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Bipolar II disorder ( BP-II ) is a mood disorder on the bipolar spectrum , characterized by at least one episode of hypomania and at least one episode of major depression . Diagnosis for BP-II requires that the individual must never have experienced a full manic episode . Otherwise, one manic episode meets the criteria for bipolar I disorder (BP-I).

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90-414: BP2 may refer to: Bipolar II disorder (BP-II) South View LRT station (BP2), Singapore BPD, also known as BP2, a Mazda B engine BP2 combination problem, a Binding problem in neuroscience, cognitive science and philosophy of mind BASIC Plus 2 programming language See also [ edit ] The Blueprint 2: The Gift & The Curse ,

180-577: A "well-being plan" serves several purposes: it informs the patients, protects them from future episodes, teaches them to add value to their life, and works toward building a strong sense of self to fend off depression and reduce the desire to succumb to the seductive hypomanic highs. The plan has to aim high. Otherwise, patients will relapse into depression. A large part of this plan involves the patient being very aware of warning signs and stress triggers so that they take an active role in their recovery and prevention of relapse. Several studies have shown that

270-581: A 2002 album by Jay-Z Black Panther: Wakanda Forever , also known as Black Panther 2 [REDACTED] Topics referred to by the same term This disambiguation page lists articles associated with the same title formed as a letter–number combination. If an internal link led you here, you may wish to change the link to point directly to the intended article. Retrieved from " https://en.wikipedia.org/w/index.php?title=BP2&oldid=1126910042 " Category : Letter–number combination disambiguation pages Hidden categories: Short description

360-421: A chronic relapsing nature. It has been suggested that BP-II patients have a higher degree of relapse than BP-I patients. Generally, within four years of an episode, around 60% of patients will relapse into another episode. Some patients are symptomatic half the time, either with full on episodes or symptoms that fall just below the threshold of an episode. Because of the nature of the illness, long-term therapy

450-569: A class, the first generation antipsychotics are associated with movement disorders , along with anticholinergic side effects compared with second generation antipsychotics. There is evidence to support the use of SSRI and SNRI antidepressants in BP-II, but the use of these treatments is controversial. Potential risks of antidepressant pharmacotherapy in patients with bipolar disorder include increased mood cycling, development of rapid cycling, dysphoria , and switch to hypomania. In addition,

540-801: A comprehensive history, medication review, and laboratory work are key to diagnosing BP-II and differentiating it from other conditions. The differential diagnosis of BP-II is as follows: unipolar major depression , borderline personality disorder , posttraumatic stress disorder , substance use disorders , and attention deficit hyperactivity disorder . Major differences between BP-I and BP-II have been identified in their clinical features, comorbidity rates and family histories. During depressive episodes, BP-II patients tend to show higher rates of psychomotor agitation , guilt, shame, suicidal ideation , and suicide attempts. BP-II patients have shown higher lifetime comorbidity rates of phobias , anxiety disorders , substance use, and eating disorders . In addition, there

630-476: A decrease in brain excitation due to blockage of low-voltage sodium-gated channels, decrease in glutamate and excitatory amino acids, and potentiation of levels of GABA . There is evidence that lamotrigine decreases the risk of relapse in rapid-cycling BP-II. It is more effective in BP-II than BP-I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100 to 200 mg have been reported to have

720-406: A depressive episode. It is during depressive episodes that BP-II patients often seek help. Symptoms may be syndromal or subsyndromal . Depressive episodes in BP-II can present similarly to those experienced in unipolar depressive disorders . Patients characteristically experience a depressed mood and may describe themselves as feeling sad, gloomy, down in the dumps, or hopeless, for most of

810-501: A depressive period, or simply to better organize one's life by setting boundaries for one's perceptions and behaviors. There is evidence to suggest that BP-II has a more chronic course of illness than BP-I. This constant and pervasive course of the illness leads to an increased risk in suicide and more hypomanic and major depressive episodes with shorter periods between episodes than BP-I patients experience. The natural course of BP-II, when left untreated, leads to patients spending

900-554: A direct and persisting impact on psychosocial functioning. An abnormal semantic memory organization can manipulate thoughts and lead to the formation of delusions and possibly affect speech and communication problems, which can lead to interpersonal issues. BP-II patients have also been shown to present worse cognitive functioning than those patients with BP-I, though they demonstrate about the same disability when it comes to occupational functioning, interpersonal relationships, and autonomy . This disruption in cognitive functioning takes

