BACKGROUND: Young people in out-of-home care are more likely to experience poorer mental and physical health outcomes related to their peers. Stable care environments are essential for ameliorating impacts of disruptive early childhood experiences, including exposure to psychological trauma, abuse and neglect. At present there are very few high quality data regarding the placement stability history of young people in out-of-home care in Australia or other countries. OBJECTIVES: To undertake the first systematic census of background, care type and placement stability characteristics of young people living in the out-of-home care sector in Australia. METHODS: Data was collected from four non-government child and adolescent community service organisations located across metropolitan Melbourne in 2014. The sample comprised 322 young people (females 52.8%), aged between 12 - 17 years (mean age=14.86 [SD=1.63] years). RESULTS: Most young people (64.3%) were in home-based care settings (i.e., foster care, therapeutic foster care, adolescent care program, kinship care, and lead tenant care), relative to residential care (35.7%). However, the proportion in residential care is very high in this age group when compared with all children in out-of-home care (5%). Mean age of first removal was 9 years (SD=4.54). No gender differences were observed for care type characteristics. Three quarters of the sample (76.9%) had a lifetime history of more than one placement in the out-of-home care system, with more than a third (36.5%) having experienced ≥5 lifetime placements. Relative to home-based care, young people in residential care experienced significantly greater placement instability (χ2=63.018, p<0.001). CONCLUSIONS: Placement instability is common in the out-of-home care sector. Given stable care environments are required to ameliorate psychological trauma and health impacts associated with childhood maltreatment, well-designed intervention-based research is required to enable greater placement stability, including strengthening the therapeutic capacities of out-of-home carers of young people.

Arterial coronary grafts can be used in the majority of patients and have better patencies than saphenous vein grafts (SVGs), resulting in excellent perioperative and superior long-term outcomes. Barriers to their extensive use include potential for trauma and spasm, extra-operating time, unfamiliarity, concerns over hypoperfusion and deep sternal wound infection in patients in whom bilateral internal thoracic arteries are used-especially diabetics. This presentation addresses these concerns with particular attention to the radial artery, and skeletonized right internal thoracic artery harvest and construction of the proximal anastomoses of these grafts to the ascending thoracic aorta. The facile handling of these grafts and techniques identical to SVG grafting are emphasized. Avoidance of competitive flow and the importance of spasm prophylaxis cannot be overstated. Arterial grafts have patencies >90% at 10 years (SVG 50-60% at 10 years) and once functioning normally, remain free of atheroma. Long-term results are excellent, especially freedom from recurrent cardiac events and reoperations, even in patients with significant preoperative comorbidities such as diabetes and renal dysfunction. Depending on age, long-term survival is between 85 and 90% at 10 years and 75 and 80% at 15 years, and is always better than for one arterial graft plus SVG in all long-term risk-adjusted or propensity-matched studies.

OBJECTIVE: While risk factors for depression are increasingly known, there is no widely utilised depression risk index. Our objective was to develop a method for a flexible, modular, Risk Index for Depression using structural equation models of key determinants identified from previous published research that blended machine-learning with traditional statistical techniques. METHODS: Demographic, clinical and laboratory variables from the National Health and Nutrition Examination Study (2009-2010, N = 5546) were utilised. Data were split 50:50 into training:validation datasets. Generalised structural equation models, using logistic regression, were developed with a binary outcome depression measure (Patient Health Questionnaire-9 score ⩾ 10) and previously identified determinants of depression: demographics, lifestyle-environs, diet, biomarkers and somatic symptoms. Indicative goodness-of-fit statistics and Areas Under the Receiver Operator Characteristic Curves were calculated and probit regression checked model consistency. RESULTS: The generalised structural equation model was built from a systematic process. Relative importance of the depression determinants were diet (odds ratio: 4.09; 95% confidence interval: [2.01, 8.35]), lifestyle-environs (odds ratio: 2.15; 95% CI: [1.57, 2.94]), somatic symptoms (odds ratio: 2.10; 95% CI: [1.58, 2.80]), demographics (odds ratio:1.46; 95% CI: [0.72, 2.95]) and biomarkers (odds ratio:1.39; 95% CI: [1.00, 1.93]). The relationships between demographics and lifestyle-environs and depression indicated a potential indirect path via somatic symptoms and biomarkers. The path from diet was direct to depression. The Areas under the Receiver Operator Characteristic Curves were good (logistic:training = 0.850, validation = 0.813; probit:training = 0.849, validation = 0.809). CONCLUSION: The novel Risk Index for Depression modular methodology developed has the flexibility to add/remove direct/indirect risk determinants paths to depression using a structural equation model on datasets that take account of a wide range of known risks. Risk Index for Depression shows promise for future clinical use by providing indications of main determinant(s) associated with a patient's predisposition to depression and has the ability to be translated for the development of risk indices for other affective disorders.

