The British Journal of Psychiatry (2008) 192: 92-97. doi: 10.1192/bjp.bp.106.032102
© 2008 The Royal College of Psychiatrists
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REVIEW ARTICLE

Semantic priming in schizophrenia: systematic review and meta-analysis

E. Pomarol-Clotet, MD, PhD

Benito Menni C.A.S.M., Sant Boi de Llobregat, Barcelona, Spain

T. M. S. S. Oh, PhD

Department of English Language and Literature, National University of Singapore, Singapore

K. R. Laws, PhD

School of Psychology, University of Hertfordshire, Hatfield, UK

P. J. McKenna, MB, ChB, MRCPsych

Department of Psychological Medicine, University of Glasgow, Gartnavel Royal Hospital, Glasgow, UK

Correspondence: Professor P. J. McKenna, Department of Psychological Medicine, Trust HQ Building, 1055 Great Western Road, Glasgow G12 0XH, UK. Email: peter.mckenna{at}virgin.net

Declaration of interest

None.


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ABSTRACT
 
Background

Increased semantic priming is an influential theory of thought disorder in schizophrenia. However, studies to date have had conflicting findings.

Aims

To investigate semantic memory in patients with schizophrenia with and without thought disorder.

Method

Data were pooled from 36 studies comparing patients with schizophrenia and normal controls in semantic priming tasks. Data from 18 studies comparing patients with thought disorder with normal controls, and 13 studies comparing patients with and without thought disorder were also pooled.

Results

There was no support for altered semantic priming in schizophrenia as a whole. Increased semantic priming in patients with thought disorder was supported, but this was significant only in comparison with normal controls and not in comparison with patients without thought disorder. Stimulus onset asynchrony (SOA) and general slowing of reaction time moderated the effect size for priming in patients with thought disorder.

Conclusions

Meta-analysis provides qualified support for increased semantic priming as a psychological abnormality underlying thought disorder. However, the possibility that the effect is an artefact of general slowing of reaction time in schizophrenia has not been excluded.


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INTRODUCTION
 
Increased semantic priming or semantic hyperpriming is currently one of the most influential theories of thought disorder, the incoherent speech seen in some patients with schizophrenia. It originated in the work of Maher, who proposed that a pathological heightening of the normal associative processes between words could lead to the intrusion into speech of material which would normally be excluded on the basis of its irrelevance in the current context.1 Maher's associative process between words was similar in all essential respects to the concept of spread of activation in network theories of semantic memory, and this meant that the proposal could be readily tested by means of the lexical decision or semantic priming task.2 In this paradigm, a string of letters is flashed up on a computer screen and the participant has to decide by a key press whether it is a word or a non-word (Fig.1). Immediately beforehand, another word – the prime – is briefly shown which may or may not be semantically related to the target word (if this happens to be a real word). The time taken to decide that the letter string is a word is significantly reduced when the prime is related to the target, a phenomenon that is most easily explained as the prime producing spread of activation to associated words in semantic memory, and so reducing the amount of additional network activation needed to identify that the target is a real word.


Figure 1
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  		Fig. 1 The lexical decision task.

Over 30 studies of semantic priming in schizophrenia have now been carried out. Influential early studies by Manschreck et al3 and Spitzer et al4 found evidence for increased semantic priming in patients with thought disorder. Other studies, for example by Ober and co-workers,5,6 also suggested that priming is reduced in schizophrenia as a whole. The basic priming design has been subjected to many variations across the studies, one of the most important of which has concerned the use of a short or a long prime–target interval (stimulus onset asynchrony or SOA). Priming at SOAs of up to approximately 400 ms captures the `automatic' process of spread of activation in semantic memory. However, it is clear that other `controlled' processes become important at longer SOAs.2

In a review by Minzenberg et al,7 findings were divided over whether priming was increased in patients with thought disorder. However, a relatively consistent finding was reduced priming at long SOAs in schizophrenia as a whole. This review also drew attention to the fact that few studies had corrected for a well-recognised psychometric artefact whereby, if patients with schizophrenia are slower to respond on both the unprimed and primed versions of the task, the value for priming will tend to be spuriously inflated.


