Is syntax based on spatial Image Schemas in the ...

Squibs Paradox lost*

JOSEPH HILFERTY, JAVIER VALENZUELA, and OSCAR VILARROYA

Introduction

The question of whether or not language is an emergent property of general cognitive abilities is an intriguing topic that has given rise to much debate. In various recent publications, Jackendoff (1993, 1996, 1997) maintains that our capacity for language cannot be based solely on the specialization of other, more basic cognitive processes. Instead he argues that our faculty for language must ultimately be grounded in the principles of a genetically endowed Universal Grammar. To back his claim up, JackendofF briefly enumerates some favorite Chomskyan themes (i.e., neurological pathologies, the poverty-of-stimulus argument, the development of creoles, the critical-period hypothesis, etc.); he then confidently asserts that the clearest evidence in favor of nativism has to do with the failure of linguists the world over to come up with complete grammars. In what follows, we show that what Jackendoff contends to be the clearest proof of the existence of Universal Grammar is, in reality, very weak evidence, because it rests on several seriously flawed major assumptions. The putative paradox

Before we assess Jackendoff's argument, let us take a look at his actual Claims. These are laid out in the following passage: To my mind, [...] the most compelling evidence [for the innate basis of Universal Grammar] comes from a "transcendental" argument that I like to couch äs the Paradox o/Language Requisition. E very normal child acquires the mental grammar of his or her own language within seven or eight years, with little direct instruction or consultation. Yet the Community of linguistics, working collectively, with oodles of cross-linguistic evidence, has not succeeded in writing the grammar of a single language, despite decades of research, backed by centuries of traditional grammar. Since linguists are presumably bringing their highly developed general purpose problem solving ability to bear on the problem, such ability is evidently not enough. Children must know something unconsciously that we linguists can't Cognitive Linguistics 9-2 (1998), 175-188

Brought to you by | Purdue University Libraries Authenticated Download Date | 1/6/16 4:28 PM

0936-5907/98/0009-0175 © Walter de Gruyter

·*

176 /. Hilferty, J. Valenzuela, and O. Vilarroya know consciously, namely a search space of hypotheses. They don't have to decide between [Chomskyan] generative grammar and cognitive grammar and LFG and HPSG and tagmemics, let alone alternatives yet to be developed. They know which one is right, even if we don't. So—even if every bit of, say, Langacker's (1987, 1991) is correct, the fact that it took till 1991 to find it and till 20?? to convince everyone etse demonstrates conclusively that there must be a rieh Universal Grammar! (JackendofT 1996: 95; the italics are Jackendoff's.)

The gist of Jackendoff 's thesis can be summarized äs follows: If (a) scholars have so far failed to elucidate grammar in any convincing way, despite their numbers, man-hours, and effort, then (b) a child cannot learn the rules or principles that constitute such a grammar.

We contend that this argument is a non sequitur, for reasons that we develop below. In fact, it is clearly an argument made from resignation and despair (cf. Jackendoff 1993 [1994: 33]) and not from careful reasoning based on positive evidence. This strikes us äs a rather frail foundation for a theory of language acquisition. Underlying assumptions

At the heart of Jackendoff's Paradox of Language Acquisition argument is the implication that language and grammar are descriptively so intricate that they cannot be acquired by a child without the aid of some genetically prewired guidelines. In essence, this line of argument assumes that: (a) there is a direct correspondence in complexity between the (external) behavior or abilities of a System and its causal structure (i.e., the system's inner workings that actually produce or account for the behavior or abilities in question); and (b) learning, if unhelped by genetically inherited knowledge structures, is both analytical and explicit in nature. We take each of these assumptions up in turn. Assumption (a) states that, if the behavior exhibited by a given System is complex on a descriptive level, then this implies that the internal mechanisms that produce this complex behavior must necessarily be complex äs well. We believe that this assumption embraces a fallacy, viz. that it is legitimate to project the properties of an effect onto the cause, äs if the properties could be read back. Applied to Jackendoff's argument, this amounts to projecting the complexity of a theoretical description (which depends on the specific epistemological stance of the linguist) onto the internalized grammar of Speakers and hearers. The grounds for this strategy are dubious, because it is genuinely possible that the grammar


