344 J. Ogar et al. / Brain and Language 97 (2006) 343–350

dysarthria in that AOS is not caused by muscle weakness.Also, errors heard in dysarthric speech are usually consis-tent and predictable, while errors heard in apraxic speechare unpredictable (Wertz et al., 1984). AOS diVers fromaphasia in that speech errors indicative of AOS are non-lin-guistic in nature and therefore, distinct from those heard inaphasia. AOS can occur independently of language-relatedimpairments in auditory comprehension, reading compre-hension and writing (Darley, Aronson, & Brown, 1975).

In speech production models, AOS is typically regardedas a problem that occurs at an intermediate level of speechproduction, between utterance formulation (where aphasicerrors occur) and the muscular execution of motor plans inthe articulation of speech (where dysarthric errors occur)(Darley et al., 1975). Darley Wrst conceived of AOS as aproblem at the level of the “motor speech programmer.” Inhis model, the motor speech programmer receives theabstract phonological/phonetic representation of a portionof the linguistic message, interprets this code, selects andsequences movement routines, sends the orchestrated sen-sorimotor commands to the articulators and internallymonitors the execution of the plan (Darley et al., 1975).Following this view, DuVy deWnes AOS as:

“ƒ a motor speech disorder resulting from the impair-ment of the capacity to program sensorimotor commandsfor the positioning and movements of muscles for the voli-tional production of speech. It can occur without signiWcantweakness or neuromuscular slowness, and in the absence ofdisturbances of thought or language.” (DuVy, 1995).

The motor speech evaluation (MSE) has been widelyused in the diagnosis of AOS (see Wertz et al., 1984). TheMSE elicits speech samples with such tasks as vowel prolon-gation, repetition of syllables, words, and phrases, oral read-ing, and picture description. Typically, a speech–languagepathologist determines the presence or absence of AOS and/or dysarthria by analyzing patient performance on thesetasks. Salient symptoms that emerge in patients with AOSinclude one or more of the following: “(1) eVortful, trial anderror groping with attempts at self-correction; (2) dyspro-sody unrelieved by extended periods of normal rhythm,stress and intonation; (3) articulatory inconsistency onrepeated productions of the same utterance, and/or (4) obvi-ous diYculty initiating utterances” (Wertz et al., 1984).

In a previous paper, we analyzed behavioral and lesiondata from 25 chronic stroke patients diagnosed with AOSand compared them to 19 patients without AOS (Dronkers,1996). In that study, all patients with AOS were found tohave lesions in the left superior precentral gyrus of theinsula (SPGI), an area medial to frontal and temporal cor-tex. Moreover, this study showed that 19 patients withoutAOS spared the same circumscribed SPGI area despite hav-ing large middle cerebral artery lesions that involved ante-rior areas. Such a dissociation is strong evidence that thissmall region within the insula plays a signiWcant role incoordination of articulatory movements.

In the current study we sought (1) to explore whetherpatients with AOS produce distinct error proWles on the

MSE; and (2) to investigate the relationship between sever-ity of AOS and the extent of the lesion. To do this, we eval-uated stroke patients with and without AOS for whomvideotaped MSEs were available. Performance on nine sub-tests of the MSE was analyzed to ascertain which taskswere particularly sensitive to the presence of AOS. Thesepatients’ scores on aphasia and dysarthria measures werealso evaluated to determine if there was a relationshipbetween AOS and these two disorders. Finally, lesion vol-umes were calculated and correlated with AOS severity toexamine the relationship between lesion size and severityratings.

2. Methods

2.1. Participants

We evaluated videotaped MSEs for 18 patients with AOSand 8 patients without AOS. Patients were recruited from adatabase of 150 patients at the Center for Aphasia andRelated Disorders in Martinez, CA. Inclusionary criteria forall patients included: a single, left hemisphere cerebralvascular accident (CVA), right-handed, at least one-yearpost-CVA, native English-speakers, normal or corrected-to-normal hearing, and no prior history of neurologic, psychiat-ric or substance abuse problems. Inclusion criteria alsorequired a complete, videotaped MSE and available lesionreconstruction data for each patient. Only 26 patients metthese strict criteria; all others were excluded due to lack of avideotaped MSE. Data from some of the patients with AOS(56%) were used in an earlier study (Dronkers, 1996). Demo-graphic information on all patients, as well as speech andlanguage severity scores are presented in Table 1.