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Method
 
Papers reporting semantic priming studies in patients with schizophrenia were searched electronically from 1988 (the year of the publication of the first study3) to April 2007. Studies were identified initially through PubMed, and then MEDLINE, PsycINFO and EMBASE, using the keywords schizophrenia, priming and semantic priming. The electronic search was supplemented by checking of review articles and the reference lists of all research papers obtained. To be included, studies had to report reaction time data in patients with schizophrenia and normal controls in any type of semantic priming paradigm. Age and gender matching was not required. Use of diagnostic criteria for schizophrenia was also not required. Non-English language papers and unpublished studies (e.g. theses) were included.

Most studies reported data on the lexical decision task; however, a few used the alternative procedure of word pronunciation (where the subject speaks the target word or string, and reaction time is recorded by a voice key). Most studies reported `subtractive' values for priming, that is, mean unprimed reaction time minus mean primed reaction time. Some studies instead reported priming as `percentage gain' in reaction time, in an attempt to avoid the above-mentioned tendency for overall slowing of reaction time to artefactually increase the value for priming when calculated by subtraction. As less than a third of studies used this technique, subtractive measures were used in the analyses, unless percentage gain was the only measure reported. Other variations in experimental design were either examined as moderator variables or ignored.

Data obtained from each study were converted into an effect size Cohen's d, the difference between the means for the patient and control groups divided by their pooled standard deviation. Hedges' correction was used; this corrects for the tendency of studies with small sample sizes to overestimate the effect size. Where means and standard deviations were not available, effect sizes were derived from t-values, F-values or P-values. In some cases, priming effects were presented only as interaction F-values in a two-by-two (between and within) ANOVA on the raw reaction times in the primed and unprimed conditions. In such cases, the interaction effect is comparable to one-way ANOVA using difference scores – the sums of squares are half those obtained from one-way analysis, and thus the ratio of sum of squares, degrees of freedom, F ratios and {eta}2 should be the same (M. Aitken, personal communication, 2007). For some studies, data were extracted from graphs or scatter plots using a digitising program (UnGraph; http://www.biosoft.com). Authors were contacted if effect sizes could not be extracted from any of the published data. All effect sizes were extracted a second time and differences resolved.

The meta-analysis was carried out using DSTAT 1.108 which uses a fixed-effects model. Individual effect sizes were combined to produce an overall effect size, with each d-value weighted by the reciprocal of its variance. Analysis of moderator variables was based on the weighted effect size for each study using the Q statistic for categorical variables and Rosenthal's focused comparison for continuous variables.9 Moderator variables included SOA, age, duration of illness and neuroleptic treatment. The potential confounding effect of general slowing of reaction time was also examined.


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Results
 
Thirty-six studies were located.4–6,10–42 This number included two studies that each reported two experiments on separate samples of patients and controls14,38 and three unpublished PhD theses.10,33,37 The studies are summarised in the online data supplement to this paper, which shows sample sizes, values for mean patient age and duration of illness, the SOA or SOAs used and how patients were dichotomised into those with and without thought disorder. Some studies additionally measured performance on a variety of neuropsychological tests but this information is not shown because of the relatively small number of such studies. All studies except two12,21 employed diagnostic criteria for schizophrenia.

In two studies the standard deviations reported for priming appeared to be standard errors of the mean, based on the fact that they were much smaller than the means (standard deviations for difference scores in priming studies are typically as large as or larger than the means). The authors of one of these studies agreed that this was the case,16 and in the other this interpretation was supported by calculating the effect size from other data provided in the paper.30

Priming in schizophrenia
For this analysis, when studies examined two or more groups of patients with schizophrenia (e.g. patients with and without thought disorder), these were combined. Similarly, when studies examined priming at two or more SOAs, the effect sizes were averaged. A positive effect size indicates that priming is increased.

The pooled effect size from the 36 studies was non-significant at 0.07 (95% CI –0.02 to 0.16). The data were significantly heterogeneous (Q(35)=59.82, P=0.008), but homogeneity was achieved by excluding two studies with outlying effect sizes. This made little difference to the effect size (pooled d=0.08, 95% CI –0.02 to 0.17). Excluding the three studies which used pronunciation rather than lexical decision16,20,29 also made little difference (pooled d=0.07, 95% CI –0.02 to 0.17).