Paradox lost 177 need not incorporate all the properties of the description. Assumption (a) is therefore logically unsound because it begs the question äs to whether or not descriptions map biuniquely onto objects of study. The foregoing argument suggests that the presumption of complexity implicit in Jackendoff's argument should not be taken uncritically. While we concedc that such a supposition is perhaps not uncalled for, it is by no means the only logical possibility. This is true because there are several wcll-known examples of Systems in which descriptive complexity does not correlate with actual complexity. Consider just two cases in point: (i)

Gravity. The ways in which physical objects interact in space are highly complex and varied. This is the case of planetary orbits, the speed of falling objects, ocean tides, and black holes. Nevertheless, such complexity can be reasonably described by a few fundamental physical laws such äs Newton's Law of Universal Gravitation (F — Gmmld2) and Einstein's Relativity Formula (e = mc2). (ii) The yenetic code. The complexity of life forms on Earth is almost infinite. Yet the System that encodes such complexity makes use of a simple mechanism that combines sequences of four nucleotides: adenine, cytosine, guanine, and thymine. These cases show that is not inconceivable to have a mismatch between Systems that manifest complex behaviors and their causal structure. Consequently, in the case of language acquisition it should not be assumed a priori that the complexity inherent in the description of linguistic behavior should correspond isomorphically to the actual cognitive processes in our brains (i.e., the grammar that accounts for observable linguistic behavior). Assumption (b) maintains that, if unaided by domain-specific innate knowledge, learning can only be achieved through explicit and analytical methods. This assumption is problematic at best. Even if we grant the existence of a complex System regulating linguistic behavior, it does not follow that the only way that a child can master (i.e., learn) such a System is through step-by-step analytical procedures that crystallize in the form of explicit rules (cf. Seidenberg 1997). In this regard, consider the case of the social-interaction System. In terms of descriptive complexity, this System is arguably much like the previous naturalistic cases of gravity and the genetic code, but of course with the added property of being a human ability. Now, sociobiological speculation notwithstanding, there seems to be little reason to presuppose that the specific rules or principles (or whatever) that might govern Systems of social interaction are genetically transmitted. Yet children do attain to the basic social skills that allow them to function in their respective communities. Furthermore,


178 / Hilferty, J. Valenzuela, and O. Vilarroya ^

they do so, despite the fact that only the smallest fraction of social-interaction precepts are ever explicitly taught. This suggests that learning can take place even without recourse t o explicit analytical rules or innate ideas. To exemplify what we are trying to get across, let us briefly examine a specific instance of nonexplicit learning: that of gift-giving. Indisputably, the appropriateness of a gift is highly context dependent, and, hence, many variables have to be calculated. To wit: (1) the age, sex, interests, socio-economic Status of the recipient; (2) the relationship between the giver and the recipient (e.g., parentchild, boss-employee, teacher-student, friends, lovers, ex-lovers, spouses, neighbors, acquaintances, etc.); (3) the reason for the gift (e.g., birthday, graduation, reconciliation, surprise, reward, thanks, Christmas, family tradition, etc.); (4) the appropriate amount of money to be spent on the gift; (5) etc., etc. Therefore, in order to give a present to the neighbor's daughter on the day of her tenth birthday, all of the above variables (which, to say the least, is a very partial taxonomy) play a role in choosing the appropriate gift. In the Situation at hand, a submachine gun, a car, a ham sandwich, a potato, a copy of Carnap's Meaning and Necessity, or leather lingerie would normally be thought of äs unsuitable gifts. It is doubtful that a set of explicit rules could be stipulated that generates all and only the appropriate presents for such an occasion, let alone for all possible variants thereof. Moreover, even if it were possible to write "a generative gramrnar of gift-giving", there is absolutely no guarantee that a person would, or could, actually use such a set of explicit rules. Such a conjecture would, then, require an act of faith. Conclusion

