Aphasia and Related Neurogenic Language Disorders Leonard L. LaPointe Fourth Edition ae) %) ThiemeThieme Medical Publishers, Inc 333 Seventh Ave. New York, NY 10001 ‘Acquisitions Eaitor: Emily Ekle Managing Editor: Dominick Pucek Faitorial Director, Clinical Reference: Michael Wachinger International Production Director: Andreas Schabert Provluction Editor: Heidi Gravel, Maryland Composition ‘Vice President, Incernational Marketing and Sales: Cornelia Schulze (Chief Financial Office: James W. Mitos President: Bran D. Scanlan Compositr: Maryland Composition Printer Len Paper USA Library of Congress Cataloging-in-Publication Data ‘Aphasia and related neurogenic language disorder [edited by] Leonard L.LaPointe ~Ath ed scm. Includes bibliographical references and index. ISBN 978-1-60405-261-8 1. Aphasia 2. Language disorders. 3. Central nervous system—Diseases—Complications. LaPointe, Leonard L. IDNIM: 1, Aphasia. 2. Language Disorders, 3 Central Nervous ystem Diseases-complications: WL 3405] RCA2S.ABIS 2011 5168552—dc22 2010032191 Copyright © 2011 by Thieme Medical Publishers, Inc. This book. incuding al pars thereo. is legally protected by ‘copyright. Any use, exploitation, or commercialization outside the narow limits set by copyright legislation without the publishers consen is illegal and llable to prosecution. This applies in particular to photsta reproduction, copying. mimeographing or duplication of any king, translating, preparation of microflms, and electronic data processing and storage Important note: Medical knowledge is ever-changing. As new research and clinical experience broaden our knowledge, changes in treatment and drug terapy may be requite, The authors and eitors ofthe material herein have consulted Sources believe tbe reliable in their eflors to provide information that is complete and in accord with the standards accepted at he time of publication. However, n view ofthe possiblity of human error by the authors, editors, or publisher af the work herein or changes in medical knowledge, neither the authors, editors, oor publisher. nor any other Party who has been involved in the preparation ofthis work, warrants thatthe information contained herein sin every Tespect aecurate oF complet, and they ae nat responsible for any errors or omissions or forthe results obtained from tse of such information, Readers are encouraged to confirm the information contained herein with other sources. For trample. readers are advised to check the product information sheet included in the package ofeach drug they plan to Sdminister tobe certain tha the information concained in this publication i accurate and that changes have not been ‘made inthe recommended dose or inthe contraindication for administration, Ths recommendation is of particular importance in connection with new or infrequently used drugs Some of the product names, patents, and reistered designs referred to inthis book are in fac registered trademarks or proprietary names eventhough specific reference to tis facts not always made inthe text. Therefor, the appearance bra name without designation as proprietary isnot tobe construed asa representation by the publisher that itis inthe public domain, Printed in China 978-1-60406-261-8,Chapter 3 Aphasia Theory, Models, and Classification Malcolm R. McNeil and David A. Copland Aphasia Theories Theories are nets cast to catch what we call ‘the world”: to rationalize, to explain, and to master it. We endeavour to make the mesh even finer and finer Popper (1968, p. 59) Prior to considering specific theories and models of aphasia or relevant models of language fun tion, it may be instructive to reflect on what con- stitutes a theory or model and what it might be used for. A theory is generally understood to be “a system of ideas or statements held as an ex- planation or account of a group of facts or phe- nomena” (Michie, Johnston, Abraham, Lawton, Parker, & Walker, 2005, . 33). Although a range of criteria has been proposed regarding what con- stitutes a proper theory, any theory should allow generalization and should be testable. This is an important point, as a theory is of limited use if itexplains only a restricted set of prior observa tions. although this increased understandings of itself valuable. In essence, a theory should allow predictions beyond the data upon which it was based, and should be able tobe falsified. There is considerable variation in the scope of theories— from mechanistic explanations of a restricted set ‘or single phenomenon to macro-theories that encompass a broad spectrum of phenomena and have a unifying purpose. There is no generally agreed-upon unified theory of aphasia, although a few have been pro- Posed. That is, there is no single theory that has gained acceptance in the scientific communities and that accounts for the wide range of behav- iors that represent phenomena or for the array of persons to whom the term applies. The term. ‘aphasia applies to language-specific behaviors, otto the anatomy, physiology, cognitive mecha~ nisms, or even communication impairments that ‘may underlie the linguistic behaviors or are the result ofthe linguistic behaviors. Aphasiaisiden- tified by the behaviors that are allowed within its behavioral boundaries and not by its cognitive, anatomic, or physiologic substrates, or by the impairments in communication to which it gives rise. As such, aphasia is not likely to be identified or defined by the anatomic site of damage that. ‘caused the language behavior, at least not until the enormously complex cortical and subcorti- cal networks that are responsible for “doi language and for the broad array of language im- pairments have been identified and validated, Theories are closely linked to definitions, mod- els, and classification systems. A good definition is a first approximation to a theory. Although Sometimes used interchangeably in the aphasia literature, models differ in some respects from theories as they attempt to visualize or formal- ize a theory in a way that allows it to be tested in essence, the model puts the theory to work (Whyte, 2008). For practical reasons, therefore, Models tend to simplify aspects ofthe theory and may not factor in particular aspects of the related theory, as the emphasis may be placed on the utility of the model to provide a test in the real world, Some models have been propased with- ut clear reference to an overriding theory that is separable from it. In these instances the model 2728 __!_ Foundations and Practic: ies ‘may serve to highlight a particular phenomenon. that does not relate to the other phenomenon about aphasia for which the theory attempts to account. As with theories, the scope and com- plexity of models varies greatly, from a simple analogy (eg. lexical access as a file search) to complex computational modeling of elearning (Wilson, 2002). The goals of models vary accord- ingly, from simulating a specific phenomenon to providing an explanation to possibly predicting behavior. It is important to keep in mind that modeling can occur without reference to theory. For instance, a computational model may simu- late a language behavior (e.g. frequency effects in reading), but this does not necessarily ex- plain the behavior or meet the requirements of a theory (McCloskey, 1991), In aphasiology, there has been a slow increase in the development of models and less emphasis on broader unifying theories, perhaps reflecting a clinical focus and assumption that such targeted modeling will Provide a closer step toward treatment or a win- dow into the difficult encapsulation of the com plexities of aphasia within a single theory. So, for what can models and theories of apha- sia be used? The simplest answer is to explain or better understand the phenomena of aphasia. Ideally, such models and theories would enable Prediction of the characteristics of an individ- uual with aphasia, given data that constrain the theory. Theories and models of aphasia by neces- sity have grounding in conceptions ofnormallan- ‘guage function and also may seek to further this understanding by studying pathologic language. ‘Theories and models of aphasia also can incorpo- Fate neurobiologic considerations, although this is not obligatory. Some claim that certain cogni- tive neuropsychological theories seek