Psychiatry Research 178 (2010) 225229

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Psychiatry Research
j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p s yc h r e s

Review article

Schizophrenia and language Shall we look for a decit of deviance detection?

Kuzma Strelnikov
CerCo, Universit Toulouse 3, CNRS, Facult de Mdecine de Rangueil, 31062 Toulouse CEDEX9, France; Hopital Purpan, FR-31059 Toulouse, France

a r t i c l e

i n f o

a b s t r a c t
In this article, we consider the view on schizophrenia that asserts this disease originates from a decit in the hemispheric specialization for language. We suggest that a decit in the hemispheric specialization for language may be a consequence of the other recently shown neurophysiological decit of schizophrenia, namely deviance detection. We hypothesise that a decit of deviance detection related to the dysfunction of NMDA receptors in schizophrenia leads to the abnormal interaction between the parallel and sequential streams of speech processing in the brain. This hypothesis opens perspectives for genetic, molecular and pharmacological studies of the decit of deviance detection in schizophrenia, as reected by event-related potentials and neuroimaging during speech processing. 2010 Elsevier Ireland Ltd. All rights reserved.

Article history: Received 28 August 2009 Received in revised form 21 December 2009 Accepted 18 April 2010 Keywords: Schizophrenia Language Hemispheric specialization Glutamate NMDA

Contents 1. Introduction . . . . . 2. Activationverication 3. Conclusion . . . . . References . . . . . . . . . . . . . . . approach and . . . . . . . . . . . . . . . . . . . . . . . deviance detection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225 226 228 228

1. Introduction A large body of experimental and theoretical literature on the pathogenesis of schizophrenia attempts to elucidate the complex interactions of brain receptor systems involved in the disorder, including almost every known group of receptors: dopaminergic, glutaminergic, serotonergic, adrenergic, GABAergic, etc. These studies are of crucial importance because they provide perspectives for the search of new drugs that can modify these receptor systems. They are complemented by neuroimaging studies that can indicate, though with limited precision (Demirci et al., 2008), where in the brain a certain neurophysiological decit may occur. On the other hand, there is a cognitive approach in the studies of schizophrenia that investigates different psychological decits and relationships between them. These studies may be helpful in clarifying diagnostics criteria and in assessing the effect of treatment on the described cognitive decits. However, the nal goal in understanding the
Centre de Recherche Cerveau et Cognition, UMR 5549, (CNRS-Universit Paul Sabatier Toulouse 3), Facult de Mdecine de Rangueil, 133 route de Narbonne, 31062 Toulouse CEDEX9, France. E-mail addresses: kuzma@cerco.ups-tlse.fr, strelkuz@hotmail.com. 0165-1781/$ see front matter 2010 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2010.04.025

disease would be to elaborate its model, which would comprise both structural (including molecular) and cognitive aspects and construct a link between them. This perspective has inspired several approaches during recent decades. As noticed by Crow (Crow, 1995), though language disorders per se (such as decits of phonological, lexicosemantic or syntactic processing) are not a diagnostic sign in individuals with schizophrenia, the core syndrome (nuclear symptoms) of schizophrenia is determined by the dissociation between thought, speech perception, speech production and meaning. These various dissociations in schizophrenia can be discussed at the neural level as disconnectivity occurring through structural changes of association bres at the cellular level, and/or functionally, through aberrant control of synaptic plasticity at the synaptic level (Stephan et al., 2009). To consider these disconnections systematically, the rst logical step would be to analyse the possible disconnection between brain hemispheres, then disconnections between the specic macroscopic structures of each hemisphere separately, and then disconnections inside of each structure at the level of neuron populations coming down nally to the level of neural circuits. The attempt to make the rst step in this logical sequence is provided by the theory of Crow (2008), by which schizophrenia can