The moral of the story is quite simple. It is a fundamental error of judgment, we believe, to surmise that a cognitive System such äs grammar cannot be learned just because a formalized or explicit description has not yet emerged after many years of hard work by so many people. Such reasoning is clearly faulty. Furthermore, even if a given cognitive phenomenon—linguistic or otherwise—can be expressed descriptively in the form of explicit rules or principles, this does not necessarily mean that cognizers actually make use of such notions (cf. Searle 1990). In short, the very paradigm on which Jackendoff's argument is perched may well be intrinsically unable to yield an isomorphic fit with the internalized grammar of real language users. This is, of course, not to deny the enlightening heuristic value of explicit


Paradox lost

179

descriptions, but merely to recognize that they provide little basis for the postulation of innate concepts. Without a doubt, the controversy concerning nature and nurture in languagc acquisition is a highly complicated topic that should be treated with the utmost care, no matter what position one takes on the issue. From our obscrvations, we can only conclude that JackendofTs Paradox of Languagc Acquisition argument is fatally flawed, in that it rests upon sevcral unprovcn assumptions. The weaknesses of the argument stcm, in our opinion, from the failure to distinguish between mental grammar (to usc JackcndolFs own term) and theoretical grammar. Given our prescnt stutc of knowlcdge (or ignorance), to conflate the two äs if they were completely commensurable is simply unwarranted for the following reason: theoretical grammar is open to pubüc inspection, whereas mental grammar is not. It follows then that mental grammar is a type of implicit knowlt'dye and theoretical grammar is a type of explicit knowledye. To link the two notions äs equivalent can only lead to conceptual confusion. To conclude: whether or not grammar is hard-wired into the human gcnome is still an open question. In the course of this notc, we argued that, even if language is ultimately proven to be part of our innate gcnetic endowment, it plainly will not be on the basis of JackendofTs so-called "most compelling evidence". There is no Paradox of Language Acquisition, because mental grammar and theoretical grammar are two difiercnt brecds of cat. Universität de Barcelona Universidad de Murcia Universität Autönoma de Barcelona Note * The authors may be contacted at the following c-mail addresscs: Joseph Hilfcrty (Universität de Barcelona): [email protected]; Javier Valenzuela (Universidad de Murcia): [email protected]; Oscar Vilarroya (Universität Aulonoma de Barcelona): [email protected]

References JackendolT, Ray 1993 Palternfi in the Mind: Language and Human Nature. London: llarvester Wheatsheaf (also published by BasicBooks, New York, 1994). 1996 Conceptual semantics and cognitive linguistics. Cogniiive Unguistics 7: 93-129. 1997 The Architecture ofthe Language Faculty. Cambridge, M A: The M IT Press.


180 Z). Kemmerer Langacker, Ronald W. 1987 Foundations of Cognitive Grammar, vol. I: Theoretical Prerequisites. Stanford, CA: Stanford University Press. 1991 Foundations of Cognitive Grammar* vol. II: Descriptive Application. Stanford, CA: Stanford University Press. Seidenberg, Mark S. 1997 Language acquisition and use: Learning and applying probabilistic constraints. Science 275:1599-1603. Searle, John R. 1990 Consciousness, explanatory Inversion, and cognitive science. Behavioral and Brain Sciences 13: 585-596. (Also published in: Macdonald, Cynthia and Graham Macdonald (eds.), Philosophy of Psychology: Debates on Psychological Exploitation, vol. 1. Oxford: Basil Blackwell, 1995, 331-355.)

