Bipolar Disorder - an overview (original) (raw)
Chapters and Articles
You might find these chapters and articles relevant to this topic.
URL:
https://www.sciencedirect.com/science/article/pii/S0020748910000805
Treatment of Bipolar Depression
Steven L. Dubovsky MD, in Psychiatric Clinics of North America, 2005
Bipolar disorder is not a unitary illness but a group of disorders with different courses and treatment responses [3]. In addition to categorical subgroups such as bipolar I and bipolar II disorder, conditions associated with a childhood onset, psychotic symptoms, a prominent affective family history, or comorbid substance abuse or contamination of the personality may be different disorders from adult-onset bipolar disorder in a patient without a family history of a mood disorder or significant comorbidity. Furthermore, features such as rapid or ultradian cycling may represent evolution of a mood disorder with a different pathophysiology and course than earlier stages of the disorder [8].
URL:
https://www.sciencedirect.com/science/article/pii/S0193953X05000249
Mental health in adult congenital heart disease
Philip Moons, ... Koen Luyckx, in International Journal of Cardiology Congenital Heart Disease, 2023
2.1.2 Bipolar disorder
Bipolar disorders are a group of brain disorders that cause extreme fluctuation in a person's mood, energy, and ability to function [7]. Empirical evidence on bipolar disorders in CHD is scarce. In research, bipolar disorders are often pooled with other mood-affective disorders. A study in adolescents with transposition of the great arteries (d-TGA) in the US found that 1 out of 139 patients (0.7%) presented with bipolar disorder [19]. A study in 4206 patients with tetralogy of Fallot in Taiwan found that bipolar disorders occurred in 36.7/100,000 patient years [20]. This rate was 2.4 times higher than in the general Taiwanese population [20].
URL:
https://www.sciencedirect.com/science/article/pii/S2666668523000174
Severe Mental Illness and Cardiovascular Disease
Michael Goldfarb MD, MSc, ... Petter Andreas Ringen MD, PhD, in Journal of the American College of Cardiology, 2022
Bipolar disorder
Bipolar disorders are a group of brain disorders that cause extreme fluctuation of a person's mood, energy, and functional ability. Bipolar I disorder is a manic-depressive disorder, considered the most severe form, and may be accompanied by psychotic episodes.9 There are currently 7 million Americans with bipolar disorder, and the lifetime prevalence of bipolar disorder is about 1%-3%.10 In longitudinal studies, bipolar disorder is associated with a 1.5- to 2.5-fold increased risk of cardiovascular disease compared with the general population.12 Cardiovascular disease is the most common cause of death in people with bipolar disorder and is responsible for 35%-40% of the excess mortality.20
People with bipolar disorder have a cardiovascular risk profile comparable to those with schizophrenia. Studies have reported similar prevalences of smoking, inadequate exercise, poor nutrition, and obesity, as well as hypertension, diabetes, and metabolic syndrome.14,21-24
Commonly used pharmacotherapy for bipolar disorder can also increase cardiovascular risk. Both lithium and valproic acid can cause weight gain and impaired insulin resistance.19 Antipsychotics may also be used in bipolar disorder along with their impact on weight, lipid, and insulin metabolism. People with bipolar disorder are more likely than people without psychiatric disease to have issues with medication adherence, substance abuse, and poor self-care.25
URL:
https://www.sciencedirect.com/science/article/pii/S0735109722054213
Functional Connectivity
John M. Billings MD, ... Christopher T. Whitlow MD, PhD, MHA, in Neuroimaging Clinics of North America, 2017
Bipolar Disorder
Bipolar disorder is a common psychiatric illness with significant morbidity, accounting for approximately 7% of all mental and substance use disorders.29,30 Mood disorders historically have been exclusively a clinical diagnosis, with only a limited role of neuroimaging. One of the exciting possibilities for the future of neuroimaging is using differences in structural connectivity to differentiate between different mood disorders, and therefore, help to tailor individualized treatment. For example, work by Rive and colleagues31 demonstrated the ability to differentiate between unipolar versus bipolar mood disorder, using various resting state networks, and binary gaussian process classifiers (a method similar to SVM, additionally able to predict the probability of class membership). Work by Roberts and colleagues29 implicates the inferior frontal gyrus as having a key role in bipolar disorder, showing functional dysconnectivity from multiple regions, including the bilateral insulae, ventrolateral prefrontal gyri, superior temporal gyri, and the putamen. This work demonstrated a modest ability to discriminate between bipolar disorder and healthy controls with an accuracy of 64.3% (chance level 40.8%), and positive predictive values ranging from 49% to 54%.