to provide information assessment, diagnosis, prognosi and treatment (Hill, Dean, & Decker, 2001) but this is a contentious issue (see below). as there are few theories or models of aphasia that actu ally provide direction regarding the treatment of the language or communication impairment. ‘The Dominant Paradigm Although there is no unified theory of aphasia, there is a scientific paradigm under which the ‘majority of the scientific community practices That paradigm is best described as the “classi- cal associative connectionist” paradigm and is best represented by the classification system Most frequently in use today around the world (discussed in greater detail below). There are, however, challenges to this paradigm. Before addressing them, we will briefly describe the neoclassical connectionist model of aphasia that underpins this paradigm, Following the Pioneering work of Broca, the models proposed by Wernicke and by Lichtheim and the later re- formulation of Geschwind generally assume the existence of language centers located in discrete regions of the brain. A fundamental tenet of this paradigm is that these centers, composed of as- sociation cortex, hold representations required for particular language functions (eg, speak- ing, listening, repeating, writing. reading), and that information Flows between these centers via dedicated pathways (see Schuell, Jenkins, & Jimenez-Pabon [1964] and Caplan [1987] for detailed descriptions and cogent reviews). In this formulation, a posterior language center (the posterior superior temporal cortex, now known as the Wernicke area) holds auditory language representations. A lesion of this center impairs auditory comprehension but also influ- ences production. An anterior language center (third frontal convolution of the left hemisphere Or Broca area) was said to hold speech motor representations. Lesions of this center disrupt spoken word production but leave auditory ‘Comprehension intact. Disruption of the arcuate fasciculus connecting the posterior and anterior language centers is assumed to cause auditory repetition deficits. These models and the rise of the “diagram makers” have been profoundly influential in both neurologic aphasiology and clinical aphasiology and still hold sway in vari- us ways today, despite considerable criticism (see Darley, 1982; Poeppel & Hickok, 2004), One key limitation of this dominant paradigm is its attempt to link broad aphasic signs and symptoms to discrete anatomic structures. The Classification of aphasia derived from this sys~ ‘tem (discussed below) vastly oversimplified the ‘complex array of signs in an individual and does ot account fora large majority of patient symp. tom complexes. There is now clear evidence that language functions are not solely housed in ese discrete i Be these areas a Seficits in these Sally, language i ief these rudime Several identi leading to this e Garring in one-o hart contribute emergence of th evelopment of models of langua Seely new parad (iscussed below BS specify langu: ecssion, and i ed treatment ef Beason for the ris me models is tha Bemction to discr \zeeiding the pitf SSS (see Colthe: Beeoretical persp. Be departures f SEmnectionist mo Bt theory, the ypesspective, and Modeling aphasia Sze presented | peek discussed in t QB that a very Sabai has been | 2 2 single, uni Spective was first 9505) and later seinforced by her 2 was defended s1 bis view, the core at crosses allan ments of language Bcommon underly he core of the und ‘ef auditory proces McNeil. Odell, anc Gee involving the Support language | Hal mechanisms), fas received some Support. it has not Eajority of aphasiChapter 3_Aphasia Theory, Models, and Classification 29 these discrete language centers or that lesions in these areas are consistently associated with deficits in these functions (or vice versa). Criti- cally, language is no longer understood in terms Of these rudimentary functions but instead as several identifiable processing components leading to this end point, with breakdowns oc curring in one or more of the subcomponents that contribute to the overall function. The emergence of this approach underpinned the development of cognitive neuropsychological models of language that have emerged as a rela- tively new paradigm for understanding aphasia (discussed below). Besides offering the chance to specify language impairments with greater precision, and in doing so guide assessment and treatment efforts more practically, one key reason for the rise of these information process~ ing models is that they rarely attempt to attach function to discrete neural structures, thereby avoiding the pitfalls of earlier “diagram mak ers” (see Coltheart & Langdon, 1998). Three theoretical perspectives that represent substan: tive departures from the classical associative connectionist model include Brown's microge~ netic theory, the cognitive neuropsychological perspective, and computational approaches to ‘modeling aphasia. These theoretical approach- es are presented below. Additionally, although not discussed in this chapter, itis important to note that a very different theoretical view of aphasia has been presented: namely, that apha- sia is a single, unitary phenomenon. This per- spective was first articulated by Pierre Marie (1906) and later championed by Schuell and reinforced by her aphasia classification schema. It was defended still later by Darley (1982). In this view, the core impairment in aphasia is one that crosses all language modalities and compo- nents of language and can be accounted for by a common underlying impairment. For Schuell, the core of the underiying impairment was one of auditory processing. For McNeil (1982) and McNeil, Odell, and Tseng (1991), the core is cone involving the cognitive mechanisms that support language (eg. attentional or memo- rial mechanisms). Although this latter notion has received some experimental attention and support, it has not gained the support of the majority of aphasiologists and thus might be classified as a competing paradigm in aphasia It is, however, not a dominant paradigm. Brown's Microgenetic Theory In contrast othe classical associative connection- ist approach, Jason Brown's microgenetic theory arose from the holist tradition and represented both a. process and hierarchical theory. At its heart, this theory details a brain-language system that is characterized by its temporal dynamism. Brown (1988) proposed that ‘the mental state isa recurring process of flow from the archaic to the recent forebrain evolution that retraces, ina fraction of a second (microgenesis), formations in the evolution of the human brain (phylogenesis) and patterns in the growth ofthe individual (on- togenesis).” According to this view, aphasic signs and symptoms such as paraphasias are temporary disruptions that actually reflect a previously con- cealec earlier phase of normal language processing that suddenly emerges. This proposalin some ways echoes the continuity hypothesis, as proposed in various forms by Freud, Pick, and Jackson (see McNeil, 1988), which holds that linguistic errors (particulary paraphasias and some forms of sen- tence comprehension) observed in persons with aphasia are no different in kind from errors made by healthy individuals under certain conditions such as fatigue or divided attention. This hypoth. esis isnot, however, equivalent tothe “regression hypothesis ist proposed by Ribot (1883) and ater by Freud (1953) and Jackson (1958) and more re- cently formalized by Jakobson (1968), Weprnan and jones (1969), ane Goodslass(1978). hasbeen investigated in various forms by Caramazza and 2urif (1978), Gleason (1978), MeNel. Brauer, and Pratt (1990), Parisi and Pizzamiglio (1970), Petit, MeNell, and Keith (1989), Whitaker and Selnes (1978), Poeck, Orgas, Kerschensteiner, and Hartie 1974), and De Villiers (1978). In its simplest form, it states that persons with aphasia “ose” language in the inverse order to which it was learned when they were children. Tis theoretical perspective has not gained wide acceptance. Brown urged a step back to consider the un- derpinnings that connect and encompass rather than the superficial or easily observed phenom- ena thatdrive and test most theories and models. Earlier versions of Brown's theory proposed a30___1_ Foundations