990-466: A greater risk of substance use, anxiety disorders, and suicidality. In addition, they are associated with increased treatment resistance compared to non-mixed episodes. Bipolar disorder is often a lifelong condition, and patients should be followed up regularly for relapse prevention. Although BP-II is thought to be less severe than BP-I in regard to symptom intensity, BP-II is associated with higher frequencies of rapid cycling and depressive episodes. In

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1080-586: A high potential for painful consequences (engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments.) Hypomania is distinct from mania . During a typical hypomanic episode, patients may present as upbeat, may show signs of poor judgment or display signs of increased energy despite lack of sleep, but do not meet the full criteria for an acute manic episode. Patients may display elevated confidence, but do not express delusional thoughts as in mania. They can experience increase in goal-directed activity and creativity , but do not reach

1170-440: A major cause of psychosocial disability. There is evidence that shows the mild depressive symptoms, or even sub-syndromal symptoms, are responsible for the non-recovery of social functioning, which furthers the idea that residual depressive symptoms are detrimental for functional recovery in patients being treated for BP-II. It has been suggested that symptom interference in relation to social and interpersonal relationships in BP-II

1260-402: A major depressive episode, the best chance for recovery is to have therapeutic interventions that focus on the residual depressive symptoms and to aim for improvement in psychosocial and cognitive functioning. Even with treatment, a certain amount of responsibility is placed in the patient's hands; they have to be able to assume responsibility for their illness by accepting their diagnosis, taking

1350-549: A neighboring synapse creates extrasynaptic signaling/ volume transmission . In addition, glutamate plays important roles in the regulation of growth cones and synaptogenesis during brain development as originally described by Mark Mattson . Extracellular glutamate in Drosophila brains has been found to regulate postsynaptic glutamate receptor clustering, via a process involving receptor desensitization. A gene expressed in glial cells actively transports glutamate into

1440-581: A patient with depression with mixed features may have a depressed mood, but has simultaneous symptoms of rapid speech, increased energy, and flight of ideas. Conversely, a patient with hypomania with mixed features will present with the full criteria for a hypomanic episode, but with concurrent symptoms of decreased appetite, loss of interest, and low energy. Episodes with mixed features can last up to several months. They occur more frequently in patients with an earlier onset of bipolar disorder, are associated with higher frequency of episodes, and are associated with

1530-454: A patient's prognosis, long-term therapy is most favorably recommended for controlling symptoms, maintaining remission and preventing relapses. With treatment, patients have been shown to present a decreased risk of suicide (especially when treated with lithium ) and a reduction of frequency and severity of their episodes, which in turn moves them toward a stable life and reduces the time they spend ill. To maintain their state of balance, therapy

1620-518: A person's life can trigger a relapse in patients with BP-II. These include stressful life events, criticism from peers or relatives, and a disrupted circadian rhythm. In addition, the addition of antidepressant medications can trigger a hypomanic episode. Comorbid conditions are extremely common in individuals with BP-II. In fact, individuals are twice as likely to present a comorbid disorder than not. These include anxiety , eating , personality (cluster B) , and substance use disorders . For BP-II,

1710-454: A result of the high suicide risk for this group, reducing the risk and preventing attempts remains a main part of the treatment; a combination of self-monitoring, close supervision by a therapist, and faithful adherence to their medication regimen will help to reduce the risk and prevent the likelihood of suicide. Suicide is a common endpoint for many patients with severe psychiatric illness. The mood disorders (depression and bipolar) are by far

1800-436: A toll on their ability to function in the workplace, which leads to high rates of work loss in BP-II patient populations. After treatment and while in remission, BP-II patients tend to report a good psychosocial functioning but they still score less than patients without the disorder. These lasting impacts further suggest that a prolonged period of untreated BP-II can lead to permanent adverse effects on functioning. BP-II has

1890-422: Is C 5 H 9 NO 4 . Glutamic acid exists in two optically isomeric forms; the dextrorotatory L -form is usually obtained by hydrolysis of gluten or from the waste waters of beet -sugar manufacture or by fermentation. Its molecular structure could be idealized as HOOC−CH( NH 2 )−( CH 2 ) 2 −COOH, with two carboxyl groups −COOH and one amino group − NH 2 . However, in

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1980-526: Is a higher correlation between BP-II patients and family history of psychiatric illness, including major depression and substance-related disorders compared to BP-I. The occurrence rate of psychiatric illness in first degree relatives of BP-II patients was 26.5%, versus 15.4% in BP-I patients. Although BP-II is a prevalent condition associated with morbidity and mortality, there has been an absence of robust clinical trials and systematic reviews that investigate

