Amusia Due to Rhythm Agnosia in a Musician with Left Hemisphere Damage: A Non-Auditory Supramodal Defect

Amusia Due to Rhythm Agnosia in a Musician with Left Hemisphere Damage: A Non-Auditory Supramodal Defect

NOTE AMUSIA DUE TO RHYTHM AGNOSIA IN A MUSICIAN WITH LEFT HEMISPHERE DAMAGE: A NON-AUDITORY SUPRAMODAL DEFECT Ludmil Mavlov (Bulgarian Academy of Sci...

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AMUSIA DUE TO RHYTHM AGNOSIA IN A MUSICIAN WITH LEFT HEMISPHERE DAMAGE: A NON-AUDITORY SUPRAMODAL DEFECT Ludmil Mavlov (Bulgarian Academy of Sciences, Central Laboratory for Brain Research, Sofia 31, Bulgaria)

Tonal pitch and rhythm are considered to be the basic components of music (Wertheim, 1969; Henkin, 1955; Gordon, 1970, 1978b; Gates and Bradshaw, 1977). "Rhythm sense" is most often associated with musical functions, that is why many authors assume that rhythm perception requires an auditory analysis, and its disorder ("rhythm agnosia"), respectively, is a type of auditory agnosia (Luria, 1969; Kaydanova, 1967; Baru and Karaseva, 1971; Frederiks, 1969; Sterritt, Camp and Lipman, 1966; Albert, Sparks, von Stockert and Sax, 1972; and others). The localization of brain damage responsible for such a disturbance is also asserted to be in the temporal (auditory) region (Luria, 1969; Semernitskaya, 1945; Baru and Karaseva, 1971). Indeed, in daily life rhythm structures are usually perceived and produced as sequences of sound stimuli, and music and dances are the major means for the development of "rhythm sense". Although music cannot exist without the integration of tonality and rhythm, their independent functioning has been confirmed in some studies. Gordon and Bogen (1974) found that the depression of the right hemisphere by sodium amytal destroyed the tonal-melodic aspects of singing severely, while the rhythmic ones seemed unaffected. Bentley (1968) pointed out that the performance of "monotones" as a group revealed significant deficiencies in both pitch discrimination and tonal memory, but not in rhythm memory. This dissociation was convincingly disclosed also in the case described in the present paper. The patient was a professional musician who developed severe difficulty in recognizing and producing rhythms, and at the same time his abilities for recognition and production of individual tones and tone sequences were completely preserved. The most important finding in this case was the fact that the recognition and reproduction of rhythm patterns were equally disturbed no matter whether they were perceived auditorily, visually, or tactually, and that this supramodal disorder caused a severe amusia despite the preserved ability to recognize and produce tones.

CASE REPORT

A 61-year old man, right-handed, professional mUSICIan (violin player and music teacher), suddenly suffered a cerebral vascular accident and fell into a coma on December 19, 1968. Several hours later consciousness returned but he had motor difficulties in the right extremities, as well as speech disorders. On Cortex (1980) 16, 331-338.

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December 20, he was admitted to the Neurological Clinic of the Medical Academy in Sofia_ Physical and neurological examination (on admission)

The patient was alert, cooperative, well-oriented. Blood pressure was normal, and he had never had arterial hypertension. Cranial nerves were intact. Motor examination demonstrated no paresis, and there were no asymmetries of tone and reflexes. There was pronounced right hemihypaesthesia for touch, pain, and temperature. Position sense, graphaesthesia, and two-point discrimination were severely disturbed in the right extremities. There was no hemianopia. Lumbar puncture yielded clear CSF without any pathological changes. Left carotid angiography provided evidence for an occlusion of the posterior parietal artery (an avascular zone in the territory of the artery). Diagnosis was: ischaemic vascular stroke (embolism?) in the left cerebral hemisphere. Neuropsychological examination 25 days after the stroke (january 3, 1969) Spontaneous speech was severely impaired, poor, almost lacking nouns, with hesitations, perseverations and pauses. Series speech was good. Oral repetition was impossible even for single phonemes. After producing an inadequate sound, he was aware of the error and attempted self-corrections. After each failure he said: "You see, 1 can't", "I failed again, why?" He pronounced these phrases easily, fluently, and without any phonemic errors. Naming, too, was impossible - he exhibited gross phonemic defects, hesitation, and finally he gave up. The patient confirmed that he was not only unable to utter the name but he could not recall it, either. Reading aloud was analogous to his oral repetition and showed hesitations, phonemic paraphasias, and attempts at self-correction. Difficulties were manifested even when he read single letters and short words. After that, however, he declared flunetly: "Everything is clear to me, but 1 can't", "It doesn't work; 1 know it very well but I can't". Spontaneous writing was not possible at all. Writing to dictation could be performed only for single letters, but not always. He could not write a single entire word, even a short one. He could write one- and two-digit numbers, but he failed with three-digit ones. Writing to dictation by arranging block-letters was also disturbed even for shorter words. Writing by copying (with the unaffected left hand) was preserved, although too slowly, letter by letter. Comprehension of· spoken language was surprisingly well preserved for yesno questions, commands (including the Pierre Marie's test with three pieces of paper), matching spoken words to pictures, and understanding syntactic relations in longer phrases. Comprehension of written material and performance of written commands were altogether intact. Calculation (namely addition and subtraction) with one- and two-digit numbers was grossly disordered even when carried out with written digits. Left-right orientation was severely disturbed. He had difficulties in imitating finger, limb and mouth positions. Finger gnosis was mildly impaired.

