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Major depressive disorder

Major depressive disorder
For other depressive disorders, see Types of psychological depression.
Major depressive disorder Classification and external resources

Vincent van Gogh’s 1890 painting At Eternity’s Gate

ICD-10 ICD-9 OMIM DiseasesDB MedlinePlus eMedicine MeSH

F32., F33. 296 608516 3589 003213 med/532 D003865

Major depressive disorder (also known as clinical depression, major depression, unipolar depression, or unipolar disorder) is a mental disorder characterized by an all-encompassing low mood accompanied by low self-esteem, and loss of interest or pleasure in normally enjoyable activities. The term "major depressive disorder" was selected by the American Psychiatric Association to designate this symptom cluster as a mood disorder in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders

(DSM-III) classification, and has become widely used since. The general term depression is often used to describe the disorder, but as it can also be used to describe other types of psychological depression, more precise terminology is preferred for the disorder in clinical and research use. Major depression is a disabling condition which adversely affects a person’s family, work or school life, sleeping and eating habits, and general health. In the United States, approximately 3.4% of people with major depression commit suicide, and up to 60% of all people who commit suicide have depression or another mood disorder. The diagnosis of major depressive disorder is based on the patient’s self-reported experiences, behavior reported by relatives or friends, and a mental status exam. There is no laboratory test for major depression, although physicians generally request tests for physical conditions that may cause similar symptoms. The most common time of onset is between the ages of 30 and 40 years, with a later peak between 50 and 60 years. Major depression is reported about twice as frequently in women as in men, although men are at higher risk for suicide. Most patients are treated in the community with antidepressant medication and some with psychotherapy or counseling. Hospitalization may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. A minority are treated with electroconvulsive therapy (ECT), under a short-acting general anaesthetic. The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Depressed individuals have shorter life expectancies than those without depression, in part because of greater susceptibility to medical illnesses. Current and former patients may be stigmatized. The understanding of the nature and causes of depression has evolved over the centuries, though many aspects of depression remain incompletely understood and are the subject of discussion and research. Psychological, psycho-social, evolutionary and


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biological causes have been proposed. Psychological treatments are based on theories of personality, interpersonal communication, and learning theory. Most biological theories focus on the monoamine chemicals serotonin, norepinephrine, and dopamine that are naturally present in the brain and assist communication between nerve cells. Monoamines have been implicated in depression, and most antidepressants work to increase the active levels of at least one.

Major depressive disorder
show varying symptoms depending on age and situation.[8] Most exhibit a loss of interest in school and a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure.[4] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[3]

The biopsychosocial model proposes that biological, psychological, and social factors all play a role to varying degrees in causing depression.[9] The diathesis–stress model posits that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[10][11] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[12] These interactive models have gained empirical support. For example, a prospective, longitudinal study uncovered a moderating effect of the serotonin transporter (5-HTT) gene on stressful life events in predicting depression. Specifically, depression may follow such events, but is more likely to appear in people with one or two short alleles of the 5-HTT gene.[10] A Swedish study estimated the heritability of depression—the degree to which individual differences in occurrence are associated with genetic differences—to be approximately 40 percent for women and 30 percent for men,[13] and evolutionary psychologists have proposed that the genetic basis for depression lies deep in the history of naturally selected adaptations. A substance-induced mood disorder resembling major depression has been causally linked to long-term drug use or abuse or withdrawal from certain sedative and hypnotic drugs.[14][15]

Symptoms and signs
Major depression is a serious illness that affects a person’s family, work or school life, sleeping and eating habits, and general health.[1] Its impact on functioning and wellbeing has been equated to that of chronic medical conditions such as diabetes.[2] A person suffering a major depressive episode usually exhibits a very low mood that pervades all aspects of life and an inability to experience pleasure in activities that formerly were enjoyed. Depressed people may be preoccupied with, or ruminate over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self hatred.[3] Other symptoms include poor concentration and memory, withdrawal from social situations and activities, reduced sex drive, and thoughts of death or suicide. Insomnia is common: in the typical pattern, a person wakes very early and is unable to get back to sleep.[4] Hypersomnia, or oversleeping, is less common.[4] Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.[3] The person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries according to the World Health Organization’s criteria of depression.[5] Family and friends may notice that the person’s behavior is either agitated or lethargic.[4] Older depressed persons may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.[6] In severe cases, depressed people may have symptoms of psychosis such as delusions or, less commonly, hallucinations, usually of an unpleasant nature.[7] Depressed children often display an irritable rather than a depressed mood,[3] and

Monoamine hypothesis
Most antidepressant medications work by increasing the levels of one or more of the monoamines—the neurotransmitters serotonin, norepinephrine and dopamine—in the synaptic cleft between neurons. Some medications affect the monoamine receptors directly.


