- Email: [email protected]
Phonemic Vowel Length Contrasts in Cerebellar Disorders
Brain and Language 67, 95–109 (1999) Article ID brln.1998.2044, available online at http://www.idealibrary.com on
Phonemic Vowel Length Contrasts in Cerebellar Disorders Hermann Ackermann,* Susanne Gra¨ber,* Ingo Hertrich,* and Irene Daum† *Department of Neurology, University of Tu¨bingen, Tu¨bingen, and †Faculty of Psychology, University of Bochum, Bochum, Germany Apraxia of speech and Broca’s aphasia both affect voice onset time (VOT) whereas phonemic vowel length distinctions seem to be preserved. Assuming a close cooperation of anterior perisylvian language zones and the cerebellum with respect to speech timing, a similar profile of segment durations must be expected in ataxic dysarthria. In order to test this hypothesis, patients with cerebellar atrophy or cerebellar ischemia were asked to produce sentence utterances including either one of the German lexial items ‘‘Rate’’ (/ra:t he/, ‘installment’), ‘‘Ratte’’ (/rat he/, ‘rat’), ‘‘Gram’’ (/gra:m/, ‘grief’), ‘‘Gramm’’ (/gram/, ‘gramm’), ‘‘Taten’’ (/t hatn/, ‘actions’), or ‘‘Daten’’ (/datn/, ‘data’). At the acoustic signal, the duration of the target vowels /a/ and /a:/ as well as the VOT of the word-initial alveolar stops /d/ and /t/ were determined. In addition, a master tape comprising the target words from patients and controls in randomized order was played to three listeners for perceptual evaluation. In accordance with a previous study, first, the cerebellar subjects presented with a reduced categorical separation of the VOT of voiced and unvoiced stop consonants. Second, vowel length distinctions were only compromised in case of the minimal pair ‘‘Gram’’/‘‘Gramm.’’ In contrast to ‘‘Rate’’/‘‘Ratte’’, production of the former lexical items requires coordination of several orofacial structures. Disruption of vowel length contrasts would, thus, depend upon the complexity of the underlying articulatory pattern. 1999 Academic Press Key Words: vowel length; VOT; ataxic dysarthria; cerebellum; apraxia of speech.
INTRODUCTION
Voice onset time (VOT), i.e., the time lag between consonant burst and vowel onset, provides a critical contrast between voiced and voiceless stop consonants: the former have a shorter VOT than their unvoiced cognates or This study was supported by grants from the DFG (SFB 307) and the BMFT (01 KL9001 O). The authors thank Dr. M. M. Schugens and Dr. S. Spieker for critical discussion and helpful comments. Address correspondence and reprint requests to Hermann Ackermann, M. D., M. A., Department of Neurology, University of Tu¨bingen, Hoppe-Seyler-Strasse 3, D-72076 Tu¨bingen, Germany. Fax: (Germany) 7071-296507. 95 0093-934X/99 $30.00 Copyright 1999 by Academic Press All rights of reproduction in any form reserved.
96
ACKERMANN ET AL.
even present with a voicing lead, i.e., glottal vibrations prior to stop consonant release burst (Lisker & Abramson, 1964, 1967). For example, the VOT of /d/, as a rule, amounts to less than 20 ms at the initial position of isolated English words whereas the values of the respective /t/ productions exceed 30 ms. Similar data have been reported for German stop consonants (Stock, 1971; Haag, 1979; Ziegler & von Cramon, 1986). Broca’s aphasia and apraxia of speech (AOS)—syndromes which reflect damage to the inferior dorsolateral frontal lobe, the subjacent white matter, or the anterior insula (Alexander, Benson, & Stuss, 1989; Kertesz, 1984; Dronkers, 1996)—give rise to a significant overlap of the VOT of voiced and unvoiced stops (Blumstein, Cooper, Zurif, & Caramazza, 1977; Freeman, Sands, & Harris, 1978; Blumstein, Cooper, Goodglass, Statlender, & Gottlieb, 1980; Itoh, Sasanuma, Tatsumi, Murakami, Fukusako, & Suzuki, 1982; Hoit-Dalgaard, Murry, & Kopp, 1983; Tuller, 1984). A former study of our group revealed similar VOT patterns in patients with ataxic dysarthria due to cerebellar atrophy (Ackermann & Hertrich, 1997). Since reciprocal pathways connect the left frontal lobe with the contralateral cerebellar hemisphere, these data might indicate a close cooperation of these structures with respect to the specification of VOT. Besides VOT, a variety of other durational parameters of the acoustic signal serve phonological functions and, therefore, must be adequately controlled (Klatt, 1976). In English, e.g., the voicing contrast of syllable-final stop consonants is signaled by the preceding vowel length and syllable-initial voiced and voiceless fricatives differ in noise duration. Both reduced and increased absolute vowel durations were observed in patients with damage to the anterior perisylvian language zones (Duffy & Gawle, 1984; Bauman, Wangler, & Prescott, 1975; Collins, Rosenbek, & Wertz, 1983; Ryalls, 1986). As a rule, however, speech apraxics and Broca aphasics vary the length of vocalic segments as a function of the voicing characteristics of the following stop consonant, i.e., produce a similar durational contrast to that of normal speakers (Duffy & Gawle, 1984; Baum, Blumstein, Naeser, & Palumbo, 1990). Furthermore, these patients display an unimpaired distinction of noise segments in voiced and unvoiced frictives (Code & Ball, 1982; Kent & Rosenbek, 1983; Harmes, Daniloff, Hoffman, Lewis, Kramer, & Absher, 1984). Similar findings could be obtained from native Thai speakers presenting with nonfluent aphasia: the relative duration of phonologically short and long vowel targets was largely undistorted (Gandour & Dardarananda, 1984). Since both Broca’s aphasia and AOS compromise VOT in the presence of intact phonemic vowel length distinctions and since VOT may be considered an acoustic parameter of the temporal coordination of orofacial and laryngeal muscle activity during speech production (Keller, 1990), these syndromes seem to specifically disrupt the adjustment of phonatory and articulatory functions (Blumstein, 1988; Buckingham, 1991). Assuming a close interaction of the cerebellum and the anterior perisylvian
VOWEL LENGTH IN ATAXIC DYSARTHRIA
97
language zones with respect to the specification of VOT, the question arises whether ataxic dysarthria also spares vowel length contrasts. A native Thai speaker who suffered from a right-sided ischemic cerebellar lesion showed markedly prolonged vowel durations (Gandour & Dardarananda, 1984). Yet, the temporal relation of short and long vowel targets, i.e., the respective durational phonemic contrast, was revealed to be preserved. Comprehensive studies on vowel length distinctions in ataxic dysarthria are not yet available. In order to examine the influence of ataxic dysarthria on the duration of vocalic segments, native German speakers suffering from cerebellar atrophy or ischemia were asked to produce minimal pairs primarily differing in vowel length. Stimuli differing in voicing of the word-initial alveolar stop were included as well to allow for a comparison with previous findings on VOT in ataxic dysarthria (Ackermann & Hertrich, 1997). Subjects with Parkinson’s disease (PD) show an overlap of the VOT of voiced and unvoiced stops at syllable-initial position similar to the pattern observed in Broca’s aphasia (Lieberman, Kako, Friedman, Tajchman, Feldman, & Jiminez, 1992). These VOT disruptions were attributed to an impairment of striatal pathways acting on the prefrontal cortex. Thus, the implementation of VOT seems to depend on the basal ganglia as well. It is unknown whether these dysfunctions also compromise vowel length contrasts. Therefore, PD patients were examined in addition to the cerebellar subjects. Dysfunction of the dopaminergic pathways projecting from the substantia nigra to the striatum and/or the prefrontal cortex represents the core pathomechanism of PD. However, in later stages the disease process extends to other cerebral areas. In order to assess the contribution of a specific functional–neuroanatomic system, i.e., the dopaminergic nigrostriatal and -frontal pathways, to the adjustment of vowel length, early PD patients (stages I–II; Hoehn & Yahr, 1967) were considered. MATERIALS AND METHODS
Subjects The present investigation—part of a larger study involving the evaluation of speech perception and production in ataxic dysarthria—examined ten patients with cerebellar pathology (see Ackermann, Gra¨ber, Hertrich, & Daum, 1997a). Eight individuals (five males, three females; age 28–72 years; median, 62 years) showed diffuse atrophy of the cerebellum at magnetic resonance imaging (MRI). To a variable degree, all of them presented with ataxia of gait, dyscoordination of voluntary arm movements, oculomotor disorders, and speech difficulties; none had any clinical signs of extracerebellar motor dysfunctions. Transcranial magnetic stimulation of the motor cortex further confirmed the integrity of the corticospinal tracts to the distal arm and leg muscles. In addition, extensive investigations of blood serum and cerebrospinal fluid were unremarkable. Taken together, these findings warranted the diagnosis of an idiopathic cerebellar atrophy (IDCA; Harding, 1984). Two subjects (C04 and C02) had already participated in a previous study of ataxic dysarthria (patients CA5 and CA7; Ackermann et al., 1997a). Patient C04 showed a few small ischemic lesions within the periventricular white
98
ACKERMANN ET AL.