A funnel plot of the studies is shown in Fig. 2a and does not suggest publication bias.


Figure 2
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  		Fig. 2 Funnel plot of effect sizes for semantic priming in studies of schizophrenia and studies of patients with thought disorder.

Semantic priming in patients with thought disorder
The pooled effect size for 18 studies which compared patients with schizophrenia and thought disorder with normal controls was 0.16 (95% CI 0.01 to 0.31), indicating significantly increased priming. These studies were again heterogeneous (Q(17)=52.31, P<0.0001) and the effect size climbed further to 0.38 (95% CI 0.21 to 0.55) when five studies with outlying effect sizes were excluded. As shown in Fig. 2b, the funnel plot of these studies was asymmetrical, but it suggested a lack of small studies with positive findings, rather than the pattern typical of publication bias, where there is an absence of small studies with negative findings. Also, it should be noted that this analysis did not include the study of Manschreck et al,3 because an effect size could not be extracted from any of the data in the paper. This study had a small sample size and positive findings and so would have tended to make the funnel plot more symmetrical.

In contrast, pooling the 14 studies which compared patients without thought disorder with controls yielded an effect size of 0.00 (95% CI –0.15 to 0.16) for semantic priming. These studies were not significantly heterogeneous (Q(13)=21.29, P=0.07).

Thirteen studies allowed comparisons between patients with and without thought disorder. The pooled effect size was 0.06 (95% CI –0.12 to 0.24). This was non-significant, but once again the findings were heterogeneous (Q(12)=28.79, P=0.004). The value increased after excluding two outliers (pooled d=0.16, 95% CI –0.02 to 0.35) reaching trend level (P=0.08).

Indirect semantic priming
In this version of the semantic priming paradigm the target words are only indirectly related to the prime, usually via a mediating word, for example, lemon – sweet (mediating word sour), black – chalk (mediating word white). This experimental design aims to examine the hypothesis that activation of associations is not just greater than normal in schizophrenia, but that it extends to more distant associations.

The pooled effect size for nine studies which employed an indirect semantic priming condition was 0.19 (95% CI 0.03 to 0.36), a significant increase. These studies were homogeneous (Q(8)=4.67, P=0.80). Six of these studies included comparisons of patients with thought disorder with controls, and in these the pooled effect size was greater (pooled d=0.56 (95% CI 0.31 to 0.80). These studies were also homogeneous (Q(5)=7.74, P=0.17).

Stimulus onset asynchrony as a moderator variable
The studies employed a wide range of SOAs, from zero (i.e. the prime and target were presented simultaneously) to 1500 ms. In order to examine this factor, studies were coded as employing a short SOA (<=400 ms) or long SOA (>400 ms).

Schizophrenia as a whole
The pooled effect size for 23 studies with short SOAs was 0.09 compared with 0.00 in 22 studies using long SOAs. This difference was not significant (QB(1)=1.30, P=0.25). The larger number of studies in the analyses reflects the fact that some studies tested their subjects at both short and long SOAs, or at multiple SOAs.

We was also examined SOA as a continuous variable. This analysis indicated that effect sizes tended to become more negative with increasing SOA, but once again the effect was not significant (for 45 studies Z=–1.07, P=0.29). A plot of the effect size for priming against SOA is shown in Fig. 3 and, despite the lack of significance, suggests that there may be a more complex pattern of interaction. At very short SOAs (0–200 ms), there is little evidence of increased priming in schizophrenia. As SOA increases beyond 200 ms, positive effect sizes start to appear as well as negative ones. After around 600–800 ms, negative effect sizes are in the majority, and they then incline back towards 0 at >=1000 ms.


Figure 3
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  		Fig. 3 Plot of studies of semantic priming in schizophrenia as a function of stimulus onset asynchrony (SOA). Two studies where the prime was self-terminated by the subject after a minimum period of time were excluded: Aloia et al,20 SOA `>=350 ms, effect size =–0.17; Baving et al,36 SOA >=800 ms, effect size=0.85.

Patients with thought disorder
When compared with normal controls, the pooled effect size for ten studies with a short SOA was 0.25 compared with –0.14 in seven studies with a long SOA; this difference was significant (QB(1)=6.33, P=0.01). When patients with thought disorder were compared with those without thought disorder the difference was significant at trend level (pooled d for eight studies with short SOA and six studies with long SOA=0.15 v. –0.17 respectively; QB(1)=3.39, P=0.06).

