Indirect speech acts, figurative language and theory of mind Some suggestive indications from three genetic syndromes

Jean-Adolphe Rondal & Amaryllis Quiros Ramirez

University of Lige, Belgium

Abstract Three genetic syndromes are analyzed regarding language development and functioning: autism, fragile X, and Asperger syndrome. A common symptomatology is uncovered though varying in severity regarding the semantic-pragmatic aspects of language. It is proposed that the language difficulties in these syndromes find their origin in an underdevelopment of theory of mind for neurogenetic reasons.

Key words : theory of mind, intersubjectivity, language, autism, fragile X, Asperger syndrome, genetic background, figurative language, mental verbs, metaphores, metonymies, illocutory acts, proverbs.

1. THEORY OF MIND So-called theory of mind was proposed as a way to explain basic interpersonal difficulties in infantile autism (Baron-Cohen et al;, 1985; Baron-Cohen, 1991; Flavell, 2004). The hypothesis is rooted in a work by Premack and Woodruff (1978) suggesting that the chimpanzees and the other nonhuman primates actually dispose of the necessary cognitive abilities for reading the states of mind and decode the intentions of the members of their own species. De Waal (2006) has supplied an empirical demonstration that this is indeed the case. He traces the origin of this ability to the affective link associated with collaborative needs in social mammals. Presently the expression theory of mind (a curious label perhaps better substituted with intersubjectivity) refers to a whole domain of the human mental organization subsuming a series of mechanisms allowing to interpret the state of mind of the social partners. It is likely that this ability finds its origin in the so-called mirror-neurons recently identified in primates brain. One is speaking of particular structures represented in several areas of the brain (in particular the frontal and parietal cortices; Rizzolati, Fogassi, & Gallese, 2006). These neurons fight whenever a social partner executes an action alerting the neuronal structures responsible for the same movements in the observer. They supply a sort of inner experience and from there an intuitive comprehension of the actions and states of mind of the alter ego. They may also underlie the ability to learn by observation (Bandura, 1976). A strong link seems to exist between the motor organization of intentional acts and the ability to understand the same actions in others. Given that humans and other primates are social beings, it is easy to see in it a mechanism that is evolutionary advantageous. Moreover the brain mirror-system contains Broca area the relevance of which for language is well known. If, as agreed by many specialists (cf. Rondal, 2000), human communication has started with the use of gestures and facial mimics, it is likely that the mirror-system also played an important role in language evolution. 2. AUTISM It may be suggested that autism is caused by a basic deficiency at the level of the mirror-neurons which are either lacking or insufficiently functional. There is common agreement that autism is

a severe pathology of intersubjectivity. The syndrome is affecting roughly one child in 1,000 and 4 boys for 1 girl (Gilberg & Coleman, 1992). It is not an early version of schizophrenia or a psychogenic condition as previously thought. Autism corresponds to a severe disorder of the interpersonal ontogenesis where neurocognitive and language deficits prevail (Tager-Flusberg, 2000). These children suffer from an important communicative dysfunction already identifiable in the second year of life (Stone et al., 1999), judging from the absence of ocular contacts with caretakers, absence of social smile in the first months, and a lack of language development in the first years (Rapin & Dunn, 2003). The child with autism typically exhibits stereotyped behaviors, behavioral routines and rituals of the obsessive type (Bailey et al., 1996). In three-quarter of the cases, there is also some degree of mental retardation (Rutter, 1979), most often as a secondary consequence of a lack of proper social development. In 3% of the cases, however, a fragile-X pathology is associated with autism (Bailey et al., 1996) (see below for the genetic correlation between the two entities). Neurofunctional anomalies of the hippocampal and amydgalia systems are usually observed together with an abnormal organization of the polysensorial integration at the level of the temporal and parietal brain areas. These anomalies are responsible for the exaggerated processing of sensorial representation and the perturbation of perceptual integration (Bailey et al, 1996). They corrode the affective meaning of the stimuli, modify attention processes, reduce the social bonds and the affiliative motivations (cf. the review by Waterhouse et al., 1996). A serious deficit of theory of mind accounts well for the major developmental difficulties in autism regarding social development and the language pragmatic aspects (Tager-Flusberg et al., 1990). Usually, the grammatical aspects of the language system are not primarily disturbed (Cantwell et al., 1978; Tager-Flusberg, 2000). There remains a doubt as to the semantic aspects of language. Lexical distribution in formal categories (particularly with regard to verbs and modifiers) is described as abnormal by some researchers (for example, Hobson, 1989) but as basically normal by others (for example, Tager-Flusberg et al., 1990). Curiously, there seems to be no systematic data on the contents of the lexical terms used by children with autism despite the fact that Kanner (1946) already suggested the existence of what he called metaphoric language, i.e., semantic incongruities, seeming neologisms, and other

