What is Bipolar Disorder


Bipolar disorder or manic-depressive disorder, which is also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes. The elevated moods are clinically referred to as mania or, if milder, hypomania. Individuals who experience manic episodes also commonly experience depressive episodes, or symptoms, or mixed episodes in which features of both mania and depression are present at the same time. These episodes are usually separated by periods of “normal” mood; but, in some individuals, depression and mania may rapidly alternate, which is known as rapid cycling. Extreme manic episodes can sometimes lead to such psychotic symptoms as delusions and hallucinations. The disorder has been subdivided into bipolar I, bipolar II, cyclothymia, and other types, based on the nature and severity of mood episodes experienced; the range is often described as the bipolar spectrum.

Genetic factors contribute substantially to the likelihood of developing bipolar disorder, and environmental factors are also implicated. Bipolar disorder is often treated with mood stabilizing medications and, sometimes, other psychiatric drugs. Psychotherapy also has a role, often when there has been some recovery of the subject’s stability. In serious cases, in which there is a risk of harm to oneself or others, involuntary commitment may be used. These cases generally involve severe manic episodes with dangerous behavior or depressive episodes with suicidal ideation. There are widespread problems with social stigma, stereotypes, and prejudice against individuals with a diagnosis of bipolar disorder. People with bipolar disorder exhibiting psychotic symptoms can sometimes be misdiagnosed as having schizophrenia, another serious mental illness.

The current term “bipolar disorder” is of fairly recent origin and refers to the cycling between high and low episodes (poles). A relationship between mania and melancholia had long been observed, although the basis of the current conceptualization can be traced back to French psychiatrists in the 1850s. The term “manic-depressive illness” or psychosis was coined by German psychiatrist Emil Kraepelin in the late nineteenth century, originally referring to all kinds of mood disorder. German psychiatrist Karl Leonhard split the classification again in 1957, employing the terms unipolar disorder (major depressive disorder) and bipolar disorder.



The causes of bipolar disorder likely vary between individuals. Twin studies have been limited by relatively small sample sizes but have indicated a substantial genetic contribution, as well as environmental influence. For bipolar I, the (probandwise) concordance rates in modern studies have been consistently put at around 40% in monozygotic twins (same genes), compared to 0 to 10% in dizygotic twins. A combination of bipolar I, II and cyclothymia produced concordance rates of 42% vs 11%, with a relatively lower ratio for bipolar II that likely reflects heterogeneity. The overall heritability of the bipolar spectrum has been put at 0.71. There is overlap with unipolar depression and if this is also counted in the co-twin the concordance with bipolar disorder rises to 67% (Mz) and 19% (Dz). The relatively low concordance between dizygotic twins brought up together suggests that shared family environmental effects are limited, although the ability to detect them has been limited by small sample sizes.



Genetic studies have suggested many chromosomal regions and candidate genes appearing to relate to the development of bipolar disorder, but the results are not consistent and often not replicated. Although the first genetic linkage finding for mania was in 1969, the linkage studies have been inconsistent. (Genetic linkage studies may be followed by fine mapping searching for the phenomenon of linkage disequilibrium with a single gene, then DNA sequencing; using this approach causative DNA base pair changes have been reported for the genes P2RX7 and TPH1. Recent meta-analyses of linkage studies detected either no significant genome-wide findings or, using a different methodology, only two genome-wide significant peaks, on chromosome 6q and on 8q21. Genome-wide association studies have also not brought a consistent focus — each has identified new loci, while none of the previously identified loci were replicated. Findings did include a single-nucleotide polymorphism in DGKH; a locus in a gene-rich region of high linkage disequilibrium (LD) on chromosome 16p12; and a single-nucleotide polymorphism in MYO5B.  A comparison of these studies, combined with a new study, suggested an association with ANK3 and CACNA1C, thought to be related to calcium and sodium voltage-gated ion channels. Diverse findings point strongly to heterogeneity, with different genes being implicated in different families. Numerous specific studies find various specific links. Advanced paternal age has been linked to a somewhat increased chance of bipolar disorder in offspring, consistent with a hypothesis of increased new genetic mutations. A review seeking to identify the more consistent findings suggested several genes related to serotonin (SLC6A4 and TPH2), dopamine (DRD4 and SLC6A3), glutamate (DAOA and DTNBP1), and cell growth and/or maintenance pathways (NRG1, DISC1 and BDNF), although noting a high risk of false positives in the published literature. It was also suggested that individual genes are likely to have only a small effect and to be involved in some aspect related to the disorder (and a broad range of “normal” human behavior) rather than the disorder per se.



