Major depressive disorder ( MDD ), also known simply as depression , is a mental disorder characterized by at least two weeks of low mood present in partial great situation. Often accompanied by low self-esteem, loss of interest in normally fun activities, low energy, and pain without obvious cause. People may also sometimes have false beliefs or see or hear things that other people can not. Some people experience periods of depression that are separated by years in which they are normal, while others almost always have symptoms. Major depressive disorders can negatively impact a person's private, work, or school life as well as sleep, eating habits, and general health. Between 2-7% of adults with major depression die from suicide, and up to 60% of people who die of suicide experience depression or other mood disorders.
The cause is believed to be a combination of genetic, environmental, and psychological factors. Risk factors include family history of the condition, major changes in life, certain medications, chronic health problems, and substance abuse. Approximately 40% of the risk appears to be related to genetics. The diagnosis of major depressive disorder is based on reported experiences of people and mental status checks. There are no laboratory tests for severe depression. Testing, however, can be done to rule out any physical condition that can cause similar symptoms. The great depression must be distinguished from sadness, which is part of normal and less severe life. The US Prevention Services Task Force (USPSTF) recommended screening for depression among those over the age of 12, while an earlier Cochrane review found that routine use of filtering questionnaires had little effect on detection or treatment.
Usually, people are treated with counseling and antidepressant drugs. The drug appears to be effective, but the effect may be only significant in the most severe depression. It is unclear whether the drug affects the risk of suicide. Types of counseling used include cognitive behavioral therapy (CBT) and interpersonal therapy. If other measures are not effective electroconvulsive therapy (ECT) can be tried. Hospitalization may be necessary in cases with a risk of danger to yourself and can sometimes occur against a person's wishes.
The major depressive disorder affects about 216 million people (3% of the world's population) by 2015. The percentage of people affected at one point in their lives varies from 7% in Japan to 21% in France. Lifetime rates are higher in developed countries (15%) compared to developing countries (11%). This causes the second year mostly to live with disability, after a low back pain. The most common onset time is in a person's 20s and 30s. Women are affected about twice as often as men. The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorder (DSM-III) in 1980. It was a split from the previous depressive neurosis in DSM-II, which also included conditions now known as dysthymia and adjustment disorders with depressed mood. Those who are currently or previously affected can be stigmatized.
Video Major depressive disorder
Signs and symptoms
Severe depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health. Its impact on function and well-being has been compared with other chronic medical conditions such as diabetes.
A person who has a major depression episode usually shows a very low mood, covering all aspects of life, and an inability to experience pleasure in activities previously enjoyed. The depressed person may be preoccupied with, or thinking of, unworthy thoughts and feelings, unintentional guilt or regret, helplessness, despair, and self-loathing. In severe cases, a depressed person may have symptoms of psychosis. These symptoms include delusions or, more rarely, hallucinations, usually unpleasant. Other depressive symptoms include poor concentration and memory (especially in those with melancholy or psychotic features), withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common among the depressed. In a typical pattern, a person wakes up very early and can not go back to sleep. Hypersomnia, or excessive sleep, can also occur. Some antidepressants may also cause insomnia because of their stimulatory effects.
Depressed people can report some physical symptoms like fatigue, headaches, or digestive problems; Physical complaints are the most common problems in developing countries, according to World Health Organization criteria for depression. Appetite often decreases, with the resulting weight loss, although increased appetite and weight gain sometimes occur. Family and friends may notice that the person's behavior is anxious or lethargic. People with older depression may have cognitive symptoms from recent onset, such as forgetfulness, and slower movements. Depression often coincides with common physical disorders among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.
Depressed children may often display an irritable mood rather than a depressed mood, and show symptoms depending on age and situation. Most lost interest in school and showed a decline in academic performance. They can be described as clinging, demanding, dependent, or insecure. Diagnosis may be delayed or missed when symptoms are interpreted as normal moods.
Related conditions
Severe depression often coincides with other psychiatric problems. The 1990-92 National Comorbidity Survey (US) reported that half of those with major depression also had lifelong anxiety and related disorders such as generalized anxiety disorder. Symptoms of anxiety can have a major impact on the course of depressive illness, with delayed recovery, increased risk of relapse, greater disability, and increased suicide attempts. There is an increased level of alcohol and drug abuse and especially dependency, and about one-third of individuals diagnosed with ADHD develop comorbid depression. Post-traumatic stress disorder and depression often occur together. Depression can also occur along with attention deficit hyperactivity disorder (ADHD), complicating both diagnosis and treatment. Depression is also often comorbid with alcohol abuse and personality disorders.
Depression and pain often occur together. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 to 85% of patients with pain will suffer from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialized clinics. The diagnosis of depression is often delayed or missed, and the results may worsen if depression is known but completely misunderstood.
Depression is also associated with an increased risk of cardiovascular disease 1.5 to 2-fold, regardless of other known risk factors, and itself is directly or indirectly associated with risk factors such as smoking and obesity. People with severe depression are less likely to follow medical recommendations to treat and prevent cardiovascular disorders, which further increases the risk of medical complications. In addition, cardiologists can not recognize the underlying depression that complicates cardiovascular problems under their care.
