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Background: Major depressive disorder (MDD) commonly co-occurs with clinically significant levels of anxiety. However, anxiety symptoms are varied and have been inconsistently associated with clinical, functional, and antidepressant treatment outcomes. We aimed to identify and characterise dimensions of anxiety in people with MDD and their use in predicting antidepressant treatment outcome. Method: 1008 adults with a current diagnosis of single-episode or recurrent, nonpsychotic, MDD were assessed at baseline on clinical features and cognitive/physiological functioning. Participants were then randomised to one of three commonly prescribed antidepressants and reassessed at 8 weeks regarding symptom change, as well as remission and response, on the 17-item Hamilton Rating Scale Depression (HRSD17) and the 16-item Quick Inventory of Depressive Symptomatology (QIDS-SR16). Exploratory factor analysis was used on items from scales assessing anxiety symptoms, and resulting factors were assessed against clinical features and cognitive/physiological functioning. Factors were also assessed on their ability to predict treatment outcome. Results: Three factors emerged relating to stress, cognitive anxiety, and somatic anxiety. All factors showed high internal consistency, minimal cross-loadings, and unique clinical and functional profiles. Furthermore, only higher somatic anxiety was associated with poorer QIDS-SR16 remission, even after adjusting for covariates and multiple comparisons. Conclusions: Anxiety symptoms in people with MDD can be separated onto distinct factors that differentially respond to treatment outcome. Furthermore, these factors do not align with subscales of established measures of anxiety. Future research should consider cognitive and somatic symptoms of anxiety separately when assessing anxiety in MDD and their use in predicting treatment outcome. [ABSTRACT FROM AUTHOR]

Objectives: Schizophrenia is a debilitating psychiatric illness associated with positive and negative symptoms as well as significant impairments in cognition. Current antipsychotic medications do not alleviate these cognitive deficits, and more effective therapeutic options are required. Increased oxidative stress and altered antioxidant levels, including glutathione (GSH) have been observed both in individuals with cognitive impairment and in people with schizophrenia. A GSH precursor, the antioxidant N-acetylcysteine (NAC) has been investigated as a novel treatment for the cognitive symptoms of schizophrenia, and recent research suggests that NAC may be a promising adjunctive treatment option. However, the current literature lacks integration as to why NAC may effectively improve cognition in schizophrenia. The present theoretical synthesis aimed to address this gap by examining the processes by which NAC may improve cognitive function in schizophrenia. Methods: The schizophrenia literature was reviewed in three key domains: cognitive impairment, the relationship between oxidative stress and cognition, and the efficacy of NAC as a novel treatment. This led to a theoretical analysis of the neurobiological processes by which NAC may improve cognition in schizophrenia. Results: This theoretical review concluded that improved cognition may result from a combination of factors, including decreased oxidative stress, neuroprotection of cognitive networks and an increase in glutamatergic modulation of the N-methyl-d-aspartate receptor system. Whilst a number of mechanisms by which NAC may improve cognition and symptoms in schizophrenia have been proposed, there is still limited understanding of the specific metabolic pathways involved and how they interrelate and modify specific symptomology. Discussion: Exploration of how NAC treatment may act to improve cognitive function could guide clinical trials by investigation of the specific neurotransmitter systems and processes involved, allowing for targeted neurological outcome measures. Future research would benefit from the investigation of both in vivo cortical GSH concentration and peripheral plasma GSH in a population of individuals with chronic schizophrenia. [ABSTRACT FROM AUTHOR]