2070-459: Is called glutamyl . The one-letter symbol E for glutamate was assigned as the letter following D for aspartate , as glutamate is larger by one methylene –CH 2 – group. When glutamic acid is dissolved in water, the amino group (− NH 2 ) may gain a proton ( H ), and/or the carboxyl groups may lose protons, depending on the acidity of the medium. In sufficiently acidic environments, both carboxyl groups are protonated and

2160-513: Is catalyzed by glutamate decarboxylase (GAD). GABA-ergic neurons are identified (for research purposes) by revealing its activity (with the autoradiography and immunohistochemistry methods) which is most abundant in the cerebellum and pancreas . Stiff person syndrome is a neurologic disorder caused by anti-GAD antibodies, leading to a decrease in GABA synthesis and, therefore, impaired motor function such as muscle stiffness and spasm. Since

2250-763: Is different from Wikidata All article disambiguation pages All disambiguation pages Bipolar II disorder Hypomania is a sustained state of elevated or irritable mood that is less severe than mania yet may still significantly affect the quality of life and result in permanent consequences including reckless spending, damaged relationships and poor judgment. Unlike mania, hypomania cannot include psychosis . The hypomanic episodes associated with BP-II must last for at least four days. Commonly, depressive episodes are more frequent and more intense than hypomanic episodes. Additionally, when compared to BP-I, type II presents more frequent depressive episodes and shorter intervals of well-being. The course of BP-II

2340-530: Is directly tied to poor psychosocial functioning, a common side-effect in patients with BP-II. The impact on a patient's psychosocial functioning stems from the depressive symptoms (more common in BP-II than BP-I). An increase in these symptoms' severity seems to correlate with a significant increase in psychosocial disability. Psychosocial disability can present itself in poor semantic memory , which in turn affects other cognitive domains like verbal memory and (as mentioned earlier) executive functioning leading to

2430-402: Is gradual; the two forms are in equal concentrations at pH 2.10. At even higher pH, the other carboxylic acid group loses its proton and the acid exists almost entirely as the glutamate anion OOC−CH( NH 3 )−( CH 2 ) 2 −COO , with a single negative charge overall. The change in protonation state occurs at pH 4.07. This form with both carboxylates lacking protons is dominant in

2520-415: Is involved in cognitive functions such as learning and memory in the brain. The form of plasticity known as long-term potentiation takes place at glutamatergic synapses in the hippocampus , neocortex , and other parts of the brain. Glutamate works not only as a point-to-point transmitter, but also through spill-over synaptic crosstalk between synapses in which summation of glutamate released from

2610-510: Is more chronic and consists of more frequent cycling than the course of BP-I. Finally, BP-II is associated with a greater risk of suicidal thoughts and behaviors than BP-I or unipolar depression . BP-II is no less severe than BP-I, and types I and II present equally severe burdens. BP-II is notoriously difficult to diagnose. Patients usually seek help when they are in a depressed state, or when their hypomanic symptoms manifest themselves in unwanted effects, such as high levels of anxiety , or

2700-423: Is more common than BP-I, while BP-II and major depressive disorder have about the same rate of diagnosis. Of all individuals initially diagnosed with major depressive disorder , between 40% and 50% will later be diagnosed with either BP-I or BP-II. Substance use disorders (which have high co-morbidity with BP-II) and periods of mixed depression may also make it more difficult to accurately identify BP-II. Despite

2790-399: Is often a useful one as well, which can contribute as fuel or as a substrate for further metabolism processes. Examples are as follows: Both pyruvate and oxaloacetate are key components of cellular metabolism, contributing as substrates or intermediates in fundamental processes such as glycolysis , gluconeogenesis , and the citric acid cycle . Glutamate also plays an important role in

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2880-695: Is often continued indefinitely, as around 50% of the patients who discontinue it relapse quickly and experience either full-blown episodes or sub-syndromal symptoms that bring significant functional impairments. The deficits in functioning associated with BP-II stem mostly from the recurrent depression that BP-II patients experience. Depressive symptoms are much more disabling than hypomanic symptoms and are potentially as, or more disabling than mania symptoms. Functional impairment has been shown to be directly linked with increasing percentages of depressive symptoms, and because sub-syndromal symptoms are more common—and frequent—in BP-II, they have been implicated heavily as

2970-502: Is often used as an alignment medium to control the scale of the dipolar interactions observed. The drug phencyclidine (more commonly known as PCP or 'Angel Dust') antagonizes glutamic acid non-competitively at the NMDA receptor . For the same reasons, dextromethorphan and ketamine also have strong dissociative and hallucinogenic effects. Acute infusion of the drug eglumetad (also known as eglumegad or LY354740), an agonist of

