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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The existence of a genetic background is now a well admitted notion in schizophrenia, but some individuals at genetic risk for that disease could never manifest it at a clinical level. However, several vulnerability models could help us to identify such individuals. According to them, when similar perturbations at a given test are observed both in clinically stable schizophrenics and their nonschizophrenic first degree relatives, this test could be qualify as an indicator of the vulnerability to schizophrenia. In literature, that seems the case for several neuropsychological tasks, exploring attentional abilities (degraded version of the Continuous Performance Task [DS-CPT], and Span Of Apprehension task [SOA]) and executive functions (Wisconsin Card Sorting Test [WCST]). Our study was undertaken to replicate literature data and to further explore the relationship between these three neuropsychological markers. For that purpose, performances at DS-CPT, SOA and WCST were assessed among 18 clinically stable schizophrenics, 18 of their biological full siblings and 15 unrelated control subjects matched with the two others groups for several socio-demographic factors. Comparisons were performed by non parametric analysis (Kruskal-Wallis one way ANOVA, and Mann-Whitney). Compared to controls, the siblings group performances were significantly impaired on the three tasks, while they did not statistically differ from the schizophrenic ones. No relationship was observed between the markers, except for the "d'" index at DS-CPT and the number of successfully performed categories at the WCST. Results from the sibling group suggested that the observed impaired neuropsychological performances may actually represent indicators of the genetic vulnerability to schizophrenia. Moreover, the generally admitted relationship between WCST poor performances and an impairment of the prefrontal cortex, lead us to hypothesize some role of this brain area in schizophrenia vulnerability.
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PMID:[Vulnerability to schizophrenia. I: Familial nature of of neuropsychologic indicators]. 985 Aug 18

This study was aimed, first, at detecting neuropsychological markers that assess vulnerability to schizophrenia in siblings of patients with schizophrenia, and second, at exploring possible relationships between markers. For these purposes, performances were assessed in 18 clinically stabilized patients with schizophrenia, 18 of their unaffected full siblings, and 15 controls on attentional abilities (the Degraded Stimuli-Continuous Performance Task [DS-CPT] and the Span of Apprehension [SOA] task) and on executive functions (the Wisconsin Card Sorting Test [WCST]). Both patients and siblings were impaired on the three tasks, leading to the conclusion that these poor performances may represent markers of genetic vulnerability to schizophrenia. Furthermore, significant relationships were found between DS-CPT and WCST performance in patients only, suggesting a possible implication of prefrontal brain areas for the two tasks. In spite of the lack of similar relationships between DS-CPT and WCST in siblings, this raises the question of a putative role of prefrontal areas in vulnerability to schizophrenia.
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PMID:Neuropsychological deficit in siblings discordant for schizophrenia. 1108 21

The central auditory system of the human brain uses a variety of mechanisms to analyze auditory scenes, among others, preattentive detection of sudden changes in the sound environment. Electroencephalography (EEG) and magnetoencephalography (MEG) provide a measure to monitor neuronal cortical currents. The mismatch negativity (MMN) or field (MMNm) reflect preattentive activation in response to deviants within a sequence of homogenous auditory stimuli. Functional magnetic resonance imaging (fMRI) allows for a higher spatial resolution as compared to the extracranial electrophysiological techniques. The image encoding gradients of echo planar imaging (EPI) sequences, however, elicit an interfering background noise. To circumvent this shortcoming, the present study applied multi-echo EPI mimicking an auditory oddball design. The gradient trains (SOA = 800 msec, 94.5 dB SPL, stimulus duration = 152 msec) comprised amplitude (-9 dB) and duration (76 msec) deviants in a randomized sequence. Moreover, the scanner noise was recorded and applied in a whole-head MEG device to validate the properties of this specific material. Robust fMRI activation patterns emerged in response to the deviant gradient switching. Changes in amplitude activated the entire auditory cortex, whereas the duration deviants elicited right-lateralized signal increase in secondary areas. The recorded scanner noise evoked reliably right-lateralized mismatch MEG responses. Source localization was in accordance with activation of secondary auditory cortex. The presented paradigm provides a robust and feasible tool to study the functional anatomy of early cognitive auditory processing in clinical populations such as schizophrenia.
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PMID:Mismatch responses to randomized gradient switching noise as reflected by fMRI and whole-head magnetoencephalography. 1211 73