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be attributed as a failure in the hemispheric specialization for language. This theory presents evolutionary and genetic insights on the origins of schizophrenia by claiming that specic changes occurred in the human genotype after a certain speciation event, which led to the appearance of the dominant hemisphere for language. Individuals with schizophrenia may fail in the process of establishing hemispheric dominance for some key aspect of language. This theory has some interesting conrmations at various levels anatomical and functional signs of disturbed hemispheric asymmetry in individuals with schizophrenia, indications to the mostly genetic risk for the development of schizophrenia (see Crow, 2008 for a detailed review). However, several important points still remain unresolved; some of them are pointed out by Crow. Linearity of the phonological sequence (phonological forms can be represented as linear strings of symbols) as one of the principles of language (Chomsky, 1964) discussed by Crow does not necessarily imply linearity of processing of this sequence by the dominant hemisphere. A great amount of data shows bilateral phonological processing in the brain (see Zatorre and Gandour, 2008 for a review). Some authors suggest that the temporal properties of speech sounds are processed more in the left hemisphere, while spectral properties are processed more on the right side, though both types exist in both hemispheres (Zatorre et al., 2002). Other authors assert that speech is just processed in smaller time windows in the left hemisphere than in the right (Hickok and Poeppel, 2007). Thus, hemispheric dominance for phonological processing is unlikely; a distribution of this job between the hemispheres is actually more likely. Lexico-semantic analysis also may be bilateral and the conceptual network may be widely distributed across the cortex (Hickok and Poeppel, 2007). Considering the existing models of hemispheric interaction during language processing, one can come to the conclusion that Crow's proposed link between schizophrenia and language may lie not in the vague domain of hemispheric dominance, but in some other brain mechanisms that may be linked to some extent to hemispheric interaction. In the light of the above-mentioned data, normal language processing is not divided easily between the dominant and non-dominant hemispheres; the idea of Crow seems plausible in the sense that there may be a certain misconnectivity (Crow, 1998) between hemispheres in schizophrenia resulting in its nuclear symptoms. The next level to clarify disconnections in schizophrenia is the brain mapping level that of interactions of different brain areas within one hemisphere, as well as bilateral interactions of particular brain areas. At this level, an important role of the excessive dopamine activity in the mesolimbic pathway was indicated for the delusions and hallucinations in schizophrenia (Cohen and Servan-Schreiber, 1992). Cognitive dysfunction and disorganization of schizophrenia may be related to a functional decit in the dorsolateral prefrontal cortex (Brodmann's areas 46/9), where decient dopamine activity may be related to reduced working memory and language disorder associated with schizophrenia (Perlstein et al., 2001, 2003). Temporal lobe volume reduction is a very consistent nding in schizophrenia (e.g., Takahashi et al., 2007; Collinson et al., 2009; Sun et al., 2009). Many of the frontal ndings in schizophrenia could stem from abnormalities in processing at an earlier stage in posterior regions such as the temporal and inferior parietal cortex due to a profound disruption of large-scale prefrontotemporal interactions (Friston and Frith, 1995). A relative increase of the temporal lobe activation in schizophrenia has also been demonstrated in a number of word perception studies (Frith et al., 1995; Kubicki et al., 2003). In addition, although there is a debate about the ndings, a facilitated semantic priming effect has been found repeatedly in schizophrenia and could be interpreted as result of a certain disinhibition in temporal and perhaps some other regions (Moritz et al., 2001, 2003; Wentura et al., 2008; Kreher et al., 2009). This inuences other levels of speech processing, e.g.