Other moderator variables
Among the other moderator variables examined, age was not significant (Z=0.31 in 34 studies, P=0.76). Duration of illness was also not significant (Z=–0.97 in 26 studies, P=0.33) – priming tended to be greater with a shorter length of illness, but nowhere near significantly so. Only four studies were carried out with unmedicated patients, or included a subsample of unmedicated patients, and so it was not considered appropriate to examine medication status as a moderator variable.

The effect of overall slowing
It is universally accepted that reaction time is slower than normal in patients with schizophrenia.43 However, this in itself will tend to inflate the value for priming due to a simple arithmetical artefact: the difference between a mean reaction time of, say, 900 ms in the unprimed condition and 600 ms in the primed condition is numerically greater than that for the difference between, say, values 600 ms and 400 ms in controls, even though the proportional increase is the same.

To examine this potential confounding effect, a value for general slowing of reaction time in schizophrenia was first calculated for each study. This was taken as the difference between schizophrenia and control means in the unprimed (unrelated word) condition. If data for the unprimed reaction time were not available, reaction time across both unprimed and primed conditions was used. This was standardised across the studies by converting it to an effect size and this was then entered as a moderator variable in the analysis. For obvious reasons, studies which reported percentage priming were not included in the analysis.

General slowing of reaction time was a significant moderator of effect size in schizophrenia as a whole (for 29 studies Z=2.82, P=0.004), with the positive sign indicating that the greater the slowing the greater the amount of priming. This also held true in the comparison between patients with thought disorder and controls (for 16 studies Z=3.23, P=0.001).


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Discussion
 
The proposal that associative processes in semantic memory are pathologically altered in schizophrenia has now been tested in over 30 studies using the semantic priming paradigm. Meta-analysis of these studies provides no evidence to support the view that priming (at least direct semantic priming) is increased or decreased in the disorder as a whole, but there is support, albeit qualified, for increased priming in patients with thought disorder. This increase is seen particularly at short SOAs, consistent with an underlying mechanism of increased spread of activation.

Altered priming only in patients with thought disorder?
Considering priming in schizophrenia as a whole, the negative findings of our meta-analysis broadly mirror the results of Minzenberg et al's `vote counting' review which found that the studies were approximately evenly divided into those reporting increased, normal and reduced semantic priming.7 However, they commented that studies which employed long SOAs were relatively consistent in finding reduced priming. A similar pattern was discernible in our plot of effect sizes against SOA in which slightly more studies had positive than negative values for priming at short SOAs, but from around 600–800 ms negative effect sizes became increasingly the rule. Furthermore, at least some of the strategic or `controlled' processes that have been proposed to take place at longer SOAs require a degree of conscious attention and effort,2 and impairment might, therefore, be expected in schizophrenia. Nevertheless, appearances may be deceptive: the two meta-analytic procedures we carried out provided no grounds to support reduced semantic priming at long SOAs in schizophrenia as a whole.

In relation to thought disorder, Minzenberg et al7 again found that the studies were divided among those finding increased, normal and decreased priming and concluded that `it is presently unclear how semantic priming disturbances (should they be reliably demonstrated) may be related to thought disorder as manifested clinically'. Meta-analysis, by contrast, yields clearer results here: the effect size for priming in patients with thought disorder compared with controls was small but significant at 0.16, rising to 0.38 in a homogeneous set of studies. This finding could be considered to be strengthened by the facts that: (a) the comparison of patients without thought disorder with controls found no increase in priming; and (b) the meta-analysis of smaller sets of studies of indirect semantic priming also found that the effect size was increased, with this being particularly marked in patients with thought disorder. However, it is weakened again by the fact that the analysis comparing patients with and without thought disorder had ambiguous results: the pooled effect size was positive, but only substantially so after outliers were excluded and even then it still did not reach significance, although by this time there were relatively few studies.

