The relationship between irritability as a subjective experience and the behavioural indicators typically used to measure the construct are not known. Its links to mood, and contextual relationships, vary with age and are yet to be thoroughly examined.

First, to interrogate the relationship between the subjective experience of irritability and mood, and that with its behavioural indicators. Second, to determine how these relationships vary with age and over time.

This study examined data from a previous clinical trial of adolescents and young adults (N = 82) with bipolar disorder, who received a psychological intervention over 18 months. Participants completed a battery of questionnaires, which included assessments of irritability. Analyses of covariance were conducted to examine the interaction between mood symptoms, subjective measures of irritability, behavioural measures of irritability and age over time.

Subjective irritability scores differed significantly over time when controlling for manic, but not depressive, symptom scores. Further, subjective irritability significantly differed when controlling for behavioural measures of irritability (temper outbursts and argumentativeness). There were significant interactions between scores of depressive symptoms, temper outbursts and subjective irritability with age, wherein younger participants showed no correlation between depressive symptoms and temper outbursts. In addition, younger participants showed lower correlations between subjective irritability and both depressive and temper outburst scores, than older participants.

Subjective irritability is linked to mood morbidity and behavioural outbursts, and these relationships are contingent on age. Our novel findings suggest that subjective irritability should be assessed in greater detail in patients with mood disorders.

Emotional cognition and effective interpretation of affective information is an important factor in social interactions and everyday functioning, and difficulties in these areas may contribute to aetiology and maintenance of mental health conditions. In younger people with depression and anxiety, research suggests significant alterations in behavioural and brain activation aspects of emotion processing, with a tendency to appraise neutral stimuli as negative and attend preferentially to negative stimuli. However, in ageing, research suggests that emotion processing becomes subject to a ‘positivity effect’, whereby older people attend more to positive than negative stimuli.

This review examines data from studies of emotion processing in Late-Life Depression and Late-Life Anxiety to attempt to understand the significance of emotion processing variations in these conditions, and their interaction with changes in emotion processing that occur with ageing.

We conducted a systematic review following PRISMA guidelines. Articles that used an emotion-based processing task, examined older persons with depression or an anxiety disorder and included a healthy control group were included.

In Late-Life Depression, there is little consistent behavioural evidence of impaired emotion processing, but there is evidence of altered brain circuitry during these processes. In Late-Life Anxiety and Post-Traumatic Stress disorder, there is evidence of interference with processing of negative or threat-related words.

How these findings fit with the positivity bias of ageing is not clear. Future research is required in larger groups, further examining the interaction between illness and age and the significance of age at disease onset.

Cognitive impairment is a core feature of depression and has a negative effect on a person's functioning, in psychosocial and interpersonal areas, and on workforce performance. Cognitive impairment often persists, even with the remittance of mood symptoms. One potential way of improving treatment of cognitive impairment would be to identify variables that predict cognitive change in patients with depression.

To systematically examine findings from studies that investigate baseline variables and how they predict, or correlate with, cognitive change in mood disorders, and to examine methodological issues from these studies.

Studies that directly measured associations between at least one baseline variable and change in cognitive outcome in patients with current major depressive episode were identified using PubMed and Web of Science databases. Narrative review technique was used because of the heterogeneity of patient samples, outcome measures and study procedures. The review was registered on PROSPERO with registration number CRD42020150975.

Twenty-four studies met the inclusion criteria. Evidence from the present review for prediction of cognitive change from baseline variables was limited for demographic factors, with some preliminary evidence for depression, cognitive and biological factors. Identification of patterns across studies was difficult because of methodological variability across studies.

Findings from the present review suggest there may be some baseline variables that are useful in predicting cognitive change in mood disorders. This is an area warranting further research focus.

Cognitive impairment is considered a core feature of major depressive disorder (MDD) and research into psychological treatments aiming to address cognitive impairment are gaining momentum. Compared with the well-established research base of cognitive treatment trials in schizophrenia, including meta-analyses, mood disorder research is much more preliminary.

To focus on identifying the important factors to consider in developing larger-scale psychological treatment trials targeting cognitive impairment in mood disorders. Trial design recommendations have been published for cognitive treatment trials in bipolar disorder.

An in-depth discussion of methodological considerations in the development of cognitive treatment trials for MDD.

Methodological considerations include: screening for, and defining, cognitive impairment; mood state when cognitive intervention begins; medication monitoring during cognitive interventions; use of concomitant therapy; level of therapist involvement; duration and dose of treatment; choice of specific cognitive training exercises; home practice; improving adherence; appropriate comparison therapies in clinical trials; and choice of primary outcomes.