Objective: Posttraumatic stress disorder and childhood trauma frequently co-occur. Both are associated with abnormal neural responses to salient emotion stimuli. As childhood trauma is a risk factor for posttraumatic stress disorder, differentiating between their neurophysiological effects is necessary to elucidate the neural pathways by which childhood trauma exposure contributes to increased posttraumatic stress disorder risks. Methods: Face-specific N170 evoked response potentials for backward-masked (non-conscious) and conscious threat (fear, angry) and non-threat (happy) faces were measured in 77 adults (18–64 years old, 64% women, 78% right-handed) symptomatic for posttraumatic stress disorder. Differences in N170 peak amplitudes for fear-versus-happy and angry-versus-happy faces at bilateral temporo-occipital (T5, T6) sites were computed. The effect of cumulative exposure to childhood interpersonal trauma, other childhood trauma, adult trauma, depression and posttraumatic stress disorder symptom severity on the N170 response was assessed using hierarchical multiple regression analyses. Results: T5 N170 peak amplitudes for non-conscious fear-versus-happy faces were inversely related to cumulative childhood interpersonal trauma after accounting for socio-demographic, clinical symptom and other trauma factors. Posttraumatic stress disorder Avoidance was positively associated with N170 peak amplitudes for non-conscious fear-versus-happy faces, primarily due to reduced N170 responsivity to happy faces. Conclusion: Childhood interpersonal trauma exposure is associated with reduced discrimination between fear and happy faces, while avoidance symptom severity is associated with dampened responsivity to automatically processed happy faces in posttraumatic stress disorder adults. Results are discussed in terms of the likely contributions of impaired threat discrimination and deficient reward processing during neural processing of salient emotion stimuli, to increased risks of posttraumatic stress disorder onset and chronicity in childhood interpersonal trauma–exposed adults. [ABSTRACT FROM AUTHOR]

Objectives: To compare clinical outcomes and adverse effects between Bitemporal (BT) and Right Unilateral Ultrabrief (RUL(UB)) electroconvulsive therapy (ECT) in an elderly population.Methods: Patients over the age of 65 years admitted to a tertiary referral hospital over a seven month period requiring ECT received RUL(UB) ECT. They were compared with those who received BT ECT over these and the preceding seven months.Results: Twenty-three patients entered the study. No significant differences was observed between the groups in demographic and clinical characteristics or clinical improvement. However, patients who received BT ECT were significantly more likely to be confused post treatment compared with the RUL(UB) group.Conclusions: This pilot study found RUL(UB) ECT to be an effective treatment in elderly patients. These patients also suffered significantly less confusion than patients who received BT ECT. [ABSTRACT FROM AUTHOR]

The diagnostic boundary between schizophrenia and bipolar disorder can be unclear, particularly with early onset. We assessed if emotion brain circuits differentiate psychosis versus mania symptoms in a series of six early onset patients. Symptoms were dissociated by direction, awareness condition, and brain regions. Greater psychosis symptoms were correlated with greater prefrontal, anterior cingulate, amygdala, and fusiform face area activation during masked fear processing. By contrast, greater mania symptoms were correlated with less amygdala activation during unmasked fear and happy processing. This suggests emotion dysfunction in schizophrenia versus bipolar disorder may arise from partially distinct neural mechanisms of susceptibility. [ABSTRACT FROM PUBLISHER]

Objective: To evaluate the efficacy, safety, and impact on hospitalizations of long-acting injectable paliperidone palmitate (PP) treatment, in patients with recent-onset schizophrenia who had not responded satisfactorily to oral antipsychotics. Methods: In this 18-month, open-label, Phase-IIIb study from Asia-Pacific region, patients (18-50 years) with recent-onset (⩽5 years) schizophrenia unsatisfactorily treated with previous oral antipsychotics were initiated on PP 150 mg eq on day 1, 100 mg eq on day 8, followed by flexible once monthly maintenance doses of 50-150 mg eq. The number and duration of hospitalizations were compared using a mirror analysis method between two periods: retrospective (12 months before PP initiation) and prospective (12 and 18 months after PP treatment) periods. Results: A total of 303 out of 521 (58%) patients (mean age, 28.7 years; 65.5% men, 92.5% Asian) completed the study. Positive and Negative Syndrome Scale (PANSS) total score improved significantly from baseline to month 18 (mean [standard deviation, SD] change: -11.3 [21.38], P<0.0001, primary endpoint). Subgroup analysis revealed greater improvements among patients with worse disease severity at baseline: PANSS ⩾70 versus <70 (mean [SD] change: -23.1 [24.62] vs -4.7 [15.98], P<0.0001 each). Secondary efficacy endpoints such as Clinical Global Impression of Schizophrenia (CGI-SCH), Medication Satisfaction Questionnaire (MSQ) scores showed significant improvements (P<0.0001) from baseline; 33.3% patients achieved symptom remission. In mirror analyses set (N=474), PP significantly (P<0.0001) reduced mean number of hospitalization days/person/year (12-month: 74.3 vs 19.7; 18-month: 74.3 vs 18.9) as well as percentage of patients requiring hospitalization in past 12 months (12-month: 39.7% vs 24.6%; 18-month: 39.7% vs 25%), and PP treatment increased the proportion of patients not requiring hospitalization (12-month: 60.3% vs 75.4%; 18-month: 60.3% vs 75%) from retrospective to prospective period. Adverse events (⩾15%) were extrapyramidal symptoms-related (31.3%), injection-site pain (18.6%), and insomnia (15.2%). Conclusion: PP was efficacious and generally tolerable with significant reductions observed in both number of hospitalizations and days spent in hospital. [ABSTRACT FROM AUTHOR]