Maps Major depressive disorder
Cause
The cause of major depressive disorder is unknown. The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The stress-diathesis model determines that depression results when pre-existing vulnerabilities, or diathesis, are activated by stressful life events. The existing vulnerability may be genetic, implying an interaction between nature and nurture, or schematic, resulting from a world view learned in childhood.
Child abuse, whether physical, sexual or psychological, is all of the risk factors for depression, among other psychiatric problems that occur together such as anxiety and drug abuse. Childhood trauma is also correlated with the severity of depression, lack of response to treatment and duration of illness. However, some are more prone to develop mental illness such as depression after trauma, and various genes have been suggested to control vulnerability.
Genetics
The 5-HTTLPR, or serotonin promoter serotonin promoter allele has been associated with an increased risk of depression. However, since the 1990s the results have been inconsistent, with three recent reviews finding effects and two non-existent findings. Other genes that have been associated with gene-environment interactions include CRHR1, FKBP5 and BDNF, the first two are associated with stress reactions of the HPA axis, and the latter involved in neurogenesis.
Other health issues
Depression can also come as a result of chronic medical conditions or terminals such as HIV/AIDS, or asthma and can be labeled "secondary depression". It is unknown whether the underlying disease induces depression through effects on quality of life, through joint etiology (such as basal ganglia degeneration in Parkinson's disease or immune dysregulation in asthma). Depression can also be iatrogenic (the result of health care), such as drug-induced depression. Depression-related therapy including interferon, beta-blocker, isotretinoin, contraceptive, cardiac, anticonvulsant, antimigrain, antipsychotic, and hormonal agents as hormone agonists release gonadotropin. Drug abuse at an early age is also associated with an increased risk of developing depression later in life. The depression that occurs as a result of pregnancy is called postpartum depression, and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be the result of a decrease in sunlight.
Pathophysiology
The pathophysiology of depression is not yet understood, but current theories are centered around the monoaminergic system, circadian rhythms, immunological dysfunction, HPA axis dysfunction and structural or functional abnormalities of the emotional circuit.
Monoamine theory, derived from the efficacy of monoaminergic drugs in treating depression, is the dominant theory to date. This theory postulates that insufficient activity of monoamine neurotransmitters is a major cause of depression. The evidence for the theory of monoamines comes from various fields. First, acute tryptophan thinning, the required serotonin precursor, monoamine, can cause depression in those who have remission or relatives of depressed patients; this suggests that decreased serotonergic neurotransmission is important in depression. Second, the correlation between the risk of depression and polymorphism in the 5-HTTLPR gene, which encodes serotonin receptors, indicates a relationship. Third, decrease in the size of the coeruleus locus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptors, and evidence from the mouse model showed decreased adrenergic neurotransmission in depression. Furthermore, decreased levels of homovanillic acid, changes in response to dextroamphetamine, the response of depressive symptoms to dopamine receptor agonists, decreased dopamine D1 receptor binding striatum, and dopamine receptor gene polymorphisms involving dopamine in depression. Finally, increased activity of monoamine oxidase, which decreases monoamine, has been associated with depression. However, this theory is inconsistent with the fact that the depletion of serotonin does not cause depression in healthy people, the fact that antidepressants instantly increase levels of monoamines but takes weeks to work, and the presence of atypical antidepressants that can be effective even if they do not target these pathways.. One of the proposed explanations for lag therapy, and further support for monoamine deficiency, is the desensitization of self-inhibition in raphe nuclei by an increase in serotonin mediated by antidepressants. However, the disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan thinning, resulting in a depressed state mediated by increased serotonin. Further opposition to the monoamine hypothesis is the fact that mice with lesions in dorsal rapica are no more depressive in control, findings of a 5-HIAA jugular increase in normalized depression patients with SSRI treatment, and a preference for carbohydrates in depressed patients. Already limited, the monoamine hypothesis has been further simplified when presented to the general public.
Abnormalities of the immune system have been observed, including elevated levels of cytokines involved in producing ill behavior (which share overlap with depression). The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in the treatment of depression, and normalization of cytokine levels after successful treatment further indicate immune system abnormalities in depression.
HPA axis abnormalities have been suggested in depression given the association of CRHR1 with depression and increased frequency of dexamethasone test non-suppression in depressed patients. However, this disorder is inadequate as a diagnostic tool, because the sensitivity is only 44%. This stress related disorder has been hypothesized to be the cause of the decrease in hippocampal volume seen in depressed patients. Furthermore, meta-analysis results in decreased suppression of dexamethasone, and an increased response to psychological stress. Further abnormal results have been obscured by the response of cortisol awakening, with increased responses attributed to depression.
The theory that unites neuroimaging findings has been proposed. The first proposed model is the "Limbic Cortical Model", which involves the hyperactivity of the paralimbic ventral region and hypoactivity of the frontal regulatory areas in emotional processing. Another model, "Corito-Striatal model", suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures produce depression. Another model proposes a hyperactivity structure of significance in identifying negative stimuli, and the hypoactivity of cortical regulatory structures produces a negative emotional bias and depression, consistent with the study of emotional bias.