Is syntax based on spatial Image Schemas in the inferior parietal cortex? Evidence against Deane's Parietal Hypothesis* DAVID KEMMERER

In a series of recent publications, Paul Deane has argued that syntax is based on spatial image Schemas that are implemented in the left inferior parietal cortex, a view that he calls the Parietal Hypothesis (Deane 1991, 1992, 1996). I will argue that the Parietal Hypothesis is inconsistent with data that do not show any close relation between syntactic competence and the left inferior parietal cortex. These data come from neuropsychological studies of several populations of brain-damaged patients and from functional neuroimaging studies of normal subjects. The organization of the paper is äs follows: first I will summarize the Parietal Hypothesis, then I will present the evidence against it, and finally I will briefly address some implications of this discussion for the question of where syntax is localized in the brain. The Parietal Hypothesis

Deane's proposal is an extension of LakofFs (1987) Spatialization of Form Hypothesis, which states that grammatical concepts are organized in terms


Evidence against Deane's Parietal Hypothesis

181

of spatial image Schemas—specifically, that sentences are organized in terms of the OBJECT schema, constituency is organized in terms of the PART-WHOLE schema, grammatical relations are organized in terms of the LINK schema, and head-dependent relations are organized in terms of the CENTER-PERIPHERY schema. According to Deane, if Lakoff's proposal is on the right track, it predicts that syntax should be implemented in the same region of the brain that is dedicated to representing spatial image Schemas. Deane argues that the region that is most likely to serve this function is the inferior parietal cortex (i.e., the supramarginal and angular gyri), since damage to this region, especially in the right hemisphere, impairs a variety of congnitive functions that he believes are associated with spatial image Schemas—for example, bodily awareness, somatosensory Integration, the representation of high-level spatial relationships, and the ability to recognize and draw physical objects that are composed of multiple parts arranged in certain configurations (e.g., Critchley 1953). Deane argues that, in accordance with the predicted neural association between grammatical and spatial concepts, the inferior parietal cortex, especially in the left hemisphere, also appears to be crucial for syntax. He adduces two main kinds of evidence in support of this view. First, damage to this brain region has been reported to impair syntactic processing in both production and comprehension. In particular, cases have been reported where left inferior parietal damage is implicated in global aphasia (Hecaen 1967) and agrammatism (Mohr 1976; Kolk et al. 1985). Second, a number of functional neuroimaging studies have found activation in the left inferior parietal region when normal subjects perform tasks that require syntactic processing (see the references cited in Deane 1996: 58-59). Evidence against the Parietal Hypothesis

The Parietal Hypothesis is clearly a very intriguing proposal that deserves careful consideration. An especially valuable feature of the proposal is that it can easily be tested, since it makes two strong predictions: (1) that damage to the left inferior parietal cortex should consistently result in syntactic deficits in both production and comprehension, and (2) that functional neuroimaging studies of syntactic processing in normal subjects should consistently reveal activation in the left inferior parietal cortex. In what follows I will argue that both of these predictions are disconfirmed by existing data. A language disorder that frequently results from damage to the left inferior parietal cortex, especially the supramarginal gyrus, is conduction aphasia (Kohn 1992). The most prominent characteristics of this disorder