matter at MRI. In consideration of unremarkable neuropsychological tests and electrophysiological investigations, silent lacunar infarctions were assumed. MRI of the spinal cord revealed syringomyelia in subject C02. This disorder represents a distinct disease entity unrelated to the patient’s cerebellar pathology. The remaining IDCA patients did not show any evidence of extracerebellar pathology at MRI. Two participants of the present study suffered from an unilateral lesion: one subject (male, 27 years) underwent removal of nearly the complete left cerebellar hemisphere because of a tumor about 10 years before testing, the other patient (male, 69 years) had suffered right-sided cerebellar ischemia within the region of blood supply of the right superior cerebellar artery 5 years prior to the present investigation. Both these subjects had initially shown an unilateral ataxic syndrome which had improved during further follow-up. Nine PD patients participated in the present study (five males, four females; age 34–69 years; median, 57 years). Diagnosis was based on unilateral onset of symptomatology and the presence of two of the three signs, rest tremor, rigidity, and akinesia, as well as a significant response to L-dopa (Gibb & Lees, 1989). Disease duration extended from 2 to 6 years. Neuroleptic therapy prior to onset of the disease or during follow-up, a history of strokes, or pyramidal and/or ataxic signs at clinical examination were exclusion criteria. All subjects received L-dopa, a dopamine agonist, and a MAO-B inhibitor. A few patients were, in addition, treated with the new antiparkinsonian drug budipine. In subjects with motor fluctuations kinematic investigation was performed during the off-phase. On the basis of clinical findings, five patients were assigned to stage I and four to stage II according to the scale of Hoehn and Yahr (1967). These early levels of PD reflect a relatively selective dopaminergic deficit. All cerebellar and PD patients were fully able to cooperate. Neuropsychological screening, including a short version of the Wechsler Adult Intelligence Scale as well as tests of memory and so-called frontal lobe functions, revealed unimpaired performance in all clinical subjects (see Daum & Ackermann, 1997). Thus, incipient or overt dementia could be ruled out. Furthermore, clinical examination did not yield any indications of emotional disturbances. Using the dysarthric dimensions introduced by Darley, Aronson, and Brown (1975), one of the authors (I.H.) performed a perceptual evaluation of the recorded test materials and samples of spontaneous speech prior to acoustic analysis. All cerebellar subjects showed— to a varying degree—articulatory impreciseness in terms of either reduced consonant clusters, incomplete occlusions, voicing errors or distorted (centralized) vowels. Perceived /d/ in case of a /t/ target most often occurred in patient C01. Six of the 10 cerebellar individuals (C01, C02, C05, C06, C09, C10) showed a slight to moderate decrease of speech tempo. Besides lengthened words, prolonged interword pauses contributed to these perceived abnormalities. Markedly reduced speech rate, concomitant with ‘‘scanning’’ rhythm, was noted in subject C03. Apart from a single individual (C04), all ataxic dysarthrics presented with harsh and/ or breathy voice quality. As concerns the PD patients, two individuals showed a tendency toward rather accelerated speech rate concomitant with incomplete stop occlusions (P06 and P07). Articulatory performance was unremarkable in the remaining cases. Seven of the PD subjects had breathy and/or harsh voice quality, with reduced voice volume in three instances. Five male and four female subjects (age 30–72 years; median, 61 years) who did not have a history of neurological or psychiatric disorders served as control group.
Speech Material Two minimal pairs differing in the duration of the vowel ‘‘a’’ were considered for analysis: ‘‘Ratte’’ (/rat he/, ‘rat’) and ‘‘Rate’’ (/ra:t he/, ‘installment’) as well as ‘‘Gramm’’ (/gram/, ‘gram’) and ‘‘Gram’’ (/gra:m/, ‘grief’). These stimuli represent German lexical items. In case of the bisyllabic units, the vowels /a/ and /a:/ bear the word stress. Indeed, formant measurements revealed some short vowels of standard German to be more centralized (diphthongized) than their long cognates, and these effects even may outweigh durational contrasts (Jessen,
VOWEL LENGTH IN ATAXIC DYSARTHRIA
99
1993). Nevertheless, duration does represent the strongest acoustic correlate of the short/long distinction of the German vowels /a/ and /a:/ in a stressed position (Hertrich & Ackermann, 1997). In order to compare the effects of cerebellar dysfunctions on vowel length contrasts and VOT, the German nouns ‘‘Daten’’ (/da:tn/, ‘data’) and ‘‘Taten’’ (/t ha:tn/, ‘deeds’) were also included. As a rule, the German stop /t/, when produced in vowel context, represents an aspirated and voiceless sound with /d/ as its voiced cognate. Usually, the latter consonant is not produced with voicing lead, i.e., glottal vibrations preceding burst release, in southern German dialects. Word stress is located on the first syllable of the target word, i.e., ‘‘da’’ and ‘‘ta,’’ respectively.
Recording Procedure The stimuli were printed in bold large letters on separate cards and presented by the experimenter five times each in a quasi-randomized order. Subjects had to produce the visually displayed target embedded into the carrier phrase ‘‘Ich habe . . . gelesen’’ (‘‘I have read . . .’’). Since the testing session also included a range of other neuropsychological tests, the production task was restricted to only five repetitions of each stimulus in order to avoid fatigue effects. Speech examination took place in a sound-treated room using a DAT recorder (JVC XD Z505) and a condenser microphone (Sennheiser, ME62). The mouth-microphone distance amounted to about 20 cm. Prior to analysis, the recordings were bandpass filtered (50–8000 Hz), digitized at a sampling rate of 20 kHz, and stored on a personal computer (486 IBM compatible).
Perceptual Evaluation A master tape was generated for perceptual evaluation of the stimuli obtained from the patients and their controls. The recorded utterances were combined to a single sequence, randomized across groups but blocked by individual. Prior to this procedure, one of the authors (I.H.) checked the recordings with respect to dysfluencies such as iterations or audible inspirations, incomplete stop consonant production, and devoicing of vocalic intervals. Two utterances (‘‘Gram’’, ‘‘Gramm’’) of a control speaker were discarded from further analysis because of misspelling with following self-correction (e.g., ‘‘Gramm . . . a¨h . . . Gram’’). Three certified speech pathologists, unacquainted with the patients and the controls, rated the items which were presented by a loudspeaker adjusted to comfortable loudness. As a measure of perceived vowel length and voicing contrasts, the frequency of misassignments was calculated, e.g., the number of long vowel targets classified as the respective short cognate and vice versa. The number of judgments for each item amounted to n ⫽ 15 (3 raters ⫻ 5 repetitions). When, thus, one of the three experts misclassifies a single target, error frequency equals 6.6% (1/15). Perceptual evaluation of the recordings yielded an interrater reliability of the three speech pathologists of 86% (Cohen’s κ ⫽ 0.86, chance ⫽ 50%).
Acoustic Measurements Vowel duration was determined from the onset of periodic energy to the change in waveform associated with the initiation of the word-final bilabial nasal in ‘‘Gram’’/‘‘Gramm’’ or vowel offset in ‘‘Ratte’’/‘‘Rate’’. In accordance with the definition of Lisker and Abramson (1964), VOT of the initial alveolar stop of the target words ‘‘Daten’’ and ‘‘Taten’’ was defined as the time interval between the beginning of the burst and vowel onset (see Ackermann & Hertrich, 1997). A former investigation using similar recording and signal analysis procedures had deter-
100
ACKERMANN ET AL.
mined reliability measures with respect to VOT (Hertrich & Ackermann, 1994): Patients with Huntington’s chorea and control speakers showed a similar error magnitude (VOT measurement error in normals ⫽ 2.3 ms; VOT measurement error in patients with Huntington’s chorea ⫽ 2.1 ms; error of vowel duration ⬍ 4 ms).
RESULTS
Perceptual Data Table 1 (second and fifth columns) illustrates the results of the identification task in terms of the number of misassignments, i.e., the percentage of items which are perceived as the cognate of the visually displayed stimulus. Only a few utterances obtained from the controls and the PD patients were incorrectly classified with respect to the voicing and vowel length characteristics of the respective target: two of the three raters misidentified the same ‘‘Daten’’ target of a PD subject; in all other instances, a single speech pathologist incorrectly classified one token each. Compared to the maximum error frequency in the control group, four cerebellar subjects showed an increased number of misassignments of ‘‘Taten’’ and ‘‘Gram’’ targets whereas erroneous classification of short vowel targets occurred in a single repetition only (target ‘‘Gramm’’ from subject C03). At the perceptual level, a subgroup of the cerebellar patients, thus, had a tendency to shorten the VOT of unvoiced stops and to reduce the duration of long vowel targets, predominantly in case of ‘‘Gram’’ utterances. Acoustic Data Figure 1 shows the distribution of the individual measurements of VOT and vowel length separately for each participant. The control group exhibited a clear-cut segregation of the voiced and unvoiced targets across all speakers at about 40 ms, i.e., all /t/ productions had a VOT above and the respective voiced stops below this value. With respect to the minimal pairs ‘‘Gram’’/ ‘‘Gramm’’ and ‘‘Rate’’/‘‘Ratte’’ a similar strict distinction at 120 and 140 ms, respectively, was observed. The data plots of two of the three minimal pairs obtained from the cerebellar group revealed compromised category boundaries in about half of the subjects. As concerns ‘‘Taten’’/‘‘Daten’’, five patients (C02, C03, C05, C09, C10) showed an overlap of the produced /d/ and /t/ targets and a single one (C01) a complete assimilation of the unvoiced cognate to the voiced one. Furthermore, five individuals presented—as compared to the controls—with a disruption of the category boundary of the ‘‘Gram’’ and ‘‘Gramm’’ targets (C03, C04, C05, C06, C09). Apart from patients C06 and C10, all cerebellar subjects maintained the category boundary of ‘‘Rate’’/‘‘Ratte.’’ The various phonemic durational contrasts were rather well preserved within the PD group. A single patient each produced the long vowel targets ‘‘Rate’’ and ‘‘Gram,’’ respectively, with a vowel length largely below the
TABLE 1 Perceptual and Acoustic Data Obtained from Patients with Cerebellar Atrophy (C01–C10), Parkinson’s Disease (PD), and Control Subjects A. Minimal pair ‘‘Daten’’/‘‘Taten’’: VOT VOT/d/ VOT/t/ Err/d/ (%)
Mean (ms)
SD
Err/t/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 0.0 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 20.0 PD subjects (N ⫽ 9) Min 0.0 Max 13.2 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 0.0 Mean — SD —
29.9 17.5 27.0 14.9 46.0 29.7 22.5 21.8 36.1 74.1
2.0 2.7 6.8 2.1 23.2 6.5 3.6 5.2 29.6 51.9
53.4 20.0 0.0 0.0 0.0 6.6 0.0 0.0 40.0 0.0
30.4 53.5 198.0 59.2 63.4 104.1 89.4 72.8 48.7 140.5
5.6 40.5 21.0 6.1 23.0 38.6 18.6 19.6 19.2 44.1
0.19 a 6.82 2.28 a 17.18 17.37 1.21 a 5.11 a 11.13 1.18 a 2.34 a
15.5 34.5 24.4 5.1
1.6 9.8 4.4 2.6
0.0 6.6 — —
52.5 111.9 79.4 20.3
4.5 15.6 10.3 5.0
5.67 20.91 12.37 5.24
15.2 28.2 21.7 5.1
1.4 6.5 3.6 2.0
0.0 0.0 — —
49.2 88.5 74.5 12.9
2.8 22.9 10.7 6.1
5.49 24.04 14.15 6.52
Sub
B. Minimal pair ‘‘Gramm’’/‘‘Gram’’: Vowel length Vowel/a/ Vowel/a:/ Err/a/ (%)
Mean (ms)
SD
Err/a:/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 13.2 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 0.0 PD subjects (N ⫽ 9) Min 0.0 Max 0.0 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD —
74.6 63.6 121.4 53.8 82.3 62.4 49.0 68.9 91.7 61.4
9.5 2.7 3.1 7.1 12.7 8.9 6.9 15.4 26.7 17.1
0.0 0.0 0.0 86.6 60.0 13.2 0.0 0.0 20.0 0.0
195.3 249.5 215.7 81.8 169.2 107.1 183.8 152.8 186.9 219.3
12.2 49.9 43.4 10.2 95.9 25.7 41.6 14.5 84.2 40.2
15.61 6.16 a 4.08 a 5.10 a 2.33 a 4.25 a 10.37 6.69 a 2.27 a 8.75
35.5 91.3 72.0 16.0
3.0 30.6 11.8 8.1
0.0 0.0 — —
106.9 250.8 180.1 47.4
6.8 34.0 18.4 10.2
5.07 20.33 12.54 4.62
58.5 98.1 74.3 13.0
7.2 18.5 11.2 3.5
0.0 6.6 — —
145.2 233.6 197.2 30.3
9.4 78.6 27.7 22.2
7.01 20.44 11.76 4.59
Sub
102
ACKERMANN ET AL.