Patients’ lesions were evaluated based on CT or MRIimages obtained at least three weeks post-onset of thestroke. Lesions were reconstructed onto 11 templates basedon the brain atlas of DeArmond, Fusco, and Dewey (1989)(see Fig. 1). Reconstructions were completed by a board-certiWed neurologist, experienced in using these templates.Lesion reconstructions were then entered into a Macintoshcomputer with software developed at the Veterans AVairsNorthern California Health Care System (VANCHCS) inMartinez, California (Frey, Woods, Knight, Scabini, &Clayworth, 1987).

All participants read and signed consent forms prior totesting. The data were collected as part of a larger studyapproved by the Institutional Review Board at the VANC-HCS, Martinez, CA.

2.2. Materials and procedures

The motor speech evaluation (MSE) was administeredto patients in a noise-attenuated testing room. The MSEconsists of nine subtests, which include:

(1) Vowel Prolongation. The examinee is asked to take amedium-sized breath and prolong the vowel “ah,” as

J. Ogar et al. / Brain and Language 97 (2006) 343–350 345

long as possible. This subtest helps determine whetheradequate breath support is present for speech and tolisten for tremor or Xuctuations in volume.

(2) Sequential Diadochokinesis. The examinee repeatsone-syllable strings multiple times (“pa, pa, paƒ”,“ta, ta, taƒ”, and “ka, ka, kaƒ”).

(3) Alternating Diadochokinesis. The examinee alternatesbetween the three-syllable utterance “pataka” as rap-idly and smoothly as possible.

(4) Single Repetition of Multisyllabic Words. The exam-inee repeats three multisyllabic words (‘gingerbread’,‘snowman’, and ‘television’) one time after the exam-

Table 1Demographic information and speech and language scores for AOS and non-AOS patients

Note. AQ, Aphasia Quotient on the Western Aphasia Battery.a Non-AOS group comprised of (5) Wernicke’s Aphasia, (2) Anomic, and (1) WNL based on WAB classiWcation. Fluency, Auditory Comprehension,

Repetition and Naming scores are subtests of the WAB.

Patient Age (years)

TPO (months)

Edu (years)

Aphasia type

AOS (0–7)

Dysarthria (0–7)

AQ (0–100)

Fluency (0–10)

Aud Comp(0–10)

Repetition (0–10)

Naming (0–10)

Lesion vol. (ccs)

Mild AOS1 55 55 14 WNL 1.5 2.5 95.5 9 9.5 9.8 9.7 33.12 58 34 14 Anomic 2.5 2 91.5 9 9.7 9.7 8.3 128.13 75 99 20 Anomic 2 1.5 92 8 10 9.8 10 58.54 68 73 16 Anomic 2.5 1 86.7 6 9.8 9.9 9.7 129.6

Moderate AOS5 68 16 Broca’s 4.5 5.5 26.1 0 8 3.2 2 159.76 31 16 13 Broca’s 4 1 69.8 4 9.2 4.5 9.3 1697 70 112 18 Conduction 4 3.5 77.1 5 9.4 6.6 9.3 107.28 70 251 12 Broca’s 5 2 26.7 1 6.2 1.6 1.7 198.89 62 21 13 Broca’s 4.5 3 44.2 4 7.7 3.2 4.3 64.9

10 48 44 14 Broca’s 4.5 1 61.8 4 8.6 5.3 6.7 12111 79 99 12 WNL 4 4 94.2 9 10 8.5 10 116.812 66 152 10 Broca’s 5.5 2.5 44.3 2 7 3.9 5.2 148

Severe AOS13 45 10 16 Broca’s 6 1 35.8 2 9 2.5 4 152.714 77 25 14 Global 7 3.5 7.8 0 3.9 0 0 84.315 80 33 9 Broca’s 7 10.4 0 3.2 0 0 232.816 49 11 12 Broca’s 7 0 9.6 0 2.3 0 0 238.417 79 131 16 Broca’s 6 0 34.1 0 7.2 0 0 261.718 56 131 13 Broca’s 7 27.5 1 6.5 1.8 3.5 141.9

AOS average 63.1 72.9 13.9 4.7 2.1 52.0 3.6 7.6 4.5 5.2 141.5Non-AOS average 69.6 29.5 16.0 a 0.0 0.1 63.2 8.3 6.5 5.2 5.4 68.3

Fig. 1. Comparison of computerized lesion overlapping in patients with and without apraxia of speech (AOS). (A) Overlapping the lesions of 18 patientswith AOS lesions shows a common area of infarction (in bright yellow). (B) Overlapping the lesions of 8 patients without AOS lesions shows damage tomuch of the left hemisphere, but not the superior precentral gyrus of the insula (SPGI). (For interpretation of the references to colour in this Wgure legend,the reader is referred to the web version of this paper.)

