BRAIN

AND

LANGUAGE

39, 33-56 (1990)

Temporal Dimensions of Consonant and Vowel Production: An Acoustic and CT Scan Analysis of Aphasic Speech SHARI

R. BAUM,*‘$ SHEILA E. BLUM.STEIN,*‘? MARGARET A. NAESER,?§ AND CAROLE L. PALUMBO?,§

*Depurtment of Cognitive and Linguistic Sciences, Brown University; tAphasia Research Center, VA Medical Center, SSchool of Human Communication Disorders, McGill University; and BDepartment of Neurology, Boston University School of Medicine

This study explored a number of temporal (durational) parameters of consonant and vowel production in order to determine whether the speech production impairments of aphasics are the result of the same or different underlying mechanisms and in particular whether they implicate deficits that are primarily phonetic or phonological in nature. Detailed analyses of CT scan lesion data were also conducted to explore whether more specific neuroanatomical correlations could be made with speech production deficits. A series of acoustic analyses were conducted including voice-onset time, intrinsic and contrastive fricative duration, and intrinsic and contrastive vowel duration as produced by Broca’s aphasics with anterior lesions (A patients), nonfluent aphasics with anterior and posterior lesions (AP patients), and fluent aphasics with posterior lesions (P patients). The constellation of impairments for the anterior aphasics including both the A and AP patients suggests that their disorder primarily reflects an inability to implement particular types of articulatory gestures or articulatory parameters rather than an inability to implement particular phonetic features. They display impairments in the implementation of laryngeal gestures for both consonant and vowel production. These patterns seem to relate to particular anatomical sites involving Broca’s area, the anterior limb of the internal capsule, and the lowest motor cortex areas for larynx and tongue. The posterior patients also show evidence of subtle phonetic impairments suggesting that the neural instantiation of speech may require more extensive involvement, including the perisylvian area, than previously suggested. 0 1990 Academic Press, 1~.

Recent years have seen renewed interest in the speech production deficits exhibited by aphasic patients. The long-standing issue as to This research was supported in part by Grant DC00314 to Brown University and DC00081 to the Boston University School of Medicine. Many thanks to Felicia Gershberg for her assistance in the preparation of the manuscript. Send reprint requests to Sheila E. Blumstein, Department of Cognitive and Linguistic Sciences, Box 1978, Brown University, Providence, RI 02912. 33 0093-934x/90 $3.08 Copyright 0 19% by Academic Press, Inc. All rights of reproduction in any form reserved.

34

BAUM

ET AL.

whether various clinical types of aphasics manifest speech production impairments which are due to different underlying-mechanisms remains controversial (Blumstein, 1973; Blumstein, Cooper, Zurif, & Caramazza, 1977; Blumstein, Cooper, Goodglass, Statlender, & Gottlieb, 1980; Kohn, 1984; Kent & Rosenbek, 1983; Trost & Canter, 1974). Most recent acoustic/phonetic research has demonstrated that anterior (Broca’s) aphasics generally display articulatory implementation deficits, whereas posterior (Wernicke’s) aphasics exhibit deficits in phonological planning (Alajouanine, Ombredane, & Durand, 1939; Blumstein et al., 1977; Blumstein et al., 1980; Tuller, 1984). In particular, acoustic analyses have shown that anterior patients have problems with the temporal control of articulatory gestures, especially those requiring the coordination of two independent articulators, e.g., the larynx and the tongue or lips in the production of voicing in stop consonants, and the velum and the tongue or lips in the production of nasal consonants (Blumstein et al., 1977; Blumstein et al., 1980; Itoh, Sasanuma, Hirose, Yoshioka, & Ushijima, 1980; Itoh, Sasanuma, Tatsumi, Murakami, Fukusako, & Suzuki, 1982; Itoh, Sasanuma, & Ushijima, 1979). Posterior (Wernicke’s) aphasics, in general, do not show such deficits. However, several recent studies have attributed a subtle phonetic deficit to these patients, in addition to the earlier postulated phonemic deficit (Blumstein et al., 1977; Ryalls, 1986; Tuller, 1984). These studies have revealed potential abormalities in the production of several phonetic parameters including voice-onset time as a cue to voicing in stop consonants (Tuller, 1984), vowel duration as a cue to syllablefinal voicing (Duffy & Gawle, 1984; Tuller, 1984), and overall variability in the production of vowels (Ryalls, 1986). In fact, a number of researchers have suggested that even some of the phonemic substitutions produced by Wernicke’s aphasics could reflect subtle motor disturbances rather than impairments in phonological planning (cf. Buckingham & Yule, 1987; McNeilage, Hutchinson, & Lasater, 1981). In this view, subtle motor impairments could influence the production of particular acoustic cues which are subsequently misperceived by the listener as phoneme substitutions. Thus, much recent evidence points to a subclinical phonetic or motoric impairment in posterior (Wernicke’s) aphasia. In nearly all studies where production impairments have been revealed in both anterior and posterior aphasics, temporal parameters of speech have been implicated. Consideration of temporal parameters provides a means of exploring the nature of the production deficits in aphasic patients. There are a number of durational parameters that may serve either a phonological or phonetic function in English. Phonological parameters function contrastively in the language whereas phonetic ones do not. For example, duration of the fricative noise is a critical attribute distinguishing voiced from voiceless fricatives (Klatt, 1976; Nartey, 1982). In this

SPEECH

PRODUCTION

IN APHASIA

35

case, duration has a contrastive function, distinguishing one sound segment from another, and it thus serves a phonological role. Duration also serves a phonetic role in fricative consonants. Each fricative has its own characteristic duration with [f 01 in English being shorter in duration than [s S]. Because this duration parameter characterizes an intrinsic property of these fricatives, yet is not used in the language system to distinguish among the class of fricatives, duration in this case is a phonetic feature. There are a number of temporal parameters which function contrastively in English. These include differences in VOT signalling the voicedvoiceless contrast in initial stop consonants, differences in vowel duration signalling the voicing contrast in syllable-final stop consonants, and differences in noise-onset time (or the duration of the frication noise) signalling voicing contrasts in fricative consonants. Those temporal parameters which have an intrinsic but no contastive value in English include differences in intrinsic vowel length (e.g., tense vowels such as [i] are longer than lax vowels such as [I]), and intrinsic fricative noise duration (e.g., [fJ and [8] are inherently shorter than [s] and [S]). Both intrinsic and contrastive duration may be examined using the same categories of speech sounds, allowing a direct comparison between the aphasics’ ability to produce durational cues as they serve various phonological-phonetic functions in the language. If patients’ deficits are primarily phonological in nature, then only those durational cues that signal phonological contrasts should be compromised, and those durational parameters that reflect intrinsic phonetic characteristics should be spared. In contrast, if the deficit is primarily phonetic in nature, then all durational attributes should be compromised regardless of their phonological (contrastive) or phonetic (intrinsic) status. The results of several recent studies are relevant here. As already mentioned, many studies have replicated the early VOT results reported by Blumstein et al. (1977), demonstrating an overlap in category boundaries for anterior aphasics and a great deal of prevoicing and paraphasia evident in the speech of posterior aphasics (Blumstein et al., 1980; Itoh et al., 1982; Shewan, Leeper, & Booth, 1984; Tuller, 1984). The results of these studies have led to the conclusion that anterior aphasics have a deficit in the coordination of articulators required for the accurate production of voicing contrasts, while posterior aphasics manifest a phonological planning deficit (producing many phonemic paraphasic errors). Studies of fricative consonants have focused on the production of [s] and [z] in anterior aphasics. Kent and Rosenbek (1983) reported duration measures for normals and for seven apraxic speakers for [s z] in wordinitial position. Their results demonstrate some overlap in the duration values for the voiced and voiceless fricatives produced by the apraxic speakers, but a clear distinction for the normals (cf. Klatt, 1976; Nartey,

