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Apraxia of Speech: Concepts and Controversies

Wolfram Ziegler,a Ingrid Aichert,a and Anja Staigera
Purpose: This article was written as an editorial to a collection of original articles on apraxia of speech (AOS) in which some of the more recent advancements in the understanding of this syndrome are discussed. It covers controversial issues concerning the theoretical foundations of AOS. Our approach was motivated by a change of perspective on motor speech that has taken place in neurobiology, neurolinguistics, phonology, and phonetics during the past few decades. Method: The literature on AOS is reviewed from 3 different but overlapping perspectivesthat is, a disconnection, a motor memory, and a fine motor skill perspective. Separate sections are devoted to the delimitations of AOS from oral facial apraxia, dysarthria, and phonological impairment. Conclusions: We conclude that many of the still unresolved conceptual issues about AOS arise from an underspecification of existing models of spoken language production. We suggest that phonological and motor impairments of sound production should be studied by an integrated approach. Key Words: apraxia of speech, oral facial apraxia, dysarthria, phonological impairment, phonetics, speech motor control, speech sound disorders, aphasia

ost of the current research on apraxia of speech (AOS) is rooted in the heritage of Frederic Darley and his scholars, and many clinicians and researchers still refer to the definitions and the diagnostic criteria formulated by these authorities (Darley, Aronson, & Brown, 1975; Wertz, Lapointe, & Rosenbek, 1984). Since Darley s time, however, a considerable amount of new evidence has been accumulated. Thinking about AOS has become more model-driven, modern experimental paradigms have been employed, and more data are available. Some of the new findings are in accordance with the older theories, but new ideas have also emerged; in some accounts, the old diagnostic criteria were subject to considerable modification (Wambaugh, Duffy, McNeil, Robin, & Rogers, 2006). The achievements of the last decades are multifaceted, but it is not clearly visible whether and where they converge. Hence, there is a strong need to discuss the current state-of-theart in research on AOS and to pinpoint the issues on which there is consensus or disagreement.

The collection of articles on AOS published in this issue of the Journal of Speech, Language, and Hearing Research is intended to take a step toward this aim.1 They summarize some of the advancements made during the past years and discuss and eventually consolidate diverging ideas. The contributions are focused on theoretical and diagnostic issues in acquired AOS in adults, with two articles discussing the relationship between phonetic and phonological impairment (Buchwald & Miozzo, 2012; Laganaro, 2012) and another article discussing the role of error variability (Staiger, Finger-Berg, Aichert, & Ziegler, 2012); two articles also review clinical and experimental assessment methods (Haley, Jacks, de Riesthal, Abou-Khalil, & Roth, 2012; Maas & Mailend, 2012), and two contributions cover new developments in primary progressive AOS (Croot, Ballard, Leyton, & Hodges, 2012; Duffy & Josephs, 2012). In our introductory article, we attempt to sketch old and new battle lines in the discussion of AOS and seek to explain why we consider the debate about this clinical condition particularly important at the present time. The discourse on AOS has always been caught in a seemingly inescapable circle of trying to get a grip on something that we are still unable to define unequivocally (McNeil, Robin, & Schmidt, 2009). Our approach here

a Clinical Neuropsychology Research Group (EKN), Clinic for Neuropsychology, City Hospital Mnchen, Germany Correspondence to Wolfram Ziegler: wolfram.ziegler@extern.lrz-muenchen.de Editor: Anne Smith Associate Editor: Julie Liss Received April 18, 2012 Accepted May 21, 2012 DOI: 10.1044/1092-4388(2012/12-0128)

1 The articles in this supplement originated from presentations given at the Apraxia of Speech: Mechanisms and Symptoms satellite workshop (which was organized by the authors of the current article) during the 6th International Conference on Speech Motor Control in Groningen, the Netherlands, June 2011.

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attempts at escaping this circle, not by postulating new axioms or proposing an update of diagnostic criteria but rather through a synopsis of different perspectives of why patients with AOS cannot speak properly. Admittedly, the selection of topics in this appraisal is neither balanced nor exhaustive but rather reflects the subjective weighting and emphasis of its authors and may therefore be blamed for a neglect of other important viewpoints.

The Flesh and Blood of Speaking

Major exponents of 20th century linguistics had construed the building blocks of speech as purely symbolic units without any motor or acoustic substance. It was one of the major achievements of structuralist phonology that it divested the speech sounds from their flesh and blood (Jakobson, 1937, Lecture 1) and transformed them into purely contrastive, immaterial units, which are keineswegs lautlich [not sound-like in any way] (De Saussure, 1967, p. 142). Later, generative phonology conceived phonological representations of words as feature matrices of an abstract sort, figuring solely as the arguments of a set of algebraic rules (Chomsky & Halle, 1991, p. 9) Likewise, in some of the more recent computational models of word production, the phonological forms of words were construed as linear strings of abstract segments, generated through activation flows in a network of equally abstract syllabic and subsyllabic nodes, without any acoustic or motor constraints influencing the functioning of this machinery (e.g., Dell, Schwartz, Martin, Saffran, & Gagnon, 1997). Common to these approaches is the understanding that a physical record of speech performance has very little to offer those who are primarily concerned with the structure of language (Chomsky & Halle, 1991, p. 293). In this dualist tradition, the consequences of lesions to the speech motor centers of the human brain have not attracted much attention by neurolinguists and aphasiologists in the last century. Conventional aphasiology has considered the motor domain of speech production as entirely disjunct from and irrelevant to the processing stages pertaining to the linguistic module (Alexander & Hillis, 2008, p. 287), implying a clear-cut demarcation of a conceived abstract, amodal phonology from the motor mechanisms of speaking, and a complete relegation of motor constraints from neurolinguistic theories. Overall, the structuralist invention of the phoneme as an immaterial entity had a massive and enduring impact on linguistic and neurobiological theories about language, concomitant with a far reaching neglect of the material basis of human communicationthat is, the auditory and motor aspects of speaking.

During the last decades, however, the perspective has changed remarkably, and the flesh and blood of spoken language have started to arouse new interest. Modern phonetic theories, for instance, attempt to explain the dynamics of phonological cognition by unmasking discrete phonological representations as surface phenomena arising from the continuous, physical motor substrates of speaking (e.g., Gafos & Benus, 2006). Articulatory phonology considers the abstract representations of words as bundles of gestural units thatunlike the phonemes of structuralist or generative phonology have a temporal dimension and are characterized by a transparent relationship with the unfolding speech movements (Goldstein, Byrd, & Saltzman, 2006). Other recent substance-based phonological models have sought to disclose the structural regularities of phonological form as emerging from the constraints of the motor and sensory systems implied in speaking (Sol, Beddor, & Ohala, 2007). In a similar vein, the motor side of speaking receives more and more interest in neurobiology and neurolinguistics. The most advanced neurogenetic findings relating to human languagethat is, evidence related to the FOXP2 genepoint at a crucial role of motor speech capacities and motor learning in the evolution of language (Enard, 2011). Mutations of this gene may cause a condition predominantly characterized by impaired oral and speech motor functions in the absence of any significant paresis (Vargha-Khadem, Gadian, Copp, & Mishkin, 2005). Human speech is considered distinct from nonhuman communication systems in that it is anchored in motor cortical areas with an exquisite potential for planning and learning and with strong interconnections with auditory and somatosensory association areas in the left temporo-parietal cortex. New methods for the study of overt speaking in the magnetic resonance imaging scanner as well as recent developments of techniques for the in vivo analysis of fiber tract systems have created substantial gains in understanding this network (Ziegler & Ackermann, in press). One of the major aims of these studies is to discover the neural centers involved in the planning of speech movementsthat is, the neural substrate of AOS (Bohland & Guenther, 2006; Brendel et al., 2010; Shuster & Lemieux, 2005). On the background of the described change of perspective, AOS gains increasing relevance as a clinical model of how the faculty of articulate language can break down. Considering that the reasoning about the relationship of abstract representations of word forms to their phonetic counterparts is currently undergoing a substantial change, our thinking about the neurological condition interfering with phonologyphonetics boundary processes must keep up with these new ideas and with the prospering research in linguistics, psychology, and neurobiology.

