Academic literature on the topic 'Inflammatory response in mood disorders'
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Journal articles on the topic "Inflammatory response in mood disorders"
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Haroon, E., X. Chen, Z. Li, X. P. Hu, J. C. Felger, and A. H. Miller. "Multimodal neural signature of inflammatory response in mood disorders." Brain, Behavior, and Immunity 66 (November 2017): e38-e39. http://dx.doi.org/10.1016/j.bbi.2017.07.140.
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Moya, Gonzalo E., Phillip D. Rivera, and Kristin E. Dittenhafer-Reed. "Evidence for the Role of Mitochondrial DNA Release in the Inflammatory Response in Neurological Disorders." International Journal of Molecular Sciences 22, no. 13 (June 29, 2021): 7030. http://dx.doi.org/10.3390/ijms22137030.
Full textAbstract:
Mitochondria are regarded as the metabolic centers of cells and are integral in many other cell processes, including the immune response. Each mitochondrion contains numerous copies of mitochondrial DNA (mtDNA), a small, circular, and bacterial-like DNA. In response to cellular damage or stress, mtDNA can be released from the mitochondrion and trigger immune and inflammatory responses. mtDNA release into the cytosol or bloodstream can occur as a response to hypoxia, sepsis, traumatic injury, excitatory cytotoxicity, or drastic mitochondrial membrane potential changes, some of which are hallmarks of neurodegenerative and mood disorders. Released mtDNA can mediate inflammatory responses observed in many neurological and mood disorders by driving the expression of inflammatory cytokines and the interferon response system. The current understanding of the role of mtDNA release in affective mood disorders and neurodegenerative diseases will be discussed.
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Chang, Hui H., and Po S. Chen. "Inflammatory Biomarkers for Mood Disorders - A Brief Narrative Review." Current Pharmaceutical Design 26, no. 2 (March 4, 2020): 236–43. http://dx.doi.org/10.2174/1381612826666200115100726.
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Background: The nervous system and the immune system interact consistently in the brain and peripheries. Inflammation in the brain not only alters the metabolism of neurotransmitters, but also causes network dysfunction, structural changes, and the development of mood symptomology in patients with mood disorders. In addition, the dysregulation of the neuroimmune axis in mood disorders drives multiple-system comorbidities. Furthermore, patients with low-grade inflammation are more likely to exhibit treatment resistance with both pharmacotherapy and non-pharmacotherapy. Objective: The aim of this review was to examine the available data regarding not only evidence of inflammation in the pathophysiology of mood disorders and their comorbid conditions, but also potential inflammatory biomarkers of mood disorders. Methods: Studies of the use of adjunct anti-inflammatory medications in mood disorders, and inflammatory biomarkers that may guide treatment outcomes in mood disorders, were summarized. Results: Studies have demonstrated that certain adjunct anti-inflammatory medications might help to improve mood symptoms and reduce comorbidities, and the baseline levels of inflammatory biomarkers, such as peripheral C-reactive protein (CRP), could be used to stratify the treatment outcome. All results suggested that the identification of peripheral and brain inflammatory biomarkers for the diagnosis, outcome prediction, staging, and stratification of interventions of mood disorders has emerged as an important area of translational research in psychiatry. Conclusion: Inflammatory biomarkers could guide interventions and enhance treatment response in patients with mood disorders. The main challenge is that substantial complexities might hamper the attainment of this goal.
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Dominiak, Monika, Adam Gędek, Michalina Sikorska, Paweł Mierzejewski, Marcin Wojnar, and Anna Z. Antosik-Wójcińska. "Acetylsalicylic Acid and Mood Disorders: A Systematic Review." Pharmaceuticals 16, no. 1 (December 31, 2022): 67. http://dx.doi.org/10.3390/ph16010067.
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The effects of acetylsalicylic acid (ASA) on mood disorders (MD) and on inflammatory parameters in preclinical and clinical studies have not yet been comprehensively evaluated. The aim of this study was to systematically summarize the available knowledge on this topic according to PRISMA guidelines. Data from preclinical and clinical studies were analyzed, considering the safety and efficacy of ASA in the treatment of MD and the correlation of inflammatory parameters with the effect of ASA treatment. Twenty-one studies were included. Both preclinical and clinical studies found evidence indicating the safety and efficacy of low-dose ASA in the treatment of all types of affective episodes in MD. Observational studies have indicated a reduced risk of all types of affective episodes in chronic low-dose ASA users (HR 0.92, 95% CI:0.88, 0.95, p < 0.0001). An association between ASA response and inflammatory parameters was found in preclinical studies, but this was not confirmed in clinical trials. Further long-term clinical trials evaluating the safety and efficacy of ASA in recurrent MD, as well as assessing the linkage of ASA treatment with inflammatory phenotype and cytokines, are required. There is also a need for preclinical studies to understand the exact mechanism of action of ASA in MD.
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Bauer, Moisés E., and Antônio L. Teixeira. "Neuroinflammation in Mood Disorders: Role of Regulatory Immune Cells." Neuroimmunomodulation 28, no. 3 (2021): 99–107. http://dx.doi.org/10.1159/000515594.
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Mood disorders are associated with chronic low-grade systemic (sterile) inflammation, with increased plasma levels of pro-inflammatory mediators targeting all tissues including the brain. Importantly<b>,</b> pro-inflammatory cytokines (ex., tumor-necrosis factor alpha [TNF-α], interleukin [IL]-6) regulate mood behavior and cognition by influencing neurotransmitter levels, activating stress-responsive endocrine axes, among other effects. However, the mechanisms underlying this enhanced inflammation are not well understood. There is increasing evidence indicating that impaired immunoregulatory mechanisms may play a role in this context. Patients with mood disorders (major depression [MDD] and bipolar disorder [BD]) have reduced numbers of major regulatory cells of both innate (natural killer regulatory cells and myeloid-derived suppressor cells [MDSCs]) and adaptive immune responses (CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup>, B regulatory cells). Dysfunctional regulatory immune cells might contribute to systemic and neuroinflammation observed in mood disorders via different mechanisms, such as: (i) failure to develop adequate stress-related responses, (ii) indirectly through microglial activation, (iii) lack of trophic support and pro-cognitive functions of T cells in the brain, and (iv) dysbiosis. In conclusion, maladaptive immunoregulatory mechanisms seem to be involved with both onset and progression of mood disorders. A deeper understanding of these mechanisms may lead to the development of new therapeutic strategies.
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Squassina, Alessio, Claudia Pisanu, and Roberta Vanni. "Mood Disorders, Accelerated Aging, and Inflammation: Is the Link Hidden in Telomeres?" Cells 8, no. 1 (January 15, 2019): 52. http://dx.doi.org/10.3390/cells8010052.
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Mood disorders are associated with an increased risk of aging-related diseases, which greatly contribute to the excess morbidity and mortality observed in affected individuals. Clinical and molecular findings also suggest that mood disorders might be characterized by a permanent state of low-grade inflammation. At the cellular level, aging translates into telomeres shortening. Intriguingly, inflammation and telomere shortening show a bidirectional association: a pro-inflammatory state seems to contribute to aging and telomere dysfunction, and telomere attrition is able to induce low-grade inflammation. Several independent studies have reported shorter telomere length and increased levels of circulating inflammatory cytokines in mood disorders, suggesting a complex interplay between altered inflammatory–immune responses and telomere dynamics in the etiopathogenesis of these disorders. In this review, we critically discuss studies investigating the role of telomere attrition and inflammation in the pathogenesis and course of mood disorders, and in pharmacological treatments with psychotropic medications.
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Silberstein, Susana, Ana Clara Liberman, Paula Ayelén dos Santos Claro, Maria Belén Ugo, Jan M. Deussing, and Eduardo Arzt. "Stress-Related Brain Neuroinflammation Impact in Depression: Role of the Corticotropin-Releasing Hormone System and P2X7 Receptor." Neuroimmunomodulation 28, no. 2 (2021): 52–60. http://dx.doi.org/10.1159/000515130.
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Depression and other psychiatric stress-related disorders are leading causes of disability worldwide. Up to date, treatments of mood disorders have limited success, most likely due to the multifactorial etiology of these conditions. Alterations in inflammatory processes have been identified as possible pathophysiological mechanisms in psychiatric conditions. Here, we review the main features of 2 systems involved in the control of these inflammatory pathways: the CRH system as a key regulator of the stress response and the ATP-gated ion-channel P2X7 receptor (P2X7R) involved in the control of immune functions. The pathophysiology of depression as a stress-related psychiatric disorder is depicted in terms of the impact of CRH and P2X7R function on inflammatory pathways in the brain. Understanding pathogenesis of affective disorders will lead to the development of therapies for treatment of depression and other stress-related diseases.
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Leite Dantas, Rafael, Jana Freff, Oliver Ambrée, Eva C. Beins, Andreas J. Forstner, Udo Dannlowski, Bernhard T. Baune, Stefanie Scheu, and Judith Alferink. "Dendritic Cells: Neglected Modulators of Peripheral Immune Responses and Neuroinflammation in Mood Disorders?" Cells 10, no. 4 (April 19, 2021): 941. http://dx.doi.org/10.3390/cells10040941.