36

BAUM

ET AL.

1982; but see Baum and Blumstein, 1987 who failed to find a clear duration distinction for normals). In addition, they cite problems with the coordination of the onset of frication and the onset of voicing simultaneous with the frication noise in the apraxic patients. The frication noise often preceded the onset of voicing. Another study which examined both durational and spectral properties of the fricatives [s z] was conducted by Harmes, Daniloff, Hoffman, Lewis, Kramer, and Absher (1984). In contrast to Kent and Rosenbek (1983), Harmes et al. (1984) found that the four Broca’s aphasics tested showed normal control of duration, including the production of a duration distinction signalling the voicing contrast between [s] and [z]. However, they note that all of their aphasic subjects devoiced [z] in some instances. Harmes et al. contend that the major differences between the aphasics and normals were found in the spectral characteristics which they examined. Although not without controversy, the conclusions based on studies of fricative duration in aphasia, point to a potential temporal coordination impairment for anterior aphasics. As regards studies of vowel duration, three are particularly noteworthy in the present context. As mentioned earlier, Tuller (1984) compared the contrastive use of vowel duration to signal final consonant voicing with the results of her VOT analyses on both Broca’s and Wernicke’s aphasics. Although the data were quite variable, she showed that not all subjects who produced a bimodal distribution of VOT values did so with vowel duration. Further, vowel durations for the aphasic subjects were longer, overall, than those for normals. Based on the variation between the VOT results and the results of the vowel duration measures. Tuller concluded that neither anterior nor posterior aphasics demonstrate a deficit in the production of voicing per se since the phonetic parameters contributing to the voicing contrast were not similarly compromised. Rather, she suggests that the deficit is primarily a phonetic one. Duffy and Gawle (1984) examined vowel duration in CVC syllables as produced by normal speakers, aphasics, and aphasics with apraxia of speech. They found that the duration distributions for the aphasics and the apraxics failed to consistently fall within normal limits. Furthermore, the apraxic subjects deviated more from the normal baseline than did the aphasics without apraxia. All subjects did, nevertheless, maintain the voicing distinction by varying vowel durations. Contrary to most other studies though (e.g., Ryalls, 1986; Tuller, 1984), Duffy and Gawle found that the apraxic speakers’ vowel durations were shorter than normal. Finally, Ryalls (1986) found no significant differences between anterior, posterior, and normal subjects’ vowel durations (although in general the aphasic productions were longer), but found that standard deviations of the durations measures were significantly larger in the anterior aphasic group than in the normals. No differences were found between the an-

SPEECH PRODUCTION IN APHASIA

31

terior and posterior groups. Ryalls (1986) concludes that the greater acoustic variability exhibited by both groups, coupled with the increased duration measures, suggests a phonetic deficit in both anterior and posterior aphasic speakers. Despite the inconsistency of some of the results obtained in the duration parameters of speech, most suggest that aphasic patients display impairments in the production of temporal parameters. Nevertheless, these studies have not focused on a comparison of a number of temporal parameters produced by the same patients. As a result, it is difficult to determine whether the nature of such deficits is primarily phonological or phonetic. The aim of the current study is to determine whether both anterior and posterior aphasics exhibit deficits in temporal coordination, and if so, whether these deficits are the result of the same or different underlying mechanisms. Furthermore, detailed analyses of lesion data may provide more specific neuroanatomical correlations with speech production deficits. To this end, the following series of analyses were conducted. They include measures of VOT, intrinsic and contrastive fricative duration, and intrinsic and contrastive vowel duration, as produced by Broca’s aphasics with anterior lesions, nonfluent aphasics with anterior and posterior lesions, and fluent aphasics with posterior lesions. METHOD Subjects A total of 13 aphasic patients served as subjects. They were grouped into three categories on the basis of clinical diagnosis (Boston Diagnostic Aphasia Examination, Goodglass & Kaplan, 1972)and lesion site as determined by CT scan.’ There were four Broca’s aphasics with anterior lesions (group A), four nonfluent aphasics with lesions that involved both anterior and posterior structures (group AP), and five fluent aphasics, four Wernicke’s aphasics and one Conduction/Wemicke’s aphasic, with posterior lesions (group P). CT scans were unavailable for two Wernicke’s aphasics and the Conduction/Wernicke’s aphasic. All subjects had suffered a unilateral left hemisphere CVA at least 1 month prior to testing. Table 1 summarizes individual subject histories. The subjects, all native speakers of English, were outpatients at the Boston VA Medical Center.

Stimuli For the VOT analyses, the stimuli consisted of five tokens each of the syllables [daC] and [taC]. The final consonant varied so as to create five different real word tokens for both the voiced and voiceless series. The fricative stimuli consisted of CV syllables in which the six fricatives [f 0 s 5 v z] preceded each of the five vowels [i e a o u]. These CV syllables did not always form real words in English. Finally, two series of vowels were analyzed. To examine intrinsic vowel duration, the seven syllables [hid], [bed], [hId], [hEd], [hud], [hUd], and [hod] were elicited (cf. Peterson & Barney, 1952). To examine contrastive vowel duration (i.e., vowel duration as a cue to final consonant voicing), the vowels [i I e E ae o u] were elicited in the context of [bVd] and[bVt].

’ Results of an in-depth analysis of CT scan lesion information and correlations with acoustic analyses are reported in the Results section.

