DISARTRIA

J. COMMUN. DISORD. 19 (1986) 347-366

CLINICAL AND ACOUSTICAL VARIABILITY IN HYPOKINETIC DYSARTJ3RIA

E. JEFFREY METTER and WAYNE R. HANSON Veterans Administration Medical Center, Sepulveda, California

Ten male patients with parkinsonism secondary to Parkinsons disease or progressive supranuclear palsy had clinical neurological, speech, and acoustical speech evaluations. In addition, seven of the patients were evaluated by x-ray computed tomography (CT) and (F- 18)-fluorodeoxyglucose (FDG) positron emission tomography (PET). Extensive variability of speech features, both clinical and acoustical, were found and seemed to be independent of the severity of any parkinsonian sign, CT, or FDG PET. In addition, little relationship existed between the variability across each measured speech feature. What appeared to be important for the appearance of abnormal acoustic measures was the degree of overall severity of the dysarthria. These observations suggest that a better understanding of hypokinetic dysarthria may result from more extensive examination of the variability between patients. Emphasizing a specific feature such as rapid speaking rate in characterizing hypokinetic dysarthria focuses on a single and inconstant finding in a complex speech pattern.

The clinical syndrome of hypokinetic dysarthria as presented by Darley et al. (1975) suggested that the speech abnormality represented a relatively uniform syndrome that occurred with Parkinsons disease and more re- cently has been noted in progressive supranuclear palsy (PSP) (Hanson and Metter, 1980). PSP is a chronic progressive neurologic disorder of unknown etiology that occurs in middle or late life. The clinical features first described by Steele, Richardson, and Olezewski (1964) included ophthalmoplegia (mainly of vertical gaze), dystonic rigidity of the neck, pseudobulbar palsy, mild dementia, and dysarthria. Subsequent reports have described prominent parkinsonian features (Klawans and Ringel, 1971; Blumenthal and Miller, 1969; Behrman et al. 1969). Pathologic features are different from Parkinsons disease and include nerve cell loss, gliosis, neurofibrillary tangles, and demyelination in the basal ganglia and cerebellum. Marked atrophy of the midbrain and pontine tegmentum usu- ally exists (Steele et al., 1964).

Although the hypokinetic dysarthria is distinctive in these disorders, it has primarily been described from selected subjects with severe dysar-

Address correspondence to E. Jeffrey Metter, Department of Neurology, Veterans Ad- ministration Medical Center, 16111 Plummer Street, Sepulveda, CA 91343.

0 1986 by Elsevier Science Publishing Co., Inc. 347 52 Vanderbilt Ave., New York, NY 10017 002 l-9924/86/$03.50

348 E. J. METTER and W. R. HANSON

thria. Some speech features may vary greatly in parkinsonian patients who have less severe dysarthria, particularly in measures of speaking rate, fundamental frequency, and vocal intensity. Marked variability is also present in other clinical features that may occur in patients with hypokinetic dysarthria, including bradykinesia, tremor, rigidity, and overall degree of disability. Additionally, little information has been available con- cerning the agreement between speech adequacy and the overall degree of disability associated with the disease in these patients. Likewise, little emphasis has been placed on how the dysarthria relates to other features of the basal ganglia disorders.

The purpose of this study was to compare the clinical syndromes, brain anatomy, and glucose metabolism with speech characteristics in parkinsonian patients with varying degrees of hypokinetic dysarthria. Of interest was whether or not specific clinical, metabolic, or structural findings relate to some aspect of the dysarthria. Also of interest was the extent of variability that may exist between patients across the studied features.

