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Background: Formal thought disorder (FTD) in schizophrenia is related to a disturbance in the representation of contextual information. This study aimed to assess the extent to which the 'context module' is disturbed in patients with schizophrenia. The context module is needed to mediate an appropriate behavioral response. It comprises 2 cognitive functions, namely working memory and behavioral inhibition, and is linked to networks in the prefrontal cortex. We compared patients with enhanced FTD (n = 15) to ones with low levels and a control group (n = 21, respectively). We hypothesized that FTD patients would have greater degradation of the context module by presenting both working memory and inhibition deficits, while in low FTD patients mild degradation of the context module would be present with working memory deficits only., Methods: Using a within-subjects design, subjects underwent a battery of neuropsychological tests with different demands on the context module. We also divided patients according to first-episode versus chronic course., Results: Our results confirmed our predictions on FTD. However, first-episode patients showed working memory deficits more than those with several episodes., Conclusion: We conclude that the context module is more degraded in FTD patients, although our results have to be interpreted with caution because of the small sample size., (Copyright 2010 S. Karger AG, Basel.)

Formal thought disorder (TD) is a core symptom in schizophrenia, but the underlying neurocognitive mechanisms have yet to be determined. This pilot study tested the hypothesis that unconscious semantic activation in conceptual memory is increased in thought disordered patients with schizophrenia. Twenty-eight right-handed individuals with a DSM-IV diagnosis of schizophrenia or schizophreniform disorder (2 patients) and 14 healthy comparison participants performed lexical decisions on target words that were preceded by semantically related and unrelated unconsciously perceived masked prime words (masked priming paradigm). Fourteen patients showed more severe thought disorder symptoms (TD patients), 14 patients showed weaker TD symptoms (non-TD patients). Groups did not differ significantly with regard to gender, age, education and premorbid verbal intelligence. Rigorous tests demonstrated that the masked word could not be consciously identified in either group. Schizophrenia patients with TD showed increased masked semantic priming in comparison to non-TD schizophrenia patients and healthy comparison participants. The present results suggest that the unconscious automatic spread of activation within semantic memory is increased in schizophrenia patients with TD. Increased unconscious activation of several related concepts may interfere with conscious goal-directed thinking in TD patients.

Objective: To study the mesolimbic dopamine system during expectation and receipt or omission of rewards in partially remitted patients with schizophrenia treated with the atypical antipsychotic olanzapine., Methods: We studied 16 patients with a current episode of schizophrenia, all treated with the atypical drug olanzapine, and 16 healthy subjects using functional magnetic resonance imaging. Subjects performed a delayed incentive paradigm with monetary rewards., Results: During reward expectation, both, patients with schizophrenia and healthy control subjects, showed activation of the ventral striatum and midbrain in the vicinity of the ventral tegmental area. Significant categorical group differences emerged in the anterior cingulate cortex with only healthy controls showing increasing activation with increasing reward. In the patients, activation of this region was inversely correlated with positive symptoms. During outcome, both, patients with schizophrenia and healthy controls, showed activation of the ventral striatum and the mesial prefrontal cortex. Significant categorical group differences emerged in the right ventrolateral prefrontal cortex for the salience contrast with healthy controls showing a U-shaped activation curve, i.e., higher activation for either omission or receipt of reward compared to no reward., Conclusions: Our findings partially support the current concept of dopaminergic dysfunction in schizophrenia, suggesting a rather hyperactive mesolimbic dopamine system and reduced prefrontal activation, at least in partially remitted patients treated with atypical antipsychotics.

Studies on working memory (WM) dysfunction in schizophrenia have reported several functionally aberrant brain areas including the lateral prefrontal cortex, superior temporal areas and the striatum. However, less is known about the relationship of WM-dysfunction, cerebral activation, task-accuracy and diagnostic specificity. Using a novel WM-task and event-related functional magnetic resonance imaging (fMRI), we studied healthy control subjects (n=17) and partially remitted, medicated inpatients meeting DSM-IV criteria for schizophrenia (n=19) and major depressive disorder (n=12). Due to the event-related technique, we excluded incorrectly performed trials, thus controlling for accuracy-related activation confounds. Compared with controls, patients with schizophrenia showed less activation in frontoparietal and subcortical regions at high cognitive load levels. Compared with patients with depression, schizophrenic patients showed less prefrontal activation in left inferior frontal cortex and right cerebellum. In patients with schizophrenia, a lack of deactivation of the superior temporal cortex was found compared to both healthy controls and patients with depression. Thus, we could not confirm previous findings of impaired lateral prefrontal activation during WM performance in schizophrenic patients after the exclusion of incorrectly performed or omitted trials in our functional analysis. However, superior temporal cortex dysfunction in patients with schizophrenia may be regarded as schizophrenia-specific finding in terms of psychiatric diagnosis specificity.