URL:
https://www.sciencedirect.com/science/article/pii/S1052514917300680
Cellular Plasticity Cascades: Targets for the Development of Novel Therapeutics for Bipolar Disorder
Carlos A. ZarateJr, ... Husseini K. Manji, in Biological Psychiatry, 2006
Bipolar disorder is one of the most severely debilitating of all medical illnesses and affects the lives and functioning of millions worldwide. Recent studies indicate that for a large percentage of patients, outcome is poor. Patients afflicted with bipolar disorder generally experience high rates of relapse, chronicity, lingering residual symptoms, cognitive and functional impairment, psychosocial disability, and diminished well-being (Fagiolini et al 2005; Revicki et al 2005; Tohen et al 2003). In addition many deleterious health-related effects are now being recognized. Bipolar disorder is increasingly being viewed as an illness not only with purely psychologic manifestations but as a systemic disease frequently associated with cardiovascular disease, diabetes mellitus, obesity, and thyroid disease (Kupfer 2005). Despite these facts, little is known about the precise neurobiological underpinnings of bipolar disorder, which is essential for the development of specific-targeted therapies that are more effective, work rapidly, and are better tolerated than existing therapies. In this perspectives article, we discuss the prospect of developing new medications for bipolar disorder based on two approaches:
1
Understanding the presumed therapeutically relevant biochemical targets of medications currently in use and using that knowledge to design new drugs directed at these targets. This includes not only direct biochemical targets, but also downstream targets that are regulated by chronic drug administration (i.e., consistent with the clinical temporal profile).
2
Understanding the pathophysiology of the illness (admittedly in its infancy) and using that knowledge to design therapeutics to attenuate or prevent those pathologic processes.
URL:
https://www.sciencedirect.com/science/article/pii/S0006322305014253
Dual Disorders in Cannabis Misuse
F. Arias-Horcajadas, ... B. Mesías, in Handbook of Cannabis and Related Pathologies, 2017
Bipolar Disorder
Bipolar disorder is one of the conditions most related with cannabis dependence, as epidemiological studies on the general population confirm, such as the ECA or the NESARC, along with many clinical studies. On one hand, there is a high prevalence of use and dependence in bipolar patients. On the other, cannabis use inducing manic phases is also described. The increased risk of appearance of a bipolar disorder has been related to the dosage of cannabis and use beginning at an earlier age. Likewise, cannabis use brings forward the age of onset of bipolar disorder (Lagerberg et al., 2011), which supports the view that it has at least a role in precipitating the symptoms.
Cannabis use has been associated with clinical changes in bipolar disorder, such as more mixed episodes, rapid cycling, more suicide attempts, greater functional limitations, more psychotic symptoms, and an increase in the number of relapses. In the NESARC study, an association is indicated, and it is related to an earlier age of onset of bipolar disorder and more mixed, depressive and manic episodes (Lev-Ran, Le Foll, McKenzie, George, & Rehm, 2013a).
URL:
https://www.sciencedirect.com/science/article/pii/B9780128007563000089
Neurobehavioral Manifestations of Neurological Diseases: Diagnosis and Treatment
Samantha E. Marin MD, Russell P. Saneto DO, PhD, in Neurologic Clinics, 2016
Bipolar Disorder
Bipolar disorder is a psychiatric condition in which there are extreme shifts in mood, resulting in periods of emotional highs (mania) and lows (depression), producing marked impairment in daily functioning.33 Bipolar disorder is believed to affect approximately 1% of the population. Although the etiology of bipolar disorder is unknown, it is believed to result from a combination of genetic and environmental factors.173,174 Several candidate loci have been linked with bipolar disorder175; however, no single gene has been identified as causative. Recently, there has been significant interest in the role of mitochondrial dysfunction in the pathophysiology of bipolar disorder.
