From Theory to Practice: A Qualitative Study Exploring Change Managers' Experiences Applying Change Management Frameworks in Hospital Redevelopment Across One Australian State.

Bipolar disorder (BD) is a major psychiatric condition impacting 2.4% of adults worldwide (), subsequently increasing risks of physiological disease (; ), substance use disorders (), and suicide () for millions of people. Individuals living with bipolar disorder cycle between depression and (hypo)mania, interspersed by periods of symptom remission (; ). While these affective states are defined to be categorically distinct from each other, individuals often experience states with co-existing (hypo)manic and depressive symptoms (; ). In addition, individuals diagnosed with BD experience a greater risk of suicide during depressive affective states, particular those that present with (hypo)mania symptoms (). The neurobiological underpinnings have been sought since the condition was empirically delineated in the early 1900s (). At present, significant progress has been achieved, particularly with the advent of multi-site consortia constructing large-scale datasets. Yet, a neurobiological explanation of between depression, (hypo)mania, and euthymia remains elusive. At present, it is established that BD is associated with significant inter-individual heterogeneity that creates difficulty in identifying generalizable neurobiological features (). The current perspective article presents the utility of integrating research methodology inspired by the behavioral psychopathology literature and the use of idiographic symptom network modeling. Typical research in human neuroscience investigates group-wise neurobiological characteristics within a single timeframe (i.e., cross-sectional) or across a few sessions in the timeframe of months or years (i.e., longitudinal). Idiographic symptom network modeling uses ecological momentary assessment to acquire multiple, daily samples to construct individual-specific temporal relationships between distinct symptoms. In short, we argue that increasing within subject neuroimaging data, akin to idiographic symptom network modeling, may better account for heterogeneity and subsequently provide more precise neurobiological linking to affective and behavioral symptomatology via idiographic network analysis, therefore establishing potential neurobiological causes of affective trait transitions in BD. Within the past decade, focus on large-scale datasets through meta- and mega-analyses has increased to bolster attempts at identifying neurobiological phenotypes of BD through structural and functional MRI. In brief, measures from structural MRI reveal nonspecific reductions in cortical thickness across both cerebral hemispheres (). Moreover, BD is significantly associated with reduced indices of white-matter integrity, particularly the corpus callosum and cingulum (). Furthermore, a multi-site investigation including several thousand participants found that sensorimotor and basal ganglia morphometry were the most important features distinguishing BD from major depression (). Functional neuroimaging investigations have aimed to identify trait- and affective state-specific neurocognitive mechanisms of BD. In particular, activity within the amygdalo-hippocampus complex is enhanced across affective states, including euthymia (). In contrast, frontal and parietal activity elicited by working memory or reward processing tasks appeared specific to affective state (). Frontoparietal dynamics are particularly interesting to researchers as they contribute to executive functioning (; ), one core executive function thought to underpin cognitive and affective symptomatology in BD (). In a recent meta-analysis, motoric and motivational inhibition were associated with distinct activation patterns (. Motoric inhibition underpinned by frontal, insular, and thalamic regions is more sensitive to the emotional content of environmental cues among individuals with BD in contrast to healthy individuals without a psychiatric condition. In addition, report motivational inhibition indexed by delay discounting revealed enhanced activation across the orbitofrontal cortex and striatum when selecting immediate rewards compared to delayed, yet greater rewards. Furthermore, a considerable number of individuals diagnosed with BD have taken at least one psychotropic medication (), which promotes neuroanatomical and neurofunctional changes overlapping with probable neurobiological signatures of BD pathophysiology (; ), thus presenting as a significant confounding variable and many neuroimaging studies are confounded with such effects (; ). While cross-sectional studies account for the majority of research, longitudinal studies following individuals across affective states exist within the literature, albeit sparsely. One study investigating morphometric changes over 6 years revealed cortical thinning within the prefrontal cortex that linearly scaled with the number of manic episodes (). It has been reported that dynamic co-activation of the amygdala and sensorimotor network is more frequently associated with mania while amy