Semantic priming in schizophrenia: An examination of spreading activation using word pronunciation and multiple SOAs.

Barch, Deanna M.; Cohen, Jonathan D.; Servan-Schreiber, David; Steingard, Sandra; Steinhauer, Stuart R.; Kammen, Daniël P. van

doi:10.1037/0021-843x.105.4.592

Cited by 162 publications

(159 citation statements)

References 35 publications

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“…On the other hand, using similar semantic priming experiments that sampled a range of SOA times, Barch et al (1996) failed to demonstrate 'hyper-priming' effects in schizophrenia for SOAs ranging from very short (i.e. 250 ms) to relatively long (i.e.…”

Section: Attention and Semantic Processesmentioning

confidence: 96%

Semantic disturbance in schizophrenia and its relationship to the cognitive neuroscience of attention

Nestor

Han

Niznikiewicz

et al. 2001

Biological Psychology

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We view schizophrenia as producing a failure of attentional modulation that leads to a breakdown in the selective enhancement or inhibition of semantic/lexical representations whose biological substrata are widely distributed across left (dominant) temporal and frontal lobes. Supporting behavioral evidence includes word recall studies that have pointed to a disturbance in connectivity (associative strength) but not network size (number of associates) in patients with schizophrenia. Paralleling these findings are recent neural network simulation studies of the abnormal connectivity effect in schizophrenia through 'lesioning' network connection weights while holding constant network size. Supporting evidence at the level of biology are in vitro studies examining N-methyl-D-aspartate (NMDA) receptor antagonists on recurrent inhibition; simulations in neural populations with realistically modeled biophysical properties show NMDA antagonists produce a schizophrenialike disturbance in pattern association. We propose a similar failure of NMDA-mediated recurrent inhibition as a candidate biological substrate for attention and semantic anomalies of schizophrenia.

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Section: Attention and Semantic Processesmentioning

confidence: 96%

Semantic disturbance in schizophrenia and its relationship to the cognitive neuroscience of attention

Nestor

Han

Niznikiewicz

et al. 2001

Biological Psychology

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“…In fact, whereas RT priming evidence for increased spreading activation has come from wordpair studies employing relatively short SOAs (≤300 ms), most RT priming evidence for impaired context use has come either from word-pair studies employing longer SOAs, or from studies using sentence contexts, which also build up over a longer period. For instance, schizophrenia patients displayed less priming than normal controls for closely related words at a long SOA of 950 ms, but not at shorter (200-700 ms) SOAs (Barch et al, 1996). In a sentence-context study (Kuperberg et al, 1998), both schizophrenia patients and controls were slower to recognize a sentence-final word when it was semantically incongruent with the context than when it was congruent, but patients with high thought-disorder ratings were delayed less than were either controls, or patients with low thought-disorder ratingsconsistent with impaired use of context.…”

Section: Introductionmentioning

confidence: 93%

Electrophysiological insights into conceptual disorganization in schizophrenia

Kiang

Kutas

Light

et al. 2007

Schizophrenia Research

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Disorganized speech, or thought disorder, in schizophrenia may reflect abnormal processing of meaningful concepts. To examine whether schizophrenia involves abnormalities in how a meaningful context influences processing of concepts strongly, weakly, or not related to it, we used the N400, an event-related brain potential (ERP) index of semantic relatedness. ERPs were recorded from schizophrenia patients (n=18) and normal controls (n=18) while they viewed category definitions (e.g., a type of fruit), each followed by a target word that was either a hightypicality category exemplar (apple), low-typicality exemplar (cherry), or non-exemplar (clamp). Participants' task was to indicate via button-press whether or not the target belonged to the category. In both patients and controls, N400 amplitude was largest (most negative) for nonexemplars, intermediate for low-typicality exemplars, and smallest (least negative) for hightypicality exemplars. Compared to controls, patients showed a trend toward reduced N400 amplitude differences between non-exemplars and low-typicality exemplars. Most importantly, within patients, reduced N400 amplitude differences between high-and low-typicality exemplars were correlated with psychotic symptoms. In schizophrenia patients, an N400 index of semantic processing was associated with psychotic symptoms. Psychosis may be associated with greater similarity in how concepts strongly and weakly meaningfully related to their context are processed.

