Brain and Cognition 55 (2004) 240–246 www.elsevier.com/locate/b&c Crossed apraxia of speech: A case report Venu Balasubramaniana,* and Ludo Maxb a Speech-Language Pathology and Audiology, Seton Hall University, South Orange, NJ 07079, USA b University of Connecticut, USA Accepted 12 February 2004 Available online 9 April 2004 Abstract The present study reports on the first case of crossed apraxia of speech (CAS) in a 69-year-old right-handed female (SE). The possibility of occurrence of apraxia of speech (AOS) following right hemisphere lesion is discussed in the context of known occurrences of ideomotor apraxias and acquired neurogenic stuttering in several cases with right hemisphere lesion. A current hypothesis on AOS—the dual route speech encoding (DRSE) hypothesis—and predictions based on DRSE were utilized to explore the nature of CAS in SE. One prediction based on the DRSE hypothesis is that there should be no difference in the frequency of occurrence of apraxic errors on words and non-words. This prediction was tested using a repetition task. The experimental stimuli included a list of minimal pairs that signaled voice–voiceless contrasts in words and non-words. Minimal-pair stimuli were presented orally, one at a time. SEÕs responses were recorded using audio and videotapes. Results indicate that SEÕs responses were characterized by numerous voicing errors. Most importantly, production of real word minimal pairs was superior to that of non-word minimal pairs. Implications of these results for the DRSE hypothesis are discussed with regard to currently developing perspectives on AOS. Ó 2004 Elsevier Inc. All rights reserved. 1. Introduction Liepmann (1900) hypothesized that the left hemisphere is dominant for learned skilled movements in right-handed individuals. A century of research that followed this assertion has focused on the relationship between localized lesions in the left hemisphere and a variety of apraxias, including apraxia of speech (AOS). From a historical perspective, it is interesting to note that the possible sites of lesion(s) that could cause AOS have increased from one to three different regions of the left hemisphere (Dronkers, 1996; Kuriki, Mori, & Hirata, 1999; Nagao, Takeda, Komori, Isozaki, & Hirai, 1999). AOS was initially linked to a frontal lobe lesion of the left hemisphere (Darley, Aronson, & Brown, 1975). A parietal lobe lesion was reportedly another possible site of lesion resulting in AOS (Luria, 1966). Furthermore, subcortical lesions of the left hemisphere were also reportedly associated with AOS (Kertesz, * Corresponding author. E-mail address: balasuve@shu.edu (V. Balasubramanian). 0278-2626/$ - see front matter Ó 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.bandc.2004.02.005 1984). A recent study has reported that patients with ParkinsonÕs disease may also exhibit symptoms of AOS (Howard, Binks, Moore, & Playfer, 2000). It seems that advances in neuroimaging techniques and neurocognitive modeling have begun the process of gradually revealing the intricate network of neural structures underlying motor speech programming (MSP). Findings presented here support inclusion of the right hemisphere as a critical (or maybe even dominant in some individuals) neural location for MSP in right-handed adults. Several lines of previous work are consistent with this perspective. Recent studies of ideomotor apraxia offer supportive evidence for the fractionation of cognitive systems underlying hand preference and skilled movements (Raymer et al., 1999). Several case studies have reported ideomotor apraxia following isolated dorsolateral right hemisphere and subcortical lesions (Raymer et al., 1999), right subcortical—including the striatum—and right fronto-temporal lesions (Mozaz, Marti, Carrera, & Puente, 1990), and lesions of the right mesial frontal area including the supplementary motor area and the genu of the corpus callosum (Marchetti & Della Sala, V. Balasubramanian, L. Max / Brain and Cognition 55 (2004) 240–246 1997). These case reports strongly suggest that the right hemisphereÕs role in controlling learned movements is of such a nature that a disruption of this component of the distributed bilateral neural networks underlying motor control can lead to apraxia. Another area of research that pertains to the role of the right hemisphere in motor speech production is acquired neurogenic stuttering (ANS). Acquired neurogenic stuttering, a neuromotor disorder of speech (Duffy, 1995), has been reported in a few cases following right hemisphere lesions (Ardila & Lopez, 1986; Horner & Massey, 1983; Soroker, Bar-Israel, Schechter, & Solzi, 1990). These studies confirm that the both hemispheres play an important role in MSP. Kurowski, Blumstein, and