Objective: Little is known about changes in quality of media reporting of suicide in the community following a celebrity suicide. Our objective was to compare trends in quality of media reporting of suicide, before and after the suicide of an Indian entertainment celebrity, against the World Health Organization suicide reporting guidelines.
Method: Online news portals of English and local language newspapers, as well as television channels, were searched to identify relevant suicide-related news articles. Comparison of reporting characteristics before and after the celebrity suicide was performed using chi-square test or Fisher's exact test.
Results: A total of 3867 eligible news reports were retrieved. There was a significant increase in harmful reporting characteristics, such as reporting the name, age and gender of the deceased (p < 0.001 for all comparisons), mentioning the location (p < 0.001) and reason for suicide (p = 0.04) and including photos of the deceased (p = 0.002) following the celebrity suicide. Helpful reporting practices were less affected; there was a significant rise in inclusion of expert opinion (p = 0.04) and mention of suicide-related warning signs (p = 0.02).
Conclusion: Following a celebrity suicide, significant changes in the quality of media reporting of suicide were noted with an increase in several potentially harmful reporting characteristics.
目的:在名人自杀后,媒体对社区自杀报道质量的变化知之甚少。我们的目的是比较印度一位娱乐名人自杀前后媒体对自杀报道质量的趋势与世界卫生组织自杀报道准则的对比。方法:检索英语和地方语言报纸的在线新闻门户网站以及电视频道,找出与自杀相关的新闻文章。比较名人自杀前后的报道特征采用卡方检验或Fisher精确检验。结果:共检索到3867篇符合条件的新闻报道。在名人自杀后,有害的报道特征显著增加,例如报道死者的姓名、年龄和性别(p p p = 0.04),并包括死者的照片(p = 0.002)。有益的报告做法受到的影响较小;包括专家意见(p = 0.04)和提及自杀相关警告标志(p = 0.02)的人数显著增加。结论:在名人自杀后,媒体对自杀的报道质量发生了显著变化,一些潜在有害的报道特征有所增加。
{"title":"Changing trends in quality of media reporting of suicide in the community following a celebrity suicide in India.","authors":"Vikas Menon, Sujita Kumar Kar, Ramdas Ransing, Ginni Sharma, Jigyansa Ipsita Pattnaik, Charanya Kaliamoorthy, Natarajan Varadharajan, Srijeeta Mukherjee, Aditya Agrawal, Susanta Kumar Padhy, Sm Yasir Arafat","doi":"10.1177/00048674211009618","DOIUrl":"https://doi.org/10.1177/00048674211009618","url":null,"abstract":"<p><strong>Objective: </strong>Little is known about changes in quality of media reporting of suicide in the community following a celebrity suicide. Our objective was to compare trends in quality of media reporting of suicide, before and after the suicide of an Indian entertainment celebrity, against the World Health Organization suicide reporting guidelines.</p><p><strong>Method: </strong>Online news portals of English and local language newspapers, as well as television channels, were searched to identify relevant suicide-related news articles. Comparison of reporting characteristics before and after the celebrity suicide was performed using chi-square test or Fisher's exact test.</p><p><strong>Results: </strong>A total of 3867 eligible news reports were retrieved. There was a significant increase in harmful reporting characteristics, such as reporting the name, age and gender of the deceased (<i>p</i> < 0.001 for all comparisons), mentioning the location (<i>p</i> < 0.001) and reason for suicide (<i>p</i> = 0.04) and including photos of the deceased (<i>p</i> = 0.002) following the celebrity suicide. Helpful reporting practices were less affected; there was a significant rise in inclusion of expert opinion (<i>p</i> = 0.04) and mention of suicide-related warning signs (<i>p</i> = 0.02).</p><p><strong>Conclusion: </strong>Following a celebrity suicide, significant changes in the quality of media reporting of suicide were noted with an increase in several potentially harmful reporting characteristics.</p>","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"81-90"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211009618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38942202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-06-18DOI: 10.1177/00048674211025696
Tom English, David Castle
{"title":"Treating schizophrenia: Should we emphasise 'first do no harm'?","authors":"Tom English, David Castle","doi":"10.1177/00048674211025696","DOIUrl":"https://doi.org/10.1177/00048674211025696","url":null,"abstract":"","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"8-10"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211025696","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39245389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-05-02DOI: 10.1177/00048674211010262
Gin S Malhi, Erica Bell, Darryl Bassett, Philip Boyce, Malcolm Hopwood, Greg Murray, Roger Mulder, Ajeet Singh, Richard Porter
Australian & New Zealand Journal of Psychiatry, 56(1) give misleading results guiding clinical practice. Therefore, we conducted a metaanalysis in a different way by putting NAC-risperidone combination as one group and grouping NAC supplementation to other treatments as another. Our results, which were quite different from those of that meta-analysis (Lee et al., 2021), failed to show effectiveness of NAC supplementation for improving irritability in patients with ASD (Figure 1[a]). Instead, NAC was only effective when used as add-on therapy to risperidone when compared with risperidone treatment alone in respect of improving irritability among patients with ASD (Figure 1[b]). Our findings suggest that current evidence only support the use of NAC as add-on therapy to risperidone for irritability in patients with ASD rather than as supplementation to other treatments.