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Affective disorders (AD) including major depressive disorder (MDD) and bipolar disorder (BD) are common mood disorders associated with increased disability and poor health outcomes. Altered immune responses characterized by increased serum levels of pro-inflammatory cytokines and neuroinflammation are common findings in patients with AD and in corresponding animal models. Dendritic cells (DCs) represent a heterogeneous population of myeloid cells that orchestrate innate and adaptive immune responses and self-tolerance. Upon sensing exogenous and endogenous danger signals, mature DCs secrete proinflammatory factors, acquire migratory and antigen presenting capacities and thus contribute to neuroinflammation in trauma, autoimmunity, and neurodegenerative diseases. However, little is known about the involvement of DCs in the pathogenesis of AD. In this review, we summarize the current knowledge on DCs in peripheral immune responses and neuroinflammation in MDD and BD. In addition, we consider the impact of DCs on neuroinflammation and behavior in animal models of AD. Finally, we will discuss therapeutic perspectives targeting DCs and their effector molecules in mood disorders.
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Saavedra, Juan M. "Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders." Clinical Science 123, no. 10 (July 23, 2012): 567–90. http://dx.doi.org/10.1042/cs20120078.
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The effects of brain AngII (angiotensin II) depend on AT1 receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT1 receptor activity associates with hypertension and heart failure, brain ischaemia, abnormal stress responses, blood–brain barrier breakdown and inflammation. These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT1 receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-β neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT1 receptor blockade, but also from PPARγ (peroxisome-proliferator-activated receptor γ) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury.
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Gharipour, Mojgan, Majid Barekatain, Johoon Sung, Naghmeh Emami, Ladan Sadeghian, Minoo Dianatkhah, Nizal Sarrafzadegan, and Shayesteh Jahanfar. "The Epigenetic Overlap between Obesity and Mood Disorders: A Systematic Review." International Journal of Molecular Sciences 21, no. 18 (September 15, 2020): 6758. http://dx.doi.org/10.3390/ijms21186758.
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(1) Background: Obesity and mood disorders are considered as the most prevalent morbidities in many countries. We suppose that epigenetic mechanisms may induce higher rates of obesity in subjects who suffer from mood disorders. In this systematic review, we focused on the potential roles of DNA methylation on mood disorders and obesity development. (2) Methods: This systematic review was conducted in accordance with the PRISMA statement and registered in Prospero. A systematic search was conducted in MEDLINE, Scopus, Web of Science, Cochrane Central database, EMBASE, and CINHAL. We also conducted a Grey literature search, such as Google Scholar. (3) Results: After deduplication, we identified 198 potentially related citations. Finally, ten unique studies met our inclusion criteria. We have found three overlap genes that show significant DNA methylation changes, both in obesity and depression. Pathway analysis interaction for TAPBP, BDNF, and SORBS2 confirmed the relation of these genes in both obesity and mood disorders. (4) Conclusions: While mechanisms linking both obesity and mood disorders to epigenetic response are still unknown, we have already known chronic inflammation induces a novel epigenetic program. As the results of gene enrichment, pathways analysis showed that TAPBP, BDNF, and SORBS2 linked together by inflammatory pathways. Hypermethylation in these genes might play a crucial rule in the co-occurrence of obesity and mood disorders.
Dissertations / Theses on the topic "Inflammatory response in mood disorders"
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GIORGI, MARIANI MICHELA. "MECHANISM OF ACTION OF ELECTROCONVULSIVE THERAPY (ECT): A NEUROIMMUNOCHEMICAL APPROACH." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071492.
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Background:
Electroconvulsive therapy (ECT) is one of the most effective and fast acting therapeutic options for treatment-resistant psychiatric diseases, in particular mood disorders. Mood disorders are highly heterogeneous, disabling and severe mental illness, at still unknown etiology, which have been associated with a multifaceted pathogenesis, encompassing genetic, epigenetic and metabolic vulnerabilities together psychosocial/lifestyle factors. Among the various biological patterns thought to be involved in the physiopathology of dysthymia, major depression, cyclothymia, bipolar I, II, mixed states and related disorders, alterations in the neuroendocrine and immune systems have been also evidenced. Additionally, an increasing number of studies have highlighted the relevance of impaired mechanisms of defense against reactive oxygen species (ROS) in the progression and severity of BD. Oxidative stress and redox states are indeed part of the metabolic and chemical networks of the immune/inflammation response. Despite such evidences, few studies have examined, by now, the impact of ECT on specific neuroendocrine, immune and oxidative stress paths in patients undergoing this therapy. It has been reported that ECT-induced epileptic seizures stimulate the intra-cerebral release of cytokines, including the cytokine network associated with the pathophysiology of affective disorders. It is therefore challenging to consider that the therapeutic efficacy of ECT may reside on the degree of activation of the immune/inflammatory system and that patients, under depressive, hypomanic, manic or mixed states, may change their specific profile of biochemical/immunological markers by ECT. ECT would thus act on complex biochemical cascades, formed by several neurotransmitters, neuro-hormones, neurotrophic factors and metabolic substrates, playing a significant therapeutic role.
Hypothesis:
Beside possible neurotransmitter and neurotrophin variations, mood disorder patients would also present significant changes of peripheral cytokine and oxidative stress profiles, before and after ECT; it might be thus possible to identify specific redox chemical and immune features related to the response/Non-response to this treatment. Such a result could also considerably help to detect peripheral molecular correlates of immunochemical dysregulation, refractory symptoms and ECT therapeutic benefits or adverse effects in mood disorders.
Aims:
The foremost aims of this study were: 1) to explore the degree of expression/activity of peripheral immune and oxidative stress markers during the course of ECT in bipolar patients; 2) to possibly evidence differences of these biochemical parameters among Remitter and Non-Remitter patients, assessed by means of suitable examinations and psychometric questionnaires, administered to recruited patients before, during and after ECT.
Methods:
From 2016 to 2018, we recruited and investigated 17 consecutive patients with a BD diagnosis accordingly to DSM-V diagnostic criteria, all treated by ECT at the Psychiatry section of the Department of Clinical and Experimental Medicine of the University of Pisa.
All patients were examined during three main phases of ECT course, following this schedule: 1) at T0, by both psychometric and biochemical evaluations, before the first application; 2) at T1, by biochemical evaluations carried out 3 hours after the first application; 3) at T2, at the end of the treatment, by both psychometric and biochemical examinations. A forth biochemical assessment was carried out also at T3, 3 hours after the last application, in order to possible appraise a different reactivity of immune/oxidative stress patterns at the end of ECT applications. To constantly monitor patients, psychiatric and physical examinations were always performed for the duration of the study.
Psychometric questionnaires carried out prior to (T0) and after (T3) the ECT course, consisted into: the Hamilton Depression Rating Scale-17 (HAM-D), Young Mania Rating Scale (YMRS), Brief Psychiatric Rating Scale (BPRS) and Clinical Global Improvement Impression (CGI) scale. The CGI subscale “global improvement”, final HAM-D and YMRS total scores were used to identify Remitter and Non-Remitter groups .
Biochemical investigations, performed after blood samplings carried out at the 4 scheduled times, T0, T1, T2 and T3, were: 1)-the plasma levels of the immune/inflammatory cytokines IL-6, IL-8 and TNFα; 2)-the plasma levels/ activity of the antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD), total thiols (R-SH), the ferric reducing ability of plasma (FRAP), uric acid as well as an index of oxidative damage, the advanced oxidation plasma protein products (AOPP).
Results:
At the end of therapy, about the 53% of ECT-treated BD patients was found to remit. Concerning biochemical investigation, we observed that, globally, in 17 subjects, 3 hours after ECT (T1), the activity of SOD in plasma increased nearly attaining the statistical significance, while FRAP was found significantly decreased; when analyzing Remitters and Non-Remitters separately, the nearly significant increased SOD reported in all patients at T1, after the first ECT application, was due to a greater enzyme activity in Remitters, while the global T1 FRAP reduction was due to the significant decrease of plasma ferric reducing power in Non-Remitters only. We also reported that Non-Remitters had a significantly reduced CAT activity both at T1 and in the long term, at the end of ECT course (T2), and a higher percent of responce in uric acid and IL 8 after the last ECT (T3 vs. T2). Also, Non-Remitters tended to concomitantly have, at T2, higher plasma FRAP, SOD,IL6 and lower CAT, Thiols in respect to baseline (T0) values as well as in respect to Remitters. No significant effect on the plasma level of AOPP was observed at any scheduled time in all patients, indicating that no relevant protein damage, due to ROS was reported during ECT sessions.
Limitations:
The study, at the present stage, had a small sample size; moreover the patient group was heterogeneous, consisting of treatment resistant bipolar patients in different phases of illness and with different pharmacological regimes.
Conclusions:
According to literature, we showed that ECT is an effective and safe treatment able to heal drug-resistant bipolar patients with very severe clinical presentation and risk of suicide, in all phases of the illness.