Another finding cautioning against acceptance of increased semantic priming in patients with thought disorder is that general slowing of reaction time significantly moderated the effect size. In other words, meta-analysis fails to exclude the possibility that some or all of the differences found merely reflect the fact that patients with schizophrenia have slower than normal reaction times. This does not automatically invalidate the conclusion that semantic priming is increased in patients with thought disorder – this confounding factor does not apply to the comparison of patients with v. patients without thought disorder, which had results in the same direction, although not reaching significance – but it does mean that it needs to be addressed in future studies. One simple remedy would be to use percentage gain as the index of priming, or the regression-based correction suggested by Chapman et al,44 rather than a subtractive measure. Two studies have avoided the problem altogether by examining errors rather than slowing of reaction time. Kwapil et al45 presented a prime followed by a visually degraded target and used accuracy of identification (by pronunciation) as the measure of semantic priming. They found that patients with schizophrenia unselected for presence of thought disorder showed more than twice the priming shown by the controls. In contrast, Quelen et al46 found no increase in priming in unselected patients with schizophrenia, but in this study there was an association between increased priming and presence of thought disorder.

Effect of stimulus onset asynchrony
If semantic priming is increased in patients with thought disorder, the effect is seen predominantly at short SOAs. This finding thus supports an interpretation in terms of an increase in the automatic element of the processes underlying priming in the lexical decision task, that is, increased spread of activation in semantic memory. How might this lead to thought disorder being manifested clinically? According to network theories of semantic memory, when nodes are activated, for example by hearing or reading words, the activation spreads to other nodes for words conceptually associated with them. Maher plausibly argued that the same process takes place when an individual is speaking and thinking about what to say next.1 This would then cause activation of nodes which were only distantly related to the topic of discourse, and in such circumstances it could become difficult to prevent the intrusion of irrelevant associations which, as he put it, `lie like a web of distractions around each element in the sentence'. In Maher's words, depending on the severity of the disturbance, the result would be speech that was either merely richer in associations than usual or, at the other end of the spectrum, was strewn with multiple intrusions which seriously compromised its intelligibility.1

Closing comments
The central finding of this meta-analysis is that increased semantic priming may be a psychological mechanism underlying thought disorder but is not relevant to the wider clinical picture of the disorder. In some ways, this conclusion echoes the changing status of the symptom of thought disorder in schizophrenia over the years. Originally, Bleuler considered association disturbance to be one of the fundamental symptoms of schizophrenia, `present in every case and at every period of the illness'.47 Uncritical acceptance of Bleuler's views, particularly in the USA, led to thought disorder being considered central to the understanding of the disorder, as well as a certain way to distinguish patients with and patients without schizophrenia clinically. Eventually, however, studies began to cast doubt on its universality and also made it clear that the symptom could be seen in mania and probably other disorders as well.48,49 Following influential work by Andreasen,50 thought disorder is now regarded as a relatively uncommon symptom in schizophrenia, which broadly speaking can be either present or absent in the same way as other symptoms, such as auditory hallucinations or first-rank symptoms. Nevertheless, unlike these symptoms, it is widely believed that thought disorder can also be present `subclinically' and can be detected in a greater proportion of patients than those in whom it is clinically obvious when special procedures such as interpreting proverbs are used to elicit it.

This meta-analysis touches on two final issues of relevance to semantic priming in schizophrenia. First, Maher et al51 found evidence that priming changes from hyperpriming to hypopriming with increasing duration of illness, a finding which is of considerable potential significance given the important clinical differences between patients with acute and chronic illness. This meta-analysis, however, found no evidence to support such an association. Second, dopaminergic mechanisms regularly feature in theoretical analyses of semantic priming in schizophrenia.52,53 It is, therefore, somewhat disappointing to find that the vast majority of studies have restricted their examination to patients treated with antipsychotics. This meta-analysis suggests that while there is clearly scope for further investigation of priming in schizophrenia at least some future studies should be carried out on patients who are drug-free.


