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Adding esketamine to lamotrigine to treat major depression: Combinatorial synergism, augmentation, or neither? 在拉莫三嗪中加入艾司卡胺治疗重度抑郁症:组合协同作用、增强作用,还是两者皆无?
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-23 DOI: 10.1111/bdi.13448
Gin S. Malhi, Uyen Le, Cornelia Kaufmann, Erica Bell
<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
在一项由研究者发起的研究1 中,我们对严重抑郁症患者进行了治疗,该研究旨在确定埃斯可他胺在抑郁症治疗(PoET)中的定位。由于这是一项自然研究,我们没有规定患者在开始添加埃斯开他敏治疗时正在服用哪种抗抑郁药物,而是在医生的指导下每两周对患者进行一次灌注。大多数转诊患者都在服用 SSRIs、SNRIs 或 TCAs,偶尔也会服用 MAOIs 或新型药物,如 vortioxetine。然而,有一名患者已经试用了大多数治疗方法,尽管患者没有双相情感障碍病史,但医生还是试用了拉莫三嗪,这可能是因为病情复杂(合并症多)和缺乏反应。我们在此介绍的病例是一名 44 岁的白种女性(LE),她目前的精神病史为治疗抵抗性抑郁症(TRD),同时伴有广泛性焦虑症(GAD)、强迫症(OCD)和先天性苯二氮卓类药物依赖。以前的诊断还包括恢复期的矫形厌食症和年轻时的药物滥用。她的病史包括骨质疏松症和溃疡性结肠炎,但她自2015年起就不再使用类固醇,也不吸烟、饮酒或使用药物。2018年底,时年40岁的LE被诊断为重度抑郁障碍伴焦虑。她的抑郁发作没有明显的诱因,因为疾病,她在2019年停止了工作。她的抑郁症状包括悲伤、麻木、失乐症、自我价值感低、无助感和绝望感、食欲不振、疏远和消极自杀的想法。她将自己的抑郁症描述为 "伴有难以忍受的痛苦的抑郁症",她 "看不到未来"。除了每周接受心理和饮食治疗外,她还尝试了多种药物治疗,包括 SSRIs、SNRIs、TCAs、MAOIs、非典型抗精神病药物和锂增强剂(见图 1)。她对一些药物产生了部分反应,但也出现了严重的副作用。她还接受了一个疗程的经颅磁刺激(rTMS)治疗,但她说 "对我毫无用处,我感觉比 SSRI 的作用还小"。2024 年 1 月,患者被转介到 CADE 诊所2 并接受 PoET 筛查。经过广泛的评估,我们认为该患者适合参加研究。她同意并于 2024 年 1 月开始接受研究。按照我们的治疗方案,她每周接受两次埃斯开他敏治疗,为期 4 周。入组时,LE 每天服用拉莫三嗪 200 毫克、地西泮 4.5 毫克(缓慢减量,但在试验期间保持稳定剂量)和舒眠酮(suvorexant)。她填写了一份基线调查问卷,并于2024年1月接受了首次埃斯卡胺治疗。她在二月中旬完成了疗程,总共接受了八次艾司卡胺治疗。在整个研究期间,她每周填写一次问卷,其中包括标准抑郁症状量表,以及由定制项目组成的每日问卷。为确保数据收集的准确性,对每日问卷的完成情况进行了积极监控。此外,在埃斯氯胺酮治疗4周后,还需完成一份综合治疗后问卷,其中包含与基线问卷相同的量表。PoET研究旨在确定最适合使用埃斯氯胺酮的患者的临床特征,并确定哪些抗抑郁药物最有可能对埃斯氯胺酮的增强作用产生反应。在埃斯氯胺酮治疗期间,LE出现了轻微的解离和一过性血压升高等副作用,这两种副作用都在意料之中,并在用药1小时后消失。服用埃斯氯胺酮(56 毫克)一周后,她表示 "感觉好多了,睡得也更好了"(抑郁症症状快速量表-医生评分 [QIDS-C] = 21)。服用埃斯氯胺酮(84毫克)第2周后,她报告说,治疗后情绪立即得到了提升,并持续了24小时,但这种效果没有持续到这一天(QIDS-C = 14)。服用埃斯氯胺酮(84毫克)第3周后,LE报告说她的情绪在治疗后有所好转,被动自杀念头也完全停止了(QIDS-C = 10)。服用埃斯卡胺(84毫克)第4周后,她报告说 "情绪明显好转,很久以来第一次感到饥饿",同时 "焦虑感明显下降"。她还指出,埃斯氯胺酮的效果似乎一直在持续,她这样描述道:"(我的)情绪继续保持稳定,精力充沛,(我)能够完成必要的任务"。