semanticsyntactic integration in schizophrenia may be driven primarily by semantic memory-based processes (Chernigovskaya et al., 2003; Kuperberg, 2008). Obviously, a revision of the role of speech processing in schizophrenia is needed to link the above described data to an appropriate model of speech processing and to understand what is changed in the pathological situation. It is important to note that any progress in drawing such a link in pathology is based inevitably on the appropriate conceptions concerning normal brain functioning. In the present article, we will focus on the direction of such conceptual approaches to schizophrenia with regards to the brain mechanisms of language, the specic decit of which may account for a large number of schizophrenic symptoms (Crow, 2008). We will try to show that language disorder in schizophrenia may be a consequence of a more general decit that of deviance detection which nds its grounds in the decit of NMDA receptor functioning. By deviance detection we mean the detection of deviance of the received information from the information created on the basis of previous experience that exists already in the neural network and is dened as predictive coding (Friston, 2005). 2. Activationverication approach and deviance detection In our recent model of normal continuous speech processing (Strelnikov, 2008), we suggested that it happens in two streams: sequential and parallel (Fig. 1). The sequential stream is strictly modular and unidirectional; the parallel stream is highly interactive and creates predictions (neural predictive coding (Friston, 2005) based on the available information. The parallel stream predictions are incrementally veried, accepted, or rejected on the basis of the actual linguistic information perceived by the sequential stream. The parallel stream works mainly on contextual information and on information from prior communicative and linguistic experiences. The sequential stream, in turn, works on actual information about the perceived speech. The dichotomy of perception in the proposed model corresponds to the peculiarities of the left and right hemispheres in terms of their ways of treating environmental information. Each hemisphere houses both streams of processing; however, one stream is dominant for each hemisphere the parallel stream is dominant for the right and the sequential stream for the left hemisphere. This principle of sequential and parallel streams interaction may function at various levels of speech processing. The analogy can be driven with the feedback principle that is present at various levels of brain organization: interhemispheric, intrahemispheric and inside the populations of brain cells. So, in a rst approximation, hemispheric interaction during continuous speech processing can be considered as an interaction of the sequential and the parallel streams. The next level to apply the sequential-parallel principle for speech processing is intrahemispheric. Here, this principle partially corresponds to the proposed division of speech analysis into the ventral (parallel) and dorsal (sequential) streams, with the ventral stream proposed to be bilateral and the dorsal stream lateralized to the left (Hickok and Poeppel, 2007). However, the model of Hickok and Poeppel (2007) is proposed only for word level; this explains only partial nature of correspondence with our model of continuous speech processing. As for the level of cell populations, the present techniques do not permit assessment of the principles of its functioning during speech processing. In terms of our model of speech processing, we suggest that deviance detection could be a possible mechanism of conrmation or rejection of the predictive coding that is created by the parallel stream. Having acquired the actual linguistic information, the brain compares it with several predictive coding variants at the neural level, and variants that deviate the most from the actual information are rejected. If the two streams work in an unbalanced fashion, the information predicted by the parallel stream is not corrected properly,

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Fig. 1. Activationverication model of continuous speech processing. Speech processing is considered here as being realized in two streams: sequential and parallel. The parallel stream is highly interactive, treating linguistic memory information in a predictive and integral way. The sequential stream is strictly modular, with verifying and differentiating functions. The parallel stream creates predictive coding variants at all levels of processing, based on initially missing linguistic information. This predictive coding is incrementally veried, accepted, or rejected on the basis of the actual linguistic information perceived by the sequential stream (from Strelnikov, 2008).