TABLE 1—Continued C. Minimal pair ‘‘Ratte’’/‘‘Rate’’: Vowel length Vowel/a/ Vowel/a:/ Err/a/ (%)
Mean (ms)
SD
Err/a:/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 0.0 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 0.0 PD subjects (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD —
75.3 97.8 102.4 86.6 88.7 61.2 56.9 88.4 109.2 95.3
7.1 15.7 12.4 8.4 21.8 10.3 5.6 11.1 10.1 22.7
0.0 0.0 0.0 0.0 0.0 40.0 0.0 0.0 0.0 20.0
170.5 353.5 272.9 159.1 217.8 69.3 193.7 172.0 190.6 179.2
14.1 54.2 52.2 2.6 38.9 10.1 24.1 9.1 23.3 50.6
14.46 13.45 9.40 12.25 6.64 1.24 a 17.40 10.8 7.93 3.23 a
67.0 113.6 82.0 13.7
5.0 13.1 8.4 2.4
0.0 0.0 — —
129.1 257.7 187.0 44.3
6.1 20.2 13.0 4.4
7.50 27.19 15.65 7.13
63.3 108.1 79.4 12.3
5.0 28.1 11.4 8.6
0.0 0.0 — —
151.8 215.7 186.5 21.8
9.2 30.4 18.3 7.5
5.01 25.49 12.91 6.46
Sub
Note. Err/d/ (Err/t/), /d/ targets (/t/ targets) perceived as /t/ targets (/d/ targets) in percentage of evaluated stimuli (n ⫽ 15 judgments, 3 raters ⫻ 5 repetitions); Err/a/ (Err/a:/), /a/ targets (/a:/ targets) perceived as /a:/ targets (/a/ targets) in percentage of evaluated stimuli (n ⫽ 15); Mean (columns), individual mean across five repetitions; Mean (rows), group means; SD, standard deviation; Min (Max), lower (upper) limit of the respective range. a Below normal range.
category boundary of the normal speakers (‘‘Gram,’’ patient No. 6; ‘‘Rate,’’ patient No. 4). It is noteworthy, however, that both these subjects did not show an overlap of the durations of the short and long targets. Rather, a shift of the boundary toward a lower value characterizes these individuals. As a quantitative estimate of the segregation of the minimal pair targets, the t values of the acoustic measures were calculated (Table 1). In short, the t value relates the difference of two means to their standard errors. Given an approximately equal number of repetitions for all comparisons, the t values, therefore, can be considered a measure of the distinctness of two classes of items. Using these data, statistical analysis revealed a significant difference between cerebellar and control groups for the minimal pairs ‘‘Taten’’/‘‘Daten’’ (p ⫽ .021) and ‘‘Gram’’/‘‘Gramm’’ (p ⫽ .018). All other betweengroup comparisons did not reach the 5% level.
VOWEL LENGTH IN ATAXIC DYSARTHRIA
103
FIG. 1. Scattergrams of vowel length (‘‘Gram’’/‘‘Gramm’’; ‘‘Rate’’/‘‘Ratte’’) and VOT measurements (‘‘Taten’’/‘‘Daten’’) in the cerebellar group (CERE), subjects with Parkinson’s disease (PD) and normal speakers (NC). Since only five repetitions per stimulus were obtained, the frequently used display of the number of tokens (ordinate) versus durational parameters (abscissa) did not seem to be feasible.
COMMENTS
In accordance with a previous investigation (Ackermann & Hertrich, 1997), the cerebellar patients, first, showed impaired voicing contrasts. Second, both visual inspection of the distributional patterns and calculation of a quantitative estimate of the respective category boundaries indicate a differential influence of cerebellar disorders on the two vowel length contrasts studied: whereas the minimal pair ‘‘Gram/Gramm’’ revealed to be compro-
104
ACKERMANN ET AL.
FIG. 1—Continued
mised as well, the segregation of the targets ‘‘Rate’’ and ‘‘Ratte’’ was largely undisturbed. The reduced distinction between voiced and unvoiced word-initial alveolar stops observed in ataxic dysarthria predominantly reflects disruption of long-lag VOT (Ackermann & Hertrich, 1997). Compared to voiced stops, the respective unvoiced cognates require execution of an additional laryngeal abduction gesture and are, thus, characterized by a more complex articulatory pattern. Apart from excursions of the mandible, the utterances ‘‘Rate’’ and ‘‘Ratte’’ involve—at the articulatory level—movements of the tongue only whereas coordination of lips, tongue body, and velum is required for the production of ‘‘Gram’’ and ‘‘Gramm.’’ As a rule, the various German vowels lack nasalization. Thus, an elevated velum must be expected during word-
VOWEL LENGTH IN ATAXIC DYSARTHRIA
105
FIG. 1—Continued
medial /a/ of the test stimuli. Subsequent transition from /a/ to /m/, then, involves the temporal adjustment of velum lowering and bilabial closure. In light of these suggestions, cerebellar dysfunctions seem to compromise durational parameters dependent upon the demands on speech motor coordination. Itoh, Sasanuma, and Ushijima (1979) observed enlarged variability of velar movements—determined by means of fiberoptic techniques—during speech in an AOS patient. Assuming a parallel disorder in AOS and ataxic dysarthria, increased variability of vowel duration in ‘‘Gram’’ utterances compared to ‘‘Rate’’ must be expected. Conceivably, thus, velar activity represents a critical articulatory event such as the devoicing gesture during production of unvoiced stop consonants which poses high demands on temporal control and would, thus, also be vulnerable to cerebellar disorders.
106
ACKERMANN ET AL.