METHODS

Seven male Parkinsons disease patients and one PSP patient were selected who had complete neurologic evaluations, x-ray CT, positron emission tomography (PET) and (F 18)-fluorodeoxyglucose (FDG), and motor speech evaluations. These eight subjects included one with severe and one with moderately severe dysarthrias. For this reason, two other subjects were included with severe hypokinetic dysarthrias who had complete motor speech and neurological evaluation but who were without CT or FDG-PET. Of the latter two patients, one had progressive supranuclear palsy and the other Parkinsons disease. The ten subjects had a mean age of 62 years, and the range was from 54 to 76 years. Age-matched controls for comparison of FDG scans were taken from the study of Kuhl et al (1982). Each subject had a neurologic examination that included ratings from 0 (normal) to 3 (severe) of bradykinesia, tremor, rigidity, and dementia. They were also rated by the staging scale of Hoehn and Yahr (1958), and by the scale of Webster (1979). All subjects were receiving medication at the time of testing. The eight subjects with Parkinsons disease were all taking levodopa. Neither PSP subject had responded to levodopa. One was receiving methylsergide, the other was taking anti- cholinergics. A clinical note was made for the degree of dyskinesia in each case.

Acoustic speech measurements including speaking rate, mean fundamental frequency, relative intensity, and vowel phonation time were made from tape-recorded speech samples. The recordings were analyzed using a microprocessor-controlled speech analyzer (PM 301, Voice Identifi- cation, Inc.), which we have described in a previous publication (Hanson

HYPOKINETIC DYSARTHRIA 349

and Metter, 1983). Each subject was recorded while seated in a sound- treated test room (IAC model 403A) directly in front of a microphone (Electrovoice model RE-15) that was coupled to an Ampex tape recorder (AF 600B) located in an adjacent test room. The mouth-to-microphone distance was 8 inches. The speech samples consisted of reading aloud the Grandfather Passage, and maximum sustained phonation of ah. Ten age-matched normal controls were tape recorded for comparison of acoustic speech measures.

The authors agreed on a rating of overall intelligibility, dysphonia, articulation, prosody, and hypernasality using the methods of Darley et al. (1975) for each connected speech sample. Each characteristic was graded on a seven-point scale (1 = normal to 7 = most severe deviation from normal). An index of total dysarthria severity was derived by adding together the scores for each of the five measures, resulting in a dysarthria scale ranging from 5 to 35.

X-ray computed tomography (CT) was done as part of the clinical evaluation and was evaluated qualitatively. Positron emission tomography (PET) was done on the ECAT II (Ortec, Oakridge, Tennessee) (Phelps et al., 1978). (Fl8)-fluorodeoxyglucose (FDG) was used as the isotope to examine glucose metabolism as modeled by Phelps et al. (1979). The resulting scans of the brain were projected onto a monitor, regions of interest were outlined, and corresponding local cerebral metabolic rate for glucose (LCMRGlc) were determined by the computer. Quantitative comparison of CT, PET, and clinical symptomatology of the Parkinsons disease subjects have been reported by Kuhl, Metter, and Riege (1984).

RESULTS

A number of measured speech parameters showed extensive variation in our subjects. To examine whether or not pattern to the variation existed, we focused on several features that were of particular interest, including: the clinical status (ratings of physical disability), severity of overall dysarthria, and speaking rate. These features were then compared across a number of variables.

Clinical Status: General Features

Clinical severity of parkinsonism was evaluated using the Webster scale, because it showed a strong correlation with the scales of Hoehn and Yahr (1958) and with the clinical scales from the neurologic examination. The Webster scale is linear with a range of 0 (normal) to 30 (most severe). Mild parkinsonism ranges from 0 to 10, moderate from 11 to 20, and severe 21 to 30. Comparing the level of clinical disability to the severity of dysarthria as judged by the dysarthria scale (Figure 1) demonstrated that


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Figure 1. Scattergram showing relations between perceptual index of total dysarthria severity and Parkinson disability as judged by the Webster scale (1979).

the most severe dysarthrias occurred with both mild and severe parkinsonian disability ratings. One subject with severe dysarthria but mild clinical disability was a 58-year-old male with a 6-to-g-year history of Par- kinsons disease. He initially presented complaining of a change in his speech, which was interfering with his ability to work as a traveling sales- man. He was noted by the examining physician to have a dysarthria and very mild features of parkinsonism. Over the years, the dysarthria became progressively worse more rapidly than other features of his disease. He is now essentially unable to communicate by speech, but he is independent in activities and is able to drive while being treated with levodopa. In contrast to this patient were two patients with severe clinical features who also displayed severe dysarthria. Both of these individuals had PSP.