thereby leading the person to hear what is not really said or to read what is not really written. This prediction of the model naturally evokes reexions on schizophrenia If deviance detection in the brain may serve to eliminate the irrelevant (to the external world) ideas, most of the nuclear symptoms can be interpreted from this position. On the other hand, if deviance detection is a mechanism of hemispheric interaction during speech processing, its failure may underlie a failure of hemispheric specialization as outlined in Crow's theory. However, we argue that the lack of lateralization approach to schizophrenia is over-simplistic. It is not the lack of lateralization, but the decit of interaction between hemispheres that seems to be really important. This decit may lead in some cases to the increase or decrease in the activation of the particular hemisphere (e.g., an increase when it works on its own in an uncontrolled fashion, a decrease when it does not receive proper information from the other hemisphere). According to recent fMRI studies, brain activity in language specic temporal and frontal areas is more lateralised to the right than in healthy controls (Sommer et al., 2001; Dollfus et al., 2005; Razamandimby et al., 2007). In addition, the shift of brain asymmetry to the right as observed in fMRI was signicantly associated with more severe hallucinations (Sommer et al., 2001). Thus, a shift to the right hemisphere in schizophrenia may indicate the increased activity of the parallel stream of processing because deviance from the actual information is not detected properly by the sequential stream. At present, the role of the right hemispheric activations observed in the studies of normal speech processing often remains unexplained (Van Lancker Sidtis, 2006). Furthermore, it should be noted that brain activations for speech processing in the right hemisphere methodologically may be more difcult to detect than in the left hemisphere because of their more distributed and variable nature. As we suggest in our activationverication model (Strelnikov, 2008), since the sequential stream passes speech information through certain stages of processing, the specialized neural networks at each stage may be conglomerated in the left hemisphere cortex so that information passes in an orderly fashion from one conglomeration of neurons to another. In contrast, the high interconnection of the parts of the parallel stream may predict that the neural networks in the right hemisphere cortex are more spatially dispersed and less segregated.

Distributed activations are only beginning to be discussed in terms of the statistical methodology of their detection in the brain (Friston et al., 2008). At the other level of brain organization, applying the sequential parallel model to intrahemispheric relations, the decreased activation in the left prefrontal cortex may correspond to the decit in the dorsal (sequential) stream of speech processing and a certain overactivation of temporal regions (Frith et al., 1995; Kubicki et al., 2003) may correspond to the increased activity in the parallel stream in schizophrenia. These studies were restricted only to word processing; there was not any actual linguistic information on the syntactic and suprasegmental phonological (prosodic) speech properties for the sequential stream. However, some individually variable linguistic predictions in the parallel stream of the model still could be generated. As speech processing by the parallel stream is highly contextdependent, some ndings showing facilitation of semantic priming in schizophrenia (Moritz et al., 2001, 2003; Wentura et al., 2008; Kreher et al., 2009) conrm the increased activity of this stream. This disinhibition of the parallel stream may arise from the lack of control by the sequential stream. Thus, the above considerations may lead to the idea that there is an abnormality, a certain imbalance, in the cooperation between the two streams of speech processing in schizophrenia at several neurofunctional levels. We suggest that a key factor to understanding this imbalance may be a decit in the mechanisms of deviance detection. Is any experimental evidence of the decit of deviance detection in schizophrenia available? A widely spread electrophysiological measurement for automatic deviance detection by the brain is mismatch negativity (MMN), as observed in event-related potentials (ERPs). MMN is a component of event-related potentials that is elicited by the violation of some regularity in the perceived sensory stream. If there is a discordance between the regularity representation established by the preceding stimulation and the novel stimulus, MMN is generated automatically even when attention is not allocated to stimulation, thus it reects neural processing at the pre-attentive level (see Naatanen et al., 2007 for a review). Initial studies of MMN used sensory (mostly auditory) stimulation, but during the last decade many studies supported the existence of this phenomenon for the processing of linguistic properties, MMN was described for lexico-