{"title":"The 2020 mood disorders clinical practice guidelines: Dazzlingly bedazzling!","authors":"Gin S Malhi, Erica Bell, Darryl Bassett, Philip Boyce, Malcolm Hopwood, Greg Murray, Roger Mulder, Ajeet Singh, Richard Porter","doi":"10.1177/00048674211010262","DOIUrl":"https://doi.org/10.1177/00048674211010262","url":null,"abstract":"Australian & New Zealand Journal of Psychiatry, 56(1) give misleading results guiding clinical practice. Therefore, we conducted a metaanalysis in a different way by putting NAC-risperidone combination as one group and grouping NAC supplementation to other treatments as another. Our results, which were quite different from those of that meta-analysis (Lee et al., 2021), failed to show effectiveness of NAC supplementation for improving irritability in patients with ASD (Figure 1[a]). Instead, NAC was only effective when used as add-on therapy to risperidone when compared with risperidone treatment alone in respect of improving irritability among patients with ASD (Figure 1[b]). Our findings suggest that current evidence only support the use of NAC as add-on therapy to risperidone for irritability in patients with ASD rather than as supplementation to other treatments.","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"92-93"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211010262","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38942197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-12-09DOI: 10.1177/00048674211065669
Julia M Lappin
Australian & New Zealand Journal of Psychiatry, 56(1) Substance misuse is common among people who experience psychotic illness, with approximately one-third diagnosed with lifetime comorbid substance misuse (Toftdahl et al., 2016). Detecting and intervening in comorbid substance use is important because it is associated with poorer outcomes across a range of domains including increased rates of not only relapse and re-hospitalisation but also violence, suicide and all-cause mortality (reviewed in Darke et al., 2019). This significant negative prognostic indicator is frequently overlooked both in research, where people with comorbid substance use are often excluded from randomised controlled trials or other experimental studies, and in the clinical setting where substance issues may be considered to fall in the domain of drug and alcohol services. Furthermore, it is possible, even likely, that problematic use of many substances may go undetected in our severe mental illness populations because we do not see substance misuse as our core business, or because we are not exploring all possible drugs that may be in use. So, is it time for us to start to get better at detecting and intervening in substance use? For those clinicians who are motivated to enquire about comorbid substance use as part of a holistic assessment, what are the major substances that we should be inquiring about? Likely, the first drugs that spring to mind in association with psychosis will be cannabis and methamphetamine. It is undoubtedly true that most cases of new-onset psychosis in the context of substance use in Australia, at least in those aged below 30, are related to cannabis, and/or to stimulants, predominantly methamphetamine. The potential for cannabis to increase risk for psychosis has been comprehensively researched and debated over recent decades. Meta-analytic evidence suggests that cannabis use is associated with increased risk for psychosis and in a dose-dependent manner (reviewed in Darke et al., 2019). High-potency cannabis (‘skunk’) contains high concentrations of Δ9tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis. Use is associated with both a higher risk for psychosis and a younger age of its onset. Based on evidence that cannabis use is associated with an earlier onset of psychotic illness, it has also been argued that use may hasten the onset of psychosis in those who are otherwise vulnerable by dint of, for example, familial risk, genetic predisposition and/or environmental factors such as childhood trauma or social deprivation. Methamphetamine is the most common illicitly used amphetamine, with an estimated 37 million users globally (Lappin and Sara, 2019). Use is predominantly of ‘ice’, the high potency crystalline form of methamphetamine. Methamphetamine and its active metabolite amphetamine have long been known to induce psychotic symptoms during use, likely due to their ability to powerfully increase synaptic dopamine. P