Preliminary results suggest that ECT can induce changes of the antioxidant system: an increased ROS scavenging activity at T1 seems to be an index of favorable response. The diminuition of antioxidant defense system would be conversely linked to reduced benefits deriving from this therapy. The recruitment of a larger cohort of patients is needed to confirm and pursue this useful investigation of peripheral biomarkers of ECT response. This will permit to perform more robust statistical tests as multivariate regression or principal component analyses and to possibly define peculiar immunochemical changes related to the clinical response.
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Cattaneo, Carlo Ignazio. "Mood Disorders and Inflammatory Markers: Pathophysiology and Implications for Treatment." Doctoral thesis, Università del Piemonte Orientale, 2018. http://hdl.handle.net/11579/97206.
Full textAbstract:
INTRODUCTION: Mood disorders are chronic disorders, responsible for disability worldwide. In recent years a growing body of literature has proposed a psycho-neuro-immunological hypothesis, according to which inflammation may play a role in the development and response to treatment of such diseases. Both Major Depressive Disorder and Bipolar Disorder have been associated with peculiar patterns of cytokine alterations and, on the other hand, some psychotropic drugs showed the ability to affect cytokines production, making an immunomodulatory action of these drugs plausible.
METHODS: Our research also included a comparison of Neurokinin-1Receptor (NK-1R) expression and Substance P (SP) ability to induce NF-κB activation in monocytes from BD patients and healthy donors (HD). A further study was conducted on human monocytes, which were used as such or differentiated into M1 and M2 macrophages. Cells were treated with vortioxetine before or after differentiation, and their responsiveness, in terms of included oxy-radical and TNFα production, TNFα and PPARγ gene expression, and NF-κB translocation was evaluated.
RESULTS: An increase in pro-inflammatory cytokines such as IL-4, TNF-α, soluble interleukin-2receptor (sIL2-R), IL-1β, IL-6, soluble receptor of TNF-alpha type1 (STNFR1) and C-reactive protein (CRP) is reported in BD patients, during all phases of the disease. IL‐1β, IL‐6, and TNF‐α serum levels are elevated and an increased microglial activation can be observed in some brain regions in MDD patients. NK-1R expression showed relevant alterations in BD patients and SP involvement appeared plausible. Vortioxetine showed anti-inflammatory effect.
CONCLUSIONS: Neuro-immunomodulation must be taken into consideration when dealing with the pathophysiology of psychiatric disorders and in the choice of antidepressants; the effect of medications affecting the serotoninergic pathway on the innate immune system should be further investigated, also in a disease-specific context.
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Husain, Muhammad Ishrat. "The role of anti-inflammatory agents in the treatment of mood disorders." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-antiinflammatory-agents-in-the-treatment-of-mood-disorders(54f2b6e8-a03f-4be9-80e7-fa77d6b3f360).html.
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Background: Multiple reviews have demonstrated that mood disorders are associated with abnormal pro- and anti-inflammatory immunological markers and recent studies suggest that anti-inflammatory medication may play an important role in the treatment of mood disorders. Aims: 1. To evaluate current evidence on the efficacy and acceptability of anti-inflammatory drugs in patients with major depressive disorder (MDD) and bipolar disorder. 2. To determine whether the anti-inflammatory tetracycline antibiotic minocycline, added to treatment as usual (TAU) for 3 months in patients with treatment-resistant depression leads to an improvement in depressive symptoms and if so, to estimate effect sizes to inform the development of a larger, hypothesis-testing study. Methods: A systematic review and meta-analysis of published trials of anti-inflammatory agents in mood disorders was conducted. The Cochrane Central Register of Controlled Trials, PubMed, EMBASE, PsychINFO and Clinicaltrials.gov were searched from inception until April 15, 2017 for completed and on-going clinical trials of anti-inflammatory agents for MDD and bipolar disorder. Data from randomized controlled trials (RCTs) assessing the antidepressant and antimanic effect of adjunctive mechanistically diverse anti-inflammatory agents were pooled to determine standard mean differences (SMDs) compared with placebo and/or treatment as usual. To address the second aim a multi-site, 12-week, double blind, placebo-controlled, pilot trial was conducted. The trial was of minocycline added to treatment as usual for patients suffering from DSM-5 major depressive disorder whose current episode has failed to respond to at least 2 antidepressants. The primary outcome measure was mean change in Hamilton Depression Rating Scale (HAMD-17) scores from baseline to week 12. Secondary measures were the Clinical Global Impression scale (CGI), Patient Health Questionnaire-9 (PHQ-9), the Generalised Anxiety Disorder scale (GAD-7) and EuroQoL (EQ-5D). Side effects checklists were also used. Minocycline was started at 100 mg once daily (OD) and increased to 200 mg OD after two weeks. Results: The meta-analysis found that patients receiving anti-inflammatory agents showed lower post-treatment depressive symptom scores compared with those receiving placebo with a SMD of -0.71 (6 RCTs, n=214, 95% CI -1.24 to -0.17, p=0.009). Anti-inflammatory treatment was found to reduce post-treatment manic symptom scores with a SMD of -0.72 (3 RCTs, n=96, 95% CI -1.31 to -0.13, p=0.02). Anti-inflammatory treatment was found to yield an improvement in depressive symptom scores from baseline to outcome with a SMD of -0.52 (5 RCTs, n=194, 95% CI -1.01 to 0.05) but this was not statistically significant (p=0.07). In the pilot RCT, a total of 41 participants were randomised, with 21 in the minocycline group and 20 in the placebo group. A large decrease in HAMD scores was observed in the minocycline group compared to the placebo group (Standardized effect size -1.21, p < 0.001). CGI scores in the minocycline group also showed a large improvement compared with placebo (OR: 17.6, p < 0.001). PHQ-9 (ES -0.43), GAD-7 (ES -0.46) and EQ-5D total (ES -0.48) showed more moderate improvements. Conclusions: Anti-inflammatory treatments may confer benefit for both depressive and manic symptoms however current studies are limited by small sample sizes, short durations, differing baseline symptomatology and poorly defined illness durations. The findings of the pilot RCT indicate that adjunctive minocycline leads to improvement in symptoms of treatment-resistant depression. However, the findings require replication in a larger sample. Overall, further high-quality trials are needed before making recommendations for the routine clinical use of anti-inflammatory interventions including minocycline, in the treatment of mood disorders.
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Mauch, Christoph Peter. "The startle response as a measure in mouse models of mood disorders." Diss., Ludwig-Maximilians-Universität München, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-176487.
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Ein großer Teil der Fragestellungen in den Neurowissenschaften beschäftigt sich mit dem Thema, wie das Säugerhirn Verhalten auslöst und steuert. Die Schreckreaktion ist ein relativ einfaches Verhalten, welches bei Säugetieren ohne großen Aufwand ausgelöst werden kann und variabel auf eine Vielfalt von experimentellen Behandlungen reagiert.
Das Ziel der vorliegenden Arbeit war es, Schreckreaktions-Messungen am Max-Planck-
Institut für Psychiatrie in München (MPI-P) zu etablieren. Vor dem Hintergrund aktueller Fragestellungen sollten die Experimente zu einsatzbereiten Messmethoden und Verhaltensparadigmen führen.
In der vorliegenden Arbeit gelang es nicht, das Paradigma der furchtpotenzierten Schreckreaktion (FPS) zuverlässig in einem häufig am MPI-P eingesetzten Mausstamm anzuwenden. Das FPS maskierende Phänomen, daß die Präsentation eines unkonditionierten Tons bereits zu einer deutlich verstärkten Schreckreaktion in diesen Mäusen führt ("tone enhanced startle", TES) wurde dann charakterisiert und im Folgenden als ergänzendes Paradigma zur Messung und Abschätzung des Hörvermögens, der Stimulus Adaptation und der Aufmerksamkeit in Mäusen vorgeschlagen.
Eine Literaturrecherche ergab, daß im Paradigma der Furchtkonditionierung ("fear conditioning", FC) und deren aktives Verlernen ("extinction of FC", ExFC) verwendete Stimulus-Parameter eine hohe Varianz zwischen verschiedenen Laboratorien aufweisen. Der im Verhalten ausgelesene Lernerfolg während einer FC wie auch einem ExFC hingen in den vorliegenden Experimenten wesentlich von der verwendeten Stimulusqualität ab
(d.h. sinus-Ton oder weißes Rauschen). Im Umkehrschluß empfiehlt die vorliegende Arbeit einen überlegteren Umgang mit den eingetzten Stimulus-Parametern.
Es zeigte sich, daß eine erhöhte Schreckreaktion (Übererregbarkeit) ohne weiteres in einem Tiermodell der Posttraumatischen Belastungsstörung ("posttraumatic stress disorder",PTSD) gemessen werden kann. Im Weiteren konnte gezeigt werden, daß verändertes Hippocampus-Volumen in diesen Tieren, gemessen über ultramikroskopische Aufnahmen und analog zu Hippocampusveränderungen in Patienten, unabhängig von anderen PTSD-ähnlichen Symptomen dieser Mäuse ist.