Schizophrenia is characterized by deficits in face and facial emotion processing. This is the first study using event-related potentials (ERPs) to investigate the corresponding neural activation in first onset psychosis. ERPs for 108 first onset psychosis participants and 108 matched healthy controls were recorded while they viewed facial expressions. Group differences on general (neutral) face processing and emotional valence were examined under both unmasked (conscious) and backward-masked (nonconscious implicit) conditions over frontal and temporo-occipital regions. Clinical significance was assessed by comparing diagnoses and correlating ERPs with symptoms. During general face processing, patients showed reduced activation within 70 ms and exaggerated later processing from 160 ms over the frontal region, with a negative shift in voltage over left temporal and occipital regions across the time course. In addition, from 70 ms onwards, patients showed a positive shift in voltage for disgust whereas controls showed a negative shift in voltage for fear and anger (both compared to happy) over temporo-occipital regions. Effects were related to disorganization and depression symptoms and (preliminarily) were apparent across psychotic diagnoses. These results suggest that first onset psychosis is characterized by general as well as emotion-specific face processing impairments from the earliest, automatic processing period. [ABSTRACT FROM AUTHOR]

The article presents a research on psychotic disorders and premorbid functioning among children and adolescents. The article includes psychotic disorders like post-traumatic stress disorder (PTSD) with auditory hallucination symptoms, pervasive developmental disorder (PDD) and childhood-onset schizophrenia (COS). The article also includes study of schizophrenia spectrum disorders (SSD) and mood disorder (MD) and discusses treatment by paediatric mental health services.

Background: Schizophrenia may be understood as a disorder of neural synchrony. There is also increasing evidence that emotional and social cognitive impairments are central to this disorder. In patients with first-episode schizophrenia, we examined whether emotion perception is associated with disruptions to high-frequency (40 Hz) gamma synchrony and whether these disruptions predict selfregulatory adaptive compensations reflected in social cognitive behaviours. Methods: We obtained electroencephalography recordings from 28 patients with first-episode schizophrenia and matched healthy controls during perception of facial emotion under both conscious and nonconscious conditions. We extracted gamma-band synchrony from the electroencephalogram. We also used behavioural measures of emotion identification, emotional intelligence, negativity bias and social function, along with ratings of first-episode schizophrenia symptoms. We analyzed group differences and predicted social cognition to assess the potential contribution of medication. Results: Within 200 ms poststimulus, patients with first-episode schizophrenia showed alterations in gamma synchrony during both conscious and nonconscious emotion perception. Stimulus-locked synchrony was reduced in patients, particularly over the temporal cortex, whereas complementary enhancements in absolute gamma synchrony (independent of stimuli) were more distributed over temporal and left parieto-occipital regions. This pattern of altered synchrony predicted poor performance on each measure of social cognition among these patients. Medication dosage did not correlate significantly with either gamma synchrony or behavioural measures in this group. Limitations: Limitations to our study include the lack of comparison between medicated and unmedicated patients or between types of medication. Conclusion: These findings suggest that disruptions in integrative processing of motivationally important stimuli show promise as a potential biological marker of social cognitive impairments, present from the first episode of schizophrenia, and their outcomes. [ABSTRACT FROM AUTHOR]