{"title":"Comorbid substance use in psychosis: Someone else's problem?","authors":"Julia M Lappin","doi":"10.1177/00048674211065669","DOIUrl":"https://doi.org/10.1177/00048674211065669","url":null,"abstract":"Australian & New Zealand Journal of Psychiatry, 56(1) Substance misuse is common among people who experience psychotic illness, with approximately one-third diagnosed with lifetime comorbid substance misuse (Toftdahl et al., 2016). Detecting and intervening in comorbid substance use is important because it is associated with poorer outcomes across a range of domains including increased rates of not only relapse and re-hospitalisation but also violence, suicide and all-cause mortality (reviewed in Darke et al., 2019). This significant negative prognostic indicator is frequently overlooked both in research, where people with comorbid substance use are often excluded from randomised controlled trials or other experimental studies, and in the clinical setting where substance issues may be considered to fall in the domain of drug and alcohol services. Furthermore, it is possible, even likely, that problematic use of many substances may go undetected in our severe mental illness populations because we do not see substance misuse as our core business, or because we are not exploring all possible drugs that may be in use. So, is it time for us to start to get better at detecting and intervening in substance use? For those clinicians who are motivated to enquire about comorbid substance use as part of a holistic assessment, what are the major substances that we should be inquiring about? Likely, the first drugs that spring to mind in association with psychosis will be cannabis and methamphetamine. It is undoubtedly true that most cases of new-onset psychosis in the context of substance use in Australia, at least in those aged below 30, are related to cannabis, and/or to stimulants, predominantly methamphetamine. The potential for cannabis to increase risk for psychosis has been comprehensively researched and debated over recent decades. Meta-analytic evidence suggests that cannabis use is associated with increased risk for psychosis and in a dose-dependent manner (reviewed in Darke et al., 2019). High-potency cannabis (‘skunk’) contains high concentrations of Δ9tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis. Use is associated with both a higher risk for psychosis and a younger age of its onset. Based on evidence that cannabis use is associated with an earlier onset of psychotic illness, it has also been argued that use may hasten the onset of psychosis in those who are otherwise vulnerable by dint of, for example, familial risk, genetic predisposition and/or environmental factors such as childhood trauma or social deprivation. Methamphetamine is the most common illicitly used amphetamine, with an estimated 37 million users globally (Lappin and Sara, 2019). Use is predominantly of ‘ice’, the high potency crystalline form of methamphetamine. Methamphetamine and its active metabolite amphetamine have long been known to induce psychotic symptoms during use, likely due to their ability to powerfully increase synaptic dopamine. P","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"5-7"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39958645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-05-18DOI: 10.1177/00048674211010327
Esther Hanssen, Mariët van Buuren, Nienke Van Atteveldt, Imke Lj Lemmers-Jansen, Anne-Kathrin J Fett
Objective: Recent findings suggest that diminished processing of positive contextual information about others during interactions may contribute to social impairment in the schizophrenia spectrum. This could be due to general social context processing deficits or specific biases against positive information. We studied the impact of positive and negative social contextual information during social interactions using functional neuroimaging and probed whether these neural mechanisms were associated with real-life social functioning in schizophrenia spectrum disorders.
Methods: Patients with a schizophrenia spectrum disorder (N = 23) and controls disorder (N = 25) played three multi-round trust games during functional magnetic resonance imaging scanning, with no, positive and negative information about the counterpart's trustworthiness, while all counterparts were programmed to behave trustworthy. The main outcome variable was the height of the shared amount in the trust game, i.e. investment, representing an indication of trust. The first investment in the game was considered to be basic trust, since no behavioural feedback was given yet. We performed region-of-interest analyses and examined the association with real-life social functioning using the experience sampling method.
Results: Social contextual information had no effect on patients' first investments, whereas controls made the lowest investment after negative and the highest investments after positive contextual information was provided. Over trials, patients decreased investments, suggesting reduced social reward learning, whereas controls increased investments in response to behavioural feedback in the negative context. Patients engaged the dorsolateral prefrontal cortex less than controls during context presentation and showed reduced activity within the caudate during repayments. In patients, lower investments were associated with more time spent alone and social exclusion and lower caudate activation was marginally significantly associated with higher perceived social exclusion.
