St Vincents Mental Health

Fitzroy, Australia

St Vincents Mental Health

Fitzroy, Australia
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Sankaranarayanan A.,Hunter Valley Mental Health Service | Sankaranarayanan A.,Hamad Medical Corporation | Mancuso S.,St Vincents Mental Health | Castle D.,St Vincents Hospital Melbourne | Castle D.,University of Melbourne
Psychiatry Research | Year: 2014

Cigarette smoking has been associated with an increased risk of suicide. Patients with psychosis are more likely to smoke cigarettes and are also at an increased risk of suicide. The aim of this study was to compare risk for suicidal behavior among patients with psychosis who were current smokers, previous smokers and nonsmokers. We studied 1812 of the 1825 participants who took part in the Australian Survey of High Impact Psychosis (SHIP) for whom smoking data was available. We identified predictors for lifetime suicide attempts using univariate logistic regression analysis. These variables were retained for the multiple logistic regression models if they were a significant predictor of lifetime suicide attempts. A series of multiple logistic regressions were then conducted to predict lifetime suicide attempts using current smoking status and lifetime smoking status as independent variables, respectively, while controlling for the retained predictor variables. Current smoking and lifetime smoking were statistically significant predictors of lifetime suicide attempts. However adding the covariates to a logistic regression model reduced this association to non-significance. The strongest predictors were self-harm in the past 12 months, the presence of lifetime depressive symptoms and a diagnosis of psychotic depression. Identification of suicide risk factors is essential for successful suicide prevention. While previous research highlights the importance of cigarette smoking as an important risk factor for suicidal behaviors including in patients with psychosis, these results must be interpreted within the context of methodological issues. © 2013.

Toh W.L.,University of Melbourne | Toh W.L.,Monash University | Rossell S.L.,University of Melbourne | Rossell S.L.,Monash University | And 3 more authors.
Comprehensive Psychiatry | Year: 2011

The human visual system is comprised of an array of complex organs, which jointly decode information from visible light to construct a meaningful representation of the surrounding environment. The study of visual scanpaths transpired in a bid to enhance our understanding of the role of eye movements underpinning adaptive functioning as well as psychopathology and was further aided by the advent of modern eye-tracking techniques. This review provides a background to the nature of visual scanpaths, followed by an overview and critique of eye movement studies in specific clinical populations involving the psychotic, anxiety, and mood disorders, and concludes with suggested directions for future research. We performed a Medline and PsycInfo literature search, based on variations of the terms "visual scanpath," "eye-tracking," and "eye movements," in relation to articles published from 1986 to the present. Eye-tracking studies in schizophrenia mostly concurred with the existence of a "restricted" scanning strategy, characterized by fewer number of fixations of increased durations, with shorter scanpath lengths, and a marked avoidance of salient features, especially in relation to facial emotion perception. This has been interpreted as likely reflecting dual impairments in configural processing as well as gestalt perception. Findings from the anxiety and mood disorders have conversely failed to yield coherent results, with further research warranted to provide corroborating evidence and overcome identified methodological limitations. Future studies should also look toward applying similar techniques to related disorders as well as conducting parallel neuroimaging investigations to elucidate potential neurobiological correlates. © 2011 Elsevier Inc.

Mancuso S.G.,St Vincents Mental Health | Mancuso S.G.,Swinburne University of Technology | Knoesen N.P.,St Vincents Mental Health | Castle D.J.,St Vincents Mental Health | Castle D.J.,St Vincents Hospital
Comprehensive Psychiatry | Year: 2010

This study assessed demographic and clinical features in 65 subjects with body dysmorphic disorder (BDD) and compared the 39 (60%) with the delusional form (receiving an additional diagnosis of delusional disorder, somatic type) with those who did not meet delusionality criteria. Delusional and nondelusional patients did not statistically differ on most demographic and clinical variables. Delusional patients, however, had significantly more severe BDD symptoms at both baseline and follow-up assessments than those of nondelusional patients. Furthermore, poorer insight was significantly associated with more severe BDD symptoms at both baseline and follow-up. Overall improvement in BDD symptom severity was similar for the 2 groups. Our results support other studies in the view that BDD and its delusional variant have more similarities than differences and that the delusional variant may be simply a more severe form of BDD. Implications for the diagnostic classification of BDD and future research directions are discussed. Crown Copyright © 2010.