Diagnosis
Clinical assessment
Diagnostic assessments may be performed by a well-trained general practitioner, or by a psychiatrist or psychologist, who records the current state of a person, biographical history, current symptoms, and family history. The broad clinical goal is to formulate relevant biological, psychological and social factors that may impact an individual's mood. Assessors can also discuss how people currently regulate mood (healthy or not) such as alcohol and drug use. Assessment also includes an examination of the mental state, which is an assessment of one's current mood and content, in particular the presence of a theme of despair or pessimism, self-harm or suicide, and no positive thought or plan. Specialist mental health services are rare in rural areas, so diagnosis and management are mostly left to primary care physicians. This problem is even more marked in developing countries. Mental health checks may include the use of assessment scales such as the Hamilton Assessment Scale for Depression or Inventory Beck Depression or the Suicide-Revised Behavior Questionnaire. Scores on the assessment scale alone are not sufficient to diagnose depression for DSM or ICD satisfaction, but provide an indication of symptom severity for an extended period of time, so that people who score above a given cut-off point can be more carefully evaluated for the diagnosis of depressive disorder. Some assessment scales are used for this purpose.
Primary care physicians and other non-psychiatric physicians have more difficulty with less recognition and depression treatment than psychiatric physicians, partly because of the physical symptoms that often accompany depression, in addition to the many potential patients, providers, and system barriers that the authors portray. A review found that non-psychiatrists missed about two-thirds of cases, although this has improved somewhat in more recent studies.
Before diagnosing major depressive disorders, doctors generally perform medical examinations and investigations are selected to rule out other causes of symptoms. These include blood tests that measure TSH and thyroxine to rule out hypothyroidism; basic electrolytes and serum calcium to exclude metabolic disorders; and complete blood count includes ESR to rule out systemic infection or chronic disease. Adverse affective reactions to drugs or alcohol abuse are often ruled out, as well. Testosterone levels can be evaluated to diagnose hypogonadism, the cause of depression in men. Vitamin D levels may be evaluated, as low levels of vitamin D have been associated with a greater risk of depression.
Subjective cognitive complaints appear in older depressed people, but they can also be an indication of demented disorders, such as Alzheimer's disease. Cognitive tests and brain imaging may help to distinguish depression from dementia. CT scans can exclude brain pathology in those with psychotic symptoms, rapid onset or unusual symptoms. In general, the investigation is not repeated for the next episode unless there is a medical indication.
There are no biological tests that confirm severe depression. Depression biomarkers have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including Neurotropic Rice Brain Factors and various functional MRI techniques. One study developing a decision tree model interprets a series of fMRI scans taken during various activities. In their subjects, study authors were able to achieve 80% sensitivity and 87% specificity, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative possibility ratios were 6.15, 0.23, respectively). However, more research is needed before this test can be used clinically.
DSM-IV-TR and ICD-10 Criteria
The most widely used criteria for diagnosing depression are found in the fourth edition of the American Psychiatric Association's revision of the Diagnostic and Statistical Manual of Mental Disorder (DSM-IV-TR), and the World Health Organization International Statistical Classification of Diseases and Related Health Problems (ICD-10), which uses the name depressive episode for one episode and repeated depressive disorder to repeat episodes. The latter system is commonly used in European countries, while the former is used in the US and many other non-European countries, and the authors of both have worked to tailor one another.
Both DSM-IV-TR and ICD-10 marked typical symptoms of depression (major). ICD-10 defines three typical symptoms of depression (depressed mood, anhedonia, and reduced energy), two of which must be present to determine the diagnosis of depressive disorder. According to DSM-IV-TR, there are two major symptoms of depression - feelings of depression and anhedonia. At least one of these must be present to make a diagnosis of major depressive episodes.
Major depressive disorder is classified as a mood disorder in DSM-IV-TR. Diagnosis depends on the presence of a single or recurrent major episode of depression. Further qualifications are used to classify both the episode itself and the course of the disturbance. Category Depression Disorder Not Declared Determined if the manifestations of depressive episodes do not meet the criteria for episodes of major depression. The ICD-10 system does not use the term major depressive disorder but lists very similar criteria for the diagnosis of depressed episodes (mild, moderate or severe); repeated terms may be added if there are multiple episodes without mania. The episode of major depression
A major depressive episode is characterized by a very depressed mood that lasts for at least two weeks. Episodes can be isolated or repetitive and categorized as mild (some symptoms exceed minimum criteria), moderate, or severe (a real impact on social or occupational function). Episodes with psychotic features - commonly referred to as psychotic depression - are automatically rated as weight. If the patient has an episode of mania or increased mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because mood persists in an emotional or "polar" state.
DSM-IV-TR excludes cases in which the symptoms are the result of mourning, although it may be for normal mourning to evolve into episodes of depression if mood persists and characteristic features of a major depressive episode develop. Criteria have been criticized because they do not take into account other aspects of the personal and social context in which depression can occur. In addition, several studies have found little empirical support for the DSM-IV cut-off criteria, suggesting that they are a forced diagnostic convention in a series of depressive symptoms with varying degrees of severity and duration: Excluded are the associated diagnoses, including dysthymia, which involve chronic but lighter mood disorders; a brief, recurrent depression, consisting of a brief depressive episode; mild depressive disorder, where only a few of the symptoms of major depression are present; and adjustment disorders with depressed moods, indicating a low mood resulting from a psychological response to an identifiable event or stressor.