182 D, Kemmerer are impaired word and sentence repetition, phonemic paraphasias (i.e., transpositions, substitutions, deletions, or insertions of phones or syllables), and impaired auditory verbal short-term memory (STM). This last feature is consonant with recent functional neuroimaging studies that show activation in the left inferior parietal cortex when normal subjects perform auditory verbal STM tasks (e.g., Frackowiak 1994). For present purposes, the most important characteristic of conduction aphasia is that syntactic competence is typically preserved in both production and comprehension, contrary to the prediction of the Parietal Hypothesis. For example: four detailed case studies have been reported of conduction aphasics who have lesions encompassing the left inferior parietal cortex (Warrington et al. 1971; Shallice and Butterworth 1977; Butterworth et al. 1990; McCarthy and Warrington 1987; Vallar and Baddeley 1984, 1987; Vallar et al. 1990). These patients are described äs having fluent and grammatical spontaneous speech and äs performing normally on several tests of sentence production. They also display good receptive sentence processing äs measured by syntactic comprehension tests and grammaticality judgement tests. The only tests of receptive sentence processing on which the patients performed poorly were those that required them to retain a verbatim record of a sentence in auditory verbal STM. Of course this result is hardly surprising, given that all of the patients had severe STM deficits. It is worth adding that Palumbo et al. (1992) describe nine other conduction aphasics, eight of whom had lesions that included the left inferior parietal cortex. These eight patients are reported to have intact syntactic abilities in both production and comprehension äs measured by standardized tests. All of these findings contradict the Parietal Hypothesis, since it predicts that damage to the left inferior parietal cortex in conduction aphasia should impair syntax in both Output and input modalities. Another large population of patients who have inferior parietal damage yet spared syntactic abilities are patients with Alzheimer's disease (AD). There are t wo main types of evidence for inferior parietal damage in AD. First, this brain region has an extremely high density of neurofibrillary tangles (an anatomical marker of AD) compared to other cortical areas (Arnold et al. 1991); and second, this brain region has a greater amount of hypometabolism than other cortical areas—in fact, the degree of inferior parietal hypometabolism correlates with the degree of impairment on a wide ränge of neuropsychological tests (Keilp et al. 1996). Numerous studies have shown that one of the few cognitive domains that is preserved in AD is syntax. The speech and writing of AD patients is often semantically shallow or even incoherent, but it is nonetheless


Evidence against Deane's Parietal Hypothesis

183

syntactically well-formed (e.g., Bayles 1982; Hier et al. 1985; Blanken et al. 1987; Kempler et al. 1987; Illes 1989; Kemper et al. 1993; Croisile et al. 1996). In addition, while AD patients do not correct semantic errors in sentence repetition tasks, they frequently correct syntactic errors (Bayles 1982). They also make better use of syntactic cues than semantic cues in disambiguating spoken homophones (Schwartz et al. 1979; Kempler et al. 1987). With respect to syntactic comprehension, Rochon et al. (1994) tested 23 AD patients on a large battery of constructions that included actives, passives, datives, conjoined objects, relatives, clefts, and conjoined verb phrases. The patients performed within normal limits on all of the constructions except for relatives, clefts, and conjoined verb phrases, and the authors argue that these constructions were difficult for the patients not because the patients have a parsing impairment, but rather because the constructions contain two propositions and hence exceeded the patients' semantic STM capacity. All of these studies contradict the Parietal Hypothesis, since it predicts that the inferior parietal damage in AD should impair syntactic competence in both production and comprehension. I turn now to functional neuroimaging studies that challenge the Parietal Hypothesis. Although Deane cites a number of positron emission tomographic (PET) studies in support of his proposal, none of these studies were specifically designed to distinguish between the cortical areas that are involved in syntactic processing and those that are involved in other aspects of linguistic processing. In fact, at the time of this writing, I am only aware of two imaging studies that have attempted to do this, and neither of them is fully consistent with the Parietal Hypothesis. (It is worth noting, however, that PET studies äs well äs functional magnetic resonance imaging studies of language processing are now appearing in the literature at an extremely rapid pace, so it is likely that we will soon have many more studies available that are relevant to the issue under discussion here.) First, Mazoyer et al. (1993) conducted a PET study in which subjects were presented with sentences that had disrupted semantics but intact syntax. No significant activation was found in the left inferior parietal cortex. Second, Stromswold et al. (1996) conducted a study in which subjects were presented with syntactically complex sentences in one condition and syntactically simpler sentences in another condition. Both types of sentences elicited activation in the supramarginal gyrus; however, contrary to what the Parietal Hypothesis would predict, this activation was not significantly greater for the complex sentences than for the simpler sentences. The only cortical areas that were activated significantly more in the former condition than in the latter were Broca's area and the anterior cingulate gyrus.