38

BAUM ET AL. TABLE PROFILES OF APHASIC

Subject Al A2 A3 A4

Age 62 67 55 67

SUBJECTS

Diagnosis

1 TESTEDIN TPO

Nonfluent Broca’s

6 mos 9 yrs

Atypical

1 yr 4 yrs

Broca’s

API AP2 AP3 AP4

61

Broca’s

59

Atypical

52 57

Broca’s Broca’s

PI P2 P3

72 58 77

P4

49

P5

57

Wernicke’s Wernicke’s Wernicke’s (recovered) Wernicke’s/ conduction Wernicke’s

PRESENT STUDY

AARb

PL

ACSd

5 3 3.5

6 4 2 1

+0.34 +0.81 +1.04 -0.50

2

3 yrs 2 mos 13 yrs 8 yrs

6 5.5 4

1 7 4 3

-0.21 +0.84 +0.55

2 yrs 1 yr 4 yrs

7 6.5 7

7 7 7

-0.24 -0.33 +0.80

1 mo

6

I

- 1.19

6 yrs

7

7

-0.35

3

-0.22

n Time post onset when tested. ’ Articulatory agility rating from the BDAE: 1 (always impaired) to 7 (never impaired). c Phrase length rating from the BDAE (1 to 7 words). * Auditory comprehension z score from the BDAE. All stimuli were printed in orthographic form on 3 x 5 cards. They were presented to subjects blocked by analysis series (i.e., VOT, fricatives, intrinsic vowel duration, contrastive vowel duration). Within each block, the stimuli were randomized, and the full series was elicited a total of five times. There were thus a total of 50 tokens for each subject in the VOT series, 150 in the fricative series, 35 in the intrinsic vowel series, and 70 in the contrastive vowel series. If the subject was unable to read a stimulus, the token was produced by the examiner and repeated by the aphasic patient. As expected, the repetition procedure was more often necessary for those stimuli which did not form real words in the language. The syllables were recorded in a quiet room with a high quality reel-to-reel tape recorder. These stimuli were digitized onto disk via a PDP 1l/34 computer at the Brown University Phonetics Laboratory and edited from the waveform display. Tokens were sampled at a 20 kHz sampling rate with a 9 kHz low-pass filter setting and a IO-bit quantization. The utterances produced by the aphasic patients formed the data set for acoustic analysis. Because the acoustic analyses focused on only certain acoustic dimensions. it was necessary to insure that the patients’ productions corresponded to the broad phonetic category of the target consonant or vowel, on the one hand, and that the perceptual judgments of the listener did not eliminate or skew the analysis of the acoustic dimension in question, on the other. As a result, if the patient’s utterance maintained all phonetic dimensions as the target phoneme save the dimension under investigation, the utterance was analyzed. In contrast, if the production modified other phonetic features corresponding to the target phoneme, then the segment was eliminated from the data analysis. Following these criteria, consonant productions were eliminated from the data analysis if the patient’s productions did not correspond to the correct place or manner of articulation of the target consonant. There was no attempt to classify the voicing dimension on the basis of perceptual judg-

SPEECH PRODUCTION IN APHASIA

39

ments of the examiners. For example, if a subject was to produce an [s] and it sounded like a [z] (a voicing error), the duration of the fricative noise was analyzed as a target [s] production; in contrast, if the patient’s production was perceived as an [fl (a place of articulation error), this utterance was not analyzed for voicing. Similarly for vowel productions, utterances were eliminated from the data analysis if they were perceived as either errors along the front/back dimension or vowel height dimension. For example, if the subject was to produce [bit] and produced either [but] (a front/back error) or [bet] (a vowel height error), the vowel was not analyzed; in contrast, if the utterance was perceived as [bItI, it was analyzed for vowel duration.

Duration Analyses Durations were measured in all cases by both visual inspection of the acoustic waveforms and auditory perception. For the [daC] and [taC] tokens, VOT for the initial stop consonants was measured as the time from the onset of the burst to the onset of periodic energy. Therefore both burst and aspiration noise were included in the VOT values. For those tokens which were prevoiced, VOT was measured from the onset of periodic energy to the onset of the burst. The value of these VOT tokens is negative. For the fricative syllables, durations of both the frication noise and the vocalic nucleus were measured. For the voiceless fricatives, a cursor was placed at the start of frication noise, defined by a greater than 5 dB increase in spectral energy at or above 2 kHz as compared to the background noise level (as shown by discrete Fourier analysis). The offset of the fricative was also demarcated by a cursor placed at the end of the noise segment which usually coincided with the onset of periodicity corresponding to the vowel transition. In some cases, frication noise continued into the onset of the vowel. In these instances, only the frication noise prior to that point was included in the duration measures. Voiced fricatives proved somewhat more difficult to analyze. Again both the fricative and vowel durations were calculated separately. The onset of the voiced fricative was readily determined by visual inspection of the waveform; its offset was defined as a decrease or loss of high-frequency noise in the region between 4 and 6.5 kHz (as determined by Fourier analysis). The duration of the vocalic nucleus was determined by placing one cursor at the onset of periodicity (corresponding to the vowel transition) and the other at the point where noticeable periodicity diminished. Vowel durations were measured from the onset of periodicity up to the end of periodic energy in the waveform. For the two vowel series, the end of periodicity generally corresponded to the onset of the closure for the final stop consonant.

Results

Voice Onset Time The mean VOT (and standard deviation) for the production of [d] and [t] for each of the three aphasic groups is as follows: The Broca’s (group A) aphasics showed a mean VOT of 19 msec (44.2) for [d] and a mean VOT of 85 msec (27.3) for [t]; the nonfluent (group AP) aphasics showed a mean VOT of 15 msec (19.1) for [d] and a mean VOT of 60 msec (21.9) for [t]; and the posterior (group P) aphasics showed a mean VOT of 1.1 msec (22.8) for [d] and a mean VOT of 75.9 msec (22.6) for [t]. VOT analyses could not be conducted for one anterior patient (A4) who was unable to produce a full closure in the production of stop consonants, and as a consequence, in the acoustic analyses, there were no bursts corresponding to the release of the consonant closure.

40

BAUM ET AL.

Earlier findings have shown contrasts between the VOT distribution of nonfluent and fluent patients. Typically, nonfluent patients show overlap of VOT in the production of voiced and voiceless stop consonants, whereas fluent patients, similar to normals, show two distinct VOT distributions corresponding to the voiced and voiceless phonetic categories, with minimal, if any, overlap between the boundaries of these categories. For both groups of patients, some of the VOTs of voiced targets occur in the voiceless category and vice versa. Figures 1-3 display the distribution of VOT productions for each of the patients by group. On balance, the results shown in Figs. l-3 replicate SUBJ Al [‘f/D]

SUBJ

&!

[T/U]

VOT IN MS

VOT IN MS

SUUJ

A3 [‘l’/D]

lo-

VOT IN MS

FIG. 1. The distribution of VOT productions of alveolar stop consonants for each patient in the anterior (A) lesion group. The abscissa represents voice-onset time (in msec), and the ordinate represents the number of responses produced at each VOT value. The target voiced stops [d] are indicated by the white bars, and target voiceless stops [t] by the striped bars. Solid bars indicate target voiced and voiceless stop consonants occurring at the same VOT value.