Subtype
The DSM-IV-TR recognizes five further subtypes of MDD, called specifiers , in addition to noting the length, severity and presence of psychotic features:
- Melancholy depression is characterized by a loss of pleasure in most or all activities, failure of reactivity to pleasant stimuli, the quality of depression is more pronounced than sadness or loss, worsening of morning symptoms, , psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt. Atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positive, significant weight gain or increased appetite (comfort), excessive sleep or drowsiness (hypersomnia), weight sensation in legs known as leaden paralysis, and significant social disorders as a consequence of hypersensitivity to perceived interpersonal rejection.
- Catatonic depression is a rare and severe form of severe depression involving impaired motor behavior and other symptoms. Here, the man is mute and almost stupor, and either remains immobile or shows aimless or even weird movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.
- Postpartum depression , or postpartum mental and behavioral disorders, not classified elsewhere , refers to the intense, ongoing and sometimes paralyzing depression experienced by women after childbirth. Postpartum depression has an incidence rate of 10-15% among new mothers. DSM-IV mandates that, to qualify as postpartum depression, onset occurs within a month of delivery. It is said that postpartum depression can last for three months.
- Seasonal affective disorder (SAD) is a form of depression in which depressive episodes come in autumn or winter, and disappear in the spring. The diagnosis is made if at least two episodes have occurred in colder months with none at any other time, over a period of two years or longer.
Screening
In 2016, the United States Prevention Services Task Force (USPSTF) recommended screening in adult populations with evidence that it improves detection of people with depression and with appropriate treatment improves outcomes. They recommend screening for those aged between 12 and 18 years as well.
A Cochrane review from 2005 found the screening program did not significantly improve detection rates, treatment, or outcomes.
Differential diagnosis
To confirm major depressive disorder as the most likely diagnosis, other potential diagnoses should be considered, including dysthymia, adjustment disorders with depressed mood, or bipolar disorder. Dysthymia is a chronic and mild mood disorder in which a person reports low mood almost daily for a span of at least two years. The symptoms are not as severe as major depression, although people with dysthymia are susceptible to severe episodes of severe depression (sometimes referred to as double depression ). The deviation of adjustment to depressed mood is a mood disorder that appears as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for major depressive episodes. Bipolar disorder, also known as manic-depressive disorder, is a condition in which the depressive phase alternates with the period of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate as individuals who are diagnosed with severe depression often experience some hypomanic symptoms, suggesting a continuous mood disorder. A further differential diagnosis involves chronic fatigue syndrome.
Other disorders should be ruled out before diagnosing major depressive disorder. They include depression due to physical illness, drugs, and substance abuse. Depression due to physical illness was diagnosed as a mood disorder due to a general medical condition. This condition is determined by history, laboratory findings, or physical examination. When depression is caused by drugs, drug abuse, or exposure to toxins, it is then diagnosed as a specific mood disorder (previously called Substance induced mood in DSM-IV-TR).
Prevention
Prevention efforts can lead to a decrease in the level of conditions between 22 and 38%. Eating fish in large quantities can also reduce the risk.
Behavioral interventions, such as interpersonal therapy and behavior-cognitive therapy, effectively prevent new onset depression. Because such interventions seem most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their most targeted audiences most efficiently via the Internet.
However, previous meta-analyzes have found prevention programs with components that improve competence to excel from behavior-oriented programs as a whole, and find behavioral programs that are specifically unhelpful for older people, for whom the social support program is uniquely rewarding. In addition, the best program to prevent depression consists of more than eight sessions, each lasting between 60 and 90 minutes, provided by a combination of lay and professional workers, has a high quality research design, reports erosion levels, and has an Intervention-defined well.
The Dutch mental health care system provides preventive interventions, such as "Coping with Depression" (CWD) courses for people with sub-threshold depression. This course is claimed to be the most successful psychoeducation intervention for the treatment and prevention of depression (both for its adaptability to various populations and outcomes), with 38% reduction in risk of severe depression and efficacy as a treatment compared with both. to other psychotherapy.
Management
The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice (over drugs) for people under 18 years of age. The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines suggest that antidepressants should not be used for the initial treatment of mild depression, because of the poor risk-benefit ratio. The guidelines recommend that antidepressant treatment in combination with psychosocial interventions should be considered for:
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- People with a history of moderate or severe depression
- Those with mild depression have been present for a long time
- As second-line treatment for mild depression that continues after another intervention
- As a first-line treatment for moderate or severe depression.
The guidelines further note that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.
The American Psychiatric Association's treatment guidelines recommend that initial care should be individually adjusted based on factors including symptom severity, existing disorders, previous care experience, and patient preferences. Options may include pharmacotherapy, psychotherapy, exercise, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) or light therapy. Antidepressant drugs are recommended as an initial treatment option in people with mild, moderate or severe depression, and should be given to all patients with severe depression unless ECT is planned.
Treatment options are much more limited in developing countries, where access to mental health staff, medications, and psychotherapy is often difficult. The development of mental health services is minimal in many countries; depression is seen as a phenomenon of the developed world despite contradictory evidence, and not as a life-threatening condition. The 2014 Cochrane Review found insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.