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REFERENCES
 
    1
  1. Maher BA. A tentative theory of schizophrenic utterance. In Progress in Experimental Personality Research, vol. 12 : Personality (eds BA Maher, WB Maher). Academic Press, 1983.
    2. 2
  2. McNamara TP. Semantic Priming: Perspectives from Memory and Word Recognition. Psychology Press, 2005 .
    3. 3
  3. Manschreck TC, Maher BA, Milavetz JJ, Ames D, Weisstein CC, Schneyer ML. Semantic priming in thought disordered schizophrenic patients. Schizophr Res 1988; 1: 61-6.[CrossRef][Medline]
    4. 4
  4. Spitzer M, Braun U, Hermle L, Maier S. Associative semantic network dysfunction in thought-disordered schizophrenic patients: direct evidence from indirect semantic priming. Biol Psychiatry 1993; 34: 864 -77.[CrossRef][Medline]
    5. 5
  5. Vinogradov S, Ober BA, Shenaut GK. Semantic priming of word pronunciation and lexical decision in schizophrenia. Schizophr Res 1992; 8: 171 -81.[CrossRef][Medline]
    6. 6
  6. Ober BA, Vinogradov S, Shenaut GK. Automatic versus controlled semantic priming in schizophrenia. Neuropsychology 1997; 11: 506 -13.[CrossRef][Medline]
    7. 7
  7. Minzenberg M, Ober BA, Vinogradov S. Semantic priming in schizophrenia: a review and synthesis. J Int Neuropsychol Soc 2002; 8: 699 -720.[CrossRef][Medline]
    8. 8
  8. Johnson BT. DSTAT 1.10: Software for the Meta-Analytic Review of Research Literatures. Erlbaum, 1993 .
    9. 9
  9. Rosenthal R. Meta-Analytic Procedures for Social Research. Sage, 1991.
    10. 10
  10. Meyer PC. Semantic priming, thought disorder and laterality in schizophrenia. Unpublished PhD thesis. Department of Psychology, Harvard University, 1991.
    11. 11
  11. Chapin K, McCown J, Vann L, Kenney D, Youssef I. Activation and facilitation in the lexicon of schizophrenics. Schizophr Res 1992; 6: 251 -5.[CrossRef][Medline]
    12. 12
  12. Spitzer M, Weisker I, Winter M, Maier S, Hermle L, Maher BA. Semantic and phonological priming in schizophrenia. J Abnorm Psychology 1994; 103: 485 -94.[CrossRef][Medline]
    13. 13
  13. Blum NA, Freides D. Investigating thought disorder in schizophrenia with the lexical decision task. Schizophr Res 1995; 16: 217 -24.[CrossRef][Medline]
    14. 14
  14. Henik A, Nissimov E, Priel B, Umansky R. Effects of cognitive load on semantic priming in patients with schizophrenia. J Abnorm Psychology 1995; 104: 576 -84.[CrossRef][Medline]
    15. 15
  15. Ober BA, Vinogradov S, Shenaut GK. Semantic priming of category relations in schizophrenia. Neuropsychology 1995; 9: 220 -8.[CrossRef]
    16. 16
  16. Barch DM, Cohen JD, Servan-Schreiber D, Steingard S, Cohen JD, Steinhauer SS, van Kammen DP. Semantic priming in schizophrenia: an examination of spreading activation using word pronunciation and multiple SOAs. J Abnorm Psychology 1996; 105: 592 -601.[CrossRef][Medline]
    17. 17
  17. Besche C, Passerieux C, Segui J, Sarfati Y, Laurent JP, Hardy-Bayle MC. Syntactic and semantic processing in schizophrenic patients evaluated by lexical-decision tasks. Neuropsychology 1997; 11: 498 -505.[CrossRef][Medline]
    18. 18
  18. Passerieux C, Segui J, Besche C, Chevalier JF, Widlocher D, Hardy-Bayle MC. Heterogeneity in cognitive functioning of schizophrenic patients evaluated by a lexical decision task. Psychol Med 1997; 27: 1295 -1302.[CrossRef][Medline]
    19. 19
  19. Spitzer M, Weisbrod M, Winkler S, Maier S. Event-related potentials in semantic speech processing by schizophrenia patients. [Ereigniskorrelierte Potentiale bei semantischen Sprachverarbeitungsprozessen schizophrener Patienten.] Nervenarzt 1997; 68: 212-25.[CrossRef][Medline]
    20. 20