nonconventional uses. Given what we know today of lexical development in general and the relational difficulties in autism, there is nothing but expectable in such semantic idiosyncrasies. However, except for Rutters 1987 wrong suggestion but on the right track so to speak (see below), nobody to our knowledge has acknowledged it. Concerning particularly those lexical terms that are semantically less transparent, the construction of conventional reference (the denotatum) demands a number of encounters with the object or the event-referent in situation whereby a member of the linguistic community supplies the appropriate label. Hearing uttering a word in the presence of a particular object or in the course of an event only one time, one cannot usually be sure of its meaning. The word can refer to the form of the object, anyone of its parts, its function, color, use, etc. One is able to disambiguate the reference only gradually following several such encounters whereby the denotated characteristics remains constant whereas the other aspects vary (cf. Rondal, 2002). Someone not disposing of an adequate interactive capacity is clearly at a disadvantage in this process. Hence the likely recourse at connotative meanings (a type of meaning personal, affective, tied to idiosyncratic experience, and deprived of genuine communicative value) easily giving an impression of strangeness or figurativity. Without a minimum of relational ability, conventional lexical development (hence linguistic) is difficult or impossible. Rutter (1987) has suggested that characteristics of the type could be explained by a lack of corrective feedback from the parents or other adults part. There is no reason (nor data) supporting the hypothesis of a lack of evaluative or corrective feedback in typically developing, retarded or disturbed children (cf. Rondal, 1985, 2006). Lack of appropriate personal relationships, it may be thought, is what prevents most children with autism to take into account the information originating from the interlocutors or their feedbacks depriving them of the semantic calibrating necessary for learning conventional word meaning. 3. FRAGILE X SYNDROME Fragile X syndrome is more severe in male subjects with a prevalence of approximately .90 for 1,000 living births. Most male subjects are mentally retarded (from mild to severe retardation) (cf. Hagerman, 1996, for a review). Their behavioral phenotype includes

anomalies of the same kind as those observed in autism but less marked; for example, a tendency to avoid ocular and social contacts, impulsive speech with perseverations, relatively high rates of dysfluencies and omission or substitution of vocalic and consonantal phonemes (Hagerman, 1995) . The receptive and productive lexicon is relatively preserved. Grammatical development follows with mental age. Pragmatic development is deficient, not so much as to basic functioning (conversational turn taking, elementary speech acts) but regarding more sophisticated illocutory acts such as indirect requests and figurative language uses (Sudhalter et al., 1991). A research conducted in our laboratory by Marcucci (2006) illustrates these deficiencies. A group of male subjects with fragile X (aged 15 to 24 years) received a series of tasks assessing comprehension of sentences and short paragraphs containing proverbs, metaphors (conventional and new ones), metonymies (forms substituting one term with another holding a particular relationship with the first; for example, container for content in the expression drink a glass of water), as well as requests (explicit, implicit, indirect, in action, in information). The fragile X subjects were matched for mental age with a group of typically developing children. Results showed a good receptive ability for the explicit requests as well as for literal language in all subjects. In the tasks involving indirect speech acts, non conventional metaphors (particularly psychological ones, for example,This boys is an angel), metonymies, and proverbs, the individuals with fragile X scored significantly lower than the typically developing children. These data can not be explained by a difference in cognitive ability given that the two groups were matched for mental age. We will see later with Asperger syndrome another indication ruling out a purely cognitive explanation of the pragmatic limitations under scrutiny. These limitations relate overall to a specific ability (or lack of it) distinct from global cognitive level as well as from other language components; the capacity to go beyond literal language towards contemplating reasonable hypotheses as to the states of mind of the interlocutors and their communicative intents whenever a literal interpretation is not yielding a relevant meaning. Garner et al. (1999) have given the classical false belief tasks (Perner & Wimmer, 1985; Perner et al., 1989) to a group of boys with fragile X, aged 10 to 16 years, and a group of subjects with a corresponding mental retardation of unknown etiology. A