346 J. Ogar et al. / Brain and Language 97 (2006) 343–350

iner provides a model. Stimuli contain consonantclusters and require movement between diVerentplaces of articulation.

(5) Multiple Repetitions of Multisyllabic Words. Theexaminee repeats three polysyllabic words (‘artillery,’‘impossibility’, and ‘catastrophe’) Wve times each.Words include consonant clusters and require rapidmovement between multiple places of articulationduring productions of each word.

(6) Single Repetition of Monosyllabic Words. The exam-inee is asked to repeat single, monosyllabic words onetime after the tester provides a model. Each wordbegins and ends with the same consonant (e.g., ‘nine’,‘judge’), so that minimal movement is requiredbetween places of articulation.

(7) Words of Increasing Length. The examinee repeatssimilar words that increase in number of syllables(e.g., ‘jab,’ ‘jabber,’ and ‘jabbering’). This subtest mea-sures the ability to sequence the correct number ofsyllables in the proper order. Some speakers of AOShave shown a tendency to make more errors onlonger words than on shorter words (Wertz et al.,1984).

(8) Repetition of Sentences. The examinee repeats sen-tences composed of frequent and infrequent wordchoices (e.g. ‘In the summer they sell vegetables,’‘Arthur was an oozy, oily sneak’).

(9) Reading of “Grandfather Passage .” The examineereads a brief, phonetically balanced paragraph thatcontains most of the sounds produced by Englishspeakers. This test was included as a means to com-pare speech during oral reading to speech on repeti-tion and more purposeful, volitional tasks (Wertzet al., 1984).

Two licensed speech–language pathologists (SLP), bothof whom were blind to lesion information, reviewed video-taped administrations of the MSE for each patient selectedfor study. The SLPs independently scored patients’ MSEperformance, using a severity scale (0–7, with ‘0’ indicatingno deWcit and ‘7’ a severe impairment) on each subtest. Inaddition, the SLPs assigned an overall AOS and dysarthriascore, based on the same severity scale described above.Results below are averages of the two clinicians’ scores. Theinter-rater correlation for overall AOS severity was veryhigh, r (18)D .95.

3. Results

Overall severity ratings for the patients with AOSranged from one to seven, indicating deWcits that rangedfrom mild to severe. Of those patients, four were rated ashaving mild AOS (with a score of 1–3), eight presented withmoderate AOS (with a score of 4–5), and six were rated ashaving a severe AOS (score of 6–7). These classiWcationswere veriWed by K-means cluster analysis, with the excep-tion of one patient who, with a severity score of 5.5, classi-

Wed statistically as having severe, rather than moderateAOS.

AOS patients had mean severity scores greater than 1.00on all MSE subtests, with scores ranging from 1.44 to 5.42.Four of the nine subtests were especially diYcult for AOSpatients. These included: Alternating Diadochokinesis(MeanD 5.42), Multiple Repetitions of MultisyllabicWords (MD 4.96), Repetition of Sentences (MD4.70), andReading of ‘The Grandfather Passage’ (MD4.89). All pair-wise t tests on the data from the AOS patients were per-formed to compare diVerences in patients’ performance foreach pair of subtests. SigniWcant diVerences were foundbetween each of these four subtests and each of the remain-ing Wve, indicating that tasks in these four tests posed themost diYculty for apraxic speakers (tD3.37, p 6 .005 forall comparisons). None of these four subtests diVered sig-niWcantly from each other (tD 1.59, p 7 .13, NS). Thesefour subtests all involve the production of multisyllabicwords and sentences that require immediate shifting inplace and manner of articulation (e.g., repeating the word‘catastrophe’ Wve times).

