Males and females with first episode psychosis present distinct profiles of social cognition and metacognition.

Deficits in social cognition and metacognition impact the course of psychosis. Sex differences in social cognition and metacognition could explain heterogeneity in psychosis. 174 (58 females) patients with first-episode psychosis completed a clinical, neuropsychological, social cognitive, and metacognitive assessment. Subsequent latent profile analysis split by sex yielded two clusters common to both sexes (a Homogeneous group, 53% and 79.3%, and an Indecisive group, 18.3% and 8.6% of males and females, respectively), a specific male profile characterized by presenting jumping to conclusions (28.7%) and a specific female profile characterized by cognitive biases (12.1%). Males and females in the homogeneous profile seem to have a more benign course of illness. Males with jumping to conclusions had more clinical symptoms and more neuropsychological deficits. Females with cognitive biases were younger and had lower self-esteem. These results suggest that males and females may benefit from specific targeted treatment and highlights the need to consider sex when planning interventions.

Persons with first episode psychosis have distinct profiles of social cognition and metacognition.

Subjects with first-episode psychosis experience substantial deficits in social cognition and metacognition. Although previous studies have investigated the role of profiles of individuals in social cognition and metacognition in chronic schizophrenia, profiling subjects with first-episode psychosis in both domains remains to be investigated. We used latent profile analysis to derive profiles of the abilities in 174 persons with first-episode psychosis using the Beck's Cognitive Insight Scale, the Faces Test, the Hinting Task, the Internal, Personal and Situational Attributions Questionnaire, and the Beads Task. Participants received a clinical assessment and a neuropsychological assessment. The best-fitting model was selected according to the Bayesian information criterion (BIC). We assessed the importance of the variables via a classification tree (CART). We derived three clusters with distinct profiles. The first profile (33.3%) comprised individuals with low social cognition. The second profile (60.9%) comprised individuals that had more proneness to present jumping to conclusions. The third profile (5.7%) presented a heterogeneous profile of metacognitive deficits. Persons with lower social cognition presented worse clinical and neuropsychological features than cluster 2 and cluster 3. Cluster 3 presented significantly worst functioning. Our results suggest that individuals with FEP present distinct profiles that concur with specific clinical, neuropsychological, and functional challenges. Each subgroup may benefit from different interventions.

Influence of social cognition as a mediator between cognitive reserve and psychosocial functioning in patients with first episode psychosis.

BACKGROUND: Social cognition has been associated with functional outcome in patients with first episode psychosis (FEP). Social cognition has also been associated with neurocognition and cognitive reserve. Although cognitive reserve, neurocognitive functioning, social cognition, and functional outcome are related, the direction of their associations is not clear. Therefore, the main aim of this study was to analyze the influence of social cognition as a mediator between cognitive reserve and cognitive domains on functioning in FEP both at baseline and at 2 years. METHODS: The sample of the study was composed of 282 FEP patients followed up for 2 years. To analyze whether social cognition mediates the influence of cognitive reserve and cognitive domains on functioning, a path analysis was performed. The statistical significance of any mediation effects was evaluated by bootstrap analysis. RESULTS: At baseline, as neither cognitive reserve nor the cognitive domains studied were related to functioning, the conditions for mediation were not satisfied. Nevertheless, at 2 years of follow-up, social cognition acted as a mediator between cognitive reserve and functioning. Likewise, social cognition was a mediator between verbal memory and functional outcome. The results of the bootstrap analysis confirmed these significant mediations (95% bootstrapped CI (-10.215 to -0.337) and (-4.731 to -0.605) respectively). CONCLUSIONS: Cognitive reserve and neurocognition are related to functioning, and social cognition mediates in this relationship.

Volumetric and morphological characteristics of the hippocampus are associated with progression to schizophrenia in patients with first-episode psychosis.

BACKGROUND: Abnormalities in the hippocampus have been implicated in the pathophysiology of psychosis. However, it is still unclear whether certain abnormalities are a pre-existing vulnerability factor, a sign of disease progression or a consequence of environmental factors. We hypothesized that first-episode psychosis patients who progress to schizophrenia after one year of follow up will display greater volumetric and morphological changes from the very beginning of the disorder. METHODS: We studied the hippocampus of 41 patients with a first-episode psychosis and 41 matched healthy controls. MRI was performed at the time of the inclusion in the study. After one year, the whole sample was reevaluated and divided in two groups depending on the diagnoses (schizophrenia vs. non-schizophrenia). RESULTS: Patients who progressed to schizophrenia showed a significantly smaller left hippocampus volume than control group and no-schizophrenia group (F=3.54; df=2, 77; P=0.03). We also found significant differences in the morphology of the anterior hippocampus (CA1) of patients with first-episode psychosis who developed schizophrenia compared with patients who did not. CONCLUSIONS: These results are consistent with the assumption of hyperfunctioning dopaminergic cortico-subcortical circuits in schizophrenia, which might be related with an alteration of subcortical structures, such as the hippocampus, along the course of the disease. According with these results, hippocampus abnormalities may serve as a prognostic marker of clinical outcome in patients with a first-episode psychosis.