Mathison (1998) study of consonant and vowel production in right hemisphere lesioned subjects offers further support for the same notion. Advances in neuroimaging have further enhanced our understanding of the neural substrates of motor speech. In a recent functional magnetic resonance imaging (fMRI) study of speech production (Riecker et al., 2000), it was found that repetition of CV and CCCV monosyllables elicited bilateral symmetric hemodynamic responses in the primary sensorimotor cortex. However, repetition of polysyllabic lexical items led to a lateralized hemodynamic response in the left hemisphere. Hence, speech production may involve bilateral and/or unilateral left hemisphere hemodynamic activation depending on the degree of articulatory complexity/sequencing required by the specific speech tasks. Taken together, the neuroimaging data, lesion data from studies of ideomotor apraxias in right hemisphere patients, and ANS in right hemisphere damaged dextrals, seem to suggest that AOS may also occur as a result of right hemisphere lesions. Indeed, such occurrence was reported in recent studies (McNeil, Doyle, & Wambaugh, 2000). However, neither descriptive information nor theoretical discussions on such cases are available in the existing literature on apraxia of speech. If AOS can occur as a result of right hemisphere lesions, how shall we account for the nature of crossed apraxia of speech (CAS)? Apraxia of speech is ‘‘an articulatory disorder resulting from impairment, as a result of brain damage, of the capacity to program the positioning of speech musculature and the sequencing of muscle movements for the volitional production of phonemes. No significant weakness, slowness, or incoordination in reflex and automatic acts. Prosodic alterations may be associated with the articulatory problem, perhaps in compensation for it’’ (Darley et al., 1975). Although DarleyÕs definition of apraxia of speech is a widely used one, there is no commonly agreed upon definition in this area of study. Three major classes of characteristics of AOS are related to the domains of (1) articulation, (2) prosody, and (3) fluency. Some of the commonly observed articulation 241 characteristics of AOS include the following: (1) substitutions of sounds are more frequent than other types of errors, (2) bilabials are better preserved than other sounds, (3) phonetically complex sounds such as affricates and fricatives are more frequently affected than other sounds, (4) difficulty in consistently realizing speech sounds, (5) more errors on nonsense syllables and nonsense words than on meaningful words, (6) more articulation errors on volitional speech than on automatic speech, (7) less frequent sounds could increase articulatory errors. Prosodic characteristics that are commonly encountered in persons with AOS include: (1) restricted intonation contours, (2) dysprosody, (3) syllable segregation, and (4) Ôforeign accent.Õ Speech fluency may be disrupted by repetition of sounds/syllables, (2) multiple attempts at producing target words, (3) speech initiation difficulty, and (4) groping for placement of articulators for speech sound production. Various combinations of these characteristics may occur in any given individual with this condition. But no single apraxic will evidence all the symptoms listed here. Besides, rarely does AOS occur in its pure form. On the contrary, it commonly co-occurs with aphasia and/or other apraxias. The co-occurrence of aphasia and AOS will certainly raise questions about the nature of AOS. Therefore, it is not at all surprising to encounter conceptual problems in the study of the nature of AOS as expressed in numerous theories of AOS, including those arguing that AOS may be a language based disorder and not a pure motor speech problem. A recent suggestion among contemporary theories is the dual route speech encoding (DRSE) hypothesis (Varley & Whiteside, 1998, 1999; Whiteside & Varley, 1998) which uses a psycholinguistic model to account for the characteristics of AOS. Unlike the Ôserial-orderingÕ models of speech production that characterized speech production in terms of assembling of individual sounds (Dell, 1988; Shattuck-Hufnagel, 1979), this particular psycholinguistic model proposed that frequently used words/syllables are stored as movement gestalts or verbo-motor patterns that can be accessed via a direct route (DR; Levelt & Wheeldon, 1994). Given that the DR would rely more on storage and less on online computation, it is in this regard more efficient than an indirect route (IR). Phonetic encoding could take place on the basis of the verbo-motor patterns of words or syllables, without an intervening Ôserial-orderingÕ of individual sounds. Employment of the DR