3060-419: Is responsible for umami , one of the five basic tastes of the human sense of taste . Glutamic acid often is used as a food additive and flavor enhancer in the form of its sodium salt , known as monosodium glutamate (MSG). All meats, poultry, fish, eggs, dairy products, and kombu are excellent sources of glutamic acid. Some protein-rich plant foods also serve as sources. 30% to 35% of gluten (much of

3150-407: Is strongly associated with atypical depression . A mixed episode is defined by the presence of a hypomanic or depressive episode that is accompanied by symptoms of the opposite polarity. This is commonly referred to as a mood episode with mixed features (e.g. depression with mixed features or hypomania with mixed features), but can also be referred to as mixed episodes or mixed states. For example,

3240-403: Is that the mood episodes cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (from the depressive symptoms or the unpredictability of cycling between periods of depression and hypomania). A hypomanic episode is established if a patient's symptoms last for most of the day each day for at least four days. Furthermore, three or more of

3330-463: Is the best option and aims to not only control the symptoms but to maintain sustained remission and prevent relapses from occurring. Even with treatment, patients do not always regain full functioning, especially in the social realm. There is a very clear gap between symptomatic recovery and full functional recovery for both BP-I and BP-II patients. As such, and because those with BP-II spend more time with depressive symptoms that do not quite qualify as

3420-502: Is the only mood stabilizer to demonstrate a decrease in suicide and self-harm in patients with mood disorders. Due to lithium's narrow therapeutic index , lithium levels must be monitored regularly for prevention of lithium toxicity . There is also evidence that the anticonvulsants valproate, lamotrigine, carbamazepine, and topiramate are effective in the reduction of symptoms of hypomanic and depressive episodes of bipolar disorder. Potential mechanisms contributing to these effects include

3510-564: Is the standard of care for treatment of both BP-I and BP-II, additional non-pharmaceutical therapies can also help those with the illness. Benefits include prevention of relapse and improved maintenance medication adherence. These include psychotherapy (e.g. cognitive behavioral therapy , psychodynamic therapy , psychoanalysis , interpersonal therapy , behavioral therapy , cognitive therapy , and family-focused therapy ), social rhythm therapy , art therapy , music therapy , psychoeducation , mindfulness , and light therapy . Meta-analyses in

3600-464: Is usually a manifestation of severe psychiatric distress that is often associated with a diagnosable and treatable form of depression or other mental illness. In a clinical setting, an assessment of suicidal risk must precede any attempt to treat psychiatric illness. The global estimated lifetime prevalence of bipolar disorder among adults range from 1 to 3 percent. The annual incidence is estimated to vary from 0.3 to 1.2 percent worldwide. According to

3690-494: Is very recurrent and results in severe disabilities, interpersonal relationship problems, barriers to academic, financial, and vocational goals, and a loss of social standing in their community, all of which increase the likelihood of suicide. Mixed symptoms and rapid-cycling, both very common in BP-II, are also associated with an increased risk of suicide. The tendency for BP-II to be misdiagnosed and treated ineffectively, or not at all in some cases, leads to an increased risk. As

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3780-449: Is worse than symptom interference in other chronic medical illnesses such as cancer. This social impairment can last for years, even after treatment that has resulted in a resolution of mood symptoms. The factors related to this persistent social impairment are residual depressive symptoms, limited illness insight (a very common occurrence in patients with BP-II), and impaired executive functioning. Impaired ability in executive functions

3870-417: The d form occurs in some special contexts, such as the bacterial capsule and cell walls of the bacteria (which produce it from the l form with the enzyme glutamate racemase ) and the liver of mammals . Although they occur naturally in many foods, the flavor contributions made by glutamic acid and other amino acids were only scientifically identified early in the 20th century. The substance

3960-594: The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) . In addition, alternative diagnostic criteria is established in the World Health Organization's International Classification of Diseases-11th Revision (ICD-11)]. The diagnostic criteria are established from self-reported experiences from patients or their family members, the psychiatric assessment , and

4050-649: The ICD-11 , a BP-II patient will have experienced episodic experiences of one or more hypomaniac episodes and one or more major depressive episodes , and no history of a manic episode or mixed episode. These symptoms cannot be explained by other diagnoses such as: The specifiers are the same as the DSM-5 with the exception of catatonic features and if symptoms have occurred with or without psychosis about 6 weeks after childbirth . The signs and symptoms of BP-II may overlap significantly with those of other conditions. Thus,