  20. Aloia MS, Gourovitch ML, Missar D, Pickar D, Weinberger DR, Goldberg TE. Cognitive substrates of thought disorder, II: specifying a candidate cognitive mechanism. Am J Psychiatry 1998; 155: 1677 -84.[Abstract/Free Full Text]
    21. 21
  21. Weisbrod M, Maier S, Harig S, Himmelsbach U, Spitzer M. Lateralised semantic and indirect semantic priming effects in people with schizophrenia. Br J Psychiatry 1998; 172: 142-6.[Abstract/Free Full Text]
    22. 22
  22. Barch DM, Carter CS, Perlstein W, Baird J, Cohen JD, Schooler N. Increased stroop facilitation effects in schizophrenia are not due to increased automatic spreading activation. Schizophr Res 1999; 39: 51 -64.[CrossRef][Medline]
    23. 23
  23. Condray R, Steinhauer SR, Cohen JD, van Kammen DP, Kasparek A. Modulation of language processing in schizophrenia: effects of context and haloperidol on the event-related potential. Biol Psychiatry 1999; 45: 1336 -55.[CrossRef][Medline]
    24. 24
  24. Condray R, Siegle GJ, Cohen JD, van Kammen DP, Steinhauer SR. Automatic activation of the semantic network in schizophrenia: evidence from event-related brain potentials. Biol Psychiatry 2003; 54: 1134 -48.[CrossRef][Medline]
    25. 25
  25. Rossell SL, Shapleske J, David AS. Direct and indirect semantic priming with neutral and emotional words in schizophrenia: relationship to delusions. Cognit Neuropsychiatry 2000; 5: 271-92.[CrossRef]
    26. 26
  26. Baving L, Wagner M, Cohen R, Rockstroh B. Increased semantic and repetition priming in schizophrenic patients. J Abnorm Psychology 2001; 110: 67 -75.[CrossRef][Medline]
    27. 27
  27. Moritz S, Mersmann K, Kloss M, Jacobsen D, Wilke U, Andresen B, Naber D, Pawlik K. `Hyper-priming' in thought-disordered schizophrenic patients. Psychol Med 2001; 31: 221-9.[CrossRef][Medline]
    28. 28
  28. Surguladze S, Rossell S, Rabe-Hesketh S, David AS. Cross-modal semantic priming in schizophrenia. J Int Neuropsychol Soc 2002; 8: 884 -92.[CrossRef][Medline]
    29. 29
  29. Moritz S, Woodward TS, Kuppers D, Lausen A, Schickel M. Increased automatic spreading activation in thought-disordered schizophrenic patients. Schizophr Res 2003; 59: 181-6.[CrossRef][Medline]
    30. 30
  30. Besche-Richard C, Passerieux C. Semantic context-processing deficit in thought-disordered schizophrenic patients: evidence from new semantic priming paradigms. Cognit Neuropsychiatry 2003; 8: 173 -89.[CrossRef][Medline]
    31. 31
  31. Gouzoulis-Mayfrank E, Vöss T, Morth D, Thelen B, Spitzer M, Meincke U. Semantic hyperpriming in thought-disordered patients with schizophrenia: state or trait? A longitudinal investigation. Schizophr Res 2003; 65: 65-73.[CrossRef][Medline]
    32. 32
  32. Hokama H, Hiramatsu K, Wang J, O'Donnell BF, Ogura C. N400 abnormalities in unmedicated patients with schizophrenia during a lexical decision task. Int J Psychophysiology 2003; 48: 1 -10.[CrossRef][Medline]
    33. 33
  33. Irwin SAM. Patterns of excitation and inhibition in patients with schizophrenia. Unpublished PhD thesis. Department of Psychology, University of Massachussetts, 2003.
    34. 34
  34. Minzenberg MJ, Poole JH, Vinogradov S, Shenaut GK, Ober BA. Slowed lexical access is uniquely associated with positive and disorganized symptoms in schizophrenia. Cognit Neuropsychiatry 2003; 8: 107 -27.[CrossRef][Medline]
    35. 35
  35. Chenery HJ, Copland DA, McGrath J, Savage G. Maintaining and updating semantic context in schizophrenia: an investigation of the effects of multiple remote primes. Psychiatry Res 2004; 126: 241 -52.[CrossRef][Medline]
    36. 36
  36. Rossell SL. Affective semantic priming in patients with schizophrenia. Psychiatry Res 2004; 129: 221-8.[CrossRef][Medline]
    37. 37