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引用次数: 0
ChatGPT in academic psychiatry 精神病学的 ChatGPT。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-20 DOI: 10.1111/bdi.13451
Hinpetch Daungsupawong, Viroj Wiwanitkit
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引用次数: 0
ADHD medications for cognitive impairment in bipolar disorders 治疗双相情感障碍认知障碍的 ADHD 药物。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-20 DOI: 10.1111/bdi.13459
Virginio Salvi
<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
双相情感障碍(BD)患者通常表现出认知功能障碍,尤其是在言语和工作记忆、处理速度和执行功能方面,这比残留症状更容易导致不良的职业后果。因此,人们一直在努力寻找可以改善认知功能并最终改善 BD 整体功能的治疗方法。一些观察结果表明,多巴胺能低下状态是 BD 认知功能障碍的驱动因素;因此,人们尝试将提高多巴胺水平作为改善认知功能的策略。刺激性和非刺激性 ADHD 药物均可提高大脑多巴胺和去甲肾上腺素水平,因此是治疗 BD 认知功能障碍的理想药物。基于这些前提,国际双相情感障碍协会(ISBD)"以认知为目标 "工作组对多动症药物治疗双相情感障碍患者认知功能障碍的疗效和耐受性进行了系统回顾。该综述对耐受性给予了肯定,认为在 BD 得到适当稳定的情况下,因使用兴奋剂或非兴奋剂 ADHD 药物而导致治疗引发躁狂发作的风险并不比使用安慰剂或其他对照条件高。因此,除非对 BD 进行药物稳定,否则可以安全地使用哌醋甲酯、利眠宁、阿莫达非尼、莫达非尼或安非他明。除了来自随机对照试验的审查证据外,瑞典的一项大型登记研究也发现,在同时服用情绪稳定剂的患者中,没有证据表明哌醋甲酯与治疗引发的躁狂症之间存在关联,该研究针对的是 2307 名患有 BD 的成年人,他们后来开始服用哌醋甲酯治疗并发多动症。3 因此,我们可以说,有足够的证据表明,在病情充分稳定的 BD 患者中,并不妨碍使用 ADHD 药物。然而,最引人注目的研究目的是审查 ADHD 药物作为 BD 认知增强剂的疗效:作者根据三项研究的证据得出结论,认为没有足够的数据可以断言 ADHD 药物可以改善 BD 的认知能力。第一项研究旨在评估哌醋甲酯辅助治疗对减轻急性躁狂症患者躁狂症状的疗效。出于安全考虑,研究持续了 2.5 天,之后哌醋甲酯被认为无效,因此停止了研究。观察时间很短很可能是哌醋甲酯对认知缺乏影响的原因。第二项研究评估了氯硝柳胺对躁狂症受试者的认知促进作用,该研究采用了小型精神状态检查(Mini-Mental State Examination),这是一种针对老年痴呆症的通用认知筛查工具,很可能缺乏评估特定认知功能细微变化的敏感性。值得注意的是,这两项研究都对急性躁狂症发作时的认知能力进行了评估。由于躁狂症患者注意力分散、易冲动,而且经常缺乏合作,因此对其认知能力进行评估本身就很困难。此外,有人认为,躁狂症核心症状影响或导致的认知障碍大多会在发作结束后消失;因此,正如 ISBD 专家小组本身所指出的那样,最好在躁狂症的恢复期而非急性期对认知能力进行评估。这项研究的对象是抑郁症患者或轻度抑郁症患者,并采用了全面的认知评估方法。然而,与安慰剂相比,莫达非尼对处理速度和言语学习的改善仅有轻微的显著性,这显然是由于样本量非常小(总共 12 名受试者)、6 虽然在儿童/青少年中,哌醋甲酯的剂量效应相关,剂量越大,改善越大,但在处理速度、记忆痉挛和工作记忆等领域的影响很小。尽管如此,这两篇论文都得出结论,ADHD 药物对 ADHD 症状的影响程度远大于对认知功能的影响程度,在大多数情况下,只能得出小到中等的效应大小。从这些元分析和 Miskowiak 等人的系统综述中可以得出的一个教训是,未来评估认知增强剂对 BD 认知影响的研究应采用更合理的方法。
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引用次数: 0
