Cognition In Psychiatric Disorders Research Articles

Efficacy of Transcranial Magnetic Stimulation (TMS) on cognition in psychiatric disorders: A systematic review

Efficacy of Transcranial Magnetic Stimulation (TMS) on cognition in psychiatric disorders: A systematic review

Assessment of Stress Effects on Cognitive Flexibility using an Operant Strategy Shifting Paradigm.

Stress affects cognitive function. Whether stress enhances or impairs cognitive function depends on several factors, including the 1) type, intensity, and duration of the stressor; 2) type of cognitive function under study; and 3) timing of the stressor in relation to learning or executing the cognitive task. Furthermore, sex differences among the effects of stress on cognitive function have been widely documented. Described here is an adaptation of an automated operant strategy shifting paradigm to assess how variations in stress affect cognitive flexibility in male and female Sprague Dawley rats. Specifically, restraint stress is used before or after training in this operant-based task to examine how stress affects cognitive performance in both sexes. Particular brain areas associated with each task in this automated paradigm have been well-established (i.e., the medial prefrontal cortex and orbitofrontal cortex). This allows for targeted manipulations during the experiment or the assessment of particular genes and proteins in these regions upon completion of the paradigm. This paradigm also allows for the detection of different types of performance errors that occur after stress, each of which has defined neural substrates. Also identified are distinct sex differences in perseverative errors after a repeated restraint stress paradigm. The use of these techniques in a preclinical model may reveal how stress affects the brain and impairs cognition in psychiatric disorders, such as post-traumatic stress disorder (PTSD) and major depressive disorder (MDD), which display marked sex differences in prevalence.

Cognition in psychiatric disorders: from models to management

Cognition in psychiatric disorders: from models to management

P01-190 - Theory of mind and neurocognitive functioning in patients with bipolar disorder

ObjectivesStudies into social cognition in psychiatric disorders have recently been expanded to address the questions whether or not “theory of mind” (ToM), that is, the ability to represent own and others’ mental states, is impaired in bipolar affective disorder (BPD).Results have been mixed so far, mainly due to possible confounding effects of neurocognition, as well as, clinical factors such as acuity and current mood. Here, we explored ToM and its associations with neurocognitive functioning in BPD.Methods33 patients with bipolar I disorder (of which 12 were currently depressed, 10 manic, and 11 remitted) and 29 healthy controls were assessed using a test battery that was identical to the one that was used in previous studies into schizophrenia, comprising diverse neurocognitive tasks, including measures of intelligence, executive functioning, and ToM tasks.ResultsThe bipolar patient group as a whole, as well as all three clinical subgroups, were impaired on all measures of ToM relative to controls, but did not differ from each other in most ToM scores. Patients’ poorer performance on executive tasks did not fully explain ToM differences between patients and controls, suggesting a partially selective ToM deficit in BPD.ConclusionsPatients with BPD are impaired in ToM, partially independent of other cognitive dysfunctions and current mood.

Theory of mind and neurocognitive functioning in patients with bipolar disorder

Studies into social cognition in psychiatric disorders have recently been expanded to address the question of whether or not theory of mind (ToM), i.e., the ability to represent ones own and others mental states, is impaired in bipolar affective disorder (BPD). Results have been mixed so far, mainly due to possible confounding effects of neurocognition, as well as clinical factors such as acuity and current mood. Here, we explored ToM and its associations with neurocognitive functioning in BPD. A total of 33 patients with bipolar I disorder (of whom 12 were currently depressed, 10 manic, and 11 remitted) and 29 healthy controls were assessed using a test battery that was identical to the one that was used in previous studies in schizophrenia, comprising diverse neurocognitive tasks, including measures of intelligence, executive functioning, and ToM tasks. The bipolar disorder patient group as a whole and all three clinical subgroups were impaired on all measures of ToM relative to controls, but did not differ from each other in most ToM scores. Patients poorer performance on executive tasks did not fully explain ToM differences between patients and controls, suggesting a partially selective ToM deficit in BPD. Patients with BPD are impaired in ToM, partially independent of other cognitive dysfunctions and current mood.

Social cognition and its neural correlates in schizophrenia and autism.

The study of social cognition in psychiatric disorders has become increasingly popular in recent years. This is due to the its proposed link to social functioning and the inability of general neurocognitive skills to explain the spectrum of impairments observed in patients. This article reviews research into two of the processes thought to underlie social cognition (emotion perception and theory of mind) in schizophrenia and autism. This is followed by a look at neuroimaging studies and their efforts to localize the neural correlates of emotion perception and theory of mind in the two disorders. We concluded that while a specific impairment in emotion perception and theory of mind skills cannot be generalized to all individuals with autism and schizophrenia, there are subpopulations that have lingering deficits of social cognition tasks. Neuroimaging work consistently points to the involvement of the fusiform gyrus and amygdala in emotion processing, while the medial prefrontal and frontal cortex are implicated in tasks invoking theory of mind. We propose that deficits of social cognition may benefit from cognitive remediation therapy and pharmacological cognitive enhancers.