Studies on working memory (WM) dysfunction in schizophrenia have reported several functionally aberrant brain areas including prefrontal and temporal cortex. Longitudinal studies have shown changes in prefrontal activation during treatment. We used event-related functional magnetic resonance imaging and a parametric verbal WM task to investigate cerebral function during WM performance in healthy subjects and medicated patients with schizophrenia with an acute symptom exacerbation. Patients were scanned twice: within the first week after admission to the hospital and after 7-8 weeks of a multimodal treatment including atypical antipsychotic agents. There were no differences in activation of lateral prefrontal regions in patients relative to healthy controls neither at baseline nor after 7-8 weeks. Controls showed relatively more activation in parietal, striatal and cerebellar regions. In patients with schizophrenia, frontotemporal function was bilaterally enhanced after 7-8 weeks. This activation change was associated with improved accuracy in a verbal WM task, improved verbal WM-span and symptom reduction as measured by the BPRS global score and the BPRS factor for thought disturbance. Although we could not replicate findings of functional hypofrontality in the patients with schizophrenia, frontotemporal activation changed with treatment and was associated with verbal WM performance and significant reduction of psychopathology.

Background: Antipsychotic treatment in schizophrenia is frequently associated with extrapyramidal side effects. Objective behavioural measures to evaluate the severity of extrapyramidal side effects in the clinical setting do not exist., Objectives: This study was designed to investigate grasping movements in five drug naive and 13 medicated subjects with schizophrenia and to compare their performance with that of 18 healthy control subjects. Deficits of grip force performance were correlated with clinical scores of both parkinson-like motor disability and psychiatric symptom severity, Methods: Participants performed vertical arm movements with a handheld instrumented object and caught a weight that was dropped into a handheld cup either expectedly from the opposite hand or unexpectedly from the experimenter's hand. The scaling of grip force and the temporospatial coupling between grip and load force profiles was analysed. The psychiatric symptom severity was assessed by the positive and negative symptom score of schizophrenia and the brief psychiatric rating scale. Extrapyramidal symptoms were assessed by the unified Parkinson's disease rating scale., Results: Drug naive subjects with schizophrenia performed similar to healthy controls. In contrast, medicated subjects with schizophrenia exhibited excessive grip force scaling and impaired coupling between grip and load force profiles. These performance deficits were strongly correlated with the severity of both extrapyramidal side effects related to antipsychotic therapy and negative symptoms related to the underlying pathology., Conclusions: These data provide preliminary evidence that deficits of sensorimotor performance in schizophrenia are, at least in part, related to the side effects of antipsychotic treatment. The investigation of grasping movements may provide a sensitive measure to objectively evaluate extrapyramidal side effects related to antipsychotic therapy.

Auditory verbal hallucinations in schizophrenia may be due to dysfunctional inner speech-related cortical areas. Repetitive transcranial magnetic stimulation (rTMS) has been reported to be an effective treatment of hallucinations. In a cross-over sham controlled study, we guided rTMS stereotactically to inner speech-related cortical areas in hallucinating patients. These areas were identified individually prior to rTMS using fMRI in a subgroup of our patients. Active stimulation was applied over Broca's area and over the superior temporal gyrus as determined by fMRI, or according to structural images in the remaining patients. rTMS did not lead to a significant reduction of hallucination severity. Conclusively, rTMS has to be regarded critically as a possible novel tool for the treatment of hallucinations.

Enhanced semantic priming (SP) has been reported in individuals with schizophrenia who exhibit positive formal thought disorder (TD) and it has been linked to heightened automatic spreading activation in semantic networks of these patients. However, the state or trait nature of semantic hyperpriming in schizophrenia and its relation to clinical features (e.g., length of illness, symptom shifts) is not clear. To explore these issues, we administered a lexical decision task with semantically related, indirectly related or unrelated prime-target pairs to acutely ill inpatients with schizophrenia shortly after admission and again after 12-16 weeks, while most patients were already in (partial) remission (n=33). In addition, we examined 20 healthy control subjects twice (2 weeks apart). Relative to control subjects, TD patients with schizophrenia exhibited hyperpriming only in the acute psychotic state, but not during the follow-up examination, when TD and other positive symptoms had resolved. There were no associations between priming effects and length of illness or number of previous psychotic episodes. In conclusion, semantic hyperpriming in TD patients with schizophrenia appears to be clearly state-dependent and might be viewed as an episode marker of psychosis with TD.

