter, including the arcuate fasciculus, bipolar electrical stimulation on the cortical surface below the 15-mA range produces a limited spread of activation, and induces cortical dysfunction, but does not produce structural damage to the cortex (Gordon et al. 1990; Nathan, Sinha, Gordon, Lesser, & Thakor, 1993; Ojemann, 1991; Ojemann & Mateer, 1979; Boatman, Lesser, & Gordon, 1995). Gordon et al.’s (1990) histopathologic study of cortical tissue stimulated at below 15 mA for no greater than 5 s duration and subsequently removed in a temporal lobe resection revealed no structural damage in the areas that had received the stimulation. Nathan et al.’s (1993) model of the current density distributions generated by electrical stimulation revealed that bipolar cortical stimulation produced only localized current flows unlikely to have any impact on white matter functioning. Recently, we had an opportunity to test a patient who was being evaluated for seizure surgery by stimulation of the posterior portion of the left perisylvian region. This patient provided the opportunity to learn if cortical dysfunction alone could induce conduction aphasia. METHODS Case report. The patient (JC), was a 48-year-old right handed woman who was referred to our Epilepsy service for the potential surgical treatment of intractable seizure disorder. She had a 13-year history of her complex partial seizures characterized by an alteration of consciousness and a decreased ability to spontaneously produce speech during seizure activity. She demonstrated a baseline anomia during nonstimulated testing and in spontaneous speech

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FIG. 3. Location of grid placements over the lateral surface of the subject’s left hemisphere. Only electrode 5 and 10 from the 4 ⫻ 5 temporal–parietal grid were stimulated during experimental trials. as demonstrated by a score of ⫹42/60 on the Boston Naming Test (Kaplan, Goodglass, & Weintraub, 1983). The patient underwent functional cortical mapping procedures as part of the standard clinical diagnostic protocol for her medically intractable epilepsy. The standard protocol included prolonged video/scalp/sphenoidal EEG monitoring, MRI with volumetric assessment, neuropsychological testing, and cerebral angiography as part of a Wada test. Left hemispheric dominance for language function was confirmed during the Wada test. Electrode array placement. Verification of electrode locations were determined by a combination of intraoperative photographs, plain skull films, and MRI scans. Information from previous scalp/sphenoidal EEG surface recordings was used to determine the sites to be covered by the subdural electrodes. The grids were surgically placed in the subdural space over the left hemisphere according to a protocol established at an institutional epilepsy management conference using principles articulated by Lesser et al., (1987) and Luders et al., (1989). The 2.3-mm platinum–iridium electrodes (Ad-tech, Racine, WI) were 10 mm apart (center to center) and were embedded in medical grade silastic. Three grids (4 x 5, 4 x 8, and 3 ⫻ 3 electrodes) and five (1 ⫻ 4 electrode) strips were placed (Fig. 3). The 4 x 8 grid was placed over the left lateral frontal lobe, the 4 x 5 grid was placed over the left temporal/inferior parietal region, and the 3 x 3 grid was placed in the left orbital frontal region. Two electrode strips were placed over the lateral parietal cortex and three strips were also placed, equidistantly, along the inferior portion of the temporal lobe. Electrical stimulation testing procedures. After sufficient seizures for focus localization were obtained, cortical mapping procedures were initiated. At that time the patient had fully recovered, had minimal edema, and did not experience discomfort from either the surgery or

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the indwelling electrode arrays. One pair of electrodes, located over the subject’s left hemisphere’s posterior superior temporal gyrus, was stimulated during the experimental trials of this report. This pair was chosen for experimental manipulation because of strong disruption of repetition abilities elicited during clinical testing. Other electrode pairs nearby produced repetition deficits, but these were not as robust as at this site. This pair comprised electrodes 5 and 10 from the 4 x 5 temporal/parietal grid (Fig. 3). We used a Grass S-12 cortical stimulator (Grass Instrument Co., Quincy, MA) to produce 5-s trains of 300-µs square wave pulses of alternating polarity generated at a rate of 50 Hz. Stimulation was initiated at 1.5 mA and increased in 1-mA increments to a maximum of 15.5 mA (Lesser, Gordon, & Uematsu, 1994). Before each stimulation session, the threshold current for after-discharges was established. If after-discharges were seen, testing was performed at the next lowest current level at which after-discharges were not seen. If no after-discharges were present, the current was set to a maximal level of 15.5 mA. Testing procedures. The patient was tested in quiet but not soundproof conditions. During stimulated trials, target visual or auditory stimuli were presented approximately 1 s after current onset. The current was maintained for approximately 5 s during each trial. The 5 s stimulation response period was considered adequate in light of the patient’s baseline response times when there was no electrical stimulation. All auditory and visual stimuli were presented and then removed prior to cessation of the cortical stimulation. During nonstimulated trials, the timing of stimuli, the personnel and equipment present in the room matched the conditions during the stimulated trials. During both stimulated and nonstimulated trials the patient was unable to view the hand of the clinician upon the soundless remote switch of the stimulator. Tests of repetition, verbal picture naming, naming to definition, and auditory comprehension were given to the patient in an equal number of stimulated and nonstimulated (control) trials, randomly presented over 3 days of testing. The auditory comprehension (word/picture matching), verbal picture naming, naming to definition, and repetition of word tasks utilized the same matching set of words, pictures, and definitions. The nonwords used in the repetition task were phonologically similar to the words used in the repetition of words task. The number of trials given each day was variable because of the subject’s fatigue. The patient’s responses were recorded by video tape for later analysis.