Randomized control trial to assess the efficacy of metacognitive training compared with a psycho-educational group in people with a recent-onset psychosis.

BACKGROUND: Aims were to assess the efficacy of metacognitive training (MCT) in people with a recent onset of psychosis in terms of symptoms as a primary outcome and metacognitive variables as a secondary outcome. METHOD: A multicenter, randomized, controlled clinical trial was performed. A total of 126 patients were randomized to an MCT or a psycho-educational intervention with cognitive-behavioral elements. The sample was composed of people with a recent onset of psychosis, recruited from nine public centers in Spain. The treatment consisted of eight weekly sessions for both groups. Patients were assessed at three time-points: baseline, post-treatment, and at 6 months follow-up. The evaluator was blinded to the condition of the patient. Symptoms were assessed with the PANSS and metacognition was assessed with a battery of questionnaires of cognitive biases and social cognition. RESULTS: Both MCT and psycho-educational groups had improved symptoms post-treatment and at follow-up, with greater improvements in the MCT group. The MCT group was superior to the psycho-educational group on the Beck Cognitive Insight Scale (BCIS) total (p = 0.026) and self-certainty (p = 0.035) and dependence self-subscale of irrational beliefs, comparing baseline and post-treatment. Moreover, comparing baseline and follow-up, the MCT group was better than the psycho-educational group in self-reflectiveness on the BCIS (p = 0.047), total BCIS (p = 0.045), and intolerance to frustration (p = 0.014). Jumping to Conclusions (JTC) improved more in the MCT group than the psycho-educational group (p = 0.021). Regarding the comparison within each group, Theory of Mind (ToM), Personalizing Bias, and other subscales of irrational beliefs improved in the MCT group but not the psycho-educational group (p < 0.001-0.032). CONCLUSIONS: MCT could be an effective psychological intervention for people with recent onset of psychosis in order to improve cognitive insight, JTC, and tolerance to frustration. It seems that MCT could be useful to improve symptoms, ToM, and personalizing bias.

Daytime Ayahuasca administration modulates REM and slow-wave sleep in healthy volunteers.

OBJECTIVES: Ayahuasca is a traditional South American psychoactive beverage and the central sacrament of Brazilian-based religious groups, with followers in Europe and the United States. The tea contains the psychedelic indole N,N-dimethyltryptamine (DMT) and beta-carboline alkaloids with monoamine oxidase-inhibiting properties that render DMT orally active. DMT interacts with serotonergic neurotransmission acting as a partial agonist at 5-HT(1A) and 5-HT(2A/2C) receptor sites. Given the role played by serotonin in the regulation of the sleep/wake cycle, we investigated the effects of daytime ayahuasca consumption in sleep parameters. MEASUREMENTS AND RESULTS: Subjective sleep quality, polysomnography (PSG), and spectral analysis were assessed in a group of 22 healthy male volunteers after the administration of a placebo, an ayahuasca dose equivalent to 1 mg DMT kg(-1) body weight, and 20 mg d-amphetamine, a proaminergic drug, as a positive control. Results show that ayahuasca did not induce any subjectively perceived deterioration of sleep quality or PSG-measured disruptions of sleep initiation or maintenance, in contrast with d-amphetamine, which delayed sleep initiation, disrupted sleep maintenance, induced a predominance of 'light' vs 'deep' sleep and significantly impaired subjective sleep quality. PSG analysis also showed that similarly to d-amphetamine, ayahuasca inhibits rapid eye movement (REM) sleep, decreasing its duration, both in absolute values and as a percentage of total sleep time, and shows a trend increase in its onset latency. Spectral analysis showed that d-amphetamine and ayahuasca increased power in the high frequency range, mainly during stage 2. Remarkably, whereas slow-wave sleep (SWS) power in the first night cycle, an indicator of sleep pressure, was decreased by d-amphetamine, ayahuasca enhanced power in this frequency band. CONCLUSIONS: Results show that daytime serotonergic psychedelic drug administration leads to measurable changes in PSG and sleep power spectrum and suggest an interaction between these drugs and brain circuits modulating REM and SWS.