4140-520: The extracellular space , while, in the nucleus accumbens -stimulating group II metabotropic glutamate receptors , this gene was found to reduce extracellular glutamate levels. This raises the possibility that this extracellular glutamate plays an "endocrine-like" role as part of a larger homeostatic system. Glutamate also serves as the precursor for the synthesis of the inhibitory gamma-aminobutyric acid (GABA) in GABA-ergic neurons. This reaction

4230-425: The glutamatergic system , and hormonal regulation play a role in the pathophysiology of the disease. The cause of Bipolar disorder can be attributed to misfiring neurotransmitters that overstimulate the amygdala, which in turn causes the prefrontal cortex to stop working properly. The bipolar patient becomes overwhelmed with emotional stimulation with no way of understanding it, which can trigger mania and exacerbate

4320-664: The mental status examination . In addition, Screening instruments like the Mood Disorders Questionnaire are helpful tools in determining a patient's status on the bipolar spectrum. In addition, certain features have been shown to increase the chances that depressed patients have a bipolar disorder, including atypical symptoms of depression like hypersomnia and hyperphagia , a family history of bipolar disorder, medication-induced hypomania, recurrent or psychotic depression , antidepressant refractory depression , and early or postpartum depression . According to

4410-528: The metabotropic glutamate receptors 2 and 3 ) resulted in a marked diminution of yohimbine -induced stress response in bonnet macaques ( Macaca radiata ); chronic oral administration of eglumetad in those animals led to markedly reduced baseline cortisol levels (approximately 50 percent) in comparison to untreated control subjects. Eglumetad has also been demonstrated to act on the metabotropic glutamate receptor 3 (GRM3) of human adrenocortical cells , downregulating aldosterone synthase , CYP11B1 , and

4500-405: The physiological pH range (7.35–7.45). At even higher pH, the amino group loses the extra proton, and the prevalent species is the doubly-negative anion OOC−CH( NH 2 )−( CH 2 ) 2 −COO . The change in protonation state occurs at pH 9.47. Glutamic acid is chiral ; two mirror-image enantiomers exist: d (−), and l (+). The l form is more widely occurring in nature, but

4590-431: The DSM-5, a patient diagnosed with BP-II will have experienced at least one hypomanic episode , at least one major depressive episodes , and no manic episode . Furthermore, the occurrence of the mood episodes are not better explained by schizoaffective disorder , schizophrenia , delusional disorder , or other specified or unspecified schizophrenia spectrum and other psychotic disorder. The final criteria that must be met

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4680-777: The World Mental Health Survey Initiative, the lifetime prevalence of BP-II was found to be 0.4%, with a 12-month prevalence of 0.3%. Other meta-analyses have found lifetime prevalence of BP-II up to 1.57%. In the United States, the estimated lifetime prevalence of BP-II was found to be 1.1%, with a 12-month prevalence of 0.8%. The mean age of onset for BP-II was 20 years. Thus far, there have been no studies that have conclusively demonstrated that an unequal distribution of bipolar disorders across sex and ethnicity exists. Glutamatergic neurotransmission Glutamic acid (symbol Glu or E ;

4770-542: The anionic form is known as glutamate ) is an α- amino acid that is used by almost all living beings in the biosynthesis of proteins . It is a non-essential nutrient for humans, meaning that the human body can synthesize enough for its use. It is also the most abundant excitatory neurotransmitter in the vertebrate nervous system . It serves as the precursor for the synthesis of the inhibitory gamma-aminobutyric acid (GABA) in GABAergic neurons. Its molecular formula

4860-439: The body in the form of urea. Glutamate is also a neurotransmitter (see below), which makes it one of the most abundant molecules in the brain. Malignant brain tumors known as glioma or glioblastoma exploit this phenomenon by using glutamate as an energy source, especially when these tumors become more dependent on glutamate due to mutations in the gene IDH1 . Glutamate is the most abundant excitatory neurotransmitter in

4950-448: The body's disposal of excess or waste nitrogen . Glutamate undergoes deamination , an oxidative reaction catalysed by glutamate dehydrogenase , as follows: Ammonia (as ammonium ) is then excreted predominantly as urea , synthesised in the liver . Transamination can thus be linked to deamination, effectively allowing nitrogen from the amine groups of amino acids to be removed, via glutamate as an intermediate, and finally excreted from

