Defining pharmacy and its practice: a conceptual model for an international audience

Background: There is much fragmentation and little consensus in the use of descriptors for the different disciplines that make up the pharmacy sector. Globalization, reprofessionalization and the influx of other disciplines means there is a requirement for a greater degree of standardization. This has not been well addressed in the pharmacy practice research and education literature. Objectives: To identify and define the various subdisciplines of the pharmacy sector and integrate them into an internationally relevant conceptual model based on narrative synthesis of the literature. Methods: A literature review was undertaken to understand the fragmentation in dialogue surrounding definitions relating to concepts and practices in the context of the pharmacy sector. From a synthesis of this literature, the need for this model was justified. Key assumptions of the model were identified, and an organic process of development took place with the three authors engaging in a process of sense-making to theorize the model. Results: The model is “fit for purpose” across multiple countries and includes two components making up the umbrella term “pharmaceutical practice”. The first component is the four conceptual dimensions, which outline the disciplines including social and administrative sciences, community pharmacy, clinical pharmacy and pharmaceutical sciences. The second component of the model describes the “acts of practice”: teaching, research and professional advocacy; service and academic enterprise. Conclusions: This model aims to expose issues relating to defining pharmacy and its practice and to create dialogue. No model is perfect, but there are implications for what is posited in the areas of policy, education and practice and future research. The main point is the need for increased clarity, or at least beginning the discussion to increase the clarity of definition and consistency of meaning in-and-across the pharmacy sector locally, nationally and internationall

Exploring an increased role for Australian community pharmacy in mental health professional service delivery: evaluation of the literature

Background: Australian general practitioners primarily treat mental health problems by prescribing medication dispensed by community pharmacists. Pharmacists therefore have regular interactions with mental health consumers and carers.Aims: This narrative review explored the potential role of community pharmacy in mental health services.Method: Medline, CINAHL, ProQuest, Emerald, PsycINFO, Science Direct, PubMed, Web of Knowledge and IPA were utilised. The Cochrane Library as well as grey literature and “lay” search engines such as GoogleScholar were also searched.Results: Four systematic reviews and ten community pharmacy randomised controlled trials were identified. Various relevant reviews outlining the impact of community pharmacy based disease state or medicines management services were also identified.Conclusion: International studies involving professional service interventions for mental health consumers could be contextualised for the Australian setting. Australian studies of pharmacy professional services for chronic physical health conditions provided further guidance for the expansion of community pharmacy mental health professional services

Neurocognitive Predictors of Treatment Response to Randomized Treatment in Adults with Tic Disorders

Tourette\u27s disorder (TS) and chronic tic disorder (CTD) are neurodevelopmental disorders characterized by involuntary vocal and motor tics. Consequently, TS/CTD have been conceptualized as disorders of cognitive and motor inhibitory control. However, most neurocognitive studies have found comparable or superior inhibitory capacity among individuals with TS/CTD relative to healthy controls. These findings have led to the hypothesis that individuals with TS/CTD develop increased inhibitory control due to the constant need to inhibit tics. However, the role of cognitive control in TS/CTD is not yet understood, particularly in adults. To examine the role of inhibitory control in TS/CTD, the present study investigated this association by assessing the relationship between inhibitory control and treatment response in a large sample of adults with TS/CTD. As part of a large randomized trial comparing behavior therapy versus supportive psychotherapy for TS/CTD, a battery of tests, including tests of inhibitory control was administered to 122 adults with TS/CTD at baseline. We assessed the association between neuropsychological test performance and change in symptom severity, as well as compared the performance of treatment responders and non-responders as defined by the Clinical Global Impression Scale. Results indicated that change in symptoms, and treatment response were not associated with neuropsychological performance on tests of inhibitory control, intellectual ability, or motor function, regardless of type of treatment. The finding that significant change in symptom severity of TS/CTD patients is not associated with impairment or change in inhibitory control regardless of treatment type suggests that inhibitory control may not be a clinically relevant facet of these disorders in adults

Dynamics of Cortical Degeneration Over a Decade in Huntington's Disease

BACKGROUND: Characterizing changing brain structure in neurodegeneration is fundamental to understanding longterm effects of pathology and ultimately providing therapeutic targets. It is well established that Huntington’s disease (HD) gene carriers undergo progressive brain changes during the course of disease, yet the long-term trajectory of cortical atrophy is not well defined. Given that genetic therapies currently tested in HD are primarily expected to target the cortex, understanding atrophy across this region is essential. METHODS: Capitalizing on a unique longitudinal dataset with a minimum of 3 and maximum of 7 brain scans from 49 HD gene carriers and 49 age-matched control subjects, we implemented a novel dynamical systems approach to infer patterns of regional neurodegeneration over 10 years. We use Bayesian hierarchical modeling to map participant- and group-level trajectories of atrophy spatially and temporally, additionally relating atrophy to the genetic marker of HD (CAG-repeat length) and motor and cognitive symptoms. RESULTS: We show, for the first time, that neurodegenerative changes exhibit complex temporal dynamics with substantial regional variation around the point of clinical diagnosis. Although widespread group differences were seen across the cortex, the occipital and parietal regions undergo the greatest rate of cortical atrophy. We have established links between atrophy and genetic markers of HD while demonstrating that specific cortical changes predict decline in motor and cognitive performance. CONCLUSIONS: HD gene carriers display regional variability in the spatial pattern of cortical atrophy, which relates to genetic factors and motor and cognitive symptoms. Our findings indicate a complex pattern of neuronal loss, which enables greater characterization of HD progression

