Biomedical subjects

James M Gold

Publications and source records attributed to James M Gold.

At least 19 recordsLinked to original sources

PubMed2026

The effect of monetary versus point-based rewards on effort-cost decision making in individuals at clinical high risk for psychosis.

OBJECTIVE: The dissemination of inexpensive computerized behavioral tasks indexing amotivation may enhance the assessment of clinical high risk (CHR) across settings. However, the impact of varying reward value in such tasks is unclear. If point-based rewards engage participants, this could improve the scalability of computerized assessments. We tested how point-based rewards versus money impacted effort-cost decision-making in CHR individuals. We further assessed how negative symptom severity and household income interacted with reward-type to impact behavior. METHODS: Participants completed the Effort Expenditure for Reward Task (EEfRT). Participants were randomly assigned to receive either money or points for their performance during the EEfRT. Data from a large sample of CHR (N = 233) individuals and healthy controls (HC; N = 157) were collected. RESULTS: Across diagnostic groups, we observed heightened effort expenditure when money was used as a reward (b = 0.13, p = 0.018). We did not find an interaction of CHR status (b = 0.07, p = 0.845) or negative symptoms (b = 0.01, p = 0.429) with reward-type. Within CHR individuals, heightened negative symptom severity was associated with reduced expended effort (b = -0.03, p = 0.016), regardless of reward type. In an exploratory analysis, we found that individuals in the money condition with relatively high household income expended less effort during high reward, high probability trials (b = -0.24, p = 0.046). CONCLUSIONS: Across CHR and HC individuals, individuals pursuing money expended greater effort. While we did not find a group by reward type interaction, CHR individuals with heightened negative symptom severity expended less effort across trials, replicating prior work. Present findings support further study of point-based rewards in tasks indexing amotivation.

Humans↗

PubMed2006

Social/communication skills, cognition, and vocational functioning in schizophrenia.

Deficits in social/communications skills have been documented in schizophrenia, but it is unclear how these deficits relate to cognitive deficits and to everyday functioning. In the current study, social/communication skills performance was measured in 29 schizophrenia patients with a history of good vocational functioning (GVF) and 26 with a history of poor vocational functioning (PVF) using a role-play-based social skills assessment, the Maryland Assessment of Social Competence (MASC). A battery of standard cognitive tasks was also administered. MASC-indexed social skills were significantly impaired in PVF relative to GVF patients (odds ratio = 3.61, P < .001). Although MASC social skills performance was significantly associated with cognitive performance in domains of verbal ability, processing speed, and memory, the MASC nevertheless remained an independent predictor of vocational functioning even after controlling for cognitive performance. Social/communications skills predict vocational functioning history independently of cognitive performance, and social skills measures should be considered for inclusion in test batteries designed to predict everyday functioning in schizophrenia.

Activities of Daily Living↗

PubMed2006

Neuropsychology of the deficit syndrome: new data and meta-analysis of findings to date.

The deficit syndrome is thought to characterize a pathophysiologically distinct subgroup of patients with schizophrenia. Supporting this notion, prior research examining the neuropsychological correlates of the deficit syndrome has suggested the presence of a differential impairment in frontal and parietal functions. This article reports findings from 2 studies attempting to replicate and extend previous reports of a differential neuropsychological impairment in deficit schizophrenia. In the first study, we administered a comprehensive neuropsychological battery to 20 deficit and 25 nondeficit patients with schizophrenia and 25 normal healthy controls. In the second study, a meta-analysis was conducted of 13 separate studies examining the neuropsychology of the deficit syndrome. There was little evidence from either of the present studies that the deficit syndrome is associated with a selective impairment in frontal and parietal lobe functions. The first study failed to find significant differences in frontal or parietal abilities for deficit vs nondeficit patients. The meta-analytic findings revealed that deficit patients were globally more neuropsychologically impaired than nondeficit patients (effect size [ES] = 0.41). Relative to nondeficit patients, deficit patients performed poorest on tests of olfaction (ES = 1.11), social cognition (ES = 0.56), global cognition (ES = 0.52), and language (ES = 0.51). The neuropsychological impairments associated with the deficit form of schizophrenia do not follow an obvious anatomically defined pattern of impairment. The question of whether deficit patients exhibit a unique cognitive impairment profile will require a more sophisticated and rigorous examination of the neuropsychology of the deficit syndrome.

Adult↗

PubMed2006

Schizophrenia in translation: the presence of absence: habenular regulation of dopamine neurons and the encoding of negative outcomes.