The Wve remaining MSE subtests that rendered numeri-cally lower severity scores did not involve multiple repetitionsof consonant clusters or words that required rapid coordina-tion of the lips, tongue, velum, and larynx (e.g., repetition ofsingle syllable words, such as ‘mom’). These subtests were:Vowel Prolongation (MD1.44), Sequential Diadokinesis(MD3.53), Single Repetitions of Multisyllabic Words(MD3.34), Single Repetitions of Monosyllabic Words(MD2.31), and Words of Increasing Length (MD3.43).

To further characterize performance on the MSE, scoreswere compared between mild, moderate, and severelyaVected speakers with AOS. All patients showed the sameoverall pattern of having the most diYculty with the foursubtests noted above. Severely aVected patients had diY-culty across all nine subtests, while mildly aVected AOSspeakers had diYculty with subtests requiring rapid alter-nation between places of articulation, including AlternatingDiadochokinesis and Multiple Repetitions of MultisyllabicWords. This suggests that performance on these two sub-tests, particularly when compared to performance onSequential Diadochokinesis and Single Repetition ofMonosyllabic Words, can detect AOS in even the mildestpatients.

Patients without AOS had little diYculty with any of theMSE subtests. They scored 0 on all subtests except Alter-nating Diadochokinesis, which yielded a mean severityscore near 1. Severity scores for each MSE subtest for allpatients are shown in Fig. 2. Due to non-overlapping diVer-ences between the AOS and non-AOS groups and the lackof variance in the non-AOS group, the need for statisticalanalysis was obviated.

3.1. Aphasia and dysarthria

All but two of the patients with AOS also presented withaphasia. A correlation was performed measuring the rela-

J. Ogar et al. / Brain and Language 97 (2006) 343–350 347

tionship between AOS severity and aphasia severity (basedon Aphasia Quotient scores from the Western Aphasia Bat-tery (WAB)). This relationship was signiWcant, r (18)D .90,p6 .05, suggesting that participants with more severe AOStended to have more severe aphasia. Patients with severeAOS presented with Broca’s or global aphasia. Patients withmild AOS had anomic aphasia or performed within normallimits on the WAB. Moderately impaired AOS speakers pre-sented with Broca’s aphasia, conduction aphasia or per-formed within normal limits. Of the patients without AOS,Wve had Wernicke’s aphasia, 2 had Anomic aphasia and onescored within normal limits. See Table 1 for AOS, dysar-thria, aphasia ratings, and other demographic information.

A dysarthria rating was obtained for AOS patientsbased on the MSE. (In two cases, the two raters did notagree on the presence of dysarthria so scores were omittedfrom the analysis). Of these 16 patients, 14 presented withdysarthria ranging in severity from 1 to 6. A correlationalanalysis revealed that the relationship between AOS anddysarthria severity was not signiWcant, r (16)D .32, p 6 .05,suggesting that there is no relationship between AOS anddysarthria severity.

To address the second question, we examined the relation-ship between AOS severity and the extent of the lesion. Totallesion volumes for AOS patients were calculated and rangedfrom 33 to 261 cubic centimeters (cc). The average lesion vol-ume for AOS patients was 141.5cc and the median was 135.75.(For the non-AOS patients, the range was 7.4–166.5cc. Theaverage lesion volume was 68.3cc and the median was 55.2cc).There was a signiWcant correlation in the 18 AOS patients

between lesion volume and AOS severity, r (18)D .61, p<.01,indicating that patients with larger lesions tended to havemore severe deWcits. Mild AOS speakers had an average lesionvolume of 68.8cc, moderately aVected patients had an averagevolume of 113.0cc, and severely impaired AOS patients hadan average lesion volume of 140.0cc.

To investigate the eVect of lesion site, overlays of MRIreconstructions were generated for each of the AOS sever-ity groups. Consistent with Dronkers (1996), all AOSpatients had lesions that involved the SPGI (see Fig. 3).Mildly aVected patients tended to have lesions restricted tothe insula and immediately surrounding areas. Moderately-impaired patients had lesions encompassing the SPGI andmiddle frontal gyrus, with most lesions also involvingBroca’s area, the basal ganglia, external capsule, and inter-nal capsule. Severely-aVected patients had lesions involvingall of these areas, as well as Wbers of the superior longitudi-nal fasciculus (SLF). Some severe patients also had involve-ment of primary auditory cortex (Brodmann’s areas 41 and42) and of anterior Brodmann’s area 22. In general, patientswithout AOS had more posterior lesions.