Conclusion: The failure to adapt trust to positive and negative social contexts suggests that patients have a general insensitivity to prior social information, indicating top-down processing impairments. In addition, patients show reduced sensitivity to social reward, i.e. bottom-up processing deficits. Moreover, lower trust and lower neural activation were related to lower real-life social functioning. Together, these findings indicate that improving trust and social interactions in schizophrenia spectrum needs a multi-faceted approach that targets both mechanisms.
{"title":"Neural, behavioural and real-life correlates of social context sensitivity and social reward learning during interpersonal interactions in the schizophrenia spectrum.","authors":"Esther Hanssen, Mariët van Buuren, Nienke Van Atteveldt, Imke Lj Lemmers-Jansen, Anne-Kathrin J Fett","doi":"10.1177/00048674211010327","DOIUrl":"https://doi.org/10.1177/00048674211010327","url":null,"abstract":"<p><strong>Objective: </strong>Recent findings suggest that diminished processing of positive contextual information about others during interactions may contribute to social impairment in the schizophrenia spectrum. This could be due to general social context processing deficits or specific biases against positive information. We studied the impact of positive and negative social contextual information during social interactions using functional neuroimaging and probed whether these neural mechanisms were associated with real-life social functioning in schizophrenia spectrum disorders.</p><p><strong>Methods: </strong>Patients with a schizophrenia spectrum disorder (<i>N</i> = 23) and controls disorder (<i>N</i> = 25) played three multi-round trust games during functional magnetic resonance imaging scanning, with no, positive and negative information about the counterpart's trustworthiness, while all counterparts were programmed to behave trustworthy. The main outcome variable was the height of the shared amount in the trust game, i.e. investment, representing an indication of trust. The first investment in the game was considered to be basic trust, since no behavioural feedback was given yet. We performed region-of-interest analyses and examined the association with real-life social functioning using the experience sampling method.</p><p><strong>Results: </strong>Social contextual information had no effect on patients' first investments, whereas controls made the lowest investment after negative and the highest investments after positive contextual information was provided. Over trials, patients decreased investments, suggesting reduced social reward learning, whereas controls increased investments in response to behavioural feedback in the negative context. Patients engaged the dorsolateral prefrontal cortex less than controls during context presentation and showed reduced activity within the caudate during repayments. In patients, lower investments were associated with more time spent alone and social exclusion and lower caudate activation was marginally significantly associated with higher perceived social exclusion.</p><p><strong>Conclusion: </strong>The failure to adapt trust to positive and negative social contexts suggests that patients have a general insensitivity to prior social information, indicating top-down processing impairments. In addition, patients show reduced sensitivity to social reward, i.e. bottom-up processing deficits. Moreover, lower trust and lower neural activation were related to lower real-life social functioning. Together, these findings indicate that improving trust and social interactions in schizophrenia spectrum needs a multi-faceted approach that targets both mechanisms.</p>","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"59-70"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211010327","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38913238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-03-16DOI: 10.1177/0004867421998774
Shu-Bin Li, Ze-Tian Li, Zhi-Hong Lyu, Xiao-Yuan Zhang, Lai-Quan Zou
Objective: Olfactory deficits have been reported in bipolar disorder, but this finding is controversial. This study investigated whether olfactory deficit can serve as a specific marker for bipolar disorder by comparing olfactory function in different mood episodes of bipolar disorder. We also compared olfactory function in bipolar disorder and other mental disorders - namely, major depressive disorder and schizophrenia.
Methods: The study consisted of two experiments. Experiment 1 enrolled 175 bipolar disorder patients (70 depressed subgroup, 70 manic subgroup and 35 euthymic subgroup) and 47 controls. Experiment 2 enrolled the participants from Experiment 1, along with 85 major depressive disorder and 90 schizophrenia patients. The Sniffin' Sticks test was used to evaluate odour identification ability and odour threshold (as a measure of odour sensitivity). The Hamilton Depression Rating Scale and Young Mania Rating Scale were used to assess depressive symptoms in all subjects and manic symptoms in bipolar disorder patients, respectively. We also used the Positive and Negative Syndrome Scale to assess clinical symptoms in schizophrenia patients.