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Serotonin is hypothesized to help regulate other neurotransmitter systems; decreased serotonin activity may allow these systems to act in unusual and erratic ways.[16] According to this "permissive hypothesis", depression arises when low serotonin levels promote low levels of norepinephrine, another monoamine neurotransmitter.[17] Some antidepressants enhance the levels of norepinephrine directly, whereas others raise the levels of dopamine, a third monoamine neurotransmitter. These observations gave rise to the monoamine hypothesis of depression. In its contemporary formulation, the monoamine hypothesis postulates that a deficiency of certain neurotransmitters is responsible for the corresponding features of depression: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life."[18] The proponents of this theory recommend the choice of an antidepressant with mechanism of action that impacts the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine- and dopamine-enhancing drugs.[18] In the past two decades, research has revealed multiple limitations of the monoamine hypothesis, and its explanatory inadequacy has been criticized within the psychiatric community.[19] Intensive investigation has failed to find convincing evidence of a primary dysfunction of a specific monoamine system in patients with major depressive disorders. The medications tianeptine and opipramol have long been known to have antidepressant properties despite lacking any effect on the monoamine system. Experiments with pharmacological agents that cause depletion of monoamines have shown that this depletion does not cause depression in healthy people nor does it worsen symptoms in depressed patients—although an intact monoamine system is necessary for antidepressants to achieve therapeutic effectiveness.[20] According to an essay published by the Public Library of Science (PLoS), the monoamine hypothesis, already limited, has been further oversimplified when presented to the general public.[21]

Major depressive disorder

Schematic of a synapse between an axon of one neuron and a dendrite of another. Synapses are specialized gaps between neurons. Electrical impulses arriving at the axon terminal trigger release of packets of chemical messengers (neurotransmitters), which diffuse across the synaptic cleft to receptors on the adjacent dendrite temporarily affecting the likelihood that an electrical impulse will be triggered in the latter neuron. Once released the neurotransmitter is rapidly metabolised or pumped back into a neuron. Antidepressants influence the overall balance of these processes.

Other theories
MRI scans of patients with depression have reported a number of differences in brain structure compared to those without the illness. Although there is some inconsistency in the results, meta-analyses have shown there is strong evidence for smaller hippocampal[22] volumes and increased numbers of hyperintensive lesions.[23] Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.[24] There may be a link between depression and neurogenesis of the hippocampus,[25] a center for both mood and memory. Loss of hippocampal neurons is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Drugs may increase serotonin levels in the brain, stimulating neurogenesis and thus increasing the total mass of the hippocampus. This increase may help to restore mood and memory.[26][27] Similar relationships have been observed between depression and an area of the anterior cingulate cortex implicated in the modulation of emotional behavior.[28] One of the neurotrophins responsible for neurogenesis is the brain-derived


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neurotrophic factor (BDNF). The level of BDNF in the blood plasma of depressed subjects is drastically reduced (more than threefold) as compared to the norm. Antidepressant treatment increases the blood level of BDNF. Although decreased plasma BDNF levels have been found in many other disorders, there is some evidence that BDNF is involved in the cause of depression and the mechanism of action of antidepressants.[29] Major depression may also be caused in part by an overactive hypothalamic-pituitaryadrenal axis (HPA axis) that is similar to the neuro-endocrine response to stress. Investigations reveal increased levels of the hormone cortisol and enlarged pituitary and adrenal glands, suggesting disturbances of the endocrine system may play a role in some psychiatric disorders, including major depression. Oversecretion of corticotropin-releasing hormone from the hypothalamus is thought to drive this, and is implicated in the cognitive and arousal symptoms.[30]

Major depressive disorder
SSRIs may directly depend on the increase of central serotonergic neurotransmission for their therapeutic effect, the same system that impacts cycles of sleep and wakefulness.[31] Research on the effects of light therapy on treating seasonal affective disorder suggests that light deprivation is related to decreased activity in the serotonergic system and to abnormalities in the sleep cycle, particularly insomnia. Exposure to light also targets the serotonergic system, providing more support for the important role this system may play in depression.[32] Sleep deprivation and light therapy both target the same brain neurotransmitter system and brain areas as antidepressant drugs, and are now used clinically to treat depression.[33] Light therapy, sleep deprivation and sleep time displacement (sleep phase advance therapy) are being used in combination quickly to interrupt a deep depression in hospitalized patients.[32] The hormone estrogen has been implicated in depressive disorders due to the increase in risk of depressive episodes after puberty, the antenatal period, and reduced rates after menopause.[34] Conversely, the premenstrual and postpartum periods of low estrogen levels are also associated with increased risk.[34] The use of estrogen has been under-researched, and although some small trials show promise in its use to prevent or treat depression, the evidence for its effectiveness is not strong.[34] Estrogen replacement therapy has been shown to be beneficial in improving mood in perimenopause, but it is unclear if it is merely the menopausal symptoms that are being reversed.[34] Other research has explored potential roles of molecules necessary for overall cellular functioning: cytokines and essential nutrients. Major depressive disorder is nearly identical to sickness behavior, the response of the body when the immune system is fighting an infection.[35] This raises the possility that depression can result from a maladaptive manifestation of sickness behavior as a result of abnormalities in circulating cytokines.[36][37][38] Deficiencies in certain essential dietary nutrients, particularly vitamin B12 and folic acid, have been associated with depression;[39] other agents such as the elements copper and magnesium,[40] and vitamin A have also been implicated.[41]

Depression may be related to the same brain mechanisms that control the cycles of sleep and wakefulness. Depression may be related to abnormalities in the circadian rhythm, or biological clock. For example, the REM stage of sleep, the one in which dreaming occurs, may be quick to arrive, and intense, in depressed people. REM sleep depends on decreased serotonin levels in the brain stem,[31] and is impaired by compounds, such as antidepressants, that increase serotoninergic tone in brain stem structures.[31] Overall, the serotonergic system is least active during sleep and most active during wakefulness. Prolonged wakefulness due to sleep deprivation activates serotonergic neurons, leading to processes similar to the therapeutic effect of antidepressants, such as the selective serotonin reuptake inhibitors (SSRIs). Depressed individuals can exhibit a significant lift in mood after a night of sleep deprivation.


