2001
DOI: 10.1017/s0033291701003105
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‘Hyper-priming’ in thought-disordered schizophrenic patients

Abstract: 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.

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Cited by 87 publications
(66 citation statements)
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References 30 publications
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“…Greater priming is thought to reflect greater activation of the target by the prime. Consistent with increased spread of activation to weak associates, an abnormally large priming effect for indirectly related words has been found in thought-disordered schizophrenia patients, although only when the prime-target interval (or stimulus-onset asynchrony (SOA)) is relatively short (≤300 ms) (Moritz et al, 2001;Moritz et al, 2003;Spitzer et al, 1993).…”
Section: Introductionmentioning
confidence: 74%
“…Greater priming is thought to reflect greater activation of the target by the prime. Consistent with increased spread of activation to weak associates, an abnormally large priming effect for indirectly related words has been found in thought-disordered schizophrenia patients, although only when the prime-target interval (or stimulus-onset asynchrony (SOA)) is relatively short (≤300 ms) (Moritz et al, 2001;Moritz et al, 2003;Spitzer et al, 1993).…”
Section: Introductionmentioning
confidence: 74%
“…A contribution of controlled processes to the observed result is highly unlikely, since postlexical matching strategies are not thought to be involved in pronunciation tasks 5,45 and expectancy-based priming is unlikely to occur at such short SOAs. 5 Thus, this finding can be paralleled to observations of hyperpriming under automatic access conditions and for weak or indirect stimulus dimensions in patients with thought disorder, [9][10][11][18][19][20][21] rendering dopaminergic hyperactivity a plausible basis for priming abnormalities in patients with schizophrenia.…”
Section: Discussionmentioning
confidence: 68%
“…However, in patients with schizophrenia, hyperpriming ceases to exist at such "very short" SOAs, 18 possibly because of perceptual processing abnormalities. 9 Thus, although the investigation of healthy young participants under such "ideal" conditions might provide more accurate insights into the mechanisms governing priming, the generalizability of our findings to clinical populations should be confirmed in further studies.…”
Section: Limitationsmentioning
confidence: 78%
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