Results: All three bipolar disorder patient subgroups (depressed, manic and euthymic subgroup) showed reduced odour identification ability compared to controls; however, only patients in the acute phase of a mood episode (depressed, and manic subgroup) showed impaired odour sensitivity. Clinical symptoms were negatively correlated with odour sensitivity but not odour identification ability. Bipolar disorder and major depressive disorder patients showed less odour identification and sensitivity impairment than schizophrenia patients.
Conclusion: Odour sensitivity is a potential dopaminergic marker for distinguishing between bipolar disorder patients in acute phase vs remission, while odour identification is a trait but a nonspecific marker of bipolar disorder.
{"title":"Odour identification impairment is a trait but not a disease-specific marker for bipolar disorders: Comparisons of bipolar disorder with different episodes, major depressive disorder and schizophrenia.","authors":"Shu-Bin Li, Ze-Tian Li, Zhi-Hong Lyu, Xiao-Yuan Zhang, Lai-Quan Zou","doi":"10.1177/0004867421998774","DOIUrl":"https://doi.org/10.1177/0004867421998774","url":null,"abstract":"<p><strong>Objective: </strong>Olfactory deficits have been reported in bipolar disorder, but this finding is controversial. This study investigated whether olfactory deficit can serve as a specific marker for bipolar disorder by comparing olfactory function in different mood episodes of bipolar disorder. We also compared olfactory function in bipolar disorder and other mental disorders - namely, major depressive disorder and schizophrenia.</p><p><strong>Methods: </strong>The study consisted of two experiments. Experiment 1 enrolled 175 bipolar disorder patients (70 depressed subgroup, 70 manic subgroup and 35 euthymic subgroup) and 47 controls. Experiment 2 enrolled the participants from Experiment 1, along with 85 major depressive disorder and 90 schizophrenia patients. The Sniffin' Sticks test was used to evaluate odour identification ability and odour threshold (as a measure of odour sensitivity). The Hamilton Depression Rating Scale and Young Mania Rating Scale were used to assess depressive symptoms in all subjects and manic symptoms in bipolar disorder patients, respectively. We also used the Positive and Negative Syndrome Scale to assess clinical symptoms in schizophrenia patients.</p><p><strong>Results: </strong>All three bipolar disorder patient subgroups (depressed, manic and euthymic subgroup) showed reduced odour identification ability compared to controls; however, only patients in the acute phase of a mood episode (depressed, and manic subgroup) showed impaired odour sensitivity. Clinical symptoms were negatively correlated with odour sensitivity but not odour identification ability. Bipolar disorder and major depressive disorder patients showed less odour identification and sensitivity impairment than schizophrenia patients.</p><p><strong>Conclusion: </strong>Odour sensitivity is a potential dopaminergic marker for distinguishing between bipolar disorder patients in acute phase vs remission, while odour identification is a trait but a nonspecific marker of bipolar disorder.</p>","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"71-80"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0004867421998774","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25485428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-05-13DOI: 10.1177/00048674211011259
Mark George, Saxby Pridmore
Malhi et al. (2021) have given reasons for transcranial magnetic stimulation (TMS) not being prominently positioned on the 2020 Royal Australian and New Zealand College of Psychiatrists (RANZCP) mood disorders guidelines algorithm. They state positioning is based on clinical effect, ‘(b)ut rTMS has been posited as a treatment for depression largely because of its mechanism of action and not because of its clinical effect’. It is not stated who or when this positing was performed. We have been involved with TMS since the early 1990s and offer historical facts. For much of the 20th century, it was known that (1) ECT is effective in the treatment of MDD and (2) because the skull is a poor conductor, current electricity cannot be focused and spreads out across the brain causing the side-effects of memory loss and seizure. Psychiatrists around the world explored the application of focused electrical energy (electromagnetic technology) to the brain of people with MDD (with fingers crossed that depolarization would not spread). There was no extravagant expectation of replacing ECT – rather, it was hoped to harness some ECT magic with fewer side-effects. The first study of TMS in MDD was conducted in Germany in 1993 – stimulation was applied over the vertex. In 1995, based on the pathophysiology of MDD, Mark George and colleagues conducted a trial with TMS applied to the left dorsolateral prefrontal cortex – this has remained a potent option for the last quarter century. From the beginning, TMS has been offered to people who have not responded to psychotherapy and medication – treatments which are widely available, proven and relatively inexpensive. TMS involves set-up costs and professional clinical supervision. In the early years, in addition to expense, TMS was reserved for nonresponders to other treatments because of the possibility (unrealized) of side-effects. With each failed treatment, the chance of a subsequent treatment achieving a good outcome is greatly reduced. This is sometimes overlooked when the general outcome of TMS is being evaluated – because most of those who come to TMS have failed at least two other treatments, the achievement of >40% response (Fitzgerald et al., 2016) is remarkable and valuable. While ECT may be more efficacious, TMS has a better balance of efficacy and acceptability. If TMS is to be positioned on an algorithm, for the last two decades, the general recommendation and specific requirement of insurers has been – after two failed treatment attempts and before ECT. This position could be reasonably retained.