Clinical Status: Specific Features

The lack of an absolute relationship between total parkinsonian disability and the severity of dysarthria raised the question of whether or not specific features of the parkinsonian syndrome might show association with the dysarthria. To answer this question, each subcategory of the Webster disability scale was studied independently. Ratings for three of these independent features, bradykinesia, rigidity, and facial motility, were compared to total dysarthria scores and no relationships were apparent. Like- wise, no relationship was observed between tremor, dyskinesia, or duration of parkinsonism and severity of dysarthria. The duration of disease for the ten subjects ranged from 2 to 18 years. Two subjects with severe dysarthria had had their illnesses for 2 and 10 years, respectively. Subjects with mild to moderate dysarthria showed great variation in the duration of their disease.

Speaking Rate

One of the most interesting and seemingly variable features of hypokinetic dysarthria is speaking rate. Our subjects, when compared to controls, form a continuum from much slower (77 wpm) than normal to much faster (263 wpm) than normal speaking rates. Rate did not relate to either the severity of clinical symptoms or severity of dysarthria as seen in Figures 2 and 3. Of three subjects with mild parkinsonism (Webster score < 1 l), one had an abnormally fast (245 wpm), one had a slow (96 wpm), and one a normal rate (168 wpm) as compared to normal controls (range 118 to 186 wpm). Of two subjects with the most severe clinical parkinsonism, one had a very rapid rate (263 wpm) and the other a slow rate (77 wpm). Normal speech rates were not observed in subjects with either severe clinical parkinsonism or with severe dysarthria. Both subjects with progressive supranuclear palsy had severe dysarthrias, one with a rapid rate, the other with a slower than normal rate. Likewise, of the subjects with Parkinsons disease, speech rates were found that were slower and faster than normal. Thus, extremes of rate were not specific for either disorder. No relationship was found between the degree of rigidity or bradykinesia and speaking rate.

Fundamental Frequency

Mean fundamental frequency for the reading passage was examined in relation to the clinical and dysarthria scales. Figure 4 demonstrates mean fundamental frequency in relation to the total dysarthria score and Webster scale for each patient. Data are also shown for normal control subjects.


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Figure 2. Scattergram between speech rate in words per minute and perceptual total dysarthria score. x = normal subjects, 0 = total dysarthria scores.

Mean fundamental frequency for each patient was within the normal range, though there was a tendency for fundamental frequency to increase with increased clinical disability and with increased severity of the dysarthria. Also, six of 10 subjects had a mean fundamental frequency greater than 130 Hz, whereas only one control was above this frequency.

Variability of Fundamental Frequency

Clinically, hypokinetic dysarthria is characterized by monopitch and hy- poprosody. To examine monopitch, the variation of fundamental frequency for each subject was examined during the reading of the Grand- father Passage. In Figure 5, coefficients of variability for frequency (the ratio of individual mean fundamental frequency standard deviation by the mean fundamental frequency) are plotted in relationship to dysarthria score, speech rate, and parkinsonian score. Some degree of inverse re-

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Figure 3. Scattergram between speech rate in words per minute and Parkinson disability score (Webster, 1979). x = normal subjects, 0 = Parkinson disability score.

Figure 4. Scattergrams between mean fundamental frequency and total dysarthria scores and Parkinson disability scores.

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Figure 5. Scattergrams between frequency CV (coefficient of variability) and total dysarthria score, speech rate, and Parkinson disability scores. x = normal, 0 = clinical group.

lation was apparent between FF-CV and both dysarthria severity and clinical disability, but not with speaking rate. Subjects with severe dysarthria showed FF-CV less than normal subjects. A low FF-CV was also seen in one subject with only a mild to moderate dysarthria, so that the change was not absolutely related to severity. Abnormal FF-CVs were observed in the presence of mean fundamental frequencies that were within the range of the normal controls, demonstrating the specificity of the problem of fundamental frequency variation.