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Visual recognition of objects, faces, and embedded pictures was well preserved. Auditory recognition of environmental sounds, and tactual recognition (with left hand) of objects were also intact. Examination of musical abilities 25 days after the stroke (January 3, 1969)

(a) Melodies. A severe amusia, both expressive and receptive, was revealed. The patient could not identify popular songs, even though they sounded familiar to him. He could not either name such a melody or choose the correct name from several alternatives presented. He failed to sing any of the melodies which he had frequently listened to and performed. He could not reproduce a melody he had just heard. On few occasions he managed to reproduce a melody fragment with uniform times, but the first shift in note duration broke his performance. (b) Single tones and random tone sequences. Both single (i.e., isolated) tones and random tone sequences (with equal tone durations) were recognized and named adequately by the patient, and he was able to sing them out correctly. He managed to sing out without error all the notes being pointed to at random on the scale. He was, however, unable to sing to music since he had to produce each note for the proper duration. (c) Rhythms. Rhythm recognition and production were completely lost. He could not reproduce rhythm patterns with most simple structures on hearing them. He could not judge whether two rhythms he had heard were the same or different. (At that time, the examination was carried out only through auditory rhythm patterns). Reexamination 2 years 10 months after the stroke (November 9-11, 1971) Neurological examination showed that the disturbance of kinaesthesic sensation in the right extremities still persisted. Neuropsychological examination demonstrated that spontaneous speech and repetition almost completely recovered. Rare hesitations in articulation of longer or unfamiliar words were observed. Naming was normal. Reading aloud was normal as well. Spontaneous writing, and writing to dictation were possible, although with difficulty, and letters were often omitted. Forming words with blockletters was even more disturbed and almost impossible. Finger gnosis was mildly impaired. Imitating finger and limb positions (with the unaffected left hand) remained moderately deficient. Left-right disorientation and acalculia were easily demonstrated. Musical abilities

(a) Melodies. The patient complained that he could not recognize the melodies he heard on the radio. He could not distinguish different musical rhythms, i.e. waltz, tango, march, etc. On examination, his amusia persisted almost unchanged. He could not recognize the Bulgarian national anthem, familiar opera arias, natural songs, or popular country songs. Sometimes he managed to reproduce a part of a melody just presented to him, but at the first pause or a note of a longer duration, the reproduction collapsed altogether. (b) Single tones and random tone sequences. Recognition and reproduction (through imitation, or on verbal command, or on pointing to notes on the scale) of single tones and tone sequences, regardless of duration, were as intact as they were during the first exami~ation.

