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Bipolar depression Bipolar Disorder (BAP), known as manic depression (MDP), is a serious mental disorder that alternates between mania and depression. (Baldessarini et. al 2015) A significant characteristic of bipolar disorder is mood change. Bipolar disorder is manifested by alternating mania (manic episode) and depression (bipolar depression). A depressive or manic phase may take several days to weeks, sometimes months, for one cycle. Ultra-fast cycling (5-364 cycles per year), sometimes even ultra-cycling cycles (more than 365 cycles per year, or two or more cycles per day) may occur. The episodes of mania and depression are not continuous. (Baldessarini et. al 2015) Examples of depression symptoms are sadness, reduced energy, sleep disturbances (insomnia or excessive sleepiness), appetite disturbances (loss of appetite or overeating) or decreased interested in everything. These symptoms can lead to feelings of hopelessness, despair, thoughts of death to suicide. The danger of suicide culminates when depression subsides, and the victim no longer appears symptomatic of his surroundings (gaining the power to commit suicide). (Tsitsipa et. al 2015) Examples of mania symptoms are increased euphoria, disproportionately cheerful mood, increased self-esteem and self-esteem, overestimation of their abilities, accelerated thinking, accelerated speech, accelerated movements, relativity, annoyance, loss of social restraints, conflicting, reduced appetite, reduced need for sleep. (Tsitsipa et. al 2015) A significant difference between states is that in a mania episode one feels completely healthy, often stops using (appropriate or prescribed) medicines, and therefore usually doesn't even seek help while depression usually feels or knows that something is happening to him and therefore more often seeks help during a depressive episode. (Tsitsipa et. al 2015) There are 3 types of bipolar disorder. Type I Bipolar Disorder: It is characterized by fully developed manic phases that may be accompanied by psychotic symptoms. Bipolar Disorder II. Type: It is more difficult to diagnose. The patient does not experience fully developed manic phases, but only the hypomanic phase (a lighter form of mania), which usually does not cause him serious problems, and therefore often does not mention them. There is a likelihood of confusion with unipolar depression and the use of inappropriate treatment, which may worsen the course of the disease, and antidepressant therapy without mood stabilization may cause a switch to hypomania or cause ultra-fast or ultradial cycling. Compared to type BAP, depressive episodes occur more frequently and the course of the disease is more chronic. Several studies also showed a higher risk of suicide in patients with BAP II. type. Cyclothythmia: Persistent mood instability including numerous periods of depression or mild mania, but none is severe or long to warrant diagnosis of bipolar affective disorder or periodic depressive disorder. According to ICD-10, the diagnosis of cyclothymia is not a bipolar disorder, but is often seen as part of the bipolar spectrum. (Baldessarini et. al 2015) Biological psychology (also referred to as physiological psychology, psychobiology or behavioural neuroscience) is one of the basic disciplines of psychology and one of the current key approaches. It deals with the role of physiological factors in constituting psychic phenomena, physiological determinants of psyche. Localization of psychic functions in the vertical or lateral structure of the brain, elucidation of the effect of hormones and neurotransmitters or the effect of drugs on the human psyche, research of the proper functioning of "biological clocks" or identification of REM and non-REM phases of sleep belong to the knowledge of physiological psychology. Other psychological disciplines use instrumental methods. (Thomas 1993)