and Practicalities ee eee SSS euroanatomic framework underpinning lan- guage that reflected the involvement of particu- lar regions in a sequence dictated by evolution and development, progressing from. primitive to complex, with more basic language func- tions being performed by more primitive struc- tures (Brown, 1977). There are some similarities with classical connectionist models in terms of the neural substrates purported to be involved however, the dynamic nature of the theory, the inclusion of limbic structures, and consider- ing the automaticity of language and linguistic structures beyond single words were novel (see Caplan, 1987). The inherent nature of the theory hhas proven difficult to test, and itis hard to con- ceptualize a way to falsify or validate the theory. More recently, Brown (2001) has argued that the theory cannot be tested by psychological experi- ‘ments, as they require proof in terms of “quanti- ty, reproducibility, and changelessness,” which is at odds with the central tenets of the theory, but suggests that emerging techniques such as rapid ‘metabolic scanning may prove more fruitful. Cognitive Neuropsychological Models Cognitive neuropsychological models assume that the study of individuals with brain injury can inform our understanding of normal lan- {guage processes. According to this approach the language faculty is understood to be represented and organized in modules that are composed of several separable components that are domain specific in the sense that they are specialized to process only a certain type of input or represen- tation (see Fodor [1983] fora comprehensive pro: Posal regarding modularity). These modules are assumed fo operate in an encapsulated manner, such that information is processed within a mod- ule independent of information processed else- ‘where in the system. Critically, it is assumed that brain damage can disrupta module or processing component selectively leaving other components to operate normally. The use of such models then allows the identification of the locus of the defi cit through hypothesis-criven testing, which may then provide a starting point for therapy. Several such models have been proposed for single word processing (e.g, Ellis & Young, 1988; Patterson & Shewell, 1987) and sentence processing (e.g. Garrett, 1984; Schwartz, 1987). A typical model of single word processing (eg, Lesser & Milroy, 1993) provides a means of understanding break- downs in auditory and visual word processing and includes several discrete modules represent- ing stages of acoustic or visual word analysis, Phonologic and orthographic input lexicons, a semantic system, phonologic and orthographic output lexicons, and assembly buffers leading to written or spoken forms. Input and output routes are specified between modules, and alternative routes are assumed to exist for orthographic and. phonologic conversion without accessing the lex- icon. Such models provide a useful means of vi- sualizing the locus of word processing deficits in an individual through hypothesis-driven testing, focusing in part on those tasks that purportedly allow some fractionation of the system, ‘These information processing models have been particularly influential in providing a framework for assessment and treatment that links clinical concerns with theoretical consid- erations, as well as providing the psychological underpinnings for the most common signs and symptoms in aphasia. These models, however, are not without their limitations. There is con- siderable debate regarding the independence or true modularity of the various processing com- nents, and, if not truly modular, exactly how different processors interact and what actually happens within a processing module. The devel- ‘opment of these models has been largely built on single case studies, meaning that an assumption is necessarily made that the functional architec- ture is identical in all brains (Patterson & Plaut, 2003). Questions have also been raised about the overreliance on somewhat rare double dissocia- tions to confirm fractionation of functions, and it has been argued that in a complex and adaptive neurologic system responding to insult, language functions may still be performed but in a way that does not have clear implications for normal function (Seidenberg, 1988). Accommodation, adaptation, and neural reorganization following brain injury pose challenges to some of the ba- sic assumptions of some of the models that fall within this class of cognitive neuropsychological models. One method for disentangling the near impenetrable complexity of “doing” language and of the consequences of impairments to it has SS Bases aspects of eens of activit [Seple neuron-lik Bea competitive a Sex 2000: Plaut Be neuronal stru (Seputational mo Bien regarding ae cerain advant Bee characteris SS Setian this archite Beatially weighte imay be manus iat activation m Seapervised learnin, seorrecting proc yberedy repeated Peetper of 2 given s SS made and conn Feber errors (Hark S61 Representa Bedets may be cis Se kecalized, where Wee is linked toa Sse of interactc $F thax propose se Moe and bottom v Bee models, suchas Bess, have been u NBER Schwartz, Mar Setmartz, Dell, MarChapter 3_Aphasia Theory, Models, and Classification 31 been the development and use of computational connectionist modeling. Although computational approaches do not represent models or theories of aphasia per se, their use has enlightened the Psychological and neurologic models that have been proposed for various aspects of the language impairment that is aphasia, Computational Models Criticisms have been levied regarding the lack of detail or specificity of the interactions between ‘modules of cognitive neuropsychological models. A more precise understanding of the processing involved has been approached in computational connectionist, interactive, or parallel distributed. processing models that have been applied to aphasia. Computational connectionism holds that various aspects of language can be represented as patterns of activity over interconnected sets of simple neuron-like processing units that occur ina competitive and cooperative fashion (see Na- eau, 2000; Plaut, 1996). It should be noted that the neuronal structure is an analogy, and such computational models do not necessarily make claims regarding neurobiology, although there are certain advantages to applying a model with some characteristics of actual neural structures tothe study of brain disorders. Patterns of activity within this architecture are enabled through dif- ferentially weighted connections between units that may be manually fixed (e.g. in certain inter- active activation models) or may develop through supervised learning. commonly involving an er- Tor correcting procedure or “back-propagation,* whereby repeated comparisons between the output of a given system and the desired target are made and connection weights are altered to reduce errors (Harley, 1996; Nadeau, 2000; Plaut, 1996). Representations within computational ‘models may be distributed (as described above) oF localized, where the representation such as a word is linked to a specific processing unit. The degree of interaction also varies between mod- els that propose several steps that are both top own and bottom up. That is, interactive activa tion models, such as the two-step model oflexical access, have been used to model aphasic errors Dell, Schwartz, Martin, Saffran, & Gagnon, 1997: Schwartz, Dell, Martin, Gahl, & Sobel, 2006), and highly interactive models have been used that involve a single settling upon a representation through a pattern of activity across connected processing units (eg, Plaut & Shallice, 1993), ‘Aspects of aphasia have been addressed in com- putational models where “lesions” are introduced by impairing units, weakening or destroying the connections between units, introducing noise, or accelerating the rate of decay. The value of com- utational models in aphasia has been tested pri- marily in terms of how well they accommodate aphasic data. For instance, Martin, Dell, Saffran, and Schwartz (1994) demonstrated that increas- ing the decay rate in an adaptation of Del's localist interactive spreading activation model replicated the errors observed in an individual with deep dysphasia (characterized by semantic errors in repetition), and, impressively, that changes in er- rors with recovery also could be simulated. More recently, two different adaptations of this model were compared in their ability to fit naming er ‘ors ima large case series of people with aphasia twas demonstrated that “lesions” weakening se mantic or phonologic connections were more ac- curate in modeling variable aphasic naming errors (Schwartz et al, 2006). Such computational mod- els also have been employed to make predictions regarding aphasia treatment and recovery (Code, Rowley, & Kertese, 1994; Martin, Fink, Laine, ‘Ayala, 2004), and have provided new insights into how treatment may be approached (eg. Plaut 1996). Limitations of computational models have been observed. They include the observation that forms of learning involved in certain models are not consistent with actual learning mechanisms and cannot account for certain patient data (Na- eau, 2000; Ruml, Caramazza, Shelton, & Chial- ant, 2000), that the phenomena modeled are necessarily simplistic or narrow interpretations of aphasia, and that damaging these models to elicit language deficits sometimes occurs in ways that are biologically implausible. Theories and Models of Aphasia Rehabilitation Although a comprehensive model may provide a convincingexplanation ofhow particularlanguageChapter 3_Aphasia Theory, Models, and Classification 31 been the development and use of computational connectionist modeling. Although computational approaches do not represent models or theories of aphasia per se, their use has enlightened the psychological and neuralogic models that have been proposed for various aspects ofthe language impairment that is aphasia, Computational Models Criticisms have been levied regarding the lack of detail or specificity of the interactions between ‘modules of cognitive neuropsychological models, ‘A more precise understanding of the processing involved has been approached in computational connectionist, interactive, or parallel distributed Processing models that have been applied to aphasia. Computational connectionism holds that Various aspects of language can be represented as patterns of activity over interconnected sets of simple neuron-like processing units that occur ina competitive and cooperative fashion (see Na- 07 wo © pauunsaxd nq, _yeuis 10 10U29604 eysouedns oat) Suypuong, e1iousdns 814 0101804, Payuapii0N —puesousuy e2ni02qns 40 uonunf eon105 jews eomi09 2607, ews jeruedoroduiay AWENUON pax urego19 uo.ow eomsoosuen, (Hop40 Foundations and Practicalities fluent group had poor comprehension, whereas the nonfluent group had good comprehension, equating sensory and motor aphasia to fluent and nonfluent aphasia. The terms and the di- chotomous classification remained dormant and essentially buried for almost a century. Benson (1967) was instrumental in its revival. He con- sidered the characteristics of speaking rate, prosody, pronunciation (articulation), phrase length, speech effort, pauses, press of speech, word choice, paraphasia (phonemic, semantic, neologistic), and verbal stereotypes (recurring utterances) as the cardinal features to consider in differentiating persons according to their flu- ency. Perhaps the appeal of Benson's study and the eventual influence it has had on the wide- spread adoption of the classification system was derived from the correlation of lesion location (based on isotope brain scans) with fluency. He concluded that patients with lesions anterior to the fissure of Rolando had nonfluent signs, and patients with lesions posterior to the fissure of Rolando had fluent signs. Using factor analyses and the ten categories of Benson (1967) and Kerschensteiner, Poeck, and Brunner (1972) verified the presence of two distinct behavioral clusters corresponding. {in part to Benson's fluent and nonfluent catego- ries with the hierarchically arranged features of phrase length, pauses, prosody, speaking rate, and effort. Linguistic processing impairments ‘can reduce the number of words or morphemes that are produced before a pause or breakin the phrase occurs, A language impairment could also increase the number of pauses inserted ina connected speech sample or decrease the over- all rate of speech because of semantic, syntac- tic, lexical, or phonologic impairments impair the prosodic contour and increase the perceived effort used to speak. Speech motor impairments also can create each of these features of speech production that are attributed to the language system, and in the absence of careful exclu- sion of motor speech disorders that frequently co-occur with aphasia (even in persons with lesions posterior to the rolandic fissure), the classification can be applied to persons with aphasia but for the wrong reasons. For example, the features of phrase length, pauses, prosody, speaking rate, and effort are all associated with, and in some instances used to define, the pres- ence of apraxia of speech (Wertz, LaPointe, & Rosenbek, 1984). Apraxia of speech, in the ab- sence of co-occurring aphasia, has been found with lesions occurring posterior to the fissure of Rolando (McNeil, Weismer, Adams, & Mul- ligan, 1990). The probability of misdiagnosis cr misattribution of signs in the application of the nonfluent category seems to be high. This does not appear to be the case for the use of the fluent category; however, its application fre- quently results from the absence of nonfluent signs rather than the assessment of the same parameters used to determine nonfluency. Nonfluency, even when carefully objectified with explicit and measurable criteria that have been employed to date, is difficult to unambig- uuously label any level of the speech production system. That is, deficits of the motor system are at least as likely (if not more likely) candidates for explaining the nonfluency characteristics of the spoken language of the aphasic individual as deficits of the language processing system, Short phrases, poor articulatory agility, and oor melodic line (characteristics used in the Boston classification system) are all potential products of an impaired motor system and not necessarily a linguistic system. Careful diagno- sis can differentiate these very different disor- ders, but itis rarely done in the assignment of aphasia categories, and there is scarce evidence that the differential diagnosis was done in the selection of the subjects on which the classifi- cations were formed. The criteria for the classification of fluent or nonfluent aphasia are frequently undefined by researchers and clinicians, and the criteria are not universally agreed upon. Nonetheless, it is ‘sometimes possible to infer the author's inten- tions from patient descriptions, Some define nonfluent aphasia by the presence of agram: ‘matic or paragrammatic speech. Itis sometimes used as a substitute for the previously rejected motor aphasia category or as shorthand for Broca, transcortical motor, or global categories, ‘Some have used it as a substitute for the pres- ence of co-occurring motor speech impairments, Others define fluent aphasia by the absence Of agrammatic or paragrammatic speech, as a substitute for the previously rejected sensory primarily 1 which m thany class dichoChapter 3_Aphasia Theory, Models, and Classification __41 aphasia category, or as shorthand for any one of the Wernicke, transcortical sensory, anomic, oF conduction categories or by the absence of 4 concomitant motor speech disorder. Kertesz (1979) attempted to set specific criteria for the iagnosis of fluent and nonfluent aphasia as Dart of the WAB, He attempted to rate fluency from primarily language variables, attempting to minimize “disturbances of prosody and d arthria, which may not be aphasic features in all cases.” He incorporated constructs such as meaningfulness (propositionality), number of words, agrammatism (telegraphic speech), pho- Remic paraphasias (jargon), recurring stereo: typie utterances, intonation (rhythmic pattern), and mumbling and low vocal intensity. Good- slass (1981) suggests that the strictest definition Of fluency was in terms of the number of words Der uninterrupted group (usually less than four words per string, excluding stereotyped expres- sions) that the patient can occasionally produce. In this sense, nonfluency