Language and thought disorders are core symptoms in schizophrenia. We therefore studied language comprehension processes in patients with schizophrenia and control subjects during a sentence processing paradigm using event-related potentials (ERPs). In the ERP, assignment of syntactic structure to a string of words is reflected by an early left anterior negativity (ELAN) at about 80 ms after stimulus onset. Integration of syntactic and semantic information into a coherent representation is indexed by a positive potential at 600 ms (P600). Amplitudes of the ELAN and the P600 components are higher for grammatically incorrect sentences. Semantic processes are associated with a negative deflection peaking at 400 ms (N400). N400 amplitude is higher in semantically incongruent sentences. Nineteen patients with DSM IV schizophrenia and 19 healthy controls were presented with correct, semantically incorrect (semantic mismatch) and grammatically incorrect sentences (syntactic mismatch). Syntactic mismatch elicited an ELAN component in both subject groups. However, only controls but not patients with schizophrenia exhibited a P600 syntactic mismatch effect. Semantic mismatch was associated with a larger N400 potential which did not differ between groups. These results suggest that patients with schizophrenia are not impaired in syntactic structure assignment as reflected by the ELAN, but show deficits in semantic-syntactic integration processes underlying the P600.

Hypofrontality and decreased lateralization have been two major, albeit controversial, results from functional neuroimaging studies of schizophrenia. We used fMRI to study cortical activation during a verbal and spatial working memory (WM) task (2-back) in 15 inpatients acutely ill with schizophrenia and 15 matched control subjects. We hypothesized (i) hypofrontality in patients in both tasks and (ii) decreased lateralization of prefrontal activation in patients under the assumption that, in controls, left prefrontal cortex (PFC) is engaged preferentially in the verbal task (verbal domain dominance) and the right prefrontal cortex is engaged preferentially in the spatial task (spatial domain dominance). Our results showed no significant differences in frontal activation between controls and patients, i.e. no hypofrontality in patients, even at a very liberal threshold (p<0.01). This may be explained by the fact that nearly all patients studied received atypical neuroleptics. Nonetheless, we found evidence for more subtle, domain-related prefrontal dysfunction. Whereas controls showed verbal WM domain dominance in left inferior frontal cortex and spatial WM domain dominance in right prefrontal cortex, these domain dominance effects were absent in the patient group, i.e. there were no lateralization effects. Finally, only patients showed an inverse correlation between performance and right prefrontal activation in verbal WM. We conclude that the finding of hypofrontality may depend on the medication of the patients and that there is prefrontal dysfunction even in the absence of hypofrontality.

In schizophrenia, inhibitory control is reported to be disturbed and has been associated with formal thought disorder (TD). The negative priming task (NP) is used as a measure for inhibition; however, controversial results are found in the literature. The aim of this study was to evaluate cognitive inhibition in schizophrenia and TD. Additionally, the influence of the course of disease and of medication were evaluated. The NP was used to compare TD patients (n = 17) with non-TD (n = 19) and healthy controls (n = 21). Results showed similar performance among TD and non-TD patients, and controls. No influence of the course of disease or medication was found. Our results are in line with recent studies, where patients, irrespective of TD, show normal performance in the NP., (Copyright 2003 S. Karger AG, Basel)

Background: Schizophrenic patients suffer from cognitive and attentional deficits, particularly from failure of executive control functions., Methods: This study investigated the cortical organization of executive control in schizophrenic patients and healthy control subjects using event-related potentials (ERPs). Event-related potentials were collected while subjects performed an auditory Go/NoGo task that required response inhibition. To exclude stimulus discriminability and early stimulus processing to confound results, stimuli were adjusted to the subject's individual discrimination ability and were presented in a simple and a difficult version., Results: Schizophrenic patients performed similar to control subjects in the Go condition but worse than control subjects in the NoGo condition that required response inhibition. Event-related potentials revealed the neurophysiological substrate of this dysfunction. In the Go conditions, both healthy control subjects and schizophrenic patients showed the same voltage pattern. In the NoGo condition, control subjects and patients showed similar cortical activation only during early processing (N2 time window). However, in later stages of processing (P3 time window), healthy subjects showed left lateralization of ERPs over frontal areas while schizophrenic patients did not., Conclusions: We conclude that schizophrenic patients exhibit deficient processing in a neuronal network, including left frontal areas, that is involved in later stages of executive control function.