Lifestyle
Physical exercise is recommended for mild depression management, and has a moderate effect on symptoms. Exercise has also been shown to be effective for severe depression (unipolar). This is equivalent to the use of drugs or psychological therapy in most people. In the older person it seems to reduce depression. Exercise can be recommended to people who are willing, motivated, and physically fit enough to participate in an exercise program as a treatment.
There is a small amount of evidence that skipping a night's sleep can increase the symptoms of depression, with effects usually appearing within a day. This effect is usually temporary. In addition to drowsiness, this method can cause side effects of mania or hypomania.
In observational studies, quitting smoking has a benefit in depression of greater than or greater than drugs.
In addition to exercise, sleep and diet can play a role in depression, and intervention in this area can be an effective add-on for conventional methods.
Counseling
Psychotherapy can be given to individuals, groups, or families by mental health professionals. Review 2015 found that cognitive behavioral therapy seems to be similar to antidepressant drugs in terms of effects. The 2012 review found psychotherapy to be better than no treatment but no other treatments. With more complex and chronic forms of depression, a combination of drugs and psychotherapy can be used. The 2014 Cochrane Review found that work-led interventions in combination with clinical interventions help reduce sick days taken by people with depression. There is evidence of moderate quality that psychological therapy is a useful adjunct to standard antidepressant treatment of drug-resistant depression in the short term.
Psychotherapy has proven to be effective in the elderly. Successful psychotherapy seems to reduce the recurrence of depression even after being discontinued or replaced by occasional booster sessions.
Cognitive behavioral therapy
Current cognitive behavioral therapy (CBT) has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are the preferred therapies for teenage depression. In people under 18, according to the National Institute for Health and Clinical Excellence, drugs should be offered only in conjunction with psychological therapy, such as CBT, interpersonal therapy, or family therapy. Cognitive behavioral therapy has also been shown to reduce the number of sick days taken by people with depression, when used in conjunction with primary care.
The most widely studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-destructive, but long-lasting ways of cognition and change counter-productive behavior. Research that began in the mid-1990s shows that CBT can perform as well as or better than antidepressants in patients with moderate to severe depression. CBT may be effective in depressed adolescents, although its effect on severe episodes is not known definitively. Some variables predict the success of cognitive behavioral therapy in adolescents: higher levels of rational thought, less despair, less negative thoughts, and less cognitive distortion. CBT is very useful in preventing relapse.
Cognitive behavioral therapy and work programs (including modification of work and relief activities) have been shown to be effective in reducing the sick days taken by workers with depression.
Variant
Several variants of cognitive behavioral therapy have been used in those with depression, the most prominent being rational emotional behavioral therapy, and cognitive-based cognition. An awareness-based stress reduction program can reduce symptoms of depression. Awareness programs also appear to be promising interventions in youth.
Psychoanalysis
Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients who are severely depressed. More practiced therapy, called psychodynamic psychotherapy, is a psychoanalytic but less intensive tradition, meeting once or twice a week. It also tends to focus more on a person's immediate problem, and has an additional social and interpersonal focus. In a meta-analysis of three controlled trials of Short Psychodynamic Support Psychotherapy, these modifications were found to be as effective as medications for mild to moderate depression.
Antidepressants
Conflicting results have emerged from studies looking at the effectiveness of antidepressants in people with acute, mild to moderate depression. Strong evidence supports the usefulness of antidepressants in the treatment of chronic (dysthymia) or severe depression.
While small benefits are found, researchers Irving Kirsch and Thomas Moore state that they may be due to problems with trials rather than the actual effects of the drug. In later publications, Kirsch concluded that the overall effect of a new generation antidepressant drug under recommended criteria for clinical significance. Similar results were obtained in the meta analysis by Fornier.
A review commissioned by the National Institute for Health and Care Excellence concluded that there is strong evidence that SSRIs have greater efficacy than placebo in achieving a 50% reduction in depression scores for moderate and severe depression, and that there is some evidence for similar. effects in mild depression. Similarly, Cochrane's systematic review of clinical trials of tricyclic antidepressant amitriptyline concluded that there is strong evidence that efficacy is superior to placebo.
In 2014 the US FDA published a systematic review of all trials of antidepressant treatments submitted to agencies between 1985 and 2012. The authors concluded that treatment care reduced the risk of relapse by 52% compared with placebo, and that this effect was mainly due to recurrent depression in the placebo group rather than the drug withdrawal effect.
To find the most effective antidepressant drugs with minimal side effects, the dosage can be adjusted, and if necessary, a combination of various classes of antidepressants can be tried. The response rate to the first antidepressant delivery range is 50-75%, and it can take at least six to eight weeks from start of treatment to remission. Treatment of antidepressant drugs is usually continued for 16 to 20 weeks after remission, to minimize the possibility of recurrence, and even up to a year of continuation is recommended. People with chronic depression may need to take unlimited medication to avoid relapse.
Selective Serotonin Reuptake Inhibitors (SSRIs) are the main drugs prescribed, because of their relatively mild side effects, and because they are less toxic in overdose than other antidepressants. People who do not respond to one SSRI can be diverted to another antidepressant, and this results in an increase of nearly 50% of cases. Another option is to switch to atypical antidepressant bupropion. Venlafaxine, an antidepressant with different mechanisms of action, may be slightly more effective than SSRIs. However, venlafaxine is not recommended in the UK as first-line treatment because the evidence suggests that the risks may outweigh the benefits, and are not particularly recommended in children and adolescents.