will result in ‘‘articulatory cohesion’’ as expressed in a high degree of coarticulation. However, non-words, new words, and less frequent words will not have verbo-motor patterns stored in memory. In the encoding of such words, an indirect route that will perform a Ôserial-orderingÕ of the sound segments of words and non-words would be used. The IR relies more on on-line computation than on storage, and as result phonetic encoding via IR will 242 V. Balasubramanian, L. Max / Brain and Cognition 55 (2004) 240–246 show less cohesion and reduced coarticulation. According to DRSE, patients with apraxia will rely heavily on the indirect route for phonetic encoding. Therefore, even existing words and syllables will be encoded via the IR. However, such an increase in demands for computational resources is also problematic for these patients. Consequently, apraxic speech will exhibit symptoms of inconsistent voice onset patterns, articulatory prolongations, syllable segregation, variable vowel formant patterns, and reduced coarticulation. Moreover, these symptoms should be indistinguishable during the production of words versus non-words, because the apraxic speakers are assumed to use exclusively the indirect route (McNeil et al., 2000). Although this interpretation represents only a very strong version of the DRSE hypothesis, it provides predictions that can be subjected to empirical testing. To the best of our knowledge, there are no case reports of CAS in the literature, except for a mentioning of the occurrence of apraxia of speech in adults with right hemisphere lesions (Square-Storer, Roy, & Hogg, 1990). Hence, the present case report and study may lead to considerable gains in our understanding of AOS. Furthermore, there is a need for the DRSE hypothesis to be tested empirically. Indeed, the literature in the field of motor speech disorders ‘‘reflects a limitation in the amount and variety of data’’ (Kent, 2000, p. 412). The objectives of the present work are (1) to report a case of crossed apraxia of speech and (2) to verify one particular prediction based on the DRSE hypothesis, viz. the hypothesis that there will be no difference in the occurrence of apraxic breakdowns of speech on words and non-words. 2. Method 2.1. Subject SE, a 69-year-old right-handed female had a sudden onset of speechlessness and left-sided hemiplegia on 722-89. A repeat CT scan revealed hemorrhagic cerebrovascular accident that lesioned the right frontal lobe under the anterior horn of the lateral ventricle, the head of caudate and putamen of the right hemisphere (Fig. 1). The left hemisphere was spared. In the acute stage, SEÕs communication status was characterized by global aphasia. In the subacute stage, global aphasia began to resolve. At 1 month post-onset, SEÕs language impairment resembled the profile of BrocaÕs aphasia. In addition, SEÕs speech was characterized by moderate to severe apraxia of speech. Neuropsychological evaluation revealed severely impaired executive functions. On RavenÕs Progressive Matrices (performance test), SEÕs score was within normal limits. Subsequent speech-language evaluation carried out at 6 and 11 years post-onset revealed persistent crossed agrammatic BrocaÕs aphasia and AOS. The Apraxia Battery for Adults (ABA; Dabul, 2000) and Boston Diagnostic Aphasia Examination (BDAE; Fig. 1. SEÕs CT scan showing right hemisphere lesion involving the head of caudate and putamen. V. Balasubramanian, L. Max / Brain and Cognition 55 (2004) 240–246 Goodglass & Kaplan, 1983) were administered to obtain information on the presence and severity of apraxia of speech and aphasia. SEÕs performance profile on BDAE is given in Table 1. Results for subtests of the ABA are given in Table 2. Speech-language pathologists often use the ABA for clinical diagnostic purposes. However, this battery is not a compendium of tasks that can adequately sample apraxic breakdowns in articulation, prosody, and fluency components of speech production. Its major focus is on articulation performance. For instance, the increasing word-length subtest consists of 10 sequences of words that increase in number of syllables (e.g., thickthicken-thickening). The examiner presents each sequence and the patient will repeat after the examiner. Table 1 SEÕs BDAE test scores Boston Diagnostic Apasia Examination (BDAE) test scores Spontaneous speech No. of words per phrase (7) Grammatical form (7) Articulatory agility (7) 4 4 3 Auditory comprehension Word discrimination (72) Body part identification (20) Commands (15) Complex ideational material (12) 57 19 10 6 Repetion Single words (10) High probability phrases (8) Low probability phrases (8) 6 4 3 Naming Pictures (105) Animal naming Oral reading Oral sentence reading (10) Understanding written language Symbol and word discrimination (10) Phonetic Association: Word recognition (8) Comprehension of oral spelling (8) Word picture matching (10) Reading sentences and paragraphs (10) Writing Mechanics of writing (Rating) Recall of written symbols Serial writing (47) Primer level dictation (15) Written word finding Spelling to dictation (10) Written confrontation naming (10) Written formulation Narrative writing (Rating) Music Singing (2) Rhythm (2) 102 5 6 8 5 3 10 6 4 37 13 7 8 4 1 1 Maximum possible scores are given in parentheses. 