Many patients with schizophrenia have pronounced deficits in the use of negative feedback to guide problem solving and learning, as seen on tasks like the Wisconsin Card Sorting Test. There is now a compelling body of evidence from nonhuman primates that suggests transient decreases in dopamine cell activity may reflect the occurrence of unexpected negative outcomes, such as the absence of an expected reward, and, generalizing to the human, the occurrence of negative feedback or the absence of expected reward. We present preliminary evidence that habenula projections to the midbrain are capable of producing a transient, but nearly complete, inhibition of dopamine neurons at a population level similar to that observed in behaving primates following an unexpected negative outcome. Human functional imaging studies offer further evidence that the habenula is activated following receipt of unexpected negative feedback or the absence of expected positive feedback. We present initial evidence that patients with schizophrenia lack appropriate modulation of habenula activity in response to feedback. Collectively, these data suggest that the habenula may play a critical role in mediating the feedback-processing deficits of schizophrenia.

Cognition Disorders↗

PubMed2006

The speed of visual attention in schizophrenia: electrophysiological and behavioral evidence.

Schizophrenia is characterized by a substantial slowing of manual response times and by impairments in attention. However, prior research has not investigated whether attention itself is slowed in schizophrenia, and this was the goal of the present study. In Experiment 1, the N2pc component of the event-related potential waveform-an electrophysiological correlate of the focusing of attention-was recorded from 24 schizophrenia spectrum patients and 13 control subjects. Although behavioral response times were delayed by over 100 ms in the patient group, the onset latency of the N2pc component was virtually identical across groups, and no reduction in N2pc amplitude was observed in the patient group. In Experiment 2, a new cueing paradigm was developed to provide a behavioral measure of the speed of attention in 22 schizophrenia spectrum patients and 13 control subjects. We found that the average time required to allocate attention to a cued location was only 19 ms greater for the patient group than for the control group, with most patients within the range of the control subjects. Together, these experiments revealed little or no slowing of the allocation of visual-spatial attention in patients with schizophrenia. Thus, the mechanisms responsible for allocating attention to salient visual targets appear to be largely unaffected by the illness, and the well documented slowing of manual response times in schizophrenia cannot easily be explained by a slowing of attention.

Adult↗

PubMed2006

Spatial working memory as a cognitive endophenotype of schizophrenia: assessing risk for pathophysiological dysfunction.

Research suggests that first-degree relatives and individuals with schizophrenia spectrum personality disorders (SSPD) may represent nonpenetrant carriers of the genetic diathesis for schizophrenia. This study examined visuospatial working memory (SWM) as a cognitive endophenotype of schizophrenia by expanding the concept of risk for pathophysiological dysfunction beyond overt psychosis. Risk was thus defined by familial status and the presence or absence of SSPD. SWM was assessed in the following groups, in order of decreasing likelihood of genetic vulnerability: 23 patients with schizophrenia, 17 SSPD relatives of patients with schizophrenia, 23 non-SSPD relatives of patients with schizophrenia, 14 SSPD community members with no family history of psychosis, and 36 non-SSPD community members. SWM performance during a computer task was quantified by A-Prime. Relative risk ratios for SWM deficits were compared among the groups. Compared with community non-SSPD volunteers, relative risk (RR) of SWM deficits was significantly elevated in patients with schizophrenia (RR = 3.76, p = .002) and SSPD family members (RR = 2.97, p = .027), but not in the family non-SSPD (RR = 1.88, p = .241) or community SSPD (RR = 1.03, p = .971) groups. The pattern of SWM performance deficits reflected the proposed model of latent genetic liability, upholding SWM as a viable cognitive endophenotype. The results underscore the importance of including both familial liability and the schizophrenia spectrum when considering risk for schizophrenia and schizophrenia-related traits. This is particularly relevant for research efforts to identify pathophysiological components of the disease.

Adult↗

PubMed2006

Cognitive rehabilitation for schizophrenia and the putative role of motivation and expectancies.