implies a preponder- ance of paraphasias and word-finding problems. He defined fluency by preserved articulatory facility (agility), preserved prosody (rhythm, rate, and melodic line over the span of single words, phrases, or entire sentences, noting syllabic stress and monotone), and preserved grammatical skills (including the presence of ‘markers of grammatical relationships; morpho- logic markers of verb tense, person, and num- ber; word order; subordinating constructions: bound morphemes; and omissions or substitu- tions of functor words). Aswithany classification system, the fluency) nonfluency dichotomy needs to account for a reasonable array and pattern of phenom- ena such as lesion locations, psycholinguistic deficits, modality involvements, communica- tive deficits, and appropriate and differential treatments. In fact, the fluency/nonfluency categorization does not correspond well to the gross esion localization of pre- or post-rolandic fissure—perhaps the easiest of the criteria to meet. Knopman, Selnes, Niccum, Rubens, Yock, and Larson (1983) reported persistent nontlu ency with critical amounts of left-hemisphere rolandic cerebral cortex and underlying fron- toparietal white matter lesions. Broca area involvement was not necessary for persistent nonfluency. Basso, Lecours, Moraschini, and Vanier (1985) reported a substantive number of fluent patients with anterior lesions. Basso, Bracchi, Capitani, Laiacona, and Zanobio (1987) reported a high number of patients with fluent aphasia and lesions in the dominant frontal lobe. Marshall and Tompkins (1982) found no differences in verbal self-corrections between fluent and nonfluent subjects at equivalent severity. The fluencyjnonfluency classification does not differentiate modality deficits between the two categories. The classification criteria of Goodglass and Kaplan for fluent aphasia speci- fied the demonstration of poorer auditory com- prehension than nonfluent aphasic patients, Poeck, Kerschensteiner, and Hartje (1972) dem- onstrated no difference between groups on ati- ditory comprehension on a version of the Token Test. Likewise, Odell (1983) demonstrated no differences between fluent and nonfluent apha- sic subjects on either the listening or a reading version of the Revised Token Test, assessing not the type of language comprehension impair- ments but the overall assertion of more or less impairment between categories. Penn (1983) investigated fluency relative to Pragmatic competence and overall communica- tive appropriateness. The behaviors considered Were interjections, repetitions, revisions, incom- plete phrases, false starts, pauses, and word- finding difficulties. she concluded that “there ‘as not always a correlation between the clinical formof aphasia and type offluency rating," Penn’s results were supportive of Deloche, Jean-Louis, and Seron's (1979) findings and conclusions that many aspects of fluency provide no clear-cut differentiation in terms of aphasic types. Poeck (1989) posed and answered two ques- tions about the fluent/nonfluent dichotomy in aphasia. He asked about the heuristic (scien tifie) and practical value of this classification compared with other widely used systems, and about the value the classification holds for re- search. His answers were essentially “in the neg- ative” and something approaching “none.” He viewed the adoption of this classification system as a conceptual and methodologic step back- ward. Further, Poeck speculated that everybody assumes to know what fluent and nonfluenta2 Foundations and Practicalities 42_!_ Foundations and Practicalities speech production is. However, the fact is that it is a highly unreliable diagnosis among profes- sionals, and thus as a shorthand for communi- cating core characteristics ofa patient it not only has the limitations and invalidities of all classifi- cation systems, but also is insidiously dangerous because ofits presumed simplicity. ‘There seems to be a legitimate and perhaps helpful use of the term fluency as applied to language competence/processing and motor be- haviors. There may be a legitimate and useful application for the differentiation of normal speakers of a particular language. For example, many people are described as fluent or hyper~ fluent speakers. There is, however, little agree- ment among professionals on the characteristics ‘of fluent speakers. The clinical and research use of the fluent and nonfluent aphasia classifica tion is a conceptual step backward and should be discontinued until the construct can be objectified, theoretically justified, empirically validated, found reliable, broadly taught to all relevant disciplines, and found useful clinically for prognosis or some other purpose. Schuell et al (1964) reported a classification system for aphasia that proposed that apha- sia was a unitary disorder, This proposition followed Marie (1906) and preceded simi lar ones by Bay (1964) and Darley (1982). In spite of this theoretical and experimentally derived position on the nature of aphasia and its unidimensionality, Schuell et al constructed a classification for persons with aphasia that recognized that the language impairment that defines aphasia is often accompanied by other sensory, motor, and cognitive disorders that are not in and of themselves aphasia. As such, the categories of the classification are not so much a taxonomy of aphasia per se, but rather ‘classification of aphasia as a sensory, a motor, or a cognitive disorder that by accident of the co-occurring neurologic damage and shared or adjacent neurologic organization, creates com- mon patterns of language and communication performance. Based on a factor analytic study of 155 per~ sons with aphasia, assessed on a battery of 68 tests with 595 test items, organized around the assessment of all of the language modali- ties (listening, reading, writing, speaking, and gesturing), five factors were identified and interpreted: 1, language behavior; 1M, visual discrimination, recognition, and recall; Il, visuospatial behavior: IV, gross movements of the speech musculature; and V, recognition of stimulus equivalence. Two minor factors were identified by one or two tests. The first factor crossed all language modalities and all areas of language behaviors that were sampled by the large battery of tests, Importantly, the battery decisively excluded nonlinguistic tests such as copying, matching, object assembly, and speech movement tests. This factor became group 1 and was labeled simple aphasia that was char- acterized by a reduction of available language in all modalities and without concomitant perceptual, sensorimotor, or dysarthric com- ponents, Group 2 was labeled aphasia with Central involvement of visual processes. This group is indistinguishable from simple aphasia except that it has inordinately larger deficits in reading and writing that were attributed to nnonlinguistic-specific impairments of recog- nition, discrimination, and recall of learned visual symbols. Group 3, aphasia with senso- rimotor involvement affecting speech, includes individuals with severe reduction of language in all modalities, as may be the case with sim- ple aphasia; however, these individuals have co-occurring dysarthria. Careful reading of the description of these individuals (Schuell et al, 1964, p. 197) suggests that persons with apraxia of speech (a term that these authors did not tse) were excluded from this category and placed into one of the minor syndromes. ‘This category then presented with more spo- ken language deficits, but they were attributed to the sensorimotor component of speech pro- duction and not to the language deficit per se, ‘which addresses a recurring problem with both the neoclassical association and the fluent) nonfluent classification systems. Group 4 was labeled aphasia with scattered findings, usually including both visual involvement and dysar= thria, In essence, this category includes sub- stantive features of groups 1, 2, and 3. Group 5 ‘was termed severe impairment, amounting to almost complete skills in all modal Parallels to the ist classification s Schuell classifica efined aphasia a that crosses all la ferences across m Impairments of b cognitive (eg. 1 categories wepe d about lesion loca specific or psyd impairments. that associative and