significantly larger proportion of the first subjects failed the firstorder tasks (e.g., comprehension of sentences such as Andrew thinks that Mary has fallen in love for Chuck. There was no statistically significant difference between the two groups in the second-order tasks (e.g., sentences such as Andrew thinks that Mary thinks that he has fallen in love for Sandra, although the raw data were not in favor of the boys with fragile X also in this latter task. Two registers play a major role in the comprehension of indirect speech acts and figurative language: a cognitive register (this does not contradict the indication above) and a linguistic one. For example, nonpsychological metaphors are treated correctly by typically developing children before psychological ones (Brdart & Rondal, 1982). In order to understand a metaphoric meaning, one needs to find a link between plausible concepts. Implicit requests (for example, It is quite windy here to get someone concerned to close the door or the window) demand a comparative analysis of the utterance and the linguistic and/or extralinguistic context. Proverbs are even more delicate to deal with because they do not contain a direct reference to the real meaning. Beyond the cognitive component (necessary but not sufficient), there is the need to activate an intuitive strategy for reconstructing the semantic relationship intended by the interlocutor. Subjects with fragile X are in difficulty in this type of task. This suggests two levels of theory of mind: a first level, basic, severely disturbed in autism, and a second one, more sophisticated, the mental analysis of other peoples intentions.

4. ASPERGER SYNDROME Research on Asperger syndrome (affecting between 3 and 7 persons in one thousand) suggests a third level of theory of mind. In this syndrome, sometimes defined as higher level autism (BaronCohen, 2000), one records qualitative anomalies of the social interactions, a limited register of personal interests, and repetitive activities. The major difference with autism is that there is no delay in language development. The anamnesis of patients with Asperger syndrome often reveals language precocity and superior intellectual abilities but they exhibit a marked tendency to interpret literally all discourse with a limited understanding of figurative language

(Attwood, 2003). Such a profile is confirmed in a study by Rosano (2006) in our laboratory showing that persons with Asperger syndrome have difficulties in understanding indirect speech acts, metaphors, and more generally in reading the mind of the interlocutor. Adults with Asperger syndrome report that they have had difficulties in figuring out the other persons intentions and private meanings, as long as they can remember. They do not quite succeed in telling the difference between fact and fiction. They are little able to read between the lines and to grasp humor. These persons express their emotions little; nonverbal expression is impoverished and speech tends to be monotonous. They have difficulties in perceiving and understanding other peoples emotions. Their intellectual strategies lack flexibility. In spite of their important intellectual abilities, they have difficulties in understanding the social rules particularly the more arbitrary ones; hence their somewhat eccentric behaviors or behaviors interpreted as such by other people. A number of famous artists and scientists have presented the major symptoms of Asperger syndrome without being diagnosed as such most of the time. The syndrome was identified in the years 1940 by the Austrian psychiatrist Hans Asperger, at the beginning as a subcategory of autism (following Kanners seminal work on this last syndrome). Alan Turing, one of the inventors of informatics and modern computer science, clearly had Asperger syndrome. His detailed biography established by Leavitt (2006) including numerous excerpts of letters exchanged between Turing and his mother, illustrates the peculiar nature of the personal and social difficulties that he encountered all his life despite extraordinary intellectual abilities.

