Bipolar Disorder encompasses a wide spectrum of symptoms and is classified according to the types of mood episodes exhibited, including: manic, hypomanic, major depressive and mixed episodes.
Bipolar I disorder involves a manic or mixed episode in contrast to Bipolar II disorder, which involves at least one major depressive episode and at least one hypomanic episode, but no full manic or mixed episodes.
Bipolar Disorder should be differentiated from Major Depressive Disorder (MDD), which is diagnosed when a patient experiences one or more major depressive episodes without any lifetime episodes of hypomania or mania.
Depicted here is a life chart (or mood chart), which follows the patient's lifetime history of mood episodes. This permits the identification of mood episodes that are the most prevalent and important to prevent.
In this patient, as with many patients with bipolar disorder, depressive episodes become the more prominent aspect of the illness as the person ages.
Several morphometric differences have been observed in the brains of Bipolar Disorder patients relative to healthy subjects.
White matter hyperintensities and reduction in grey matter volume, identified with MRI, have been described in patients with Bipolar Disorder.
Increased ventricular size and decreased frontal cortical area volumes may also be observed in Bipolar Disorder patients.
The pathophysiology of Bipolar Disorder encompasses environmental, behavioural, neuronal, cellular, and molecular levels.
At the molecular level, aberrant signaling cascades alter synaptic plasticity. Strong evidence supporting the importance of second messenger signaling has come from studying the targets of mood stabilizing drugs such as lithium.
GSK-3 and IP3 signaling cascades are known to mediate axonogenesis, synaptogenesis, neuronal growth and cone spreading. Other downstream effects may also be involved.
The heritability of bipolar disorder is around 80%. Monozygotic twins are reported to have a higher incidence of developing Bipolar Disorder, approximately 40%, whereas the incidence is only 10% in dizygotic twins.
Although the process of developing bipolar disorder likely arises from complex interactions between genes and environmental factors, the specific genes that contribute to this risk are not known with certainty. Variations of several genes have been identified as potential contributors to the pathophysiology of bipolar disorder.
Among the identified genes are those associated with serotonin signaling (SLC6A4, TPH2), dopamine signaling (SLC6A3, DRD4), glutamate transmission (DAOA, DTNBP1), and cell maintenance and growth (NRG1, BDNF, DISC1).
The most significant environmental triggers of mood episodes among patients with bipolar disorder include use of drugs with mood-altering properties, changes in circadian rhythm, and life stressors.
Successful management of bipolar disorder requires particular attention to minimizing the effects of these influences.
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