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Major depressive disorder
An examination of depression in women indicates that vulnerability factors—such as early maternal loss, lack of a confiding relationship, responsibility for the care of several young children at home, and unemployment—can interact with life stressors to increase the risk of depression.[52] For older adults, the factors are often health problems, changes in relationships with a spouse or adult children due to the transition to a caregiving or care-needing role, the death of a significant other, or a change in the availability or quality of social relationships with older friends because of their own health-related life changes.[53] The understanding of depression has also received contributions from the psychoanalytic, existential, and humanistic branches of psychology. From the classical psychoanalytic perspective of Austrian psychiatrist Sigmund Freud, depression, or melancholia, may be related to interpersonal loss[54][55] and early life experiences.[56] Existential psychologists have connected depression to the lack of both meaning in the present[57] and a vision of the future.[58] [59] The founder of humanistic psychology, American psychologist Abraham Maslow, suggested that depression could arise when people are unable to attain their needs or to self-actualize, to realize their full potential.[60][61]

Various aspects of personality and its development appear to be integral to the occurrence and persistence of depression.[42] Although depressive episodes are strongly correlated with adverse events, a person’s characteristic style of coping may be correlated with their resilience.[43] Additionally, low self-esteem and self-defeating or distorted thinking are related to depression. Depression may be less likely to occur, as well as quicker to remit, among those who are religious.[44] It is not always clear which factors are causes or which are effects of depression; however, depressed persons who are able to make corrections in their thinking patterns often show improved mood and self-esteem.[45] American psychiatrist Aaron T. Beck developed what is now known as a cognitive model of depression in the early 1960s. He proposed three concepts which underlie depression: a triad of negative thoughts comprising cognitive errors about oneself, one’s world, and one’s future; recurrent patterns of depressive thinking, or schemas; and distorted information processing.[46] From these principles, he developed the structured technique of cognitive behavioral therapy.[47] According to American psychologist Martin Seligman, depression in humans is similar to learned helplessness in laboratory animals, who remain in unpleasant situations when they are able to escape, but do not because they initially learned they had no control.[48] Depressed individuals often blame themselves for negative events,[49] and—as reflected in a study of hospitalized adolescents with self-reported depression—those who do this may not take credit for positive outcomes.[50] This tendency is characteristic of a depressive attributional, or pessimistic explanatory style.[49] According to Albert Bandura, a Canadian social psychologist associated with social cognitive theory, depressed individuals have negative beliefs about themselves, based on experiences of failure, observing the failure of social models, a lack of social persuasion that they can succeed, and their own somatic and emotional states including tension and stress. These influences may result in a negative self-concept and a perceived lack of self-efficacy; that is, they do not believe they can influence events or achieve personal goals.[51]

Poverty and social isolation are associated with increased risk of psychiatric problems in general.[42] Child abuse (physical, emotional, sexual, or neglect) is also associated with increased risk of developing depressive disorders later in life.[62] Disturbances in family functioning, such as parental (particularly maternal) depression, severe marital conflict or divorce, death of a parent, or other disturbances in parenting are additional risk factors.[42] In adulthood, stressful life events are strongly associated with the onset of major depressive episodes;[63] a first episode is more likely to be immediately preceded by stressful life events than are recurrent ones.[64] The relationship between stressful life events and social support has been a matter of some debate; the lack of social support may increase the likelihood that life stress will lead to depression, or the absence of social support may constitute a form of strain


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that leads to depression directly.[65] There is evidence that neighborhood social disorder, for example, due to crime or illicit drugs, is a risk factor, and that a high neighborhood socioeconomic status, with better amenities, is a protective factor.[66] Adverse conditions at work, particularly demanding jobs with little scope for decision-making, are associated with depression, although diversity and confounding factors make it difficult to confirm that the relationship is causal.[67]

Major depressive disorder
"the direct physiological effects of a substance" because sedative hypnotic drugs such as alcohol and benzodiazepines increase the risk of a syndrome that is similar to major depression. This increased risk may be due in part to the effects of drugs on neurochemistry, such as decreased levels of serotonin and norepinephrine.[73][15] Alcoholism or excessive alcohol consumption significantly increases the risk of developing this syndrome.[74][75][76] Chronic use of benzodiazepines, a class of medication that is commonly used to treat insomnia, anxiety and muscular spasms, also increases the risk.[77] Chronic, severe depression can develop as a result of chronic use of benzodiazepines or as part of a protracted withdrawal syndrome.[15][78][79][80]