Revisiting cariprazine for bipolar I disorder maintenance treatment 重新审视卡哌嗪用于双相情感障碍 I 的维持治疗。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-15 DOI: 10.1111/bdi.13453
Maxwell Z. Price, Richard L. Price
<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
我们饶有兴趣地阅读了麦金太尔(McIntyre)等人的研究报告:"卡哌嗪作为一种维持疗法,用于预防成人双相情感障碍 I 的情绪发作 "1 ,结论是卡哌嗪在预防复发方面并不优于安慰剂。然而,根据我们成功使用卡哌嗪治疗双相情感障碍 I 急性抑郁、躁狂和混合发作的临床经验,我们也发现卡哌嗪在预防复发方面很有帮助。作为一种部分多巴胺激动剂,它对 D3 受体的亲和力是 D2 受体的八倍,D3 受体的亲和力高于内源性多巴胺3 ,因此卡培拉嗪是一种动态药物,找到正确的剂量对于优化疗效和减少副作用至关重要。3 相反,4.5 毫克和 6 毫克等批准剂量较高的药物具有多巴胺拮抗剂的作用,可以在数天内迅速控制躁狂症和精神病。3 毫克的剂量介于两者之间;对于某些抑郁症患者来说,它的多巴胺阻断作用可能过强,但又不足以控制躁狂症和精神病。卡培拉嗪独特的药效学特征使处方者可以根据患者的需要调整精确的剂量:双相抑郁 I 期患者可使用较低剂量;双相躁狂症和混合发作患者可使用较高剂量,作为一种耐受性相对较好的单一疗法,卡培拉嗪有可能实现全方位治疗。3 有时,对于晚期出现的副作用,如失眠,可适当减少剂量。此外,停药 12 周后才能检测不到卡哌嗪的总代谢物,对于 3A4 代谢较差或服用 3A4 抑制剂(如大麻(本研究允许))的患者来说,这段时间甚至更长。对于那些不能耐受每日服药、3 偏爱间歇服药或在服药依从性方面面临挑战的患者来说,这一特点可以实现有效的间歇服药计划。与许多其他抗精神病药物不同,由于卡培拉嗪与乙酰胆碱和组胺的结合亲和力较低,我们通常不会遇到停药效应。3 根据我们的经验,服用卡培拉嗪数月的躁郁症患者在停药后的数月内可能会保持稳定,这是因为卡培拉嗪具有长效作用。3 在这一阶段,导致停药的不良事件(67 例)可能归因于这种激进的用药计划。相反,为什么不允许双相 I 型躁狂症和混合型患者按照 FDA 指南服用 4.5 毫克或 6 毫克?3 在这一阶段,因疗效不佳而停药的比例(35)可能归因于治疗剂量不足。未能达到随机化标准(143 例)也可能反映出缺乏个体化用药。半数以上的开放标签患者在双盲随机化之前停药,这限制了样本对那些服用 3 毫克疗效最好的患者的普适性,这就引出了下一个问题:为什么要把剂量降到 1.5 毫克?更有效的设计应该是根据指数发作情况进行剂量滴定,并在双盲阶段进行调整,以解决复发的早期迹象和/或耐受性问题,口服4 和长效注射阿立哌唑5 的双相 I 型维持治疗研究就是这样设计的。此外,卡哌嗪代谢物的作用时间比口服阿立哌唑的作用时间更长,后者的维持治疗研究时间为 74 周,为什么仅在 39 周后就停止研究呢?卡普兰-梅耶曲线在 36 周时开始出现分叉,包括复发时间和躁狂复发时间,这可能反映了躁狂症所需的卡哌嗪剂量较高,而抑郁症的药效学效应则较低。从现实世界的临床背景来看,这项研究同样可以得出结论:服用 3 毫克卡哌嗪 16 周,可以持久预防双相情感障碍 I 的抑郁、躁狂和混合发作的复发,其效果与剂量减至 1.5 毫克、继续服用 3 毫克或停药 39 周的效果相当,"所有症状和功能的改善均得以维持"。
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引用次数: 0
The efficacy of lamotrigine in bipolar disorder: A systematic review and meta-analysis 拉莫三嗪对躁郁症的疗效:系统回顾和荟萃分析。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-15 DOI: 10.1111/bdi.13452
N. Haenen, A. M. Kamperman, A. Prodan, W. A. Nolen, M. P. Boks, R. Wesseloo