SPEECH

PRODUCTION

41

IN APHASIA

SUBJ API[T/D]

SC

1150

-100

-50

0

50

100

150

VOT IN MS

SUBJ Al’3

\‘l’/D]

SUDJ

AF’4[‘1‘/D]

LO

0 -150 VOT IN

MS

-100

-50

0

50

100

VOT IN MS

FIG. 2. The distribution of VOT productions for alveolar stop consonants patient in the anterior/posterior (AP) lesion group. See legend for Fig. 1.

for each

these earlier findings. Nevertheless, some interesting differences also emerged. The results for the posterior patients, as shown in Fig. 3, are consistent with earlier results. All patients show two clear-cut categories of VOT, and a region of separation between the two categories in which few, if any, tokens fall. The nonfluent AP patients, shown in Fig. 2, also show VOT distributions characteristic of earlier findings, with substantial overlap between the voiced and voiceless phonetic categories, and minimal separation of the two categories. What appears to differ from previous findings is the pattern of results for one of the Broca’s (A) patients (see Fig. 1). In particular, this patient (A3) displays a VOT distribution similar to normals-there are two distinct categories separating the voiced and voiceless target productions, and there is a clear-cut region between the two categories where no productions fall.

I50

BAUM ET AL.

42

VOT IN MS

VOT IN MS

SUDJ

P4 l’l’/D]

10

6

6

4

2

0 -150 "OT

IN MS

-100

-50

0 'JOT IN MS

50

100

VOT IN MS

FIG. 3. The distribution of VOT productions for alveolar stop consonants for each patient in the posterior (P) lesion group. See legend for Fig. 1.

150

SPEECH

PRODUCTION

IN APHASIA

43

Fricatives Intrinsic duration. Mean fricative duration was calculated for each subject for each of the fricatives [f 13s S] in each vowel environment ([i e a o u]). The mean durations collapsed across the vowels are presented in Table 2 for the three aphasic groups. Although there is considerable variability across the subjects in the absolute durations of the fricative noise, all patients (with the exception of patient A2) show longer fricative noise durations in the production of [s] and [S] compared to [fl and [0]. Statistical tests confirmed these observations. A Group x Fricative analysis of variance* showed a significant main effect for fricative duration [F(3, 30) = 18.31, p < .OOl]. No other significant effects emerged. Thus, while the duration of the fricative noise varied as a function of the particular fricative, similar results emerged for the three groups. Post hoc Newman Keuls tests revealed that the duration of the fricatives [fl and [8] differed significantly from [s] and [S] (p < .Ol), [fl differed from [0] (p < .05), but [s] and [S] did not differ from one another. It is worthwhile to compare the aphasic data to some normative results. On balance, normals show individual variability in the duration of fricative noise, although considerably less so than do the aphasics. The overall means (and standard deviations) for normals are 149 msec (27) for [fJ, 134 msec (34) for [e], 174 msec (15) for [s], and 175 msec (16) for [S] (Behrens & Blumstein, 1988). Thus, compared to normals, aphasics show similar patterns with [s] and [S] being longer than [fl and [13]. Absolute durations show differences from normals. They display shorter durations for [fl and [0] and longer durations for [s] and [S]. However, owing to the large individual variation among the patients, this generality does not hold for all patients. While there seem to be differences in the absolute durations of the frication noise produced by aphasics compared to normals, it is possible that the relative duration of the fricative noise as a function of syllable duration may not differ. That is, patients who produce longer (or shorter) fricative durations than normals may also produce longer (or shorter) vowels, thus maintaining a relatively normal CV ratio. To explore this possibility, the frication durations were also analyzed as a proportion of the vowel durations (i.e., fricative/vowel ratio) for each syllable. Results of this analysis are shown in Table 3. For all groups, there is a similar rank order of fricative/vowel proportions. A two-way ANOVA (Group x Fricative) confirmed these findings. There was a main effect for Fricative [F(3, 30) = 26.36, p < .Ol], but neither a significant main effect ’ Some subjects were unable to produce some syllables, and as a result did not produce any adequate tokens for analysis even using the repetition procedure. Therefore, the analysis of variance used the mean of the group data for the missing values. This procedure was used for all subsequent analyses containing missing values.

44

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ET AL.