Studies suggested that an abnormality in mitochondrial function existed in a subset of patients with bipolar owing to (1) structural abnormalities in mitochondria identified in patients with bipolar disorder, (2) abnormal brain phosphorus metabolism detected by 31P magnetic resonance spectroscopy (MRS), (3) altered markers of oxidative stress in bipolar disorder, (4) possible contribution of parent-of-origin effect in the transmission of bipolar disorders in families, (5) increased levels of mitochondrial polymorphisms, point mutations, and deletions in serum or post mortem brain samples from patients with bipolar disorder, (6) phenotypes of animal models with mitochondrial dysfunction, and (7) comorbidity of affective disorders in patients with established primary mitochondrial disease diagnoses.
Mitochondrial structural and functional abnormalities in bipolar disorder
One of the first lines of evidence suggesting a link between mitochondrial dysfunction and bipolar disorder is the demonstration of structural abnormalities of the mitochondria in bipolar disorder affected patients.176–178 Uranova and colleagues176,177 investigated the ultrastructural appearance of pathologic samples from patients with bipolar disorder and schizophrenia. They found decreased numbers and size of mitochondria within oligodendrocytes in the caudate nucleus and prefrontal cortex.177 However, it is unclear whether these changes were related directly to their underlying diagnosis or if they were secondary to medication effect. Subsequently, Cataldo and colleagues178 investigated the appearance of mitochondria in post mortem brain and peripheral samples from patients with bipolar disorder. They found changes in mitochondrial size and distribution: intracranial mitochondria were significantly smaller in area compared with controls and extracranial mitochondria were concentrated within the perinuclear region. These changes seemed to be independent of lithium exposure and independent of changes of surrounding neuropil structure. Further studies are required to delineate the structural changes of mitochondria found in larger populations of patients with bipolar disorder.
Additional support for abnormal oxidative phosphorylation in patients with bipolar disorder comes from neuroimaging studies. Studies using 31P MRS in patients with bipolar disorder have demonstrated decreased intracellular pH in the euthymic state and decreased phosphocreatine in the depressed state within the frontal lobes, which is hypothesized to be secondary to mitochondrial dysfunction.179–181 Dager and colleagues182 demonstrated that patients with bipolar disorder exhibited significantly increased gray matter lactate levels compared with healthy controls, suggesting a shift from oxidative phosphorylation toward glycolysis. However, these findings are inconsistent; other studies using proton MRS have failed to find similar changes in patients with bipolar disorder compared with controls.183 One of the most convincing lines of neuroradiologic evidence suggesting that mitochondrial dysfunction in specific brain regions can give psychiatric symptoms is from Anglin and associates.184 These authors demonstrated that there were altered metabolite signals in the hippocampus and cingulate cortex on proton MRS in patients with mitochondrial disease and concurrent psychiatric diagnoses. Overall impairment of functioning owing to the psychiatric symptoms correlated with metabolic markers in the cingulate cortex.
Altered markers of oxidative stress in bipolar disorder
There is some evidence that oxidative stress is thought to mediate neuropathologic processes of a number of neuropsychiatric disorders, including bipolar disorder. The mitochondria play a role in producing reactive oxygen species (ROS). Under normal conditions, the mitochondria are a major source of ROS, produced in the complexes of the respiratory chain. However, if sufficient ROS are generated to overwhelm the innate antioxidant systems, oxidative stress results in inhibition of the respiratory chain, resulting in a decreased production of ATP and cellular dysfunction. The brain is particularly vulnerable to ROS production because it metabolizes 20% of total body oxygen and has a limited amount of antioxidant capacity.185 Multiple studies have reported increased products of lipid peroxidation and alterations of the major antioxidant enzymes in patients with bipolar disorder.186–194 Wang and colleagues190 demonstrated a significant increase of 4-hydroxynonenal (a product of lipid peroxidation) in post mortem samples from the anterior cingulate in patients with bipolar disorder, suggesting a role for oxidative dysfunction. Decreased levels of mitochondrial complex I subunits and increased protein oxidation and nitration in post mortem samples from the prefrontal cortex in patients with bipolar disorder was subsequently found by other groups.192,195 Although oxidative stress markers as a means to determine bipolar disorder vulnerability have generated interest,196 further studies are required before implementation in clinical practice.