Previous cross-sectional studies on covert orienting of visual attention in schizophrenia have been inconsistent. In the present longitudinal study, we examined 40 medicated acutely ill inpatients with a covert orienting of attention task (COVAT) shortly after admission, and again 12-16 weeks after the initial examination, while most patients were in (partial) remission. We administered a COVAT with nonpredictive peripheral cues and two stimulus-onset asynchronies (SOA; 100 and 800 ms). In addition, we examined 34 healthy control subjects twice (2 weeks apart). The most important finding was a lack of inhibition of return (IOR) in patients with schizophrenia, both at the first examination in an acute psychotic state and at the follow-up examination after considerable clinical improvement. The IOR deficit was unrelated to psychopathology, length of illness, number of previous psychotic episodes, and type of neuroleptic (NL) medication. Deficient IOR in patients with schizophrenia appears to be state-independent and might be viewed as a trait or vulnerability marker of the disorder. Subsequent studies with never-medicated populations and with schizotypal or high-risk subjects are needed in order to further analyze the possible role of NL medications and to clarify whether blunted IOR might represent a vulnerability marker of schizophrenia.
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PMID:Blunted inhibition of return in schizophrenia-evidence from a longitudinal study. 1475 38

Previous studies on spatial orienting of attention in schizophrenia demonstrated a deficit of Inhibition of Return (IOR). However, other studies reported a delay in the manifestation, but an overall normal amount of IOR in patients with schizophrenia. However, the latter studies used a cue-back manipulation which is known to reinstate or speed up IOR. Hence, it is not clear whether even very long cue target intervals would allow IOR to develop in patients with schizophrenia in the absence of a cue-back manipulation. The aim of the present study was to study IOR in patients with schizophrenia using a single cue paradigm and a very long cue target interval of >1 s in order to differentiate between blunted and delayed IOR. We examined 32 inpatients with schizophrenia and 16 healthy controls with a covert orienting of attention task (COVAT) with non-predictive peripheral cues and three stimulus onset asynchronies (SOA: 100 ms, 800 ms and 1050 ms). We found a lack of Inhibition of Return (IOR) in patients with schizophrenia with both long SOAs of 800 and 1050 ms. As in a previous study of our group, the IOR deficit was unrelated to psychopathology, length of illness, number of previous psychotic episodes and type of neuroleptic medication. In summary, our study confirms and extends previous reports of deficient IOR in patients with schizophrenia. IOR seems to be not just delayed, but rather profoundly disturbed in schizophrenia. Deficient IOR in patients with schizophrenia might be viewed as a trait or alternatively as a vulnerability marker of the disorder.
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PMID:Deficient inhibition of return in schizophrenia-further evidence from an independent sample. 1601 19

The ability to detect the direction of another person's gaze and to shift our own attention reflexively in the same direction facilitates the sharing of attention with other people. Such sharing of attention would seem critical for the maintenance of normal social cognition. Social cognition is severely impaired in people with schizophrenia. So, we used spatial cuing paradigms to investigate reflexive (Experiment 1) and controlled (Experiment 2) attentional orienting triggered by gaze in schizophrenia. In Experiment 1, 30 patients and 24 controls detected targets appearing right or left of a central image of a head turned right, left, or straight-ahead. These gaze-cues were non-predictive. Patients, but not controls, showed a significant congruency advantage at 100 ms SOA. The congruency advantage was similar in patients and controls at 300-800 ms SOA. In Experiment 2, 20 patients and 24 controls detected targets 300-800 ms after a central gaze-cue that pointed away from the target on 80% of trials. Controls, but not patients, were able to reverse the reflexive congruency advantage at 800 ms SOA. This study provides the first evidence that people with schizophrenia show abnormally sensitive gaze-triggered reflexive orienting. Findings are discussed in light of recent neuroimaging work investigating the neural basis of social orienting and social cognition.
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PMID:Attentional orienting triggered by gaze in schizophrenia. 1604 44

Semantic processing deficits are present in schizophrenia and are particularly evident on semantic priming tasks. Using high schizotypes (psychosis-prone individuals) can overcome some confounds involved in studying actively symptomatic schizophrenics. In the current study, 26 high and 32 low scorers on the O-LIFE schizotypy scale (from a sample of 251 students) were selected for testing. All subjects were administered a lexical-decision semantic priming task where half the stimuli had a short 200 ms stimulus onset asynchrony (SOA, length of time from onset of prime to onset of target) and half the stimuli had a long 750 ms SOA. In addition, half the words were of high frequency and half of a low frequency. There were no group differences in priming for words of different frequencies. Low schizotypes showed greater priming at the 200 ms SOA than at the 750 ms SOA, whilst individuals with high schizotypy showed the opposite pattern. The pattern shown by the low schizotypes replicates earlier work by the authors using other normal control samples; establishing that there is greater priming under conditions of automatic spreading of activation. Furthermore, the data shows there is not an increase in automatic spreading of activation in individuals with high schizotypy. There has been controversy in the schizophrenia literature over whether there is increased priming under automatic conditions. The current study suggests that, when confounds are controlled for, schizophrenia-like symptoms are not related to an increase in automatic spreading of activation.
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PMID:Evidence of semantic disorganisation using semantic priming in individuals with high schizotypy. 1656 82