TABLE MEAN

2

FRICATIVE DURATION COLLAPSED ACROSS VOWELS FOR ANTERIOR ANTERIOR/POSTERIOR (AP), AND POSTERIOR (P) SUBJECTS

(A),

H-l

[Ol

ISI

El

Al A2 A3 A4 Mean SD

102.5 69.2 58.7 136.6 91.8 35.3

149.8 348.0 110.3 202.7 127.4

205.0 194.1 278.1 164.3 210.4 48.3

216.2 214.2 322.1 250.8 61.7

API AP2 AP3 AP4 Mean SD

64.5 50.5 103.6 108.2 81.7 28.6

80.2 73.3 48.6 95.4 74.4 19.5

138.0 132.4 204.0 215.4 172.5 43.3

142.8 126.5 205.9 237.2 178.1 52.2

PI P2 P3 P4 P5 Mean SD

54.6 89.6 165.8 176.1 42.6 105.7 62.1

119.1 167.6 214.6 70.0 142.8 62.3

174.0 164.0 238.2 379.9 273.5 245.9 87.5

166.6 150.2 241.6 357.5 279.4 239.1 84.9

Subject

TABLE FRICATIVE/VOWEL

3

RATIOS FOR THE ANTERIOR (A), ANTERIOR/POSTERIOR POSTERIOR (P) APHASICS

Subject

rfl

to1

Al A2 A3 A4 Mean SD

.365 .286 .154 .525 .333 ,155

API AP2 AP3 AP4 Mean SD PI P2 P3 P4 P5 Mean SD

(AP), AND

bl

El

.573 .349 .286 .403 .151

.905 .727 .763 .565 .740 ,140

.945 ,736 ,873 ,851 ,106

.347 .275 .486 .295 .351 .095

.339 .401 .199 .332 .318 .085

.592 .799 .977 .627 .749 .177

.641 ,790 ,902 .659 ,748 ,122

.192 .353 ,600 ,514 ,221 .376 ,179

.437 ,601 ,706 ,374 ,530 .152

.593 .627 .943 1.246 1.423 .966 .368

,520 .574 .847 1.520 1.473 .987 ,482

SPEECH

PRODUCTION

45

IN APHASIA

for Group [F(2, 10) = 1.37, p < .30] nor a significant Group x Fricative interaction [F(6, 30) = .405, p < .87]. The effect for Fricative reflects the fact that the ratios were larger for [s] and [S] compared to [fl and [(I]. Data for normal subjects extrapolated from Behrens and Blumstein (1988) reveal the following CV ratios: [fl .488, [fI] .421, [sl S84, and [S] S74. The larger ratio for [sl and [S] compared to [fl and [Ol is not unexpected given the longer absolute durations of the fricatives for [s] and [S] compared to [fl and [e]. If vowels are produced at relatively the same duration across the different fricatives, then the ratios would vary as in the obtained data. Nevertheless, it is noteworthy that the largest discrepancies between the aphasic data and the normal data emerge in the CV ratio for [s] and [S], and particularly for the posterior aphasics where the ratio values approached 1.00. These differences could reflect differences in speaking rate between the aphasics and normals. However, given the lack of significant differences among the aphasic groups and the similar patterns obtained to normals, the results suggest that the aphasics maintain relatively normal CV ratios. Contrastive duration. The mean durations of the voiced fricatives [v] and [z] were calculated and compared to their voiceless counterparts [fl and [s] for both aphasic groups. These values collapsed across vowel contexts are listed by subject in Table 4. It is clear from the Table that no group of aphasic subjects consistently maintained the expected duTABLE 4 MEAN FRICATIVE DURATION FOR VOICED AND VOICELESSCOUNTERPARTS

VI

[VI

[sl

[zl

Al A2 A3 A4 Mean SD

102.5 69.2 58.7 136.6 91.8 35.3

98.2 74.2 173.4 115.3 51.8

205.0 194.1 278.1 164.3 210.4 48.3

204.4 116.0 302.6 207.7 93.3

API AP2 AP3 AP4 Mean SD

64.5 50.5 103.6 108.2 81.7 28.6

43.3 132.4 57.4 77.7 47.9

138.0 132.4 204.0 215.4 172.5 43.3

146.2 104.5 207.0 210.2 167.0 51.0

Pl P2 P3 P4 P5 Mean SD

54.6 89.6 165.8 176.1 42.6 105.7 62.1

100.5 86.6 174.8 176.0 67.6 121.1 50.9

174.0 164.0 238.2 379.9 273.5 245.9 87.5

165.0 139.4 266.8 250.3 243.8 213.1 56.9

Subject

46

BAUM

ET AL.

rational difference between voiced and voiceless fricative consonants (i.e., voiced fricatives are typically shorter than voiceless in normal productions (Klatt, 1976; Nartey, 1982)). Although the overall means for [s] and [z] for each group of aphasics showed the expected differences, namely that [z] was shorter than [s], the differences were small for the two nonfluent groups, and two out of three A patients, two out of four AP patients, and one P patient did not show this pattern. Moreover, neither the overall means for [fl and [v] showed the expected durational differences for the A and P patients, nor did the individual patient data, with two out of three A, one out of three AP, and four out of five P patients failing to show the expected pattern. The durations of the voiced ([v z]) and voiceless ([f s]) fricatives were compared in a Group x Place x Voicing ANOVA. Results showed no main effect for group [F(2, 10) = 1.211 or for voicing [F(l, 10) = .Ol]. With respect to the failure to show a significant effect for voicing, it should be pointed out that although normals show reliable differences between the duration of the frication noise for voiced and voiceless fricatives (Baum & Blumstein, personal communication), they also show a great deal of overlap in the durations of individual voiced and voiceless tokens (Baum & Blumstein, 1987). There were no significant interactions [Group x Voicing-F(2, 10) = .16; Group x Place-F(2, 10) = .33; Group x Voicing-F(2, 10) = .36; Group x Voicing x Place-F(2, 10) = .77], indicating that the three groups of patients produced similar patterns. There was a significant main effect for place of articulation confirming the intrinsic fricative noise analyses reported earlier, but now including voiced fricatives as well [F(l, 10) = 61.761. Nevertheless, despite the fact that all three aphasic groups failed to maintain the duration contrast for voiced and voiceless fricatives, acoustic analysis of these utterances did reveal some important differences. In particular, in examining the waveforms for the production of voice fricatives, it was observed that some of the patients with anterior lesions (in groups A and A/P) exhibited inconsistent periodicity throughout the duration of the fricative noise. Namely, they produced voiced fricative tokens with periodicity starting and stopping during the course of the frication noise. Moreover, unlike the production of voiced utterances in citation form by normal subjects, anterior patients tended to delay the onset of voicing, often not beginning periodicity until the vicinity of the release of the frication noise (cf. Kent & Rosenbek, 1983). In contrast to the patients with anterior lesions, the posterior aphasics did not demonstrate this pattern of inconsistent laryngeal control; rather they showed a pattern close to that shown by normals. Vowels Intrinsic duration. Means and standard deviations of the durations of the seven vowels [i I e E o u U] were computed for each aphasic subject

SPEECH

PRODUCTION

47

IN APHASIA

group. These values are displayed in Table 5. As the Table indicates, for all patients, tense vowels are longer than lax vowels. A Group x Vowel ANOVA confirmed these findings. There was a main effect for vowel duration [F(6, 60) = 38.18, p < .OOll. Post hoc analyses revealed significant differences @ < .Ol) between the vowels [i] and [I], [e] and [El, and [u] and [U] across the three subject groups. In addition, there was a main effect for Group [F(2, 10) = 4.73, p < .04]. This effect was due to the fact that the overall duration of vowels produced by the anterior aphasics was longer than those produced by both the anterior/posterior aphasic group and the posterior aphasic group. Contrastive duration. The mean durations of the seven vowels as produced in the context preceding a voiced and voiceless consonant ([d t]) were calculated for each subject. These values are displayed in Table 6 for the three aphasic groups separately. As the Table shows, all patients displayed longer vowel durations preceding the voiced stop [d] compared to the voiceless stop [t] for each vowel comparison. A Group x Consonant Voicing x Vowel ANOVA was conducted on these duration measures. Significant main effects were found for Vowel duration [F(6, 60) = 63.13, p < .OOl] and for Voicing [F(l, 10) = 245.85, p < .OOl]. The main effect for Vowel confirms the differences in the production of intrinsic vowel durations for tense and lax vowels noted above, but with TABLE MEAN