In einem weiteren Abschnitt widmet sich die vorliegende Arbeit der laufenden Charakterisierung der Rolle von Dopaminrezeptoren (DR) in der Präpulsinhibition (PPI) und -Faszilitierung (PPF) der Schreckreaktion. Durch lokale injektion von DR-Antagonisten konnte gezeigt werden, daß die Blockade von DR1 wiederholbar PPI verstärkt, während die Rolle von DR2, getestet mit zwei verschiedenen Antagonisten, als ambivalent gedeutet werden muß.
Basierend auf diesen Experimenten wurden optogenetische Methoden in die Schreckreaktionsmessung eingeführt. Transgenen Mäusen, die lichtsensitive Ionenkanäle in ihren neuronalen Zellmembranen bestimmter Zellpopulationen tragen, wurden Lichtblitze ins Gehirn appliziert. Auf diese Weise konnten PPI und PPF unabhängig voneinander manipuliert werden. Daraus folgend, und im Unterschied zur populären Summationshypothese der PPF, schlägt die vorliegende Arbeit einen eigenständigen, von der PPI unabhängigen PPF-Schaltkreis vor, der Pyramidenneuronen der präfrontalen Kortexschicht V beinhaltet.
Die vorliegende Arbeit konnte erfolgreich verschiedene Protokolle und Verhaltensparadigmen der Schreckreaktionsmessung am MPI-P etablieren und zur sofortigen Nutzung zur Verfügung stellen. Es wurden nicht nur neue Techniken wie z.B. optogenetische Methoden in die Schreckreaktionsmessung eingeführt, die vorliegenden Experiemente leisten auch ihren Beitrag zur aktiven Forschung, in dem sie z.B. die große Bedeutung der Stimulus-Parameter für den Lernerfolg von Versuchstieren nachweisen.In neuroscience major efforts are focused on the question of how the mammalian brain generates and controls behaviour. The startle response is a relatively simple behaviour that can be easily elicited in mammals and is sensitive to a variety of experimental treatments. The aim of the present work was to establish startle response measures at the Max-Planck-Institute of Psychiatry (MPI-P), Munich, providing a set of readily applicable methods and paradigms, and contributing to questions in behavioural neuroscience. While the present thesis failed to robustly elicit fear potentiated startle (FPS) in a commonly used mouse strain at the MPI-P, strong unconditioned startle enhancement by acoustic stimulus presentation in that mouse strain was capitalised to propose tone enhanced startle (TES) as an additional paradigm to assess hearing capability, stimulus adaptation and attention in mice. A literature survey revealed considerably varying parameters used in fear conditioning (FC) and extinction of conditioned fear (ExFC). In the present work, FC, ExFC as well as FPS/TES highly depended on the stimulus quality (i.e. sine wave or white noise), demanding a more careful handling of stimulus parameters. Hyper-arousal was readily tested in a mouse model of posttraumatic stress disorder (PTSD). Additionally it was shown that altered hippocampal volume in these animals, assessed by ultramicroscopic measures and mimicking patient data, was independent of other symptoms present in this model. The present thesis contributes to the ongoing characterisation of the role of dopamine receptors (DR) in prepulse inhibition (PPI) and prepulse facilitation (PPF) of startle, manipulating PPI/F by injections of DR-antagonists into the prefrontal cortex of mice. It was found that blockade of DR1 reliably increases PPI, while the effect of DR2 was inconsistent, using to different DR2-antagonists. Based on this work, optogenetic methods were established. Applying intracerebral light flashes to transgenic mice carrying light sensitive ion channels on their neuronal cell membrane, PPI and PPF were manipulated independently, proposing the existence of a discrete PPF mediating pathway including prefrontal layer V pyramidal neurons, contrasting the popular summation hypothesis of PPF. The present work established and developed successfully different startle paradigms that are ready to use for animal characterisation and testing. Apart from combining startle measures with new techniques such as optogenetic methods, the present thesis points out the stimulus parameter dependence of animal learning, suggesting a fundamental discussion about fear conditioning and extinction learning protocols.
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ROFEY, DANA LYNN. "BULIMIC SYMPTOMS AND MOOD PREDICT FOOD RELEVANT STROOP INTERFERENCE IN WOMEN WITH TROUBLED EATING PATTERNS." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1027948284.
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Mauch, Christoph Peter [Verfasser], and Carsten [Akademischer Betreuer] Wotjak. "The startle response as a measure in mouse models of mood disorders / Christoph Peter Mauch. Betreuer: Carsten Wotjak." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1062877314/34.
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Aldoori, Ayat Dhia. "Elucidation of signaling mediators between adipose and neural tissue." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1407845819.
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Werncke, Daíse. "Relação entre restrição nutricional e acidose ruminal com as alterações na produção e composição do leite." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/163326.
Full textAbstract:
O estudo consistiu de dois experimentos com o objetivo de avaliar os efeitos da acidose ruminal e restrição nutricional na ocorrência de processos inflamatórios nos animais e relacionar com as alterações na produção e composição do leite. Foram utilizadas doze vacas Holandês e Mestiças Holandês Jersey. Experimento 1: Na fase de adaptação, os animais receberam uma dieta formulada para atender 100% das necessidades nutricionais de energia e proteína. Na indução foi administrada uma dieta com restrição de 50% das necessidades em energia e proteína. Na recuperação os animais receberam uma das três dietas experimentais, para recuperar a estabilidade do leite: (1) suprimento somente de energia; (2) suprimento somente de proteína; (3) suprimento de energia e proteína. A restrição nutricional em energia e/ou proteína afeta negativamente a produção de leite, o peso vivo e o escore de condição corporal. Além de reduzir a eficiência de utilização de proteína da dieta e provocar uma maior instabilidade do leite ao teste do álcool. Entretanto, não altera o perfil sanguíneo e metabólico. Experimento 2: Os animais foram divididos em dois grupos (1) controle e (2) acidose. O delineamento experimental foi reversível simples com dois tratamentos e dois períodos experimentais. Foram analisados parâmetros referente às características físico-quimica, saúde da glândula mamária, medidas fisiológica, perfil metabólico e parâmetros sanguíneos. A indução da acidose ruminal subaguda (SARA) causou redução da produção e estabilidade do leite ao teste do álcool, pH urinário, pH fecal, pH ruminal. Entretanto, a indução a SARA não alterou os parâmetros sanguíneos avaliados. A SARA altera as características físico-químicas do leite, sem influenciar nas concentrações proteínas de fase aguda, caracterizando uma resposta inflamatória. A SARA pode acometer os animais sem apresentar mudanças no perfil sanguíneo dos mesmos.The study consisted of two experiments with the aim of evaluating the effects of ruminal acidosis and nutritional restriction on the occurrence of inflammatory processes in animals and correlate with changes in milk production and composition. Twelve Holstein and cross bred Holstein and Jersey cows were used. In the first study, in the adaptation phase, the animals received a diet formulated to supply 100% of the nutritional needs of energy and protein. In the induction, a diet composed by 50% restriction of energy and protein requirements was administered. In the recuperation, the animals received one of the three experimental diets to recover milk stability: (1) only energy supply; (2) supply only of protein; (3) supply of energy and protein. The nutritional restriction in energy and / or protein can affects negatively milk production, weight and condition score body. In addition to reduce the efficiency of protein utilization of the diet and cause greater instability of the milk to the alcohol test. However, it does not changed the blood and metabolic profile. In second study, the animals were divided into two groups (1) control and (2) acidosis. The experimental design was simple reversible with two treatments and two experimental periods. Physiochemical characteristics, health of the mammary gland, physiological measures, metabolic profile and blood parameters were analyzed. Losses in milk production, reduction of alcohol stability test, urinary pH, fecal pH, ruminal pH were caused by Subacute ruminal acidosis (SARA) induction. However, induction of SARA did not changed the blood parameters evaluated. SARA changes the physical-chemical characteristics of the milk, without influencing the acute phase proteins concentrations, characterizing an inflammatory response. SARA can affect the animals without demostrate changes in the blood profile of the animals.
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Leahan, K. E. "Photic stimulation and the treatment of mood and sleep disorders." Phd thesis, 2004. http://hdl.handle.net/1885/148546.
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Subramaney, Ugasvaree. "Personality style, cortisol secretion and the inflammatory response to trauma exposure in a cohort of South African metro police cadets: a prospective, longitudinal study." Thesis, 2012. http://hdl.handle.net/10539/11051.
Full textAbstract:
Literature investigating trauma exposure, Posttraumatic stress disorder (PTSD) and
cortisol secretion has produced conflicting results with regard to whether cortisol is
increased or decreased. With trauma there is also a pro- inflammatory response which
is intimately linked with the hypothalamic pituitary axis (HPA). The police population can
offer useful information in this regard as they represent a sample that will undergo
exposure to traumatic events as part of their normal duties. In South Africa few studies
have examined biological correlates of the traumatic stress response in the police
population.
This study sought to determine whether correlations exist between cortisol and the
inflammatory response in terms of the cytokines Interleukin 6 (IL6) and Tumour Necrosis
Factor (TNF) in response to trauma exposure in a cohort of newly enrolled metro police
officers, previously naïve to the duty related trauma exposure. Personality styles were
assessed, as coping skills and personality have been suggested as factors determining
responses to trauma.