Background: Tumors of the central nervous system (CNS) have physical and psychological effects that commonly interact and change over time. Although well suited to addressing problems at the interface between physical and psychological medicine, the role of the consultation-liaison psychiatrist has not been previously described in the management of these patients. The purpose of this paper is to summarize the experience of psychiatry liaison attachment within a CNS tumor service and to reflect on its utility within a complex multidisciplinary environment. Methods: A retrospective file review was performed on all cases seen by a psychiatrist in a CNS tumor service over the previous 5 years. A simple thematic inductive analysis was conducted of the common problems experienced by patients and their management by the psychiatrist and within the team. Results: Five common themes were identified: (i) facilitating adaptation to diagnosis; (ii) supporting living with lower-grade tumors; (iii) managing mental disorders; (iv) neuropsychiatric symptoms of tumor progression; and (v) grief and uncertainty in the advanced stages of illness. The capacity of the psychiatrist to understand and integrate the clinical, pathological, radiological, and treatment information, in communication with colleagues, helped address these challenges. Conclusions: Psychological challenges in CNS tumor patients have both psychological and neurological underpinnings. In our experience, the addition of a liaison psychiatrist to a CNS tumor service was efficient and effective in improving patient management and led to enhanced communication and decision-making within the team.

Illness staging is widely utilized in several medical disciplines to help predict course or prognosis, and optimize treatment. Staging models in psychiatry in general, and bipolar disorder in particular, depend on the premise that psychopathology moves along a predictable path: an at-risk or latency stage, a prodrome progressing to a first clinical threshold episode, and one or more recurrences with the potential to revert or progress to late or end-stage manifestations. The utility and validity of a staging model for bipolar disorder depend on its linking to clinical outcome, treatment response and neurobiological measures. These include progressive biochemical, neuroimaging and cognitive changes, and potentially stage-specific differences in response to pharmacological and psychosocial treatments. Mechanistically, staging models imply the presence of an active disease process that, if not remediated, can lead to neuroprogression, a more malignant disease course and functional deterioration. Biological elements thought to be operative in bipolar disorder include a genetic diathesis, physical and psychic trauma, epigenetic changes, altered neurogenesis and apoptosis, mitochondrial dysfunction, inflammation, and oxidative stress. Many available agents, such as lithium, have effects on these targets. Staging models also suggest the utility of stage-specific treatment approaches that may not only target symptom reduction, but also impede illness neuroprogression. These treatment approaches range from prevention for at-risk individuals, to early intervention strategies for prodromal and newly diagnosed individuals, complex combination therapy for rapidly recurrent illness, and palliative-type approaches for those at chronic, late stages of illness. There is hope that prompt initiation of potentially disease modifying therapies may preclude or attenuate the cognitive and structural changes seen in the later stages of bipolar disorder. The aims of this paper are to: a) explore the current level of evidence supporting the descriptive staging of the syndromal pattern of bipolar disorder; b) describe preliminary attempts at validation; c) make recommendations for the direction of further studies; and d) provide a distillation of the potential clinical implications of staging in bipolar disorder within a broader transdiagnostic framework.

BACKGROUND: Current group-average analysis suggests quantitative but not qualitative cognitive differences between schizophrenia (SZ) and bipolar disorder (BD). There is increasing recognition that cognitive within-group heterogeneity exists in both disorders, but it remains unclear as to whether between-group comparisons of performance in cognitive subgroups emerging from within each of these nosological categories uphold group-average findings. We addressed this by identifying cognitive subgroups in large samples of SZ and BD patients independently, and comparing their cognitive profiles. The utility of a cross-diagnostic clustering approach to understanding cognitive heterogeneity in these patients was also explored. METHOD: Hierarchical clustering analyses were conducted using cognitive data from 1541 participants (SZ n = 564, BD n = 402, healthy control n = 575). RESULTS: Three qualitatively and quantitatively similar clusters emerged within each clinical group: a severely impaired cluster, a mild-moderately impaired cluster and a relatively intact cognitive cluster. A cross-diagnostic clustering solution also resulted in three subgroups and was superior in reducing cognitive heterogeneity compared with disorder clustering independently. CONCLUSIONS: Quantitative SZ-BD cognitive differences commonly seen using group averages did not hold when cognitive heterogeneity was factored into our sample. Members of each corresponding subgroup, irrespective of diagnosis, might be manifesting the outcome of differences in shared cognitive risk factors.