INTRINSIC

VOWEL

5

DURATIONS FOR ANTERIOR (A), ANTERIOR/POSTERIOR POSTERIOR (P) APHASICS

(AP),

AND

Subject

[hid]

bldl

lhedl

Wdl

lhudl

1hW

[hod1

Al A2 A3 A4 Mean SD

335.2 470.8 335.6 297.0 359.7 76.3

212.2 305.8 227.2 248.4 50.3

356.6 413.2 466.0 411.9 54.7

261.8 289.5 261.2 270.8 16.2

315.4 385.0 358.0 369.0 356.9 29.8

207.4 284.0 297.4 262.9 48.6

321.4 416.2 461.2 399.6 71.4

API AP2 AP3 AP4 Mean SD

308.8 272.7 234.6 383.0 299.8 63.2

199.8 176.6 173.6 198.6 187.2 14.0

251.2 273.0 233.4 393.2 287.7 72.2

238.5 210.4 194.6 235.4 219.7 21.0

246.2 280.3 249.8 421.2 299.4 82.7

186.0 210.8 165.6 225.0 196.9 26.3

289.4 323.5 313.3 396.8 330.8 46.3

Pl P2 P3 P4 P5 Mean SD

307.7 336.0 283.0 297.4 306.0 22.4

154.3 211.4 177.4 165.2 201.8 182.0 24.1

296.3 301.8 295.0 432.7 432.2 351.6 73.9

236.3 209.0 174.2 238.6 214.5 30.1

243.7 305.4 263.6 319.0 325.4 291.4 35.9

122.7 186.3 168.8 217.6 173.9 39.6

246.0 285.8 286.2 482.0 408.0 341.6 99.3

48

BAUM ET AL. TABLE 6

MEAN

Subject Al A2 A3 A4 Mean SD

Mean SD

API AP2 AP3 AP4 Mean

SD Mean

SD

Pl P2 P3 P4 PS Mean SD

Mean SD

CONTRASTIVE

VOWEL

DURATION FOR ANTERIOR (A), ANTERIOR/POSTERIOR POSTERIOR (P) APHASICS

(AP),

AND

[bit] [bid]

PItI

bet1

bldl

[bed1

bEtI [bEdI

[baet] [baed]

btl bdl

[bud1

174.6 300.6 262.8 311.5 247.0 315.8 200.6 323.8 221.3 40.8 312.9 9.7

101.4 204.6 182.3 265.0 189.0 218.0 145.4 180.2 154.5 40.3 217.0 35.7

224.2 363.4 290.0 474.5 238.2 353.2 204.6 363.4 239.3 36.5 388.6 57.5

145.0 234.8 179.2 235.8 179.6 230.5 158.3 226.4 165.5 16.9 231.9 4.3

224.0 357.4 286.8 245.6 344.0 208.4 313.3 241.2 34.0 338.2 22.6

233.8 335.8 251.6 406.0 226.2 424.8 266.2 386.4 244.5 18.0 388.3 38.3

200.8 354.6 261.4 404.3 219.4 450.3 274.6 308.5 239.1 34.7 379.4 61.3

143.2 317.4 130.0 195.7 165.6 246.8 219.8 299.0 164.7 39.6 264.7 54.9

120.8 205.2 107.0 188.3 138.8 159.6 149.4 200.0 129.0 18.8 188.3 20.4

202.4 314.4 170.3 241.3 165.2 268.0 238.4 371.2 194.1 33.8 298.7 57.0

153.6 265.6 157.5 169.6 183.0 165.2 230.8 161.5 7.3 226.5 41.5

195.0 306.4 209.0 222.0 223.4 313.0 329.8 386.4 239.3 61.4 307.0 67.3

214.4 330.6 166.3 268.3 192.4 315.4 242.0 379.2 203.8 32.2 323.4 45.7

177.0 244.2 172.3 193.0 180.4 223.6 228.6 396.0 189.6 26.2 264.2 90.4

160.0 270.0 211.4 319.2 181.6 275.8 136.0 177.8 224.3 173.4 27.9 272.3 38.8

133.7 175.7 178.2 215.4 120.2 194.6 84.8 138.7 141.0 187.0 131.6 33.9 182.3 28.3

229.0 340.7 228.6 352.8 176.0 326.6 320.0 175.4 380.4 202.3 30.7 344.1 23.9

164.0 189.0 166.6 225.4 148.8 191.2 97.0 172.0 146.0 225.8 144.5 28.0 200.7 23.9

282.7 364.3 251.6 319.4 192.8 257.2 275.3 180.4 424.5 226.9 48.5 328.1 68.0

160.0 318.7 255.6 315.4 215.6 271.2 148.3 327.5 186.2 373.4 193.1 43.5 321.2 36.4

169.7 250.0 221.8 324.4 169.0 284.8 141.3 345.5 152.8 332.6 170.9 30.8 307.5 39.3

WI

a different set of data. The significant effect for voicing indicates that vowels produced in the environment preceding a voiced consonant were significantly longer than those preceding a voiceless consonant. A significant Voicing x Vowel duration interaction was also found [F(6, 60) = 6.54, p < .OOl], suggesting that not all of the vowels showed the

Ti

Wernicke’s

Sensory Anterior % PVWM Middle % PVWM Posterior % PVWM Anterior SMG

Motor

ALIC

Medial SCF

Al

0 0 0 0 0 0 0

0

0 0 0 0 0 0

SM

SM SM+l B/W W

3 4 0.0 3.5 1 4 5 5 5 5 3.75 2

4 5 5 5 3.75 3.75 3.5 3.5

AND

A2

2

B B/W

TABLE 7 Two

0 2 0 0 0 0

0

0

0 0 0 0 0 1 2 2 4 2

0

A3

POSTERIOR

0 0 0 0 0 0

0

1

0 I 2.5 1 4 5

4

3.8

1 5

1

5 5 3.5 4.0 4.5 5 5 5 3

API

Subject

2 0 2.5 0 3.75 1.5

1

3.75

2

1

5 5 1 1.5 5 4 3.75 4.75 3

5 4.8 5 4.5 5 5

4.9

4.8

4.75 4.85 5 5 5 5 5 4.5 3.75 3 4.8

AP3

5 4 0 I 4 5

4.25

4.85

2 5 5 5 5 5 5 5 4.85 4.25 5

AP4

FOUR ANTERIOR/POSTERIOR

AP2

(A),

APHASIC PATIENTS

3.5

5 4 3.75 2 5 5 5 4 0

A4

(P)

(NO LESION) TO 5 (TOTAL LESION)) FOR FOUR ANTERIOR

5 5 0

(0

SM

SM SM SM

W

W

B B/W B B/W B B/W

Broca’s

SCALES

CT Slice

RATING

Region

CT

(AP),

5 4.85 5 4 5 5 3.5

I 0 0 1 2.5 0 0

1

2 0

0 0 0 0 0 0 0 0 0

P5

0

0 0 0 0 0 0 0 0 0 0 0

P3

50

BAUM

ET AL.