{"title":"Positioning TMS.","authors":"Mark George, Saxby Pridmore","doi":"10.1177/00048674211011259","DOIUrl":"https://doi.org/10.1177/00048674211011259","url":null,"abstract":"Malhi et al. (2021) have given reasons for transcranial magnetic stimulation (TMS) not being prominently positioned on the 2020 Royal Australian and New Zealand College of Psychiatrists (RANZCP) mood disorders guidelines algorithm. They state positioning is based on clinical effect, ‘(b)ut rTMS has been posited as a treatment for depression largely because of its mechanism of action and not because of its clinical effect’. It is not stated who or when this positing was performed. We have been involved with TMS since the early 1990s and offer historical facts. For much of the 20th century, it was known that (1) ECT is effective in the treatment of MDD and (2) because the skull is a poor conductor, current electricity cannot be focused and spreads out across the brain causing the side-effects of memory loss and seizure. Psychiatrists around the world explored the application of focused electrical energy (electromagnetic technology) to the brain of people with MDD (with fingers crossed that depolarization would not spread). There was no extravagant expectation of replacing ECT – rather, it was hoped to harness some ECT magic with fewer side-effects. The first study of TMS in MDD was conducted in Germany in 1993 – stimulation was applied over the vertex. In 1995, based on the pathophysiology of MDD, Mark George and colleagues conducted a trial with TMS applied to the left dorsolateral prefrontal cortex – this has remained a potent option for the last quarter century. From the beginning, TMS has been offered to people who have not responded to psychotherapy and medication – treatments which are widely available, proven and relatively inexpensive. TMS involves set-up costs and professional clinical supervision. In the early years, in addition to expense, TMS was reserved for nonresponders to other treatments because of the possibility (unrealized) of side-effects. With each failed treatment, the chance of a subsequent treatment achieving a good outcome is greatly reduced. This is sometimes overlooked when the general outcome of TMS is being evaluated – because most of those who come to TMS have failed at least two other treatments, the achievement of >40% response (Fitzgerald et al., 2016) is remarkable and valuable. While ECT may be more efficacious, TMS has a better balance of efficacy and acceptability. If TMS is to be positioned on an algorithm, for the last two decades, the general recommendation and specific requirement of insurers has been – after two failed treatment attempts and before ECT. This position could be reasonably retained.","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"98-99"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211011259","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38988044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-05-10DOI: 10.1177/00048674211011246
Tarun Bastiampillai, Wini Wei Lam Woo, Sherry Kit Wa Chan, Pramod C Nair
1 Department of Psychiatry, Monash University, Clayton, VIC, Australia 2 Discipline of Psychiatry, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia 3 Mental Health Division, Southern Adelaide Local Health Network, Adelaide, SA, Australia 4 Department of Psychiatry, LKS Faculty of Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR 5 Discipline of Clinical Pharmacology, Flinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia
{"title":"Why does clozapine cause increased rebound psychosis and catatonia, compared to quetiapine?","authors":"Tarun Bastiampillai, Wini Wei Lam Woo, Sherry Kit Wa Chan, Pramod C Nair","doi":"10.1177/00048674211011246","DOIUrl":"https://doi.org/10.1177/00048674211011246","url":null,"abstract":"1 Department of Psychiatry, Monash University, Clayton, VIC, Australia 2 Discipline of Psychiatry, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia 3 Mental Health Division, Southern Adelaide Local Health Network, Adelaide, SA, Australia 4 Department of Psychiatry, LKS Faculty of Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR 5 Discipline of Clinical Pharmacology, Flinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"98"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211011246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38887226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-08-30DOI: 10.1177/00048674211043443
William Lugg
Australian & New Zealand Journal of Psychiatry, 56(1) robust testing. For example, our Windows of Antidepressant Response Paradigm (WARP) may be useful in devising future clinical trials, especially where agents purported to have rapid actions are investigated. This would also test the utility of the paradigm and allow it to be further refined, if found to be useful. Similarly, our Channelling Response Paradigm (CRP) can perhaps provide a framework for naturalistic treatment studies conducted in real-world populations, in a similar vein to landmark studies such as STAR*D (Rush et al., 2004). Dr Rosenman’s description of the guidelines as ‘intellectually dazzling’ is balanced by his well-founded concern that psychiatric diagnoses of disorders and paradigms for psychiatric management need to constantly evolve and strive harder to better capture reality. While we share his, and arguably mainstream psychiatry’s, belief that the current binary diagnoses do not adequately capture the descriptive landscape of mental health (which has prominent dimensional components like A, C and E), we have had to be pragmatic and construct a guideline on the available evidence which derives principally from a taxonomy based on binary diagnoses. We thus extend an invitation to everyone to assist us in further bedazzling future iterations of the guidelines and help us escape the confines of our thinking.