5040-407: The body. A key process in amino acid degradation is transamination , in which the amino group of an amino acid is transferred to an α- ketoacid , typically catalysed by a transaminase . The reaction can be generalised as such: A very common α-keto acid is α-ketoglutarate , an intermediate in the citric acid cycle . Transamination of α-ketoglutarate gives glutamate. The resulting α-ketoacid product

5130-495: The case of a relapse, patients may experience new onset sleep disturbance, racing thoughts and/or speech, anxiety, irritability , and increase in emotional intensity. Family and/or friends may notice that patients are arguing more frequently with them, spending more money than usual, are increasing their binging on food, drugs, or alcohol, and may suddenly start taking on many projects at once. These symptoms often occur and are considered early warning signs. Psychosocial factors in

5220-452: The compound is prevalent in neutral solutions. The glutamate neurotransmitter plays the principal role in neural activation . This anion creates the savory umami flavor of foods and is found in glutamate flavorings such as MSG . In Europe, it is classified as food additive E620 . In highly alkaline solutions the doubly negative anion OOC−CH( NH 2 )−( CH 2 ) 2 −COO prevails. The radical corresponding to glutamate

5310-515: The day, nearly every day. In children, this can present with an irritable mood. Most patients report significant fatigue , loss of energy, or tiredness. Patients or their family members may note diminished interest in usual activities such as sex, hobbies, or daily routines. Many patients report a change in appetite along with associated weight change. Sleep disturbances may be present, and can manifest as problems falling or staying asleep, frequent awakenings, excessive sleep, or difficulties getting up in

5400-566: The difficulties, it is important that BP-II individuals be correctly assessed so that they can receive the proper treatment. Antidepressant use, in the absence of mood stabilizers, is correlated with worsening BP-II symptoms. Multiple factors contribute to the development of bipolar spectrum disorders, although there have been very few studies conducted to examine the possible causes of BP-II specifically. While no identifiable single dysfunctions in specific neurotransmitters have been found, preliminary data has shown that calcium signal transmission,

5490-732: The effects of depression. Bipolar disorder is characterized by marked swings in mood, activity, and behavior. BP-II is characterized by periods of hypomania, which may occur before, after, or independently of a depressive episode . Hypomania is the signature characteristic of BP-II, defined by an experience of elevated mood. A patient's mood is typically cheerful, enthusiastic, euphoric, or irritable. In addition, they can present with symptoms of inflated self-esteem or grandiosity, decreased need for sleep, talkativeness or pressured speech, flight of ideas or rapid cycling of thoughts, distractibility, increased goal-directed activity, psychomotor agitation, and/or excessive involvement in activities that have

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5580-440: The efficacy of pharmacologic treatments for the hypomanic and depressive phases of BP-II. Thus, the current treatment guidelines for the symptoms of BP-II are derived and extrapolated from the treatment guidelines in BP-I, along with limited randomized controlled trials published in the literature. The treatment of BP-II consists of the following: treatment of hypomania, treatment of major depression, and maintenance therapy for

5670-436: The evidence for their efficacy in bipolar depression is mixed. Thus, in most cases, antidepressant monotherapy in patients with BP-II is not recommended. However, antidepressants may provide benefit to some patients when used in addition to mood stabilizers and antipsychotics, as these drugs reduce the risk of manic/hypomanic switching. However, the risk still exists, and should be used with caution. Although medication therapy

5760-468: The field have attempted to find reliable differences between BP-I depressive episodes and episodes of major depressive disorder, but the data is inconsistent. However, some clinicians report that patients who came in with a depressive episode, but were later diagnosed as having bipolar disorder often presented with hypersomnia , increased appetite, psychomotor retardation , and a history of antidepressant -induced hypomania. Evidence also suggests that BP-II

5850-412: The following symptoms must be present: Inflated sense of self-esteem or grandiose thoughts, feeling well rested despite getting low amounts of sleep (3 hours), talkativeness, racing thoughts, distractibility, and increase in goal-directed activity or psychomotor agitation, or excessive involvement in activities with high risk of painful consequences. Per DSM-5 criteria, a major depressive episode consists of

5940-406: The frequency and severity of depressive episodes. Lithium prevents mood relapse and works especially well in BP-II patients who experience rapid-cycling. Almost all BP-II patients who take lithium have a decrease in the amount of time they spend ill and a decrease in mood episodes. Along with medication, other forms of therapy have been shown to be beneficial for BP-II patients. A treatment called

6030-400: The ineffable but undeniable flavor he detected in many foods, most especially in seaweed. Professor Ikeda termed this flavor umami . He then patented a method of mass-producing a crystalline salt of glutamic acid, monosodium glutamate . Glutamic acid is produced on the largest scale of any amino acid, with an estimated annual production of about 1.5 million tons in 2006. Chemical synthesis

