General practitioners’ experiences and perceptions of mild moderate depression management and factors influencing effective service delivery in rural Australian communities: a qualitative study

Background

Rural communities in Australia face significant disadvantages relating to geographical isolation and limited access to mental health services. Documenting general practitioners’ (GP) experiences and perception of mental health services in rural Australia may be useful to gain insight into rural GP management of mild to moderate depression.

Aims

To explore GPs’ experience and views on which factors influence access to mental health services for mild to moderate depression.

Method

This qualitative study was conducted in 2014 in the Northern Rivers, NSW, Australia. Data were obtained from semi-structured in-depth face-to-face interviews with ten GPs, and analyses were performed using a general inductive method of thematic analysis.

Results

Most GPs believed that the current services for managing mild-moderate depression were adequate, however they also identified the need for better access and more services that were free for patients. GPs had a positive perception of management of depression in a rural setting, identifying advantages including better doctor-patient relationships, continuity of care and the proximity of services. However, GPs also identified several barriers to access to mental health services in a rural setting, including long waiting-times, inadequate patient rapport with referred professionals, cost of treatment, transportation, geographical location, stigma, and lack of education about available mental health services. As a result, GPs frequently self-managed patients in addition to referring them to other community mental health service providers where possible.

Conclusion

Overall, GPs appeared relatively satisfied with the resources available in their communities but also identified numerous barriers to access and room for improvement. Rural GPs often self-managed patients in addition to referring patients to other mental health services providers. This should be taken into account when designing mental health policies, developing new services or re-designing current services in rural communities.

     

A neural mediator of human anxiety sensitivity

Advances in the neuroscientific understanding of bodily autonomic awareness, or interoception, have led to the hypothesis that human trait anxiety sensitivity (AS)—the fear of bodily autonomic arousal—is primarily mediated by the anterior insular cortex. Despite broad appeal, few experimental studies have comprehensively addressed this hypothesis. We recruited 55 individuals exhibiting a range of AS and assessed them with functional magnetic resonance imaging (fMRI) during aversive fear conditioning. For each participant, three primary measures of interest were derived: a trait Anxiety Sensitivity Index score; an in‐scanner rating of elevated bodily anxiety sensations during fear conditioning; and a corresponding estimate of whole‐brain functional activation to the conditioned versus nonconditioned stimuli. Using a voxel‐wise mediation analysis framework, we formally tested for ‘neural mediators’ of the predicted association between trait AS score and in‐scanner anxiety sensations during fear conditioning. Contrary to the anterior insular hypothesis, no evidence of significant mediation was observed for this brain region, which was instead linked to perceived anxiety sensations independently from AS. Evidence for significant mediation was obtained for the dorsal anterior cingulate cortex—a finding that we argue is more consistent with the hypothesized role of human cingulofrontal cortex in conscious threat appraisal processes, including threat‐overestimation. This study offers an important neurobiological validation of the AS construct and identifies a specific neural substrate that may underlie high AS clinical phenotypes, including but not limited to panic disorder. Hum Brain Mapp 36:3950–3958, 2015. © 2015 Wiley Periodicals, Inc.     

The effect of Lorenzo's oil on oxidative stress in X-linked adrenoleukodystrophy

X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder biochemically characterized by the accumulation of very long chain fatty acids (VLCFA), particularly hexacosanoic acid (C(26:0)) and tetracosanoic acid (C(24:0)), in tissues and biological fluids. Although patients affected by this disorder predominantly present central and peripheral demyelination as well as adrenal insufficiency, the mechanisms underlying the brain damage in X-ALD are poorly known. The current treatment of X-ALD with glyceroltrioleate (C(18:1))/glyceroltrierucate (C(22:1)) (Lorenzo's oil, LO) combined with a VLCFA-poor diet normalizes VLCFA concentrations, but the neurological symptoms persist or even progress in symptomatic patients. Considering that free radical generation is involved in various neurodegenerative disorders and that in a previous study we showed evidence that oxidative stress is probably involved in the pathophysiology of X-ALD symptomatic patients, in the present study we evaluated various oxidative stress parameters, namely thiobarbituric acid reactive species (TBA-RS) and total antioxidant reactivity (TAR) in plasma, as well as the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) in erythrocytes from symptomatic and asymptomatic X-ALD patients and verified whether LO treatment and a VLCFA restricted diet could change these parameters. We observed a significant increase of plasma TBA-RS in symptomatic and asymptomatic X-ALD patients, reflecting induction of lipid peroxidation even before the disease was manifested. In addition, LO treatment did not alter this profile. Furthermore, plasma TAR measurement of X-ALD patients was not different from that of controls. Similarly, the antioxidant enzyme activities CAT, SOD and GPx were not altered in erythrocyte from X-ALD patients as compared to controls. We also examined the in vitro effects of hexacosanoic acid (C(26:0)) and tetracosanoic acid (C(24:0)) alone or combined with oleic (C(18:1))/erucic (C(22:1)) acids on various oxidative stress parameters in cerebral cortex of young rats, namely chemiluminescence, TBA-RS, TAR, CAT, SOD and GPx in order to investigate whether those fatty acids were able to induce oxidative stress. We found that there was a significant increase of TBARS and of chemiluminescence in rat cerebral cortex exposed to C(26:0)/C(24:0), and that the addition of C(18:1)and C(22:1) to the assays did not prevent this effect. Furthermore, TAR measurement was not altered by C(26:0) and C(24:0) acids in rat cerebral cortex. Taken together, our results indicate that lipid peroxidation occurs in X-ALD and that LO treatment does not attenuate or prevent free radical generation in these patients. Therefore, it may be presumed that antioxidants should be considered as an adjuvant therapy for X-ALD patients.     