{"title":"The case for discontinuation of the 'discontinuation syndrome'.","authors":"William Lugg","doi":"10.1177/00048674211043443","DOIUrl":"https://doi.org/10.1177/00048674211043443","url":null,"abstract":"Australian & New Zealand Journal of Psychiatry, 56(1) robust testing. For example, our Windows of Antidepressant Response Paradigm (WARP) may be useful in devising future clinical trials, especially where agents purported to have rapid actions are investigated. This would also test the utility of the paradigm and allow it to be further refined, if found to be useful. Similarly, our Channelling Response Paradigm (CRP) can perhaps provide a framework for naturalistic treatment studies conducted in real-world populations, in a similar vein to landmark studies such as STAR*D (Rush et al., 2004). Dr Rosenman’s description of the guidelines as ‘intellectually dazzling’ is balanced by his well-founded concern that psychiatric diagnoses of disorders and paradigms for psychiatric management need to constantly evolve and strive harder to better capture reality. While we share his, and arguably mainstream psychiatry’s, belief that the current binary diagnoses do not adequately capture the descriptive landscape of mental health (which has prominent dimensional components like A, C and E), we have had to be pragmatic and construct a guideline on the available evidence which derives principally from a taxonomy based on binary diagnoses. We thus extend an invitation to everyone to assist us in further bedazzling future iterations of the guidelines and help us escape the confines of our thinking.","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"93-95"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39370920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-01-01Epub Date: 2021-05-10DOI: 10.1177/00048674211011243
Tarun Bastiampillai, Sherry Kit Wa Chan, Stephen Allison, David Copolov, Jeffrey Cl Looi
1 Department of Psychiatry, Monash University, Clayton, VIC, Australia 2 College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia 3 Consortium of Australian-Academic Psychiatrists for Independent Policy and Research Analysis (CAPIPRA), Canberra, ACT, Australia 4 Department of Psychiatry, LKS Faculty of Medicine, University of Hong Kong, Hong Kong SAR 5 The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pok Fu Lam, Hong Kong 6 Academic Unit of Psychiatry and Addiction Medicine, The Australian National University Medical School, Canberra Hospital, Canberra, ACT, Australia
{"title":"Antipsychotic treatment in clinical high risk for psychosis: Iatrogenesis related to dopamine supersensitivity psychosis?","authors":"Tarun Bastiampillai, Sherry Kit Wa Chan, Stephen Allison, David Copolov, Jeffrey Cl Looi","doi":"10.1177/00048674211011243","DOIUrl":"https://doi.org/10.1177/00048674211011243","url":null,"abstract":"1 Department of Psychiatry, Monash University, Clayton, VIC, Australia 2 College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia 3 Consortium of Australian-Academic Psychiatrists for Independent Policy and Research Analysis (CAPIPRA), Canberra, ACT, Australia 4 Department of Psychiatry, LKS Faculty of Medicine, University of Hong Kong, Hong Kong SAR 5 The State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pok Fu Lam, Hong Kong 6 Academic Unit of Psychiatry and Addiction Medicine, The Australian National University Medical School, Canberra Hospital, Canberra, ACT, Australia","PeriodicalId":117457,"journal":{"name":"The Australian and New Zealand journal of psychiatry","volume":" ","pages":"97"},"PeriodicalIF":4.6,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/00048674211011243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38967228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}