Abnormal language in schizophrenia has been regarded as a hallmark of this disorder. Language abnormalities include loose and unusual associations, tangentiality, and inability to maintain a topic. Recent theories of language dysfunction have invoked working memory abnormalities, as well as abnormal processes within semantic memory in schizophrenia. Two views, often construed as opposing, have been offered to account for language peculiarities in schizophrenia: one holds that initial processes of activation are abnormal while the other holds that late processes of context utilization might be disturbed. We suggest that these views may be complementary rather than mutually exclusive. Given the relative paucity of data on the early processes within semantic networks, we present new evidence using ERP short SOA paradigm that these processes are abnormal in schizophrenia. Furthermore, reduced N400 in the unrelated condition found in this study suggests that the abnormality was related to inefficient early inhibitory processes.
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PMID:Abnormal inhibitory processes in semantic networks in schizophrenia. 1984 Aug 22

Deficits in visual processing are well established in schizophrenia. However, there is conflicting evidence about whether these deficits start before the formation of percepts because visual processing studies in schizophrenia have typically examined the processing of consciously registered stimuli. In this study, we used nonconscious color priming to evaluate the very early visual processing stages in schizophrenia. Nonconscious and conscious color priming was assessed in 148 schizophrenia patients and 54 healthy control subjects. In both conditions, subjects identified the color of a ring preceded by a disk (prime) in the same color (congruent) or a different color (incongruent). The ring rendered the disk invisible in the nonconscious condition (SOA of 62.5 ms) or did not mask the disk (SOA of 200 ms) in the conscious condition. Schizophrenia patients exhibited a color priming effect (longer reaction times in the incongruent vs. congruent trials) that was similar to healthy controls in both the nonconscious and conscious priming conditions. Healthy controls had a significantly larger priming effect in the nonconscious vs. conscious condition, but patients did not show a significant difference in priming effects between the two conditions. Our results indicate that schizophrenia patients do not have deficits at the nonconscious, pre-perceptual stages of visual processing, suggesting that the feed forward sweep of information processing (from retina to V1) might be intact in schizophrenia. These results imply that the well-documented visual processing deficits in this illness likely occur at later, percept-dependent stages of processing.
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PMID:Nonconscious and conscious color priming in schizophrenia. 2315 1

People with schizophrenia show deficits in processing visual stimuli but neural abnormalities underlying the deficits are unclear and it is unknown whether such functional brain abnormalities are present in other severe mental disorders or in individuals who carry genetic liability for schizophrenia. To better characterize brain responses underlying visual search deficits and test their specificity to schizophrenia we gathered behavioral and electrophysiological responses during visual search (i.e., Span of Apprehension [SOA] task) from 38 people with schizophrenia, 31 people with bipolar disorder, 58 biological relatives of people with schizophrenia, 37 biological relatives of people with bipolar disorder, and 65 non-psychiatric control participants. Through subtracting neural responses associated with purely sensory aspects of the stimuli we found that people with schizophrenia exhibited reduced early posterior task-related neural responses (i.e., Span Endogenous Negativity [SEN]) while other groups showed normative responses. People with schizophrenia exhibited longer reaction times than controls during visual search but nearly identical accuracy. Those individuals with schizophrenia who had larger SENs performed more efficiently (i.e., shorter reaction times) on the SOA task suggesting that modulation of early visual cortical responses facilitated their visual search. People with schizophrenia also exhibited a diminished P300 response compared to other groups. Unaffected first-degree relatives of people with bipolar disorder and schizophrenia showed an amplified N1 response over posterior brain regions in comparison to other groups. Diminished early posterior brain responses are associated with impaired visual search in schizophrenia and appear to be specifically associated with the neuropathology of schizophrenia.
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PMID:Abnormal early brain responses during visual search are evident in schizophrenia but not bipolar affective disorder. 2660 66


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