Some limited long-term studies indicate that children who later receive a diagnosis of bipolar disorder may show subtle early traits such as sub threshold cyclical mood abnormalities, full major depressive episodes, and possibly ADHD with mood fluctuation. There may be hypersensitivity and irritability. There is some disagreement whether the experiences are necessarily fluctuating or may be chronic. A history of stimulant use in childhood is found in high numbers of bipolar patients and has been found to cause an earlier onset of bipolar disorder and a worse clinical course, independent of attention deficit hyperactivity disorder.



Evidence suggests that environmental factors play a significant role in the development and course of bipolar disorder, and that individual psychosocial variables may interact with genetic dispositions. There is fairly consistent evidence from prospective studies that recent life events and interpersonal relationships contribute to the likelihood of onsets and recurrences of bipolar mood episodes, as they do for onsets and recurrences of unipolar depression. There have been repeated findings that between a third and a half of adults diagnosed with bipolar disorder report traumatic/abusive experiences in childhood, which is associated on average with earlier onset, a worse course, and more co-occurring disorders such as PTSD. The total number of reported stressful events in childhood is higher in those with an adult diagnosis of bipolar spectrum disorder compared to those without, particularly events stemming from a harsh environment rather than from the child’s own behavior. Early experiences of adversity and conflict are likely to make subsequent developmental challenges in adolescence more difficult, and are likely a potentiating factor in those at risk of developing bipolar disorder.




Hyperintensities (bright areas on MRI scans above)

are 2.5 times more likely to occur in bipolar disorder


Researchers hypothesize that abnormalities in the structure and/or function of certain brain circuits could underlie bipolar and other mood disorders. Some studies have found anatomical differences in areas such as the amygdala, prefrontal cortex and hippocampus. However, despite 25 years of research involving more than 7,000 MRI scans, studies continue to report conflicting findings and there remains considerable debate over the neuroscientific findings. Two fairly consistent abnormalities found in a meta-analysis of 98 MRI or CT neuroimaging studies were that groups with bipolar disorder had lateral ventricles which were on average 17% larger than control groups, and were 2.5 times more likely to have deep white matter hyperintensities. Given the size of the meta-analysis, it was concluded that the relatively small number of significant findings was perhaps surprising, and that there may be genuinely limited structural change in bipolar disorder, or perhaps heterogeneity has obscured other differences. In addition, it was noted that averaged associations found at the level of multiple studies may not exist for an individual.



It has been suggested that a hypersensitivity of the melatonin receptors in the eye could be a reliable indicator of bipolar disorder, in studies called a trait marker, as it is not dependent on state (mood, time, etc.). In small studies, patients diagnosed as bipolar reliably showed a melatonin-receptor hypersensitivity to light during sleep, causing a rapid drop in sleeptime melatonin levels compared to controls. Another study showed that drug-free, recovered, bipolar patients exhibited no hypersensitivity to light. It has also been shown in humans that valproic acid, a mood stabilizer, increases transcription of melatonin receptors and decreases eye melatonin-receptor sensitivity in healthy volunteers while low-dose lithium, another mood stabilizer, in healthy volunteers, decreases sensitivity to light when sleeping, but doesn’t alter melatonin synthesis. The extent to which melatonin alterations may be a cause or effect of bipolar disorder are not fully known.


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