fl is important to a these assumption truly objectively ¢ The behaviors on tem was derived v basic assumption: and other behavi feading, speaking even likely, that selected for mea the factor analysi have emerged. On tal replications, u f2n the unidimen ality of aphasia ate, there is insu fo accept one cla ail others. It may assifying person rent classiicati senified theoretic main elusive. Wh: sification system: t date leave the Search of an ade fhe purposes for {20 additional lab 2 Until consid sembled, the pers served by careful Symptoms that a IRand for which 2 That is, lesion loc Bape is substantiv ipaistication andChapter3 _Aphasia Theory, Models, and Classification 43 almost complete loss of functional language skills in all modalities. Parallels to the neoassociative connection- ist classification system are not evident in the Schuell classification system because Schuell defined aphasia as a unidimensional disorder that crosses all language modalities, with dif- ferences across modalities being attributed to impairments of basic sensorimotor and other cognitive (eg, memory) impairments. The categories were derived without assumptions about lesion localization or about modality- specific or psycholinguistic process-specific Impairments that underlie the neoclassical associative and fluent/nonfluent categories. It is important to acknowledge that the lack of these assumptions is not synonymous with a truly objectively derived classification system. The behaviors on which the classification sys- tem was derived were selected because of some basic assumptions about the nature of aphasia and other behaviors that can affect listening reading, speaking, and writing. It is possible, even likely, that if other behaviors had been selected for measurement and entered into the factor analysis, different categories would have emerged. Only through many experimen: tal replications, using a variety of instruments, can the unidimensionality or multidimension: ality of aphasia classification be settled. To date, there is insufficient converging evidence to accept one classification system and reject all others. It may be that different purposes for classifying persons with aphasia will yield dif ferent classification systems and that a single unified theoretically derived system will re main elusive. What is apparent is that the clas sification systems proposed and investigated to date leave the theorist and the clinician in search of an adequate taxonomy for any of the purposes for which one might want to put an additional label on the diagnosis of apha sia. Until considerably more evidence is as sembled, the person with aphasia may be best served by careful description of the signs and symptoms that are relevant to the problem at hand for which a label would be substituted. That is, lesion location implied by the aphas: type is substantively unnecessary given the so- phistication and availability of brain imaging technology. Treatments have not been validated that can be applied to a specific aphasia type. Classification assignment has not been shown to provide prognostic information about ex pected recovery from aphasia, either assisted (with treatment) or unassisted. In summary, we believe that all classifica- tion systems proposed to date fail to provide the theoretical justification or the clinical util- ity for any purposes to which they might serve thus, their adoption and use are not justified. There remains, however, a need to communi- cate among professionals the salient aspects of the individuals’ language and communica- tion abilities and impairments. In spite of the logic and evidence that the classification sys- tems proposed to date fail at every turn, history suggests that is unlikely that professionals will abandon the notion of “aphasia with adjectives.” There are, however, some cautions that require consideration when persons with aphasia are assigned a “type.” As suggested nearly three decades ago, three temptations arise, however, when clinicians classify their patients. The first is a tendency to see behaviors in terms of clas: sification categories, which forces them into a mold even when the behaviors are disparate The second problem is to ignore sometimes critical assessment in areas which the clas sification does not cover. (It should be noted that the areas of assessment which forms the basis of Benson's [sie; the neo-classical asso: ciative] classification of his patients is but a small part of the information on which most contemporary speech-language pathologists assess and treat.) The third potential problem. is related to the other two but highlights the fact that the physiologic, perceptual, cogni tive, linguistic and communicative abilities and disabilities, and the strategies imple mented to overcome the aphasic deficits, are very individualized. Thus the dimensions on Which the patient is classified will not predict these other more salient treatment variables for any individual, In other words, within- foup variance is likely to be as large or larger than between-group variance for many di- ‘mensions on which treatment is based. In summaty, if aphasic patients are classified, classification should be done with an aware- ness of the temptations to see what is not there, to miss what is there and to ignore in- dividual differences. (McNeil, 1982, p. 698)44 __1_ Foundations and Practicalities Chapter Review 1. Properly constituted theories of aphasia A. should be able to be falsified, B. must be simplified in models. . need to include consideration of brain ‘mechanisms. D. cannot be modified on the basis of new incompatible data, F. all of the above. 2, Classical and neoclassical associative con- nectionist models ‘A. are underspecified in terms of current conceptions of language processing components. B, are well supported by clinical-anatomic correlations. . have declined in influence since the rise ‘of competing approaches. D. are based on the holist tradition, E, none of the above. 3. Cognitive neuropsychological models ‘A. donotmake claims regarding the brain. mechanisms’ underpinning language processes. B. are based on the assumption that the language faculty is modular in organi- zation. . provide information on what tasks to use in treating language deficits. ). Aand B. Band ¢. mS 4, The fluent/nonfluent classification system A. is the most reliable system to use be- ‘cause itis a simple dichotomy. B, captures the communication impaii ment in aphasia better than the other systems. C. is firmly grounded in site of lesion evi- dence with fluent aphasia related to posterior lesions. D, none of the above. E. AandC, 5, The Schuell classification system A. is the only truly objectively derived aphasia classification system. B, is based on tasks and behaviors that allow for and consider the differential diagnosis of motor speech impairments from language impairments. G. is the aphasia classification most ap- propriate for employment by speech- language pathologists but not psycholo- gists, linguists, or neurologists. D. Band. none of the above, ‘Answers: 1: A; 2: A; 3:D; 4:D; 5:B. References ‘Adams, RD. & Victor, M. (1977). Principles of neurol- ‘ogy. New York: McGraw-Hill ‘Akbarzadeh, MR, & Moshtagh-Khorasani, M. (2007, (Oct). A hierarchical fuzzy rule-based approach to aphasia diagnosis, journal of Biomedical Informatics, 40, 465-475, Baddeley, A. Logie, R, Nimmo-Smith, 1, & Brereton, 'N. (1985) Components of fluent reading. Journal of ‘Memory and Language, 24, 119-131 Basso, A. (2003). Aphasia and its therapy. Oxford: ‘Oxford! University Press Basso, A, Bracchi, M, Capitani, E, Laiacona, M, & Zanobio, M. E (1987, Sep). Age and evolution of language area functions. study on adult stroke pa tients, Cortet, 23, 475-483, Basso, A. Lecours, A. R, Moraschini, S. 8 Vanier, M (1985, Nov). Anatomeclinical correlations of the aphasias as defined through computerized tomog raphy exceptions, Brain and Language, 26,201-228, Bastian, H.C. (1869). On the various forms of loss of speech in cerebral disease. British Foreign Medical Chirurg Review, 43, 209-236. Bay. (1964). Principles ofdassifiation and thir influ ence an our concepts of aphasia In A.V. S. De Reuck ‘&M, OConner (Eds), Ciba Foundation symposium on disorders of language. Boston: Little, Brown, Benson, DF (1967). Fluency in aphasia: Correlation with ‘adioactive scan localization. Cortex, 3, 373-394 Benson. D. F_(1979). Aphasia, olexia, and agraphia, ‘New York: Churchill Livingstone Ree we (1961) — BBisez (1965). Sur =—r iPers 6, 337-395, een |W. (1972 MGical and ther iehearies € Thomas. Been |W. 197 Dhew York: Academs fee |W. (1988) WEaerence Eribaum. Pee |W. (2001) Seemplex sentences Sef the regression h WB ort (Es), Lar Beestdown: Paral ees Hopkins Uni Jie: M_ & Fiytche PSs of disconnect ane 2739, =a Sp Pesyivian languag Aan of Neurology Heide Rowiey.D.1 Sing recovery f Seetworks: prelimin feeession. Cortex Sounders Compary. Bec S. Schwarez. Heeger. D. A (195 sae nonaphasic sp 01-338 (Betocte. C_ Jean-Lo ‘Seedy of the tempo speech of five aph Imterview and des 2 Be Wiles, j 6. (197 iphemes in acquisi BEB Zurif(Eds freakdown: Paral Jobns Hopkins Uni PEeerson,j. (1954). 