Background: Previous studies on semantic priming have suggested that schizophrenic patients with language disturbances demonstrate enhanced semantic and indirect semantic priming effects relative to controls. However, the interpretation of semantic priming studies in schizophrenic patients is obscured by methological problems and several artefacts (such as length of illness). We, therefore, used a psychometric high-risk approach to test whether healthy subjects reporting language disturbances resembling those of schizophrenics (as measured by the Frankfurt Complaint Questionnaire subscale 'language') display increased priming effects. In addition, the Schizotypal Personality Questionnaire was used to cover symptoms of schizotypal personality. Enhanced priming was expected to occur under conditions favouring automatic processes., Methods: One hundred and sixty healthy subjects performed a lexical decision semantic priming task containing two different stimulus onset asynchronicities (200 ms and 700 ms) with two experimental conditions (semantic priming and indirect semantic priming) each., Results: Analyses of variance revealed that the Frankfurt Complaint Questionnaire-' language' high scorers significantly differed from low scorers in three of the four priming conditions indicating increased automatic spreading activation. No significant results were obtained for the Schizotypal Personality Questionnaire total and subscales scores., Conclusions: In line with Maher and Spitzer it is suggested that increased automatic spreading activation underlies schizophrenia-typical language disturbances which in our study cannot be attributed to confounding variables such as different reaction time baselines, medication or length of illness. Finally, results confirm that the psychometric high-risk approach is an important tool for investigating issues relevant to schizophrenia.

Repetition blindness is the failure to report the detection of repeated items in rapid visually presented lists. It can be explained in terms of either a processing limitation or an active inhibitory process. In two studies conducted in either English or German language we set out to induce repetition blindness under various conditions in a total of 47 control subjects and 30 schizophrenic patients. The patients displayed the phenomenon to at least the same degree as normal control subjects. These results render unlikely accounts of repetition blindness which involve processes known to be dysfunctional in schizophrenic patients. Moreover, the study provides an example of how the performance of schizophrenic patients can constrain theories of normal cognition.

The general reduction of P300 amplitude in response to auditory oddball stimuli is one of the most consistently replicated biological observations in schizophrenic patients. Several groups have reported a P300 asymmetry in schizophrenic patients, others have not been able to replicate this finding. In order to clarify this issue, we examined the effect of stimulus discriminability on P300 amplitude distribution in schizophrenic patients and in age-matched normal control subjects, using two different auditory oddball paradigms. The detection of the target tone was either simple or difficult, due to manipulation of pitch disparity. The P300 amplitude was comparatively smaller in the schizophrenic patient group compared to the healthy controls and in the difficult task compared to the simple. The schizophrenic patients showed a specific P300 amplitude reduction over left temporal electrode sites when the simple paradigm was used. The difficult paradigm did not elicit asymmetrical P300 amplitudes in schizophrenic patients.

Event-related potentials (ERPs) can be used for high-resolution mental chronometry. For about 15 years, this method has been applied to the study of linguistic phenomena. Semantic incongruency produces a negative component at about 400 ms after stimulus onset, the N400. We measured the N400 component in 20 schizophrenic patients and 20 normal control subjects performing a lexical decision task in which semantic distance between prime and target was varied. The results provide evidence of dysfunctional semantic information processing in schizophrenic patients, and reaction time data from previous studies can be interpreted within an electrophysiological framework. The N400 amplitude and latency data support recent spreading activation models of schizophrenic language dysfunction.

The experimental association psychology approach to mental associations has been the conceptual background for the concept of schizophrenia. Cognitive neuroscience methods and concepts can be used to study various forms of schizophrenic thought disorder. In particular, the concepts of semantic associative and working memory can be applied fruitfully to schizophrenia research. Semantic associative networks can be simulated with self-organizing feature maps. Dysfunctional lexical access can be modeled in terms of low signal-to-noise ratio in intra- or between-network information processing. Evidence for the crucial role of dopamine in this function is presented, and a general neurocomputational model of schizophrenic thought disorder is developed. This model capitalizes on basic aspects of neural information processing (i.e., neuromodulation and neuroplasticity) and allows a parsimonious explanation of a number of otherwise inexplicable or unrelated clinical phenomena and experimental results.