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(c) Rhythms. Recognition ,and reproduction of simple rhythm patterns composed of 2 to 5 elements were again grossly disturbed. On this occasion, rhythm perception was investigated presenting the patterns auditorily (by clicks), visually (by flashes), and tactually (by taps on the hand). Stimulation was performed manually. In each of the three modalities a standard series of 12 simple rhythm patterns was presented. The patient reproduced correctly only 2 rhythms presented auditorily, 1 rhythm visually, and 1 tactually. Thus, the disturbance was confirmed in all modalities. Reexamination 4 years 9 months after the stroke (September 25, 1973) Neurological and neuropsychological examinations disclosed no further improvement of the patient's condition. The same pronounced deficit of position sense in his right extremitjes was present. Speech and reading were normal. In writing, he omitted letters. Finger agnosia was still evident. Imitation of finger and hand positions was moderately disturbed. Left-right disorientation and acalculia were conspicuous; the patient himself had commented on this. Musical abilities (a) Melodies. The severe receptive and expressive amusia manifested no improvement. The patient again complained that he could not recognize melodies he had heard and played before. He said, however, that he enjoyed listening to pleasant melodies. Examination showed the same difficulties in recognizing and reproducing popular melodies. He stated that they sounded fairly familiar to him. Of a famous Bulgarian country song having a typical national rhythm he commented that it was "something like a dance". Asked whether it was popmusic he replied: "I think it is". When he was required to name the musical rhythms of the presented melodies, he said he could not. (b) Single tones and random tone sequences. Examination again confirmed the perfect recognition and production of tonal pitches. , (c) Rhythm abilities. A detailed study of the patient's abilities for rhythm discrimination and reproduction was carried out. Rhythm patterns were perceived via audition, vision and touch, employing new methods designed for this purpose (Mavlov and Dascalov, 1973). Rhythm patterns were fairly simple and consisted of 2 to 5 stimulus elements delimiting 1 to 4 short and long empty interstimulus intervals. The patterns were programmed by an electronic programmer, recorded on a magnetic tape, and presented by sound clicks, light flashes and mechanical taps. Adapting amplifiers, actuating light sources or electromagnetic transducers, were applied for visual and tactual presentation. The parameters building up the patterns were the following: stimulus-element duration (click, flash, or tap) of 10 msec, short interval duration of 200 msec, and long interval duration of 400 msec. In rhythm discrimination 68 rhythm pattern pairs of equal pattern duration for same-different judgement were presented. There was a pause of 1 sec between the two patterns in a pair. The pause between two pattern pairs lasted 5 sec, and during that time a same-different judgement had to be made. For reproduction 40 single rhythm patterns were administered with a pause of 10 sec after each pattern. During the pause the pattern had to be reproduced. The patient preferred oral reproduction. Each of the above pattern sets was presented three times once for each modality. The following results were obtained: Rhythm discrimination - a) by audition .-...... 23 errors (a poor score but above chance level which is 50%, i.e. 34 errors); b) by vision - 37 errors (chance level performance); c) by touch - 34 errors (chance level performance). Rhythm reproduction - a) on

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auditory perception - 37 incorrect out of 40 presented; b) on visual perception38 incorrect out of 40 presented; c) on tactual perception - 36 incorrect out of 40 presented. It is worth mentioning that these rhythm pattern sets were not difficult and when they were administered to normal subjects of different age and education far better results than the patient's ones were obtained . . A great number of subjects achieved 100% correct responses (Mavlov and Pentcheva, 1977). Briefly, in this case, evidence of an amusia concomitant with a severe and persistent rhythm agnosia and apraxia was found. The rhythm disturbances were manifested regardless of the sensory channel through which they were tested.

DISCUSSION

In the presented case it has been shown that after . a left hemisphere stroke a professional musician developed a severe receptive and expressive amusia persisting for many years. Recognition and reproduction of tonal pitches were fairly well preserved, and it would be suggested that amusia was the result of the concomitant severe disturbance of the patient's rhythm abilities. The discrimination of two simple rhythm patterns as same or different, as well as the reproduction of perceived single rhythm patterns were consistently impaired. It is noteworthy that the defect was demonstrated regardless of the modality of perception, i.e. whether rhythm structures were perceived through audition, vision, or touch. In addition, the patient had at the beginning a marked but transient conduction aphasia which disappeared later on. In addition to the amusia and rhythm agnosia some other neurological and neuropsychological deficiencies persisted as well: proprioceptive hypaesthesia in the right extremities, pronounced left-right disorientation and acalculia, moderate impairment in imitating finger and limb positions, finger agnosia, and spatial agraphia (a Gerstmann's syndrome). Both the clinical picture and carotid angiography gave evidence for a left posterior parietal (or maybe partially parieto-temporal) localization of the lesion. There is no agreement in the world literature concerning the role of the left and right hemisphere in amusia. Amusia is considered to occur with left hemisphere damage (Henschen, 1926; Kleist, 1962; Wertheim and Botez, 1961), as well as with right hemisphere damage (Botez and Wertheim, 1959; Pittrich, 1956, cited by Spreen, Benton and Fincham, 1965; Bogen and Gordon, 1971; Gordon and Bogen, 1974; Wiirtzen, 1903, Jossmann, 1927, and Jellinek, 1956, all cited by Gordon and Bogen, 1974). On the other hand, according to Wertheim (1969), left hemisphere lesions cause a "receptive" amusia, while right hemisphere lesions - an "expressive" one. It is possible, of course, that amusia should arise from both left and right hemisphere lesions, with different clinical features. However, it does not seem likely that the dichotomy is "receptive" versus "expressive" musical impairment. In my view, it is more probable that different components of musical abilities are disordered: in one type of amusia it is tonality that is disordered, and in another - it is rhythm. It may be suggested that right hemisphere damage impairs predominantly the tonal aspect of musical functions. This is supported by the evidence for disturbance of tonal memory only after right, and not left, temporal lobectomies (Milner, 1962; Berlin, Chase, Dill and Hagepanos, 1965), as well as by some dichotic listening experiments with musical pitch in normals (Kallman and Corballis, 1975; Gordon, 1970, 1978a; Darwin, 1969, cited by Gordon, 1970; Kimura, 1964) and in brain