Fármacos que pueden producir somnolencia excesiva / Drugs promoting excessive sleepiness

La somnolencia es un acontecimiento frecuente y fisiológico en ciertas circunstancias. La somnolencia excesiva durante el día se caracteriza por una sensación anormal de sueño con fuerte tendencia a dormirse en situaciones o momentos inapropiados, que debe diferenciarse de la fatiga. Entre las posibles causas de una somnolencia excesiva diurna está el consumo de fármacos. Hay dos posibilidades por las que los fármacos pueden considerarse como agentes etiológicos: a) a través de un mecanismo indirecto (compuestos que alteran la cantidad y la calidad del sueño y condicionan su fragmentación o deprivación) o b) por un efecto directo que propicia de forma mediada un aumento de la somnolencia diurna. Este favorecimiento de la somnolencia diurna debería identificarse como reacción adversa. Se describen los nuevos términos que la investigación de los mecanismos implicados en el control de la sucesión de sueño-vigilia está introduciendo en la farmacología de los fármacos productores de sueño: hipnóticos, promotores del sueño, intensificadores del sueño, modificadores de la biestabilidad y cronobióticos. Se identifican los factores farmacocinéticos que principalmente determinan la duración del efecto hipnótico tras administración única (volumen de distribución) y tras administración múltiple (eliminación) y se expone la importante variación interindividual en la frecuencia e intensidad con que los fármacos inducen una somnolencia excesiva. Por último, se completa la visión del posible impacto de los fármacos sobre el ciclo sueño-vigilia refiriendo los posibles efectos durante la noche de los fármacos tomados por la mañana, enfatizando la importancia de considerar el proceso como un todo continuo y no como compartimentos estancos (AU)

In certain circumstances sleepiness is a frequent and physiological event. Excessive daytime sleepiness is characterized by an abnormal sleep sensation with a strong tendency to fall asleep in inappropriate situations and time moments, which should be differentiated from fatigue. Among the possible causes of excessive daytime sleepiness there is drug consumption. There are two different possibilities to consider drugs as etiological agents: a)thought an indirect mechanism (compounds disrupting sleep quantity and quality resulting in sleep fragmentation or deprivation) or b) by a straight effect directly promoting an increase of daytime sleepiness. This promotion of daytime sleepiness should be identified as an adverse reaction. The new terms that research on the mechanisms which control the wake-sleep cycle is introducing in the pharmacology of drugs favouring sleep are described: hypnotics, sleep promoters, sleep enhancers, bi-stability modifiers and chronobiotics. The pharm acokinetic factors which mainly determine the duration of the hypnotic effects are identified, either after a single administration (volume of distribution) or after a repetitive administration (elimination) and the important interindividual variation in frequency and intensity of drug induced excessive sleepiness is explained. Lastly, the description of the potential drug impact on the wake-sleep cycle is completed by referring thee ventual effects that drug ingestion at morning time could induce during the night, highlighting the importance to consider the process as a continuum non-compartmental one (AU)

Effects of tobacco smoking on the kinetics of the pupillary light reflex: a comparison between smokers and non-smokers.

BACKGROUND: The time course of the pupillary light reflex (PLR) is determined by the successive activation of parasympathetic and sympathetic innervations of the iris, latency and amplitude reflecting parasympathetic activity and recovery time showing mainly sympathetic activity. OBJECTIVE: To determine the effects of tobacco cigarette smoking on the PLR in smokers after an abstinence period of at least 12 h. METHODS: Ten smokers (mean 15.7 cigarettes/day) and 10 non-smokers participated in a randomised, non-intervention controlled, cross-over study that included a parallel control group. Smokers underwent two sessions with a time interval between 3 and 8 days; two recordings were taken at each session, separated by 20 min: session 1, without smoking, and session 2, smoking 3 cigarettes within a 30-min period. Non-smokers underwent one session; two recordings were taken separated by 20 min. At each recording, in both groups, PLR was elicited with four light flashes of increasing luminance. RESULTS: The relationship between PLR parameters and light intensity was linear in each subject. The slope of the regression line for relative amplitude increase versus intensity was significantly flatter in abstinent smokers than in non-smokers (p=0.033); the slope returned significantly after smoking (p=0.043). No other significant effects were obtained. CONCLUSIONS: Kinetic parameters of PLR provide a sensitive pharmacological test to detect cholinergic neurotransmission manipulation effects, as they seem to detect changes in moderate smokers after 12 h of abstinence, and their reversal on return to smoking. These results suggest an enhancement in the suppression of the parasympathetic oculomotor reflex arc rather than a facilitation of the sympathetic drive to the iris.