Mancuso S.G.,Swinburne University of Technology | Knoesen N.P.,St Vincents Mental Health | Castle D.J.,St Vincents Hospital
Australian and New Zealand Journal of Psychiatry | Year: 2010

Objective: The purpose of this study was to investigate the use of the Dysmorphic Concerns Questionnaire (DCQ) as a screening measure for body dysmorphic disorder (BDD) and to derive DCQ cutoff scores to facilitate the screening procedure. Method: The DCQ was completed by 244 undergraduates (mean = 20.80, SD = 3.10 years) and 57 BDD outpatients (mean = 29.60, SD = 9.44 years) in Melbourne, Australia. The undergraduate sample was screened for eating disorders using the Eating Attitudes Test-26, and for BDD using the Body Dysmorphic Disorder Questionnaire. Results: The BDD outpatients obtained significantly higher scores on the DCQ than the undergraduates. This difference remained statistically significant after controlling for the severity of depression and social anxiety symptoms. A DCQ cutoff score of 9 resulted in the correct classification of 96.4% of BDD patients and 90.6% of undergraduates. Conclusions: The results supported the use of the DCQ as a brief, sensitive, and specific screening instrument for BDD. © 2010 The Royal Australian and New Zealand College of Psychiatrists.

Haydock M.,St Vincents Mental Health | Cowlishaw S.,University of Bristol | Cowlishaw S.,Australian National University | Harvey C.,North Western Mental Health | And 3 more authors.
Comprehensive Psychiatry | Year: 2015

Objective There are few published studies on the comorbidity of psychosis and problem gambling. This paper provides estimates of the prevalence and clinical correlates of problem gambling in a representative sample of people with psychotic disorders. Method The second Australian national survey of psychosis was undertaken in 2010 and included adults (18-64 years) attending mental health services. Problem gambling was measured using the Canadian Problem Gambling Index (CPGI) at two sites of this study, with 442 participants providing data suitable for analysis. Results There were 151 participants who screened positive to past-year gambling. 4.1% of the total sample was classified as low risk gamblers, 6.4% were moderate risk gamblers and 5.8% were problem gamblers. Moderate risk/problem gamblers were more likely to be male, have left school with no qualifications and have sought financial assistance in the last year. There was a significant association with substance use, including alcohol use disorders and use of cannabis and 'other' drugs (excluding cannabis). Conclusions People with psychosis are four times more likely to have a gambling problem than the general population. The association of gambling with substance use disorders is consistent with community studies, while the increased need for financial assistance suggests that problem gambling increases the likelihood of financial harm for this population. Clinicians should screen for comorbid gambling problems in people with psychosis, while there is also a need for additional research into this area. © 2015 Elsevier Inc. All rights reserved.

Castle D.,Australian Catholic University | Bosanac P.,St Vincents Mental Health | Bosanac P.,University of Melbourne | Rossell S.,Swinburne University of Technology
Australasian Psychiatry | Year: 2015

Objective: To provide a clinically-focused review of the biological treatment of treatment-resistant obsessive compulsive disorder (OCD). Conclusions: There is a paucity of research on how to manage OCD patients who fail to respond adequately to first line therapies. High-dose selective serotonin reuptake inhibitors (SSRIs) and clomipramine have good evidencebased data. Combinations of SSRIs have little support in clinical trials, but the combination of SSRIs and clomipramine can be helpful: careful clinical and cardiac monitoring is required. Certain adjunctive antipsychotics have a reasonable evidence base in OCD, but their use also needs to be weighed against the potential side effect burden. In patients with substantial generalised anxiety symptoms, clonazepam is worth considering. Of the other augmenting strategies, memantine and ondansetron appear useful in some cases, and are well tolerated. Topiramate might ameliorate compulsions to some degree, but it is less well tolerated. If all these strategies, along with expert psychological therapy, fail, careful consideration should be given to deep brain stimulation (DBS), which has an emerging evidence base and which can result in dramatic benefits for some individuals. For some patients, gamma radiosurgery might also still have a place.

Cardamone L.,University of Melbourne | Salzberg M.R.,University of Melbourne | Salzberg M.R.,St Vincents Mental Health | O'Brien T.J.,University of Melbourne | Jones N.C.,University of Melbourne
British Journal of Pharmacology | Year: 2013