Objective

To provide up-to-date clinical guidance on the efficacy of lamotrigine in bipolar disorder (BD).

Methods

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).

Results

We included 20 RCTs (n = 1166 lamotrigine users) and 20 cohort studies (n = 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, p = 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, p = 0.488).

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, p = 0.037). Relapse/recurrence rates did not differ significantly between lamotrigine and lithium (RR 1.06 [95% CI = 0.89, 1.25], df = 2, p = 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.

Conclusions

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.

目的:就拉莫三嗪对双相情感障碍(BD)的疗效提供最新的临床指导:就拉莫三嗪对双相情感障碍(BD)的疗效提供最新的临床指导:根据PRISMA指南,通过系统文献检索确定了符合条件的研究。我们纳入了定量评估拉莫三嗪对躁狂症疗效的随机对照试验(RCT)和队列研究。我们将纳入的研究分为三组:1.抑郁症的急性治疗;2.躁狂症和躁狂症的急性治疗;3.维持治疗。根据对照组(安慰剂与活性比较药)和治疗策略(单药治疗与附加治疗)进行分层分析:我们纳入了 20 项 RCT(n = 1166 名拉莫三嗪使用者)和 20 项队列研究(n = 11141 名拉莫三嗪使用者)。其中24项研究被纳入荟萃分析。在抑郁发作期间,开始使用拉莫三嗪作为附加治疗与安慰剂相比,抑郁症状的减少幅度更大(SMD -0.30 [95% CI = -0.51, -0.10],df = 3,p = 0.004)。拉莫三嗪与活性比较药在抑郁症状的减少方面没有显著差异(SMD -0.28 [95% CI = -1.06, 0.50], df = 3, p = 0.488)。作为一种维持治疗方法,拉莫三嗪的复发/复发率明显低于安慰剂(风险比 (RR) 0.84 [95% CI = 0.71, 0.99], df = 2, p = 0.037)。拉莫三嗪和锂盐的复发/复发率差异不大(RR 1.06 [95% CI = 0.89, 1.25],df = 2,p = 0.513)。对高质量登记研究的定性评估发现,与其他常用治疗方案相比,拉莫三嗪的入院率较低:有大量证据表明拉莫三嗪对 BD 具有疗效,特别是作为急性抑郁发作期间的附加治疗和预防复发的维持治疗。
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引用次数: 0
Back to the future: May Kleine-Levin syndrome be an emerging psychiatric disorder? 回到未来:克莱因-莱文综合征可能是一种新出现的精神疾病吗?
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-15 DOI: 10.1111/bdi.13455
Sacha Koutsikas, Antoine Yrondi, Laura Hatchondo, Rachel Debs
<p>Since the 20th century, atypical cases of recurrent hypersomnia are no longer related to mood disorders but are grouped together in the new Kleine-Levin syndrome (KLS).</p><p>Between neurology and psychiatry, the KLS symptoms include hypersomnia (up to 20 h of sleep/day), which may or may not be accompanied by disinhibition, derealisation, extreme apathy, cognitive dysfunction, childishness, anxiety, hallucinations, ideas of reference and delusions of grandeur. At the point of diagnosis, additional examinations (biology, imaging) are not diagnostic and are even less pathognomonic, just as is the case for psychiatric disorders.</p><p>The indication for long-term treatment based on thymoregulatory depends on the intensity and frequency of the episodes.</p><p>Today, the international literature insists on a dichotomy between BPD and very recent KLS despite the redundancy of such a distinction<span><sup>1</sup></span> (Figure 1).</p><p>KLS is commonly recognised as a neurological disease with inflammatory markers on functional imaging during episodes, between episodes and post-mortem. This has enabled it to be distinguished from mood disorders. However, recent studies on BPD have shown that it too.</p><p>In addition, studies of both patients with BPD and their relatives have found that cognitive impairment and sleep problems appear 5–6 years before the first decompensation.