6120-422: The literature has shown that psychotherapy plus pharmacotherapy was associated with a lower relapse rate compared with patients treated with pharmacotherapy alone. However, relapse can still occur, despite continued medication and therapy. People with bipolar disorder may develop dissociation to match each mood they experience. For some, this is done intentionally, as a means by which to escape trauma or pain from

6210-422: The majority of their lives with some symptoms, primarily stemming from depression . Their recurrent depression results in personal distress and disability. This disability can present itself in the form of psychosocial impairment, which has been suggested to be worse in BP-II patients than in BP-I patients. Another facet of this illness that is associated with a poorer prognosis is rapid cycling , which denotes

6300-425: The molecule becomes a cation with a single positive charge, HOOC−CH( NH 3 )−( CH 2 ) 2 −COOH. At pH values between about 2.5 and 4.1, the carboxylic acid closer to the amine generally loses a proton, and the acid becomes the neutral zwitterion OOC−CH( NH 3 )−( CH 2 ) 2 −COOH. This is also the form of the compound in the crystalline solid state. The change in protonation state

6390-593: The morning. Around half of depressed patients develop changes in psychomotor activity, described as slowness in thinking, speaking, or movement. Conversely, they may also present with agitation, with inability to sit still or wringing their hands. Changes in posture, speech, facial expression, and grooming can be observed. Other signs and symptoms include changes in posture and facial expression, slowed speech, poor hygiene, unkempt appearance, feelings of guilt, shame, or helplessness, diminished ability to concentrate, nihilistic thoughts, and suicidal ideation . Many experts in

6480-430: The most common psychiatric conditions associated with suicide. At least 25% to 50% of patients with bipolar disorder also attempt suicide at least once. Aside from lithium—which is the most demonstrably effective treatment against suicide—little is known about contributions of specific mood-altering treatments to minimizing mortality rates in persons with either major mood disorders or bipolar depression specifically. Suicide

6570-401: The most conservative estimate of lifetime prevalence of alcohol or other substance use disorders is 20%. In patients with comorbid substance use disorder and BP-II, episodes have a longer duration and treatment compliance decreases. Preliminary studies suggest that comorbid substance use is also linked to increased risk of suicidality. BP-II is diagnosed according to the criteria established in

6660-400: The most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicenter trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of BP-II, although lithium was superior in individuals with BP-I. There is also some evidence for the use of valproate and topiramate, although

6750-402: The occurrence of four or more major Depressive, Hypomanic, and/or mixed episodes in a 12-month period. Rapid cycling is quite common in those with BP-II, much more so in women than in men (70% vs. 40%), and without treatment leads to added sources of disability and an increased risk of suicide. Women are more prone to rapid cycling between hypomanic episodes and depressive episodes. To improve

6840-431: The pancreas has abundant GAD, a direct immunological destruction occurs in the pancreas and the patients will have diabetes mellitus . Glutamic acid, being a constituent of protein, is present in foods that contain protein, but it can only be tasted when it is present in an unbound form. Significant amounts of free glutamic acid are present in a wide variety of foods, including cheeses and soy sauce , and glutamic acid

6930-472: The presence of a depressed mood or loss of interest/pleasure in activities ( anhedonia ). In addition to the former symptoms, five out of the nine following symptoms must occur for more than two weeks (to the extent in which it impairs functioning): weight loss/gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue, feelings of worthlessness/inappropriate guilt, decreased concentration, or thoughts of death/suicide. Specifiers: According to

7020-474: The prevention of relapse of hypomania or depression. As BP-II is a chronic condition, the goal of treatment is to achieve remission of symptoms and prevention of self-harm in patients. Treatment modalities of BP-II include medication-based pharmacotherapy, along with various forms of psychotherapy. The most common pharmacologic agents utilized in the treatment of BP-II includes mood stabilizers , antipsychotics , and antidepressants . Mood stabilizers used in

7110-458: The production of adrenal steroids (i.e. aldosterone and cortisol ). Glutamate does not easily pass the blood brain barrier , but, instead, is transported by a high-affinity transport system. It can also be converted into glutamine . Glutamate toxicity can be reduced by antioxidants , and the psychoactive principle of cannabis , tetrahydrocannabinol (THC), and the non psychoactive principle cannabidiol (CBD), and other cannabinoids ,