For child and adolescent depression, fluoxetine is recommended if medication is used. Fluoxetine; However, it appears to have little benefit in children, while other antidepressants have not proven effective. There is also sufficient evidence to determine their effectiveness with depression complicated by dementia. Any antidepressant may cause low serum sodium levels (also called hyponatremia); However, it has been reported more frequently with SSRIs. Not infrequently SSRI cause or worsen insomnia; sedation of a mirtazapine antidepressant may be used in such cases.
Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by dietary interactions and potentially life-threatening drugs. They are still rarely used, although newer and better tolerated agents of this class have been developed. Safety profiles differ from reversible monoamine oxidase inhibitors such as moclobemide in which the risk of serious dietary interactions is negligible and dietary restriction is less restrictive.
For children, adolescents, and possibly young adults between 18 and 24 years, there is a higher risk of both suicidal ideation and suicidal behavior in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicide. One review did not find the connection; another increased risk; and thirdly there is no risk to those aged 25-65 years and the risk of decline in those over 65. A black box warning was introduced in the United States in 2007 about SSRIs and other antidepressant drugs due to an increased risk of suicide in patients younger than age 24 years. A revision of similar prudential notices is implemented by the Japanese Ministry of Health.
Other drugs
There is some evidence that omega-3 fatty acid fish supplement containing high levels of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) is effective in treatment, but not the prevention of severe depression. However, Cochrane's review determined that there was not enough high-quality evidence to suggest that Omega-3 fatty acids were effective in depression. There is limited evidence that vitamin D supplementation is of value in reducing symptoms of depression in individuals with vitamin D deficiency. There is some early evidence that COX-2 inhibitors have a beneficial effect on severe depression. Lithium appears effective in lowering the risk of suicide in those with bipolar disorder and unipolar depression to levels similar to that of the general population. There is a narrow range of effective and safe lithium doses so rigorous monitoring may be necessary. Low-dose thyroid hormones can be added to existing antidepressants to treat persistent depression symptoms in people who have tried several treatment programs. Limited evidence suggests stimulants such as amphetamines and modafinils may be effective in the short term, or in addition to therapy. Also, it is recommended that folate supplements may have a role in depression management.
Electroconvulsive Therapy
Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which electrical spasms are induced in patients to provide relief from psychiatric illness. ECT is used with informed consent as the last line of intervention for major depressive disorder.
One round of ECT is effective for about 50% of people with severe depression who are resistant to treatment, whether unipolar or bipolar. Follow-up treatment is still poorly studied, but about half of the people who respond recur within twelve months.
In addition to effects in the brain, the general physical risk of ECT is similar to the general short anesthesia. Immediately after treatment, the most common side effects are confusion and memory loss. ECT is considered one of the most harmless treatment options available for pregnant women with severe depression.
Usually ECT involves a lot of administration, usually given two or three times per week until the patient no longer suffers symptoms. ECT is administered under anesthesia with muscle relaxants. Electroconvulsive therapy may differ in its application in three ways: electrode placement, maintenance frequency, and the electrical waveform of the stimulus. These three forms of application have significant differences in both side effects and remission of symptoms. After treatment, drug therapy is usually continued, and some patients receive ECT treatment.
ECT seems to work in the short term through most anticonvulsant effects in the frontal lobe, and long-term through neurotropic effects especially in the medial temporal lobes.
Transcranial magnetic stimulation
Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small areas of the brain. TMS was approved by the FDA for major drug-resistant depressive disorders in 2008 and in 2014 evidence supports that it may be effective. The American Psychiatric Association, the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have authorized the rTMS for trMDD.
More
Bright light therapy reduces the severity of depressive symptoms, with benefits found for seasonal affective disorder and for non-elderly depression, and effects similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to standard antidepressant treatment is not effective. For the non-seasonal depression in which light is used mostly in combination with antidepressants or moderate effects wake therapy is found, with a better response than control treatment in high-quality research, in studies that apply morning light therapy, and with those who respond total or partial sleep deprivation. Both analyzes recorded poor quality, short duration, and small size of most studies reviewed. There is not enough evidence for Reiki and dance therapy therapy in depression.
Prognosis
The episodes of major depression often recover from time to time whether they are treated or not. Outpatient on the waiting list showed a 10-15% decrease in symptoms within a few months, with approximately 20% no longer meeting the complete criteria for depressive disorders. The median duration of an episode is estimated to be 23 weeks, with the highest recovery rate in the first three months.
Research has shown that 80% of those who suffer from their first major episode of depression will suffer at least 1 more during their lifetime, with an average lifetime of 4 episodes. Other general population studies show that about half of those who have episodes recover (whether treated or not) and stay healthy, while the other half will have at least one more, and about 15% of them experience chronic relapse. Recruiting studies from selective inpatient homes showed lower recovery and higher chronicity, while most outpatient studies showed that almost all recovered, with an average 11-month episode duration. About 90% of those with severe or psychotic depression, most of whom also meet the criteria for other mental disorders, experience recurrence.
Recurrence is more likely to occur if symptoms are not fully resolved with treatment. The current guidelines recommend continuous antidepressants for four to six months after remission to prevent recurrence. Evidence from many randomized controlled trials suggests that sustained antidepressant drugs after recovery may reduce the chances of relapse by 70% (41% in placebo versus 18% in antidepressants). Preventive effects may last for at least the first 36 months of use.