From the standpoint of evolutionary theory, major depression is hypothesized, in some instances, to increase an individual’s ability to reproduce. Evolutionary approaches to depression and evolutionary psychology posit specific mechanisms by which depression may have been genetically incorporated into the human gene pool, accounting for the high heritability and prevalence of depression by proposing that certain components of depression are adaptations,[68] such as the behaviors relating to attachment and social rank.[69] Current behaviors can be explained as adaptations to regulate relationships or resources, although the result may be maladaptive in modern environments.[70] From a counseling psychology viewpoint, the therapist may see depression, not as a biochemical illness or disorder, but as "a species-wide evolved suite of emotional programmes that are mostly activated by a perception, almost always over-negative, of a major decline in personal usefulness, that can sometimes be linked to guilt, shame or perceived rejection".[71] This suite may have manifested in aging hunters in humans’ foraging past, who were marginalized by their declining skills, and may continue to appear in alienated members of today’s society. The feelings of uselessness generated by such marginalization could hypothetically prompt support from friends and kin. Additionally, in a manner analogous to that in which physical pain has evolved to hinder actions that may cause further injury, "psychic misery" may have evolved to prevent hasty and maladaptive reactions to distressing situations.[72]

Clinical assessment
Further information: Rating scales for depression A diagnostic assessment may be conducted by a general practitioner, licensed clinical social worker, or by a psychiatrist or psychologist,[1] who records the person’s current circumstances, biographical history and current symptoms, and a family medical history to see if other family members have suffered from a mood disorder, and discuss the person’s alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person’s current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans.[1] Specialist mental health services are rare in rural areas, and thus diagnosis and management is largely left to primary care clinicians.[81] This issue is even more marked in developing countries.[82] The score on a rating scale alone is not sufficient to diagnose depression, but it provides an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis.[83] Several rating scales are used for this purpose.[83] Screening programs have been advocated to improve detection of depression, but there is evidence that they do not improve detection rates, treatment, or outcome.[84]

Drug use
See also: Substance induced mood disorder The DSM precludes a diagnosis of major depressive disorder for those presenting with


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Before diagnosing a major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease.[85] Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men.[86] Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer’s disease.[87] Depression is also a common initial symptom of dementia.[88] Cognitive testing and brain imaging can help distinguish depression from dementia.[89] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[90] No biological tests confirm major depression.[91] Investigations are not generally repeated for a subsequent episode unless there is a medical indication.

Major depressive disorder
depressive disorder, but lists very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.[96]

Major depressive episode
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[3] Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe. If the patient has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead.[97] Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[98] DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a major depressive episode develop.[99] The criteria have been criticized because they do not take into account any other aspects of the personal and social context in which depression can occur.[100] In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration:[101] excluded are a range of related diagnoses, including dysthymia which involves a chronic but milder mood disturbance,[102] Recurrent brief depression which involves briefer depressive episodes,[103][104] minor depressive disorder which involves only some of the symptoms of major depression,[105] and adjustment disorder with depressed mood which involves low mood resulting from a psychological response to an identifiable event or stressor.[106]

DSM-IV-TR and ICD-10 criteria
The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association’s revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), and the World Health Organization’s International Statistical Classification of Diseases and Related Health Problems (ICD-10) which uses the name recurrent depressive disorder.[92] The latter system is typically used in European countries, while the former is used in the US and many other non-European nations,[93] and the authors of both have worked towards conforming one with the other.[94] Major depressive disorder is classified as a mood disorder in DSM-IV-TR.[95] The diagnosis hinges on the presence of a single or recurrent major depressive episode.[3] Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Depressive disorder not otherwise specified is diagnosed if the depressive episode’s manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term Major

The DSM-IV-TR recognizes five further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:


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• is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.[107] • is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.[108] • is a rare and severe form of major depression involving disturbances of motor behavior and other symptoms. Here the person is mute and almost stuporose, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.[109] • (Mild mental and behavioral disorders associated with the puerperium, not elsewhere classified in ICD-10[110]) refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10–15% among new mothers, typically sets in within three months of labor, and lasts as long as three months.[111] • (SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.[112]

Major depressive disorder
person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression).[102] Adjustment disorder with depressed mood is a mood disturbance appearing 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 a major depressive episode.[106] Bipolar disorder, previously known as manic-depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.[113]

The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice for people under 18, while electroconvulsive therapy is only used as a last resort. Care is usually given on an outpatient basis, while treatment in an inpatient unit is considered if there is a significant risk to self or others. A significant number of recent studies have indicated that physical exercise has beneficial effects. Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.[114]

Psychotherapy can be delivered, to individuals or groups, by mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and psychiatric nurses. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[115] In children and young

Differential diagnoses
To confer major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a


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people under 18, medication should only be offered in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy.[116] Psychotherapy has been shown to be effective in older people.[117][118] Successful psychotherapy appears to reduce the recurrence of depression even after it has been terminated or replaced by occasional booster sessions. The most studied form of psychotherapy for depression is cognitive behavioral therapy (CBT), thought to work by teaching clients to learn a set of useful cognitive and behavioral skills. Earlier research suggested that CBT was not as effective as antidepressant medication; however, research in 1996 suggests that it can perform as well as antidepressants in patients with moderate to severe depression.[119] Overall, evidence shows CBT to be effective in depressed adolescents,[120] although one systematic review noted there was insufficient evidence for severe episodes.[121] Combining fluoxetine with CBT appeared to bring no additional benefit,[122][123] or, at the most, only marginal benefit.[124] Several variants have been used in depressed patients, most notably rational emotive behavior therapy,[125] and more recently mindfulness-based cognitive therapy.[126] Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. The therapy takes a structured course with a set number of weekly sessions (often 12) that focus on relationships with others. Therapy can be used to foster interpersonal skills that allow people to communicate more effectively and to reduce stress.[127] Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[128] is used by its practitioners to treat clients presenting with major depression.[129] A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[130] In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.[131] Logotherapy, a form of existential psychotherapy developed by Austrian psychiatrist Viktor Frankl, addresses the filling of an