The study participants were followed up for one year with repeated measures analysis of
urine, blood, and saliva cortisol as well as blood cytokine determination every 3 months.
Measures for PTSD [the Clinician Administered Scale for Posttraumatic stress disorder
(CAPS) and the revised version of the Impact of Event Scale (IES-R)] as well as for
depression [the Hamilton Depression Rating Scale (HAM-D)] were undertaken.
145 new recruits volunteered for the study, of which 120 completed all 5 visits. There
were slightly more females than males in the sample and almost 50% of the sample admitted to alcohol abuse. Trauma exposure on entry into the police force was
remarkably high with 99% having been exposed to at least one traumatic event in their
lives. The majority (61.1 %) had been exposed to more than one traumatic event. There
was evidence for the influence of prior trauma on responses to current traumatic events.
MVA’s were very common, both duty and non duty related. Certain traumas were
associated with greater changes in scores for PTSD and depression in relation to
baseline. Over the 5 visits, only a third submitted valid 24 hour urine samples. Of these,
the profile of the entire group indicated that 24 hour urine cortisol tended to initially
decrease, and then increase with time. Saliva and blood cortisol, which were more
reliably measured, tended to decrease with time.
Scores for depression and post traumatic stress disorder were generally low in response
to duty related traumatic events, and tended to decrease over time. However, the
prevalence of lifetime PTSD as measured by the CAPS was high.
There was a strong linear correlation between TNF and IL6. Results indicate a
proinflammatory response, particularly with regard to IL6. There were no significant
correlations between blood cortisol and HAM-D and between blood cortisol and CAPS
(lifetime). There was an inverse relationship between CAPS (current scores) and blood
cortisol. Cortisol and IES-R scores were significant at visit 3 (inverse relationship). For
saliva, there were no significant associations with any of the variables for PTSD and
depression.
For personality styles, aggressive and antisocial clinical patterns were associated with
lower current CAPS scores, while schizoid clinical pattern and the severe syndrome
scale of thought disorder showed an association with lower lifetime CAPS score. For the
IES-R, only narcissistic clinical pattern was associated with lower scores. A further analysis of those with low (less than 25% of the median) and high (greater than 25% of
the median) cortisol responses was undertaken.
The results indicate a similar trend to some studies showing lowered cortisol levels with
chronic trauma exposure, but this did not correlate with sufficiently high scores for PTSD
as measured by the CAPS. Similarly, proinflammatory cytokine increases are evident
with trauma exposure, but not with scores for PTSD and depression. There were more
variables significantly associated with the low cortisol responders than the high cortisol
responders; with a suggestion of cumulative trauma exposure correlating with low
cortisol response and a corresponding pro inflammatory response in terms of IL6.
The results are discussed with a view to assisting the metro police force with recruitment
and counseling strategies and important future research is recommended.
Books on the topic "Inflammatory response in mood disorders"
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1950-, Goodnick Paul J., ed. Predictors of treatment response in mood disorders. Washington, D.C: American Psychiatric Press, 1996.
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Stoddard, Frederick J., and Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.
Full textAbstract:
Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound healing is increased cortisol secretion secondary to depression and/or stress, and impaired immune response, in addition or together with the other factors such as genetic or epigenetic risk for depression. Cellular models relate both to wound healing and to depression include cytokines, the inflammatory response (Miller et al, 2008), and cellular aging (Telgenhoff and Shroot, 2005) reflected in shorter leukocyte telomere length (LTL) (Verhoeven et al, 2016). Another model of stress impacting wound healing investigated genetic correlates—immediate early gene expression or IEG from the medial prefrontal cortex, and locomotion, in isolation-reared juvenile rats. Levine et al (2008) compared isolation reared to group reared samples, and found that, immediate gene expression in the medial prefrontal cortex (mPFC) was reduced, and behavioral hyperactivity increased, in juvenile rats with 20% burn injuries. Wound healing in the isolation reared rats was significantly impaired. They concluded that these results provide candidates for behavioral biomarkers of isolation rearing during physical injury, i.e. reduced immediate mPFC gene expression and hyperactivity. They suggested that a biomarker such as IEGs might aid in demarcating patients with resilient and adaptive responses to physical illness from those with maladaptive responses
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Rao, Narsing A., Uwe Pleyer, Jorge L. Alió, Talin Barisani-Asenbauer, and Phuc Le Hoang. Immune Modulation and Anti-Inflammatory Therapy in Ocular Disorders: IOIS Guidelines. Springer, 2014.
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Rao, Narsing A., Uwe Pleyer, Jorge L. Alió, Talin Barisani-Asenbauer, and Phuc Le Hoang. Immune Modulation and Anti-Inflammatory Therapy in Ocular Disorders: IOIS Guidelines. Springer, 2016.
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Rao, Narsing A., Uwe Pleyer, Jorge L. Alió, Talin Barisani-Asenbauer, and Phuc Le Hoang. Immune Modulation and Anti-Inflammatory Therapy in Ocular Disorders: IOIS Guidelines. Springer London, Limited, 2014.
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Hasbun, Rodrigo, Richard Dunham, Joseph S. Kass, Rituparna Das, Karen Nunez-Wallace, Lydia J. Sharp, and Doris Kung. HIV-Associated Neurocognitive Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0038.
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HIV causes a chronic form of encephalitis (HIVE) that is clinically characterized by either dementia or mild neurocognitive impairment. Since the introduction of antiretroviral therapy in 1996, the incidence of HIV dementia has decreased by 50%, but the prevalence of mild neurocognitive disorder has increased up to 39%. HIVE is the result of direct microglial infection, interruption of trophic factors, or caused by inflammatory cytokines. HIV enters the brain primarily by the “Trojan horse mechanism”; it is carried by monocytes and lymphocytes that cross the blood–brain barrier. HIV has a predilection for the basal ganglia, deep white matter, and hippocampus, resulting in a subcortical dementia. HIV dementia is a diagnosis of exclusion and other co-infections, cerebrovascular disease, malnutrition, and drug abuse should be ruled out before making the diagnosis. In patients receiving antiretroviral therapy with immunological response, a novel condition termed CD8+ T cell encephalitis was recently described.
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Ménard, Caroline, Madeline L. Pfau, Georgia E. Hodes, and Scott J. Russo. Immune Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0028.
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Mood disorders such as major depressive disorder (MDD) are diagnosed largely based upon behavioral symptoms rather than biological factors. Some have argued that a lack of rigorous biomarker-based diagnosis is the reason why 30%–50% of MDD patients are unresponsive to traditional antidepressant medications. Over the past few decades, MDD has been shown to be highly prevalent in patients suffering from chronic inflammatory conditions, such as lupus erythematosus, multiple sclerosis, etc. Moreover, subgroups of MDD patients have shown consistently higher levels of circulating pro-inflammatory cytokines. Together, these clinical findings suggest that alterations within the immune system might contribute to the behavioral symptoms of MDD. In this chapter, we review the growing literature in both humans with MDD and in rodent stress models of depression that support a role for the immune system in depression.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 63-Year-Old Male with Severe Flaccid Weakness Post Motor Vehicle Accident. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0009.
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Neuromuscular disorders are important causes of newly acquired weakness in the intensive care unit. Although evaluation usually begins with physical examination findings, these can be compromised in the intensive care unit environment. Therefore, electrodiagnostic study becomes even more important as a tool in localizing weakness to nerve, muscle or neuromuscular junction. Critical illness neuropathy and myopathy occurs in the setting of sepsis and multiple organ failure where sepsis is accompanied by the systemic inflammatory response syndrome. Additional, intensive care unit-specific risk factors exist, predominantly relating to administration of high-dose steroids, nondepolarizing neuromuscular blocking agents, and sedating agents such as propofol. There is no specific treatment except for optimizing medical management of the underlying disorder, including prevention and management of sepsis, systemic inflammatory response syndrome, and organ damage, as well as avoidance of exacerbating medications.
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Patel, Sameer, and Julia Wendon. Pathophysiology and causes of acute hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0194.
Full textAbstract:
Acute liver failure (ALF) is a rare, life-threatening clinical syndrome, resulting in loss of hepatic metabolic and immunological function, in a person with no prior history of liver disease. Mortality can still exceed 50%. ALF is characterized by hepatic encephalopathy (HE) and coagulopathy, occurring within days or weeks. Establishing aetiology is essential for treatment, prognostication, and liver transplantation consideration. Viral hepatitis and drug-induced liver failure are the two commonest causes worldwide. Aetiology and time of onset of encephalopathy determines prognosis. Disease progression can rapidly result in multi-organ failure. Ammonia has been postulated in the development of HE, cerebral oedema and intracranial hypertension. Coagulopathy can be highly variable, with some patients prothrombotic, or exhibiting balanced coagulation disorders. Systemic inflammatory response syndrome (SIRS) and associated infection are frequently observed. Significant haemodynamic changes are common while renal failure is an independent risk factor for mortality. Respiratory failure is less common. Deranged homeostasis results in severe hypoglycaemia, and metabolic disturbance.