4. Discussion

In this paper, we set out to answer two questions. OurWrst purpose was to determine whether mild, moderate andsevere AOS patients with lesions to the SPGI showed char-acteristic patterns of performance on the MSE. Our secondaim was to explore how AOS severity was inXuenced bylesion volume and the extent of the lesion.

Fig. 2. Mean severity scores and conWdence intervals on the motor speech evaluation (MSE) for patients with mild, moderate and severe apraxia of speech(AOS). All patients showed the same pattern of having diYculty on the four subtests noted in this Wgure. Severe patients had diYculty with all subtests,while mildly aVected patients had diYculty on two tests in particular: Alternating Diadochokinesis and Multiple Repetitions of Multisyllabic Words, bothof which require rapid alternation between places of articulation.

Vowel Prolongation

Sequential Diadochokinesis

Alternating Diadochokinesis

Single Reps of Multisyl Words

Multiple Reps of Multisyl Words

Single Reps of Monosyl Words

Words of Increasing Length

Repetition of Sentences

Grandfather Passage

MSE Subtest

mea

n

seve

rity

sco

re

348 J. Ogar et al. / Brain and Language 97 (2006) 343–350

To explore the Wrst question, we analyzed motor speechevaluation (MSE) performance and showed that patientswith AOS had the most diYculty with four of the nine sub-tests: Alternating Diadochokinesis, Multiple Repetitions ofMultisyllabic Words, Repetition of Sentences, and theReading of The Grandfather Passage. Though other sub-tests elicited apraxic errors as well, the tasks in these sub-tests rendered poorest performances as indicated by thehighest severity scores.

AOS patients had less diYculty with Vowel Prolonga-tion, Sequential Diadochokinesis, and Single Repetitionsof Single Words (both mono- and multisyllabic). In otherwords, simple articulation was not enough to causespeech errors for AOS patients. Even mildly aVected AOSpatients performed poorly on two tests in particular:Alternating Diadochokinesis and Multiple Repetitions ofMultisyllabic Words. We hypothesize that it is the com-plexity of the articulatory movements required on thesesubtests that most reliably evoke speech errors in anapraxic speaker. Thus, these two subtests on the MSE,when compared to Sequential Diadochokinesis and Sin-gle Repetitions of Monosyllabic Words, may serve as aquick clinical means of assessing for AOS, as the discrep-ancy between these pairs of tests is typical of all our

patients with AOS, even those with a mild form of thedisorder.

The authors of the MSE considered complexity whenthey chose the words, phrases and sentences that comprisethe MSE (Wertz et al., 1984). Subtests were designed spe-ciWcally to elicit apraxic errors because it had already beenacknowledged that AOS speakers would have diYcultywith multisyllabic words, words of increasing length andthose containing consonant clusters. Wertz et al. (1984)have noted that descriptions of AOS have evolved andexpanded over the years since they were Wrst detailed byDarley—so much so that AOS is now associated withnearly 30 diVerent articulatory, rate, and prosody charac-teristics (DuVy, 1995).

Since Darley’s time, a number of perceptual, acousticand physiologic studies have further enhanced our under-standing of complexity as it relates to AOS (Kent & Rosen-bek, 1983); (McNeil, Hashi, & Southwood, 1984); (Square-Storer & Apeldoorn, 1991). These studies have shown thathigh frequency words are easier for apraxic speakers thanlow frequency words, meaningful words are easier thannon-meaningful words, and bilabial and lingual–alveolarplaces of articulation are easier than other places ofarticulation (DuVy, 1995). Research has also shown that

Fig. 3. Comparison of computerized lesion overlapping in patients with mild, moderate and severe apraxia of speech (AOS), as determined by severityscores on the motor speech evaluation (MSE). Patients with mild AOS had lesions restricted to the superior precentral gyrus of the insula (SPGI) or imme-diately adjacent areas. Moderately aVected patients had lesions encompassing the SPGI, middle frontal gyrus and, in most cases, Broca’s area, the basalganglia, and the internal and external capsules. Patients with severe AOS had lesions in all the areas, as well as the superior longitudinal fasciculus (SLF),primary auditory cortex, and anterior Brodmann’s area 22.

J. Ogar et al. / Brain and Language 97 (2006) 343–350 349

oral–nasal distinctions are easier to articulate than voicingdistinctions, which are easier than manner distinctions,which are easier than place distinctions (DuVy, 1995).