Slowed orofacial gestures represent a salient feature of ataxic dysarthria (Kent & Netsell, 1975). Using an optoelectronic device, a previous study measured lower lip movements during production of a /pap/ sequence: apart from a single exception, all those cerebellar subjects—comparable in severity to the patients of the present study—presented with velocity/amplitude ratios outside the normal range (Ackermann, Hertrich, Daum, Scharf, & Spieker, 1997b). This mechanism cannot account for the observed tendency toward reduced vowel length of the produced ‘‘Gram’’ targets. Slowed articulatory gestures should rather give rise to lengthened vocalic segments. In addition to slowed articulatory performance a second pathomechanism must be assumed in ataxic dysarthria. Recent models conceptualize the cerebellum as an ‘‘internal clock’’ which provides temporal computations within the motor, perceptual, and cognitive domains (Keele & Ivry, 1990; Ivry, 1997). The reciprocal pathways connecting the frontal cortex with the contralateral cerebellar hemisphere might serve the neuroanatomical basis of a close interaction between anterior perisylvian language zones and cerebellum with respect to speech timing. The findings of the present study indicate, however, that these assumed cerebrocerebellar loops are, as a rule, only required for the control of movement patterns comprising the coordination of several distinct articulators. Besides motor control, Leiner, Leiner, and Dow (1993) discussed a contribution of the cerebellum to cognitive aspects of speech production. Functional imaging revealed activation of lateral aspects of the right cerebellar hemisphere during a verb generation task (Petersen, Fox, Posner, Mintun, & Raichle, 1989; Fiez & Raichle, 1997), and a patient with right-sided cerebellar infarction showed impaired performance under these conditions (Fiez, Petersen, Cheney, & Raichle, 1992). Furthermore, agrammatism in the absence of other cognitive impairments has been observed following a similar ischemic lesion (Silveri, Leggio, & Molinari, 1994). Rather than a cognitive deficit in terms of a phonological disorder, the observed abnormalities of the sound structure of the produced utterances seem to reflect disturbed articulatory processes. First, perceived errors were, as a rule, restricted to the substitution of unvoiced stops and long vowels by the respective voiced and short cognates. In case of a phonological disorder, the reverse would also be expected. Second, articulatory complexity determined the occurrence of impaired durational contrasts rather than phonemic criteria. The patients with early PD were unimpaired with respect to the various acoustic measures considered by the present study. In accordance with these findings, the mildly impaired PD subjects (stages I and II according to Hoehn & Yahr, 1967) studied by Lieberman and co-workers (1992) showed in a single instance only an overlap of the VOT of voiced and unvoiced stop consonant targets. Conceivably, disorders of phonetic timing depend upon later stages of PD. Under these conditions other transmitter systems than the dopaminergic pathways such as noradrenergic projections are also compro-
VOWEL LENGTH IN ATAXIC DYSARTHRIA
107
mised. It is noteworthy that two PD patients showed a shift in category boundary toward lowered values. It remains to be settled whether more advanced stages of the disease would show a higher frequency of this abnormality. REFERENCES Ackermann, H., & Hertrich, I. 1997. Voice onset time in ataxic dysarthria, Brain and Language, 56, 321–333. Ackermann, H., Gra¨ber, S., Hertrich, I., & Daum, I. 1997a. Categorical speech perception in cerebellar disorders. Brain and Language, 60, 323–331. Ackermann, H., Hertrich, I., Daum, I., Scharf, G., & Spieker, S. 1997b. Kinematic analysis of articulatory movements in central motor disorders. Movement Disorders, 12, 1019– 1027. Alexander, M. P., Benson, D. F., & Stuss, D. T. 1989. Frontal lobes and language. Brain and Language, 37, 656–691. Baum, S. R., Blumstein, S. E., Naeser, M. A., & Palumbo, C. L. 1990. Temporal dimensions of consonant and vowel production: An acoustic and CT scan analysis of aphasic speech. Brain and Language, 39, 33–56. Bauman, J., Wangler, H. H., & Prescott, T. 1975. Durational aspects of continuous speech: Comparative measurements based on vowel and consonant production by normal and apraxic speakers. Paper presented at the Annual Convention of the American Speech and Hearing Association, Washington, DC (cited in Collins et al., 1983). Blumstein, S. E., Cooper, W. E., Zurif, E. B., & Caramazza, A. 1977. The perception and production of voice-onset time in aphasia. Neuropsychologia, 15, 371–383. Blumstein, S. E., Cooper, W. E., Goodglass, H., Statlender, S., & Gottlieb, J. 1980. Production deficits in aphasia: A voice–onset time analysis. Brain and Language, 9, 153–170. Blumstein, S. E. 1988. Approaches to speech production deficits in aphasia. In F. Boller & J. Grafman (Eds.), Handbook of neuropsychology (Vol. 1, pp. 349–365). Amsterdam: Elsevier. Buckingham, H. W., Jr. 1991. Explanations for the concept of apraxia of speech. In T. Sarno (Ed.), Acquired aphasia (2nd ed., pp. 271–312). New York: Academic Press. Code, C., & Ball, M. 1982. Fricative production in Broca’s aphasia: A spectrographic analysis. Journal of Phonetics, 10, 325–331. Collins, M., Rosenbek, J. C., & Wertz, R. T. 1983. Spectrographic analysis of vowel and word duration in apraxia of speech. Journal of Speech and Hearing Research, 26, 224–230. Darley, F. L., Aronson, A. E., & Brown, J. R. 1975. Motor speech disorders. Philadelphia: Saunders. Daum, I., & Ackermann, H. 1997. Neuropsychological abnormalities in cerebellar syndromes: Fact of fiction? In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 455– 471). San Diego: Academic Press. (International Review of Neurobiology, 41) Dronkers, N. F. 1996. A new brain region for coordinating speech articulation. Nature, 384, 159–161. Duffy, J. R., & Gawle, C. A. 1984. Apraxic speakers’ vowel duration in consonant–vowel– consonant syllables. In J. C. Rosenbek, M. R. McNeil & A. E. Aronson (Eds.), Apraxia of speech: Physiology, acoustics, linguistics, management (pp. 167–196). San Diego: College–Hill. Fiez, J. A., Petersen, S. E., Cheney, M. K., & Raichle, M. E. 1992. Impaired non-motor learning
108
ACKERMANN ET AL.
and error detection associated with cerebellar damage: A single case study. Brain, 115, 155–178. Fiez, J. A., & Raichle, M. E. 1997. Linguistic processing. In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 233–254). San Diego: Academic Press. (International Review of Neurobiology, 41) Freeman, F. J., Sands, E. S., & Harris, K. S. 1978. Temporal coordination of phonation and articulation in a case of verbal apraxia: A voice onset time study. Brain and Language, 6, 106–111. Gandour, J., & Dardarananda, R. 1984. Prosodic disturbance in aphasia: Vowel length in Thai. Brain and Language, 23, 206–224. Gibb, W. R., & Lees, A. J. 1989. The significance of the Lewy body in the diagnosis of idiopathic Parkinson’s disease. Neuropathology and Applied Neurobiology, 15, 27–44. Haag, W. K. 1979. An articulatory experiment on voice onset time in German stop consonants. Phonetica, 36, 169–181. Harding, A. E. 1984. The hereditary ataxias and related disorders. Edinburgh: Churchill Livingstone. Harmes, S., Daniloff, R. G., Hoffman, P. R., Lewis, J., Kramer, M. B., & Absher, R. 1984. Temporal and articulatory control of fricative articulation by speakers with Broca’s aphasia. Journal of Phonetics, 12, 367–385. Hertrich, I., & Ackermann, H. 1994. Acoustic analysis of speech timing in Huntington’s disease. Brain and Language, 47, 182–196. Hertrich, I., & Ackermann, H. 1997. Articulatory control of phonological vowel length contrasts: Kinematic analysis of labial gestures. Journal of the Acoustical Society of America, 102, 523–536. Hoehn, M. M., & Yahr, M. D. 1967. Parkinsonism: Onset, progression, and mortality. Neurology, 17, 427–442. Hoit-Dalgaard, J., Murry, T., & Kopp, H. G. 1983. Voice onset time production and perception in apraxic subjects. Brain and Language, 20, 329–339. Itoh, M., Sasanuma, S., & Ushijima, T. 1979. Velar movements during speech in a patient with apraxia of speech. Brain and Language, 7, 227–239. Itoh, M., Sasanuma, S., Tatsumi, I. F., Murakami, S., Fukusako, Y., & Suzuki, T. 1982. Voice onset time characteristics in apraxia of speech. Brain and Language, 17, 193–210. Ivry, R. 1997. Cerebellar timing systems. In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 555–573). San Diego: Academic Press. (International Review of Neurobiology, 41) Jessen, M. 1993. Stress conditions on vowel quality and quantity in German. Working Papers of the Cornell Phonetics Laboratory, 8, 1–27. Keele, S. W., & Ivry, R. Y. 1990. Does the cerebellum provide a common computation for diverse tasks? A timing hypothesis. In A. Diamond (Ed.), The development and neural bases of higher cognitive functions (pp. 179–211). New York: New York Academy of Sciences (Annals of the New York Academy of Sciences, 608) Keller, E. 1990. Speech motor timing. In W. J. Hardcastle & A. Marchal (Eds.), Speech production and speech modelling (pp. 343–364). Dordrecht: Kluwer. Kent, R. D., & Netsell, R. 1975. A case study of an ataxic dysarthric: Cineradiographic and spectrographic observations. Journal of Speech and Hearing Disorders, 40, 115–134. Kent, R. D., & Rosenbek, J. C. 1983. Acoustic patterns of apraxia of speech. Journal of Speech and Hearing Research, 26, 231–249. Kertesz, A. 1984. Subcortical lesions and verbal apraxia. In J. C. Rosenbek, M. R. McNeil &
VOWEL LENGTH IN ATAXIC DYSARTHRIA
109
A. E. Aronson (Eds.), Apraxia of speech: Physiology, acoustics, linguistics, management (pp. 73–90). San Diego: College-Hill. Klatt, D. H. 1976. Linguistic uses of segmental duration in English: Acoustic and perceptual evidence. Journal of the Acoustical Society of America, 59, 1208–1221. Leiner, H. C., Leiner, A. L., & Dow, R. S. 1993. Cognitive and language functions of the human cerebellum. Trends in Neurosciences, 16, 444–447. Lieberman, P., Kako, E., Friedman, J., Tajchman, G., Feldman, L. S., & Jiminez, E. B. 1992. Speech production, syntax comprehension, and cognitive deficits in Parkinson’s disease. Brain and Language, 43, 169–189. Lisker, L., & Abramson, A. S. 1964. A cross-language study of voicing in initial stops: Acoustical measurements. Word, 20, 384–422. Lisker, L., & Abramson, A. S. 1967. Some effects of context on voice onset time in English stops. Language and Speech, 10, 1–28. Petersen, S. E., Fox, P. T., Posner, M. I., Mintun, M., & Raichle, M. E. 1989. Positron emission tomographic studies of the processing of single words. Journal of Cognitive Neuroscience, 1, 153–170. Ryalls, J. H. 1986. An acoustic study of vowel production in aphasia. Brain and Language, 29, 48–67. Silveri, M. C., Leggio, M. G., & Molinari, M. 1994. The cerebellum contributes to linguistic production: A case of agrammatic speech following a right cerebellar lesion. Neurology, 44, 2047–2050. Stock, D. 1971. Untersuchungen zur Stimmhaftigkeit hochdeutscher Phonemrealisationen. Hamburg: Buske. Tuller, B. 1984. On categorizing aphasic speech errors. Neuropsychologia, 22, 547–557. Ziegler, W., & von Cramon, D. 1986. Timing deficits in apraxia of speech. European Archives of Psychiatry and Neurological Sciences, 236, 44–49.
