Acta Neurol Scand., 1987:76:422-427 Key words: conduction aphasia;arcuate fasciculus; supramarginal gyrus; cerebral infarction. Conduction aphasia and arcuate fasciculus H. Tanabe’, T. Sawada‘, N. Inoue2, M. Ogawa2,Y. Kuriyama2,J. Shiraishi’ ’Department of Health Sciences, Osaka University and ‘Cerebrovascular Division, National Cardiovascular Center, Osaka, Japan. ABSTRACT - Three patients are presented who developed conduction aphasia after a small infarction almost exclusively confined to the arcuate fasciculus. All of them were diagnosed as conduction aphasia within a week after the stroke and showed a rapid amelioration. On the basis of the 3 patients and conduction aphasics in the literature, the relation between conduction aphasia and the arcuate fasciculus is discussed. Accepted for publication Juni 23, 1987. Even though the arcuate fasciculus, a deep white fiber bundle connecting Wernicke’s area (sensory speech area) and Broca’s area (motor speech area), has been regarded as a significant anatomical basis for conduction aphasia from the veiwpoint of disconnexion hypothesis (1-5), there has been not one reported case of fonduction aphasia with a lesion exclusively resticted to this association fiber tract (4-14). We experienced 3 patients who showed conduction aphasia after a small infarction limited to the arcuate fasciculus in the parietal operculum. The investigation of these patients make it possible to reconsider more strictly the relation between conduction aphasia and the arcuate fasciculus. Case reports Case 1. A 76-year-old man, high school graduate and retired trader, is right-handed, but one of his 6 children and one of his 12 grandchildren are lefthanded. Since age 62, he has had anginal pain 5 times. One year ago, weakness of the right hand developed suddenly but cleared up within 2 days. On the morning of Nov. 11, 1983, his wife felt his speech was somewhat strange, but noticed no change in his behavior. The patient himself became aware of the speech difficulty of sutra chanting (his morning habit). That evening, he also noticed diffi- culty in writing when making an entry in his diary. He experienced no muscular weakness or numbness. The following day, he was admitted because of the sudden onset of language disturbance. He was alert, co-operative, well-oriented and demonstrated normal memory function. Neurological examination revealed no evidence of motor or sensory disturbance, apraxia, agnosia, acalculia or difficulty with right-left orientation. Spontaneous and conversational speech was fluent and entirely meaningful but with hesitations and occasional literal paraphasias generally recognized as errors by the patient. Literal paraphasias became evident in volitional speech such as repetition, reading aloud and naming, especially in repetition of polysyllabic words and sentenses. He was aware of his own mistakes and atternped frequently to correct them. Word finding difficulty and verbal paraphasia were hardly observed. Aural comprehension was normal even for syntactically organized complex materials, as was reading comprehension. Writing disturbance was as mild as spontaneous speech disturbance, but some paragraphias and hesitation were found mainly in writing Kana (Japanese language has two different types of transcriptional characters, that is, Kanji(ideogram) and Kana(phonogram)). The aphasic symptoms disappeared rapidly. On Dec. 6, while the patient was CONDUCTION APHASIA AND ARCUATE FASCICULUS still conscious of a little speech difficulty, paraphasia was hardly noticed even in repetition of complex words and sentences. No paragraphia was observed in writing long sentences. The computed tomographic (CT)scan disclosed an underlying small infarct of the left supramarginal gyrus. Case 2. A 74-year-old man, junior high school graduate and director of a company, is righthanded, but batting has always been with his left hand. He has one left-handed granddaughter. In his twenties, atrial fibrillation was pointed out and since 3 years ago he had been treated for hypertension and atrial fibrillation. When listening to a lecture on the afternoon of Nov. 15,1983, the patient noticed some difficulty in comprehending it and dropped a pen held in his right hand. Afterwards, he also noticed speech and word finding difficulties. The