Major depressive disorder
"existential vacuum" associated with feelings of futility and meaninglessness. This type of psychotherapy may be particularly useful for depressed adolescents.[132]

Prescription antidepressants are as effective as psychotherapy, although more patients cease medication than cease psychotherapy, most likely due to side effects from the medication. To find the most effective antidepressant medication with tolerable or fewest side effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50–75%, and it can take at least six to eight weeks from the start of medication to remission, when the patient is back to their normal self.[133] Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimise the chance of recurrence.[133] People with chronic depression may need to take medication indefinitely to avoid relapse.[1] The terms refractory depression or treatment-resistant depression are used to describe cases that do not respond to adequate courses of least two antidepressants.[134] Any antidepressant can cause low serum sodium levels (also called hyponatremia);[135] nevertheless, it has been reported more often with SSRIs.[136] Selective serotonin reuptake inhibitors (SSRIs), such as sertraline, escitalopram, fluoxetine, paroxetine, and citalopram are the primary medications prescribed owing to their effectiveness, relatively mild side effects, and because they are less toxic in overdose than other antidepressants.[136] Patients who do not respond to one SSRI can be switched to another, and this results in improvement in almost 50% of cases.[137] Another option is to switch to the atypical antidepressant bupropion.[138][139][140] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[141] However, venlafaxine is not recommended in the UK as a firstline treatment because of evidence suggesting its risks may outweigh benefits,[142] and it is specifically discouraged in children and adolescents.[143] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine can be used


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in such cases.[144] For adolescent depression, fluoxetine[143] and escitalopram[145] are the two recommended choices. Antidepressants have not been found to be beneficial in children.[146]

Major depressive disorder
to increase the effectiveness of antidepressant drugs, albeit offset by increased side effects.[154]

The effectiveness of antidepressants continues to be questioned. Their effectiveness has been shown to increase with the severity of the depression, and to reach clinical significance only in studies involving the most severely depressed, perhaps because the very severely depressed had a decreased response to the placebo effect rather than an increased response to the medication.[155] An editorial in the BMJ drew attention to bias in the publication of studies showing antidepressant efficacy compared to unpublished studies where the data did not support efficacy. Though these unpublished studies might have suffered methodological or other problems, the article called attention to the possibility that sponsor or journal bias might have inflated or created the apparent efficacy of antidepressants over placebo.[156] A black box warning was introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicidality in patients younger than 24 years old.[157]

Amitriptyline is a tricyclic antidepressant, so called because there are three rings in its molecular structure. Tricyclic antidepressants have more side effects than SSRIs and are usually reserved for the treatment of inpatients, for whom the tricyclic antidepressant amitriptyline, in particular, appears to be more effective.[147][148] Monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better tolerated agents of this class have been developed.[149]

Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a procedure whereby pulses of electricity are sent through the brain via two electrodes, usually one on each temple, to induce a seizure while the patient is under a short general anaesthetic. Hospital psychiatrists may recommend ECT for cases of severe major depression which have not responded to antidepressant medication or, less often, psychotherapy or supportive interventions.[158] ECT can have a quicker effect than antidepressant therapy and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has stopped eating and drinking, or where a patient is severely suicidal.[158] ECT is probably more effective than pharmacotherapy for depression in the immediate short-term,[159] although a landmark community-based study found much lower remission rates in routine practice.[160] Used on its own the relapse rate within the first six months is very high; early studies put the rate at around 50%,[161] while a more recent controlled trial found

Pharmacological augmentation
A doctor may add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance.[150] Medication with lithium salts has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[151] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[152] Addition of a thyroid hormone, triiodothyronine may work as well as lithium, even in patients with normal thyroid function.[153] Addition of atypical antipsychotics when the patient has not responded to an antidepressant is also known


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rates of 84% even with placebos.[162] The early relapse rate may be reduced by the use of psychiatric medications or further ECT[163][164] (although the latter is not recommended by some authorities[165]) but remains high.[166] Common initial adverse effects from ECT include short and long-term memory loss, disorientation and headache.[167] Although objective psychological testing shows memory disturbance after ECT has mostly resolved by one month post treatment, ECT remains a controversial treatment, and debate on the extent of cognitive effects and safety continues.[168][169]

Major depressive disorder
which are applied to the brain from outside the head. Multiple controlled studies support the use of this method in treatment-resistant depression; it has been approved for this indication in Europe, Canada, Australia, and the US.[182][183][184] rTMS appeared similarly effective for both uncomplicated depression and depression resistant to medication;[183] however, it was inferior to ECT in a side-by-side randomized trial.[185] Vagus nerve stimulation was approved by the FDA in the United States in 2005 for use in treatment-resistant depression,[186] although it failed to show short-term benefit in the only large double-blind trial when used as an adjunct on treatment-resistant patients;[187] a 2008 systematic review concluded that despite the promising results reported mainly in open studies, further clinical trials are needed to confirm its efficacy in major depression.[188] Poor diet or medical disorders leading to deficiency in certain nutrients have been linked to major depression disorder. Thus improved diet or correction of nutritional deficiency may be of value in some cases of major depression.[189]

Physical exercise
Physical exercise is recommended by U.K. health authorities,[170] and a systematic review of 23 studies indicated a "large clinical effect". Among these, three studies employing intention to treat analysis and other biasreducing measures were inconclusive.[171]