Schizophrenic patients (n = 44) and normal controls (n = 50) performed a computerized version of the Stroop color-word interference task. Schizophrenic patients generally showed more Stroop interference than normal subjects. The effect was neither related to demographic variables, nor to actual psychopathology. However, the course of the disorder was related to the Stroop effect, in that acute, chronic, and schizoaffective patients displayed a larger interference effect than patients with a recurrent episode. From a methodological perspective, the computerized version of the Stroop task proved to be more sensitive to interference effects in the patient group. The finding of enhanced reverse Stroop interference in patients strongly preoccupied with colors is discussed within the framework of MacLeod and Dunbar's (MacLeod and Dunbar, 1988) theory of Stroop interference involving differential practice effects.

The concept of noise has only recently been applied to modelling neuropsychiatric disorders. Two examples of such models are presented. 1. A phantom limb is a neurological condition after the amputation of an extremity. It consists of sensations of the presence of the lost limb and has been attributed to cortical as well as non-cortical mechanisms. A neural network model of phantom limbs is proposed which can parsimoniously account for a large number of clinical features and recent findings of cortical map plasticity after deafferentation. In trained self-organizing feature maps, deafferentation was simulated. Reorganization is shown to be driven by input noise. According to the model, the production of input noise by the deafferented primary sensory neuron drives cortical reorganization in amputees. No such noise is generated and/or conducted to the cortex in paraplegics. 2. Several clinical features of schizophrenia have been related to the ratio of signal to noise in neuronal information processing. In particular, dopamine--which has been implicated in the causation of schizophrenia for decades--has been proposed to modulate signal-to-noise ratio. Data are presented which suggest that schizophrenic thought disorder is the result of a hypodopaminergic state and concomitant increased effects of noise in semantic information processing. Possible functions of noise in the nervous systems are discussed.

This study of 70 schizophrenic patients used a lexical decision task involving the recognition of words that were preceded (primed) either by meaningfully or phonologically associated or by nonassociated words to study the intrusion of contextually inappropriate associations in thought disorder (TD). The patients were split into subgroups of TD and non-TD patients, and the data from these two groups were compared with data from 44 normal control participants. TD schizophrenic patients exhibited more semantic priming than non-TD patients and controls, and differences in phonological priming dependent on stimulus onset asynchrony (SOA) were obtained. Results support the hypotheses of an increase in activation or a decrease in inhibition in the spreading of semantic and phonological associations in TD schizophrenic patients.

The comprehension of auditorily presented sentences with a metaphoric content was investigated in three experimental studies. Experiments 1 and 2 established the time course in control subjects: At 400 ms after prime offset only the concrete meaning was activated, whereas 1200 ms after prime offset both concrete and metaphoric meaning were active. Experiment 3 demonstrated a heightened activation of the concrete meaning and no activation of the metaphoric meaning in schizophrenic patients. These results resolve the dispute over the use of concepts by schizophrenic patients (overinclusive versus underinclusive), and can be related to the neurobiology of working memory and of associative semantic memory. The three experiments may serve as paradigms of how the method of mental chronometry can be applied in the field of psychopathology.

The characteristics of the spread of semantic activation in associative networks in normal subjects, thought-disordered (TD) and nonthought-disordered (NTD) schizophrenic patients with respect to time and semantic distance are examined. Direct and indirect semantic priming effects at two stimulus onset asynchronies (SOA) in a lexical decision task reveal that semantic associations spread further and faster in TD schizophrenic patients than in normal controls and in NTD schizophrenic patients. From a methodological point of view, indirect semantic priming at short prime-target intervals appears to be the best indicator of associative network dysfunction. The findings are discussed within the framework of current research on the effect of dopamine on the signal-to-noise ratio in cortical neural networks. Data suggest that semantic associative memory operates at a comparatively lower signal-to-noise ratio in thought-disordered schizophrenic patients.

Schizophrenic patients and normal controls performed a lexical decision task involving the recognition of words which were preceded (primed) by either associated, indirectly associated, or non-associated words. In contrast to normal control subjects who showed no indirect semantic priming effect at an inter-stimulus interval (ISI) of 0 ms, a trend towards such an indirect semantic priming effect was found in schizophrenic patients. With a longer ISI of 500 ms, an indirect semantic priming effect was obtained in both groups. In the framework of network models of semantic memory, the results are interpreted as further evidence for an increase in activation or decrease in inhibition in the spreading of associational activation in schizophrenic patients.