Phonemic Vowel Length Contrasts in Cerebellar Disorders Hermann Ackermann,* Susanne Gra¨ber,* Ingo Hertrich,* and Irene Daum† *Department of Neurology, University of Tu¨bingen, Tu¨bingen, and †Faculty of Psychology, University of Bochum, Bochum, Germany Apraxia of speech and Broca’s aphasia both affect voice onset time (VOT) whereas phonemic vowel length distinctions seem to be preserved. Assuming a close cooperation of anterior perisylvian language zones and the cerebellum with respect to speech timing, a similar profile of segment durations must be expected in ataxic dysarthria. In order to test this hypothesis, patients with cerebellar atrophy or cerebellar ischemia were asked to produce sentence utterances including either one of the German lexial items ‘‘Rate’’ (/ra:t he/, ‘installment’), ‘‘Ratte’’ (/rat he/, ‘rat’), ‘‘Gram’’ (/gra:m/, ‘grief’), ‘‘Gramm’’ (/gram/, ‘gramm’), ‘‘Taten’’ (/t hatn/, ‘actions’), or ‘‘Daten’’ (/datn/, ‘data’). At the acoustic signal, the duration of the target vowels /a/ and /a:/ as well as the VOT of the word-initial alveolar stops /d/ and /t/ were determined. In addition, a master tape comprising the target words from patients and controls in randomized order was played to three listeners for perceptual evaluation. In accordance with a previous study, first, the cerebellar subjects presented with a reduced categorical separation of the VOT of voiced and unvoiced stop consonants. Second, vowel length distinctions were only compromised in case of the minimal pair ‘‘Gram’’/‘‘Gramm.’’ In contrast to ‘‘Rate’’/‘‘Ratte’’, production of the former lexical items requires coordination of several orofacial structures. Disruption of vowel length contrasts would, thus, depend upon the complexity of the underlying articulatory pattern. 1999 Academic Press Key Words: vowel length; VOT; ataxic dysarthria; cerebellum; apraxia of speech.
INTRODUCTION
Voice onset time (VOT), i.e., the time lag between consonant burst and vowel onset, provides a critical contrast between voiced and voiceless stop consonants: the former have a shorter VOT than their unvoiced cognates or This study was supported by grants from the DFG (SFB 307) and the BMFT (01 KL9001 O). The authors thank Dr. M. M. Schugens and Dr. S. Spieker for critical discussion and helpful comments. Address correspondence and reprint requests to Hermann Ackermann, M. D., M. A., Department of Neurology, University of Tu¨bingen, Hoppe-Seyler-Strasse 3, D-72076 Tu¨bingen, Germany. Fax: (Germany) 7071-296507. 95 0093-934X/99 $30.00 Copyright 1999 by Academic Press All rights of reproduction in any form reserved.
96
ACKERMANN ET AL.
even present with a voicing lead, i.e., glottal vibrations prior to stop consonant release burst (Lisker & Abramson, 1964, 1967). For example, the VOT of /d/, as a rule, amounts to less than 20 ms at the initial position of isolated English words whereas the values of the respective /t/ productions exceed 30 ms. Similar data have been reported for German stop consonants (Stock, 1971; Haag, 1979; Ziegler & von Cramon, 1986). Broca’s aphasia and apraxia of speech (AOS)—syndromes which reflect damage to the inferior dorsolateral frontal lobe, the subjacent white matter, or the anterior insula (Alexander, Benson, & Stuss, 1989; Kertesz, 1984; Dronkers, 1996)—give rise to a significant overlap of the VOT of voiced and unvoiced stops (Blumstein, Cooper, Zurif, & Caramazza, 1977; Freeman, Sands, & Harris, 1978; Blumstein, Cooper, Goodglass, Statlender, & Gottlieb, 1980; Itoh, Sasanuma, Tatsumi, Murakami, Fukusako, & Suzuki, 1982; Hoit-Dalgaard, Murry, & Kopp, 1983; Tuller, 1984). A former study of our group revealed similar VOT patterns in patients with ataxic dysarthria due to cerebellar atrophy (Ackermann & Hertrich, 1997). Since reciprocal pathways connect the left frontal lobe with the contralateral cerebellar hemisphere, these data might indicate a close cooperation of these structures with respect to the specification of VOT. Besides VOT, a variety of other durational parameters of the acoustic signal serve phonological functions and, therefore, must be adequately controlled (Klatt, 1976). In English, e.g., the voicing contrast of syllable-final stop consonants is signaled by the preceding vowel length and syllable-initial voiced and voiceless fricatives differ in noise duration. Both reduced and increased absolute vowel durations were observed in patients with damage to the anterior perisylvian language zones (Duffy & Gawle, 1984; Bauman, Wangler, & Prescott, 1975; Collins, Rosenbek, & Wertz, 1983; Ryalls, 1986). As a rule, however, speech apraxics and Broca aphasics vary the length of vocalic segments as a function of the voicing characteristics of the following stop consonant, i.e., produce a similar durational contrast to that of normal speakers (Duffy & Gawle, 1984; Baum, Blumstein, Naeser, & Palumbo, 1990). Furthermore, these patients display an unimpaired distinction of noise segments in voiced and unvoiced frictives (Code & Ball, 1982; Kent & Rosenbek, 1983; Harmes, Daniloff, Hoffman, Lewis, Kramer, & Absher, 1984). Similar findings could be obtained from native Thai speakers presenting with nonfluent aphasia: the relative duration of phonologically short and long vowel targets was largely undistorted (Gandour & Dardarananda, 1984). Since both Broca’s aphasia and AOS compromise VOT in the presence of intact phonemic vowel length distinctions and since VOT may be considered an acoustic parameter of the temporal coordination of orofacial and laryngeal muscle activity during speech production (Keller, 1990), these syndromes seem to specifically disrupt the adjustment of phonatory and articulatory functions (Blumstein, 1988; Buckingham, 1991). Assuming a close interaction of the cerebellum and the anterior perisylvian
VOWEL LENGTH IN ATAXIC DYSARTHRIA
97
language zones with respect to the specification of VOT, the question arises whether ataxic dysarthria also spares vowel length contrasts. A native Thai speaker who suffered from a right-sided ischemic cerebellar lesion showed markedly prolonged vowel durations (Gandour & Dardarananda, 1984). Yet, the temporal relation of short and long vowel targets, i.e., the respective durational phonemic contrast, was revealed to be preserved. Comprehensive studies on vowel length distinctions in ataxic dysarthria are not yet available. In order to examine the influence of ataxic dysarthria on the duration of vocalic segments, native German speakers suffering from cerebellar atrophy or ischemia were asked to produce minimal pairs primarily differing in vowel length. Stimuli differing in voicing of the word-initial alveolar stop were included as well to allow for a comparison with previous findings on VOT in ataxic dysarthria (Ackermann & Hertrich, 1997). Subjects with Parkinson’s disease (PD) show an overlap of the VOT of voiced and unvoiced stops at syllable-initial position similar to the pattern observed in Broca’s aphasia (Lieberman, Kako, Friedman, Tajchman, Feldman, & Jiminez, 1992). These VOT disruptions were attributed to an impairment of striatal pathways acting on the prefrontal cortex. Thus, the implementation of VOT seems to depend on the basal ganglia as well. It is unknown whether these dysfunctions also compromise vowel length contrasts. Therefore, PD patients were examined in addition to the cerebellar subjects. Dysfunction of the dopaminergic pathways projecting from the substantia nigra to the striatum and/or the prefrontal cortex represents the core pathomechanism of PD. However, in later stages the disease process extends to other cerebral areas. In order to assess the contribution of a specific functional–neuroanatomic system, i.e., the dopaminergic nigrostriatal and -frontal pathways, to the adjustment of vowel length, early PD patients (stages I–II; Hoehn & Yahr, 1967) were considered. MATERIALS AND METHODS
Subjects The present investigation—part of a larger study involving the evaluation of speech perception and production in ataxic dysarthria—examined ten patients with cerebellar pathology (see Ackermann, Gra¨ber, Hertrich, & Daum, 1997a). Eight individuals (five males, three females; age 28–72 years; median, 62 years) showed diffuse atrophy of the cerebellum at magnetic resonance imaging (MRI). To a variable degree, all of them presented with ataxia of gait, dyscoordination of voluntary arm movements, oculomotor disorders, and speech difficulties; none had any clinical signs of extracerebellar motor dysfunctions. Transcranial magnetic stimulation of the motor cortex further confirmed the integrity of the corticospinal tracts to the distal arm and leg muscles. In addition, extensive investigations of blood serum and cerebrospinal fluid were unremarkable. Taken together, these findings warranted the diagnosis of an idiopathic cerebellar atrophy (IDCA; Harding, 1984). Two subjects (C04 and C02) had already participated in a previous study of ataxic dysarthria (patients CA5 and CA7; Ackermann et al., 1997a). Patient C04 showed a few small ischemic lesions within the periventricular white
98
ACKERMANN ET AL.
