Australian & New Zealand Journal of Psychiatry

Neurocognitive impairment is considered a core feature of mood disorders. Research has shown that neurocognitive impairment often persists beyond mood symptom resolution and can have significant deleterious effects on interpersonal relationships, academic achievement, occupational functioning and independent living. As such, neurocognitive impairment has become an important target for intervention. In this systematic review, we aimed to examine the extant literature to ascertain whether current standard evidence-based psychotherapies can improve neurocognitive functioning in mood disorders.

Studies examining changes in neurocognitive functioning following evidence-based psychotherapy were identified using MEDLINE, PsycINFO and Web of Science databases. Given the heterogeneity of study procedures, treatment protocols and patient samples, a narrative rather than meta-analytic review technique was employed.

Nineteen studies (21 articles) met inclusion criteria. There was preliminary evidence of improved executive functioning following evidence-based psychotherapy for Major Depressive Disorder and Bipolar Disorder. There was also some signal of reduced negative biases in emotional information processing following psychotherapy in depression. Due to methodological variability across studies however, it was difficult to draw clear conclusions.

Findings from the current review suggest that evidence-based psychotherapies may influence some aspects of neurocognitive functioning in mood disorders. This continues to be an ongoing area of importance and warrants further research.

This study investigates (1) the proportion of people with psychosis who are on long-acting injectable antipsychotics; (2) the difference in the demographic, clinical, substance use and adverse drug reaction profiles of people taking long-acting injectables compared to oral antipsychotics; and (3) the differences in the same profiles of those on first-generation antipsychotic versus second-generation antipsychotic long-acting injectables.

Data were collected as part of the Survey of High Impact Psychosis. For this study, participants with diagnoses of schizophrenia or schizoaffective disorder who were on any antipsychotic medication were included (N = 1049).

Nearly a third (31.5%) of people with psychosis were on long-acting injectables, of whom 49.7% were on first-generation antipsychotic long-acting injectables and 47.9% were on second-generation antipsychotic long-acting injectables. This contrasts with oral antipsychotics where there was a higher utilisation of second-generation antipsychotics (86.3%). Of note, compared to those on the oral formulation, people on long-acting injectables were almost four times more likely to be under a community treatment order. Furthermore, people on long-acting injectables were more likely to have a longer duration of illness, reduced degree of insight, increased cognitive impairment as well as poor personal and social functioning. They also reported more adverse drug reactions. Compared to those on first-generation antipsychotic long-acting injectables, people on SGA long-acting injectables were younger and had had a shorter duration of illness. They were also more likely to experience dizziness and increased weight, but less likely to experience muscle stiffness or tenseness.

Long-acting injectable use in Australia is associated with higher rates of community treatment order use, as well as poorer insight, personal and social performance, and greater cognitive impairment. While long-acting injectables may have the potential to improve the prognosis of people with psychosis, a better understanding of the choices behind the utilisation of long-acting injectable treatment in Australia is urgently needed.

Medication cessation and service disengagement often precedes relapse in people with severe mental illnesses but currently specialist mental health services only become involved after a relapse. Early detection of non-adherence is needed to enable intervention to avert relapse. This paper aims to demonstrate how digitally automated non-adherence risk monitoring from Medicare data with active follow-up can work and perform in practice in a real-world mental health service setting.

AI² software is an automated risk monitoring tool to detect non-adherence using Medicare data. It was implemented prospectively in a cohort of 354 registered patients of a community mental health clinic between July 2019 and February 2020. Patients flagged as at risk by the software were reviewed by two clinicians. We describe the risks automatically flagged for non-adherence and the clinical responses. We examine differences in clinical and demographic factors in patients flagged at increased risk of non-adherence.

In total, 46.7% (142/304) were flagged by the software as at risk of non-adherence, and 22% (31/142) received an intervention following clinician review of their case notes. Patients flagged by the software were older in age and had more prior mental health treatment episodes. More alerts were associated with patients who had been transferred from the mental health service to the care of their general practitioners, and those with more alerts were more likely to receive a follow-up intervention.

Digitally automated monitoring for non-adherence risk is feasible and can be integrated into clinical workflows in community psychiatric and primary care settings. The technology may assist clinicians and services to detect non-adherence behaviour early, thereby triggering interventions that have the potential to reduce rates of mental health deterioration and acute illness relapse.

Subjective quality of life is an important outcome of psychotic disorders. However, longitudinal course of subjective quality of life in the early illness stage is under-studied. We aimed to investigate the patterns and baseline predictors of subjective quality of life trajectories over 3 years in early psychosis patients, utilizing growth mixing modeling analysis, in the context of a 3-year follow-up of a randomized controlled trial comparing 1-year extension of early intervention with step-down psychiatric care for first-episode psychosis.