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What Goes Wrong in AOS?

Although the syndrome termed apraxia of speech was given many different names during the last 150 years, the patients who received this diagnosis were always viewed as suffering from impairment at a high organizational level of motor speech. Clinicians consider them distinct from patients who are dysarthric because their speech pattern is inconsistent with the relatively predictable signs characterizing the elementary motor impairments resulting from paresis, ataxia, akinesia, or dyskinesia of the speech muscles (e.g., Wertz et al., 1984). Moreover, from a theoretical perspective, the existence of a motor planning stage and, accordingly, a motor planning impairment always seemed highly plausible to many scholars because the disjunct natures of a conceived symbolic phonological grammar, on the one hand, and a purely mechanical motor device, on the other, most obviously required for an efficient translation mechanism. If, in the classical dualist view, phonemes are purely symbolic and contain no motor information at all, how then could an entirely nonlinguistic motor periphery be able to interpret the phoneme strings of words without some powerful translator? After all, the idea that relatively abstract movement images need to be transformed into motor commands and that this translation process can be impaired selectively has long played an important role in motor domains other than speech (Liepmann, 1900a), and the role of abstract motor representations and their relationship to motor execution has remained one of the most challenging issues in human motor cognition and action control (Prinz, Aschersleben, & Koch, 2009). Over the decades, the presumed pathomechanism underlying the apraxic speech problem was vested in various psychological or physiological concepts. We concentrate here on three major themes that were intoned from early on and were varied depending on the zeitgeist of each particular period.

mental images of how an intended action would be perceived. Liepmann developed his theory on the basis of his observations in a patient with apraxiathat is, impairment of limb motor actions in the absence of any paresis or ataxiawhich he conceived of as resulting from a disconnection of the motor centers from the movement images. Later, he explicitly referred to speech as similar to limb motor action, with the exception that speaking is based on acoustic rather than visual movement images (Liepmann, 1913, p. 489). In this context, he also alluded to his patients speech impairment (then termed motor aphasia) as an apraxia of the language muscles, arguing that Wie die Extremittenmuskeln sind auch die einzelnen beim Sprechen thtigen Muskeln und gewisse Coordinationen derselben intact. Aber sie treten nicht in den Dienst der acustischen, optischen und tactilen Vorstellungen, wie es zu ihrem Gebrauch als Sprechwerkzeug erforderlich ist. [like the limb muscles, also the single muscles implied in speaking and certain coordinations of them are intact. But they are not brought into service by the acoustical, optical, and tactile images as it would be required for their utilization as a language tool]. (Liepmann, 1900b, p. 129) The neuro-anatomical basis of phonologymotor disconnection. Neuro-anatomically, Liepmann s (1900c) ideomotor theory was centered on the idea of a posteriorto-anterior stream of information in the left brain mediating die Herrschaft der Seele ber die Glieder [the governace of the mind over the limbs] (p. 191). Because in his thinking the images of intended actions of the limbs (also termed movement formulas) were predominantly visual, he considered them as being stored in posterior brain areas, from where they activate the appropriate motor patterns in the left frontal lobe (Goldenberg, 2009). In this model, Liepmanns ideomotor (originally ideo-kinetic) apraxia was associated with lesions disconnecting the posterior movement images from the central motor innervations. As is well-known, a similar neuro-anatomical model also exists for speech, with the dorsal stream as a core structure connecting auditory areas in superior temporal cortex with inferior-frontal motor regions through the fasciculus longitudinalis superior (Geschwind, 1965, p. 626). The prototypical disconnection syndrome related to this neural structure, corresponding with Liepmanns (1900c) ideo-kinetic apraxia, is conduction aphasiaa disorder originally characterized by an outstanding problem of word and nonword repetition, whereas auditory comprehension and motor speech are preserved (Geschwind, 1965). Hence, the concept of a speech disorder resulting from a disconnection of articulation from the (acoustic) images of intended actions applies at least equally well to conduction aphasia as it might apply to AOS.

Disconnection of the Movement From the Mind

A common characterization of the condition of AOS is that the affected patient cannot speak properly although he or she knows what he or she wants to say and how it should sound (Hillis et al., 2004, p. 1479). Linguistically, the concept of knowing how it should sound refers to the assumption that in AOS the phonological representations of words are preserved but cannot be translated into movements. Historically, knowledge of how it should sound alludes to Liepmanns (1900c, p. 191) idea that the limbs are governed by the mindthat is, purposeful movements (of the limbs) are controlled by

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Modern accounts of the posterior-to-anterior stream of information in speech production are based on a more differentiated perspective of the interconnections between auditory (superior-temporal) and motor (inferiorfrontal) areas of the left hemisphere (Catani & Mesulam, 2008). First, left superior-temporal and inferior-parietal cortex has received increased attention as an interface site for the integration of sensory and motor information and as a location where lesions may cause phonological impairment (Buchsbaum et al., 2011). Second, the anterior target region of this system is not in the central (rolandic) motor cortical representation area of the vocal tract muscles itself but rather is anterior to this region that is, in the opercular and the triangular parts of Brocas area (Saur et al., 2008). These premotor regions project onto the speech motor areas of the central sulcus and precentral gyrus and may therefore be understood to represent a further intermediate processing step between the acoustic and the (elementary) motor modalities of speaking, conveying higher order motor information to the speech motor execution system. As an apparently straightforward conclusion, AOS might be associated with damage to this preparatory motor system in left inferior frontal cortex (Hillis et al., 2004), whereas phonological impairment results from lesions more upstreamthat is, to the inferior-parietal or temporal-parietal areas or to connecting fibers (Buchsbaum et al., 2011). However, the role of Brocas area in the development of AOS is controversial because lesions restricted to this region are not necessarily associated with enduring speech impairment (cf. Ziegler, 2008). Alternatively, the left anterior insular cortex (Dronkers, 1996) and also the lower left precentral motor strip seem to play a role in the origin of AOS (Schiff, Alexander, Naeser, & Galaburda, 1983), but the specific function of these areas in the transformation of acoustically based word form information into articulation and as a part of the left dorsal stream is unclear. Limitations and perspectives. Summarizing, the view that speakers with apraxia know what they intend to say but cannot transform this knowledge into appropriate articulations borrows from Liepmanns (1900a, 1900b, 1900c) idea of a disconnection of the movements from the mind. It is appealing because it builds on the widely acknowledged assumption that speakers with apraxia comparable with patients with limb apraxiahave a functioning elementary motor system and a preserved access to the more abstract mental (i.e., phonological) representations of speech. However, the processing stages expanding between these two levels still need to be clarified to understand, for example, how AOS can be distinguished from conduction aphasia (see the Phonological Impairment section). Further inquiries following this perspective suggest themselves for more systematic lesion and imaging studies, with the aim of disentangling

how the auditory-based phonological representation of a word is transformed into the motor innervation pattern of its articulation. Equally vague is our knowledge of what exactly needs to be planned in the left premotor areas because we have no deep insight into the degree of coordination and spatial-temporal patterning regulated at the levels of the left primary motor cortex, the cerebellum, and the basal ganglia. The DIVA model (Directions Into Velocities of Articulators ) developed by Guenther, Hampson, and Johnson (1998) qualifies as a theoretical framework guiding such inquiries, and steps toward a clarification of the interaction between motor and somatosensory processes within such a framework and in AOS have already been taken (Hickok, 2012; Jacks, 2008).