Tracheostomized patients care: efficacy of a brief theoretical education program for nursing personnel

Introduction  Tracheostomized cancer patients require a special nursing care involving specifically related procedures. The goal of this study was to evaluate the results of a brief theoretical education program on tracheostomized patients care for nursing personnel. Materials and methods  One hundred and ten professionals have participated in this before and after-intervention one group study, and the program was carried out in a Brazilian hospital, a national reference center in oncology treatment. The questionnaire outcomes were compared to assess the theoretical knowledge level of the participants. Results and discussion  Statistical analysis showed that this program was efficient to enhance knowledge skills on specific nursing procedures related to care of the traqueostomized cancer patients. The low costs and simple structure required in the program may encourage the spread of similar practices to improve quality of nursing assistance in the hospital environment.     

Cytological criteria to predict basal phenotype of breast carcinomas

Breast carcinoma is a heterogeneous disease. It can be classified into phenotypes based on the expression of certain proteins, with distinct differences in prognosis. The basal phenotype is associated with worse prognosis and it still remains without specific treatment. However, there is currently no international consensus on the cytological criteria that could predict this phenotype. The purpose of the study was to evaluate the cytological criteria in fine‐needle aspiration biopsy and to identify their association with the basal phenotype of breast carcinoma. Fine‐needle aspiration biopsy specimens and tissue sections (mastectomy specimen) from 74 cases of high‐grade invasive ductal breast carcinomas were consecutively retrieved from the files of three institutions. Breast carcinomas were studied using the tissue microarray technique, being classified into phenotypes: luminal A, luminal B, HER2 overexpression, and basal. The cytological criteria for all cases were reviewed blindly by two pathologists according to five cytological criteria: cellularity, cell pattern, presence of necrosis, nucleoli, and nuclear atypia. Exact Fisher test was used to test the association between cytological criteria and the phenotypes of breast carcinoma. Necrosis was present in 64.7% of basal breast carcinomas, and 31.1% of nonbasal breast carcinomas, and that result was statistically significant, showing an odds ratio (OR) of 3.80. The basal phenotype, compared with the luminal A, showed more necrosis (OR = 6.97), present/prominent nucleoli (OR = 8.18), and cellularity more frequently (OR = 18.03). Necrosis, as well as present/prominent nucleoli and abundant cellularity are criteria more frequently associated to the basal phenotype of breast carcinoma. Diagn. Cytopathol. 2009. © 2009 Wiley‐Liss, Inc.     

A Golgi fragmentation pathway in neurodegeneration

The Golgi apparatus processes intracellular proteins, but undergoes disassembly and fragmentation during apoptosis in several neurodegenerative disorders such as amyotrophic lateral sclerosis and Alzheimer's disease. It is well known that other cytoplasmic organelles play important roles in cell death pathways. Thus, we hypothesized that Golgi fragmentation might participate in transduction of cell death signals. Here, we found that Golgi fragmentation and dispersal precede neuronal cell death triggered by excitotoxins, oxidative/nitrosative insults, or ER stress. Pharmacological intervention or overexpression of the C-terminal fragment of Grasp65, a Golgi-associated protein, inhibits fragmentation and decreases or delays neuronal cell death. Inhibition of mitochondrial or ER cell death pathways also decreases Golgi fragmentation, indicating crosstalk between organelles and suggesting that the Golgi may be a common downstream-effector of cell death. Taken together, these findings implicate the Golgi as a sensor of stress signals in cell death pathways.     

Transcranial direct current stimulation in refractory continuous spikes and waves during slow sleep: a controlled study

Cathodal transcranial direct current stimulation (tDCS) decreases cortical excitability. The purpose of the study was to investigate whether cathodal tDCS could interrupt the continuous epileptiform activity. Five patients with focal, refractory continuous spikes and waves during slow sleep were recruited. Cathodal tDCS and sham stimulation were applied to the epileptic focus, before sleep (1 mA; 20 min). Cathodal tDCS did not reduce the spike-index in any of the patients.     

High expression of MeCP2 in JC virus‐infected cells of progressive multifocal leukoencephalopathy brains

Mutations of the methyl CpG binding protein 2 (MeCP2) gene are a major cause of Rett syndrome. To investigate whether the expression of this gene was related to JC virus (JCV) infection, we examined brains of four progressive multifocal leukoencephalopathy (PML) patients. JCV infection was confirmed by immunohistochemical labeling with antibodies against JCV VP1, agnoprotein and large T antigen. MeCP2 expression was examined by immunohistochemistry using a specific polyclonal antibody against MeCP2. In normal brains and uninfected cortices of PML brains, MeCP2 expression was observed in the nuclei of neurons, but not observed in glial and endothelial cell nuclei. However, in PML brains intense immunolabeling was observed in abnormally enlarged glial nuclei of JCV‐infected cells. Double immunolabeling using antibodies against large T antigen (visualized as blue) and MeCP2 (visualised as red) revealed dark red JCV‐infected nuclei, which confirmed that the JCV infected nuclei expressed MeCP2. We conclude that MeCP2 is highly expressed in the JCV‐infected nuclei of PML brain and these results may provide a new insight into the mechanism which regulates the MeCP2 expression in glial cells by the infection of JCV.