Variability of Intensity

Mean relative intensity measures for the reading passage showed no apparent differences between the hypokinetic patients and controls. A comparison of variability of intensity (I-CV) to dysarthria scores, however, demonstrated that only the parkinsonian subjects with severe dysarthria showed a decreased variation in intensity as compared to controls (see Figure 6). Comparing I-CV to the rate of speech, loss of normal intensity

Figure 6. Scattergrams between intensity variability (coefficient of variability) and total dysarthria score, speech rate, and Parkinson disability score. x = normal, 0 = clinical group.

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variability was associated with both slow and fast rates but did not appear in the normal range of speaking rates.

Vowel Phonation Time

The ability to sustain phonation of ah was highly variable in our subjects. The range of phonation time varied from 6.12 to 37.89 seconds, as compared to the normal subjects who ranged from 11.72 to 33.94 seconds. Four parkinsonian subjects had phonation times less than 10 seconds, but the longest vowel prolongation for the 20 subjects was a parkinsonian individual (37.89 seconds). Three of four parkinsonian subjects with abnormally short vowel prolongation had only mild dysarthria (scale scores of 8, 14, and 14). No relationship was noted between vowel phonation time and degree of disability or severity of dysarthria.

Pause Time

An observation commonly made in hypokinetic dysarthria is the presence of abnormal pause time in connected discourse. This abnormality ranges from a complete lack of pauses, as seen in the rapid, fused form of the dysarthria, to the extended pauses noted in some speakers with very slow speaking rate. To illustrate the variations in pause time that may exist in

Figure 7. Fundamental frequency, relative intensity, and duration for the phrase a long flowing beard clings to his chin spoken by three subjects with hypokinetic dysarthria.


different hypokinetic speakers, tracings of a phrase from the Grandfather Passage are presented in Figure 7. Outputs (fundamental frequency and relative intensity) from the Pitch Analyzer (PM301) are displayed simul- taneously on two separate channels of a Mingograph (Model 805), op- erated at a paper speed of 50 mm per second. From these tracings the total duration of each phrase, indicative of the great variability in speaking rate, can be clearly seen. Also apparent is the variability in the location and extent of pauses within each phrase. The rapid, fused, aprosodic pattern without pauses displayed by patient A stands in marked contrast to the slow, prolonged pause pattern of patient C. However, common to both tracings is a flat fundamental frequency contour consistent with the reduced coefftcient of variability noted earlier, which seems to be characteristic of many speakers with hypokinetic dysarthria. To examine pauses further, we measured the percentage of the speech sample that represented pause time for each subject (Figure 8). In both normal and

Figure 8. Scattergrams of the percentage of the speech sample that was pause time and total dysarthria score and speech rate. x = normal, 0 = clinical group.

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hypokinetic subjects, we found an inverse relationship between the pause time and speech rate, although the slopes of the two relationships seem to be different. In general, for a given speech rate, the hypokinetic subjects had a greater percentage of pausing than did corresponding normal subjects. The degree of abnormal percentage of pause time was independent of the degree of dysarthria, occurring even in the subjects with the mildest degrees of dysarthria.

Effect of Treatment: Individual Case Study

One issue in hypokinetic dysarthria is the effect that medication, particularly levodopa, may have on speech. Drug treatment appears to exert differential influence on various features of the dysarthria. This can be demonstrated by considering a 58-year-old patient (Patient D) studied on and off medication. He had a 3-year history of mild Parkinsons disease based on the Webster scale (total score = 4) with mild rigidity, decreased arm swing, facial immobility, and dysarthria while on levodopa. In addition, he had dyskinesias and on-off phenomena that was treated with a drug holiday. On stopping his levodopa he became clinically worse, with a Webster score of 19. He was able to ambulate slowly and with great difficulty. He had severe loss of arm swing, moderate bradykinesia, rigidity, facial immobility, and he required moderate assistance in most activities of daily living.