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“…This is consistent with other experimental findings, most notably those that have demonstrated schizophrenic patients tend to respond to the strongest associate of a word, regardless of context (e.g., "pen" as writing instrument even though the context suggests a fence, see Chapman and Chapman 1973). In addition, the enhanced priming effect demonstrated in several (Manschreck et al 1988;Kwapil et al 1990;Spitzer et al 1994), albeit not all (Barch et al 1996), word-priming studies of patients with schizophrenia, may also reflect evidence of problems with modulating associative links. Thus, schizophrenic thought processes may be unduly influenced by the activation, or priming, of strong associates, and impervious to the normal constraint of contextual information on the train of thought.…”

Section: A Connectionist Model Of Disturbed Associations In Schizophrmentioning

confidence: 98%

Cognitive dysfunction in schizophrenia: unifying basic research and clinical aspects

McCarley

Niznikiewicz

Salisbury

et al. 1999

European Archives of Psychiatry and Clinical Neurosciences

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Seeking to unite psychological and biological approaches, this paper links cognitive and cellular hypotheses and data about thought and language abnormalities in schizophrenia. The common thread, it is proposed, is a dysregulated suppression of associations (at the behavioral and functional neural systems level), paralleled by abnormalities of inhibition at the cellular and molecular level, and by an abnormal anatomical substrate (reduced MRI gray matter volume) in areas subserving language.At the level of behavioral experiments and connectionist modeling, data suggest an abnormal semantic network connectivity (strength of associations) in schizophrenia, but not an abnormality of network size (number of associates). This connectivity abnormality is likely to be a preferential processing of the dominant (strongest) association, with the neglect of preceding contextual information.At the level of functional neural systems, the N400 event-related potential amplitude is used to index the extent of "search" for a semantic match to a word. In a short stimulus-onset-asynchrony condition, both schizophrenic and schizotypal personality disorder subjects showed, compared with controls, a reduced N400 amplitude to the target words that were related to cues, e.g. cat-dog, a result compatible with behavioral data. Other N400 data strongly and directly suggest that schizophrenics do not efficiently utilize context. At the level of anatomical system substrates, considerable MRI data indicate abnormalities in the temporal lobe structures that subserve language and verbal associations. Gray matter volume is reduced in the posterior portion of the dominant superior temporal gyrus in both chronic and first episode schizophrenics (but not in manic-depressive psychosis), with the magnitude of reduction correlating with the degree of thought disorder.At the level of in vitro cellular and molecular analysis, NMDA receptors on inhibitory neurons are much more sensitive to blockade than are excitatory projections. A resulting failure of recurrent inhibition may account for the psychotomimetic effects of such NMDA receptor blockers as ketamine and phencyclidine, and may also be present in schizophrenia, where an endogenous NMDA receptor blocker, NAAG, is increased, and where other abnormalities of recurrent inhibition may be present. A biophysical simulation of this circuit abnormality in a model of learned pattern recognition produced, because of the reduction in recurrent inhibition, aberrant spread of excitation, resulting in confusion of normally distinguishable patterns. We suggest the neural circuit failure of inhibition and consequent aberrant spread of activation may be the substrate for an inability to use context, with the behavioral and functional consequences just described. Furthermore, there is the possibility that the unbalanced excitation might lead to progressive, neurodegenerative changes in gray matter, marked by progressive volume reduction.

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Semantic priming in schizophrenia: An examination of spreading activation using word pronunciation and multiple SOAs.

Cited by 162 publications

References 35 publications

Semantic disturbance in schizophrenia and its relationship to the cognitive neuroscience of attention

Semantic disturbance in schizophrenia and its relationship to the cognitive neuroscience of attention

Electrophysiological insights into conceptual disorganization in schizophrenia

Cognitive dysfunction in schizophrenia: unifying basic research and clinical aspects

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