Christina M. Temes, Chelsea Boccagno, Alexandra K. Gold, Hadi Kobaissi, Ingrid Hsu, Sofia Montinola, Louisa G. Sylvia
{"title":"Comorbidity of bipolar disorder and borderline personality disorder: Phenomenology, course, and treatment considerations","authors":"Christina M. Temes, Chelsea Boccagno, Alexandra K. Gold, Hadi Kobaissi, Ingrid Hsu, Sofia Montinola, Louisa G. Sylvia","doi":"10.1111/bdi.13465","DOIUrl":"10.1111/bdi.13465","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Bipolar disorder (BD) and borderline personality disorder (BPD) are both serious psychiatric conditions that elevate the risk for harmful outcomes. Although these conditions represent distinct diagnostic entities, existing research suggests that approximately 20% of individuals with BD meet the criteria for comorbid BPD. Individuals with comorbid BD/BPD appear to have a markedly more severe and phenomenologically distinct clinical course when compared with those with BD alone. However, treatments have generally not been tested in this specific population, and currently, no formal treatment guidelines exist for this subgroup of patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>In the current paper, we review the epidemiological and descriptive research characterizing those with comorbid BD/BPD and discuss the impact of this comorbidity on psychosocial treatment. We also review current findings on evidence-based treatments for BD and BPD that show promise in treating those with comorbid BD/BPD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In our review of the literature, we highlight the importance of recognizing this comorbidity and discuss avenues for developing and integrating evidence-based treatment approaches for this understudied clinical population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Although formal trials of interventions targeted to comorbid BD/BPD are limited, there is promising evidence regarding the possibility of using or integrating existing evidence-based approaches for this population. There are also several areas of clinical practice improvement and future research directions that stem from this literature.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 6","pages":"548-555"},"PeriodicalIF":5.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Raphael Cerqueira, Juliana Surjan, Acioly L. T. Lacerda, Cristiano Noto
{"title":"How far have we advanced in early intervention for bipolar disorder?","authors":"Raphael Cerqueira, Juliana Surjan, Acioly L. T. Lacerda, Cristiano Noto","doi":"10.1111/bdi.13461","DOIUrl":"10.1111/bdi.13461","url":null,"abstract":"","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 5","pages":"493-494"},"PeriodicalIF":5.0,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Bárbara Sofia Gonçalves Castro Sousa, Zoé Correia de Sá, Joana Ramos
{"title":"Decoding the enigma: Valproate encephalopathy in a bipolar affective disorder without hyperammonemia","authors":"Bárbara Sofia Gonçalves Castro Sousa, Zoé Correia de Sá, Joana Ramos","doi":"10.1111/bdi.13460","DOIUrl":"10.1111/bdi.13460","url":null,"abstract":"","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 5","pages":"507-509"},"PeriodicalIF":5.0,"publicationDate":"2024-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cultural narratives and modern psychiatry: Bridging perspectives on bipolar disorder's impact on sexual and familial dynamics","authors":"Lien-Chung Wei, Wei-Ching Huang","doi":"10.1111/bdi.13445","DOIUrl":"10.1111/bdi.13445","url":null,"abstract":"","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 6","pages":"624-625"},"PeriodicalIF":5.0,"publicationDate":"2024-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141155129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gin S. Malhi, Uyen Le, Cornelia Kaufmann, Erica Bell
{"title":"Adding esketamine to lamotrigine to treat major depression: Combinatorial synergism, augmentation, or neither?","authors":"Gin S. Malhi, Uyen Le, Cornelia Kaufmann, Erica Bell","doi":"10.1111/bdi.13448","DOIUrl":"10.1111/bdi.13448","url":null,"abstract":"<p>In an investigator-initiated study<sup>1</sup> designed to determine the positioning of esketamine in the treatment (PoET) of depression, we have treated patients with severe depression. As it is a naturalistic study, we have no stipulations as to the antidepressant treatment the person is taking when commencing add-on esketamine therapy, which is administered via bi-weekly insufflation under medical supervision. Most patients that are referred are taking SSRIs, SNRIs or TCAs, and occasionally are taking MAOIs or novel agents such as vortioxetine. However, in one patient who had trialled most treatments, the physician had resorted to trialling lamotrigine even though the patient had no history of bipolar disorder, possibly because of the complexity of the illness (number of comorbidities) and lack of response.</p><p>It is this case, of a 44-year-old Caucasian female (LE) with a current psychiatric history of treatment resistant depression (TRD), along with generalized anxiety disorder (GAD), obsessive-compulsive disorder (OCD) and iatrogenic benzodiazepine dependence that we present here. Previous diagnoses also included orthorexia in recovery and substance misuse in young adulthood. Her medical history includes osteoporosis and ulcerative colitis, but she has been off steroids since 2015, and does not smoke, consume alcohol or use substances.