On medication, the patient spoke with a slow speech rate (96 wpm), a prominent dysphonia that was hyperphonic with a relatively high fundamental frequency (mean = 142 Hz, SD = 28 Hz) for the reading sample. Off medication, his intelligibility went from good to moderately impaired, with a change in his overall dysarthria scale from 14 to 23. A change also occurred in his speech, which became slower in rate with increases in both articulation and pause time (Figure 9). This was associated with little change in his dysphonia but a moderate decrease in articulatory precision, prosody, and intensity. No changes were found in mean fundamental frequency, variability of intensity, or percentage pause time. Vowel prolongation that was short initially (7.70 seconds) fell by 51% (3.79 seconds). These observations demonstrate the differential changes that can occur in speech functions in conjunction with drug treatment with levodopa.

Variability of Severe Dysarthria in PSP

Hypokinetic dysarthria may include some speech features that are dis- tinctly different among subjects. This can be demonstrated in the two subjects with PSP (see Table 1). Both subjects were 58 years of age and showed severe disability, with Webster-scale scores of 21 and 22. Neither patient showed any improvement with L-DOPA. Both showed moderate


Figure 9. Fundamental frequency, relative intensity, and duration for the phrase a long flowing beard clings to his chin produced by a Parkinsons disease patient on and off of treatment for L-DOPA.

to severe rigidity, bradykinesia, were unable to look down, and had neck retroflexion. The first subject had been ill for at least 10 years, and for the first six years carried a diagnosis of Parkinsons disease before the full clinical picture of PSP appeared. His speech was rapid, with monopitch, monoloudness, decreased excursion of mouth movements, and decreased intensity. His reading passage showed a speaking rate of 263 wpm, the highest mean fundamental frequency observed in our patient group

Table 1. Comparison of Two Subjects with Progressive Supranuclear Palsy (PSP).

Measure Patient 1 Patient 2

Speech rate (wpm) 263 77 Articulation time (set) 22 57 Pause time (set) 8.35 45.74 % pause time 28% 45% Mean frequency (Hz) 151 147 Frequency variability .052 .040 Intensity variability 131 133 Phonation time (set) 12 7 Dysarthria score 28 26 Webster scale 22 21 Years of disease 10 2

Normal Range

118-186 35-47

7.66-25.71 18-42%

116-152 .lll-,247 188-224 12-34


(151 Hz), and a very low FF-CV (.052 compared to the normal range of . 111 to .247), indicative of his monopitch. He also showed limited ability in modifying his loudness as measured by the small coefficient of variability for intensity measures (. 131 as compared to the normal range of .188 to .224). Visual inspection of his speech tracing (Patient A, Figure 7) demonstrated almost constant voicing.

The second subject with PSP had his illness for only 2 years when studied. His dysarthria was similar in some respects to the patient just described; however, on two measures he differed greatly. First, he had a speaking rate of 77 wpm (Patient C, Figure 7), and second, he had a prolonged percentage of pause time (48%) as compared to the above case (28%) and to normal subjects (range 18-42%). The marked variability in speech rate and associated pause time in these two subjects appeared to be independent of other features of their dysarthria.

Effect of Time

Our general belief is that as parkinsonism progresses clinically a corresponding change should occur in speech. We have shown above a case in which the dysarthria was the presenting problem for a subject, consistent with a dissociation between speech and other clinical features. A second approach is to examine subjects repeatedly over time. One subject was evaluated on two occasions over a 4-year period. Clinically, the subject had shown a progression of his illness with a Webster scale increasing from 7 to 13 (mild to moderate disability). This progression was associated with increased rigidity and increased difficulty walking. The patient also began to have some on-off phenomena. At the most recent evaluation he also began to have marked problems in vertical eye movements suggesting that he may evolve a diagnosis of PSP rather than of Parkinsons disease. Over the 4-year period, his dysarthria actually showed some improvement, with the overall dysarthria severity score falling from 14 to 9. Acoustic speech measurements indicated that his speech rate slowed from 168 to 153 wpm, and mean fundamental frequency increased from 104 Hz to 124 Hz. His FF-CV showed a marked increase from .173 to .274, the latter measure being the highest observed in the 20 subjects. No change was observed in the I-CV. The principal observation in this case is that progression of clinical features of parkinsonism can be dissociated from changes occurring in the dysarthria.