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damaged subjects (Shankweiler, 1966). On the other hand, there is evidence that rhythm patterns are preferentially processed by the left hemisphere (Robinson and Solomon, 1974; Papcun, Krashen, Terbeek, Remington and Harshman, 1974; Halperin, Nachshon and Carmon, 1973; Gordon, 1978b). The case reported in the present paper demonstrating deterioration of rhythm sense after a left hemisphere lesion is consistent with this evidence. The development of amusia as a result of an isolated disturbance of rhythm sense alone is worth emphasizing. The independent importance of rhythm for melody has been stressed in a number of studies. Familiar melodies can be recognized on the basis of rhythm alone (White, 1960). Moreover, simple musical tunes remain recognizable when pitch variations are eliminated with timing relationship intact, but not vice versa (Lenneberg, cited by Sturges and Martin, 1974). And as the latter authors noticed: "a sequence (concatenation) of notes is not a tune unless the notes are in the right temporal places" (p. 383). In addition, the polymodal manifestation of the defect in the reported case contradicts the views that rhythm processing is based on auditory analysis, and that the .impairment of rhythm perception is a vari!!ty of auditory agnosia (see the introduction). Rhythm perception is rather a variety of time perception, and more precisely, it is a process of organization of temporal micro intervals in a holistic structure (temporal patterns composed of short and long time intervals'. Consequently, rhythm agnosia is probably caused by the disorder of a common supramodal time processor. Thus the physical (modal) stimuli do not have any role in the processing of temporal patterns other than delimiting the time intervals. Following this view amusia due to rhythm agnosia is, in fact, brought about by the disturbance of a component which is not auditory but supramodal in nature. This component (i.e. rhythm analysis) is, together with tonal pitch analysis, indispensable for composition, recognition and reproduction of any musical melody.

ABSTRACT

A case of a severe receptive and expressive amusia in a professional musician following a left hemisphere vascular stroke is reported. Recognition and production of single tones and random tone sequences were found to be surprisingly well preserved. In contrast, the recognition and production of simple rhythm patterns were grossly disturbed. It is suggested that amusia is due to the demonstrated rhythm disturbance. Moreover, it has been found that the defect in recognition and reproduction of rhythms was manifested regardless of the modality of perception, i.e. whether rhythm patterns were perceived by audition, vision, or touch. Therefore, the disturbance of rhythm abilities is supramodal in nature, based probably on the perception of time microintervals. Thus, this type of amusia is a result of a non-auditory supramodal defect, i.e., an impairment of temporal pattern recognition.

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SHANKWEILER, D. (1966) Effects of temporal lobe damage on perception of dichotically presented melodies, J. Comp. Physiol. Psychol., 62, 115-119. SPREEN, 0., BENTON, A. L., and FINCHAM, R. W. (1965) Auditory agnosia without aphasia, Arch. Neurol., 13, 84-92. STERRITI, G. M., CAMP, B. W., and LIPMAN, B. S. (1966) Effects of early auditory deprivation upon auditory and visual information processing, Percept. Mot. Skills, 23, 123-130. STURGES, P. T., and MARTIN, J. G. (1974) Rhythmic structure in auditory temporal pattern perception and immediate memory, J. Exptl. Psychol., 102, 377-383. WERTHEIM, N. (1969) The amusias, in Handbook of Clinical Neurology, ed. by P. J. Vinken and G. W. Bruyn, vol. 4, North-Holland, Amsterdam. - , and BOTEZ, M. I. (1961) Receptive amusia: A clinical analysis, Brain, 84, 19-30. WHITE, B. W. (1960) Recognition of distorted melodies, Amer. J. Psychol., 73, 101-107. Dr. Ludmll Mavlov, Central Laboratory for Brain Researcb, Bulgarian Academy of Sciences, G. Sofilsky Str. I, Sofia 1431, Bulgaria.