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Youngstrom, Eric, and Anna Van Meter. Comorbidity of Bipolar Disorder and Depression. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.003.
Full textAbstract:
There has been speculation about the relationship between depression and mania for centuries. Modern psychiatry and psychology have mostly viewed these as different subtypes within a “family” of mood disorders. Conceptual models of comorbidity provide an opportunity to re-examine the association between depression and other pathological mood states. We examine the evidence pertaining to rates of “comorbidity,” which, in this case, refer to the lifetime occurrence of depression and hypomanic, mixed, or manic episodes in the same individual. We explore factors that could contribute to artifactual comorbidity. We also examine data pertaining to similarities or differences in phenomenology, longitudinal course, associated features, family history, and treatment response. Multiple factors are likely involved in the comorbidity of depression and hypomania or mania, and the problems of poor reliability and inconsistent diagnostic definitions and methodology attenuate the significance of most research findings. However, evidence appears sufficient to conclude that not all depression is on the bipolar spectrum, that bipolar features moderate the course and outcome of depressive illness, and that depression and bipolar disorder most likely involve a blend of some shared and some specific mechanisms. Research and clinical work both will advance substantially by more systematically assessing for potential bipolar features “comorbid” with depression and following how these factors change the trajectory of depression over time.
Book chapters on the topic "Inflammatory response in mood disorders"
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van West, Dirk, Gunter Kenis, and Michael Maes. "Stress and Depression: The Inflammatory Hypothesis." In Mood Disorders, 211–28. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470094281.ch8.
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Burkhardt, Gerrit, Stephan Goerigk, and Frank Padberg. "Mood Disorders: Predictors of tDCS Response." In Transcranial Direct Current Stimulation in Neuropsychiatric Disorders, 481–90. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-76136-3_22.
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Rybakowski, Janusz K. "Pharmacogenetics of Mood Stabilizers." In Genetic Influences on Response to Drug Treatment for Major Psychiatric Disorders, 93–109. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27040-1_6.
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Ehlers, Stefan, and Graham A. W. Rook. "The Role of Bacterial and Parasitic Infections in Chronic Inflammatory Disorders and Autoimmunity." In The Immune Response to Infection, 521–36. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch41.
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Serretti, Alessandro, and Janusz K. Rybakowski. "Practical Application of Pharmacogenetics of Antipsychotic, Antidepressant, and Mood-Stabilizing Drugs." In Genetic Influences on Response to Drug Treatment for Major Psychiatric Disorders, 111–17. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27040-1_7.
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Dampier, Carlton, and Lamia Barakat. "Pain in sickle cell disease." In Oxford Textbook of Paediatric Pain, 248–56. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642656.003.0025.
Full textAbstract:
Sickle cell disease (SCD) presents a complex pain disorder to clinicians. Pain from vaso-occlusion of sickle erythrocytes can occur in multiple musculoskeletal locations, several internal viscera such as the spleen, as well as the penis. Such pain is typically intermittent in childhood, shares features of acute pain with other pain disorders, and often responds to non-steroidal anti-inflammatory drugs (NSAIDs) and opioid analgesics. Adolescents with SCD often experience more frequent pain, and those with bone disease in spine, hips, or shoulders may experience chronic pain. Like other chronic pain disorders, this pain often responds poorly to opioids, but there is limited current clinical or research data to support alternative medications. Many cognitive-behavioural strategies are helpful as part of multidisciplinary pain management, particularly in adolescents, who may also benefit from psychological support to treat coexistent mood disorders, to increase coping skills, and to support appropriate school and family functioning. Future advances in pharmacological and psychological therapies are needed to ameliorate the substantial burden of pain in children and adolescents with SCD.
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Dampier, Carlton, and Soumitri Sil. "Pain in sickle cell disease." In Oxford Textbook of Pediatric Pain, edited by Bonnie J. Stevens, Gareth Hathway, and William T. Zempsky, 261–71. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198818762.003.0026.
Full textAbstract:
Sickle cell disease (SCD) presents a potentially complex pain disorder to clinicians. Pain from vaso-occlusion of sickle erythrocytes can occur in multiple musculoskeletal locations, several internal viscera such as the spleen, and the penis. Such pain is typically intermittent in childhood, shares features of acute pain with other pain disorders, and often responds to nonsteroidal anti-inflammatory drugs and opioid analgesics. Adolescents with SCD often experience more frequent pain, and those with bone disease in spine, hips, or shoulders may experience chronic pain. Like other chronic pain disorders, this pain often responds poorly to opioids, but there is limited current clinical or research data to support alternative medications. Many cognitive behavior strategies are helpful as part of multidisciplinary pain management, particularly in adolescents, who may also benefit from psychological support to treat coexistent mood disorders, to increase coping skills, and to support appropriate school and family functioning. Future advances in pharmacological and psychological therapies are needed to ameliorate the substantial burden of pain in children and adolescents with SCD.
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Kemp, Andrew Haddon, André Russowsky Brunoni, and Rodrigo Machado-Vieira. "Predictors of treatment response in major depressive disorder." In Treatment-Resistant Mood Disorders, 53–60. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198707998.003.0005.
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Alam, Azeem, and Daqing Ma. "Surgery and the Inflammatory Response." In The Perioperative Neurocognitive Disorders, 101–14. Cambridge University Press, 2019. http://dx.doi.org/10.1017/9781316402504.010.
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McCombs, Jeffrey S., Glen L. Stimmel, Rita L. Hui, and T. Jeffrey White. "The economic impact of treatment non-response in major depressive disorders." In Treatment-Resistant Mood Disorders, 491–503. Cambridge University Press, 2001. http://dx.doi.org/10.1017/cbo9780511666421.022.
Full textConference papers on the topic "Inflammatory response in mood disorders"
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Appenzeller, Simone, Mariana De Barros Tozarini, Beatriz Ricato Quental, Talita Rocha Marques, and Stefanny Lopes Da Silva. "MOOD AND ANXIETY DISORDERS IN LUPUS ERYTHEMATOSUS: POSSIBLE ASSOCIATION WITH INFLAMMATORY CYTOKINES." In XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil: Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-37982.
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Lanata, Antonio, Alberto Greco, Gaetano Valenza, and Enzo Pasquale Scilingo. "A pattern recognition approach based on electrodermal response for pathological mood identification in bipolar disorders." In ICASSP 2014 - 2014 IEEE International Conference on Acoustics, Speech and Signal Processing (ICASSP). IEEE, 2014. http://dx.doi.org/10.1109/icassp.2014.6854272.
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Andrade, Dariana Rodrigues, Letícia Mendes de Lima, Luis Henrique Goes Hamati Rosa, and Edvaldo Cardoso. "Brain-gut-microbiota axis in motor disorders." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.401.
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Introduction: There seems to be a strong relationship and influence on the brain-gut- microbiota axis in the control and prevention of several diseases, including degenerative diseases that are related to motor disorders. Objectives: To analyze the relationship between movement disorders and the intestinal microbiota. Methods: Integrative review performed at PUBMED, using the descriptors Movement disorder and intestinal microbiota, in the last five years and having as inclusion criteria complete texts in English. Results: The literature suggests that the intestinal microbiota regulates the activation of microglia through the production of bacteria metabolites. Gut dysbiosis is believed to generate metabolic disorders with decreased production of neuroprotective factors, increased pro-inflammatory cytokines, production of neurotoxins, and a misdirected immune response. Metabolites produced by an altered microbiota seem to enter the circulation and affect neurological function. Braak’s hypothesis postulates that aberrant accumulation of α-synuclein (αSyn), a central component of the pathophysiology of Parkinson’s disease (PD), begins in the intestine and propagates through the vagus nerve to the brain, given that αSyn inclusions previously arise in the enteric nervous system and glossopharyngeal and vagus nerves, and vagotomized individuals have reduced risk of PD. Conclusion: The identification of the microbiota or its altered metabolites may serve as biomarkers, or even drug targets for the treatment of diseases of the central nervous system. The microbiota can be modulated through antibiotic therapy, fecal microbiota transplantation, prebiotic supplementation, dietary interventions and many other potential methods.
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Jan, Zala, Christian Gostečnik, and Veronika Kralj-Iglič. "Adverse Human Health Outcomes Associated with Psychologi-cal Trauma: A review." In Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d7.