</p><p>In late 2018, LE, then 40 years old, was diagnosed with major depressive disorder with anxiety. There was no significant precipitant for her depressive episodes and because of her illness, she stopped working in 2019. Her depressive symptoms included sadness, numbness, anhedonia, low self-worth, feelings of helplessness and hopelessness, loss of appetite, detachment and passive suicidal ideation. She described her depression as “<i>depression with unbearable pain</i>”, and she was “<i>unable to see the future</i>”. In addition to receiving psychological and dietetic treatments weekly, she also trialled multiple pharmacological treatments including SSRIs, SNRIs, TCAs, MAOIs, atypical antipsychotics and lithium augmentation (see Figure 1). She experienced a partial response with some medications but also had severe side effects. She also underwent a course of rTMS, which she reported “<i>did nothing for me, I felt like it did less than an SSRI</i>”.</p><p>In January 2024, the patient was referred to the CADE clinic<sup>2</sup> and screened for PoET. After an extensive assessment process, we deemed the patient suitable for enrolment. She consented and commenced the study in January 2024. As per our protocol, she received esketamine treatments twice weekly for 4 weeks. At the time of enrolment, LE was taking lamotrigine 200 mg daily, diazepam 4.5 mg daily (slowly weaning off, but kept at a stable dose for the duration of the trial) and suvorexant for sleep. She completed a baseline questionnaire and received her first esketamine treatment in January 2024. She completed the course by mid-February having","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 5","pages":"500-504"},"PeriodicalIF":5.0,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bdi.13448","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141086822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ADHD medications for cognitive impairment in bipolar disorders","authors":"Virginio Salvi","doi":"10.1111/bdi.13459","DOIUrl":"10.1111/bdi.13459","url":null,"abstract":"<p>People with bipolar disorders (BD) often display cognitive dysfunction, especially in verbal and working memory, processing speed and executive functions, which lead to poor occupational outcomes even more than residual symptoms.<span><sup>1</sup></span> Consequently, there is a constant effort to find treatments that might improve cognition and eventually global functioning in BD.</p><p>Several observations point to hypodopaminergic state as a driver of cognitive impairment in BD; therefore, increasing dopamine levels has been attempted as a strategy to ameliorate cognition.</p><p>Both stimulant and non-stimulant ADHD medications increase dopamine and norepinephrine brain levels, making them good candidates for treating cognitive dysfunction in BD. However, there has been a concern as to whether these medications are well tolerated, and specifically whether their use may induce (hypo)manic symptoms or episodes in persons with BD.</p><p>Stemming from these premises, the Targeting Cognition task force of the International Society for Bipolar Disorders (ISBD) conducted a systematic review on the efficacy and tolerability of ADHD medications in treating cognitive dysfunction in BD.<span><sup>2</sup></span></p><p>The review reassures on tolerability, concluding that when BD is properly stabilized, the risk of treatment-emergent manic episodes due to the use of stimulant or non-stimulant ADHD medications is not higher than with placebo or other control conditions. Thus, methylphenidate, lisdexamfetamine, armodafinil, modafinil or bupropion can be safely employed unless BD is pharmacologically stabilized. Beyond the reviewed evidence coming from Randomized Controlled Trials, a large Swedish registry study on 2307 adults with BD who later initiated methylphenidate for concurrent ADHD found no evidence for an association between methylphenidate and treatment-emergent mania among those on concomitant mood stabilizers. On the other hand, those treated with the stimulant alone had a 6.7 times increased rate of manic episodes within 3 months of medication initiation.<span><sup>3</sup></span> Hence, we might say that there is sufficient evidence not to discourage the use of ADHD medications in adequately stabilized BD.</p><p>However, the most compelling research aim was to review the efficacy of ADHD medications as cognitive enhancers in BD: the authors, based on evidence coming from three studies, concluded that there is insufficient data to assert that ADHD medications can improve cognition in BD. The first reviewed study was designed to assess the efficacy of adjunctive methylphenidate in reducing manic symptoms in acutely manic subjects. For safety reasons, the study lasted 2.5 days, after which methylphenidate was deemed ineffective and therefore stopped. The very short period of observation likely speaks for the observed lack of cognitive effect of methylphenidate. The second study, which evaluated the pro-cognitive effects of clonidine on manic subj","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 6","pages":"620-621"},"PeriodicalIF":5.0,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bdi.13459","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Progesterone for premenstrual exacerbations of bipolar disorder in a 15-year-old girl with polycystic ovary syndrome","authors":"Haixin Cen, Liuqing Zhang, Fengju Liu","doi":"10.1111/bdi.13457","DOIUrl":"10.1111/bdi.13457","url":null,"abstract":"","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 8","pages":"824-826"},"PeriodicalIF":5.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140955921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Revisiting cariprazine for bipolar I disorder maintenance treatment","authors":"Maxwell Z. Price, Richard L. Price","doi":"10.1111/bdi.13453","DOIUrl":"10.1111/bdi.13453","url":null,"abstract":"<p>We read with interest the study by McIntyre et al. “Cariprazine as a maintenance therapy in the prevention of mood episodes in adults with bipolar I disorder”<span><sup>1</sup></span> concluding that cariprazine was not superior to placebo in relapse prevention. However, based on our clinical experience successfully utilizing cariprazine to treat acute depressive, manic, and mixed episodes of bipolar I disorder, we have also found cariprazine helpful in preventing recurrence for the vast majority of patients who have remained on cariprazine over the past decade, when the dosing regimen is individualized to meet their needs.