  37. Leeson V. Semantic memory in patients wtih schizophrenia and formal thought disorder. Unpublished PhD thesis. Department of Psychology, London Guildhall University, 2004.
    38. 38
  38. Besche-Richard C, Passerieux C, Hardy-Bayle MC. Double-decision lexical tasks in thought-disordered schizophrenic patients: a path towards cognitive remediation? Brain Lang 2005; 95: 395 -401.[CrossRef][Medline]
    39. 39
  39. Nestor PG, Valdman O, Niznikiewicz M, Spencer K, McCarley RW, Shenton ME. Word priming in schizophrenia: associational and semantic influences. Schizophr Res 2006; 82: 139-42.[CrossRef][Medline]
    40. 40
  40. Rossell SL, David AS. Are semantic deficits in schizophrenia due to problems with access or storage? Schizophr Res 2006; 82: 121 -34.[CrossRef][Medline]
    41. 41
  41. Lecardeur L, Giffard B, Laisney M, Brazo P, Delamillieure P, Eustache F, Dollfus S. Semantic hyperpriming in schizophrenic patients: increased facilitation or impaired inhibition in semantic association processing? Schizophr Res 2007; 89: 243-50.[CrossRef][Medline]
    42. 42
  42. Kuperberg GR, Deckersbach T, Holt DJ, Goff D, West WC. Increased temporal and prefrontal activity in response to semantic associations in schizophrenia. Arch Gen Psychiatry 2007; 64: 138-51.[Abstract/Free Full Text]
    43. 43
  43. Schatz J. Cognitive processing efficiency in schizophrenia: generalized vs domain specific deficits. Schizophr Res 1998; 30: 41 -9.[CrossRef][Medline]
    44. 44
  44. Chapman LJ, Chapman JP, Curran TE, Miller MB. Do children and the elderly show heightened semantic priming? How to answer the question. Dev Rev 1994; 14: 159-85.[CrossRef]
    45. 45
  45. Kwapil TR, Hegley DC, Chapman LJ, Chapman JP. Facilitation of word recognition by semantic priming in schizophrenia. J Abnorm Psychology 1990; 99: 215 -21.[CrossRef][Medline]
    46. 46
  46. Quelen F, Grainger J, Raymondet P. An investigation of semantic priming in schizophrenia using a new priming paradigm. Schizophr Res 2005; 80: 173 -83.[CrossRef][Medline]
    47. 47
  47. Bleuler E. Dementia Praecox or the Group of Schizophrenias. International Universities Press, 1911 .
    48. 48
  48. Harrow M, Quinlan DM. Disordered Thinking and Schizophrenic Psychopathology. Gardner Press, 1985 .
    49. 49
  49. McKenna P, Oh T. Schizophrenic Speech: Making Sense of Bathroots and Ponds that Fall in Doorways. Cambridge University Press, 2005.
    50. 50
  50. Andreasen NC. Thought, language and communication disorders: I. Clinical assessment, definition of terms and evaluation of their reliability. Arch Gen Psychiatry 1979; 36: 1315 -21.[Abstract/Free Full Text]
    51. 51
  51. Maher BA, Manschreck TC, Redmond D, Beaudette S. Length of illness and the gradient from positive to negative semantic priming in schizophrenic patients. Schizophr Res 1996; 22: 127-32.[CrossRef][Medline]
    52. 52
  52. Spitzer M. A cognitive neuroscience view of schizophrenic thought disorder. Schizophr Bull 1997; 23: 29-50.[Abstract/Free Full Text]
    53. 53
  53. Roesch-Ely D, Weiland S, Scheffel H, Schwaninger M, Hundemer HP, Kolter T, Weisbrod M. Dopaminergic modulation of semantic priming in healthy volunteers. Biol Psychiatry 2006; 60: 604-11.[CrossRef][Medline]
Received for publication October 9, 2006. Revision received July 26, 2007. Accepted for publication August 23, 2007.


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L. Lecardeur, S. Dollfus, and E. Stip
Semantic hyperpriming in schizophrenia
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Semantic hyperpriming in schizophrenia. An artefact of general slowing of reaction time?
Laurent Lecardeur, et al.
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