243 Table 2 SEÕs performance on subtests of Apraxia Battery for Adults Increasing word length (subtest) One syllable average score Two Syllable average score Three syllable average score Deterioration in performance 1.8 0.5 0.4 1.4 Inventory of articulation characteristics Limb Apraxia score Oral Apraxia score 10/15 38/50 49/50 Each word response of the patient will be scored on a three-point scale (2 ¼ performed adequately, 1 ¼ performed with misarticulation/distortion, and 0 ¼ patient fails to perform). Any given patientÕs deterioration in performance for increase in word length can be determined by finding the average score for three-syllable word and deducting that average from that of one-syllable. Such deterioration will confirm the presence of apraxia of speech. Yet another subtest of ABA allows taking an inventory of articulation characteristics. A check-list of 15 characteristics (e.g., Ôsubject has marked difficulty in initiating speechÕ) is used for this subtest. This subtest allows the clinicians either to use a picture description task or prior observation of patientÕs speech as the bases for the determination of the presence of the articulatory characteristics in any given patient. The higher the number of articulatory characteristics observed in a given patient, the more likely that the patient has apraxia. The Limb Apraxia and Oral Apraxia subtest includes 10 limb apraxia related commands (e.g., ÔWave goodbyeÕ) and 10 oral apraxia related commands (e.g., ÔStick out your tongueÕ). On receiving each command, the patient is expected to carry out the command. A six-point scale is used to score subjectÕs performance (e.g., 5 points ¼ patientÕs response is accurate, prompt, complete, and understandable, 0 point ¼ patient is unable to perform the task even after examinerÕs demonstration). High scores are indicative of the presence of non-speech motor adequacy. Low scores are indicative of impaired non-speech motor control. The ABA does not provide normative data from non-brain damaged controls. SEÕs scores on the increasing word-length subtest and the subtest on articulation characteristics, as summarized above, indicate that SE shows speech/articulatory characteristics of apraxia of speech. Evidence of the presence of mild-moderate limb apraxia is also seen in her test scores. SEÕs language impairment resembled the profile of BrocaÕs aphasia. Word retrieval deficits, agrammatic sentence production, phonemic paraphasias and moderately impaired auditory language comprehension were the hall marks of SEÕs communication (see SEÕs BDAE test scores in Table 1). 244 V. Balasubramanian, L. Max / Brain and Cognition 55 (2004) 240–246 2.2. Materials The experimental stimuli were adopted from Varley and WhitesideÕs (1998) study. The stimuli consisted of a list of monosyllabic (CV or CVC) words and non-words. The list included 36 voice/voiceless minimal pairs. Each minimal pair signaled the voice/voiceless contrast either in the word initial or final position. The list included an equal number of real words and non-words forming minimal pairs (pen/Ben, nip/nib, pobe/bobe, gip/gib). The non-words, like the real words, obeyed the phonotactic rules of the English language. Instrumentation involved in this study included a digital minidisk audio recorder (Sharp MD-MS722) and a digital video camcorder (JVC GR-DV2000). 2.3. Procedure The stimuli were presented orally, one at a time and the subject was to repeat after the examiner. The entire test session was audiotape- and videotape-recorded. SEÕs responses to each minimal pair were perceptually rated by a speech-language pathologist. 2.4. Results SEÕs correct productions of voiced–voiceless contrasts in word versus non-word initial and final positions are shown graphically in Fig. 2. Specifically, the perceptual analyses of SEÕs responses yielded the following results: (1) SEÕs productions of minimal pairs with voiced– voiceless contrasts in the context of real and non-words included a considerable number of voicing errors. (2) SEÕs productions of real word minimal pairs were far superior to those for non-word minimal pairs. (3) Most of the articulatory errors were substitution errors. (4) Voiceless phonemes were always substituted for their voiced counter parts in the minimal pairs. (5) The non-word production task elicited reactions such as ‘‘I donÕt know’’ or ‘‘I canÕt say that’’ whereas the real word production task did not lead to such responses. 