Loss of Movement Memories

Holistic accounts. In the lexicalist spirit of the 19th century, Broca (1861) postulated that speakers with aphemia have lost le souvenir du procd quil faut suivre pour articuler les mots [the memory of the procedures for the production of words] (p. 333). Hence, in Brocas understanding, the faculty of articulate language was based on the acquired and stored procedural knowledge of how each word of a language is generated by appropriate movements of the speech organs. Aphemia resulted, in his view, from a corruption of this knowledge after lesions to left posterior inferior frontal cortex. This idea later influenced Lichtheim (1885), who hypothesized that the disorder he termed Brocas aphasia reflects a destruction of the Wortbewegungsbilder [word movement images] stored in Brocas area (p. 207). According to Lichtheim, speaking is based on die Erinnerungsbilder der Sprachbewegungen, welche wir in der Kindheit gesammelt haben [the memory images of language movements which we have acquired during childhood], and, as in Broca s view, these memories sind nicht geknpft an Laute, sondern an Worte [are not tied to sounds, but rather to words] (p. 262). Frequency of use and the acquisition of holistic motor patterns also form the theoretical basis of Levelt, Roelofs, and Meyers (1999) idea of a mental syllabary that is, a memory store comprising the phonetic plans of the most frequently occurring syllables in a speakers language. Unlike in Broca s (1861) and Lichtheim s (1885) thinking, the building blocks of speech motor planning in Levelt et al.s model are syllables, not words. This renders the motor organization of speaking more flexible and generative because new words need not always be learned from scratch but can be generated from the syllabic motor plans that have already been acquired. On the background of this theory, AOS was interpreted as resulting from a deconstruction of the stored procedural memories of how syllables are pronounced (Aichert & Ziegler, 2004; Staiger & Ziegler, 2008).

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The motor program metaphor, introduced by Darley et al. (1975) in their definitions of AOS (cf. Rosenbek, 2001), also has connotations to an implicit memory system for speech movements. Speech motor programs contain instructions prescribing the activity of the vocal tract muscles that, when unpacked, trigger the unfolding of speech movements. Speakers with apraxia, according to this approach, have lost the ability of making use of this programming capacity, and, in Darleys et al.s thinking (see p. 255), the basic programming unit was of the size of a phoneme. The assumption that the phonemes of a word can play a role as basic motor planning units has also been taken up by Varley and Whiteside (2001), although in the sense of a compensatory strategy for speakers with apraxia when their syllabic planning units are destroyed and speech movements need to be planned along an alternative, segment-by-segment route. Dynamic accounts. Notwithstanding the size of an alleged motor program or phonetic plan, the common idea in these approaches is that motor learning creates holistic motor representations of linguistic unitsthat is, words, syllables, or phonemes that are stored in the left frontal lobe. A lesion to the responsible cortical centers maypartly or completelydestroy the stored information or its retrieval and, thus, cause impairment at the word, syllable, or phoneme level of speech motor planning. Other theoretical frameworks, however, dispense with the assumption that the acquisition of speech motor skills results in a repository of crystallized units of a specific size. For instance, Liepmann (1913) described the acquisition of speech much more generally as the learning of a bestimmte Innervationsverknpfung der Gaumen-, Lippen- und Zungenkontraktionen [specific linkage of innervations of velar, labial, lingual contractions] across all levels of speech productionthat is, fr a, das u, das p, jeden Buchstaben, fr Silben und selbst kurze Worte [for a, u, p, every letter, for syllables and even short words] (p. 489). He also equated motor aphasia (i.e., Brocas aphemia) with a loss of these kinetic engrams of speaking. In modern phonetics, the kinetic engram perspective was couched in terms of a task dynamic model of action control. According to this theory, the movement dynamics of the moving vocal tract organs are entrained, during the acquisition of a motor skill, to form functional coalitions whose transient integrity is constrained by the global biodynamics of the system and by the specific goals of an action (Saltzman & Kelso, 1987). In the task dynamics approach, the acquisition of speaking skills includes not only the learning of the dynamics of each single articulatory gesture but also the tuning of the overall system to coordinate the gestural units into larger molecular structures, such as syllables or words (Goldstein et al., 2006). Hence, the acquired procedural memory of an adult speaker comprises the implicit

knowledge about how gestures are coupled in the speakers language to build larger syllabic or word molecules rather than the syllable or the word itself as a frozen motor routine. An empirical approach aiming to measure how functional synergies in speech motor coordination develop during childhood and adolescence was operationally based on the concept of stability of movement patterns as measured by a parameter termed spatiotemporal index (Smith & Goffman, 1998): With increasing age, children were shown to attain lower spatiotemporal index values that is, a higher stability of the spatial and temporal patterning of articulatory movements across multiple repetitions of an utteranceand adult-like consistency was not reached until 1416 years of age (Smith & Goffman, 1998). These data were interpreted to suggest that speech motor practice during childhood and adolescence leads to a formation and maturation of functional muscle synergies in terms of increasingly stable coordinative patterns (Smith, 2006). Regarding AOS, loss of consistency of performance has long been an important concept in the understanding of this syndrome, on the basis of the observation that speakers with apraxia are highly variable in their output: The kinematic and acoustic parameters of their utterances vary extensively across multiple trials, they can be accurate or make perceptible errors on different instances of the same word or syllable, and when they fail audibly their errors may differ between repeated productions of the same item (cf. Staiger et al., 2012). On the background of the developmental studies reported above, such inconsistent performance is interpretable as a loss of the stability of articulatory patterning, resulting from a corruption of the coordinative structures the patient had acquired over time.2 In this vein, Kelso and Tuller (1981) attempted, on the basis of the principles of task dynamics, to explain AOS as an impairment of the (learned) capacity of integrating speech movements into functional coalitions according to the goals of a specific speech task (e.g., a word). We have recently taken a similar approach in constructing a gestural model of phonetic encoding for words, which we tested in a multiple nonlinear regression analysis to predict word production accuracies in a large number of samples from speakers with apraxia (Ziegler, 2011). The coefficients of the resulting regression model described the cohesive bonds between gestures at specific locations within syllables, metrical feet, and words and revealed specifically strong intergestural cohesionsfor instance, between synchronous laryngeal-articulatory
2 The official Academy of Neurologic Communication Disorders and Sciences Treatment Guidelines for Acquired Apraxia of Speech (Wambaugh et al., 2006) have recently abandoned error variability as a diagnostic criterion, which constitutes a remarkable shift of direction in the clinical definition of the syndrome. One of the articles printed in the present issue discusses this point at some length and presents new data (Staiger et al., 2012).