6 Bsychological Corp BAB Young. a. (1 hslogy. Hove. Engl Fado.) A. (1983). 1 BMA MIT Press. eed (1953) 0m « Dew York: InternatChapter 3. Aphasia Theory, Models, and Classification __45 Brain, W. R. (1961 ‘worth, Broca, P1865), Sur le siege de la faculte du langage “rtiule, Buletin of the Society of Anthropology of Paris, 6, 337-393, Brown, | W. (1972). Aphasia, apraxia and agnosia: ‘Clinical and theoretical aspects. Springfield. 1: Charles C Thomas. Brovin, J. W. (1977). Mind, brain, and consciousness. New York: Academic Press. Brown, J. W. (1988), Life of the mind, Hillsdale, NJ Lawrence Erlbaum. Brown, J, W. (2001), Microgenetic theory: Reflections ‘nd prospects. Neuro-psychoanalysis, 3, 61~74, caplan, D. (1987), Neurolinguistics and_ linguistic “aphasiology: An introduction. New York: Cambridge University Press Caramazza, A, & Zuri B. (1978). Comprehension of ‘tomplex sentences in children and aphasis: A rest ff the regression hypothesis. in A. Caramazza & E. B. Zuri (Eds,), Language acquisition and language breakdown: Parallels and divergencies. Baltimore: Johns Hopkins University Press. Catan, M. & Fiytche,D. H. (2005, Oct). The rises and fall of disconnection syndromes. Brain, 128(Pt 10), 2224-2239, Catani, M, jones, D. K. & Fiytche, D. H, (2005, Ja). Perisyvian language networks of the human brain. ‘Annals of Neurology, 52, 8-16. Code, C. Rowley, D.T, & Kertesz, A (1994, Sep) Pre ‘icting recovery from aphasia with connectionist networks: preliminary comparisons with multiple regression. Cortex, 30, 527-532. Coltheart, M, & Langdon, R. (1998). Autism, modular ity and levels of explanation in cognitive science. Mind & Language, 13, 138-152. Darley, FL (1982), Aphasia, Philadelphia, PA: W. B Saunders Company. Dell, G-5, Schwartz, M.F, Martin, N. Safran, EM, & ‘Gagnon, D. A. (1997, Oct). Lexical access i aphasic fand nonaphasic speakers, Psychological Review, 104, 301-838. Deloche, G., Jean-Louis, J, & Seron. X. (1979, Sep) ‘Study of the temporal variables in the spontaneous Speech of five aphasic patients in two situations, interview and description, Brain and Language 8 241-250. De Villers. G. (1978), Fourteen grammatical mor- ;phemes in acquisition and aphasia In A. Caramazza EB. Zuni Eds), Language ccquistion and language breakdown: Parallels and divergencies. Baltimore: Johns Hopkins University ress, isenson, J (1954). Examining for aphasia. New York Psychological Corporation. fli A_& Young, A.( 1988), Human cognitive neuropsy- chology. Hove, England: Lawrence Erlbaum, Fodor, A.(1983).The modularity of mind. Cambridge, MA: MIT Press Freud, 5, (1953). On aphasia, Translated by E. Stengel. 'New Yorks International Universities Press. Speech disorders. london: Butter Garrett, M. (1984). The organization of processing Structure for language production; Applications to aphasic speech. in D. Caplan, A. R Lecours, & A, Smith (Fas), Biological perspectives of language pp. 172-193), Cambridge, MA: MIT Press Geschwind, N.(1965a, Jun), Disconnexion syndromes imanimals and man, | Brain, 88, 237-294, CGeschwind, N-(1965b, Sep). Disconnexion syndromes in animals and man. Brain, 88, 585-644 Gleason, J.B. (1978), Acquisition and dissolution of the English inflectional system. In A. Caramazza & EB. Zurif (Eds), Language acquisition and language breakdown: Parallels and divergencies. Baltimore: Johins Hopkins University Press Gleason, |. 8, 8 Goodglas, H.(1984). Some neurologi ‘al and linguistic accompaniments ofthe fluent and honfluent aphasias, Topics in Language Disorders, 4, 71-81 Goring. loning,K, 8 Hoff, H. (1963). Aphasia: Alii ‘al syndrome, ln L Halpern (Ed) Problems of dyaic ‘neurology. jerusalem: Hebrew University Press. Goldstein, K (1948). Afterefects of brain injuries in war, New York: Grune Stratton. Goodglass, H. (1978). Acquisition and dissolution of language in A. Caramazza & EB. Zurif (Eds), Lan- ‘guage acquisition and language breakown: Parallels and divergences. Baltimore: Johns Hopkins Univer- sity Press. GGoodelass, H.(1981).The syndromes of aphasia: Simi: Tarties and differences in neurolinguistic features. Topies in Language Disorders, 1, 1-14. GGoodslass,H. Kaplan, E, & Barresi, 8. (2001). The as ‘sessment of aphasia and related disorders (3rd ed.) Philadelphia: Lippincott Williams & Wilkins. GGoodglass, H. Quadfasel, A, & Timberlake, W. H (1964), Phrase length and the type and sever aphasia, Cortex, 1, 133-153, orno-Tempini, M,L, Brambati SM. Ginex, V. Og) ‘ML-Dronkers, N.F, Marcone, A etal-(2008, Oct) The logopeniciphonological v sive aphasia, Neurology, 71,1227 orno-Tempini, M. L, Dronkers, N. F, Rankin, K.P. ‘Ogat,} M, Phengrasamy,L, Rosen, HJ, etal. (2004, Mar). Cognition and anatomy in three variants of primary progressive aphasia. Annals of Neurology, 335-346, Harley, . A. (1996). Connectionist modeling of the recovery of language functions following brain dam- ‘age. Brain and Language, 52, 7-24 Head, (1926) Aphasia and kindred disorders, Vols. I, London: Cambridge University Pres. Hecaen, H.& Albert, ML, (1978). Human neuropsy ‘chology. New York: John Wiley & Sons. Hecaen,H, & Dubois, J. (1971). La neurotinguistique In GE. Perren & J LM. Trim (Eds.). Applications of linguists. London: Cambridge University Press. Hill. K. Dean, RS, & Decker, 5. L (2001), Integration ‘of neuropsyehological and cognitive theory in reha bilitation. The International Journal of Neuroscience, 111, 195-210.46 Foundations and Practicalities Howard, D, Patterson, K.E, Franklin, S, Orchard-Lsle, V8 Morton, (1985, Dec), Treatment of word re- trieval defcis in aphasia A comparison of two ther apy methods, Brain, 108(Pt 4), 817-829, Howes, D. (1964). Application ofthe word frequency concept to aphasia, In. V.S, De Reuck&M. O'Connor (Eds, Clba Foundation symposium on disorders of language. Boston: Lite, Brovn. Jackson, H. (1958), Selected writing of John Hughlings Jackson, Vols. 1 & 2. J. Taylor (Ed). London: tapes Press. Jakobson, R. (1968) Child language, aphasia and po ‘ological universal, Translated by A, R. Keller. The Hague: Mouton. Kerschensteiner, M., Poeck, K, & Brunner, E. (1972, ‘Jun. The Muency-non fluency dimension in the clas- sification of aphasic speech. Cortex, 8,233-247. Kertese, A. (1979). Aphasia and associated disorders: Taxonomy, localization, and recovery. New York Grune & Stratton, Kertes, A. (2007), Western Aphasia Battery (revised) San Antonio: PsychCorp. Kertesz, A. & Phipps J.B. (1977, Jan}. Numerical tax- ‘onomy of aphasia, Brain and Language, 4, 1-10. kes, K. (1934). Leitungsaphasi (Nachsprechaphasie. ink. Bonhoeffer (Ed), Hanbuch der Aertzlichen Erfahrugen im Wettriege 1914/1918, Leipzig: Barth. Knopman,D.S, Selnes, 0. A, Niccum N, Rubens, A.B, "Yoek, D.& Larson, D.