Anatomic Correlates: CT

CT scans of the head did not show any distinct changes that could be related to any clinical feature of the illness or dysarthria in the seven subjects who underwent CT scans. Most subjects showed some degree of cortical atrophy, but this was consistently mild.


Glucose Metabolic Correlates: FDG PET

The metabolic data for these subjects while on treatment showed their mean metabolism to be in the low .normal range, as were the rates for each region studied (Kuhl et al., 1984). Global metabolic rates were sig- nificantly decreased as compared to controls, but no significant differences were found for language-related cortex, thalamus, or caudate. No correlations were found between glucose metabolic rates and duration of illness, stage of illness, dementia, tremor, rigidity, or dystonia. Scaled scores of bradykinesia were correlated (r > 0.70, p < .OS) with mean cortical and caudate LCMRGlc. Correlations were calculated between the individual components of our dysarthria scale and local glucose metabolic rates for left inferior frontal and caudate regions. None were found to be significant at the .05 level uncorrected for the number of comparisons. In general, no regional explanations were found for the nature or extent of dysarthria in these subjects based on the comparison of regional glucose metabolism.

Several observations were of interest in the subject who was described on and off treatment (see Figure lo), because he had FDG-PET scans in both states. Metabolic rates for glucose were far higher while he was treated than when off of medication (a mean glucose metabolic rate of 26

Figure 10. Positron tomographs of FDG that represent the distribution of glucose utilization. Four brain sections are presented on (upper figures) and off (lower figures) of L-DOPA therapy for one subject with Parkinsons disease. The darker the region, the greater is the LCMRGlc.


Figure 11. Positron tomographs of glucose utilization in subject with progressive supranuclear palsy (PSP).

brain regions being 3.77 mg / 100 gms tissue / minute off medication and 6.18 on medication). He was the only subject of three studied both on and off treatment who showed a difference in metabolic rates. The greatest relative changes were found in both high frontal areas, Wernickes region, and in both thalamic regions. The meaning of this response is unclear.

The subject with PSP and rapid speech rate (see Figure 11) demonstrated a 10% depression in his left hemisphere compared to right hemisphere metabolism. This unilateral depression was not seen in any other subject or in 31 controls but has been seen in some stroke patients with deep lesions in which the mechanism has been assumed to involve cortical activating systems (Kuhl et al., 1982; Metter et al., 1981, 1983). Whether or not this observation can be associated with the clinical state in this subject can only be speculated.

DISCUSSION

Acoustic characterization of hypokinetic dysarthria has placed emphasis on the rapid speaking form with reduced syllable durations, monotone fundamental frequency, and continuous voicing. Such speech has been referred to as fused (Kent and Rosenbek, 1982). Our data show that other acoustic patterns exist in hypokinetic dysarthria, including one with a very slow speaking rate that is characterized by articulated islands of speech separated by extended pauses (see Figures 7 and 9). These observations are consistent with a number of other studies that have noted variability in speech rates (e.g. Canter, 1965; Kreul, 1972; Boshe, 1966). Of particular interest in our study was the observation that other measured speech features tended to show large variability without a specific relationship to the speech rate. This implies that variation in rate does not dictate differences in the overall dysarthria but rather reflects only one feature of a much more complex problem.


Mild to moderate severity of dysarthria appeared to be associated with relatively normal rates of speech. With increasing severity of the dysarthria, the speech tended to be either increased or decreased in rate. Other measures associated with more severe dysarthria seemed to vary in a similar manner independent of a fast or slow rate. These included a relative increase in mean fundamental frequency with decreased fundamental frequency variation. What appeared to be important in the appearance of a variety of abnormal acoustic measures was the degree of severity of the dysarthria.