persistence of the speech problems led him to hospitalization on Nov. 21. He was fully oriented and had no memory disturbance. Neurological examination disclosed slight diminution of pain sensitivity on the right side and a slight right-sided pronator drift of the supinated outstreched upper extremities. Motor strength was within normal bilaterally. Except for mild calculation disturbance, he had no difficulty with visuospatial construction, finger recognition and right-left orientation. Mild buccofacial and ideomotor apraxia were recognized. He had fluent and meaningful spontaneous speech with occasional literal paraphasias and word finding difficulty. By contrast, repetition and naming elicited many literal paraphasias with repeated attempts to correct them. In the latter, word finding difficulty and verbal paraphasia were occasionaly noted. Reading aloud was also impaired with literal paraphasias. Comprehension was normal for verbal and written complex commands. When compared with volitional speech difficulty, writing was disproportionately preserved but with slowness in writing Kana. The recovery of the aphasic symptoms was excellent. On discharge of Dec. 13, the patient had little difficulty in conversational speech as well as in writing, even if literal paraphasias were occasionaly noted in repetition. BarrCs sign and apraxic symptoms had then akeaay disappeared. 423 The CT scan demonstrated a small low density area in the left anterior parietal region. Case 3. A 79-year-old right-handed woman without full elementary education, and having no known left-handed relatives. Twenty years ago, cardiac enlargement was detected. Four or 5 years ago, atrial fibrillation and hypertension were pointed out. On the evening of Dec. 18,1984, speech difficulty and weakness of the right upper and lower extremities developed. During the following two days, she became unable to walk and her speech output decreased. When the patient was admitted on Dec. 21, her motor and speech functions were considerably improved. She was alert, co-operative and oriented as to place and person, but not to time. Neurological examination showed hemiparesis of the right upper and lower limbs, hypalgesia on the right and mild incoordination of the left upper and lower limbs. She had buccofacial apraxia but had no ideomotor apraxia. There was no evidence of right-left confusion or finger agnosia. Constructional ability and calculation appeared to be impaired, but her level of education prohibited us from concluding the presence of constructional apraxia and acalculia. Even though her speech output was limited, it was fluent and meaningful but with hesitation, circumlocution and some literal paraphasias. Repetition was impaired with frequent blockings and literal paraphasias. She was aware of her deficits, and her efforts to pronounce correctly or to correct them resulted in slow and careful pronunciation. Naming was equally as impaired as repetition. Verbal paraphasias and word finding difficulty were not prominent. Reading aloud was also marred by literal paralexias. She could execute the Pierre Marie’s 3-paper test without any difficulty, but comprehension was slightly impaired for verbal and written syntactically complex materials. Writing disturbance was difficult to evaluate because of her history of education and disinclination to write, but a few apparent literal paragraphias were found. The speech difficulty and right hemiparesis improved rapidly. When the patient was discharged on Feb. 16, 1985, she had a little difficulty in conversational speech, but repetition of complex words or 424 TANABE ET AL sentences still produced some literal paraphasias. Mild right hemiparesis remained. The patient could describe the history of her present illness correctly and recall of recent and remote events was excellent. The CT scan showed a small infarction in the anterior parietal region. Other than this lesion, a low density area in the superior portion of the left cerebellar hemisphere and atrophy of the frontal lobes were noted. Summary of aphasic features In the incipient stage of the illness, these 3 patients showed very similar features of aphasia. They had fluent and meaningful spontaneous speech with occasional or some literal paraphasias. The volitional speech such as reading