RESULTS

During stimulated trials the patient’s responses often continued after the 5s electrical stimulation response period had ceased. This prolonged response reflected the patients’ frequent and multiple phonemic approximations to target items. However, during none of the trials was the subject able to hear or see the stimuli after the 5-s electrical stimulation response period had passed. The patient’s responses on stimulated and nonstimulated trials for all tasks are listed in Table 1. During the electrical stimulation trials she demonstrated frequent and multiple phonemic paraphasic errors during verbal picture naming and the repetition of words and nonwords. She performed more accurately on nonstimulated compared to stimulated trials for all tasks requiring verbal production. However, in contrast to her expressive deficits during stimulated trials, she did not have a comparable problem with auditory comprehension. During stimulation, auditory comprehension of the target items was 95% accurate, demonstrating intact lexical–semantic knowledge of the verbal stimuli (Table 1).

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Table 1 JC’s Performance during Repetition, Verbal Picture Naming, Naming to Definition, and Auditory Comprehension Tasks Stimulated

Non-Stimulated

Task

Errors

% Correct

Errors

% Correct

Repetition Words Nonwords Verbal picture naming Naming to definition Auditory comprehension

7/20 11/20 20/20 13/20 1/20

65 45 0 35 95

0/20 2/20 4/20 2/20 0/20

100 90 80 90 100

Although not prompted to do so, during a number of verbal picture naming trials when she demonstrated word finding difficulties, she spontaneously produced the correct gesture of tool-like target items. During picture naming the patient also demonstrated a strategy in which she attempted to spell the target words in 65% of the trials. During the repetition of words task, she utilized this same strategy during 46% of the trials. She did not demonstrate this strategy during any of the nonstimulated trials, nor did she demonstrate this strategy to staff while spontaneously speaking during her 10 days as an inpatient. During the first three stimulated trials of the picture naming task, when the patient first utilized this oral spelling strategy, she was instructed by the tester to attempt to inhibit this behavior. She continued to utilize this strategy and the testers did not give her further instructions concerning this behavior. DISCUSSION

During electrical stimulation of the left posterior superior temporal cortex, our subject demonstrated impaired repetition and naming with frequent phonemic errors and intact comprehension. Because this language deficit did not occur when she was not stimulated, it can be assumed that the cortical stimulation induced this deficit. The language behavior noted during the electrical stimulation is consistent with the syndrome termed conduction aphasia (Geschwind, 1974). Using cognitive neuropsychological models, many investigators propose that the functional deficit of conduction aphasia is primarily at the level of the phonological output lexicon (Caramazza et al., 1981; McCarthy & Warrington, 1984; Feinberg et al., 1986; Kohn & Smith, 1991; Kohn, 1984). Subjects with conduction aphasia comprehend and are able to access lexical-semantic information about words, but demonstrate a deficit in retrieving the stored phonological representations of these same items. They frequently produce multiple, phonologically similar paraphasic errors in their attempt to self-correct, suggesting that the lexical–semantic knowledge of words is spared, but the phonologic output lexicon is impaired.