The similarity of acoustical findings between Parkinson disease patients and those with PSP suggests that hypokinetic dysarthria is not disease specific but rather reflects structural and/or functional abnormalities within the brain that are common to more than one disease. The appearance and extent of dysarthria in hypokinetic illnesses appears to be a phenomenon related to but independent of the appearance of any specific parkinsonian features. Further, our results show that severe dysarthria can occur in the presence of only mild clinical symptoms.

The lack of strong relationships between other clinical features and the dysarthria suggest that basal ganglia control of speech is somewhat different than for other movements. This may involve differences in specific locations within the basal ganglia, differences in the physiology of basal ganglia action on speech as compared to other movements, or differences in the peripheral organization of the motor system. The latter has been discussed by Hunker, Abbs, and Barlow (1982). Current techniques for studying the basal ganglia in vivo are not sensitive enough to allow for this distinction in man. Each basal ganglia nucleus is anatomically uniform in structure, but specific regions tend to receive greater innervation from specific cortical regions, and in fact cortical regions having strong cortical interconnections will tend to innervate similar regions of the caudate and putamen (Yeterian and Van Hoesen, 1978). This implies that if local areas of the basal ganglia are differentially affected, then selective involvement of speech function could occur. This would explain the findings in one of our subjects who had a severe hypokinetic dysarthria but few other clinical signs of Parkinsons disease.

From previous FDG PET studies, we have speculated that part of the function of the basal ganglia is to assist or allow cortical regions to function together in carrying out a task, acting much as a pacemaker (Metter et al., 1984). To examine caudate function, two basal ganglia diseases, Par- kinsons (PD) and Huntingtons (HD), were compared to a cortical disease, Alzheimers (AD), and to controls. Examining regional correlation matrices among 13 regions measured in each hemisphere within each disease group, the number of cortical regional reliable correlations (r values selected for p < .Ol unadjusted) was found to decrease in HD and PD


compared to age-matched controls. This differed from AD, in which an increase was found in cortical to cortical correlations. The findings suggested a loss in focusing of cortical activity related to basal ganglia pa- thology, which may account for some clinical features in HD and PD. Thus, basal ganglia damage could disrupt the ability of the cortex to in- tegrate the complexities of speech and tend to dissociate the laryngeal from articulatory functions and to disrupt prosody. Evaluation of CT and FDG PET in this study did not allow for further refinement of the earlier speculations.

To best understand hypokinetic dysarthria, a greater emphasis should be placed on the extent of variability between patients. Emphasizing a specific feature such as rapid speech rate to characterize hypokinetic dysarthria may be deceiving. Few variables specifically related to rate alone. The most meaningful understanding may result from an evaluation of a large mixed sample of parkinsonian subjects, examined using acoustical measures, with factor and cluster analysis performed in a manner similar to that used by Darley et al. (1975). It will also be necessary to study patients displaying a range of severity, whereas evaluating only subjects with moderate to severe dysarthria may be misleading. A greater emphasis should be placed on the extent of variability between patients. In our study, speech rate seemed to be independent of the severity of the parkinsonian symptoms exhibited by the subjects. In addition, few of the acoustic variables measured appeared to relate directly to speaking rate alone. It is clear that patients within the same type of dysarthria may have markedly dissimilar acoustic profiles. Univariate comparisons that em- phasize a single specific feature as characteristic of the whole group may be misleading. Multivariate approaches more accurately differentiate sub- categories of patients and should be of greater utility in identifying degrees of impairment and the effects of treatment for dysarthria. The acoustic profile method used to describe the pattern and severity of speech impairment highlights the differences that exist between patients and may result in improved treatment strategies. For the most propitious manage- ment of patients with hypokinetic dysarthria, the extreme variability in individual performance must be given due consideration. To understand the problem further, studies that include large mixed samples of parkinsonian subjects, multiple acoustic measurements, and factor and cluster analyses must be conducted. In addition, the type and severity of the impaired speech features must be identified and studied in relationship to other clinical symptoms.

The FDG studies were funded in part by Department of Energy Contract #DE-AM03-76- SSOOO12 and U.S. Public Health Service Research Grants ROl-GM-24839 and POl-NS- 15654.


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