Cognitive rehabilitation (CR) approaches seek to enhance cognitive processes or to circumvent cognitive impairments in schizophrenia in an effort to improve functional outcome. In this review we examine the research findings on the 8 evidence-based approaches to cognitive remediation listed in the 2005 Training Grid Outlining Best Practices for Recovery and Improved Outcomes for People With Serious Mental Illness, developed by the American Psychological Association Committee for the Advancement of Professional Practice. Though the approaches vary widely in theoretical orientation and methods of intervention, the results are, for the most part, encouraging. Improvements in attention, memory, and executive functioning have been reported. However, many persons with schizophrenia are more impaired in real-world functioning than one would expect given the magnitude of their cognitive deficits. We may need to look beyond cognition to other targets such as motivation to identify the reasons that many persons with schizophrenia demonstrate such marked levels of disability. Although a number of current CR approaches address motivation to varying degrees, treating motivation as a primary target may be needed to maximize CR outcomes.

Adaptation, Psychological↗

PubMed2006

Baseline neurocognitive deficits in the CATIE schizophrenia trial.

Neurocognition is moderately to severely impaired in patients with schizophrenia. However, the factor structure of the various neurocognitive deficits, the relationship with symptoms and other variables, and the minimum amount of testing required to determine an adequate composite score has not been determined in typical patients with schizophrenia. An 'all-comer' approach to cognition is needed, as provided by the baseline assessment of an unprecedented number of patients in the CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness) schizophrenia trial. From academic sites and treatment providers representative of the community, 1493 patients with chronic schizophrenia were entered into the study, including those with medical comorbidity and substance abuse. Eleven neurocognitive tests were administered, resulting in 24 individual scores reduced to nine neurocognitive outcome measures, five domain scores and a composite score. Despite minimal screening procedures, 91.2% of patients provided meaningful neurocognitive data. Exploratory principal components analysis yielded one factor accounting for 45% of the test variance. Confirmatory factor analysis showed that a single-factor model comprised of five domain scores was the best fit. The correlations among the factors were medium to high, and scores on individual factors were very highly correlated with the single composite score. Neurocognitive deficits were modestly correlated with negative symptom severity (r=0.13-0.27), but correlations with positive symptom severity were near zero (r<0.08). Even in an 'all-comer' clinical trial, neurocognitive deficits can be assessed in the overwhelming majority of patients, and the severity of impairment is similar to meta-analytic estimates. Multiple analyses suggested that a broad cognitive deficit characterizes this sample. These deficits are modestly related to negative symptoms and essentially independent of positive symptom severity.

Adult↗

PubMed2006

A comparison of cognitive structure in schizophrenia patients and healthy controls using confirmatory factor analysis.

There is evidence that cognitive task performance breaks down into the same broad domains in schizophrenia as in healthy populations. However, this does not mean that the domains are independent of one another or that the interrelationships among domains are the same between groups. We used confirmatory factor analysis (CFA) to compare the latent structure of a broad neuropsychological battery in schizophrenia patients (n = 148) and healthy controls (n = 157). Main analyses examined the fit of a hierarchical six-factor model, in which associations among the factors were assumed to reflect their strong shared relationship to a general cognitive ability factor. The model incorporated the factors of verbal comprehension, perceptual organization, verbal memory, spatial memory, processing speed, and executive/working memory. The hierarchical model provided a good overall fit to data from both groups. However multiple groups CFA revealed significant differences in factor loadings between groups, reflecting a more generalized latent structure of cognitive ability in schizophrenia. This was also evident in higher bivariate correlations among cognitive domain composite scores calculated from the observed test data. Cognitive ability, as reflected in test performance, appears to be more unitary in schizophrenia than in healthy subjects. This finding may have measurement and treatment implications.

Adult↗

PubMed2006

Impaired control of visual attention in schizophrenia.

To investigate attentional impairment in schizophrenia, the authors examined the performance of 22 patients with schizophrenia and 16 healthy control subjects in 4 visual search tasks that varied in perceptual requirements and in the need for precise attentional control. The rate of search was slowed in the patients in all tasks. However, the degree of slowing was largest in tasks requiring precise attentional control and smallest in tasks that were perceptually difficult but required less attentional control. This pattern of results indicates that the primary impairment of attention in schizophrenia lies in the control of attention and not in the selection processes that operate once attention has been directed to an object.

Adult↗

PubMed2006

Intact attentional control of working memory encoding in schizophrenia.

This study reports evidence that individuals with schizophrenia (SC) demonstrate intact attentional selection for visual working memory (WM) storage. A group of 62 participants with SC and 55 control participants without SC were studied in a series of 5 experiments that examined the ability to use top-down and bottom-up cues to guide WM encoding, as well as the ability to spontaneously select a subset of representations for storage. Participants with SC exhibited a consistent and robust ability to use selective attention in the control of WM in all 5 experiments, demonstrating a remarkable island of preserved functioning given the broad spectrum of impairments of attention and WM that have been widely reported in those with SC. These findings indicate that attention is not globally impaired in SC and make it possible to delineate more precisely the nature of the specific impairment of attention in this disorder.

