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This prospective study sought to characterise the educational experiences, mental health, and behavioural functioning of Australian children with a pre-existing learning difficulty or specific learning disorder (SLD) during the COVID-19 pandemic. The study also evaluated the potential role of parent psychological distress as a risk factor for poorer child functioning in this high-risk population. Using a prospective longitudinal design, the study involved 58 parents of children and adolescents with a pre-existing learning difficulty or specific learning disorder (M age = 11.9 years; range 7–17 years) who were initially referred to a state-wide diagnostic centre for specific learning disorders in Melbourne, Victoria, Australia. Child outcomes were assessed using the COVID-19 Wellbeing and Mental Health Survey (a modified version of the CoRonavIruS Health Impact Survey [CRISIS] tool), the Strengths and Difficulties Questionnaire (SDQ), and the Emotional Distress Scale from the Patient-Reported Outcomes Measurement Information System (PROMIS). Parents’ mental health was assessed using the CRISIS tool and the Kessler Psychological Distress Scale (K10). In keeping with initial predictions, a large proportion of parents expressed significant disruption to child educational experience and routines, including challenges related to child engagement in remote learning platforms during COVID-19. Compared to pre-pandemic mental health symptom ratings, children experienced significantly higher symptoms of worry, negative thoughts, loneliness, agitation, and aggression during the pandemic period (all p < 0.05). As expected, higher levels of parent distress predicted greater child worry symptoms (p = 0.003) and more frequent child behavioural difficulties (p = 0.004). These results help elucidate the specific psychological and educational challenges faced by children with pre-existing learning difficulty or SLD during the COVID-19 pandemic. Family-centred intervention and/or supports may help to address the unique educational and psychological needs of young people with pre-existing learning differences and their families during future global pandemics.

Deficits in memory performance have been linked to a wide range of neurological and neuropsychiatric conditions. While many studies have assessed the memory impacts of individual conditions, this study considers a broader perspective by evaluating how memory recall is differentially associated with nine common neuropsychiatric conditions using data drawn from 55 international studies, aggregating 15,883 unique participants aged 15–90. The effects of dementia, mild cognitive impairment, Parkinson’s disease, traumatic brain injury, stroke, depression, attention-deficit/hyperactivity disorder (ADHD), schizophrenia, and bipolar disorder on immediate, short-, and long-delay verbal learning and memory (VLM) scores were estimated relative to matched healthy individuals. Random forest models identified age, years of education, and site as important VLM covariates. A Bayesian harmonization approach was used to isolate and remove site effects. Regression estimated the adjusted association of each clinical group with VLM scores. Memory deficits were strongly associated with dementia and schizophrenia (p < 0.001), while neither depression nor ADHD showed consistent associations with VLM scores (p > 0.05). Differences associated with clinical conditions were larger for longer delayed recall duration items. By comparing VLM across clinical conditions, this study provides a foundation for enhanced diagnostic precision and offers new insights into disease management of comorbid disorders.

Despite evidence of a link between childhood TBI and heightened risk for depressive symptoms, very few studies have examined early risk factors that predict the presence and severity of post-injury depression beyond 1-year post injury. This longitudinal prospective study examined the effect of mild-severe childhood TBI on depressive symptom severity at 2-years post-injury. It also evaluated the potential role of sub-acute brain morphometry and executive function (EF) in prospectively predicting these long-term outcomes. The study involved 81 children and adolescents with TBI, and 40 age-and-sex matched typically developing (TD) controls. Participants underwent high-resolution structural magnetic resonance imaging (MRI) sub-acutely at five weeks post-injury (M = 5.55; SD = 3.05 weeks) and EF assessments were completed at 6-months post-injury. Compared to TD controls, the TBI group had significantly higher overall internalizing symptoms and were significantly more likely to exhibit clinically significant depressive symptoms at 2-year follow-up. The TBI group also displayed significantly lower EF and altered sub-acute brain morphometry in EF-related brain networks, including the default-mode network (DMN), salience network (SN) and central executive network (CEN). Mediation analyses revealed significant indirect effects of CEN morphometry on depression symptom severity, such that lower EF mediated the prospective association between altered CEN morphometry and higher depression symptoms in the TBI group. Parallel mediation analyses including grey matter morphometry of a non-EF brain network (i.e., the mentalising network) were not statistically significant, suggesting some model specificity. The findings indicate that screening for early neurostructural and neurocognitive risk factors may help identify children at elevated risk of depressive symptoms following TBI. For instance, children at greatest risk of post-injury depression symptoms could be identified based in part on neuroimaging of networks implicated in EF and post-acute assessments of executive function, which could support more effective allocation of limited intervention resources.

Objectives. Behavioural and psychological symptoms of dementia (BPSD) cause significant distress to both aged care residents and staff. Despite the high prevalence of BPSD in progressive neurological diseases (PNDs) such as multiple sclerosis, Huntington’s disease, and Parkinson’s disease, the utility of a structured clinical protocol for reducing BPSD has not been systematically evaluated in PND populations. Method. Staff (n=51) and individuals with a diagnosis of PND (n=13) were recruited into the study, which aimed to evaluate the efficacy of a PND-specific structured clinical protocol for reducing the impact of BPSD in residential aged care (RAC) and specialist disability accommodation (SDA) facilities. Staff were trained in the clinical protocol through face-to-face workshops, which were followed by 9 weeks of intensive clinical supervision to a subset of staff (“behaviour champions”). Staff and resident outcome measures were administered preintervention and immediately following the intervention. The primary outcome was frequency and severity of BPSD, measured using the Neuropsychiatric Inventory-Nursing Home Version (NPI-NH). The secondary outcome was staff coping assessed using the Strain in Dementia Care Scale (SDCS). Results. In SDA, significant reductions in staff ratings of job-related stress were observed alongside a statistically significant decrease in BPSD from T1 to T2. In RAC, there was no significant time effect for BPSD or staff coping; however, a medium effect size was observed for staff job stress. Conclusions. Staff training and clinical support in the use of a structured clinical protocol for managing BPSD were linked to reductions in staff job stress, which may in turn increase staff capacity to identify indicators of resident distress and respond accordingly. Site variation in outcomes may relate to organisational and workforce-level barriers that may be unique to the RAC context and should be systematically addressed in future RCT studies of larger PND samples.