Parent-of-origin effects in bipolar disorder
Multiple studies investigating the heritability of bipolar disorder in families have suggested a gender-specific mode of transmission. In early studies of bipolar disorder, male-to-male transmission was deemed rare.197 Therefore, an X-linked inheritance was presumed. In the 1960s, it was believed that X-linkage alone could not explain the pattern of inheritance of bipolar disorder and a mitochondrial inheritance was considered a possibility after the discovery of mtDNA.198 Then in the mid 1990s linkage studies suggested a maternal “parent-of-origin” effect, with affected mothers being more common than affected fathers.199–201 The parent-of-origin effect is the phenomenon in which gender of the transmitting patent affects the expression of illness in their offspring without following Mendelian laws. Further studies supported the idea of a parent-of-origin effect by showing that more maternal relatives are affected by bipolar disorder than paternal relatives.199,202 Although this finding is not universal in all studies investigating the genetic contribution to bipolar disease, there is some suggestion that maternal inheritance is present at least in some patients afflicted with the disorder.
Single nucleotide polymorphisms and haplotypes in bipolar disorder
Various mtDNA SNPs are believed to play a role in the pathophysiology of bipolar disorder.203–208 Many of those identified as playing a role in bipolar disorder involve mtDNA SNPs in complex I subunits. McMahon and associates207 investigated mtDNA SNPs in pedigrees from patients with bipolar disorder in whom maternal inheritance was evident. They identified 4 SNPs that were more common in probands. Although not significant in this study, other subsequent studies have demonstrated their significance. Studies by Kato and colleagues203,204 demonstrated that the m.10398A>G SNP was associated significantly with the bipolar disorder compared with controls. This SNP alters an evolutionarily conserved threonine into an alanine in the mitochondrial-encoded NADH dehydrogenase (complex I) subunit-3 (MT-ND3) gene. This SNP is reported at polymorphism frequencies in various ethnicities (30%–64%)209,210 and is not likely to be of etiologic importance in mitochondrial disease, although its effects on NADH dehydrogenase have not been examined.211 There is also some evidence that it plays a role in intracellular calcium dynamics212 and glucose utilization.213 There is also a suggestion that patients with this polymorphism may have better response to lithium.214
A second SNP, m.5178C>A, has also been identified as being more frequently seen in patients with bipolar disorder compared with control subjects.203 The nucleotide change results in the substitution of a methionine instead of leucine in the NADH-dehydrogenase (complex I) subunit-2 gene (ND2). This SNP was significantly more common in leukocytes in patients with bipolar disorder compared with controls.203 The presence of both the m.10398A>G and m.5178C>A polymorphisms, known as the C/A haplotype, may increase the susceptibility to bipolar disorder than each polymorphism alone.204 Kato and colleagues204 found that the coexpression of both polymorphisms was significantly more common in those with bipolar disorder. The C/A haplotype was found in 33.6% of subjects, compared with 16.8% of control patients (a relative risk of 2.4). However, more studies are required to determine the significance of the synergistic effect of these polymorphisms in the etiology of bipolar disease.
One other polymorphism that warrants mention is the m.3644T>C in the gene for a complex I NADH dehydrogenase subunit 1 subunit (ND1). This polymorphism was identified as being significantly associated with bipolar disorder. Munakata and colleagues208 identified several homoplasmic, nonsynonymous SNPs in 6 patients with bipolar disorder and symptoms suggestive of mitochondrial disorder. Multiple other mtDNA SNPs have been reported in bipolar disorder patients at a lower frequency including those in complex I subunits (m.3316G>A and m.3394T>C in the ND1 subunit; m.10084T>C and m.10398A>G in the ND3 subunit); complex V subunits (m.8537A>G, m.8563A>G in ATPase6); tRNA genes (m.1662C>T, m.5539A>G, m.5592A>G, m.5773G>A, m.5821G>A, m.10410T>C, and m.10427G>A); rRNA genes (m.63A>G, m.709G>A, m.769G>A, m.794T>C, m.3206C>T); a variant in the L-strand replication site (m.5747A>G); and several silent polymorphisms.204 Three of these variants (m.5539A>G in tRNATrp, m.5747A>G in the L-strand replication site, and m.8537A>G in ATPase6) may be of more significance because they cause amino acid substitutions at evolutionarily conserved sites and merit further investigation.204 However, it is difficult to interpret the significance of these variants without larger samples of bipolar patients.