2.5. Discussion The present case report confirms the prediction that AOS can occur following lesion to the right hemisphere in right-handed individuals. SEÕs speech was characterized by moderate to severe AOS. This study also points out the need for careful documentation and analysis of motor speech production in right hemisphere damaged cases. This work, in the context of numerous case reports on ideomotor apraxia and neurogenic stuttering in right hemisphere damaged cases, warrants further investigations along these lines. Without a doubt, future neuroimaging studies of motor speech production and developments in neurocognitive modeling of speech production will expand our understanding of the neural control of motor speech. The investigated predictions based on the DRSE hypothesis were not consistent with the obtained results. SEÕs performance on word versus non-word minimal pairs does not support the view that in AOS a ‘‘direct route’’ is impaired and both words and non-words are produced using the same ‘‘indirect route’’ for speech encoding. As pointed out earlier, the present case report addresses only a strong version of the DRSE hypothesis through a perceptual analysis of word and non-word productions in a single case. SEÕs performance when Fig. 2. SEÕs production of voiced–voiceless contrasts in real words and non-words. V. Balasubramanian, L. Max / Brain and Cognition 55 (2004) 240–246 repeating non-word minimal pairs was clearly inferior to that for real words. There could be at least two explanations for this observation. First, it is possible that, in patients with apraxia, producing real words can still benefit from a direct route even if it is functioning at a less efficient level as a result of the lesion. Second, an alternative way of accounting for the discrepant levels of success in producing words versus non-words may suggest that the on-line phonetic encoding of non-words via the indirect route is more susceptible to the interference of cognitive resources than is the phonetic encoding of real words. Nevertheless, the strong version of the DRSE hypothesis of AOS cannot unambiguously explain the performance patterns of SE. Clearly, there is a need for more research involving a larger number of apraxic subjects. The current study provides only limited data pertaining to this hypothesis. There is a need for group studies that compare the performance of apraxics and normal controls on the experimental tasks. Although providing informative pilot data to stimulate further research, a single-case study such as the one presented here remains very limited in terms of interpretation because the assumptions underlying most statistical inferential tests do no allow them to be used with data from a single subject (Max & Onghena, 1999). In addition to the need for group studies, there is also a need for more direct analyses of apraxic patientÕs speech. For example, acoustic analyses of data from experimental and control groups could offer more in-depth insights into the hypothesis discussed here. Such studies are currently underway. The DRSE hypothesis appears to be facing other problems as well. It does not specify the nature of impairment of the DR encoding in AOS. Much of the explanatory burden is shifted upon the indirect route. In addition, it appears that almost all known symptoms of AOS are attributed to the compensatory mechanism of ‘‘over-using’’ an inefficient indirect route. However, it is not clear how this proposal can explain such ameliorative effects as observed when providing apraxic patients with delayed auditory feedback. More detailed hypotheses based on neurologically and physiologically realistic models of the efferents, afferents, and internal models involved in the neuromotor control of goal-directed movements appear to be needed to explain such observations (Max, in press). Furthermore, the DRSE hypothesis does not include suggestions regarding the roles played by working memory and attentional systems in speech production. Recently, there has been some innovating work viewing AOS as a phonological disorder or as a disorder of short-term memory and other cognitive resources (Ballard, Barlow, & Robin, 2001). Along with the traditional view of AOS as a motor planning disorder, these new approaches will have to be amalgamated into a comprehensive theory of AOS for future research. 245 References Ardila, A., & Lopez, M. V. (1986). 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