Objective: Progress toward understanding brain mechanisms in psychosis is hampered by failures to account for within-group heterogeneity that exists across neuropsychological domains. We recently identified distinct cognitive subgroups that might assist in identifying more biologically meaningful subtypes of psychosis. In the present study, we examined whether underlying structural brain abnormalities differentiate these cognitively derived subgroups. Method: 1.5T T1 weighted structural scans were acquired for 168 healthy controls and 220 patients with schizophrenia/schizoaffective disorder. Based on previous work, 47 patients were categorized as being cognitively compromised (impaired premorbid and current IQ), 100 as cognitively deteriorated (normal premorbid IQ, impaired current IQ), and 73 as putatively cognitively preserved (premorbid and current IQ within 1 SD of controls). Global, subcortical and cortical volume, thickness, and surface area measures were compared among groups. Results: Whole cortex, subcortical, and regional volume and thickness reductions were evident in all subgroups compared to controls, with the largest effect sizes in the compromised group. This subgroup also showed abnormalities in regions not seen in the other patient groups, including smaller left superior and middle frontal areas, left anterior and inferior temporal areas and right lateral medial and inferior frontal, occipital lobe and superior temporal areas. Conclusions: This pattern of more prominent brain structural abnormalities in the group with the most marked cognitive impairments-both currently and putatively prior to illness onset, is consistent with the concept of schizophrenia as a progressive neurodevelopmental disorder. In this group, neurodevelopmental and neurodegenerative factors may be important for cognitive function.

OBJECTIVES: Use of appropriate face processing strategies is important for facial emotion recognition, which is known to be impaired in schizophrenia (SZ) and bipolar disorder (BD). There is preliminary evidence of abnormalities in the use of face processing strategies in the former, but there has been no explicit attempt to assess face processing in patients with BD. METHODS: Twenty-eight BD I, 28 SZ, and 28 healthy control participants completed tasks assessing featural and configural face processing. The facial inversion effect was used as a proxy of second order configural face processing and compared to featural face processing performance (which is known to be relatively less affected by facial inversion). RESULTS: Controls demonstrated the usual second-order inversion pattern. In the BD group, the absence of a second-order configural inversion effect in the presence of a disproportionate bias toward a featural inversion effect was evident. Despite reduced accuracy performance in the SZ group compared to controls, this group unexpectedly showed a normal second-order configural accuracy inversion pattern. This was in the context of a reverse inversion effect for response latency, suggesting a speed-versus-accuracy trade-off. CONCLUSIONS: To our knowledge, this is the first study to explicitly examine and contrast face processing in BD and SZ. Our findings indicate a generalized impairment on face processing tasks in SZ, and the presence of a second-order configural face processing impairment in BD. It is possible that these face processing impairments represent a catalyst for the facial emotion recognition deficits that are commonly reported in the literature. (JINS, 2016, 22, 652-661).

OBJECTIVES: Despite known overlaps in the pattern of cognitive impairments in individuals with bipolar disorder (BD), schizophrenia (SZ) and schizoaffective disorder (SZA), few studies have examined the extent to which cognitive performance validates traditional diagnostic boundaries in these groups. METHOD: Individuals with SZ (n=49), schizoaffective disorder (n=33) and BD (n=35) completed a battery of cognitive tests measuring the domains of processing speed, immediate memory, semantic memory, learning, working memory, executive function and sustained attention. RESULTS: A discriminant functions analysis revealed a significant function comprising semantic memory, immediate memory and processing speed that maximally separated patients with SZ from those with BD. Initial classification scores on the basis of this function showed modest diagnostic accuracy, owing in part to the misclassification of SZA patients as having SZ. When SZA patients were removed from the model, a second cross-validated classifier yielded slightly improved diagnostic accuracy and a single function solution, of which semantic memory loaded most heavily. CONCLUSIONS: A cluster of non-executive cognitive processes appears to have some validity in mapping onto traditional nosological boundaries. However, since semantic memory performance was the primary driver of the discrimination between BD and SZ, it is possible that performance differences between the disorders in this cognitive domain in particular, index separate underlying aetiologies.