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gestures, within syllabic rhymes, or within trochaic feet. We interpreted this pattern of cohesive bonds between speech gestures as the product of an extended motor learning process and, as a consequence, as the essential content of the procedural memory guiding the vocal tract movements for speaking (Ziegler, 2011). Familiar versus novel. Although the motor memory concept provides a rather general framework for the understanding of AOS, some more recent approaches dispense with the assumption that the disorder affects the specific, consolidated motor skills of the articulators during speaking. In these approaches, AOS is considered as an impairment of creating forward models of novel articulator movements rather than a problem of accessing existing routines for familiar motor actions (Ballard, Granier, & Robin, 2000). This view was predominantly based on visuo-motor tracking ( VMT) studies in which participants were required to track a moving target on a computer screen with appropriate movements of their jaw or lower lip. VMT tasks, which involve no prior task learning, are considered to measure a participants ability of creating a forward model of the required movement on the fly, especially when the target movement trajectory is predictable (e.g., sinusoidal; Robin, Jacks, Hageman, Clark, & Woodworth, 2008). Several patients with AOS examined in these studies had relatively impaired VMT abilities, suggesting that the patients had lost the capacity of creating the generalized motor programs that would enable them to anticipate the course of their movement trajectories (Robin et al., 2008). Proponents of this approach claim that the requirements of VMT tasks come relatively close to the motor requirements of speaking; however, on a closer look, tracking differs substantially from articulation in important dimensions, such as movement rate, rhythm, or reference frame (visual in VMT vs. acoustic in speech). More importantly, however, VMT tasks differ from speaking in that they are novel and untrained and, as a consequence, probe how a patient copes with unfamiliar motor requirements. Hence, if acquired motor skills play a role at all in VMT, they must be universal (i.e., apply to any physiologically feasible motor activity) rather than specific (i.e., involve a consolidated motor capacity of articulate language). Yet, speaking skills are far from universal because they are strongly constrained by the sound inventory and the phonotactics of a speakers language. Likewise, viewing AOS as an impairment of universal oral motor skills can hardly account for the fact that the error patterns of speakers with apraxia are so heavily influenced by speech-specific factors, such as syllable structure or frequency of use. This point is taken up again in the Oral Facial Apraxia section. Motor plasticity. The motor memory approach to AOS is based on the assumption that patients with

lesions to a particular brain region have partly or completely lost the implicit knowledge about how speech is fabricated through vocal tract movements. A core presumption implicitly underlying this view is that motor skills, such as speaking, draw on acquired procedural knowledge that is bound to a functionally specialized neural network. This premise is fully compatible with what is known about the practice-related plasticity of the motor circuitry in the human brain. Studies in adult musicians and athletes have shown that extensive practicing, especially during childhood, induces anatomically traceable structural adaptations of gray and white matter regions related to the acquired motor skill (Bengtsson et al., 2005; Gaser & Schlaug, 2003), and there is a vast amount of evidence that even short periods of massed practice in adults lead to detectable alterations in the brains motor system (cf. Adkins, Boychuk, Remple, & Kleim, 2006, for a review). These include structural and topographic changes but also include alterations at the synaptic level and a reorganization of cortical microcircuitry across all components of the neural motor network (Doyon & Benali, 2005). Although most studies on this issue relate to skill learning in the limbs, several more recent studies have also addressed the effects of oral motor exercises (Svensson, Romaniello, Wang, Arendt-Nielsen, & Sessle, 2006). Speaking is an extensively trained activity. Motor control of the respiratory muscles, the larynx, and the articulators is exercised from the 1st days of life and is very early geared toward the production of words (Smith, 2006). From all we know about neural plasticity, we can infer that the long period of speech motor learning, extending over more than the 1st decade of life, must necessarily leave an imprint on the neural network guiding the vocal tract muscles and create a neural substrate of the procedural memory of how vocal tract movements are assembled for the production of speech. Presumably, the left anterior perisylvian region discussed earlier in this article is subject to such structural and functional plasticity mechanisms during speech motor acquisition. Limitations and perspectives. As was said above, there is still a number of unresolved issues in the motor memory approach to AOS, mainly concerning the question of how the acquired procedural knowledge underlying the faculty of speaking can be described: Is it a universal, language-independent motor skill that enables us to create new internal models of any (physiologically possible) oral movement whatsoever (Robin et al., 2008)? Is it a set of holistic motor plans for the words (Broca, 1861), syllables (Levelt et al., 1999), or phonemes (Darley et al., 1975) of a speakers language? Or is it the ability of combining phonetic gestures to increasingly larger molecules, constrained by the frequency of occurrence of intergestural links in the speaker s native idiom (Ziegler, 2011)?

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A further problem must be seen in the fact that the intensive learning of a motor skill is associated with neurophysiological alterations at many different levels of the brains motor system, including not only lateral motor cortical areas but also the basal ganglia, cerebellum, supplementary motor area, and white matter structures of the neural motor network (Bengtsson et al., 2005; Doyon & Benali, 2005). Speech motor acquisition during childhood probably leads to specific changes in all these structures, implying that even the more elementary (e.g., cerebellar or striatal) stages of speech motor control draw upon acquired procedural knowledge (cf. Ziegler, 2006). Regarding AOS, we therefore need to understand which aspects of a distributed motor memory for speaking are specifically represented in left anterior perisylvian or subsylvian cortex and are compromised in patients with lesions to these areas.

thinking still prevails in modern accounts of AOS, in which simplification errors and a stronger affliction of complex as compared with simple articulations are highlighted as characteristic signs of the apraxic syndrome (McNeil et al., 2009). In a way, this perspective is reminiscent of the concept of a clumsiness of the moving organs, comparable, for instance, with handwriting impairment as a consequence of a mild paresis of the right hand. Speakers with apraxia might, on this account, simply be clumsy in their articulation because of a lesion to the (left) prerolandic representation area of the speech muscles or the underlying white matter (Lecours & Lhermitte, 1976; Tanji et al., 2001). This view poses the challenge of delimiting AOS from so-called unilateral upper motor neuron dysarthria (see the Dysarthria section below). Ease of articulation versus frequency of use. The fine motor skill perspective has no a priori relationship with the motor memory view discussed above because it emphasizes motor execution aspects and inherent spatialtemporal motor patterning requirements rather than the aspect of an acquired procedural knowledge depending on practice. However, the two concepts are confounded because phonetic structures that occur with a high frequency are often also considered easy to produce, and difficult articulations tend to occur less often. According to CELEX ( Centre for Lexical Information ) counts, for instance, frequently occurring German syllables tend to be simple in the sense that they avoid consonant clusters (Aichert, Marquardt, & Ziegler, 2005). Hence, complex syllables are not only difficult because of their intrinsic articulatory requirements but also because most of them are less overlearned. As a consequence of such confounds, certain phonetic structures may turn out to be complex for motor planning and for motor execution at the same time, which might explain why in functional imaging studies comparisons of complex versus simple conditions (e.g., clusters vs. singletons) always revealed activation of the whole speech motor system, including both the presumed planning areas (left inferior frontal cortex) and the presumed motor coordination structuresfor example, the cerebellum (Bohland & Guenther, 2006; Brendel et al., 2010). However, one may also find counterexamplesthat is, articulations that appear relatively difficult to perform but because they occur frequently, they are overlearned and should, therefore, be easy to plan or to produce. In German, for instance, the syllable [nIt] ( nicht ; English = not) is in the high-frequency range (Rank 32), although it has a cluster in the coda. To the opposite, the syllable [ ly:f ] is extremely rare in German (frequency rank > 10,000) but is not particularly complex. Such dissociating items provide an opportunity to pit the fine motor skill hypothesis of AOS against the motor memory