Not all studies have identified mtDNA SNPs in their bipolar disorder patient cohorts.206 Kirk and colleagues206 sequenced the entire mitochondrial genome in 25 probands of maternally inherited pedigrees with bipolar disorder, but found no associated polymorphisms or variants attaining significance. It should also be noted, that although associations of SNPs and bipolar disorder have been explored, it is unclear how these mtDNA polymorphisms affect the vulnerability to bipolar disorder. If and how these variants lead to changes to protein structure and function needs to be elucidated to establish any pathophysiologic significance.
In addition to polymorphisms reported in the mtDNA in patients with bipolar disorder, there is some evidence to suggest that polymorphic variants in nDNA-encoded mitochondrial genes may also have a role in bipolar genetic susceptibility.170,214–217 Several prior studies have provided evidence for the linkage of chromosome 18 with bipolar disorder.201,218–225 NDUFV2, encoding the 24-kDa subunit of complex I in the respiratory chain (NADH dehydrogenase flavoprotein 2) is located at chromosome 18p11,226,227 close to the loci identified in prior linkage studies. Therefore, it has been hypothesized that polymorphisms in NDUFV2 may be associated with psychiatric illness. Washizuka and colleagues214,216,228 identified 5 polymorphisms in NDUFV2 (c.602A>G, c.3542G>A, c.3245T>G, c.3041T>C and c.2694A>G) associated with bipolar disorder in different ethnicities. The CTAT haplotype for 4 polymorphisms in NDUFV2 that are strongly linked (c.796C>G, c.795T>G, c.602G>A, and c.233T>C) is significantly less common in those with bipolar disorder compared with control subjects.216 Although the effect of these polymorphisms on complex I activity has not been thoroughly explored, many of these polymorphisms exist around the promoter region of NDUFV2. The c.602A>G polymorphism, also associated with a higher likelihood of being diagnosed with bipolar disorder, has been shown to promote activity through a loss of binding capacity to a transcription factor.216 Doyle and colleagues215 also concluded that promoter haplotypes seem to be associated with bipolar disorder in the Caucasian population. However, the exact mechanism by which this alters complex I activity and leads to a higher susceptibility to bipolar disorder is inconclusive.
The role of mtDNA haplogroups has been investigated in patients with bipolar disorder without consensus for disease association. A particular combination of SNPs in an individual’s mtDNA (haplotype) is used to identify ancestral heritage and divide people into groups that share a common maternal ancestor. Three studies have investigated the role of haplogroups in bipolar disorder; however, no consistent findings have emerged. Kazuno and colleagues205 identified an overrepresentation of haplogroup N9a in patients with bipolar disorder compared with controls. Alternatively, Rollins and colleagues163 found a possible association between the pre-HV haplogroup and bipolar disorder. However, another study did not find any differences in haplogroup frequencies in patients with bipolar disorder.207
Mitochondrial DNA deletions and copy number variations in bipolar disorder
Deletions in the mitochondrial genome have been implicated in the pathogenesis of bipolar disorder.147,162–164,207,208,214,229–233 Kato and Takahashi147 reported that 2 of 35 patients (5.7%) with bipolar disorder harbored the common 4997 base-pair deletion in mtDNA isolated from leukocytes, suggesting that deletions of mtDNA in the brain may result in affective symptoms. Kato and colleagues234 later reported that there was a significant increase in the 4997 base-pair deletion in mtDNA in autopsied brains of patients with bipolar disorder compared with normal controls. Although the ratio of partially deleted mtDNA was small (<0.6%), this seemed to be a reflection of increased free radical generation, resulting in an increased accumulation of mtDNA deletion in these patients. These findings were replicated by Shao and colleagues,161 who identified a greater proportion of the common deletion in the dorsolateral prefrontal cortex of patients with bipolar disorder. Three subsequent studies have been unable to replicate these findings.160,233,235