People who experience recurrent episodes of depression require ongoing care to prevent more severe long-term depression. In some cases, people should take medication for long periods of time or for the rest of their lives.
Cases when adverse outcomes are associated with inappropriate treatment, severe initial symptoms that may include psychosis, early onset, previous episodes, incomplete recovery after 1 year, pre-existing mental or medical disorders, and family dysfunction as well.
Depressed people have a shorter life expectancy than those who are not depressed, in part because depressed patients are at risk of dying from suicide. However, they also have higher mortality rates than other causes, becoming more susceptible to medical conditions such as heart disease. Up to 60% of people who die of suicide experience mood disorders such as severe depression, and the risk is very high if a person has a clear sense of hopelessness or has depression and personality disorder threshold. The lifelong risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two very different numbers almost 7% for men and 1% for women (although suicide attempts are more common in women). This estimate is substantially lower than the previously accepted rate of 15%, which comes from older studies in hospitalized patients.
Depression is often associated with unemployment and poverty. The current great depression is a major cause of disease burden in North America and other high-income countries, and the fourth leading cause worldwide. By 2030, it is thought to be the second leading cause of diseases worldwide after HIV, according to the World Health Organization. Delay or failure in seeking treatment after relapse, and failure of health professionals to provide care, are two barriers to reducing disability.
Epidemiology
Major depressive disorder affects about 216 million people by 2015 (3% of the global population). The percentage of people affected at one point in their life varies from 7% in Japan to 21% in France. In most countries, the number of people depressed during their lifetime is within the range of 8-18%. In North America, the likelihood of having major depressive episodes within a one-year period is 3-5% for males and 8-10% for females. Severe depression is twice as common in women as in men, although it is unclear why this happens, and whether unknown factors contribute to this. Increased relative incidence associated with puberty development rather than chronological age, reaching adult ratios between ages 15 and 18, and appearing related to psychosocial more than hormonal factors. Depression is the leading cause of disability worldwide.
People most likely to develop their first episode of depression between the ages of 30 and 40, and there is, the peak of a smaller second incident between the ages of 50 and 60. The risk of major depression increases with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis, and during the first year after giving birth. It is also more common after cardiovascular disease, and more associated with poor outcomes than better. The study conflicts on the prevalence of depression in the elderly, but most data indicate there is a reduction in this age group. Depressive disorders are more commonly observed in urban areas than in rural populations and prevalence in groups with stronger socioeconomic factors ie homelessness.
History
Ancient Greek physician Hippocrates described the syndrome of melancholia as a disease different from certain mental and physical symptoms; he characterizes all "fears and sadness, if they last long" as a symptom of his illness. It is the same concept but much broader than today's depression; fame is given to the grouping of symptoms of sadness, disappointment, and sadness, and often fear, anger, delusion and obsession are included.
The term depression itself comes from the Latin verb deprimere , "to suppress". From the 14th century, "to suppress" was meant to subdue or lower the spirit. It was used in 1665 in the English author Richard Baker Chronicle to refer to someone who had a "great depression of the soul," and by the English writer Samuel Johnson in the same sense in 1753. The term also came into use. in physiology and economics. The earliest use refers to psychiatric symptoms was by the French psychiatrist Louis Delasiauve in 1856, and in the 1860s it appeared in a medical dictionary to refer to physiological and metaphorical emotional degradation. Since Aristotle, melancholia has been associated with people who are learning and intellectual intelligence, the dangers of contemplation and creativity. The more recent concept of abandonment of this association and through the 19th century, became more associated with women.
Although melancholia remains the dominant diagnostic term, depression is getting a currency boost in medical treatments and is a synonym at the end of this century; German psychiatrist Emil Kraepelin may be the first to use it as a comprehensive term, referring to various types of melancholia as a depressed state.
Sigmund Freud likened the melancholy state to mourning in a 1917 paper on Mourning and Melancholia. He theorizes that loss of purpose, such as losing a relationship that is rewarded through death or romantic separation, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious narcissistic process called the libidinal cathexis of the ego. Such losses cause severe melancholy symptoms deeper than mourning; not just the outside world seen negatively but the ego itself is compromised. The decrease in self-perception by the patient is expressed in his belief in error, inferiority, and inadequacy. He also emphasized early life experiences as a predisposing factor. Adolf Meyer proposes a mixed social and biological framework that emphasizes the reaction in the context of individual life, and argues that the term depression should be used rather than melancholia. The first version of DSM (DSM-I, 1952) contains depressive reactions and DSM-II (1968) depressive neuroses defined as overreacting to internal conflicts or identifiable events , and also include depressive type of depressive manic psychosis in major affective disorder.
In the mid-20th century, researchers theorize that depression is caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s on the effects of reserpine and isoniazid in altering levels of monoamine neurotransmitters and affecting depressive symptoms. The theory of chemical imbalance is never proven.
The term "unipolar" (coined with the term "bipolar") was coined by neurologist and psychiatrist Karl Kleist, and later used by his disciples Edda Neele and Karl Leonhard.