Loss of Fine Motor Skills

From its beginning, the discussion about impairments of speech motor planning involved allusions to the notion of impaired fine motor skills. For instance, one of the terms used by Broca (1861) to describe the problem of patients with aphemia was impairment of la facult de coordonner les mouvements propres au langage articul [the faculty of coordinating the movements of articulate language] (p. 333). When he had discovered that each of his aphemic cases had a lesion in the left hemisphere, Broca (1865) drew a parallel between speaking and manual fine motor skillssuch as drawing, writing, embroidery, and so forthsaying that the left hemisphere is obviously specialized for all these skillful motor activities by the same token (p. 384). This perspective differs from Brocas (1861) motor memory account described in the preceding section because it underscores the high motor coordination demands of speaking rather than the aspect of implicit learning and procedural memory. The fine motor skill view received a strong boost by the French school following Thophile Alajouanine, who coined the term phonetic disintegration to describe an impairment characterized by a neuromuscular incoordination for speech, which interferes more with difficult (e.g., fricatives) than with easier (e.g., plosives or vowels) articulations and often leads to a simplification of articulatory requirements, for example, through consonant deletions or schwa-insertions in consonant clusters (Alajouanine, Ombredane, & Durand, 1939). 3 This
3 Interestingly, the term incoordination, which played a role in Brocas (1861) understanding of aphemia and in the French phonetic disintegration concept, was later used by Darley et al. (1975) as a negative diagnostic criterion. Along with weakness and slowness, incoordination was meant to determine what is not characteristic of AOS and to delineate it from (probably ataxic) dysarthria. Hence, one and the same term was used by different authors as either an affirmative or a negative descriptor of the pathomechanism underlying AOS, demonstrating that such terms are not helpful as long as they cannot be defined unequivocally.

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hypothesis sketched in the preceding section: If their sensitivity to apraxic failure is determined by frequency more than by complexity, motor learning and memory must be more important than universal fine motor skills. This constellation was indeed observed in speakers with apraxia who had been examined for the influence of syllable frequency and syllable structure on their errors in spontaneous speech and who showed an influence of syllable frequency even when complexity was controlled for (Aichert & Ziegler, 2004; Staiger & Ziegler, 2008). Limitations and perspectives. As a conclusion, a fine motor skill approach to AOS would push the syndrome from a motor planning problem more toward a motor execution problem because sensitivity of speech impairment to the fine motor requirements of a syllable or word might simply be interpreted by a clumsiness of the speech muscles.4 Yet, the ease of articulation concept (Lindblom, 2000), which is central to this approach, is problematic for two major reasons. First, we have no objective criteria to decide, at least in adult speakers, what is easy and what is difficult to articulate. For instance, syllables with consonant clusters usually count as complex and are also more error prone in AOS when wholesyllable errors are considered (Staiger & Ziegler, 2008). However, when phonemes or phonetic gestures are taken as the primitives of motor planning, consonant clusters lose their disproportionate vulnerability to apraxic failure because they comprise more than one consonant and a larger number of gestures and, therefore, simply offer more opportunities to fail (Ziegler, 2011). Second, fine motor requirements defined in terms of ease of articulation cannot be considered independent of frequency of usage because what is difficult for speakers of one languagefor example, the fricative [ h] for speakers of Frenchmay be easy for speakers of other languages, such as English or German, simply because of the fact that [h] occurs in English and German but not in French. Despite these theoretical problems with a fine motor skill explanation of AOS, we may seek ways to differentiate between a universal ease factor, no matter how it is motivated, and a language-specific practice factor by testing speakers with apraxia for their vulnerability to ostensibly easy but infrequent versus ostensibly difficult but frequent patterns of their language.

bordering the phonetic planning processes of speech. How can we know what AOS is and where it begins or ends when we have no equally clear concepts of aphasic phonological impairment and of dysarthria? Therefore, the dispute around AOS has always also been centered on the question of how it can be delimited from its close neighborsthat is, from oral-facial apraxia, from dysarthria, and from aphasic phonological impairment.

Oral Facial Apraxia

The term apraxia of speech signals that AOS is understood as a disorder specific to speech productionthat is, the underlying impairment specifically interferes with the motor task of speaking. This perspective has been taken from the beginning: It is implicit in Brocas (1861) notion of a loss of movement memories for words and in Alajouanine et al.s (1939) phonetic disintegration concept, it lives in Liepmanns (1913) term apraxia of the language muscles and in Darley et al. s (1975) term oral-verbal apraxia, and it is part of the more recent understanding of AOS as an impairment of phonetic planning (Ziegler, 2008). The speech-specific view has recently been challenged by authors who claimed that, by and large, AOS is only a surface phenomenon of an underlying general apraxia of the vocal tract muscles (Ballard et al., 2000) oreven more universallyof an overall motor programming impairment including also, for instance, finger movements (Maas, Robin, Wright, & Ballard, 2008). This position was disputed in a series of articles (Ballard, Robin, & Folkins, 2003; Weismer, 2006; Ziegler, 2003, 2006). However, because of a lack of prospective studies focusing on this issue, there is still no general consensus. From a clinical perspective, brain lesions are rarely of the kind that they impair one function of the oral motor system and entirely spare all other functions because, macroscopically, the same brain structuresthat is, the motor cortices, basal ganglia, thalamus, cerebellum, and brainstem nucleiare involved in all movements. This may explain why in a great number of patients, we encounter impairments of speaking and swallowing, speaking and oral diadochokinesis, speaking and tongue protrusion, and so forth. Nonetheless, a large body of literature exists in which dissociations between speech and nonspeech oral movements in both directions are reported (Ziegler, 2003, 2006). Neurological models readily explain why impairment of voluntary movements of the vocal tract are often dissociated from impairments of autonomous motor activities, such as vegetative breathing or swallowing, and also from disturbances of emotional expressive movements, such as laughing or crying, but dissociations may also occur between speech and other voluntary oral motor activities (Ziegler, 2003, 2006).

The Close Neighbors of AOS

Any attempt at understanding the mechanisms underlying AOS inevitably requires also understanding the impairments arising from a disruption of processes
4

However, it should be noted that many AOS symptomsfor example, certain phoneme substitutions or occasional observations of errorless articulations cannot easily be made compatible with a fine motor skill account.

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These latter dissociations are not unexpected, considering that speaking differs from all other voluntary oral motor actions by a number of outstanding properties: its sound-producing nature and the role of an acoustic reference frame; the interlacing of pulmonal, laryngeal, and supralaryngeal mechanisms in an inherently coordinative motor organization; the motor equivalence principles constraining the interaction of these motor subsystems for the achievement of acoustic goals; the role of aerodynamic events as control parameters and as sources of afferent input; the natural chunking of sequential and simultaneous articulations into larger units; the preferential access of articulation to a specialized (verbal) working memory system; its language-specific rhythmical organization; and, most importantly, the fact that speakers have entrained the linguistic use of this complex sound-producing tool over many years of extensive motor learning. Given these unique properties of the motor activity of speaking, its distinctness from actions such as tongue-wagging, lip pursing, rhythmical jaw lifting, or VMT is virtually self-evident. It is therefore not surprising to see that oral-facial apraxia and speech impairment can dissociate and that when they co-occur, they may differ remarkably in their severity and the dynamics of their recovery (Ziegler, 2003). Proponents of a universal impairment underlying both AOS and oral apraxia concede that speakers with apraxia can be unremarkable in oral apraxia testing, arguing that this may occur because the tasks used in oral apraxia tests are much easier to perform than speech movements (Ballard et al., 2000). However, what is easier for healthy adults than moving their vocal tract organs to form words and sentences? That nonspeech oral motor tasks are not always equally easy to accomplish has for instance been shown by Bizzozero et al. (2000), whose normative data reveal that some of the items of their lower face apraxia test are so difficult to perform that healthy adults, especially older or less educated persons, often fail on them. Moreover, there are also reports of patients who, after a stroke, had oral facial apraxia without speech impairment, demonstrating that oral nonspeech motor impairment and AOS dissociate both ways (Ziegler, 2003). Theoretically, a task specific organization of speech motor control is plausible, if not mandatory, because speaking is exercised extensively from early on and the motor system in the brain is known to exhibit a considerable experience-related plasticity (see above). Lichtheim (1885) very early speculated about the task specific neural organization of speech movements, saying that Die linke Brocasche Windung und die von ihr ausgehende Leitungsbahn dient also ausschlie blich zur