7200-427: The protein in wheat) is glutamic acid. Ninety-five percent of the dietary glutamate is metabolized by intestinal cells in a first pass. Auxigro is a plant growth preparation that contains 30% glutamic acid. In recent years, there has been much research into the use of residual dipolar coupling (RDC) in nuclear magnetic resonance spectroscopy (NMR). A glutamic acid derivative, poly-γ-benzyl-L-glutamate (PBLG),

7290-412: The required medication, and seeking help when needed to do well in the future. Treatment often lasts after remission is achieved, and the treatment that worked is continued during the continuation phase (lasting anywhere from 6–12 months) and maintenance can last 1–2 years or, in some cases, indefinitely. One of the treatments of choice is Lithium , which has been shown to be very beneficial in reducing

7380-675: The results for the use of gabapentin have been disappointing. Antipsychotics are utilized as a second line option for hypomanic episodes, typically indicated patients who do not respond to mood stabilizers. However, quetiapine is the only antipsychotic that has demonstrated efficacy in multiple meta-analyses of Randomized controlled trials for treating acute BP-II depression, and is a first-line option for patients with BP-II depression. Other antipsychotics that are used to treat BP-II include lurasidone , olanzapine , cariprazine , aripiprazole , asenapine , paliperidone , risperidone , ziprasidone , haloperidol , and chlorpromazine . As

7470-567: The risk of suicide is slightly higher in patients who have BP-II than those with BP-I. In results of a summary of several lifetime study experiments, it was found that 32.4% of BP-I patients experienced suicidal ideation or suicide attempts compared to 36% in BP-II patients. Bipolar disorders, in general, are the third leading cause of death in 15- to 24-year-olds. BP-II patients were also found to employ more lethal means and have more complete suicides overall. BP-II patients have several risk factors that increase their risk of suicide. The illness

7560-524: The seeming inability to focus on tasks. Because many of the symptoms of hypomania are often mistaken for high-functioning behavior or simply attributed to personality, patients are typically not aware of their hypomanic symptoms. In addition, many people with BP-II have periods of normal affect . As a result, when patients seek help, they are very often unable to provide their doctor with all the information needed for an accurate assessment; these individuals are often misdiagnosed with unipolar depression. BP-II

7650-537: The severity of aimlessness and disorganization. Speech may be rapid, but interruptible. Patients with hypomania never present with psychotic symptoms and do not reach the severity to require psychiatric hospitalization. For these reasons, hypomania commonly goes unnoticed. Individuals often will only seek treatment during a depressive episode, and their history of hypomania may go undiagnosed. Although hypomania may increase functioning, episodes require treatment as they may indicate increasing instability and can precipitate

7740-415: The solid state and mildly acidic water solutions, the molecule assumes an electrically neutral zwitterion structure OOC−CH( NH 3 )−( CH 2 ) 2 −COOH. It is encoded by the codons GAA or GAG. The acid can lose one proton from its second carboxyl group to form the conjugate base , the singly-negative anion glutamate OOC−CH( NH 3 )−( CH 2 ) 2 −COO . This form of

7830-405: The treatment of hypomanic and depressive episodes of BP-II include lithium , and the anticonvulsant medications valproate , carbamazepine , lamotrigine , and topiramate . There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in BP-II, along with the reduction of hypomanic switch in patients treated with antidepressants. Furthermore, lithium

7920-508: The vertebrate nervous system . At chemical synapses , glutamate is stored in vesicles . Nerve impulses trigger the release of glutamate from the presynaptic cell. Glutamate acts on ionotropic and metabotropic ( G-protein coupled ) receptors. In the opposing postsynaptic cell, glutamate receptors , such as the NMDA receptor or the AMPA receptor , bind glutamate and are activated. Because of its role in synaptic plasticity , glutamate

8010-535: Was discovered and identified in the year 1866 by the German chemist Karl Heinrich Ritthausen , who treated wheat gluten (for which it was named) with sulfuric acid . In 1908, Japanese researcher Kikunae Ikeda of the Tokyo Imperial University identified brown crystals left behind after the evaporation of a large amount of kombu broth as glutamic acid. These crystals, when tasted, reproduced

8100-549: Was supplanted by the aerobic fermentation of sugars and ammonia in the 1950s, with the organism Corynebacterium glutamicum (also known as Brevibacterium flavum ) being the most widely used for production. Isolation and purification can be achieved by concentration and crystallization ; it is also widely available as its hydrochloride salt. Glutamate is a key compound in cellular metabolism . In humans, dietary proteins are broken down by digestion into amino acids , which serve as metabolic fuel for other functional roles in

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