<span><sup>2</sup></span></p><p>At the same time, studies report that KLS leads to psychiatric decompensation in 20% of cases, with some cases being premorbid.<span><sup>3</sup></span> Following the revision of the criteria for KLS,<span><sup>4</sup></span> the number of cases being diagnosed has been increasing. Of all newly diagnosed cases of KLS, the diagnosis is in doubt in 20% of these cases, that is, in those involving latent or overt psychiatric comorbidities. These cases could, therefore, involve undiagnosed psychiatric pathologies.</p><p>While there may be doubt regarding 20% of KLS cases, 80% are genuine. The question then arises as to which symptoms are useful in diagnosis: the old triad or the new paradigm of the 2000s?</p><p>For Kleine, a neurologist, Levin, a psychiatrist, and their predecessors, it was a syndrome, not a disorder, that they were investigating. Ultimately, it was not a disorder that they were referring to, but rather an invitation for the scientific community to communicate with each other and a request for help with treatment.</p><p>Recent studies have shown that the onset of BPD is associated with frustrating and unspecific symptoms, particularly anxiety, dissociative symptoms, and issues with sleeping. The mood-related component appears much later.<span><sup>5</sup></span></p><p>One might wonder why the scientific community is resistant to the idea of classifying KLS as a mood disorder, given the heterogenic nature of bipolar spectrum disorder, which covers different types of BPD (Akiskal classification).</p><p>In practice, these are young patien
自 20 世纪以来,反复嗜睡的非典型病例不再与情绪障碍有关,而是被归入新的克莱因-莱文综合征(Kleine-Levin Syndrome,KLS)。在神经病学和精神病学之间,KLS 的症状包括嗜睡(每天睡眠时间长达 20 小时),可能伴有也可能不伴有抑制、去理想化、极度冷漠、认知功能障碍、幼稚、焦虑、幻觉、参照物观念和妄想。在诊断时,其他检查(生物学、影像学)并不具有诊断意义,甚至不具有病理诊断意义,这与精神疾病的情况一样。KLS 通常被认为是一种神经系统疾病,在发作时、发作间歇期和死后的功能成像中都有炎症标记物,这使其得以与情绪障碍相区分。此外,对 BPD 患者及其亲属的研究发现,认知障碍和睡眠问题出现在首次精神失常前的 5-6 年。2 同时,研究报告显示,20% 的 KLS 会导致精神失常,部分病例在发病前就已出现。在所有新确诊的 KLS 病例中,有 20% 的病例诊断存疑,即那些有潜在或明显精神并发症的病例。因此,这些病例可能涉及未确诊的精神疾病。虽然 20% 的 KLS 病例可能存在疑点,但 80% 的病例是真实的。那么问题来了,哪些症状对诊断有用:是旧的三联征,还是 2000 年代的新范式?最近的研究表明,BPD 的发病与令人沮丧的非特异性症状有关,尤其是焦虑、分离症状和睡眠问题。5 人们可能会问,既然双相情感谱系障碍的异质性涵盖了不同类型的双相情感障碍(Akiskal 分类),为什么科学界对将 KLS 归类为情感障碍的想法持抵制态度呢?实际上,这些都是接受快速诊断的年轻患者。在必要的情况下,如果出现极端的精神失常,在成年晚期进行精神诊断是合适的。无论是对于 20% 的 KLS 病例中存在合并精神病理3 ,还是对于 100% 的 KLS 病例(如果这种综合征的存在被推翻),都已经有涉及儿童精神病学的精神保健或对这些患者进行精神监测。然而,关于在病程早期(尤其是青少年)开始药物治疗,仍有一些未解之谜:药物治疗是否能防止严重失代偿?克莱因-莱文综合征可能是双相情感障碍谱系中的一种新出现的精神障碍,其主要预防挑战在于最近的命名尚有争议,临床病例也存在问题,无法提供更好的护理。Rachel Debs、Antoine Yrondi 和 Laura Hatchondo 参与了手稿的撰写,审阅并批准了最终版本的内容,并同意对工作的所有方面负责。AY接受了阿斯利康、杨森、灵北、大冢和Servier的演讲酬金,并进行了与杨森和灵北药品开发相关的临床研究,与本工作无关。违反伦理声明规定可能导致严重后果。我同意上述声明,并声明本稿件遵循《作者指南》和《伦理声明》中规定的威利图书馆政策。
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引用次数: 0
Bipolar affective disorder in a patient with Dyke-Davidoff-Masson syndrome 戴克-大卫杜夫-马森综合征患者的躁郁症。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-14 DOI: 10.1111/bdi.13449
Aromal Shibu, Huded Swarna Rekha, Sujai Ramachandraiah, Raghavendra Kenchaiah, Arvinda Hanumanthapura Ramlingaiah, Krishna Prasad Muliyala
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引用次数: 0
Featured Cover 精选封面
IF 5.4 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-13 DOI: 10.1111/bdi.13456
Anne Duffy, Paul Grof