Innervation der Sprachbewegungen, whrend die analoge Windung der rechten Seite und die von ihr ausgehende Bahn zwar fr die Innervation der Bewegungen der Sprachorgane geeignet, nicht aber auf die Combination derselben zu Worten eingebt ist [Brocas area and its projections exclusively serve the innervation of language movements, while the analogous convolution in the right hemisphere and its efferent pathway are qualified for the innervation of the movements of the language organs but are not trained for the combination of those to words]. (p. 260) More than a century later, functional imaging studies of movement-related brain activity corroborated that speech movements predominantly activate left hemisphere cortical areas, whereas nonspeech oral movements activate bilaterally (Bonilha, Moser, Rorden, Baylis, & Fridriksson, 2006; Wildgruber, Ackermann, Klose, Kardatzki, & Grodd, 1996). Hence, the fact that AOS is strongly left-lateralized is compatible with the view that it is specific to speaking. As mentioned earlier, however, the entrenchment of speech motor patterns is probably not confined to lateralization but is rather associated with structural and functional alterations across the whole neural network engaged in this motor activity.

Dysarthria
If AOS is understood as a motor speech disorder, why should we then draw a distinction between this syndrome and the dysarthrias? Is it merely terminological sophistry, or does it make theoretical or clinical sense to keep AOS separate from paretic, ataxic, and all other dysarthria syndromes? Clinically, the separation of AOS from the dysarthrias has stood the test of time because AOS patients present a distinct clinical picture and are felt to require specific therapeutic management. They differ from most dysarthric patients by a number of neurological and neuropsychological characteristics that bring them closer to the aphasic population than to any of the populations typically suffering from dysarthria. This is due to the fact that AOS is a focal, probably cortical, syndrome of the dominant hemisphere, whereas severe and persisting dysarthria usually occurs after bilateral, often diffuse, lesions mostly involving subcortical structures. However, among the dysarthria syndromes, there also exist vast differences, for example, between the flaccid and the hyperkinetic type; nonetheless, they are grouped together under the same label. Why not AOS? Dysarthric versus apraxic symptoms. By definition, the distinction of AOS from the dysarthrias is based on negative diagnostic criterianamely, that its symptoms cannot be explained by significant weakness, slowness, or incoordination (Darley et al., 1975, p. 255). These

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restrictions are meant to exclude elementary motor impairments, much in analogy with conventional definitions of limb apraxia (Goldenberg, 2008). In fact, clumsiness, paresis, ataxia, akinesia, tremor, dyskinesia, and dystonia are not very likely to cause the dysfluent, hesitant, and groping articulation; the self-correcting behavior; or the gross misarticulations surfacing as phoneme errors that we encounter in AOS. Rather, these symptoms are reminiscent of the motor problems described in patients with limb apraxia, who, in their attempts to perform a motor action, appear similarly helpless, also show hesitations and self-corrections, and often produce faulty actions by omitting gestures or generating grossly misdirected or amorphous movements (Goldenberg, 2008). Other evidence against an elementary mechanism of impaired motor execution comes from observations that even severely impaired AOS patients may at times and rather unexpectedly produce clear and intelligible words or phrases, and their errors may vary extensively in type and location when the same utterance is produced several times (Staiger et al., 2012).5 The argument here is grounded on the assumption that speech motor execution problems cannot simply be switchedoff for a few syllables or words and that they remain more or less constant across multiple repetitions of the same utterance. However, it must be acknowledged that increased variability is a rather universal feature of immature or disordered motor control and can therefore also be foundat least to a certain degreein the dysarthrias, especially in ataxic or hyperkinetic syndromes (cf. the Loss of Fine Motor Skills section above). In summary, the distinct symptom pattern of AOS certainly calls for delineating it as a separate clinical entity, but it still needs to be determined whether there is a stringent proof in this pattern of an underlying motor planning or programming impairment. The neuro-anatomical argument. From a neuroanatomical perspective, lesion lateralization is considered relevant in this regard because it suggests that AOS resides more upstream and closer to the linguistic brain than the dysarthrias (Ziegler, 2008). Yet, the lateralization argument is weakened by the finding that also the lower motor aspects of speaking have a statistically notable (though much weaker) degree of lateralization to the left cerebral hemisphere (Urban et al., 2006). A further topographical argument is that the lesions causing AOS are considered to be located in cortical areas devoted more to motor planning than to motor executionthat is, left premotor and /or posterior inferior frontal cortex (for a review, see Ziegler, 2008). However, there is evidence that the syndrome may also
5

result from lesions to the left primary motor cortex, which was considered as an argument to classify it as a dysarthric syndrome (Bay, 1957). This claim can be countered by raising the question of whether the ventral part of the left motor strip especially its anterior portionis specialized for some higher order aspect of speech motor function as well. That neurons in primary motor cortex may encode complex and abstract movement parameters has often been suggested for other domains, as for instance by Geyer et al. (1996) or by Kakei, Hoffman, and Strick (1999). Therefore, the most critical cases upon whom the discussion about the nondysarthric nature of AOS should be focused are patients with circumscribed lesions in the left precentral cortex. In the literature, patients with such lesions have inconsistently been named apraxic, aphemic, anarthric, or dysarthric (e.g., Mori, Yamadori, & Furumoto, 1989; Schiff et al., 1983; Tanji et al., 2001; Terao et al., 2007), and the background of this taxonomic uncertainty is that it is still unclear what exactly the left motor cortical region contributes to speech. Refined analyses of the speech errors of these patients, eventually including kinematic measures of their articulation, should in the future be conducted to find out whether they are different from standard AOS cases and how they differ from unilateral upper motor neuron dysarthria, with the aim of learning more about the pathomechanism underlying their speech impairment (see the Loss of Fine Motor Skills section above). A clinical, error-based approach along this avenue has been undertaken by Haley et al. (2012). Because of the limitations of perceptual error analyses, a further fruitful way to disentangle speech planning from motor execution problems in these patients might be sought in reaction time paradigms, which may provide greater insight into the online processing of verbal responses (cf. Maas & Mailend, 2012).

Phonological Impairment
Patients with a (postlexical) phonological impairmentsuch as, for instance, in patients with conduction aphasiadiffer from speakers with apraxia in that they lack any obvious motor problems. Their speech is well-articulated and largely fluent, without visible groping, andmore or lessis prosodically unremarkable. Their core symptom is that they produce phonemic errorsthat is, substitutions, omissions, and additions of phonemes. Delineating AOS from this syndrome is one of the major clinical and theoretical challenges because on the surface there is a symptom overlap. In particular, speakers with apraxiasimilar to patients with phonological impairmentregularly produce apparently wellarticulated phoneme errors, with the only difference

Comparable observations have also been reported in patients with limb apraxia (e.g., Liepmann, 1900b, p. 119).