Association psychology research in psychiatry dates back to Kraepelin, Aschaffenburg and C.G. Jung. Findings of the 1950s and 60s in this field suggest that semantic memory is organized in the form of a network. New results of experimental psychiatric studies indicate that schizophrenic symptoms, in particular formal thought disorders, are in part the result of an unfocussed activation or disinhibition of such associational network structures: The phenomenon of semantic priming is more pronounced in schizophrenic patients than in normals. Moreover, the phenomenon of indirect semantic priming on short stimulus onset asynchrony can be seen only in schizophrenic patients. The study of spontaneous speech further suggests the activation of structures responsible for the storage and processing of meaning. Increase in semantic priming, similar to that observed in schizophrenia, can further be observed in normal subjects on awakening from REM sleep. The findings are discussed in the framework of recent findings on the neurobiological causes of schizophrenia. They can be related structurally to an involvement of the frontal lobe, and functionally to disturbances of dopaminergic transmission. Methods such as the investigation of priming effects in lexical decision tasks, as well as concepts from the domain of cognitive neuroscience such as neural networks and the spreading activation model of lexical access, can help to bridge the gap between phenomenological psychopathology and neurobiology.

Semantic priming in normal controls and schizophrenic patients can be demonstrated in lexical decision tasks. Data from such a lexical decision task are analyzed with special respect to the question as to whether associative processes in schizophrenic patients are characterized by the occurrence of entirely new associations or by the intrusion of normal associations, i.e., associations which can be found in normal subjects. The analysis of the semantic priming effects of single word pairs demonstrates little qualitative differences between the associations of normals and of schizophrenic patients. This finding provides further support for Maher's hypothesis of activated normal associations in schizophrenic patients. From a methodological perspective, the item-by-item analysis of lexical decision task data can be used to optimize this method.

A large number of psycholinguistic findings on how human beings store lexical information suggest the existence of associative memory, which may be characterized by a large capacity and a long duration. Its anatomical basis supposedly is, at least in part, the frontal lobes, and some of its functional characteristics have been tentatively linked to dopamine release. Working memory has a limited capacity, lasts only for seconds and is relevant for goal-directed behavior. Its anatomical basis in the frontal cortex is established and strong evidence suggests the involvement of dopaminergic pathways. Experimental evidence using several lexical decision tasks and a delayed response task is provided to demonstrate that some characteristic features of schizophrenic thinking--in particular the rapid shift of associations, the indirect relationship of associations, the overly abstract or overly concrete use of concepts, the lack of context-sensitivity and of general integrative function and intellectual capacity--can be explained in terms of an activation or disinhibition of associative memory, and of a dysfunctional working memory. The findings serve as an example of schizophrenia research in a cognitive neuroscience framework.

From the clinical point of view, substance-induced psychosis can be rather similar to schizophrenia. However, the question whether phenomenological resemblances represent similar underlying causal mechanisms is unsolved. Whereas the interest in experimentally induced psychosis was purely academic until the mid-1960s, the widespread use of "recreational" drugs provided this research with an important practical impact. With respect to a given case the differential diagnosis between schizophrenia and drug-induced psychosis it is often problematic. The differences in psychopathology refer to the disturbances of experience in general (Ichstörungen), the character of the hallucinations and the quality and quantity of the alterations of consciousness. Contrary to the sharp distinctions which used to be drawn between schizophrenia and drug-induced psychotic states, we hold that these states are rather similar, and may even represent a common underlying pathology. Hence, the renewed interest in the study on experimentally induced psychotic states using advanced methodology seems justified.

Background: In schizophrenia, disturbances in the development of physiological hemisphere asymmetry are assumed to play a pathogenetic role. The most striking difference between hemispheres is in language processing. The left hemisphere is superior in the use of syntactic or semantic information, whereas the right hemisphere uses contextual information more effectively.Method: Using psycholinguistic experimental techniques, semantic associations were examined in 38 control subjects, 24 non-thought-disordered and 16 thought-disordered people with schizophrenia, for both hemispheres separately.Results: Direct semantic priming did not differ between the hemispheres in any of the groups. Only thought-disordered people showed significant indirect semantic priming in the left hemisphere.Conclusions: The results support: (a) a prominent role of the right hemisphere for remote associations; (b) enhanced spreading of semantic associations in thought-disordered subjects; and (c) disorganisation of the functional asymmetry of semantic processing in thought-disordered subjects. [ABSTRACT FROM AUTHOR]

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