184 D. Kemmerer Conclusion The studies reviewed above show that, contrary to the predictions of the Parietal Hypothesis, damage to the left inferior parietal cortex does not consistently cause syntactic deficits, nor is this brain region consistently found to be activated in functional neuroimaging studies of syntactic processing. Thus it seems unlikely that syntax is localized in the parietal lobe in all individuals. This leaves us with the question of what part of the brain does represent syntax. Because space limitations preclude a detailed discussion of this issue, I will just mention that Deane's Parietal Hypothesis is by no means the only proposal regarding the localization of syntax that is currently unable to accommodate all of the available data. Any attempt to relate syntax exclusively to a particular sector of the perisylvian cortex—parietal, frontal, or temporal—faces the same problem, namely that damage to specific perisylvian cortical areas sometimes does and sometimes does not affect syntax. With respect to the inferior parietal lobe, Deane was able to cite lesion studies that relate syntax to this particular brain region, yet I was able to cite other lesion studies that do not show any close relation between syntax and this particular brain region. The same story can be told for each of the other major sectors of the perisylvian cortex. In the frontal lobe, damage in the vicinity of Broca's area often causes syntactic deficits in both production and comprehension (Caplan 1987), but there are numerous cases in which damage to Broca's area leaves syntax intact. For example, Dronkers et al. (submitted) report that of 20 patients with lesions encompassing Broca's area, 10 had good sentence production; and Caplan and Hildebrandt (1988; see also Caplan et al. 1997) describe several patients who had damage in Broca's area yet performed well on a battery of syntactic comprehension tests. Similarly, damage to the anterior or posterior superior temporal lobe sometimes disrupts syntactic processing for production and/or comprehension (e.g., Naeser et al. 1987; Variier and Caplan 1990; Dronkers et al. 1994), but sometimes superior temporal lesions leave syntactic abilities largely preserved (e.g., Caplan 1987; Caplan and Hildebrandt 1988; Caplan et al. 1997). For example, AD patients typically have severe degeneration in the anterior superior temporal lobe (Arnold et al. 1991); yet, äs shown earlier, these patients usually have intact syntax. One could infer from these findings that the specific localization of syntax within the perisylvian cortex varies across individuals, possibly due to genetic Variation (Caplan 1994). Further support for this view comes from electrical Stimulation studies which show that syntactic processing can be disrupted by Stimulation in fairly restricted perisylvian regions, but these regions vary considerably from person to person (Ojemann 1991, 1995).


Evidence against Deanes Parietal Hypothesis

185

It is important to bear in mind, however, that the issue of whether syntax has a consistent neural Implementation across the population is not yet closed. This is because the studies which suggest variable Implementation may lack the resolving power, at both linguistic and neurobiological levels of analysis, that is necessary to identify the critical brain areas. What is currently needed are more studies that combine the following features: (1) use of extensive batteries of tests that enable one to distinguishbetween patients with genuine syntactic deficits and patients with other kinds of linguistic or cognitive deficits, and (2) use of several different measures of brain damage, such äs both structural magnetic resonance imaging (MRI) and PET, in order to clearly demarcate not only areas of necrosis or degeneration but also areas of hypometabolism. As more studies of this kind are done, äs well äs more studies that use functional neuroimaging techniques to investigate syntactic processing in normal subjects, our understanding of the neural basis of syntax will undoubtedly improve. University of Iowa Note * I would like to thank Claudia Brugman and two anonymous referees for their comments on this paper. Preparation of the manuscript was supported in pari by grant T32 DC00029-07 from the National Institute on Deafness and Other Communication Disorders. Author's address: Department of Neurology, Division of Cognitive Neuroscience, 2153 RCP, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242, USA. E-mail: [email protected]