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that in AOS these perceived phonemic errors are part of an overall pattern of disfluent and phonetically distorted speech. Conversely, patients with postlexical phonological impairment may at times be considerably nonfluent, and in this respect they resemble speakers with apraxia (McNeil et al., 2009). There are still no clear criteria to resolve the diagnostic uncertainty arising from this overlap (cf. Haley et al., 2012). At the core of this diagnostic dilemma is a fundamental theoretical problem of how these two types of impairment should be delineated. The distinction between two allegedly separate postlexical output impairments phonological and phoneticdepends on how we subdivide the processing flow from lexical representations to speech movements and which symptoms we expect from impairments arising at each of the different levels (cf. Croot et al., 2012; Laganaro, 2012). There is widespread agreement that a major property of the representations implied in phonological impairment is that they are abstract. Without any further specifications, however, this property is not sufficiently distinctive because phonetic plans or motor programs are abstract as well, in the sense that they do not prescribe speech movements in their full details. A core theoretical challenge is therefore to understand in what sense phonological impairment affects more abstract representations than AOS. The motor linguistic dichotomy. Most often abstractness is explicated by saying that phonological representations pertain to a linguistic domain, whereas speech motor representations are nonlinguistic (e.g., Van der Merwe, 2009). On the basis of this distinction, the pathogenesis of speech errors has been characterized as motoric in AOS and as linguistically based in conduction aphasia (Robin et al., 2008, p. 99). Yet, it is not at all clear why these two concepts, motor and linguistic, should be mutually exclusive. Why should the phonetic plans of words not be considered linguistic entities, given that they represent important and specific properties of lexical units? Conversely, on which grounds should the phonological representations of words be radically banished from the motor domain, when we concede that they are not entirely divested from the flesh and blood of speakingthat is, that they may possess properties inherited from the speech motor system? The coexistence of fundamentally divergent motor linguistic frameworks in the literature illustrates how unconstrained this distinction really is. Neurobiologists conceive the whole peri-sylvian neural network supporting the perception and production of communicative vocal signals, including the phonological aspects of speech processing, as an action-oriented representation system (Ghazanfar, 2009), and a similar stance is

also taken in functional imaging studies charting perisylvian cortical regions and their connecting fiber tracts for their roles in the perception and production of speech (e.g., Saur et al., 2008). There is no room in these accounts for a purely linguistic domain of phonological processing beyond the neural machinery that relates superior-temporal auditory with inferior-frontal speech motor information (Hickok, 2012). In this respect, they are compatible with the common coding accounts of action knowledge, in which a common representational domain of perception and action is postulated (Prinz et al., 2009). To the extreme opposite, other researchers have used the term motor in an extremely restrictive sense for only a level on which measurable activity of speech muscles can be established by physiological recordings. As an example, Aziz-Zadeh, Cattaneo, Rochat, and Rizzolatti (2005) distinguished between two types of speech arrest occurring during transcranial magnetic stimulation in healthy participants: a nonmotor or linguistic speech arrest after stimulation of the left posterior inferior frontal region, and a motor speech arrest after stimulation of the primary motor cortical region. The authors motivated their distinction by their observation that measurable mentalis muscle activity occurred only after stimulation of the primary motor cortex, whereas stimulation of the left inferior frontal region was not accompanied by overt muscular responses. Hence, this study represents an account that obviously denies the existence of motor processes beyond the level of physiologically traceable speech movements and thereby allows extensive room for anot further specified linguistic domain. Without pondering these theories against each other, the mere existence of such extremely divergent views of how motor and linguistic domains of speaking are related obliterates the value of the motorlinguistic dichotomy as a theoretical framework for the distinction between AOS and phonological impairment. The symbolic nature of phonological impairment. Other specifications of the abstractness of phonological as opposed to motor representations claim a symbolic nature of the former, usually without providing a clear definition of what symbolic means in this context (Van der Merwe, 2009). One of the connotations of symbolic is that symbols have an arbitrary, conventional relationship with their referents. However, as already pinpointed by Jakobson, Fant, and Halle (1952), phonological categories are founded on articulatory (and acoustic) features; hence, the mapping from the phonological form of a word onto its pronunciation is by no means symbolic in the sense of arbitrary. In other words, phonological representations how abstract they may beare always constrained by the physiology implicated in speaking and understanding. The importance of such constraints was even acknowledged by

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Chomsky and Halle (1991), whose phonological entities were, as said earlier in this article, purely symbolic arguments of a strictly formal grammar: In an epilogue to their work, these authors expressed their concern about the fact that their account was in no way constrained by natural principles of human language (Chomsky & Halle, 1991, p. 400). This same concern applies to the view that phonological impairment interferes with the processing of symbolic units because it ignores the rooting of surface phonological forms in the motor and the acoustic domains.6 Discreteness. Discreteness counts as another major property characterizing processes and representations at the phonological level of speech production. The discreteness assumption emanates from the fact that lexical concepts are discrete and must therefore correspond with discrete word form representations, which finally decompose into equally discrete subunits (Pierrehumbert, 1990). Because discreteness is tacitly considered as a principle pertaining to the mental rather than the physical world, the phonology phonetics distinction has often been framed in the discretecontinuous dichotomy. As a consequence, the property of phonemic errors to involve substitutions, additions, or deletions of discrete sound categories is usually taken as an indication of their nonmotor, phonological nature, with phonemes as the primitives on which the phonological error mechanism operates. Vice versa, the occurrence of graded phonetic distortions is considered as an unmistakable sign of motor aberration and a cardinal symptom characterizing AOS (Wambaugh et al., 2006). An experimental approach to error classification based on the discreteness paradigm was, for instance, proposed by Buchwald, Rapp, and Stone (2007) in a single case study of an aphasic patient. This perspective on discreteness has been challenged by alternative accounts that contribute to a blurring of the phoneticsphonology dichotomy. In articulatory phonology (AP), for instance, discreteness is brought about by the fact that articulation derives from a limited number of abstract articulatory gestures, involving a limited number of body parts that are moved to realize a limited number of constriction types (Goldstein et al., 2006). On this account, discrete errors can occur as a consequence of, for instance, a mis-selection of one or more of these abstract gestural units. Such an error mechanism comes close to the conventional understanding of a phoneme selection error, with the difference that it is more transparent for the underlying physiology. Regarding the degree of