matter at MRI. In consideration of unremarkable neuropsychological tests and electrophysiological investigations, silent lacunar infarctions were assumed. MRI of the spinal cord revealed syringomyelia in subject C02. This disorder represents a distinct disease entity unrelated to the patient’s cerebellar pathology. The remaining IDCA patients did not show any evidence of extracerebellar pathology at MRI. Two participants of the present study suffered from an unilateral lesion: one subject (male, 27 years) underwent removal of nearly the complete left cerebellar hemisphere because of a tumor about 10 years before testing, the other patient (male, 69 years) had suffered right-sided cerebellar ischemia within the region of blood supply of the right superior cerebellar artery 5 years prior to the present investigation. Both these subjects had initially shown an unilateral ataxic syndrome which had improved during further follow-up. Nine PD patients participated in the present study (five males, four females; age 34–69 years; median, 57 years). Diagnosis was based on unilateral onset of symptomatology and the presence of two of the three signs, rest tremor, rigidity, and akinesia, as well as a significant response to L-dopa (Gibb & Lees, 1989). Disease duration extended from 2 to 6 years. Neuroleptic therapy prior to onset of the disease or during follow-up, a history of strokes, or pyramidal and/or ataxic signs at clinical examination were exclusion criteria. All subjects received L-dopa, a dopamine agonist, and a MAO-B inhibitor. A few patients were, in addition, treated with the new antiparkinsonian drug budipine. In subjects with motor fluctuations kinematic investigation was performed during the off-phase. On the basis of clinical findings, five patients were assigned to stage I and four to stage II according to the scale of Hoehn and Yahr (1967). These early levels of PD reflect a relatively selective dopaminergic deficit. All cerebellar and PD patients were fully able to cooperate. Neuropsychological screening, including a short version of the Wechsler Adult Intelligence Scale as well as tests of memory and so-called frontal lobe functions, revealed unimpaired performance in all clinical subjects (see Daum & Ackermann, 1997). Thus, incipient or overt dementia could be ruled out. Furthermore, clinical examination did not yield any indications of emotional disturbances. Using the dysarthric dimensions introduced by Darley, Aronson, and Brown (1975), one of the authors (I.H.) performed a perceptual evaluation of the recorded test materials and samples of spontaneous speech prior to acoustic analysis. All cerebellar subjects showed— to a varying degree—articulatory impreciseness in terms of either reduced consonant clusters, incomplete occlusions, voicing errors or distorted (centralized) vowels. Perceived /d/ in case of a /t/ target most often occurred in patient C01. Six of the 10 cerebellar individuals (C01, C02, C05, C06, C09, C10) showed a slight to moderate decrease of speech tempo. Besides lengthened words, prolonged interword pauses contributed to these perceived abnormalities. Markedly reduced speech rate, concomitant with ‘‘scanning’’ rhythm, was noted in subject C03. Apart from a single individual (C04), all ataxic dysarthrics presented with harsh and/ or breathy voice quality. As concerns the PD patients, two individuals showed a tendency toward rather accelerated speech rate concomitant with incomplete stop occlusions (P06 and P07). Articulatory performance was unremarkable in the remaining cases. Seven of the PD subjects had breathy and/or harsh voice quality, with reduced voice volume in three instances. Five male and four female subjects (age 30–72 years; median, 61 years) who did not have a history of neurological or psychiatric disorders served as control group.
Speech Material Two minimal pairs differing in the duration of the vowel ‘‘a’’ were considered for analysis: ‘‘Ratte’’ (/rat he/, ‘rat’) and ‘‘Rate’’ (/ra:t he/, ‘installment’) as well as ‘‘Gramm’’ (/gram/, ‘gram’) and ‘‘Gram’’ (/gra:m/, ‘grief’). These stimuli represent German lexical items. In case of the bisyllabic units, the vowels /a/ and /a:/ bear the word stress. Indeed, formant measurements revealed some short vowels of standard German to be more centralized (diphthongized) than their long cognates, and these effects even may outweigh durational contrasts (Jessen,
VOWEL LENGTH IN ATAXIC DYSARTHRIA
99
1993). Nevertheless, duration does represent the strongest acoustic correlate of the short/long distinction of the German vowels /a/ and /a:/ in a stressed position (Hertrich & Ackermann, 1997). In order to compare the effects of cerebellar dysfunctions on vowel length contrasts and VOT, the German nouns ‘‘Daten’’ (/da:tn/, ‘data’) and ‘‘Taten’’ (/t ha:tn/, ‘deeds’) were also included. As a rule, the German stop /t/, when produced in vowel context, represents an aspirated and voiceless sound with /d/ as its voiced cognate. Usually, the latter consonant is not produced with voicing lead, i.e., glottal vibrations preceding burst release, in southern German dialects. Word stress is located on the first syllable of the target word, i.e., ‘‘da’’ and ‘‘ta,’’ respectively.
Recording Procedure The stimuli were printed in bold large letters on separate cards and presented by the experimenter five times each in a quasi-randomized order. Subjects had to produce the visually displayed target embedded into the carrier phrase ‘‘Ich habe . . . gelesen’’ (‘‘I have read . . .’’). Since the testing session also included a range of other neuropsychological tests, the production task was restricted to only five repetitions of each stimulus in order to avoid fatigue effects. Speech examination took place in a sound-treated room using a DAT recorder (JVC XD Z505) and a condenser microphone (Sennheiser, ME62). The mouth-microphone distance amounted to about 20 cm. Prior to analysis, the recordings were bandpass filtered (50–8000 Hz), digitized at a sampling rate of 20 kHz, and stored on a personal computer (486 IBM compatible).
Perceptual Evaluation A master tape was generated for perceptual evaluation of the stimuli obtained from the patients and their controls. The recorded utterances were combined to a single sequence, randomized across groups but blocked by individual. Prior to this procedure, one of the authors (I.H.) checked the recordings with respect to dysfluencies such as iterations or audible inspirations, incomplete stop consonant production, and devoicing of vocalic intervals. Two utterances (‘‘Gram’’, ‘‘Gramm’’) of a control speaker were discarded from further analysis because of misspelling with following self-correction (e.g., ‘‘Gramm . . . a¨h . . . Gram’’). Three certified speech pathologists, unacquainted with the patients and the controls, rated the items which were presented by a loudspeaker adjusted to comfortable loudness. As a measure of perceived vowel length and voicing contrasts, the frequency of misassignments was calculated, e.g., the number of long vowel targets classified as the respective short cognate and vice versa. The number of judgments for each item amounted to n ⫽ 15 (3 raters ⫻ 5 repetitions). When, thus, one of the three experts misclassifies a single target, error frequency equals 6.6% (1/15). Perceptual evaluation of the recordings yielded an interrater reliability of the three speech pathologists of 86% (Cohen’s κ ⫽ 0.86, chance ⫽ 50%).
Acoustic Measurements Vowel duration was determined from the onset of periodic energy to the change in waveform associated with the initiation of the word-final bilabial nasal in ‘‘Gram’’/‘‘Gramm’’ or vowel offset in ‘‘Ratte’’/‘‘Rate’’. In accordance with the definition of Lisker and Abramson (1964), VOT of the initial alveolar stop of the target words ‘‘Daten’’ and ‘‘Taten’’ was defined as the time interval between the beginning of the burst and vowel onset (see Ackermann & Hertrich, 1997). A former investigation using similar recording and signal analysis procedures had deter-
100
ACKERMANN ET AL.
mined reliability measures with respect to VOT (Hertrich & Ackermann, 1994): Patients with Huntington’s chorea and control speakers showed a similar error magnitude (VOT measurement error in normals ⫽ 2.3 ms; VOT measurement error in patients with Huntington’s chorea ⫽ 2.1 ms; error of vowel duration ⬍ 4 ms).
RESULTS
Perceptual Data Table 1 (second and fifth columns) illustrates the results of the identification task in terms of the number of misassignments, i.e., the percentage of items which are perceived as the cognate of the visually displayed stimulus. Only a few utterances obtained from the controls and the PD patients were incorrectly classified with respect to the voicing and vowel length characteristics of the respective target: two of the three raters misidentified the same ‘‘Daten’’ target of a PD subject; in all other instances, a single speech pathologist incorrectly classified one token each. Compared to the maximum error frequency in the control group, four cerebellar subjects showed an increased number of misassignments of ‘‘Taten’’ and ‘‘Gram’’ targets whereas erroneous classification of short vowel targets occurred in a single repetition only (target ‘‘Gramm’’ from subject C03). At the perceptual level, a subgroup of the cerebellar patients, thus, had a tendency to shorten the VOT of unvoiced stops and to reduce the duration of long vowel targets, predominantly in case of ‘‘Gram’’ utterances. Acoustic Data Figure 1 shows the distribution of the individual measurements of VOT and vowel length separately for each participant. The control group exhibited a clear-cut segregation of the voiced and unvoiced targets across all speakers at about 40 ms, i.e., all /t/ productions had a VOT above and the respective voiced stops below this value. With respect to the minimal pairs ‘‘Gram’’/ ‘‘Gramm’’ and ‘‘Rate’’/‘‘Ratte’’ a similar strict distinction at 120 and 140 ms, respectively, was observed. The data plots of two of the three minimal pairs obtained from the cerebellar group revealed compromised category boundaries in about half of the subjects. As concerns ‘‘Taten’’/‘‘Daten’’, five patients (C02, C03, C05, C09, C10) showed an overlap of the produced /d/ and /t/ targets and a single one (C01) a complete assimilation of the unvoiced cognate to the voiced one. Furthermore, five individuals presented—as compared to the controls—with a disruption of the category boundary of the ‘‘Gram’’ and ‘‘Gramm’’ targets (C03, C04, C05, C06, C09). Apart from patients C06 and C10, all cerebellar subjects maintained the category boundary of ‘‘Rate’’/‘‘Ratte.’’ The various phonemic durational contrasts were rather well preserved within the PD group. A single patient each produced the long vowel targets ‘‘Rate’’ and ‘‘Gram,’’ respectively, with a vowel length largely below the
TABLE 1 Perceptual and Acoustic Data Obtained from Patients with Cerebellar Atrophy (C01–C10), Parkinson’s Disease (PD), and Control Subjects A. Minimal pair ‘‘Daten’’/‘‘Taten’’: VOT VOT/d/ VOT/t/ Err/d/ (%)
Mean (ms)
SD
Err/t/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 0.0 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 20.0 PD subjects (N ⫽ 9) Min 0.0 Max 13.2 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 0.0 Mean — SD —
29.9 17.5 27.0 14.9 46.0 29.7 22.5 21.8 36.1 74.1
2.0 2.7 6.8 2.1 23.2 6.5 3.6 5.2 29.6 51.9
53.4 20.0 0.0 0.0 0.0 6.6 0.0 0.0 40.0 0.0
30.4 53.5 198.0 59.2 63.4 104.1 89.4 72.8 48.7 140.5
5.6 40.5 21.0 6.1 23.0 38.6 18.6 19.6 19.2 44.1
0.19 a 6.82 2.28 a 17.18 17.37 1.21 a 5.11 a 11.13 1.18 a 2.34 a
15.5 34.5 24.4 5.1
1.6 9.8 4.4 2.6
0.0 6.6 — —
52.5 111.9 79.4 20.3
4.5 15.6 10.3 5.0
5.67 20.91 12.37 5.24
15.2 28.2 21.7 5.1
1.4 6.5 3.6 2.0
0.0 0.0 — —
49.2 88.5 74.5 12.9
2.8 22.9 10.7 6.1
5.49 24.04 14.15 6.52
Sub
B. Minimal pair ‘‘Gramm’’/‘‘Gram’’: Vowel length Vowel/a/ Vowel/a:/ Err/a/ (%)
Mean (ms)
SD
Err/a:/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 13.2 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 0.0 PD subjects (N ⫽ 9) Min 0.0 Max 0.0 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD —
74.6 63.6 121.4 53.8 82.3 62.4 49.0 68.9 91.7 61.4
9.5 2.7 3.1 7.1 12.7 8.9 6.9 15.4 26.7 17.1
0.0 0.0 0.0 86.6 60.0 13.2 0.0 0.0 20.0 0.0
195.3 249.5 215.7 81.8 169.2 107.1 183.8 152.8 186.9 219.3
12.2 49.9 43.4 10.2 95.9 25.7 41.6 14.5 84.2 40.2
15.61 6.16 a 4.08 a 5.10 a 2.33 a 4.25 a 10.37 6.69 a 2.27 a 8.75
35.5 91.3 72.0 16.0
3.0 30.6 11.8 8.1
0.0 0.0 — —
106.9 250.8 180.1 47.4
6.8 34.0 18.4 10.2
5.07 20.33 12.54 4.62
58.5 98.1 74.3 13.0
7.2 18.5 11.2 3.5
0.0 6.6 — —
145.2 233.6 197.2 30.3
9.4 78.6 27.7 22.2
7.01 20.44 11.76 4.59
Sub
102
ACKERMANN ET AL.