References Arnold, S., B. Hyman, J. Flory, A. Damasio, and G. V. Hoesen 1991 The topographical and neuroanatomic distribution of neurofibrillary tangles and neuritic plaques in the cerebral cortex of patients with Alzheimer's disease. Cerebral Cortex l, 103-116. Bayles, Kathryn A. 1982 Language function in senile dementia. Brain and Language 16, 265-280. Blanken, Gerhard, Jürgen Dittmann, J.-Christian Haas, and Claus-W. Wallesch 1987 Spontaneous Speech in senile dementia and aphasia: Implications for a neurolinguistic model of language production. Cognition 27, 247-274. Butterworth, Brian, Tim Shallice, and Frances L. Watson 1990 Short-term retention without short-term memory. In Shallice, Tim and Giuseppe Vallar (eds.), Neuropsychological Impairments of Short-Term Memory. Cambridge: Cambridge University Press, 208-235. Caplan, David 1987 Neurolinguistics and Linguistic Aphasiology. Cambridge: Cambridge University Press.


186 D. Kemmerer 1994

Language and the brain. In Gernsbacher, Morton Ann (ed.), Handbook of Psycholinguistics, New York: Academic Press, 1023-1053. Caplan, David and Nancy Hildebrandt 1988 Disorders of Syntactic Comprehension. Cambridge: MIT Press. Caplan, David, Nancy Hildebrandt, and Nikos Makris 1997 Location of lesions in stroke patients with deficits in syntactic processing in sentence comprehension. Brain 119, 933-949. Caplan, David and Gloria S. Waters 1990 Short-term memory and language comprehension: A critical review of the neuropsychological literature. In Shallice, Tim and Giuseppe Vallar (eds.), Neuropsychological Impairments of Short-Term Memory. Cambridge: Cambridge University Press, 337-389. Critchley, Macdonald 1953 The Parietal Lobes London: Arnold. (Reprinted 1966, New York: Haffher.) Croisile, Bernard, Bernadette Ska, Marie-Josee Brabant, Annick Duchene, Yves Lepage, Gilbert Aimard, and Marc Trillet 1996 Comparative study of oral and written picture description in patients with Alzheimer's disease. Brain and Language 53, 1-19. Deane, Paul D. 1991 Syntax and the brain: Neurological evidence for the Spatialization of Form Hypothesis. Cognitive Linguistics 2, 361-367. 1992 Grammar in Mind and Brain. New York: Walter de Gruyter. 1996 Neurological evidence for a cognitive theory of syntax: Agrammatic aphasia and the Spatialization of Form Hypothesis. In Casad, Eugene H. (ed.), Cognitive Linguistics in the Redwoods. New York: Walter de Gruyter, 55-116. Dronkers, Nina, David Wilkins, Robert Van Valin, and Brenda Redfern 1994 A reconsideration of the brain areas involved in the disruption of morphosyntactic comprehension. Brain and Language 47, 461-463. Dronkers, Nina, Johnna Shapiro, Benda Redfern, and Robert Knight submitted The third left frontal convolution and aphasia: On beyond Broca. Frackowiak, Richard S. 1994 Functional mapping of verbal memory and language. Trends in Neurosäences 17, 109-115. Hecaen, Henry 1967 Brain mechanisms suggested by studies of parietal lobes. In Darley, Frederic (ed.), Brain Mechanisms Underlying Speech and Language. New York: Grüne and Stratton, 146-255. Hier, Daniel B., Karen Hagenlocker, and Andrea Gellin Schindler 1985 Language disintegration in dementia: Effects of etiology and severity. Brain and Language 25, 117-133. Illes, Judy 1989 Neurolinguistic features of spontaneous language production dissociate three forms of neurodegenerative disease: Alzheimer's, Huntington's, and Parkinson's. Brain and Language 37, 628-642. Kemper, Susan, Emily LaBarge, F. Richard Ferraro, Hintat Cheung, Hirn Cheung, and Martha Storandt 1993 On the preservation of syntax in Alzheimer's disease. Archives of Neurology 50, 81-86.