Mitochondrial mtDNA CNVs have also been investigated in patients with various neuropsychiatric disorders. Each human cell contains hundreds to thousands of mitochondria, each of which contains multiple copies of mtDNA. Studies have suggested that maintaining an adequate mtDNA copy number may be important for cell viability.236 Two studies have investigated the role of mitochondrial mtDNA copy numbers in patients with major depression, bipolar disorder, and schizophrenia.167,233 Vawter and colleagues167 looked at mtDNA copy number in the dorsolateral prefrontal cortex and identified a nonsignificant trend toward a lower copy number in patients with bipolar disorder compared with controls, which was not seen in patients with depression. Similarly, Kakiuchi and colleagues233 found a nonsignificant trend toward decreased mtDNA copy number in patients with bipolar disorder but not schizophrenia. Overall, the current evidence for a role of mitochondrial mtDNA copy numbers in psychiatric illness is not persuasive.
Mitochondrial DNA mutations in bipolar disorder
Similar to depression, there seems to be an association between pathogenic mutations in mtDNA genes encoding for mitochondrial tRNAs and bipolar disorder. Munakata and colleagues162 reexamined the DNA microarray data from post mortem prefrontal cortices from patients with various psychiatric diagnoses, including bipolar disorder, and the mtDNA m.3243A>G mutation.237 In their series, they identified an increased expression of LARS2 (human leucyl-tRNA synthetase 2), which is responsible for the aminoacylation of tRNALeu. It is possible that LARS2 expression was a compensatory upregulation owing to accumulation of the mutation, m.3243A>G, which has been shown to decrease the efficiency of processing and aminoacylation of tRNALeu.238–240 Interestingly, the detection of the m.3243A>G mutation may be related to the sensitivity of the testing used. This mutation was not identified in the prefrontal cortex or liver using conventional restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR), but was identified using peptide nucleic acid–clamped RFLP-PCR, which has a much lower detection limit of 0.1%.162 Further studies using the more sensitive detection methodology are necessary to investigate mtRNA and bipolar disorder.
Nuclear DNA mutations in bipolar disorder
Bipolar disorder has been reported in a subset of patients diagnosed with mtDNA depletion secondary to various pathogenic nDNA mutations involved in mitochondrial integrity and maintenance.241–243 Siciliano and colleagues241 reported on a 44-year-old woman who had a history of bipolar affective disorder with an onset in her teens. Lithium therapy was ineffective and she had frequent episodes of psychotic mania. At the age of 40 years, she developed ptosis and migraine headaches. She had an exaggerated lactate elevation during moderate exercise and a muscle biopsy demonstrating increased ragged red fibers and multiple cytochrome oxidase–negative fibers (>15%). Southern blot demonstrated multiple mtDNA deletions (accounting for 28% of mtDNA). Her older sister was similarly affected. Multiple family members demonstrated different combinations of ptosis, memory difficulties, and migraine headaches. Bipolar disorder was also diagnosed in 3 additional family members. The proband and her affected family members were subsequently found to harbor a pathologic mutation in ANT1 (p. L98P), which has been seen in patients with autosomal-dominant progressive external ophthalmoplegia. Psychiatric disturbances were also reported in a large Finnish family harboring a mutation in C10orf2 (encoding for Twinkle)242 and a large Belgian family carrying a mutation in POLG1 (encoding for mitochondrial polymerase gamma).243
Differential expression of mitochondria-related nDNA genes has also been investigated in bipolar disorder. Studies have suggested that there is differential mitochondria-related gene expression in bipolar disorder compared with controls in post mortem samples from the prefrontal cortex229,244; however, these findings have not been replicated by other investigators.161,162 Other authors have demonstrated inconsistent findings with respect to the expression of nuclear genes encoding subunits of the respiratory chain.169,245,246 Authors have also investigated mRNA content as a maker of gene expression and have found significantly lower mRNA content for complex I subunits.171 However, Karry and colleagues170 reported the presence of a higher protein content of complex I subunits in the ventral parietooccipital cortex that was not associated with a higher mRNA expression.