One hundred sixty Chinese patients were recruited from specialized early intervention program for first-episode psychosis in Hong Kong after they had completed this 2-year early intervention service, and underwent 1-year randomized controlled trial as well as 2-year post–randomized controlled trial follow-up (i.e. 3-year follow-up). Assessments on premorbid adjustment, onset profile, psychopathology, functioning and treatment characteristics were conducted. Individual class membership of subjective quality of life trajectory derived from growth mixing modeling was based on the 36-Item Short Form Health Survey mental component summary scores measured at four different time-points (baseline, 1, 2 and 3 years) among 142 participants across 3-year follow-up.

Three distinct subjective quality of life trajectories were identified including higher-improving (68.3%, n = 97), lower-stable (24.6%, n = 35) and deteriorating (7%, n = 10) trajectories. Age of onset; duration of untreated psychosis; depressive, positive and negative symptoms; and intervention condition were significantly different between good (higher-improving trajectory) and poor (combined lower-stable and deteriorating trajectories) trajectory groups. Multiple regression analysis revealed that younger age of onset, more severe depression and receipt of step-down care independently predicted poor subjective quality of life trajectory.

Approximately one-third of patients displayed poor subjective quality of life trajectory in the early phase of psychotic illness. Our results affirm depression as a critical determinant of prospective subjective quality of life and underscores positive effect of extended early intervention on sustained subjective quality of life improvement. Further longitudinal research is warranted to facilitate better characterization of subjective quality of life course patterns and development of targeted intervention to optimize subjective quality of life in patients with early psychosis.

Catatonia can be life-threatening unless timely identified and treated. Lorazepam’s ubiquitous response has led to its universal acceptance as being the first-line management of catatonia and alludes to catatonia’s neurobiological underpinnings. Lorazepam challenge test (LCT) is widely used to either confirm a catatonia diagnosis or determine lorazepam sensitivity. It has a proposed schedule for administering lorazepam. However, efficacy of recommended LCT doses lack systematic evidence, resulting in variable LCT doses used in clinical and research settings contributing to findings that are challenging to generalize or assist with developing standardized lorazepam treatment protocols for catatonia. Given the same, this study aimed to objectively compare the response between two groups receiving different LCT doses and factors influencing the same.

The 6-month study in a psychiatric emergency setting at a tertiary neuropsychiatric center in India evaluated 57 catatonia patients, before and after administration of single 2 mg (n = 37; LCT-2) or 4 mg (n = 20; LCT-4) lorazepam dose, applying Bush Francis Catatonia Rating Scale (BFCRS), Mini International Neuropsychiatric Interview (MINI 5.0) and obtaining sociodemographic, clinical data.

No between-group differences (LCT-2 vs LCT-4) for sociodemographic, clinical profiles or BFCRS severity score changes to lorazepam on Mann–Whitney U test were noted. Applying Wilcoxon signed rank test comparing individual sign severity demonstrated response variability, with significant response noted to both doses (stupor, mutism, staring, posturing, withdrawal, ambitendency, automatic obedience) and others selectively to 2 mg (echolalia, rigidity, negativism, mitgehen). Notably, sign resolution (present/absent) only to 2 mg was significant for stupor, mutism, staring, posturing, echolalia, rigidity, negativism and mitgehen.

This study suggests 2 mg lorazepam may be an optimal LCT dose, given significant response to most catatonic signs thereby ensuring accurate detection and preventing misinterpretation of response. It offers future studies direction for standardizing lorazepam dosing schedules for catatonia management and exploring neurobiological underpinnings for individual catatonic signs that may be potentially different, given these findings.

Neurocognitive dysfunction is a common feature of bipolar disorder even in euthymia, and psychopharmacological treatment could have an effect on cognition. Long-term prescription of benzodiazepines in bipolar disorder is a common practice, and their effect on neurocognition has not been well studied in this population. The aim of this study was to evaluate the impact of concomitant benzodiazepine long-term use on neurocognitive function in stable euthymic bipolar disorder patients.

Seventy-three euthymic bipolar disorder outpatients and 40 healthy individuals were assessed using a neurocognitive battery. Patients were classified in two groups according to the presence of benzodiazepines in their treatment: the benzodiazepine group (n = 34) and the non- benzodiazepine group (n = 39). Neurocognitive performance was compared between the groups using a multivariate analysis of covariance, considering age, number of depressive episodes, adjuvant antipsychotic drugs, Young Mania Rating Scale score and Hamilton Depression Rating Scale score as covariates.

Both bipolar disorder groups (benzodiazepine and non-benzodiazepine) showed an impairment in memory domains (Immediate Visual Memory [p = 0.013], Working Memory [p < 0.001], and Letter-Number Sequence [p < 0.001] from the Wechsler Memory Scale-Revised-III) and slower processing speed functions (Stroop Colour [p < 0.001]) relative to the control group. Nevertheless, the benzodiazepine group showed a greater impairment in executive functions (Conceptual Level Responses [p = 0.024] from the Wisconsin Card Sorting Test and Frontal Assessment Battery [p = 0.042]).

Although memory and processing speed impairments were found in bipolar disorder, regardless of their benzodiazepine treatment, benzodiazepine users presented additional neurocognitive impairments in terms of executive functioning. These findings support restricted prescription of benzodiazepines in individuals with bipolar disorder.