The cover image is based on the Commentary Advancing clinical practice and discovery research through revised taxonomy: Case in point bipolar disorder diagnosis by Anne Duffy and Paul Grof, https://doi.org/10.1111/bdi.13415.

封面图片来自 Anne Duffy 和 Paul Grof 的评论文章《通过修订分类法推进临床实践和发现研究》:Anne Duffy 和 Paul Grof 的双相情感障碍诊断案例,https://doi.org/10.1111/bdi.13415。
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引用次数: 0
Eco-anxiety: Towards a medical model and the new framework of ecolalgia 生态焦虑症:迈向生态焦虑的医学模式和新框架。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-13 DOI: 10.1111/bdi.13446
Nausicaa Christodoulou, Karine Laaidi, Pierre A. Geoffroy

Introduction

In the context of global warming, new terms emerged in the global media and in the psychology field to embody the negative feelings which come along with climate change such as ‘eco-anxiety’ or ‘solastalgia’. The pathological character of these emotions is denied although medical opinion is often required for helping people to handle them. Also, no proper medical framework in the field exists to study and care for these patients.

Methods

In this narrative review, we aim to (1) analyse the concept of eco-anxiety by focusing on its history and developed concepts, (2) summarize the different scales built to assess eco-anxiety and (3) propose a new medical framework.

Results

We came out with a framework based on the transformation of a physiological adaptative behaviour the ‘eco-distress’. It is composed of three dimensions: eco-anger, eco-grief and eco-worry, it is not debilitating in daily life and promotes coping strategies such as management of negative emotions and pro-environmental behaviours (PEB). It can transform itself into a pathological state, the ‘ecolalgia’, composed of two core dimensions: eco-anxiety and eco-depression, leading to functional impairment and decrease in PEB. If ecolalgia maintains over 15 days, we propose to consider it as a full psychiatric disorder needing medical advice.

Conclusion

This new framework enables a novel approach that is necessary for the improved management of mental health issues related to climate change.

导言:在全球变暖的背景下,全球媒体和心理学领域出现了一些新的术语来体现气候变化带来的负面情绪,如 "生态焦虑 "或 "孤独焦虑"。尽管这些情绪往往需要医学意见来帮助人们处理,但这些情绪的病理特征却被否认了。此外,该领域也没有适当的医学框架来研究和护理这些患者:在这篇叙述性综述中,我们的目的是:(1)分析生态焦虑的概念,重点关注其历史和发展的概念;(2)总结为评估生态焦虑而建立的不同量表;(3)提出一个新的医学框架:结果:我们提出了一个基于生理适应行为转变的框架,即 "生态压力"。它由三个方面组成:生态焦虑、生态悲伤和生态忧虑,在日常生活中不会使人衰弱,并促进应对策略,如管理负面情绪和亲环境行为(PEB)。它可以转化为一种病理状态,即 "生态焦虑",由两个核心维度组成:生态焦虑和生态抑郁,从而导致功能障碍和亲环境行为(PEB)的减少。如果 "生态焦虑 "持续超过 15 天,我们建议将其视为需要医疗建议的全面精神障碍:这个新框架提供了一种新方法,对于改善与气候变化相关的心理健康问题的管理十分必要。
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引用次数: 0
First manic episode induced by abrupt discontinuation of sertraline in a patient with OCD: A case report 一名强迫症患者因突然停用舍曲林而首次躁狂发作:病例报告。
IF 5 2区 医学 Q1 CLINICAL NEUROLOGY Pub Date : 2024-05-13 DOI: 10.1111/bdi.13450
Bedirhan Şenol, Rabia Nazik Ekinci, Erol Göka
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引用次数: 0
期刊
Bipolar Disorders
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