TABLE 1—Continued C. Minimal pair ‘‘Ratte’’/‘‘Rate’’: Vowel length Vowel/a/ Vowel/a:/ Err/a/ (%)
Mean (ms)
SD
Err/a:/ (%)
Mean (ms)
SD
t value
C01 0.0 C02 0.0 C03 0.0 C04 0.0 C05 0.0 C06 0.0 C07 0.0 C08 0.0 C09 0.0 C10 0.0 PD subjects (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD — Controls (N ⫽ 9) Min 0.0 Max 6.6 Mean — SD —
75.3 97.8 102.4 86.6 88.7 61.2 56.9 88.4 109.2 95.3
7.1 15.7 12.4 8.4 21.8 10.3 5.6 11.1 10.1 22.7
0.0 0.0 0.0 0.0 0.0 40.0 0.0 0.0 0.0 20.0
170.5 353.5 272.9 159.1 217.8 69.3 193.7 172.0 190.6 179.2
14.1 54.2 52.2 2.6 38.9 10.1 24.1 9.1 23.3 50.6
14.46 13.45 9.40 12.25 6.64 1.24 a 17.40 10.8 7.93 3.23 a
67.0 113.6 82.0 13.7
5.0 13.1 8.4 2.4
0.0 0.0 — —
129.1 257.7 187.0 44.3
6.1 20.2 13.0 4.4
7.50 27.19 15.65 7.13
63.3 108.1 79.4 12.3
5.0 28.1 11.4 8.6
0.0 0.0 — —
151.8 215.7 186.5 21.8
9.2 30.4 18.3 7.5
5.01 25.49 12.91 6.46
Sub
Note. Err/d/ (Err/t/), /d/ targets (/t/ targets) perceived as /t/ targets (/d/ targets) in percentage of evaluated stimuli (n ⫽ 15 judgments, 3 raters ⫻ 5 repetitions); Err/a/ (Err/a:/), /a/ targets (/a:/ targets) perceived as /a:/ targets (/a/ targets) in percentage of evaluated stimuli (n ⫽ 15); Mean (columns), individual mean across five repetitions; Mean (rows), group means; SD, standard deviation; Min (Max), lower (upper) limit of the respective range. a Below normal range.
category boundary of the normal speakers (‘‘Gram,’’ patient No. 6; ‘‘Rate,’’ patient No. 4). It is noteworthy, however, that both these subjects did not show an overlap of the durations of the short and long targets. Rather, a shift of the boundary toward a lower value characterizes these individuals. As a quantitative estimate of the segregation of the minimal pair targets, the t values of the acoustic measures were calculated (Table 1). In short, the t value relates the difference of two means to their standard errors. Given an approximately equal number of repetitions for all comparisons, the t values, therefore, can be considered a measure of the distinctness of two classes of items. Using these data, statistical analysis revealed a significant difference between cerebellar and control groups for the minimal pairs ‘‘Taten’’/‘‘Daten’’ (p ⫽ .021) and ‘‘Gram’’/‘‘Gramm’’ (p ⫽ .018). All other betweengroup comparisons did not reach the 5% level.
VOWEL LENGTH IN ATAXIC DYSARTHRIA
103
FIG. 1. Scattergrams of vowel length (‘‘Gram’’/‘‘Gramm’’; ‘‘Rate’’/‘‘Ratte’’) and VOT measurements (‘‘Taten’’/‘‘Daten’’) in the cerebellar group (CERE), subjects with Parkinson’s disease (PD) and normal speakers (NC). Since only five repetitions per stimulus were obtained, the frequently used display of the number of tokens (ordinate) versus durational parameters (abscissa) did not seem to be feasible.
COMMENTS
In accordance with a previous investigation (Ackermann & Hertrich, 1997), the cerebellar patients, first, showed impaired voicing contrasts. Second, both visual inspection of the distributional patterns and calculation of a quantitative estimate of the respective category boundaries indicate a differential influence of cerebellar disorders on the two vowel length contrasts studied: whereas the minimal pair ‘‘Gram/Gramm’’ revealed to be compro-
104
ACKERMANN ET AL.
FIG. 1—Continued
mised as well, the segregation of the targets ‘‘Rate’’ and ‘‘Ratte’’ was largely undisturbed. The reduced distinction between voiced and unvoiced word-initial alveolar stops observed in ataxic dysarthria predominantly reflects disruption of long-lag VOT (Ackermann & Hertrich, 1997). Compared to voiced stops, the respective unvoiced cognates require execution of an additional laryngeal abduction gesture and are, thus, characterized by a more complex articulatory pattern. Apart from excursions of the mandible, the utterances ‘‘Rate’’ and ‘‘Ratte’’ involve—at the articulatory level—movements of the tongue only whereas coordination of lips, tongue body, and velum is required for the production of ‘‘Gram’’ and ‘‘Gramm.’’ As a rule, the various German vowels lack nasalization. Thus, an elevated velum must be expected during word-
VOWEL LENGTH IN ATAXIC DYSARTHRIA
105
FIG. 1—Continued
medial /a/ of the test stimuli. Subsequent transition from /a/ to /m/, then, involves the temporal adjustment of velum lowering and bilabial closure. In light of these suggestions, cerebellar dysfunctions seem to compromise durational parameters dependent upon the demands on speech motor coordination. Itoh, Sasanuma, and Ushijima (1979) observed enlarged variability of velar movements—determined by means of fiberoptic techniques—during speech in an AOS patient. Assuming a parallel disorder in AOS and ataxic dysarthria, increased variability of vowel duration in ‘‘Gram’’ utterances compared to ‘‘Rate’’ must be expected. Conceivably, thus, velar activity represents a critical articulatory event such as the devoicing gesture during production of unvoiced stop consonants which poses high demands on temporal control and would, thus, also be vulnerable to cerebellar disorders.
106
ACKERMANN ET AL.