Evidence against Deanes Parietal Hypothesis

187

Kempler, Daniel, Susan Curtiss, and Catherine Jackson 1987 Syntactic preservation in Alzheimer's disease. Journal of Speech and Hearing Research 30, 343-350. Keilp, John G., Gene E. Alexander, Yaakov Stern, and Isak Prohovnik 1996 Inferior parietal perfusion, lateralization, and neuropsychological dysfunction in Alzheimer's disease. Brain and Cognition 32, 365-383. Kohn, Susan E. (ed.) 1992 Conduction Aphasia. Hillsdale: Lawrence Erlbaum Associates. Kolk, Hermann H. J., Marianne J. F. Van Grunsven, and Antoine Keyser 1985 On parallelism between production and comprehension in agrammatism. In Kean, Mary-Louise (ed.), Agrammatism. New York: Academic Press, 166-206. Lakoff, George 1987 Women, Fire, and Dangerous Things. Chicago: Chicago University Press. Mazoyer, B. M., N. Tzourio, V. Frak, A. Syrota, N. Murayama, O. Levrier, G. Salamon, S. Dehaene, L. Cohen, and J. Mehler 1993 The cortical representation of Speech. Journal oj Cognitive Neuroscience 5, 467-479. McCarthy, Rosalyn and Elizabeth Warrington 1987 Understanding: A function of short-term memory? Brain 110, 1565-1578. Mohr, Jay P. 1976 Broca's area and Broca's aphasia. In Whitaker, Haiganoosh and Harry A. Whitaker (eds.), Studies in Neurolinguistics, L New York: Academic Press, 201-236. Naeser, M., P. Mazurski, H. Goodglass, M. Peraino, S. Laughlin, and W. Leaper 1987 Auditory syntactic comprehension in nine aphasic groups (with CT scans) and children: differences in degree but not order of difficulty observed. Cortex 23, 359-380. Ojemann, George A. 1991 Cortical organization of language. Journal of Neuroscience 11, 2281-2287. 1995 Investigatinglanguage duringawake neurosurgery. In R. D. Broadwell (ed.), Decade of the Brain. Library of Congress, 117-131. Palumbo, Carole L., Michael P. Alexander, and Margaret A. Naeser 1992 CT scan lesion sites association with conduction aphasia. In Kohn, Susan E. (ed.), Conduction Aphasia, Hillsdale: Lawrence Erlbaum Associates, 51-76. Rochon, Elizabeth, Gloria S. Waters, and David Caplan 1994 Sentence comprehension in patients with Alzheimer's disease. Brain and Language 46, 329-349. Schwartz, Myrna F., Oscar S. M. Marin, and Eleanor M. Saffran 1979 Dissociations of language function in dementia: A case study. Brain and Language 7, 277-306. Shallice, Tim and Brian Butterworth 1977 Short-term memory impairment and spontaneous Speech. Neuropsychologia 15, 729-735. Stromswold, Karin, David Caplan, Nathaniel Alpert, and Scott Rauch 1996 Localization of syntactic comprehension by positron emission tomography. Brain and Language 52, 452-473. Vallar, Giuseppe and Alan D. Baddeley 1984 Phonological short-term störe, phonological processing, and sentence comprehension: A neuropsychological case study. Cognitive Neuropsychology l, 121-141.


188 D. Kemmerer 1987

Phonological short-term störe and sentence processing. Cognitive Newopsychology 4, 417-438. Vallar, Giuseppe, Anna Basso, and Gabriella Bottini 1990 Phonological processing and sentence comprehension: A neuropsychological case study. In Shallice, Tim and Giuseppe Vallar (eds.), Neuropsychological Impairments of Short-Term Memory. Cambridge: Cambridge University Press, 418-476. Vanier, Marie and David Caplan 1990 CT-scan correlates of agrammatism. In Menn, Lise and Lorraine Obler (eds.), Agrammatic Aphasia. Amsterdam: Benjamins, 37-114. Warrington, Elizabeth KL,Valentine Logue, and R. T. C Pratt 1971 The anatomic localisation of selective impairment of auditory verbal short-term memory. Neuropsychologia 9, 377-387.