lengthening effect (preceding voiced consonants) to the same extent. Consistent with the analysis of intrinsic vowel duration, a significant Group x Vowel interaction emerged [F(12, 60) = 2.34, p < .02], indicating that the overall duration of vowels produced by anterior aphasics was longer than those produced by either anterior/posterior aphasics or posterior aphasics. Nevertheless, there was no Group x Consonant Voicing interaction [F(2, 10) = 1.221, suggesting that while the vowels produced by the anterior aphasics are longer than those produced by the two other groups, the differences between the duration of vowels as a function of consonant voicing are similar across the three groups. Correlation with Neuroanatomical Findings The extent of lesion in specific language-related neuroanatomical areas was assessed using a scale from 0 to 5 which has been used in prior studies (Naeser, Palumbo, Helm-Estabrooks, Stissny-Eder, & Albert, 1989). CT scans were evaluated for 10 of the subjects (4A, 4AP, and 2 P). Using the rating scale, 0 corresponds to no lesion and 5 corresponds to total lesion. For each neuroanatomical area, a rating of 3 or more (i.e., half of that neuroanatomical area had lesion present) was used as a cutoff for a lesion to be considered significant. Table 7 provides a summary of the extent of lesion values for each neuroanatomical area which was assessed for each of the ten subjects. Focusing first on the anterior (A) subjects, a cursory examination of Table 7 reveals that all but one of the anterior aphasics (A3) has a significant amount of lesion (>3) in both Broca’s area (slices B and B/W) and the anterior limb of the internal capsule (ALIC including slices B, B/W, and W). The lower motor cortex regions for larynx, tongue, and lips (slices W and SM) are also implicated, although less consistently so (cf. Al, A2, A4). Interestingly, the one anterior subject (A3) who had no lesion in Broca’s area, minimal involvement of the anterior limb of the internal capsule and the lower motor cortex regions for larynx, tongue, and lips, and only minimal lesion in the anterior r/3 of the periventricular white matter (PVWM) exhibited relatively normal performance on all speech measures taken. In particular, results of the VOT analysis-the one measure which revealed a clear-cut distinction between the two nonfluent groups’ performance and that of the posterior group and normals-was within normal limits for this subject. This patient’s production of voiced fricatives was also near normal and was distinguished from several of the other anterior patients in that he demonstrated consistent laryngeal control throughout the production of the frication noise. Consistent with these findings, the AP patients, all of whom displayed impairments in VOT production, also had lesion in Broca’s area, the anterior limb of the internal capsule, the lowest motor cortex area (for larynx and tongue), and the anterior % of PVWM.

SPEECH PRODUCTION IN APHASIA

51

The anterior/posterior (AP) aphasics had significant lesion in both anterior and posterior regions. All had lesion including Broca’s area, the anterior limb of the internal capsule, and the lower motor cortex areas. For all of these patients, the lesion also extended deep to include the middle r/5 PVWM, and posteriorly to include either Wernicke’s cortical area or the subcortical temporal isthmus. It is noteworthy that with the exception of patient A3, the A and AP patients displayed similar deficits in the production of VOT. The common lesion sites for these two groups include Broca’s area, the anterior limb of the internal capsule, and the lowest motor cortex areas for tongue and larynx (slice W). On the basis of these findings, it seems that Broca’s area, the anterior limb of the internal capsule and/or the lowest motor cortex area for tongue and larynx are implicated in the normal production of voice-onset time and perhaps in the coordination of two independent articulators. We by no means wish to suggest that VOT production is localized in these anatomical regions. Rather, we propose that, whatever their functional role, these structures must be intact for accurate production of this acoustic parameter, and perhaps other parameters requiring the integration of articulatory movements. For example, the fact that in these cases, lesion was present in the lowest motor cortex area for tongue and larynx is consistent with a potential impairment in VOT production. Namely, laryngeal control is a necessary prerequisite for normal production of voice-onset time. Thus, it may not be all that surprising that damage to neuroanatomical areas associated with the larynx would result in an impairment affecting a phonetic attribute of speech which requires laryngeal control and the timing of laryngeal movements. The potential role of the other damaged neuroanatomical areas should not be ignored, however. What specific role they play in articulatory implementation is not at all clear. Further research will be necessary to determine whether the difficulty in VOT production is limited to damage to only some or all of the areas thus far implicated. With respect to the two posterior patients for whom there was lesion localization data, there is virtually no overlap in lesion site in any anterior regions with either the anterior or anterior/posterior group. That they displayed normal VOT production lends further support to the importance of the anterior structures in the normal production of VOT. One patient (PS) had significant lesion in both Wemicke’s cortical area and the subcortical temporal isthmus. The other, (P3), had a less extensive lesion affecting less than half of Wernicke’s area. Nevertheless, the fact that both of these patients showed some subtle speech production impairments suggests that regions other than Broca’s area, the anterior limb of the internal capsule, and the lowest motor cortex areas contribute to the normal production of speech.

52

BAUM

ET AL.

DISCUSSION

The results of the acoustic measures used in this study may be summarized as follows. The VOT analyses essentially replicate earlier findings (cf. Blumstein et al., 1977, 1980; Itoh et al., 1982; Shewan et al., 1984; Tuller, 1984). In particular, nonfluent aphasics (including both A and AP patients) demonstrate overlap between the voiced and voiceless phonetic boundaries. In contrast, the posterior aphasics maintain a bimodal distribution of VOT. With respect to the production of fricatives, all groups maintain the intrinsic duration of the fricative noise for voiceless fricatives (i.e., [s] and [S] are longer than [fl and [f3]), although the absolute durations of the noise are variable and differ from those of normals. No group, however, reliably distinguishes voiced and voiceless fricatives on the basis of duration measures. Finally, all groups maintain intrinsic as well as contrastive durations for vowels, although the absolute duration of vowels is longer for the anterior (A) aphasics compared to either the AP or the P aphasics. (The duration values for the AP and P patients seem to be similar to those for normals.) Taken together, these results suggest that aphasic patients with anterior and/or posterior lesions present with speech production impairments. Consideration of the pattern of results displayed by the aphasics provides some evidence for the underlying basis of these deficits. Let us consider each aphasic group separately. The constellation of impairments for the anterior aphasics including both the A and AP patients suggests that their disorder primarily reflects an inability to implement particular types of articulatory gestures or articulatory parameters rather than an inability to implement particular phonetic features. If the disorder had reflected an impairment in the instantiation of a phonetic feature, then these patients should have shown deficits in the production of all of the acoustic parameters contributing to voicing in stop and fricative consonants. However, results indicated that voicing in initial stops and fricatives was impaired, whereas the production of vowel duration as a cue to postvocalic voicing was relatively normal. Thus, the articulatory implementation of the voicing feature was not compromised, but rather some of the instantiations of that feature were impaired-namely, those that involve the temporal coordination of the release of a closure or constriction and the onset of vocal cord vibration and those that involve laryngeal control. In this sense, the disorder is phonetic rather than phonological in nature. On the surface, this conclusion would seem to conflict with the data from this study showing that anterior patients evidence impairments only in the production of contrastive differences and never in the production of intrinsic differences. However, it is the case that anterior aphasics can produce contrastive differences when the articulatory maneuvers do