abstractness, there may not be a great difference between mis-selections of phonemes or of abstract gestures, but whereas the phonemic view evokes the idea of an error concerning operations on a string of symbols, the gestural view evokes a reminiscence of the notion of a parapraxic error. Because the gestural units of AP, unlike phonemes, have a temporal extension and overlap with each other in time, phonetic distortions, especially those explainable as timing errors, can arise from mechanisms afflicting the regulation of phase relationships between articulatory gestures. However, these same mechanisms may also cause perceived phonemic errors, for example, through a complete gestural overlap (Pouplier & Hardcastle, 2005). Hence, in the AP approach, the discrete units implied in phonological impairment are entirely transparent for and constrained by their associated lower level motor events. At the same time, the AP account also bears the potential of a gradual (hence, perhaps, lower level) mechanism afflicting intergestural phase relationships. On the surface, this mechanism may not only create perceived phonetic distortions but also perceived phonemic errors, and it may therefore explain why the co-occurrence of these error types in AOS need not necessarily point at two different pathomechanisms (Pouplier & Hardcastle, 2005). Context independence. A further connotation of the conceived abstractness of representations involved in phoneme errors is that they are context-independent (Buchwald & Miozzo, 2012). Segments involved in a speech error are often accommodated to their new environment. For instance, after deletion of the fricative in the initial cluster of German /S ta:l/ (steel), the syllable is produced as [tha:l]that is, with the aspirated plosiveallophone that is mandatory in syllable-initial voiceless singleton stops. Accommodation in such cases is interpreted as evidence that the error must have occurred prior to the generation of a phonetic plan (Buchwald & Miozzo, 2012). An implicit presupposition here is that such adaptations cannot occur more downstream that is, at a motor, biomechanical, or aerodynamic level. However, explanations exist in which allophonic adaptation is for instance brought about by lower level mechanisms (Browman & Goldstein, 1992), which implies that adaptation may also occur in phonetically motivated errors. A thorough discussion of the role of adaptation in error classification is included in Buchwald and Miozzos (2012) contribution to the present issue. Well-formedness. As a further aspect of their abstractness, phonologically motivated errors are considered to obey the well-formedness principles of phonological theory and to respect phonological rules. Phonemic paraphasias rarely offend phonotactic regularities, they occur more often on marked than on unmarked forms, and

This must not be confounded with the fact that phonological representations have an arbitrary relationship with their semantic referents. Yet, in this sense, speech movements are no less arbitrary/symbolic than phonological representations.

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the forms generated through such errors are often less marked than the target forms. A typical interpretation of these observations is that they reflect a speaker s knowledge of linguistic structure and that the errors must therefore originate within the phonological domain (Goldrick & Daland, 2009). A somewhat paradoxical aspect of this view is that speakersdespite their phonological impairment and while they are committing a lapseshould at the same time be able to constrain their error by optimality laws or even to launch instantaneous control mechanisms to prevent the error from breaking phonological rules. A more parsimonious alternative explanation of such error regularities might be that marked or phonologically unlicensed sound combinations do not easily cross a patients lips because their associated motor patterns are highly unfamiliar or even completely outside the patients acquired motor planning repertoire. Such a perspective can be grounded, for instance, on phonetically based theories of phonological markedness, according to which phonological constraints are rooted in phonetic knowledgethat is, acquired knowledge of the physical conditions under which speech is produced and perceived (Hayes & Steriade, 2004, p. 1). Silent phonology. The fact that phonological representations, beyond their role in producing and understanding speech, possess a potential of being maintained silently over a period of time and transformed into other modalitiesfor example, alphabetic scripthas often been taken as an indication of their abstractness and has been used to distinguish phonological from motor speech impairment. More generally, it has been proposed that any impairment interfering with the manipulation of word forms in the absence of overt speaking must have a phonological origin. Ludwig Lichtheim was probably one of the first who examined metaphonological skills to determine whether patients who are unable to produce a particular word still have access to its acoustic image : Lichtheim (1885) simply asked patients to squeeze the examiners hand once for every syllable of the critical word. Patients who performed accurately on this task were considered to possess sufficient knowledge about the acoustic image of the word they could not pronounce, and therefore their speech problem was assigned to the motor image level of speaking (Lichtheim, 1885, p. 212). Later, covert segmentation or rhyme detection tasks (silent phonology tasks) became a routine part of neurolinguistic assessment batteries, with the aim of deciding whether a patients speech problem extends to some abstract level of conscious, internal manipulation of word forms (Nickels, 1997, p. 165). The idea behind this approach is that if a patients problem is still there even when he or she does not speak overtly, his or her speech problem must originate at some higher, nonmotor level.

A major concern with this argument is that silent phonology tasks cannot be considered valid measures of phonological processing during speaking because they impose entirely different requirements: Whereas the phonological code during speaking is extremely short-lived Indefrey and Levelt (2004) estimated encoding times of approximately 25 ms per segment silent rhyming or segmentation tasks may take several seconds to complete. This implies that metaphonological reasoning is, on the one hand, less demanding than speaking because it allows a patient to take much more time to retrieve the required information and because much less phonological detail is required to tell the number of syllables of a word than to produce the word overtly. On the other hand, silent phonology tasks can also be considered more demanding because they require working memory capacities and also because they are known to rely to a large extent on the acquisition of alphabetic script. Illiterates or nonalphabetic readers /writers perform very poorly on most phonological awareness tasks, although their speaking is fully functional (e.g., Loureiro et al., 2004). To make things even more complex, interference with silent phonology tasks may also occur in AOS becauseas was said beforethese tasks draw on verbal working memory capacities involving an articulatory loop mechanism and may therefore be impaired because of slowed or inaccurate articulatory rehearsal in speakers with apraxia (Waters, Rochon, & Caplan, 1992). For all these reasons, a patients performance on such tasks is not predictive of her performance in speaking. Hence, the theoretical distinction between apraxic and phonological impairments of spoken language production cannot be based on metaphonological performance but must rather be sought in speaking. By conclusion, the distinction of aphasic phonological impairment from AOS is still not on firm grounds. Terms such as linguistic, symbolic, or discrete are not specific enough to capture the mechanisms involved in phonological impairment relative to AOS. Moreover, linguistic well-formedness and markedness principles are intricately confounded with familiarity and practice principles of motor performance. Lastly, the utmost complexity of the relationship between the phonological mechanisms implied in speaking and their explicit metaphonological derivatives limits the value of silent phonology tasks in distinguishing between phonological and speech apraxic impairments.

Conclusions
In our synopsis of theories and concepts around AOS, we have tried to illuminate the apraxic speech impairment from three different perspectives: (a) as a

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disconnection of phonology from motor execution, (b) as a disturbance of learned motor routines, and (c) as an incoordination of spatially and temporally patterned speech movements. In each of these different views, we have encountered structurally similar problems of distinguishing between the notional stages of phonological encoding, motor planning, and motor execution. Whereas the disconnection account suffers from a blurring of the boundaries between these components, the motor memory account is characterized by potential confounds between acquired aspects of motor execution skills, acquired phonetic plans/speech motor programs, and acquired knowledge about the phonological structure of a speaker s language, respectively. Finally, the fine motor skill account is challenged by the fuzziness of our distinctions between ease-of-articulation as a determinant of the motor execution requirements of speaking, frequencyof-use as a determinant of the entrenchment of alleged speech motor plans, and markedness as a factor constraining phonological mechanisms. The uncertainties arising from these conceptual overlaps have long been ascribed to a weakness of our thinking about the AOS syndrome. In effect, however, they reflect a fundamental underspecification of our models describing how stored word form representations are transformed into actual speech movements, whether and how this process can be subdivided into substages, how the alleged substages and their boundaries are represented in the brain, andas a consequencehow their clinical correlates can be delineated. The many structural similarities that exist between the factors influencing phonological encoding, phonetic planning, and motor execution impairment support the view of an integrated hierarchical action system whose higher order components have emerged from and are rooted in the physical conditions of speaking. A major obstacle that prevents us from understanding the links between phonological, apraxic, and dysarthric sound production impairment must be seen in the fact that existing theoretical accounts often cover either the phonological or the motor end of the hierarchy, but not both. One of the future challenges therefore is to overcome the hermetic division of labor between investigations of phonological and of motor speech impairment.

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Acknowledgments
This study was supported by German Research Council (Deutsche Forschungsgemeinschaft [DFG]) Grants ZI 469/9-1, 10-3, and 14-1 and by ReHa-Hilfe e.V.

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