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Until 30 years ago it was believed that psychological stress increases cortisol secretion, but later stud-ies gave contradictory results. Decrease in cortisol levels in post-traumatic stress disorder (PTSD) reflects a nonnormative and inadequate response to severe stressors, with its pathophysiology in-volving maladaptation or dysfunction in stress-regulatory systems. To have more insights in re-sponse of human body to physiological stress, inflammatory signals, oxidative stress parameters and other health parameters were measured. As for the cortisol level results, also inflammatory signals, including proinflammatory and anti-inflammatory cytokines and C-reactive protein (CRP), have been reported to increase and decrease in PTSD. Levels of interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, tumour necrosis factor (TNF)-α, interferon gamma (IFN-γ) and CRP were reported higher and lower in blood samples of individuals with PTSD. Some studies report that dysregulation of the stress axis could have direct effects on brain regions responsible for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Early-life stress, such as child-hood adversity (abuse, neglect, or family disfunction), is a potent risk factor for developing PTSD in response to later trauma, and elevated peripheral markers of inflammation are one of the best-repli-cated findings in children and adults with early-life stress. Those who develop PTSD may have an inability or failure to activate an innate immune response. PTSD can also result in other adverse outcomes, such as heightened oxidative stress (OXS), eating disorders, metabolic disorder, and car-diovascular disease (CVD). Since the results are very contradictory for PTSD and inflammation re-sponse of the human body, further research is important. Small cellular particles that can be isolated from body fluids present potential biomarkers of the clinical status and will be considered in plan-ning the future research. This contribution presents perspectives in assessment of psychological stress by objective parameters. Keywords: Cortisol; Post-traumatic stress disorder; Inflammatory response; Oxidative stress; Cyto-kines; Eating disorders; Metabolic disorder; Cardiovascular disease; Small cellular particles as stress markers, Extracellular vesicles as stress markers
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Lellis, Caio de Almeida, Marco Alejandro Menacho Herbas, Glaucia Borges Dantas, and Leonardo Rizier Galvão. "Transcranial Direct Current Stimulation in the Management of Refractory Symptoms of Parkinson’s Disease: A Systematic Review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.221.
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Introduction: Transcranial direct current stimulation (tDCS) is a non-invasive brain stimulation technique increasingly used in neurology. Objectives: To evaluate the safety and efficacy of tDCS in refractory symptoms of Parkinson’s disease (PD). Design and setting: A systematic review of the literature conducted at the Pontifical Catholic University of Goiás. Methods: A systematic review of the literature was conducted in the MedLine and Lilacs databases, with the following search strategy: “(Parkinson Disease) AND (Transcranial Direct Current Stimulation OR TDCS)”. Randomized clinical trials (10 years) were included. Results: One of the studies concluded that simultaneous tDCS of the primary motor cortex (M1) and dorsolateral prefrontal cortex (DLPC) Also, two other articles evaluated the motor response after stimulation of the left DLPC for 20 minutes, with the first realizing improved fine motor performance and attenuation of common oscillatory cortical activity in PD patients, while the second finding an improvement in balance and functional mobility when compared to placebo. Regarding cognitive and mood changes, one of the studies pointed out that a single session of tDCS on the left DLPC is insufficient to improve working memory and inhibition control. Conclusion: tDCS was shown to be a safe and effective therapeutic option in reducing gait freezing and mood disorders, as well as improving fine motor performance and cognition. It is emphasized that further studies on the subject with a larger sample are needed.
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"From poverty to depression to inflammation: a literature review." In International Conference on Public Health and Humanitarian Action. International Federation of Medical Students' Associations - Jordan, 2022. http://dx.doi.org/10.56950/ovii9740.
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Background: Depression is the most commonly presented psychiatric disorder1 . People with low socioeconomic status are more likely to experience depression compared to those with higher socioeconomic status2 . Recent studies have revealed that people experiencing depression symptoms have a greater vulnerability to infections3 . Also, it has been shown in recent studies that there is a correlation between irregular cytokine levels and an uncontrolled inflammatory response4 . Objective: The present review addresses the relationship between the immune system response and depression. In addition to the relationship between depression and low socioeconomic status. Method: We searched PubMed for relevant studies describing the relationship between inflammatory response, depression, and low-income. Our literature survey was limited to peer-reviewed articles, written in English and published from 1990 until August 2022. Results: Different studies confirmed that psychological stress causes an alteration in the level of cytokines in multiple mechanisms4,5. Hypothalamus-pituitary-adrenal axis (HPA) is a significant immunoregulatory pathway that is activated in a variety of stress circumstances, including psychological stress6,7. Chronic psychological stress results in glucocorticoid resistance due to overactivity of the HPA axis. As a result, the inflammatory response is not appropriately managed4 . (Table1) explains the changes in the level of cytokines8 . Contrastingly, antidepressant treatment may restore normal cytokine production and decrease the risk of abnormal inflammatory response9 . Conclusion: More attention should be given to the low-middle income population and their limited access to psychiatric services as they have a higher chance of experiencing mental health disorders. Depression, which is one of the most common mental health illnesses, increases the incidence of infectious diseases. Moreover, it affects the inflammatory response. Due to the shortage of clinical trials on this subject, we recommend doing more studies to identify these clinical aspects.
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Oliveira Júnior, Rocymar Rebouças, Ana Carolina Soares de Lira, Nilson Batista Lemos, Lucas Sávio Fernandes Carvalho, Maria Júlia Plech Guimarães, Marialice Pinto Viana Correia, and Luciana Karla Viana Barroso. "The Non-motor Effects of Deep Brain Stimulation of the Subthalamic Nucleus in Patients with Motor Disorders Caused by Parkinson’s Disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.655.
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Introduction: Parkinson’s disease is a disease caused by the degeneration of dopaminergic neurons in the substantia nigra, and is characterized by a triad of symptoms: bradykinesia, muscle rigidity and rest tremors; which worsen progressively, leading the patient to resort to surgical treatment to ensure a better drug response. However, surgical intervention has proven to be efficient not only to alleviate Movement Disorders, but also to control the nonmotor symptoms of the disease. Objective: To evaluate the non-motor effects of Deep Brain Stimulation (DBS) in patients who do not respond adequately to drug treatment. Methods: This is a literature review conducted by searching the electronic databases Lilacs, Scielo, Medline and Pubmed from 2011 to 2021, using the descriptors “parkinsonism”, “deep brain stimulation”, “non-motor” and “depression”. Articles and specimens from the American and Brazilian literature on the topic were considered relevant. Results: The studies showed that patients who underwent the surgical procedure showed evolution of neurophysiological and psychosocial aspects, such as improved sleep quality, reduced risk of dementia, improved mood and minimized anxiety. In this sense, it is necessary to pay attention to the stage of Parkinson’s Disease evolution that the patient is in, in order to start the surgical treatment before it no longer has the expected expressive effects. Conclusion: It is expected, therefore, a significant improvement in the quality of life of patients undergoing PCT, which is not restricted to motor gains.
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Baybuz, L. A., N. G. Perevalova, and V. Y. Makarov. "THE EFFECTIVENESS OF OZONE THERAPY IN THE REHABILITATION OF PATIENTS WITH DISORDERS OF THE CENTRAL NERVOUS SYSTEM AFTER SUFFERING COVID-ASSOCIATED PNEUMONIA." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-54-58.
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Abstract: The consequences of the transferred new coronavirus infection are currently not well understood, but the neurotropicity of SARS-CoV-2 is beyond doubt. In the manifestations of postcoid syndrome, damage to the central nervous system is dominant and requires timely diagnosis and correction, incl. at the rehabilitation stage of medical care. The introduction of highly effective non-drug methods of treatment with a small number of side effects is an urgent task of modern medicine. Such methods of treatment can include ozone therapy - the use of an ozone-oxygen mixture (ACS) for therapeutic purposes, which significantly improves blood microcirculation and oxygenation of ischemic tissues due to its fibrinolytic activity and antiaggregatory properties, and therapeutic doses of ozone are able to correct the lipid profile of patients due to reducing atherogenic lipoproteins, triglycerides and cholesterol. In the range of therapeutic concentrations, ozone exhibits immunomodulatory, anti-inflammatory, bactericidal, antiviral, and detoxification effects. This article presents the experience of using ozone therapy in patients who have undergone covid-associated pneumonia (CT1-CT4) with postcoid syndrome and a predominant lesion of the central nervous system. The analysis of the dynamics of symptoms in a group of patients who underwent a course of ozone therapy in comparison with a group where ozone therapy was contraindicated is presented. The defeat of the central nervous system was represented by the following syndromes and symptoms, both individually and in combination: - cerebrasthenic syndrome, incl. anxiety, insomnia, decreased or lack of appetite, unstable mood background, weakness, fatigue - 94% - cerebral syndrome (headaches, constant "fog in the head", less often dizziness, decreased memory and attention, impaired sensitivity like anosmia, hyposmia) - 62%, incl. loss of memory and attention was observed in 42%, anosmia and hyposmia occurred in 11% of cases. The severity of certain symptoms was manifested depending on the age, the severity of the disease, the timing of the beginning of rehabilitation measures and the comorbid background. Diagnostics of the lesion of the central nervous system by coronavirus in patients was carried out by the methods of questioning complaints, dynamic observation, using the questionnaire for assessing the quality of life EQ-5D. In addition, in both groups of patients, the assessment of the severity of the main syndromes in points from 0 to 10 was carried out using a questionnaire at the beginning of the rehabilitation course and at the end of it. Evaluation of the results at discharge was carried out using the Pearson correlation coefficient. The use of an ozone-oxygen gas mixture in a comprehensive rehabilitation program for patients with postcoid syndrome and a predominant CNS lesion can reduce the intensity or completely stop cerebroasthenic and cerebral syndromes, completely restore taste and smell, and improve certain cognitive functions. This will improve the quality of life of patients, their social adaptation and reduce the drug load. The syndromic complex of CNS lesions, which remains in a certain volume, even after a comprehensive rehabilitation program with ozone therapy, indicates the need for long-term follow-up, clinical examination and medical rehabilitation of patients after a new coronavirus infection.