Over-the-counter compounds
St John’s wort is available over-the-counter as a herbal remedy in some parts of the world;[136][172] however, the evidence of its effectiveness for the treatment of major depression is varying and confusing. Its safety can be compromised by inconsistency in pharmaceutical quality and in the amounts of active ingredient in different preparations.[173] Further, it interacts with numerous prescribed medicines including antidepressants, and it can reduce the effectiveness of hormonal contraception.[174] The issue of efficacy of omega-3 fatty acids for major depression is controversial,[175] with controlled studies and metaanalyses supporting both positive[176][177] and negative conclusions.[178][179] Reviews of short-term clinical trials of S-adenosylmethionine (SAMe) indicate that it may be effective in treating major depression in adults.[180] A 2002 review reported that tryptophan and 5-hydroxytryptophan appear to be better than placebo, but it did not recommend their widespread use owing to lack of conclusive evidence on efficacy and safety, and generally preferred the use of safer antidepressants instead.[181]

Prevention and prognosis
A 2008 meta-analysis found that behavioral interventions are effective at preventing new onset depression.[190] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested, they may be able to reach their large target audience most efficiently through the Internet.[191] However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behaviorally oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. Additionally, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes; were provided by a combination of lay and professional workers; had a high-quality research design; reported attrition rates; and had a well-defined intervention.[192] Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10–15%

Other somatic treatments
Repetitive transcranial magnetic stimulation (rTMS) utilizes powerful magnetic fields


From Wikipedia, the free encyclopedia
reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder.[193] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[194] General population studies indicate around half those who have a major depressive episode (whether treated or not) recover and remain well, while 35% will have at least one more, and around 15% experience chronic recurrence.[195] Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.[196][197] Recurrence is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.

Major depressive disorder

Depression is a major cause of morbidity worldwide.[206] Lifetime prevalence varies widely, from 3% in Japan to 17% in the US. In most countries the number of people who would suffer from depression during their lives falls within an 8–12% range.[207][208] In North America the probability of having a major depressive episode within a year-long period is 3–5% for males and 8–10% for females.[209][210] Population studies have consistently shown major depression to be about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.[211] The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.[211] People are most likely to suffer their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.[212] The risk of major depression is increased with neurological conditions such as stroke, Parkinson’s disease, or multiple sclerosis and during the first year after childbirth.[213] It is also more common after cardiovascular illnesses, and is related more to a poor outcome than to a better one.[201][214] Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group.[215] Depression is often associated with unemployment and poverty.[216] Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the World Health Organization.[217] Delay or failure in seeking treatment after relapse, and the failure of health professionals to provide treatment, are two barriers to reducing disability.[218] The World Health Organization updated its report The global burden of disease in 2004. Their "Years Lost due to Disability", or YLD, is a measurement of the equivalent years of healthy life lost through time spent in states of less than full health, and they state that in all regions, "neuropsychiatric

Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying by suicide.[199] However, they also have a higher rate of dying from other causes,[200] being more susceptible to medical conditions such as heart disease.[201] Up to 60% of people who commit suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder.[202] The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women[203] (although suicide attempts are more frequent in women).[204] The estimate is substantially lower than a previously accepted figure of 15% which had been derived from older studies of hospitalized patients.[205]


From Wikipedia, the free encyclopedia
conditions are the most important causes of disability, accounting for around one third of YLD among adults aged 15 and over." Specifically, unipolar depressive disorders are the leading cause in both males and females, in high-income countries and in low- and middle-income countries.[219]

Major depressive disorder
down".[227] From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker’s Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.[228] The term also came in to use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[229] Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.[56] Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[230] Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic breakup, 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 loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively, but the ego itself is compromised.[54] The patient’s decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[55] He also emphasized early life experiences as a predisposing factor.[56] Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individual’s life, and argued that the term depression should be used instead of melancholia.[231] The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of

Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reports that 51% of those with major depression also suffer from lifetime anxiety.[220] Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts.[221] American neuroendocrinologist Robert Sapolsky similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.[222] There are increased rates of alcohol and drug abuse and particularly dependence,[223] and around a third of individuals diagnosed with attention-deficit hyperactivity disorder develop comorbid depression.[224] Post-traumatic stress disorder and depression often co-occur.[1] Depression and pain often co-occur. One or more pain symptoms is present in 65% of depressed patients, and anywhere from five to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome worsens.[225]

The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.[226] It was a similar but far broader concept than today’s depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.[56] The term depression itself was derived from the Latin verb deprimere, "to press


From Wikipedia, the free encyclopedia
manic-depressive psychosis within Major affective disorders.[232] In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.[233] The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria),[234] and was incorporated in to the DSM-III in 1980.[235] To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes.[235][236] The ancient idea of melancholia still survives in the notion of a melancholic subtype. The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia.[237][238] There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.[239]

Major depressive disorder
feelings of powerlessness, and emotional struggle.[241][242] The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatize emotional depression (although since the early 1980s the Chinese denial of depression may have modified drastically).[243] Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression "medicalizes" sadness or misery.[244][245] Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease.[246] There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs.[247] American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as "it brings refuge, limitation, focus, gravity, weight, and humble powerlessness."[248] Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonizing a soulful state of being. Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley,[250] AmericanBritish writer Henry James,[251] and American president Abraham Lincoln.[252] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen[253] and American playwright and novelist Tennessee Williams.[254] Some pioneering psychologists, such as Americans William James[255][256] and John B. Watson,[257] dealt with their own depression. There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian

Sociocultural aspects
See also: List of people with depression Even today, people’s conceptualizations of depression vary widely, both within and among cultures. "Because of the lack of scientific certainty," one commentator has observed, "the debate over depression turns on questions of language. What we call it—’disease,’ ’disorder,’ ’state of mind’—affects how we view, diagnose, and treat it."[240] There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce


From Wikipedia, the free encyclopedia

Major depressive disorder
and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996;[265] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[266]

See also
• Types of psychological depression

[1] ^ "Depression" (PDF). National Institute of Mental Health (NIMH). publications/depression/ nimhdepression.pdf. Retrieved on 2008-09-07. [2] Hays RD, Wells KB, Sherbourne CD, et al. (1995). "Functioning and well-being outcomes of patients with depression compared with chronic general medical illnesses". Archives of General Psychiatry 52 (1): 11–19. PMID 7811158. [3] ^ American Psychiatric Association 2000a, p. 349 [4] ^ American Psychiatric Association 2000a, p. 350 [5] Patel V, Abas M, Broadhead J et al. (February 2001). "(fulltext) Depression in developing countries: Lessons from Zimbabwe". BMJ 322 (7284): 482–84. doi:10.1136/bmj.322.7284.482. 7284/482 (fulltext). Retrieved on 2008-10-05. [6] Faculty of Psychiatry of Old Age, NSW Branch, RANZCP; Kitching D Raphael B (2001) (PDF). Consensus Guidelines for Assessment and Management of Depression in the Elderly. North Sydney, New South Wales: NSW Health Department. pp. 2. ISBN 0-7347-33410. cmh/publications/depression/ depression_elderly.pdf. [7] American Psychiatric Association 2000a, p. 412 [8] American Psychiatric Association 2000a, p. 354 [9] Department of Health and Human Services (1999). "The fundamentals of mental health and mental illness" (PDF). Mental Health: A Report of the Surgeon

American president Abraham Lincoln appears to have had at least two major depressive episodes.[249] times.[258][259] British literature gives many examples of reflections on depression.[260] English philosopher John Stuart Mill experienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridge’s "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear."[261][262] English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression,[263] and it was subsequently popularized by depression sufferer former British Prime Minister Sir Winston Churchill.[263] Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly.[264] In the UK, the Royal College of Psychiatrists


From Wikipedia, the free encyclopedia
General. library/mentalhealth/pdfs/c2.pdf. Retrieved on 2008-11-11. [10] ^ Caspi A, Sugden K, Moffitt TE, et al. (2003). "Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene". Science 301: 386–89. doi:10.1126/ science.1083968. PMID 12869766. [11] Haeffel GJ; Getchell M; Koposov RA; Yrigollen CM; DeYoung CG; af Klinteberg B; et al. (2008). "Association between polymorphisms in the dopamine transporter gene and depression: Evidence for a gene-environment interaction in a sample of juvenile detainees" (PDF). Psychological Science. Haeffel%20et%20al.,%202008.pdf. Retrieved on 2008-11-11. [12] Slavich GM (September 2004). "Deconstructing depression: A diathesisstress perspective". APS Observer. observer/getArticle.cfm?id=1640. Retrieved on 2008-11-11. [13] Kendler KS, Gatz M, Gardner CO, Pedersen NL (January 2006). "A Swedish national twin study of lifetime major depression". American Journal of Psychiatry 163 (1): 109–14. doi:10.1176/ appi.ajp.163.1.109. PMID 16390897. [14] Schuckit MA, Tipp JE, Bergman M, Reich W, Hesselbrock VM, Smith TL (July 1997). "Comparison of induced and independent major depressive disorders in 2,945 alcoholics". Am J Psychiatry 154 (7): 948–57. PMID 9210745. pmidlookup?view=long&pmid=9210745. [15] ^ Professor Heather Ashton (2002). "Benzodiazepines: How They Work and How to Withdraw". bzcha03.htm. [16] Barlow 2005, p. 226 [17] Shah N, Eisner T, Farrell M, Raeder C (July/August 1999). "An overview of SSRIs for the treatment of depression" (PDF). Journal of the Pharmacy Society of Wisconsin. professional/pharmaco/depression.pdf. Retrieved on 2008-11-10. [18] ^ Nutt DJ (2008). "Relationship of neurotransmitters to the symptoms of major depressive disorder". Journal of