There is a high incidence of psychiatric comorbidity in people with epilepsy (PWE), particularly depression. The manifold adverse consequences of comorbid depression have been more clearly mapped in recent years. Accordingly, considerable efforts have been made to improve detection and diagnosis, with the result that many PWE are treated with antidepressant drugs, medications with the potential to influence both epilepsy and depression. Exposure to older generations of antidepressants (notably tricyclic antidepressants and bupropion) can increase seizure frequency. However, a growing body of evidence suggests that newer ('second generation') antidepressants, such as selective serotonin reuptake inhibitors or serotonin-noradrenaline reuptake inhibitors, have markedly less effect on excitability and may lead to improvements in epilepsy severity. Although a great deal is known about how antidepressants affect excitability on short time scales in experimental models, little is known about the effects of chronic antidepressant exposure on the underlying processes subsumed under the term 'epileptogenesis': the progressive neurobiological processes by which the non-epileptic brain changes so that it generates spontaneous, recurrent seizures. This paper reviews the literature concerning the influences of antidepressants in PWE and in animal models. The second section describes neurobiological mechanisms implicated in both antidepressant actions and in epileptogenesis, highlighting potential substrates that may mediate any effects of antidepressants on the development and progression of epilepsy. Although much indirect evidence suggests the overall clinical effects of antidepressants on epilepsy itself are beneficial, there are reasons for caution and the need for further research, discussed in the concluding section. © 2012 The British Pharmacological Society.

Cardamone L.,University of Melbourne | Salzberg M.R.,University of Melbourne | Salzberg M.R.,St Vincents Mental Health | Koe A.S.,University of Melbourne | And 3 more authors.
Neurobiology of Disease | Year: 2014

Objectives: Due to the high comorbidity of epilepsy and depression, antidepressant treatment is commonly indicated for patients with epilepsy. Studies in humans and animal models suggest that selective serotonin reuptake inhibitors (SSRIs) may reduce seizure frequency and severity, and these drugs are generally considered safe for use in epilepsy. No studies have investigated the effects of SSRIs on epileptogenesis, the neurobiological process underlying the development of the epileptic state. Methods: The effect of continuous infusion of the SSRI, fluoxetine (10mg/kg/day sc), versus vehicle control on amygdala kindling was examined in adult male Wistar rats. Seizure threshold and kindling rates were compared between SSRI-treated rats and controls. The study was then repeated examining the effect of a different SSRI, citalopram (10mg/kg/day sc), versus vehicle control. Hippocampal mRNA expression of the serotonin transporter (SERT) and the 5-HT1A receptor was examined in the brains of the rats post-mortem. Results: Treatment with either fluoxetine or citalopram significantly accelerated kindling epileptogenesis, as evidenced by fewer stimulations to reach Class V seizures compared to their respective vehicle-treated group (p. <. 0.01 for both drugs). Seizure duration was also increased in fluoxetine-treated rats. No differences in seizure threshold were observed between treatments (p. >. 0.05). mRNA analysis did not reveal any molecular changes which were common to both treatments. Conclusions: The rate of epileptogenesis in rats is enhanced by chronic treatment with SSRIs. This could potentially have implications regarding the effect of SSRIs on the development or progression of human epilepsy. © 2013.

Bosanac P.,St Vincents Mental Health | Bosanac P.,University of Melbourne | Castle D.J.,University of Melbourne
Advances in Psychiatric Treatment | Year: 2015

'Depot antipsychotics' ('long-acting injectable antipsychotic medications' or LAIs) are underused in the treatment of schizophrenia (including first episodes) and, possibly, of schizophrenia with comorbid substance use disorders. Patients' and clinicians' beliefs and attitudes, and service barriers, affect best practice and evidence-based care in LAI prescription. Poor medication adherence is a key reason for LAI prescription, but patients receiving LAIs may still relapse or experience significant side-effects. Patients' and clinicians' attitudes towards antipsychotic medication, as well as the quality of their recovery-focused relationship, are key factors in adherence. Clinicians should avoid a dichotomous 'oral v. LAI' choice: LAIs may have a place at various stages in the continuum of care and they should be one of the options discussed with any patient requiring long-term treatment, even early in the illness course. Many clinicians need better education about LAIs and greater familiarity with schizophrenia treatment guidelines.

Bosanac P.,St Vincents Mental Health | Castle D.,St Vincents Mental Health
Australasian Psychiatry | Year: 2015

Objective: We aim to provide a selective clinically focused review of the epidemiology, aetiology and management of comorbid anxiety in people with schizophrenia. Method: The following databases were reviewed: PubMed, Medline and Embase. Results: Anxiety is highly prevalent throughout course of schizophrenia, but is often not identified or its clinical significance is under-Appreciated. Also, there is a paucity of rigorous data to support specific treatment guidelines for people with schizophrenia and concurrent anxiety disorders. Psychological treatments such as cognitive behavioural therapy appear effective if targeted carefully, and preliminary data suggest that mindfulness approaches and progressive muscle relaxation may be beneficial. Pharmacological interventions need to be tailored to the individual and target specific symptom sets. There is a growing evidence base about the neurobiology of schizophrenia and concurrent anxiety symptoms or disorders which will hopefully enhance treatment options. Conclusions: Further research is required to guide treatment guidelines for anxiety in people with schizophrenia.

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