(1983, Sep. A longitudinal study ‘of speech fluency in aphasia: CT correlates of recovery and persistent nonflvency. Neurology, 33, 1170-1178. Lecours, AR. (1974). Le cerveau et le langage. LUnion Medicale du Conada, 103, 123-163, Lesser, & Milroy, L (1993) Linguistics and aphasia Psycholinguistic and pragmatic aspects of interven tion, London: Longman. turla, AR. (1964), Factors and forms of aphasia. In {A V5, De Reuck & M. O'Connor (Eds.), Ciba Foun: dltion symposium on disorders of language. Boston: Little, Brown, Lutia, A R. (1966). Higher cortical functions in man, ‘New York: Basic Books, Luria, AR, & Hutton J.T. (1977, Apr), A modern as- sessment of the basie forms of aphasia. Brain and Language, 4, 129-151. Marie, P (1906), Revision de la question de Faphasie: Ta troisieme citconvolution frontale gauche ne joue aucun role special dans la function du langage. La ‘Seraana Medica, 26, 241-247 Marshall, R.C. & Tompkins, CA. (1982, Mar), Verbal selFcorrection behaviors of fluent and noafluent aphasic subjects Brain and Language, 15, 292-306, ‘Matin, N., Dell, GS, Safran, .M. & Schwartz, M. FE (1994, Nov). Origins of paraphasias in deep dyspha- Sia: testing the consequences of a decay impairment to an interactive spreading activation model of lexi- cal retrieval. Brain and Language, 47, 609-660. Martin N, Fink, R, Laine. M, & Ayala, J (2004).Imme- diate and short-term effects of contextual priming on ‘word retrieval in aphasia, Aphasiology, 18, 867-858, Mayr, E Linsley, E.G. & Usinge, RL. (1953). Meth ‘ds and principles of systematic zoology. New York: ‘MeGraw-Hill McCloskey, M, (1991). Networks and theories: the place of connectionism in cognitive science. Psycho- logical Science, 2, 387-395, McNeil, MR (1982), The nature of aphasiain adults In N.Lass, L McReynolds, J Northern & D. Yoder (Eds), Speech language and hearing, Vol. Il (pp. 682-740) Philadelphia: W.B, Saunders McNeil, MR. (1988). Aphasia in the adult. In: N. Lass, L McReynolds, J. Northern, & D. Yoder (Eds), Hand- book of speech-language pathology and audiology (pp. 738-786). Toronto: BC. Decker. McNeil, MR, Brauer, D, & Patt. R.(1990).A test of auditory language processing regression: Adult apha- Sia versus normal children ages 5-13 years Australian Journal of Human Connurication Disorders, 18,21~39, Nell, M.R, Odell, K-H, &Tseng, C-H.(1991 Towards the integration or resource allocation into a general theory of aphasia. Clinical Aphasiology, 20, 21-39, MeNeil, MR & Pratt, SR (2001). standard defini- tion of aphasia: Toward a general theory of aphasia Aphasiology, 15.901-S11. MeNeil, M. R, Weismer, G., Adams, S, & Mulligan, M 1990, jun), Oral structure nonspeech motor control in normal, dysarthric, phasic and apraxic speakers: isometric force and static position control. Journal of Speech and Hearing Research, 23, 255-268. ‘Mesulam, MM. (1982, Jun). Slowiy progressive apha- sia without generalized dementia, Annals of Neurol gy, 11, 392-598, “Michie.S. Johnston. M., Abraham, C. Lawton, R, Parker, D.. 8 Walker, A; “Psychological Theory" Croup (2005, Feb). Making psychological theory useful for implementing evidence based practice: a consensus approach. Quality & Safety in Health Care, 14,26-33. Mohr. P, Pessn, NLS, Finkelstein, SFunkenstein, H.H, Duncan, G. W, & Davis, KR. (1978, Apr), Broca apha- sia: pathologic and clinical. Neurology, 28,311-324 Nadeau, 5. (2000). Connectionist models and lan ‘guage. In S, E, Nadeau, LJ G. Rothi, & B. Crosson Eds.) Aphasla and language: Theory fo practice (pp. 299-347), New York: Guilford Press. Nielsen JM. (1938). The unsolved problems in apha- sia: L Alexia in “motor” aphasia. Bulletin ofthe Los Angeles Neurological Society 4, 114-122. (del, KH. (1983}. Comparisons between auditory and ‘edi comprehension in aphasic adults, Unpublished ‘masters thesis, Madison, WI University of Wisconsin, Parsi D. & Pizaamiglio (1970, un). Syntactic com= prehension in aphasia. Cortex, 6 204-215, Patterson, K. 8 Plaut, D.C. (2008). "Shallow draughts intoxicate the brain”: lessons from cognitive science for cognitive neuropsychology. Topics in Cognitive Science, 1, 39-58, Patterson, K, & Shewell, C.(1987). Speak and spel: dis- sclations and word-class effect. In: M.Coltheart,G Sartori & R Job (Ed), The cognitive neuropsychology of language (pp. 273-294) London: Lawrence Erbaurn Testing assu Esof aphasia. oun cit within and 2 ‘of a psycholi Sartori & R Job ( of language HilChapter 3_Aphas Penn, C, (1983), Fluency and aphasia: a pragmatic re- Consideration, The South african Journal of Commu nication Disorder, 30, 3-8. Pettit, JM, McNeil, MLR. & Keith, RL (1989) The use ‘of novel and real-word stimuli in the assessment of English morphology in adults with aphasia. Aphasi ology 3, 655-685. ick, A. (1913), Agrammatischen Sprachstorungen Beilin: Springer. Plaut, D, C.(199, Jan}, Relearning after damage incon- nectionist networks: toward a theory of rehabilita- tion. Brain and Language, 52, 25-82. Plaut D.C. & Shale, T, (1993), Deep dyslexia: case ‘study of connectionist neuropsychology. Cognitive Neuropsychology, 10,377-500. Poeck, K (1989). Fluency, In C. Code (Ed,) The charac: teristics of aphasia (pp. 23-32), Philadelphia: Taylor Francis Poeck, K. Kerschensteiner, M & Hartje, W. (1972. Sep). ‘A quantitative study on language understanding in fluent and nonfluent aphasia. Cortex, 8, 299-304 Poeck, K, Orgass,B, Kerschensteiner, M. & Hartj, W. (1974 Jan}. A qualitative study on token test perfor- mance in aphasic and non-aphasic brain damaged patients. Neuropsyehotogia, 12, 49-54, Poeppel,D. Hickok, C, (2004, May-Jun), Towards anew functional anatomy of language Cognition. 92, 1-12 Popper, K (1958). The logic of scientific discovery (2nd 4). London: Hutchison & Co. Raymer, A.M, Beeson, P, Holland, A, Kendall, D. Ma her, LM, Martin, N, etal. (2008, Feb). Translational research in aphasia: from neuroscience to newrore- habiltation, Journal of Speech, Language. and Hear- ing Research JSLHR, 51, 5259-8275. Ribot. A. (1883), Les maladies de la memoir. Paris Librairie Germanin Bailire uml, W, Caramazza, A. Shelton JR & Chialant; D. (2000) Testing assumptions in computational theo: Fies of aphasia Journal of Memory and Language, 43, 217-248, Aussell, W.R. & Esp, MLE, (1961). Traumatic apha sia: A study of aphasia in war wounds ofthe bran. London: Oxford University Pres. Schuell, H. Jenkins, J}, & Jimenez-Pabon, E. (1964). Aphasia in adults: Diagnosis, prognosisand treatment. New York: Hoeber Medical Division, Harper & Row. Schwartz, M, (1987). Patterns of speech production deficit within and across aphasia syndromes: appli tation ofa psycholingustic model. In M. Colthear Sartori, 8 Jb (Els), The cognitive neuropsychol- gy of language. Hilsdale, NJ: Lawrence Erlbaum. Theory, Models, and Classification 47 Schwartz. M.F, DelG., Martin,N.,GahlS,& Sobel, ‘2006). A case-sries test ofthe interactive two-step ‘model of lexical acess: Evidence from picture nam- ing Journal of Memory and Language, $4, 228-264 ‘seidenberg, M.S, (1988). Cognitive neuropsychology ‘and language: The state of the art. Cognitive Newrop~ syechology, 5, 403-426. Walker-Batson, D., Curtis, S, Natarajan, R. Ford | Dronkers,N, Salmeron, E, etal (2001, Sep). A dou- ble-blind,placebo-controlied study ofthe use of am. phetamine in the treatment of aphasia Stroke, 32, 2093-2088. Weintraub, S, Rubin, N. P. & Mesulam, MM. (1990, ec), Primary progressive aphasia. Longitudinal course, neuropsychological profile, and language features, archives of Neurology, 47, 1329-1335. Weisenburg, T. M, & McBride, KE. (1935). Aphasia: ‘A clnical psychological study, New York: Common- ‘wealth Fund. Wepman, JM, & Jones, V. (1961). The language mo- daltes rest for aphasia Chicago: Education-Industry service ‘Wepman, J, M8 Jones, LV. (1968). Five aphasias: A ‘commentary on aphasia as a linguistic phenome non, nD. M,Rioch & EA. Weinstein (Eds). Research Publication Associations for Research in Nervous and Mental Disease, 42, Disorders of Communication New York: Hafner Publishing \Wernicke, (1874), Aphasische symptomkomplex. In Con, Weigart,& Breslau, Boston studies on the phi- losophy of science IV. Dordrecht: Reidel ‘Wertz, RT, Deal, J, & Robinson, A.J. (1984), Clas- ‘fying the aphasias: A comparison of the Boston Diagnostic Aphasia Examination and the Western ‘Aphasia Battery, Clinical Aphasiology, 14, 40-47, Wertz, RT, LaPointe, LL, & Rosenbek, J. C. (1984) “Aprasia of speech in adult: The disorder and its man- ‘agement, Orlando: Grune and Stratton. ‘Whitaker, H. A. & Selnes, 0. A. (1978). Token Test mea sures of language performance in normal children and aphasic patents. In A. Caramazza & €. B. Zurit (Eds), Language acmuistion and language break down: Parallels and divergencies. Baltimore: Johns Hopkins University Press. ‘Whyte J. (2008, Feb) grand unified theory of rcha bilitation (we wish), The 57th John Stanley Coulter Memorial Lecture. Archives of Physical Medicine and Rehabilitation, 89, 203-209, Wilson, 8 (2002). Tonards a comprehensive model of ‘cognitive rehabilitation, Neuropsychological Reha biltation, 12, 87-110,