'Hyper-priming' in thought-disordered schizophrenic patients.

Standard

'Hyper-priming' in thought-disordered schizophrenic patients. / Moritz, Steffen; Mersmann, K; Kloss, M; Jacobsen, D; Wilke, U; Andresen, B; Naber, Dieter; Pawlik, K.

in: PSYCHOL MED, Jahrgang 31, Nr. 2, 2, 2001, S. 221-229.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Moritz, S, Mersmann, K, Kloss, M, Jacobsen, D, Wilke, U, Andresen, B, Naber, D & Pawlik, K 2001, ''Hyper-priming' in thought-disordered schizophrenic patients.', PSYCHOL MED, Jg. 31, Nr. 2, 2, S. 221-229. <http://www.ncbi.nlm.nih.gov/pubmed/11232910?dopt=Citation>

APA

Moritz, S., Mersmann, K., Kloss, M., Jacobsen, D., Wilke, U., Andresen, B., Naber, D., & Pawlik, K. (2001). 'Hyper-priming' in thought-disordered schizophrenic patients. PSYCHOL MED, 31(2), 221-229. [2]. http://www.ncbi.nlm.nih.gov/pubmed/11232910?dopt=Citation

Vancouver

Moritz S, Mersmann K, Kloss M, Jacobsen D, Wilke U, Andresen B et al. 'Hyper-priming' in thought-disordered schizophrenic patients. PSYCHOL MED. 2001;31(2):221-229. 2.

Bibtex

@article{cbc99bb026514c0d8c1c683dcd8f11ba,
title = "'Hyper-priming' in thought-disordered schizophrenic patients.",
abstract = "BACKGROUND: A number of studies have suggested that indirect semantic priming is enhanced in thought-disordered schizophrenics. However, research on direct semantic priming has produced conflicting results. The aim of the present study was to resolve some of the ambiguities of previous findings. METHODS: For the present study, 44 schizophrenic patients were split according to the presence of associative loosening into a positive thought-disordered (TD) and non-positive thought-disordered (NTD) group. Thirty healthy subjects and 36 psychiatric patients served as controls. RESULTS: Schizophrenics displayed increased indirect semantic priming compared with psychiatric controls. When subtyping the sample, TD-patients exhibited significantly enhanced indirect semantic priming compared with healthy and psychiatric controls as well as NTD-patients. Overall slowing was found to be independent of priming effects. Medication, age and chronicity of the schizophrenic illness did not modulate priming. Conclusions: In line with Spitzer and Maher it is inferred that disinhibited semantic networks underlie formal thought disorder in schizophrenia. For future research, it would be appropriate to: employ indirect semantic priming rather than direct semantic priming conditions; and, pay more attention to potential moderators of the priming effect, most importantly, the prime display duration and the length of the stimulus onset asynchrony.",
author = "Steffen Moritz and K Mersmann and M Kloss and D Jacobsen and U Wilke and B Andresen and Dieter Naber and K Pawlik",
year = "2001",
language = "Deutsch",
volume = "31",
pages = "221--229",
journal = "PSYCHOL MED",
issn = "0033-2917",
publisher = "Cambridge University Press",
number = "2",

}

RIS

TY - JOUR

T1 - 'Hyper-priming' in thought-disordered schizophrenic patients.

AU - Moritz, Steffen

AU - Mersmann, K

AU - Kloss, M

AU - Jacobsen, D

AU - Wilke, U

AU - Andresen, B

AU - Naber, Dieter

AU - Pawlik, K

PY - 2001

Y1 - 2001

N2 - BACKGROUND: A number of studies have suggested that indirect semantic priming is enhanced in thought-disordered schizophrenics. However, research on direct semantic priming has produced conflicting results. The aim of the present study was to resolve some of the ambiguities of previous findings. METHODS: For the present study, 44 schizophrenic patients were split according to the presence of associative loosening into a positive thought-disordered (TD) and non-positive thought-disordered (NTD) group. Thirty healthy subjects and 36 psychiatric patients served as controls. RESULTS: Schizophrenics displayed increased indirect semantic priming compared with psychiatric controls. When subtyping the sample, TD-patients exhibited significantly enhanced indirect semantic priming compared with healthy and psychiatric controls as well as NTD-patients. Overall slowing was found to be independent of priming effects. Medication, age and chronicity of the schizophrenic illness did not modulate priming. Conclusions: In line with Spitzer and Maher it is inferred that disinhibited semantic networks underlie formal thought disorder in schizophrenia. For future research, it would be appropriate to: employ indirect semantic priming rather than direct semantic priming conditions; and, pay more attention to potential moderators of the priming effect, most importantly, the prime display duration and the length of the stimulus onset asynchrony.

AB - BACKGROUND: A number of studies have suggested that indirect semantic priming is enhanced in thought-disordered schizophrenics. However, research on direct semantic priming has produced conflicting results. The aim of the present study was to resolve some of the ambiguities of previous findings. METHODS: For the present study, 44 schizophrenic patients were split according to the presence of associative loosening into a positive thought-disordered (TD) and non-positive thought-disordered (NTD) group. Thirty healthy subjects and 36 psychiatric patients served as controls. RESULTS: Schizophrenics displayed increased indirect semantic priming compared with psychiatric controls. When subtyping the sample, TD-patients exhibited significantly enhanced indirect semantic priming compared with healthy and psychiatric controls as well as NTD-patients. Overall slowing was found to be independent of priming effects. Medication, age and chronicity of the schizophrenic illness did not modulate priming. Conclusions: In line with Spitzer and Maher it is inferred that disinhibited semantic networks underlie formal thought disorder in schizophrenia. For future research, it would be appropriate to: employ indirect semantic priming rather than direct semantic priming conditions; and, pay more attention to potential moderators of the priming effect, most importantly, the prime display duration and the length of the stimulus onset asynchrony.

M3 - SCORING: Zeitschriftenaufsatz

VL - 31

SP - 221

EP - 229

JO - PSYCHOL MED

JF - PSYCHOL MED

SN - 0033-2917

IS - 2

M1 - 2

ER -