<span><sup>2</sup></span> Unfortunately, this was not the case for this study protocol, which may have contributed to an incorrect conclusion.</p><p>As a partial dopamine agonist with eightfold greater affinity for D3 than D2 receptors, and higher D3 affinity than one's endogenous dopamine,<span><sup>3</sup></span> cariprazine is a dynamic medication whereby finding the correct dose is critical to optimizing effects and minimizing side effects. Lower doses function as a dopamine agonist such that 1.5 mg daily can rapidly improve bipolar I depression within 2 weeks.<span><sup>3</sup></span> In contrast, higher approved doses, such as 4.5 mg and 6 mg, which function as a dopamine antagonist, may be required for rapid control of mania and psychosis over several days.<span><sup>3</sup></span> At times, patients who are stable on 1.5 mg cannot tolerate 3 mg due to akathisia. The 3 mg dose lies somewhere in between; it may be too dopamine blocking for some depressed patients yet insufficient for control of mania and psychosis. The unique pharmacodynamic features of cariprazine allow the prescriber to dial in the precise dose to meet patients' needs: lower doses for bipolar I depression; higher doses for bipolar mania and mixed episodes, potentially achieving full spectrum coverage as a relatively well-tolerated monotherapy.</p><p>Another unique aspect of cariprazine is the exceedingly long half-life of its active metabolites, and the protracted time to reach a steady state, which can surpass 12 weeks.<span><sup>3</sup></span> Occasionally, dose reduction is appropriate for late-occurring side effects, such as insomnia. It can also take up to 12 weeks following discontinuation for total cariprazine metabolites to become undetectable, and even longer for poor 3A4 metabolizers or for those taking 3A4 inhibitors,<span><sup>3</sup></span> such as cannabis (permitted in this study). This feature enables effective intermittent dosing schedules for those who either cannot tolerate daily dosing,<span><sup>3</sup></span> prefer intermittent dosing, or face challenges with adherence. Unlike many other antipsychotics, we do not typically encounter withdrawal effects with cariprazine due to low binding affinities for acetylcholine and histamine.<span><sup>3</sup></span> In our experience, bipolar I disorder patients who have taken cariprazine ","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 5","pages":"491-492"},"PeriodicalIF":5.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/bdi.13453","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140943834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
N. Haenen, A. M. Kamperman, A. Prodan, W. A. Nolen, M. P. Boks, R. Wesseloo
{"title":"The efficacy of lamotrigine in bipolar disorder: A systematic review and meta-analysis","authors":"N. Haenen, A. M. Kamperman, A. Prodan, W. A. Nolen, M. P. Boks, R. Wesseloo","doi":"10.1111/bdi.13452","DOIUrl":"10.1111/bdi.13452","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To provide up-to-date clinical guidance on the efficacy of lamotrigine in bipolar disorder (BD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Eligible studies were identified during a systematic literature search according to PRISMA-guidelines. We included randomized controlled trials (RCTs) and cohort studies that quantitatively assessed lamotrigine's efficacy in BD. We divided the included studies into three groups: 1. acute treatment of depression, 2. acute treatment of mania and hypomania, and 3. maintenance treatment. Analyses were stratified by control group (placebo vs active comparator) and treatment strategy (monotherapy vs add-on treatment).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We included 20 RCTs (<i>n</i> = 1166 lamotrigine users) and 20 cohort studies (<i>n</i> = 11,141 lamotrigine users). Twenty-four of these studies were included in meta-analyses. During depressive episodes, greater decreases in depressive symptomatology were associated with initiation of lamotrigine as add-on treatment than with placebo (SMD −0.30 [95% CI = −0.51, −0.10], df = 3, <i>p</i> = 0.004). Decreases in depressive symptomatology did not differ significantly between lamotrigine and the active comparator (SMD −0.28 [95% CI = −1.06, 0.50], df = 3, <i>p</i> = 0.488).</p>\u0000 \u0000 <p>As a maintenance treatment, lamotrigine was associated with a significantly lower relapse/recurrence rate than placebo (risk ratio (RR) 0.84 [95% CI = 0.71, 0.99], df = 2, <i>p</i> = 0.037). Relapse/recurrence rates did not differ significantly between lamotrigine and lithium (RR 1.06 [95% CI = 0.89, 1.25], df = 2, <i>p</i> = 0.513). A qualitative assessment of high-quality register-based studies found that lamotrigine was associated with lower hospital admission rates than other commonly used treatment regimes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>There is substantial evidence for the efficacy of lamotrigine in BD, specifically as add-on treatment during acute depressive episodes and as maintenance treatment for preventing relapse and recurrence.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8959,"journal":{"name":"Bipolar Disorders","volume":"26 5","pages":"431-441"},"PeriodicalIF":5.0,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140943835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}