Group-Based Parent Training Interventions for Parents of Children with Autism Spectrum Disorders: a Literature Review

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Parents of children with autism spectrum disorders should have access to interventions to help them understand and support their child. This literature review examines the existing evidence for group-based parent training interventions that support parents of children with autism. From the literature, core intervention processes and outcomes are identified and include parenting and parent behaviour, parent health, child behaviour and peer and social support. Results show a positive trend for intervention effectiveness, but findings are limited by low-quality studies and heterogeneity of intervention content, outcomes and outcome measurement. Future research should focus on specifying effective intervention ingredients and modes of delivery, consistent and reliable outcome measurement, and improving methodological rigour to build a more robust evidence base

A Multi-Study Model-Based Evaluation of the Sequence of Imaging and Clinical Biomarker Changes in Huntington's Disease

Understanding the order and progression of change in biomarkers of neurodegeneration is essential to detect the effects of pharmacological interventions on these biomarkers. In Huntington’s disease (HD), motor, cognitive and MRI biomarkers are currently used in clinical trials of drug efficacy. Here for the first time we use directly compare data from three large observational studies of HD (total N = 532) using a probabilistic event-based model (EBM) to characterise the order in which motor, cognitive and MRI biomarkers become abnormal. We also investigate the impact of the genetic cause of HD, cytosine-adenine-guanine (CAG) repeat length, on progression through these stages. We find that EBM uncovers a broadly consistent order of events across all three studies; that EBM stage reflects clinical stage; and that EBM stage is related to age and genetic burden. Our findings indicate that measures of subcortical and white matter volume become abnormal prior to clinical and cognitive biomarkers. Importantly, CAG repeat length has a large impact on the timing of onset of each stage and progression through the stages, with a longer repeat length resulting in earlier onset and faster progression. Our results can be used to help design clinical trials of treatments for Huntington’s disease, influencing the choice of biomarkers and the recruitment of participants

Characterising white matter in Huntington's disease

Background: Investigating early white matter (WM) change in Huntington’s Disease (HD) can improve our understanding of the way in which disease spreads from the striatum. Objectives: Here, we provide a detailed characterisation of pathology-related WM change in HD. We first examined WM microstructure using diffusion-weighted imaging, then investigated both underlying biological properties of WM and products of WM damage including iron, myelin plus neurofilament light (NfL), a biofluid marker of axonal degeneration – in parallel with the mutant huntingtin protein (mHTT). Methods: We examined WM change in HD gene-carriers from the HD-CSF cohort, baseline visit. We used standard diffusion MRI to measure metrics including fractional anisotropy (FA), a marker of WM integrity, and diffusivity; a novel diffusion model (NODDI) to measure axonal density and organisation; T1 and T2 weighted structural MRI images to derive proxy iron content and myelin-contrast measures; and biofluid concentrations of NfL (in CSF and plasma) and mHTT (in CSF). Results: HD gene-carriers displayed reduced FA and increased diffusivity compared to controls, both of which were also associated with disease progression, CSF and mHTT levels. HD gene-carriers also displayed proxy measures of reduced myelin-contrast and iron in the striatum. Conclusion: Collectively, these findings present a more complete characterisation of HD-related microstructural brain changes. Correlation between reduced FA, increased axonal orientation and biofluid markers suggest that axonal breakdown is associated with increased WM degeneration, while higher quantitative T2 signal and lower myelin-contrast may indicate a process of demyelination limited to the striatum

Timing of selective basal ganglia white matter loss in premanifest Huntington’s disease

OBJECTIVES: To investigate the timeframe prior to symptom onset when cortico-basal ganglia white matter (white matter) loss begins in premanifest Huntington's disease (preHD), and which striatal and thalamic sub-region white matter tracts are most vulnerable. METHODS: We performed fixel-based analysis, which allows resolution of crossing white matter fibres at the voxel level, on diffusion tractography derived white matter tracts of striatal and thalamic sub-regions in two independent cohorts; TrackON-HD, which included 72 preHD (approx. 11 years before disease onset) and 85 controls imaged at three time points over two years; and the HD young adult study (HD-YAS), which included 54 preHD (approx. 25 years before disease onset) and 53 controls, imaged at one time point. Group differences in fibre density and cross section (FDC) were investigated. RESULTS: We found no significant group differences in cortico-basal ganglia sub-region FDC in preHD gene carriers 25 years before onset. In gene carriers 11 years before onset, there were reductions in striatal (limbic and caudal motor) and thalamic (premotor, motor and sensory) FDC at baseline, with no significant change over 2 years. Caudal motor-striatal, pre-motor-thalamic, and primary motor-thalamic FDC at baseline, showed significant correlations with the Unified Huntington's disease rating scale (UHDRS) total motor score (TMS). Limbic cortico-striatal FDC and apathy were also significantly correlated. CONCLUSIONS: Our findings suggest that limbic and motor white matter tracts to the striatum and thalamus are most susceptible to early degeneration in HD but that approximately 25 years from onset, these tracts appear preserved. These findings may have importance in determining the optimum time to initiate future disease modifying therapies in HD