Attention↗

PubMed2005

One-year double-blind study of the neurocognitive efficacy of olanzapine, risperidone, and haloperidol in schizophrenia.

Neurocognitive deficits in schizophrenia can reach 1 to 2 standard deviations below healthy controls. The comparative effect of typical and atypical antipsychotic medications on neurocognition is controversial, and based primarily on studies with small samples and large doses of typical comparator medications. The present study assessed neurocognitive efficacy. It was hypothesized that olanzapine treatment would improve neurocognitive deficits to a greater degree than either risperidone or haloperidol treatment. This was a double-blind, randomized, controlled, parallel study with neurocognition assessed at baseline, and 8, 24, and 52 weeks. Per protocol, the haloperidol arm was discontinued. Four hundred and fourteen inpatients or outpatients with schizophrenia and schizoaffective disorder were treated with oral olanzapine (n = 159), risperidone (n = 158), or haloperidol (n = 97). Individual domains (executive function, learning and memory, processing speed, attention/vigilance, verbal working memory, verbal fluency, motor function, and visuospatial ability) were transformed into composite scores and compared between treatment groups. At the 52-week endpoint, neurocognition significantly improved in each group (p < 0.01 for olanzapine and risperidone, p = 0.04 for haloperidol), with no significant differences between groups. Olanzapine- and risperidone-treated patients significantly (p < 0.05) improved on domains of executive function, learning/memory, processing speed, attention/vigilance, verbal working memory, and motor functions. Additionally, risperidone-treated patients improved on domains of visuospatial memory. Haloperidol-treated patients improved only on domains of learning/memory. However, patients able to remain in treatment for the entire 52 weeks benefited more from olanzapine or risperidone treatment than haloperidol treatment.

Adolescent↗

PubMed2005

Working memory consolidation is abnormally slow in schizophrenia.

This study reports evidence that patients with schizophrenia demonstrate a slowing of working memory (WM) consolidation, which is the process of transforming transient perceptual representations into durable WM representations. Sixteen schizophrenia patients and 16 healthy control participants performed a task measuring the visual WM consolidation rate in a change-detection paradigm. A target display containing 3 colored squares was followed by a variable delay of 17-483 ms, a pattern mask, and then a test stimulus. This pattern mask does not interfere with perception but disrupts WM consolidation. Control participants reached no-mask performance by 250 ms, indicating completed WM consolidation, whereas patients failed to reach no-mask performance by 483 ms. Slowed consolidation may play an important and largely unrecognized role in schizophrenia.

Humans↗

PubMed2005

No, it is not possible to be schizophrenic yet neuropsychologically normal.

Cognitive impairment is well documented in schizophrenia, though some reports have been interpreted to suggest that it is possible to have schizophrenia without neuropsychological impairment. The authors tested this by comparing the neuropsychological profiles of closely matched patients with schizophrenia and healthy comparison participants. Sixty-four patients with schizophrenia and 64 healthy comparison cases, matched to within 3 Full-Scale IQ points, were tested using the Wechsler Adult Intelligence Scale (3rd ed.; D. Wechsler, 1997b) and the Wechsler Memory Scale (3rd ed.; D. Wechsler, 1997c). Neuropsychological profiles for these groups were markedly different, with the group of patients with schizophrenia exhibiting performance deficits in memory and speeded visual processing but superior verbal comprehension and perceptual organization relative to the group of healthy comparison participants matched on Full-Scale IQ. Thus, scoring in the normal range does not preclude neuropsychological abnormality in schizophrenia, confirming that neuropsychological impairment is a core feature of the illness.

Adult↗

PubMed2005

Olanzapine treatment of residual positive and negative symptoms.