SPEECH PRODUCTION IN APHASIA

53

not involve the temporal coordination of two independent articulators or laryngeal timing as shown by their ability to distinguish final voiced and voiceless stop consonants on the basis of the preceding vowel duration. These results suggest that the disorder is more nearly tied to the nature of the articulatory maneuvers or instantiating a contrast rather than the functional nature of the contrast itself. In fact, earlier research has shown that anterior aphasics seem to be particularly vulnerable to those phonetic parameters requiring the temporal integration of two independent articulators. They not only show impairments in the production of voicing in initial stop consonants and fricatives (as shown in this study), but they also show deficits in the timing between the release of the closure in the oral cavity and the opening of the velum in the production of nasal consonants (Itoh et al., 1979). Difficulties with laryngeal control have also emerged for anterior aphasics, not only in the production of voiced fricatives (as shown in this study), but also in earlier research analyzing the spectral patterns for the production of place of articulation in stop consonants (Shinn & Blumstein, 1983). Thus, these studies indicate that anterior aphasics seem to have impairments in the implementation of laryngeal gestures affecting not only voicing in consonant production, but also those spectral parameters that rely on the interaction of the laryngeal system and the supralaryngeal vocal tract system. That the pattern of behavior of the nonfluent patients relates to particular anatomical structures is supported by the CT scan data. Both A and AP patients share lesions involving Broca’s area, the anterior limb of the internal capsule, and the lowest motor cortex areas for larynx and tongue. Nevertheless, there was one difference which emerged between the A and AP aphasics. In particular, analysis of vowel durations indicated that the anterior aphasics produced overall longer vowels than did either the AP aphasics or the P aphasics. These results were obtained for two independent sets of data, namely for productions of [bVt] and [bVd] as well as for productions of [hVd]. The finding that overall vowel duration is longer for anterior aphasics compared to normals has been reported by various researchers (cf. Ryalls, 1987 for a review), although this finding apparently has emerged only in polysyllabic words rather than monosyllabic stimuli as in the current study. In fact, in an earlier study, Ryalls (1986) found no difference in vowel durations between anterior and posterior patients, although their productions were longer than normals. Nevertheless, that vowel durations of anteriors are generally longer than normals is a pattern that has emerged in many studies (Ryalls, 1987). There are at least two explanations for these findings. One explanation is that the subjects’ overall production of sound segments is slower, resulting in longer vowel durations. Another explanation is that these patients are having difficulty producing the final consonant of the

54

BAUM

ET AL.

CVC utterance, and as a result, there is a consequent lengthening of the preceding vowel. Why the vowel durations for A patients were longer than normal and those for AP patients were not is not clear. The AP patients share some common lesion sites with the A patients (Broca’s area, the anterior limb of the internal capsule, the lowest motor cortex area for larynx and tongue). In addition, they have posterior lesion extension into the temporal lobe. The pattern of performance for the AP patients, however, on the vowel duration measure is similar to the P patients with whom they share common lesions in Wemicke’s area and/or the temporal isthmus. Turning to the posterior aphasics, the results of this study suggest that they have a subtle phonetic impairment. While such an impairment may not be clinically evident, it is the case that these patients showed impairments in the production of both intrinsic and contrastive fricative duration. Nevertheless, the nature of the impairment seems to be different in quality from that of the anterior aphasics. Similar to the two other aphasic groups, the posterior aphasics showed impairments in the production of the absolute duration of the fricative noise, with [fl and [O] being shorter than normal and [sl and [S] being longer than normal. However, unlike these two groups, there was a tendency for them to show a larger ratio in the duration of the fricative noise relative to the vowel in the production of [s] and [S]. Moreover, while they are similar to anterior aphasics in failing to show differences in fricative duration for voiced and voiceless fricatives, they do not display the abnormal patterns of laryngeal control revealed by the anterior aphasics. Finally, these patients show increased variability in their productions. Similar findings of increased variability in posterior aphasics have been shown not only for the parameters explored in this study, but for other phonetic parameters of consonant and vowel production as well (cf. Raylls, 1986; Kent & McNeil, 1987). What is not clear is the nature of the impairment contributing to the pattern of performance displayed by the posterior patients. A deficit in the control of temporal parameters is surely implicated. The phonetic impairment does not seem to reflect particular difficulties in implementing phonological attributes or phonetic features but rather seems to turn on more global, durational patterns of speech. It is possible that the impairment could be due to the fact that posterior areas projecting to the motor/articulatory system are damaged, resulting in a speech production impairment. Alternatively, the auditory feedback system contributing to the normal control of the articulatory parameters of speech may be impaired. These suggestions are merely speculative and are in need of further study. What is clear, however, is a phonetic deficit emerges in patients who have not sustained brain damage to Broca’s area, the an-

SPEECH PRODUCTION IN APHASIA

55

terior limb of the internal capsule, and the lowest motor cortex area for larynx and tongue, i.e., those areas of the brain typically implicated in speech production impairments in aphasic patients. These findings suggest that the neural instantiation of speech may require more extensive neural involvement including the perisylvian area than previously suggested, and that posterior areas are implicated as well in the normal production of speech. REFERENCES Alajouanine, T., Ombredane, A., & Durand, M. 1939. Le syndrome de la desintegration phonetique dans l’aphasie. Paris: Masson. Baum, S., & Biumstein, S. 1987. Preliminary observations on the use of duration as a cue to syllable-initial fricative consonant voicing in English. Journal of the Acoustical Society of America, 82, 1073-1077. Behrens, S., & Blumstein, S. 1988. Acoustic characteristics of English voiceless fricatives: a descriptive analysis. Journal of Phonetics, 16, 295-298. Blumstein, S. 1973. A phonological investigation of aphasic speech. The Hague: Mouton. Blumstein, S., Cooper, W., Goodglass, H., Statlender, S., & Gottlieb, J. 1980. Production deficits in aphasia: a voice-onset time analysis. Brain and Language. 9, 153-170. Blumstein, S., Cooper, W., Zurif, E., & Caramazza, A. 1977. The perception and pro15, 371-383. duction of voice-onset time in aphasia. Neuropsychologiu, Buckingham, H. W., & Yule, G. 1987. Phonemic false evaluation: Theoretical and clinical aspects. Clinical Linguistics and Phonetics, 1, 113-125. Duffy, J., & Gawle, C. 1984. Apraxic speakers’ vowel duration in consonant-vowel-consonant syllables. In J. C. Rosenbek, M. R. McNeil, & A. E. Aronson, (Eds.), Apraxia of speech. San Diego: College-Hill Press. Goodglass, H., & Kaplan, E. 1972. The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger Harmes, S., Daniloff, R., Hoffman, P., Lewis, J. Kramer, M., & Absher, R. 1984.Temporal and articulatory control of fricative articulation by speakers with Broca’s aphasia. Journal

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