aloud, naming and repetition was disproportionately poorly performed when compared with spontaneous or conversational speech. Especially repetition was contaminated by many literal paraphasias with attempts to correct them (conduite d’approche). The writing was also impaired with literal paragraphias. Thus, all the patients had the primary characteristics of conduction aphasia (15-18): fluent paraphasic output (primarily literal paraphasia), relatively normal comprehension of spoken language and severe disability in repetition. The other clinical features varied with the individual case, except that all cases had neither finger agnosia nor right left disorientation (Table 1). Lesion localization The CT scans were all performed with a Toshiba TCT20A. The brains were cut in 1 cm-thick sec- tions, with the plane of each section parallel to the orbito-meatal line (Fig. 1). In all the patients, lesions were found on only those 2 consective slices where the superior portion of the body of the lateral ventricle was observed and hardly observed respectively. Hence, the insula and Wernicke’s area were not damaged. The lesion on the lower C T slice was superimposed on the corresponding template of Nieuwenhuys et al. (19) (Fig. 2). The circles represent the lesions of Cases 1,2 and 3 in the order from the back to the front. This anatomical study disclosed that, in all cases, the lesions invade the arcuate fasciculus in the parietal operculum between the posterior ramus of the lateral sulcus and the central sulcus. In Cases 1 and 2, the deep subcortical lesions extended superiorly to the upper parietal lobe areas and appeared to reach the cortex partially, while the lesion on the upper slice remained subcortical in Case 3. In sum, all the patients had lesions confined to the arcuate fasciculus. Discussion It has been indicated that conduction aphasia appears mostly in the process of recovery from Wernicke’s aphasia and seldom appears at the onset in isolated fashion (4,15,20). Recently, Kertesz observed 9 acute conduction aphasics among 91 acute aphasics who were tested in the first 6 weeks after stroke (21). The aphasic type of our 3 patients was diagnosed as conduction aphasia within one week after stroke. This reconfirms that conduction aphasia can develop in the pure form at the onset of stroke. Table 1 Clinical features of the 3 conduction aphasics in the incipient stage. Case Motor deficit Sensory deficit Oral apraxia Ideomotor apraxia Constructiona1 Right-left apraxia disorientation 1 (-) R brachial weakness Rhemiparesis (-) R hypalgesia Rhypalgesia (-) (+) (-) (+) (-) (-) (-) (-) (-) (-) (+) (+) (-) (*) (--) (-) (*) 2 3 (+) - present, (-) - absent, (*) - suspected, R - right. Finger agnosia Acalculia CONDUCTION APHASIA AND ARCUATE FASCICULUS 425 P) s c 0 426 TANABE ET AL Even if conduction aphasics often show a favorable spontaneous recovery (21,22), it is noteworthy that the aphasic symptoms of Cases 1 and 2 practically cleared up within one month after onset. It may be due to such a rapid amelioration that there has been no reported case of conduction aphasia with a lesion exclusively restricted to the arcuate fasciculus. Regarding the difference of recovery rates between Cases 1 and 2, and Case 3, we might consider that Cases 1 and 2 had a family history of sinistrality and that Case 3 had another lesion and atrophy of frontal lobes. The symptoms of conduction aphasia were mild and transient in our patients whose lesions were limited to the arcuate fasciculus. O n the other hand, those are relatively severe and persist in the patients whose lesions involve not only the arcuate fasciculus but also the supramarginal gyrus (4,9,10,24,25). Accordingly, the presence of damage to the supramarginal cortex may affect the prognosis of conduction aphasics with supramarginal cortico-subcortical lesions. It is not clear whether a possible transient and secondary effect on the supramarginal cortex was related to the production of conduction aphasia in our patients or not. In any case, it is certain that a focal lesion of the arcuate fasciculus can produce a transient, mild conduction aphasia. From the C T findings of our 3 patients (Fig. 2), it appears as if conduction aphasia develops after a lesion in any portion of the arcuate fasciculus. In the literature, however, there is only one case which showed conduction aphasia after a frontal lobe le- Fig. 2. Composite representation of the low density spots of the CT scans of the three patients superimposed in the corresponding template of Nieuwenhuys et al. Circles show the lesions of Cases 1, 2 and 3 in the order from the back to the front. Numbers 3 and 4 in the figure indicate the corona radiata and the arcuate fasciculus respectively. 