OBJECTIVE: Olanzapine has been hypothesized to have superior efficacy in patients with treatment-resistant schizophrenia. The authors examined the comparative efficacy and safety of olanzapine and haloperidol in outpatients with partially responsive schizophrenia. METHOD: Sixty-three outpatients with schizophrenia who met retrospective and prospective criteria for either residual positive or residual negative symptoms entered a 16-week double-blind, parallel-groups comparison of olanzapine and haloperidol. RESULTS: There were no significant differences between the two drugs in their effect on positive or negative symptoms. There were no significant differences between the two treatment groups on measures of social and functional outcome. Olanzapine-treated patients had a significant reduction in extrapyramidal symptoms and subjective measures of stiffness and dry mouth, but the increases in systolic blood pressure and weight in olanzapine-treated patients were significantly greater than they were in haloperidol-treated patients. CONCLUSIONS: Olanzapine has limited differential benefit for either positive or negative symptoms in patients with treatment-resistant schizophrenia. Although olanzapine is associated with fewer extrapyramidal symptoms, other side effects may offset this benefit.

Adult↗

PubMed2005

Optimistic bias in the perception of personal risk: patterns in schizophrenia.

OBJECTIVE: Biases in the perception of personal vulnerability to risk could influence how individuals make decisions in many contexts. Schizophrenia patients, because of neurocognitive deficits and psychiatric symptoms, are often seen as compromised in their ability to appreciate risk information and in their decision-making capacity. The authors investigated whether schizophrenia patients share the same optimistic biases frequently demonstrated by non-ill adults in their perceptions of personal risk. METHOD: Twenty-five schizophrenic outpatients and 23 healthy comparison subjects completed a risk perception questionnaire on which they compared their own likelihood of experiencing adverse events to that of other adults. Questionnaire items were adverse events of three types: controllable, uncontrollable, and neutral. The degree to which subjects rated their own likelihood of experiencing adverse events as lower than others' was an index of optimistic bias. RESULTS: Although both groups showed an optimistic bias in general, healthy comparison subjects demonstrated a greater level of optimism than did schizophrenia patients, especially for events typically perceived as controllable. Psychiatric symptoms rated with the Brief Psychiatric Rating Scale and the Scale for the Assessment of Negative Symptoms bore little relationship to patients' ratings on the risk questionnaire. CONCLUSIONS: Results showed that an unrealistically optimistic bias in the perception of personal risk was at least as evident in a healthy comparison group as in a schizophrenia group. Such a bias could influence decision making. By identifying and responding to such biases, clinicians and researchers can promote more fully informed and rational decisions in patients and healthy adults.

Adult↗

PubMed2004

Identification of separable cognitive factors in schizophrenia.

One of the primary goals in the NIMH initiative to encourage development of new interventions for cognitive deficits in schizophrenia, Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS), has been to develop a reliable and valid consensus cognitive battery for use in clinical trials. Absence of such a battery has hampered standardized evaluation of new treatments and, in the case of pharmacological agents, has been an obstacle to FDA approval of medications targeting cognitive deficits in schizophrenia. A fundamental step in developing such a battery was to identify the major separable cognitive impairments in schizophrenia. As part of this effort, we evaluated the empirical evidence for cognitive performance dimensions in schizophrenia, emphasizing factor analytic studies. We concluded that seven separable cognitive factors were replicable across studies and represent fundamental dimensions of cognitive deficit in schizophrenia: Speed of Processing, Attention/Vigilance, Working Memory, Verbal Learning and Memory, Visual Learning and Memory, Reasoning and Problem Solving, and Verbal Comprehension. An eighth domain, Social Cognition, was added due to recent increased interest in this area and other evidence of its relevance for clinical trials aiming to evaluate the impact of potential cognitive enhancers on cognitive performance and functional outcome. Verbal Comprehension was not considered appropriate for a cognitive battery intended to be sensitive to cognitive change, due to its resistance to change. The remaining seven domains were recommended for inclusion in the MATRICS-NIMH consensus cognitive battery and will serve as the basic structure for that battery. These separable cognitive dimensions also have broader relevance to future research aimed at understanding the nature and structure of core cognitive deficits in schizophrenia.

Arousal↗

PubMed2004

Cognitive deficits as treatment targets in schizophrenia.

Cognitive impairment has emerged as an important new target in schizophrenia therapeutics in light of evidence that cognitive deficits are critically related to the functional of disability that is characteristic of the illness. Evidence is briefly reviewed supporting the idea that the cognitive impairment in schizophrenia is an attractive target for therapeutic intervention including: (1) there is a characteristic pattern of cognitive deficits that occur with very high frequency; (2) the deficits are relatively stable over time; and (3) cognitive deficits are relatively independent of the symptomatic manifestations of the illness. Thus, cognitive impairment appears to be a well-defined, reliable and distinct dimension of the illness.

Antipsychotic Agents↗