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Spinella, Toni, Sherry Stewart, Julia Naugler, Igor Yakovenko, and Sean Barrett. "The power of placebo: Does cannabidiol (CBD) expectancy alone impact acute stress and anxiety?" In 2022 Annual Scientific Meeting of the Research Society on Marijuana. Research Society on Marijuana, 2022. http://dx.doi.org/10.26828/cannabis.2022.02.000.01.
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Background. There have been notable increases in the use of cannabidiol (CBD) for therapeutic purposes, such as in the treatment of stress- and anxiety- related disorders. Preliminary research has demonstrated that CBD decreases indices of stress and anxiety. However, drug effects in humans are thought to be comprised of both pharmacological properties as well as a placebo response. Little is known about the extent to which the purported therapeutic effects of CBD result from pharmacological versus expectancy factors. Aims. The aim of this study was to evaluate whether (i) CBD expectancy alone could influence stress, anxiety, and mood, and (ii) the extent to which beliefs regarding CBD effects predicted these responses. Generalized estimating equations (GEE) were used to evaluate the research questions of interest. Methods. In this randomized crossover study, 43 health adults (23 women) attended three laboratory sessions. During the first session, they were oriented to the study and rated the extent to which they believed that CBD helped with stress, anxiety, and mood. They then participated in two identical experimental laboratory sessions, where they self-administered CBD-free hempseed oil sublingually. During one session, they were (incorrectly) informed that the oil contained CBD and in the other session, that the oil was CBD-free. Following administration, participants engaged in the Maastricht Acute Stress Test (MAST) to induce moderate levels of stress and anxiety. Heart rate variability (HRV) was assessed continuously, and subjective state (i.e., stress, anxiety, mood, other subjective states) was assessed at baseline, 90-min following oil administration, immediately following the MAST, and after a 10-min recovery period. Results. The CBD expectancy condition was associated with increased sedation as well as significant fluctuations in HRV that could indicate heightened anticipatory stress regulation. Overall, there were no observed changes in subjective stress, or anxiety, according to expectancy condition. However, participants who endorsed the strongest a priori beliefs about CBD possessing anxiolytic properties reported significantly lower anxiety in the CBD expectancy condition and higher anxiety the CBD-free expectancy condition. Conclusions. Results from this study indicated that CBD expectancy alone impacted several subjective and physiological responses. Additionally, expectancy-related factors were implicated in anxiolytic effects of CBD for those who strongly believed it was helpful for such purposes, suggesting that expectation plays some role in the purported stress- and anxiety- reducing effects of CBD. Findings from this study emphasize the need to measure and control for CBD-related expectancies in clinical research that involves the administration of CBD. Future investigations would benefit from replicating these findings and using a full balanced-placebo research design to elucidate the relative contributions of pharmacology and expectancy.
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Muflic, Lucian, and Ileana Ion. "ANTI-TUMOR NECROSIS FACTOR ALPHA BIOLOGIC THERAPY DOSE ADJUSTMENT NECESSITY IN PATIENTS WITH RHEUMATOID ARTHRITIS. A CASE PRESENTATION." In NORDSCI International Conference Proceedings. Saima Consult Ltd, 2019. http://dx.doi.org/10.32008/nordsci2019/b1/v2/36.
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Rheumatoid arthritis is an inflammatory disease characterized by chronic joint erosive processes, affecting approximately 1% of the population. [1] The pathogenic mechanisms processes involve the activation of pro-inflammatory cytokines, including TNF alpha. [2] The purpose of this case presentation is to elucidate a possible correlation between the high level of blood TNF alpha and the apparent lack of response to biologic therapy directed against this molecule. A female patient, aged 55 years, diagnosed with rheumatoid arthritis in 2006, presents an increased inflammatory biological syndrome. The patient was being treated biologically (adalimumab, and two years of etanercept previously. One year ago, the patient presents the elevation values of the blood tests commonly used to monitor the status of patients with inflammatory rheumatoid arthritis up to 2.5-3 x than normal values. Initially, this increase is considered to be due to a respiratory seasonal condition. We continued monitoring the status, after subsequent remission of these respiratory disorders, and we observed the persistence of those elevated test, this time without an obvious possible causing comorbidity. We decided to evaluate the current patient status and we obtained the following information: Biological syndrome currently moderately exceeds the maximum normal values. ESR was 47 mm/h and CRP 1.5 than the normal value. TNF alpha value determined by immunochemical methods with detection by chemiluminescence (CLIA) is 67.2 pg / mL Biological confirmation by determining serum TNF alpha and increased observation that the current level may be one explanation for the possible reactivation of the disease prompted us to continue the study in patients receiving anti-TNF alpha biologic. This study is ongoing. We can imagine this correlation between the level of TNF alpha and the degree of disease activity at least in the case of a group of patients treated with biological drugs. If this could be demonstrated, then perhaps we can expect a change in the curative approach of these patients, meaning that dose adjustment can be considered depending on the level of TNF alpha, and why not, depending on other cytokines that may be included in future studies.
Reports on the topic "Inflammatory response in mood disorders"
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Viswanathan, Meera, Jennifer Cook Middleton, Alison Stuebe, Nancy Berkman, Alison N. Goulding, Skyler McLaurin-Jiang, Andrea B. Dotson, et al. Maternal, Fetal, and Child Outcomes of Mental Health Treatments in Women: A Systematic Review of Perinatal Pharmacologic Interventions. Agency for Healthcare Research and Quality (AHRQ), April 2021. http://dx.doi.org/10.23970/ahrqepccer236.
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Background. Untreated maternal mental health disorders can have devastating sequelae for the mother and child. For women who are currently or planning to become pregnant or are breastfeeding, a critical question is whether the benefits of treating psychiatric illness with pharmacologic interventions outweigh the harms for mother and child. Methods. We conducted a systematic review to assess the benefits and harms of pharmacologic interventions compared with placebo, no treatment, or other pharmacologic interventions for pregnant and postpartum women with mental health disorders. We searched four databases and other sources for evidence available from inception through June 5, 2020 and surveilled the literature through March 2, 2021; dually screened the results; and analyzed eligible studies. We included studies of pregnant, postpartum, or reproductive-age women with a new or preexisting diagnosis of a mental health disorder treated with pharmacotherapy; we excluded psychotherapy. Eligible comparators included women with the disorder but no pharmacotherapy or women who discontinued the pharmacotherapy before pregnancy. Results. A total of 164 studies (168 articles) met eligibility criteria. Brexanolone for depression onset in the third trimester or in the postpartum period probably improves depressive symptoms at 30 days (least square mean difference in the Hamilton Rating Scale for Depression, -2.6; p=0.02; N=209) when compared with placebo. Sertraline for postpartum depression may improve response (calculated relative risk [RR], 2.24; 95% confidence interval [CI], 0.95 to 5.24; N=36), remission (calculated RR, 2.51; 95% CI, 0.94 to 6.70; N=36), and depressive symptoms (p-values ranging from 0.01 to 0.05) when compared with placebo. Discontinuing use of mood stabilizers during pregnancy may increase recurrence (adjusted hazard ratio [AHR], 2.2; 95% CI, 1.2 to 4.2; N=89) and reduce time to recurrence of mood disorders (2 vs. 28 weeks, AHR, 12.1; 95% CI, 1.6 to 91; N=26) for bipolar disorder when compared with continued use. Brexanolone for depression onset in the third trimester or in the postpartum period may increase the risk of sedation or somnolence, leading to dose interruption or reduction when compared with placebo (5% vs. 0%). More than 95 percent of studies reporting on harms were observational in design and unable to fully account for confounding. These studies suggested some associations between benzodiazepine exposure before conception and ectopic pregnancy; between specific antidepressants during pregnancy and adverse maternal outcomes such as postpartum hemorrhage, preeclampsia, and spontaneous abortion, and child outcomes such as respiratory issues, low Apgar scores, persistent pulmonary hypertension of the newborn, depression in children, and autism spectrum disorder; between quetiapine or olanzapine and gestational diabetes; and between benzodiazepine and neonatal intensive care admissions. Causality cannot be inferred from these studies. We found insufficient evidence on benefits and harms from comparative effectiveness studies, with one exception: one study suggested a higher risk of overall congenital anomalies (adjusted RR [ARR], 1.85; 95% CI, 1.23 to 2.78; N=2,608) and cardiac anomalies (ARR, 2.25; 95% CI, 1.17 to 4.34; N=2,608) for lithium compared with lamotrigine during first- trimester exposure. Conclusions. Few studies have been conducted in pregnant and postpartum women on the benefits of pharmacotherapy; many studies report on harms but are of low quality. The limited evidence available is consistent with some benefit, and some studies suggested increased adverse events. However, because these studies could not rule out underlying disease severity as the cause of the association, the causal link between the exposure and adverse events is unclear. Patients and clinicians need to make an informed, collaborative decision on treatment choices.