The Biological Approach attempts to describe and explain the emergence and treatment of bipolar disorder based on both clinical trials and biochemical and physiological changes. Focusing on the results obtained by the methods of different sciences does not mean denying psychotherapeutic approaches to these mental disorders, but merely focusing on parameters measurable and verifiable by current biological, chemical and physical methods. The corresponding hypotheses about the biological nature of affective disorders also correspond to this. (Phillips and Kupfer 2013) From the biochemical and electrophysiological point of view, there is a lot of evidence that changes in the transmission of nerve signals, especially in the synapses, contribute to the development of affective disorders. This is evidenced by changes in the concentrations of neuromediators and their metabolites in the brain, cerebrospinal fluid and plasma in some depressive patients, as well as the known effects of antidepressants. For obvious ethical reasons, the study of signal transduction and receptor and post-receptor processes in affective disorders and their therapy is still limited to the use of indirect techniques, ie, to measure changes in human post mortem brains or experiments using animal and cellular models (leukocytes, platelets, cellular cultures, liposomes, etc.). (Phillips and Kupfer 2013) Sources of knowledge leading to the formulation of affective disorder hypotheses are found primarily in the biological (genetic factors, stress effects, chronobiological aspects), immunoneuroendocrine (changes in the activity of the hypothalamic-adenohypophysis-adrenal cortex, cytokine release, etc.) and neurochemical (disruption of synaptic signal transduction) . This division is based primarily on the classical distribution of biomedical disciplines and research methods used to study systems affected by affective disorders and their therapy. It is clear that these areas are interconnected. Evidence for the existence of biochemical foundations of affective disorders was therefore primarily sought from the outset as a neuromediator system, in genetic factors, neuroendocrine changes. Biological models of bipolar disorder are based primarily on the influence of genetic or stress factors on the onset and progression of the disease. These factors may, despite immunoneuroendocrine and neurochemical effects, affect CNS signalling and lead to affective disorders. (Harrison et. al 2016) The first genetic models of bipolar disorder assumed dominant sex-linked transmission (chromosome X), but this proved unlikely. Based on the apparent heterogeneity of bipolar disease, more genemediated transmission (oligogenic transmission) is considered. However, these genes have not yet been found. Problems in determining the proportion of genetic factors in bipolar disorder are thought to be caused by disease heterogeneity. It is possible that patients with early onset or adequate treatment with lithium form a subset of higher genetic risk. Genetic factors can influence the susceptibility to bipolar disorder by contributing to the sensitivity of individuals to recurring depression-inducing events, the lack of function of certain homeostatic mechanisms. Obviously, various developmental factors and environmental effects may significantly influence genetic susceptibility to bipolar disorder. The induction or suppression of the transcription of the genetic information of the genes encoding the proteins involved in the plasticity of the synapses and neuronal growth may be essential. (Harrison et. al 2016) Stress affects the course of bipolar disorder and is believed to be involved in its formation. The mechanisms of stress effects combine biological, immunoneuroendocrine and neurochemical approaches. (Bressert 2018) The neurochemical approach to bipolar disorder is based on the assumption that the cause of t it is the disruption of signal transmission and processing in the CNS. Assuming that thoughts and feelings are related to increased or decreased activation of certain groups of neurons, then their influence is mainly possible in the area of synapses, which provide convergence and divergence of nerve signals.

Based on the mechanisms of action of psychoactive substances, it can be concluded that disorders may occur primarily during signal transduction, i.e., a change in the spreading action potential to processes resulting in the release of neuromediators into the slit, followed by activation of pre- or postsynaptic receptors and respective post-receptor changes. In receptor systems that are likely to be involved in the formation of bipolar disorder and in the therapeutic effects of antidepressants, a G protein is usually used as a transduction element. This transduction element converts the signal into an effector system, which is usually either an ion channel driven by a G protein, or an enzyme system catalysing the generation of second messengers. Second messenger activated protein kinases catalyse the phosphorylation of ion channels, binding sites, G proteins, adenylate cyclase and other enzymes, resulting in changes in cell properties. Thus, the neural signal transduction in the synapse involves a series of relatively complex processes that are normally in dynamic equilibrium. Neurochemical hypotheses of bipolar disorder suggest that disrupting this balance leads to longterm affecting of neuronal activity in certain areas of the brain responsible for feeling. The premise is that depression is related to decreased and mania with increased activity in these brain areas. (Tsitsipa & Fountoulakis 2015) In bipolar disorder, changes in the activity of the hypothalamic-pituitary-adrenal cortex (HPA) or also the hypothalamic-pituitary-thyroid axis are observed. The main focus is on the release factor for corticotropin (CRF) and hence on the HPA axis: neurons in the hypothalamus release CRF, CRF enters the adenohypophysis and stimulates the release of adrenocorticotropic hormone (ACTH), other steroids from the adrenal cortex, ACTH retroactively inhibits CRF secretion, corticosteroids feedbackinhibit the release of CRF from the hypothalamus (through the corresponding receptors) and ACTH from adenohypophysis. (Bressert 2018)

References: 1. Baldessarini R.J., Pérez J., Salvatore P., Trede K., Maggini C. History of bipolar manicdepressive disorder. In: Yildiz A., Ruiz P., Nemeroff C.B., York N., editors. The Bipolar Book: History, Neurobiology, and Treatment. New York: Oxford University Press; 2015. pp. 3–20. 2. Tsitsipa E. & Fountoulakis K. The neurocognitive functioning in bipolar disorder: a systematic review of data. Ann. Gen. Psychiatry; 2015. 14: 42 3. Thomas, R.K., "INTRODUCTION: A Biopsychology Festschrift in Honor of Lelon J. Peacock", Journal of General Psychology, 1993, vol. 120, no. 1, pp. 5. 4. Harrison PJ, Cipriani A, Harmer CJ, et al. Innovative approaches to bipolar disorder and its treatment. Ann N Y Acad Sci. 2016;1366(1):76–89. 5. Phillips ML, Kupfer DJ. Bipolar disorder diagnosis: challenges and future directions. Lancet. 2013;381(9878):1663–1671. doi:10.1016/S0140-6736(13)60989-7 6. Tsitsipa E. & Fountoulakis K.. The neurocognitive functioning in bipolar disorder: a systematic review of data. Ann. Gen. Psychiatry, 2015, 14: 42. 7. Bressert, S. Causes of Bipolar Disorder. Psych Central.2018 from https://psychcentral.com/disorders/bipolar/bipolar-disorder-causes/...