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semantic and syntactic processing (see Pulvermuller and Shtyrov, 2006 for a review; Ylinen et al., 2009). A large number of studies have found a decrease in auditory MMN in individuals with schizophrenia and even in their rst-degree relatives (see Light et al., 2007; Strelnikov, 2007 for a review). In a discussion of these ndings (Strelnikov, 2007), we suggested previously that schizophrenic cognitive impairments may arise from the same brain mechanism that causes the decrease in MMN amplitude, i.e., the impairment of glutamatergic long-term potentiation mechanisms and the decit of formation and activation of new neural circuits in response to environmental changes. The decit of deviance detection in schizophrenia also was reported using the P300 ERP component elicited by infrequent stimuli in the oddball paradigm auditory P300 amplitude was decreased and signicantly correlated with the severity of positive thought disorder (see Kirihara et al., 2005 for their original data and a review), the P3b subcomponent was shown to be responsible for this correlation (Kirihara et al., 2009). From the aforementioned predictions regarding the role of deviance detection in speech processing, the failure of these mechanisms subsequently should result in positive schizophrenic symptoms. Furthermore, a decit of deviance detection also may play an important role in the genesis of negative symptoms, i.e., as the ability to detect changes in the environment worsens, the reaction to them diminishes. The consequences include a decreased reactivity and social disadaptation of individuals with schizophrenia. MMN decit in individuals with schizophrenia is highly associated with impairments in their daily functioning, level of independence in their community living situations, and functional outcomes (Light and Braff, 2005; Kawakubo and Kasai, 2006). In addition, MMN is associated with psycho-social functioning in healthy adults (Light et al., 2007). The disruption of NMDA transmission induced by ketamine in healthy volunteers increased amphetamine-induced dopamine release as observed in individuals with schizophrenia (Kegeles et al., 2000). Behaviourally, ketamine in healthy volunteers also was shown to produce negative symptoms of schizophrenia (Krystal et al., 2005). Acute and chronic ketamine-induced changes in healthy volunteers partially mirrored the ndings on semantic priming in schizophrenia (Stefanovic et al., 2009). These data provide evidence for the role of glutamatergic long-term potentiation in the pathogenesis of schizophrenia; the decit of this glutametergic mechanism may lead to the decit of deviance detection proposed here. Additional evidence for this viewpoint is that ketamine induces a decrease of auditory MMN in healthy volunteers (Umbricht et al., 2000). An interesting question is whether the disorder of interaction between two streams of speech processing based on the decit of deviance detection is specic for schizophrenia, or is this decit common for various language disorders with unknown aetiology. For example, with a frequent disorder such as dyslexia, it is known that while processing written language the brain recodes visual speech information to phonological information (Chafe, 1988; Frost, 1998) that can also be treated by the proposed two-stream model at different levels of brain organization. Whether and to what extent the mechanisms of the decit in dyslexia are similar to those proposed here for schizophrenia remains a question for further studies. However, MMN decit is specic to schizophrenia relative to bipolar, major depressive (Catts et al., 1995; Umbricht et al., 2003) and obsessive compulsive disorders (Towey et al., 1994; Oades et al., 1997). 3. Conclusion Thus, we hypothesise that there is a decit of deviance detection related to the dysfunction of NMDA receptors in schizophrenia and this decit leads to the abnormal interaction between the parallel and sequential streams of speech processing in the brain. Our two-stream model of language processing can be used to integrate the ideas of

receptor decits, atypical lateralization, disconnectivity and structural decits into a rather coherent explanation of language in schizophrenia where the central mechanism is deviance detection. We believe that the decit of deviance detection in schizophrenia is the basic neural decit, which may manifest itself at different levels of brain organization: as the decit of hemispheric interaction, as the decit of neural populations' interactions within each hemisphere and as the decit of more subtle neural interactions within one population. To test the proposed hypothesis, more research is needed on MMN with speech stimuli in individuals with schizophrenia to conrm the decit of deviance detection for language. Further studies are needed to clarify the relationship between atypical lateralization, either structurally or functionally, and deviance detection. Another research direction involves investigating how the genetic mechanisms proposed by Crow (2008) (and perhaps some other genetic mechanisms) can inuence the glutamatergic processes that are the basis for the decit of deviance detection in schizophrenia. These studies can be complemented by the usage of pharmacological modulators of NMDA-receptors. Violations of semantic and syntactic properties are known to elicit such ERP components as Early Left Anterior Negativity (ELAN), N400 and P600. The amplitude of the N400 and P600 components in schizophrenia is decreased in many studies (see Kumar and Debruille, 2004 for a review). Molecular underpinnings of these components are much less clear than those of MMN, thus, their studies at the genetic and pharmacological levels in schizophrenia could also be useful both for the understanding of schizophrenia and normal speech processing. References
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