6.NEUROGENETIC DETERMINISM Fragile X syndrome is caused by a null mutation of the gene FMR-1 or FMR-2, both located on chromosome X. The primary etiology of Asperger syndrome involves the full mutation of two genes (NLGN3 and NLGN4), both on chromosome X (Frith, 2004). These mutations prevent the codification of an essential protein for the development and stabilization of some populations of cerebral synapses. Neurological investigation reveals an underfunctioning of the frontal and temporal superior brain regions as well as a reduced activation

of the connexions between parietal and frontal cortices, superior temporal cortex and limbic system, frontal cortex and limbic system, and frontal and occipital cortices (Happ et al., 1996). Defects of these kinds are associated with difficulties in social perception (particularly regarding the human face and gaze), ocular contacts, and the imitation of other peoples behaviors. The genetic misfits in autism are of the same type but more numerous than those in Asperger syndrome. Anomalies have been identified in 19 genes: NLGN3, NLGN4 (involved in he primary etiology of Asperger syndrome), FMR-1 (involved in the primary etiology of Fragile X syndrome), NRXN1, SHANK3, CNTNAP2, PCDH10, CNTN3, NHE9, NHE6, DIA1, A2BP1, MECP2 1 ,UBE3A, EN2, SLC6A, MET, SCN7A, et RNFB (Sutcliffe, 2008; Morrow et al., 2008), many of them on the X chromosome. The genes involved are either completely or partially mutated (in highly penetrating way), are involved in partial chromosomic translocations, are deleted, or reduplicated (modifying the number of elements copied in cell divisions). It is likely that a relatively important number of genes individually modified impact negatively on other genes and genetic territories located close or at a distance from the affected regions. They play important roles in synaptogenesis, its maturation and postnatal stabilization. Hence Morrows hypothesis stating that the autistic spectrum is mainly the result of phenotypic perturbations caused by pathological changes in the expression of dozens of genes intervening in synaptogenesis and neurotransmission in relationship with experiential events and childrens behavior. The social and pragmatic difficulties are of the same basic type in autism, fragile X, and Asperger syndrome. The X chromosome appears to be heavily involved in the primary etiology of the three pathologies. Two things vary in the three syndromes: the levels of the particular difficulties and the possibilities for compensation. Theory of mind plays at three levels that can be hierarchized. A first level is that of the perceptual mechanisms (for example, perceptionrepresentation of the human face). A second level relates to emotional functioning. A third level has to do with understanding intentionality. Cognitive abilities per se do not play a major role in these developments which depend on devoted mechanisms. It is possible, however, to mobilize the cognitive resources in such a way
This gene is also found mutated in so-called classic Rett syndrome, a progressive disorder with a severe communication and language component affecting almost exclusively females (Uchino et al. (2001).
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as to partially compensate for some of the deficits in the theory of mind. This is next to impossible in autism given the serious developmental limitations. This is difficult in males subjects with fragile X because of their mental retardation. Such a cognitive compensation can be observed in Asperger syndrome where one may witness the construction of a conscious and explicit theory of mind (as opposed to an implicit one, as normally) that has much to do with metacognitive functioning (Leslie, 1987). The key point in the psycholinguistic treatment of the illocutory speech acts (assertive, commissive, declarative, or expressive), figurative language (proverbs, metaphors, metonymies), and the socalled mental verbs (think, imagine, believe, doubt, suppose, etc.) is the ability to retrieve the meaning intended by the locutor. To this extent, the interlocutor has to consider a number of plausible mental contents in her/his communicative partner and select the one that appears to be the most appropriate to the context, either because a first attempt at literally interpreting the utterance has yielded no meaningful solution or because the interlocutor has understood from the start that the discourse received had to be interpreted figuratively. In tasks of the type, one must be flexible, opportunistic, demonstrate imagination and intuition. These abilities are mostly lacking in people with Asperger syndrome, fragile X, and even more in autism. These persons do not construct adequate perceptions of the others as equipped with mind contents that can be guessed at. A likely answer to the why question is that from the start these individuals may not have at their disposal, mostly for neurogenetic reasons, the proper mirror-neurons allowing to organize such representations and support the devoted mental mechanisms.

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