Consistent with these studies, we found that MSE sub-tests that compound these complexity factors are the sameas those that were most diYcult for patients with AOS. Forexample, when asked to repeat ‘catastrophe’ Wve times (inthe Repetitions of Multisyllabic Words subtest), the exam-inee encounters six of the complexity factors noted above.The word is repeated multiple times, is multisyllabic,involves travel between posterior and anterior points ofarticulation, includes consonants that change in place andmanner (/k/ – a velar stop - and /f/ – a labiodental fricativeboth appear), is a low frequency word, and contains a con-sonant cluster (“str”). This task elicited an average severityscore of 4.96.

MSE subtests that were relatively easy for AOS speakerscombined fewer complexity factors. For example, whenasked to produce ‘ka’ multiple times (as part of the Sequen-tial Diadochokinesis subtest), only two elements of com-plexity are confronted: stimuli are not real words and theyare repeated multiple times. This task elicited a mean sever-ity score of 3.53. Similarly, words included in the SingleRepetitions of Monosyllabic Words subtest contain onlyone of the noted complexity factors in that some of thestimuli are low frequency words, (e.g., “judge,” or “lull”).Thus, it is not surprising to Wnd that these subtests are lesslikely to elicit apraxic errors.

In this study, an item-by-item analysis of errors was notperformed, as we sought information that would be mostuseful in a busy clinical environment. Describing sucherrors would be worthwhile, as it may further guide clini-cians in designing therapy for AOS patients. For example,the Apraxia Battery for Adults-2 (ABA-2) (Dabul, 2000),provides a helpful qualitative list of error types that canguide clinicians planning therapy. For instance, in a patientwith mild AOS who presents with relatively Xuent speech,improving prosody may be more eYcacious than workingto enhance posturing for speech sounds.

Our second goal was to examine the relationshipbetween AOS severity and the extent of the lesion. As inDronkers (1996), all patients with AOS had lesions thatinvolved the SPGI. We also found that larger lesionsextending into neighboring regions such as Broca’s areaand the basal ganglia were associated with more severeAOS. This may be because other neighboring areas (e.g., thebasal ganglia, Broca’s area, and the ventral post-centralgyrus) play some role in speech praxis, or it could merely bethat co-occurring language deWcits inXuence speech pro-duction in patients with AOS. For example, speech deWcitshave also been reported in patients with damage to premo-tor areas (areas 6 and 44), the supplementary motor area(area 6), white matters regions (particularly those medial toBroca’s area), and parietal cortex (Square & Martin, 1994).

Larger lesions that extend into neighboring speech and/or language processing regions probably explain the corre-lation we found between AOS and aphasia severity (e.g.,

patients with more severe AOS tended to have more severeaphasia). We also found that AOS severity did not correlatewith dysarthria severity. That there is apparently no corre-lation between the two disorders is not entirely surprising.Though AOS and dysarthria are both motor speech disor-ders, they diVer in important ways. Dysarthria can aVectphonation, resonance, articulation or prosody as the resultof damage to the central (usually primary motor) or periph-eral nervous system (Darley et al., 1975). In AOS, however,articulation is primarily disrupted, rather than resonance orphonation, due to central nervous system damage. In mod-els of speech motor processing, dysarthria is thought to becaused by a deWcit at the end-stage execution of articula-tion, while AOS is considered to be impairment at a moreintermediate, programming stage.

In future research, it may be fruitful to view AOS as acollection of symptoms that together have traditionallybeen recognized as a singular motor speech disorder. Forexample, some of the speech deWcits related to AOS areseemingly motoric (e.g., groping) and others more lan-guage-like (e.g., transpositions). The variety of AOS-likemotor speech deWcits have been associated with an equallywide variety of lesion sites, including the insula, frontal, andtemporoparietal regions, as well as subcortical white matterareas (Square & Martin, 1994). It is conceivable that eachof these diVerent brain regions contributes in a distinct wayto motor speech production. Here, we have characterizedthe pattern seen in AOS patients with SPGI lesions. Futureresearch may beneWt from examining whether these behav-ioral diVerences may be related to functions in speciWcregions of the speech and language network.

Acknowledgments

This research was supported by NIH/NINDS 5 P01NS040813-2 and NIH/NIDCD 5 R01 DC00216-20.

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