As well as guidance for clinical trial development, this review may be helpful for clinicians wanting to provide cognitive interventions for individuals with MDD.

Electroconvulsive therapy (ECT) is recommended in treatment guidelines as an efficacious therapy for treatment-resistant depression. However, it has been associated with loss of autobiographical memory and short-term reduction in new learning.

To provide clinically useful guidelines to aid clinicians in informing patients regarding the cognitive side-effects of ECT and in monitoring these during a course of ECT, using complex data.

A Committee of clinical and academic experts from Australia and New Zealand met to the discuss the key issues pertaining to ECT and cognitive side-effects. Evidence regarding cognitive side-effects was reviewed, as was the limited evidence regarding how to monitor them. Both issues were supplemented by the clinical experience of the authors.

Meta-analyses suggest that new learning is impaired immediately following ECT but that group mean scores return at least to baseline by 14 days after ECT. Other cognitive functions are generally unaffected. However, the finding of a mean score that is not reduced from baseline cannot be taken to indicate that impairment, particularly of new learning, cannot occur in individuals, particularly those who are at greater risk. Therefore, monitoring is still important. Evidence suggests that ECT does cause deficits in autobiographical memory. The evidence for schedules of testing to monitor cognitive side-effects is currently limited. We therefore make practical recommendations based on clinical experience.

Despite modern ECT techniques, cognitive side-effects remain an important issue, although their nature and degree remains to be clarified fully. In these circumstances it is useful for clinicians to have guidance regarding what to tell patients and how to monitor these side-effects clinically.

The Treatment Algorithm Group (TAG) was supported logistically by Servier who provided financial assistance with travel and accommodation for those TAG members travelling interstate or overseas to attend the meeting in Sydney (held on 18 November 2017). None of the committee were paid to participate in this project and Servier have not had any input into the content, format or outputs from this project.

Studies using acute tryptophan depletion (ATD) to examine the effects of a rapid reduction in serotonin function have shown a reduction in global cognitive status during ATD in Alzheimer's disease (AD) and Parkinson's disease (PD). Based on the severe cholinergic loss evident in dementia with Lewy bodies (DLB) and Parkinson's disease and dementia (PDD), we predicted that a reduction of global cognitive status during ATD would be greater in these conditions than in AD.

Patients having DLB or PDD underwent ATD in a double-blind, placebo-controlled, randomized, counterbalanced, crossover design.

While the study intended to test 20 patients, the protocol was poorly tolerated and terminated after six patients attempted, but only four patients – three with DLB and one with PDD – completed the protocol. The Modified Mini-Mental State Examination (3MSE) score was reduced in all three DLB patients and unchanged in the PDD and dementia patient during ATD compared with placebo.

This reduction in global cognitive function and the poor tolerability may fit with the hypothesis that people with dementia with Lewy bodies have sensitivity to the effects of reduced serotonin function.

Impaired neuropsychological function and differences in facial emotion processing are features of major depression. Some aspects of these functions may change during treatment and may be useful in assessing treatment response, even at an early stage of treatment.

To examine early and later changes in neuropsychological functioning and facial emotion processing as potential markers of treatment response in major depression.

In total, 68 newly admitted in-patients with a primary diagnosis of major depression and 50 healthy controls completed an assessment, including mood ratings, neuropsychological measures and facial emotion processing measures at three time points (baseline, 10–14 days and 6 weeks).

Pervasive neuropsychological impairment was evident at baseline in patients with depression compared with healthy controls. During 6 weeks of treatment, only simple reaction time, verbal working memory and the recognition of angry facial expressions showed differential change in those whose depression responded to treatment compared with treatment non-responders in the depression group. None of the measures showed a significant difference between treatment responders and non-responders at 10–14 days.

Despite significant impairment in neuropsychological functioning in the depression group, most measures failed to differentiate between treatment responders and non-responders at 10–14 days or at 6 weeks. Simple reaction time, verbal working memory and recognition of angry facial expressions may be useful in assessing response in severe depression but probably not at an early stage.

Facial emotion processing was examined in patients with severe depression (n = 68) and a healthy control group (n = 50), using the Facial Expression Recognition Task. A negative interpretation bias was observed in the depression group: neutral faces were more likely to be interpreted as sad and less likely to be interpreted as happy, compared with controls. The depression group also displayed a specific deficit in the recognition of facial expressions of disgust, compared with controls. This may relate to impaired functioning of frontostriatal structures, particularly the basal ganglia.