427 CONDUCTION APHASIA AND ARCUATE FASCICULUS sion (23). Besides, the lesion was not restricted to the arcuate fasciculus. Hence, it remains to be seen whether a focal lesion of the anterior portion of the arcuate fasciculus can produce conduction aphasia. We will conclude by pointing out the following: 1) a lesion confined to the arcuate fasciculus in the parietal operculum can produce conduction aphasia in the pure form; 2) the aphasic symptoms may be mild and transient. References 1. Wernicke C. Der aphasische Symptomencomplex. Breslau: Cohn & Weigert, 1874. 2. Lichtheim L. O n aphasia. Brain 1885: 7433-484. 3. Geschwind N. Disconnexion syndromes in animals and man. Brain 1965:88:237-294,585-644. 4. Benson DF, Sheremata WA, Bouchard R, Segarra JM, Price D, Gexhwind N. Conduction aphasia, a clinicopathological study. Arch Neurol1973:28:339-346. 5 . Damasio H, Damasio AR. The anatomical basis of conduction aphasia. Brain 1980:103:337-350. 6. Green E, Howes DH. The nature of conduction aphasia, a study of anatomic and clinical features and of underlying mechanisms. In: Whitaker H et al., eds. Studies in neurolinguistics. Vol. 3. New York: Academic Press, 1976:123-156. 7. Kertesz A, Lesk D, McCabe P. Isotope localization of infarcts in aphasia. Arch Neurol 1977:34:590-601. 8. Hayward RW, Naeser MA, Zats LM. Cranial computed tomography in aphasia. Radiology 1977:123653-660. 9. Naeser MA, Hayward RW. Lesion localization in aphasia with cranial computed tomography and the Boston Diagnostic Aphasia Exam. Neurology 1978:28:545-551. 10. Kertesz A, Harlock W, Coates R. Computer tomographic localization, lesion side, and prognosis in aphasia and non-verbal impairment. Brain Lang 1979:8:34-50. 11. Mazzocchi F, Vignolo LA. Localization of lesions in aphasia: clinical CT correlations in stroke patients. Cortex 1919:15627-654. 12. Kertesz A. Localization of lesions in fluent aphasics. In: Arbib MA et al., eds. Neural Models of Language Processes. New York Academic Press, 1982327-344. 13. Naeser MA. CTscan lesion size and lesion locus in cortical and subcortical aphasias. In: Kertesz A ed. Localization in Neuropsychology. New York: Academic Press, 1983:63119. 14. Damasio H, Damasio AR. Localization of lesions in conduction aphasia. In: Kertesz A ed. Localization in Neuropsychology. New York Academic Press, 1983:231-243. 15. H b e n H, Albert ML. Human neuropsychology. New York: John Wiley & Sons, 1978:41-43,405. 16. Brown JW.The problem of repetition: a study of “conduction” aphasia and the “isolation” syndrome. Cortex 1975:11:37-52. 17. Lecours AR, Lhermitte F. L‘aphasie. Paris: Flammarion Medicine-Sciences, 1979:129-132, 340. 18. Benson DF, Aphasis. In: Heilman KM et al., eds. Clinical Neuropsychology. 2nd Edition. New York: Oxford University Press, 1985:17-47. 19. Nieuwenhuys R, Voogd J, Van Huijzen C. The human central nervous system. A synopsis and atlas. New York: Springer-Verlag, 1978. 20. Ohashi H. Clinical neuropsychology. Tokyo: Igakushoin, 1965:69-71. 21. Kertesz A. Recovery from aphasia. In: Rose FC ed. Advances in Neurology, Vol. 42. New York: Raven Press, 1984:23-39. 22. Kertesz A, McCabe P. Recovery patterns and prognosis in aphasia. Brain 1977:10&1-18. 23. Sheremata W, Andrews R, Pandya DN. Conduction aphasia from a frontal lobe lesion. Trans Am Neurol Assoc 1974:99249-252. 24. Tanabe H, Sumida T, Kitajima S , Okuda J. A case of conduction aphasia after cerebral infarction in the left anterior parietal lobe. Brain & Nerv (Tokoy) 1983:35:559-567. 25. Tanabe H, Inoue N, Sawada T, Miyakawa K, Kinugawa H, Shiraishi J. Paraphasia of conduction aphasia - from the viewpoint on the uniformity of conduction aphasia Higher brain function research (Tokyo) 1984:441-52. -. Address Hirotaka Tanabe, M.D. Department of Health Sciences Faculty of Health and Sport Sciences Osaka University 1-1, Machikaneyama, Toyonaka Osaka 560 Japan