Summary of mitochondrial dysfunction and affective disorders
Overall, multiple lines of evidence have suggested a role for mitochondrial dysfunction in some patients with depression and bipolar disorder. However, the mechanism by which mitochondrial dysfunction leads to a presentation of affective disorders is unclear. Genetic studies, particularly those investigating the genetic underpinnings of bipolar and depression, have been completed with small numbers of patients, different methodologies, and different endpoints giving inconsistent results. Considering the impact that affective disorders have on quality of life, particularly in those with a concurrent chronic illness (mitochondrial disease), it is important that large-scale, highly powered, and methodologically strong studies be completed to try to identify the link between affective disorders and mitochondrial dysfunction.
URL:
https://www.sciencedirect.com/science/article/pii/S0733861915000869
Atypical social reward anticipation as a transdiagnostic characteristic of psychopathology: A meta-analytic review and critical evaluation of current evidence
Luke Aldridge-Waddon, ... Veena Kumari, in Clinical Psychology Review, 2020
4.3.2 Bipolar disorder
Bipolar disorder is a mental illness associated with extreme and cyclical changes in mood that affect cognition, work life, and interpersonal relationships. Two studies (Dutra, Cunningham, Kober, & Gruber, 2015; Dutra, Man, Kober, Cunningham, & Gruber, 2017) were eligible for inclusion in this review. Incentive delay paradigms were used in both studies. Using neuroimaging, both studies showed that bipolar disorder is associated with hyperanticipation of social rewards, demonstrated by, in comparison to healthy individuals, increased striatal activation during social reward anticipation (Dutra et al., 2015). The bipolar disorder group also exhibited reduced orbitofrontal cortex activation during reward anticipation in comparison to healthy controls (Dutra et al., 2015), and greater ventral striatum-orbitofrontal cortex connectivity during reward receipt. The effects observed in social rewards were also observed in non-social rewards. Both studies included participants within the clinical group that were taking psychotropic medication at the time of participation (Appendix E) and all described effects remained when antipsychotic medication use was included as a covariate. Meta-analysis: Neither study was eligible for inclusion in the meta-analysis as behavioural data were not reported.
URL:
https://www.sciencedirect.com/science/article/pii/S0272735820301306
Unrecognized bipolar disorder in patients with depression managed in primary care: A systematic review and meta-analysis
John Daveney, ... Aneez Esmail, in General Hospital Psychiatry, 2019
1 Introduction
Bipolar disorder is a chronic condition, characterized by alternating episodes of mania and depression [1]. It comprises a spectrum defined by the severity and duration of mood elevation, from bipolar II (hypomania) to bipolar I (full episodes of mania) to bipolar with psychosis [1]. It is the 6th leading cause of disability worldwide [2,3] with a prevalence of up to 5% [4,5]. An increase in the number of people with bipolar disorder by 49.1% globally has been observed between 1990 and 2013, accounted for by increasing population and ageing [3]. The annual costs for bipolar disorder exceeds 45billionintheUSand45 billion in the US and 45billionintheUSand3 billion in the UK excluding lost employment [6,7].
Nearly 90% of people with depression in the UK are treated in primary care only, while the percentage of US patients with depression treated in a general medical setting is 73.3% [8,9]. There is growing evidence that a considerable percentage of primary care patients with depression have unrecognized bipolar disorder [10–13]. The identification of unrecognized cases of bipolar disorder amongst patients with depression is crucial for appropriate pharmacological management. Antidepressant monotherapy is non-optimal for patients with bipolar disorder and can lead to adverse outcomes including an increased risk of mania or hypomania and suicide [13–17].
At present, there is no up-to-date evidence concerning the prevalence of unrecognized bipolar disorder in primary care patients diagnosed with depression; this study aims to address this gap.
URL:
https://www.sciencedirect.com/science/article/pii/S0163834319300799