Slowed orofacial gestures represent a salient feature of ataxic dysarthria (Kent & Netsell, 1975). Using an optoelectronic device, a previous study measured lower lip movements during production of a /pap/ sequence: apart from a single exception, all those cerebellar subjects—comparable in severity to the patients of the present study—presented with velocity/amplitude ratios outside the normal range (Ackermann, Hertrich, Daum, Scharf, & Spieker, 1997b). This mechanism cannot account for the observed tendency toward reduced vowel length of the produced ‘‘Gram’’ targets. Slowed articulatory gestures should rather give rise to lengthened vocalic segments. In addition to slowed articulatory performance a second pathomechanism must be assumed in ataxic dysarthria. Recent models conceptualize the cerebellum as an ‘‘internal clock’’ which provides temporal computations within the motor, perceptual, and cognitive domains (Keele & Ivry, 1990; Ivry, 1997). The reciprocal pathways connecting the frontal cortex with the contralateral cerebellar hemisphere might serve the neuroanatomical basis of a close interaction between anterior perisylvian language zones and cerebellum with respect to speech timing. The findings of the present study indicate, however, that these assumed cerebrocerebellar loops are, as a rule, only required for the control of movement patterns comprising the coordination of several distinct articulators. Besides motor control, Leiner, Leiner, and Dow (1993) discussed a contribution of the cerebellum to cognitive aspects of speech production. Functional imaging revealed activation of lateral aspects of the right cerebellar hemisphere during a verb generation task (Petersen, Fox, Posner, Mintun, & Raichle, 1989; Fiez & Raichle, 1997), and a patient with right-sided cerebellar infarction showed impaired performance under these conditions (Fiez, Petersen, Cheney, & Raichle, 1992). Furthermore, agrammatism in the absence of other cognitive impairments has been observed following a similar ischemic lesion (Silveri, Leggio, & Molinari, 1994). Rather than a cognitive deficit in terms of a phonological disorder, the observed abnormalities of the sound structure of the produced utterances seem to reflect disturbed articulatory processes. First, perceived errors were, as a rule, restricted to the substitution of unvoiced stops and long vowels by the respective voiced and short cognates. In case of a phonological disorder, the reverse would also be expected. Second, articulatory complexity determined the occurrence of impaired durational contrasts rather than phonemic criteria. The patients with early PD were unimpaired with respect to the various acoustic measures considered by the present study. In accordance with these findings, the mildly impaired PD subjects (stages I and II according to Hoehn & Yahr, 1967) studied by Lieberman and co-workers (1992) showed in a single instance only an overlap of the VOT of voiced and unvoiced stop consonant targets. Conceivably, disorders of phonetic timing depend upon later stages of PD. Under these conditions other transmitter systems than the dopaminergic pathways such as noradrenergic projections are also compro-
VOWEL LENGTH IN ATAXIC DYSARTHRIA
107
mised. It is noteworthy that two PD patients showed a shift in category boundary toward lowered values. It remains to be settled whether more advanced stages of the disease would show a higher frequency of this abnormality. REFERENCES Ackermann, H., & Hertrich, I. 1997. Voice onset time in ataxic dysarthria, Brain and Language, 56, 321–333. Ackermann, H., Gra¨ber, S., Hertrich, I., & Daum, I. 1997a. Categorical speech perception in cerebellar disorders. Brain and Language, 60, 323–331. Ackermann, H., Hertrich, I., Daum, I., Scharf, G., & Spieker, S. 1997b. Kinematic analysis of articulatory movements in central motor disorders. Movement Disorders, 12, 1019– 1027. Alexander, M. P., Benson, D. F., & Stuss, D. T. 1989. Frontal lobes and language. Brain and Language, 37, 656–691. Baum, S. R., Blumstein, S. E., Naeser, M. A., & Palumbo, C. L. 1990. Temporal dimensions of consonant and vowel production: An acoustic and CT scan analysis of aphasic speech. Brain and Language, 39, 33–56. Bauman, J., Wangler, H. H., & Prescott, T. 1975. Durational aspects of continuous speech: Comparative measurements based on vowel and consonant production by normal and apraxic speakers. Paper presented at the Annual Convention of the American Speech and Hearing Association, Washington, DC (cited in Collins et al., 1983). Blumstein, S. E., Cooper, W. E., Zurif, E. B., & Caramazza, A. 1977. The perception and production of voice-onset time in aphasia. Neuropsychologia, 15, 371–383. Blumstein, S. E., Cooper, W. E., Goodglass, H., Statlender, S., & Gottlieb, J. 1980. Production deficits in aphasia: A voice–onset time analysis. Brain and Language, 9, 153–170. Blumstein, S. E. 1988. Approaches to speech production deficits in aphasia. In F. Boller & J. Grafman (Eds.), Handbook of neuropsychology (Vol. 1, pp. 349–365). Amsterdam: Elsevier. Buckingham, H. W., Jr. 1991. Explanations for the concept of apraxia of speech. In T. Sarno (Ed.), Acquired aphasia (2nd ed., pp. 271–312). New York: Academic Press. Code, C., & Ball, M. 1982. Fricative production in Broca’s aphasia: A spectrographic analysis. Journal of Phonetics, 10, 325–331. Collins, M., Rosenbek, J. C., & Wertz, R. T. 1983. Spectrographic analysis of vowel and word duration in apraxia of speech. Journal of Speech and Hearing Research, 26, 224–230. Darley, F. L., Aronson, A. E., & Brown, J. R. 1975. Motor speech disorders. Philadelphia: Saunders. Daum, I., & Ackermann, H. 1997. Neuropsychological abnormalities in cerebellar syndromes: Fact of fiction? In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 455– 471). San Diego: Academic Press. (International Review of Neurobiology, 41) Dronkers, N. F. 1996. A new brain region for coordinating speech articulation. Nature, 384, 159–161. Duffy, J. R., & Gawle, C. A. 1984. Apraxic speakers’ vowel duration in consonant–vowel– consonant syllables. In J. C. Rosenbek, M. R. McNeil & A. E. Aronson (Eds.), Apraxia of speech: Physiology, acoustics, linguistics, management (pp. 167–196). San Diego: College–Hill. Fiez, J. A., Petersen, S. E., Cheney, M. K., & Raichle, M. E. 1992. Impaired non-motor learning
108
ACKERMANN ET AL.
and error detection associated with cerebellar damage: A single case study. Brain, 115, 155–178. Fiez, J. A., & Raichle, M. E. 1997. Linguistic processing. In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 233–254). San Diego: Academic Press. (International Review of Neurobiology, 41) Freeman, F. J., Sands, E. S., & Harris, K. S. 1978. Temporal coordination of phonation and articulation in a case of verbal apraxia: A voice onset time study. Brain and Language, 6, 106–111. Gandour, J., & Dardarananda, R. 1984. Prosodic disturbance in aphasia: Vowel length in Thai. Brain and Language, 23, 206–224. Gibb, W. R., & Lees, A. J. 1989. The significance of the Lewy body in the diagnosis of idiopathic Parkinson’s disease. Neuropathology and Applied Neurobiology, 15, 27–44. Haag, W. K. 1979. An articulatory experiment on voice onset time in German stop consonants. Phonetica, 36, 169–181. Harding, A. E. 1984. The hereditary ataxias and related disorders. Edinburgh: Churchill Livingstone. Harmes, S., Daniloff, R. G., Hoffman, P. R., Lewis, J., Kramer, M. B., & Absher, R. 1984. Temporal and articulatory control of fricative articulation by speakers with Broca’s aphasia. Journal of Phonetics, 12, 367–385. Hertrich, I., & Ackermann, H. 1994. Acoustic analysis of speech timing in Huntington’s disease. Brain and Language, 47, 182–196. Hertrich, I., & Ackermann, H. 1997. Articulatory control of phonological vowel length contrasts: Kinematic analysis of labial gestures. Journal of the Acoustical Society of America, 102, 523–536. Hoehn, M. M., & Yahr, M. D. 1967. Parkinsonism: Onset, progression, and mortality. Neurology, 17, 427–442. Hoit-Dalgaard, J., Murry, T., & Kopp, H. G. 1983. Voice onset time production and perception in apraxic subjects. Brain and Language, 20, 329–339. Itoh, M., Sasanuma, S., & Ushijima, T. 1979. Velar movements during speech in a patient with apraxia of speech. Brain and Language, 7, 227–239. Itoh, M., Sasanuma, S., Tatsumi, I. F., Murakami, S., Fukusako, Y., & Suzuki, T. 1982. Voice onset time characteristics in apraxia of speech. Brain and Language, 17, 193–210. Ivry, R. 1997. Cerebellar timing systems. In J. D. Schmahmann (Ed.), The cerebellum and cognition (pp. 555–573). San Diego: Academic Press. (International Review of Neurobiology, 41) Jessen, M. 1993. Stress conditions on vowel quality and quantity in German. Working Papers of the Cornell Phonetics Laboratory, 8, 1–27. Keele, S. W., & Ivry, R. Y. 1990. Does the cerebellum provide a common computation for diverse tasks? A timing hypothesis. In A. Diamond (Ed.), The development and neural bases of higher cognitive functions (pp. 179–211). New York: New York Academy of Sciences (Annals of the New York Academy of Sciences, 608) Keller, E. 1990. Speech motor timing. In W. J. Hardcastle & A. Marchal (Eds.), Speech production and speech modelling (pp. 343–364). Dordrecht: Kluwer. Kent, R. D., & Netsell, R. 1975. A case study of an ataxic dysarthric: Cineradiographic and spectrographic observations. Journal of Speech and Hearing Disorders, 40, 115–134. Kent, R. D., & Rosenbek, J. C. 1983. Acoustic patterns of apraxia of speech. Journal of Speech and Hearing Research, 26, 231–249. Kertesz, A. 1984. Subcortical lesions and verbal apraxia. In J. C. Rosenbek, M. R. McNeil &
VOWEL LENGTH IN ATAXIC DYSARTHRIA
109
A. E. Aronson (Eds.), Apraxia of speech: Physiology, acoustics, linguistics, management (pp. 73–90). San Diego: College-Hill. Klatt, D. H. 1976. Linguistic uses of segmental duration in English: Acoustic and perceptual evidence. Journal of the Acoustical Society of America, 59, 1208–1221. Leiner, H. C., Leiner, A. L., & Dow, R. S. 1993. Cognitive and language functions of the human cerebellum. Trends in Neurosciences, 16, 444–447. Lieberman, P., Kako, E., Friedman, J., Tajchman, G., Feldman, L. S., & Jiminez, E. B. 1992. Speech production, syntax comprehension, and cognitive deficits in Parkinson’s disease. Brain and Language, 43, 169–189. Lisker, L., & Abramson, A. S. 1964. A cross-language study of voicing in initial stops: Acoustical measurements. Word, 20, 384–422. Lisker, L., & Abramson, A. S. 1967. Some effects of context on voice onset time in English stops. Language and Speech, 10, 1–28. Petersen, S. E., Fox, P. T., Posner, M. I., Mintun, M., & Raichle, M. E. 1989. Positron emission tomographic studies of the processing of single words. Journal of Cognitive Neuroscience, 1, 153–170. Ryalls, J. H. 1986. An acoustic study of vowel production in aphasia. Brain and Language, 29, 48–67. Silveri, M. C., Leggio, M. G., & Molinari, M. 1994. The cerebellum contributes to linguistic production: A case of agrammatic speech following a right cerebellar lesion. Neurology, 44, 2047–2050. Stock, D. 1971. Untersuchungen zur Stimmhaftigkeit hochdeutscher Phonemrealisationen. Hamburg: Buske. Tuller, B. 1984. On categorizing aphasic speech errors. Neuropsychologia, 22, 547–557. Ziegler, W., & von Cramon, D. 1986. Timing deficits in apraxia of speech. European Archives of Psychiatry and Neurological Sciences, 236, 44–49.