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The induction of a conduction aphasia with stimulation of the posterior superior temporal gyrus is consistent with prior studies which have documented that conduction aphasia may occur from lesions in this region (Benson et al., 1973; Damasio & Damasio, 1980; Palumbo, Alexander, & Naeser, 1992; Naeser & Hayward, 1978). During the trials in which electrical stimulation took place, JC had difficulty naming pictures and repeating words. Often JC would unsuccessfully try to spell those words. She did not utilize this oral spelling strategy during any of the nonstimulated trials, nor did she demonstrate it during spontaneous conversations that occurred during the 3 days of testing. Her oral spelling during stimulated trials may have been an attempt to use an alternative strategy that would have provided a self-cue during periods of phonologic output lexicon dysfunction (Patterson & Kay, 1982; Rapscak, Rubens, & Laguna, 1990). However, it remains possible that the electrical stimulation facilitated the orthographic output lexicon, which contains the knowledge of how words are spelled. Patients with conduction aphasia will often attempt to self-correct their phonemic paraphasic errors and frequently produce other paraphasic errors as they attempt to approximate the target word. Kohn and Smith (1991) noted that the utilization of an oral spelling strategy is frequently encountered in conduction aphasia. In a case study of a patient with conduction aphasia that spontaneously used this oral spelling strategy, Kohn and Smith (1991) assessed the accuracy of the oral spelling and its impact on speech accuracy. They found that the self-cueing provided by this strategy did not affect the accuracy of the speech production. They hypothesized that this strategy did not help because the oral spelling itself was also impaired. JC’s multiple attempts at oral spelling frequently were also in error and she usually was only able to correctly spell the first or second letter of the target word. That cortical stimulation induced conduction aphasia provides evidence that conduction aphasia can be induced by cortical (versus subcortical white matter) dysfunction. Although this finding appears to support the output lexicon hypothesis of conduction aphasia, this finding does not entirely preclude the disconnection hypothesis. Pyramidal cells that give rise to the association fibers that form the arcuate fasciculus are also found in the region of cortex that was stimulated. Therefore, electrical stimulation on the cortical surface may have caused dysfunction of these cells, thereby producing arcuate fasciculus dysfunction. Yet, it is actually the nonpyramidal cells that have rich local associations. The cortical network formed by these nonpyramidal cells, with their dense local interconnections located throughout the perisylvian language region, may actually compose the net that supports the type of parallel, distributed, reciprocal processing suggested by Dell (1986). If this lexical dysfunction hypothesis of conduction aphasia is correct, when JC’s posterior superior temporal cortex received electrical stimulation, it may have disrupted the phonologic output network operating in that region

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of cortex, rather than inducing arcuate fasciculus dysfunction. Such a disruption has the potential of degrading the phonologic processing that normally occurs in this region, inducing phonomic paraphasic errors in repetition. Unfortunately at this time it is not known whether cortical stimulation differentially induces dysfunction of pyramidal cells, nonpyramidal cells, or both. REFERENCES Bastian, H. C. 1887. On different kinds of aphasia, with special reference to their classification and ultimate pathology. British Medical Journal, 2, 931–936. Benson, D. F., Sheremata W., Bouchard, R., Segarra, J. M., Price, N., & Geschwind, N. (1973). Conduction aphasia: A clinicopathological study. Archives of Neurology, 28, 339–346. Boatman, D., Lesser, R. P., & Gordon, B. 1995. Auditory speech processing in the left temporal lobe: An electrical interference study. Brain and Language, 51, 269–290. Broca, P. 1865. Sur le siege de la faculte du language articule´. Bull. Soc. Anthropol., 6, 337– 393. Brown, J. W., & Wilson, F. R. 1973. Crossed aphasia in a dextral. Neurology, 23, 907–911. Caplan, D. (1987). Neurolinguistics and linguistic aphasiology. Cambridge: University Press. Pp. 384–389. Caramazza, A., Basili, A. G., Koller, J. J., & Berndt, R. S. 1981. An investigation of repetition and language processing in a case of conduction aphasia. Brain and Language, 14, 235– 271. Damasio, H., & Damasio, A.R. 1980. The anatomical basis of conduction aphasia. Brain, 103, 337–350. Dell, G.S. 1986. A spreading activation theory of retrieval in sentence production. Psychological Review, 93, 283–321. Demonet, J.-F., Chollet, F., Ramsay, S., Cardebat, D., Nespoulous, J.-L., Wise, R., Rascol, A., & Frackowiak, R. 1992. The anatomy of phonological and semantic processing in normal subjects. Brain and Language, 115, 1753–1768. Feinberg, T. E., Rothi, L. J. G. R., & Heilman, K. M. 1986. ‘Inner speech’ in conduction aphasia. Archives of Neurology, 43, 591–593. Freud, S. 1891. Zur Auffasung der Aphasien: Eine kritische Studie. Leipzig and Vienna: Franz Deuticke. In E. Stengel (Trans.), On aphasia: A critical study. New York: International Universities Press, 1953. Geschwind, N. 1965. Disconnection syndromes in animals and man. Brain, 88, 237–294, 585– 644. Geschwind, N. 1970. The organization of language and the brain. Science, 170, 940–944. Geschwind, N. 1974. Conduction aphasia. In N. Geschwind (Ed.), Selected papers on Language and the brain. Boston: D. Reide. Goldstein, K. 1948. Language and language disturbances. New York: Grune & Stratton. Goldstein, K. & Marmor, J. 1938. A case of aphasia with special reference to the problems of repetition and work-finding. Journal of Neurology, Neurosurgery and Psychiatry, 1, 329–339. Gordon, B., Lesser, R. P., Rance, N. E., Hart, J. Jr., Webber, R., Uematsu, S., & Fisher, R. S. 1990. Parameters for direct electrical stimulation in the human: histopathologic confirmation. Electroencephalography and Clinical Neurophysiology, 75, 371–377. Green, E., & Howes, D. H. 1978. The nature of conduction aphasia: A study of anatomic and

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