Neurocognition is severely impaired in patients with schizophrenia^1,2 independent of phase of illness.^3,4 While these impairments may appear prior to the onset of psychosis,^5-7 their severity in patients with chronic schizophrenia is about 1.5^8-10 to 2.0¹¹ SDs lower than the healthy population. Neurocognitive impairment is a central clinical feature of schizophrenia, because it is strongly associated with functional outcomes.^12,13

Investigators have an ethical responsibility not simply to disclose information to potential participants but also to ensure that the participant has the capacity to reach a decision on the basis of the information provided. How should researchers meet this ethical responsibility? Clinical assessments of decisional capacity have shown poor interrater reliability,¹ so there is a clear need for structured tools to evaluate capacity to consent to research.^2,3

THERE IS a high prevalence of neuropsychological impairment in persons with schizophrenia, ranging from mild deficits to frank dementia.^1-5 Consistent with a neurodevelopmental view, some such deficits appear to predate clinical symptoms and exacerbate with typical illness onset during late adolescence or early adulthood.^6-8

News from JAMA Psychiatry — Consensus Statement on the Upcoming Crisis in Geriatric Mental Health — Research Agenda for the Next 2 Decades

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.