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Objective: While schizophrenia has long been considered a disorder of brain connectivity, few studies have investigated white matter abnormalities in patients with first-episode schizophrenia, and even fewer studies have investigated whether there is progressive white matter pathology in the disease. Method: The authors obtained a Tiweighted structural magnetic resonance imaging (MRI) scan on 41 patients with first-episode schizophrenia. These first-episode schizophrenia patients were analyzed relative to 47 age- and sex-matched healthy comparison subjects who also underwent an MRI scan. Of the baseline participants, 25 first-episode schizophrenia patients and 26 comparison subjects returned 2 to 3 years later for a follow-up scan. To identify regional volumetric white matter differences between the two groups at baseline, voxel-based morphometry in statistical parametric mapping-2 (SPM2) was used, while tensorbased morphometry was used to identify the longitudinal changes over the follow-up interval. Results: The first-episode schizophrenia patients exhibited volumetric deficits in the white matter of the frontal and temporal lobes at baseline, as well as volumetric increases in the white matter of the frontoparietal junction bilaterally. Furthermore, these first-episode schizophrenia patients lost considerably more white matter over the follow-up interval relative to comparison subjects in the middle and inferior temporal cortex bilaterally. Conclusions: These results indicate that patients with schizophrenia exhibit white matter abnormalities at the time of their first presentation of psychotic symptoms to mental health services and that these abnormalities degenerate further over the initial years of illness. Given the role that white matter plays in neural communication, the authors suggest that these white matter abnormalities may be a cause of the dysfunctional neural connectivity that has been proposed to underlie the symptoms of schizophrenia. [ABSTRACT FROM AUTHOR]

Modelos diferentes convergen cuando describen la esquizofrenia como un síndrome de escisión que afecta, preferentemente, a la conectividad temporal de la actividad neural. La actividad sincrónica de la banda gamma (40 Hz) se ha considerado un posible mecanismo de unión de una actividad neural diseminada. Los autores creen que se trata del primer estudio que investiga la "sincronía gamma" en el primer episodio de esquizofrenia. Método: Cuarenta pacientes medicados por un primer episodio de esquizofrenia y 40 individuos sanos de control equiparados en edad y sexo participaron en un paradigma auditivo estándar "oddball. " La sincronía gamma, bloqueada temporalmente a los estímulos objeto de estudio, se extrajo de un EEG en curso. Se analizaron el alcance y la latencia de la sincronía inicial (gamma 1:-150 mseg a 150 mseg después del estímulo) y tardía (gamma2: 200-550 mseg después del estímulo) con un análisis de la varianza múltiple. Resultados: Los pacientes con un primer episodio de esquizofrenia mostraron una menor magnitud y una latencia retardada de la sincronía total gamma 1 en comparación con los individuos sanos de control. Por otro lado, no se observaron diferencias de grupo en la sincronía gamma 2. Conclusiones: Estos resultados indican que los pacientes con un primer episodio de esquizofrenia presentan una disminución general y una demora de la conectividad temporal de la actividad neural en la respuesta sensorial inicial a los estímulos que revisten interés para la prueba. Esto concuerda con las pruebas cognitivas que revelan la existencia de alteraciones de la integración perceptiva en este trastorno, sugiriendo la posibilidad de que la interrupción de la sincronía inicial entre las redes neurales diseminadas constituya un marcador del inicio de la esquizofrenia. [ABSTRACT FROM PUBLISHER]

Objective: There has been a convergence of models describing schizophrenia as a disconnection syndrome, with a focus on the temporal connectivity of neural activity. Synchronous gamma-band (40-Hz) activity has been implicated as a candidate mechanism for the binding of distributed neural activity. To the authors' knowledge, this is the first study to investigate "gamma synchrony" in first-episode schizophrenia. Method: Forty medicated first-episode schizophrenia patients and 40 age- and sex-matched healthy comparison subjects participated in a conventional auditory oddball paradigm. Gamma synchrony, time-locked to target stimuli, was extracted from an ongoing EEG. The magnitude and latency of both early (gamma 1: -150 msec to 150 msec poststimulus) and late (gamma 2: 200 to 550 msec poststimulus) synchrony were analyzed with multiple analysis of variance. Results: First-episode schizophrenia patients showed a decreased magnitude and delayed latency for global gamma 1 synchrony in relation to healthy comparison subjects. By contrast, there were no group differences in gamma 2 synchrony. Conclusions: These findings suggest that first-episode schizophrenia patients have a global decrease and delay of temporal connectivity of neural activity in early sensory response to task-relevant stimuli. This is consistent with cognitive evidence of perceptual integration deficits in this disorder and raises the possibility that a breakdown in the early synchrony of distributed neural networks is a marker for the onset of schizophrenia. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Supping with the devil? The dangers of liaisons between pharma and our profession," by P. Boyce and G. S. Malhi in a previous issue of the journal.