The term
The new definition of depression is widely accepted, albeit with some conflicting findings and views. There are several ongoing empirical based arguments for returning to melancholy diagnosis. There have been some criticisms of the expansion of diagnostic coverage, related to the development and promotion of antidepressants and biological models since the late 1950s.
Society and culture
Terminology
The term "depression" is used in several different ways. Often used to interpret this syndrome but may refer to other mood disorders or simply to a low mood. The conceptualisation of people about depression varies greatly, both within and between cultures. "Because of the lack of scientific certainty," a commentator has observed, "the debate over depression turns out to be a language question.What we call - 'illness,' 'disorder,' 'state of mind' - affects how we see, diagnose, and treat." cultural differences to the extent that serious depression is regarded as a disease that requires professional personal care, or is an indicator of something else, such as the need to address social or moral problems, the result of a biological imbalance, or the reflection of the individual. differences in understanding distress that can strengthen feelings of helplessness, and emotional struggle.
Diagnosis is less common in some countries, such as China. It has been argued that Chinese traditionally reject or disguise emotional depression (although since the early 1980s, China's rejection of depression may have changed). Or, perhaps Western culture reframing and lifting some expression of human misery into disturbance status. Australian Professor Gordon Parker and others argue that the Western concept of depression "cures" sadness or misery. Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical disease that is incorrectly perceived as an actual disease. There is also concern that DSM, as well as the field of descriptive psychiatry that it employs, tends to revise abstract phenomena such as depression, which may in fact be social constructions. American archetypal psychologist James Hillman writes that depression can nourish the soul, insofar as "it brings with it protection, boundaries, focus, gravity, weight, and humble helplessness." Hillman argues that therapeutic attempts to eliminate depression echo the theme of the Christian awakening, but have an unfortunate effect by condemning the state of a soulful soul.
Stigma
Historians are often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or because of ignorance of diagnosis or treatment. Nevertheless, the analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical figures has led to the assumption that they may have some form of depression. People who may be depressed include English writer Mary Shelley, American-English writer Henry James, and American president Abraham Lincoln. Some contemporary people are famous for possible depression including Canadian songwriter Leonard Cohen and playwright and novelist Tennessee Tennessee Williams. Some pioneering psychologists, such as the Americans William James and John B. Watson, face their own depression.
There has been ongoing discussion on whether neurological disorders and mood disorders may be related to creativity, a discussion that goes back to Aristotle's time. English literature provides many examples of reflections on depression. The English philosopher John Stuart Mill experienced a period of several months from what he called "boring neural conditions", when one "can not receive pleasurable joys or fun, one of those moments when pleasure at other times becomes bland or indifferent." He quotes the English poet Samuel Taylor Coleridge's "Rejection" as the perfect description of his case: "A sadness without pang, hollow, dark and gloomy,/A drowsiness, sadness, unintentional sadness,/Who finds no natural outlet or help/In words , or sigh, or tear. "The English author, Samuel Johnson, used the term" black dog "in the 1780s to describe his own depression, and was popularized by depressed former British Prime Minister Sir Winston Churchill.
The social stigma of severe depression is widespread, and contact with mental health services only slightly reduces this. Public opinion about treatment is very different from health professionals; alternative treatments are considered to be more helpful than pharmacologically, which is considered bad. In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a combined Combined Five Year campaign to educate and reduce the stigma from 1992 to 1996; MORI studies conducted thereafter show small positive changes in public attitudes toward depression and treatment.
Research
Trials looked at the effects of botulinum toxin on depression. The idea is that the drug is used to make the person look less frowned and that this stops the negative feedback faces from the face. By 2015 it turns out, however, that a partially positive effect that has been observed until then could be a placebo effect.
MDD has been investigated by taking MRI scans of patients with depression has revealed a number of differences in brain structure compared with those not depressed. Meta-analysis of neuroimaging studies in severe depression reported that, compared with controls, depressed patients experienced an increase in lateral ventricular volume and adrenal gland and lower basal ganglia, thalamus, hippocampus, and frontal lobes (including orbitofrontal and gyrus cortex). rectus). Hypergensity has been associated with patients with late age onset, and has led to the development of vascular depression theory.
Elderly
Depression is very common among those over 65 and an increase in frequency with age beyond this age. In addition, the risk of depression increases with respect to age and individual fragility. Depression is one of the most important factors that adversely affect the quality of life in adults and the elderly. Both symptoms and treatment among the elderly are different from those of other adult populations.
As with many other diseases it is common among parents to not present symptoms of classic depression. Diagnosis and treatment are more complicated because parents are often treated simultaneously with a number of other drugs, and often have other concurrent diseases. Different treatment in studies of SSRI drugs has shown less and often inadequate effects among older people, while other drugs with more obvious effects have adverse effects that can be very difficult to manage among the elderly. Duloxetine is an SNRI drug with documented effects on recurrent depression among the elderly, but has adverse effects in the form of dizziness, dry mouth, diarrhea, and constipation.
Problem solving therapy is in 2015 the only psychological therapy with a proven effect, and can be equated with simpler forms of cognitive behavioral therapy. However, elderly people with depression rarely offer psychological treatments, and evidence that suggests other effective treatments are incomplete. Electroconvulsive therapy (ECT or electric shock therapy) has been used as a treatment for the elderly, and research-registration shows it e
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