Major depressive disorder
Clinical Psychiatry 69 Suppl E1: 4–7. PMID 18494537. [19] Hirschfeld RM (2000). "History and evolution of the monoamine hypothesis of depression". Journal of Clinical Psychiatry 61 Suppl 6: 4–6. PMID 10775017. [20] Delgado PL (2000). "Depression: The case for a monoamine deficiency". Journal of Clinical Psychiatry 61 Suppl 6: 7–11. PMID 10775018. [21] Lacasse J, Leo J (2005). "Serotonin and depression: A disconnect between the advertisements and the scientific literature". PLoS Med 2 (12): e392. doi:10.1371/journal.pmed.0020392.g001. PMID 16268734. ?request=get-document&doi=10.1371/ journal.pmed.0020392. Retrieved on 2008-10-30. [22] Videbech, P and Ravnkilde (2004). "Hippocampal volume and depression: A meta-analysis of MRI studies". American Journal of Psychiatry 161: 1957–66.. PMID 15514393. [23] Videbech, P (1997). "MRI findings in patients with affective disorder: a metaanalysis". Acta Psychiatrica Scandinavica 96 (3): 157–68. doi:10.1111/ j.1600-0447.1997.tb10146.x. [24] Herrmann LL, Le Masurier M, Ebmeier KP (2008). "White matter hyperintensities in late life depression: a systematic review". Journal of Neurology, Neurosurgery, and Psychiatry 79: 619–24. doi:10.1136/ jnnp.2007.124651. PMID 17717021. [25] Mayberg H (July 6, 2007). "Brain pathway may underlie depression". Scientific American 17 (4): 26–31. article.cfm?id=brain-pathway-mayunderlie-depression. Retrieved on 2008-09-13. [26] Sheline YI, Gado MH, Kraemer HC (2003). "Untreated depression and hippocampal volume loss". American Journal of Psychiatry 160: 1516–18. doi:10.1176/appi.ajp.160.8.1516. PMID 12900317. [27] Duman RS, Heninger GR, Nestler EJ (1997). "A molecular and cellular theory of depression". Archives of General


From Wikipedia, the free encyclopedia

Major depressive disorder

"From inflammation to sickness and Psychiatry 54 (7): 597–606. PMID depression: when the immune system 9236543. subjugates the brain". Nat Rev Neurosci. [28] Drevets WC, Savitz J, Trimble M (August 9: 46-56 PubMed 2008). "The subgenual anterior cingulate [38] Maes, M. (2008) "The cytokine cortex in mood disorders". CNS hypothesis of depression: inflammation, Spectrums 13 (8): 663–81. PMID oxidative & nitrosative stress (IO&NS) 18704022. and leaky gut as new targets for [29] Sen S, Duman R, Sanacora G (September adjunctive treatments in depression". 2008). "Serum brain-derived Neuro Endocrinol Lett. 29: 287-291 neurotrophic factor, depression, and PubMed antidepressant medications: Meta[39] Coppen A, Bolander-Gouaille C (January analyses and implications". Biological 2005). "Treatment of depression: time to Psychiatry 64 (6): 527–32. doi:10.1016/ consider folic acid and vitamin B12". j.biopsych.2008.05.005. PMID Journal of Psychopharmacology 19 (1): 18571629. 59–65. PMID 15671130. [30] Monteleone P (2001). "(abstract) [40] Siwek M, Wróbel A, Dudek D, Nowak G, Endocrine disturbances and psychiatric Zieba A (September-October 2005). "The disorders". Current Opinion in Psychiatry role of copper and magnesium in the (Lippincott Williams & Wilkins, Inc.) 14 pathogenesis and treatment of affective (6): 605–10. ISSN 0951–7367. disorders". Psychiatria Polska 39 (5): 911–20. PMID 16358591. copsych/ [41] Bremner JD, McCaffery P (February abstract.00001504-200111000-00020.htm;jsessionid=JWdDsz1T6hhjhpsR47xrbhpTjhxhpdS64Yh8Qzp 2008). "The neurobiology of retinoic acid (abstract). in affective disorders". Progress in [31] ^ Adrien J. (October 2003). Neuropsychopharmacology and "Neurobiological bases for the relation Biological Psychiatry 32 (2): 315–31. between sleep and depression". Sleep PMID 17707566. Medicine Review 6 (5): 341–51. PMID [42] ^ Raphael B (2000). "Unmet Need for 12531125. Prevention". in Andrews G, Henderson S [32] ^ Terman M (December 2007). "Evolving (eds). Unmet Need in applications of light therapy". Sleep Psychiatry:Problems, Resources, Medicine Review 11 (6): 497–507. PMID Responses. Cambridge University Press. 17964200. pp. 138–39. ISBN 0-521-66229-X. [33] Benedetti F, Barbini B, Colombo C, [43] Sadock 2002, p. 541 Smeraldi E (October 2007). [44] Dein, Simon (2006). "Religion, "Chronotherapeutics in a psychiatric spirituality and depression: implications ward". Sleep Medicine Review 11 (6): for research and treatment" (PDF). 509–22. PMID 17689120. Primary Care and Community Psychiatry [34] ^ Cutter WJ, Norbury R, Murphy DG 11 (2): 67–72. doi:10.1185/ (July 2003). "Oestrogen, brain function, 135525706X121110. and neuropsychiatric disorders". Journal of Neurology, Neurosurgery and headeradmin/upload/0178web2.pdf. Psychiatry 74 (7): 837–40. PMID Retrieved on 2008-11-21. 12810759. PMC: 1738534. [45] Warman DM, Beck AT (June 2003). "About treatment and supports: pmidlookup?view=long&pmid=12810759. Cognitive behavioral therapy". National [35] Hart, B. L. (1988) "Biological basis of the Alliance on Mental Illness (NAMI) behavior of sick animals". Neurosci website. Biobehav Rev. 12: 123-137. PubMed Template.cfm?Section=About_Treatments_and_Supp [36] Charlton, B. G. (2000) "The malaise ContentManagement/ theory of depression: major depressive ContentDisplay.cfm&ContentID=7952. disorder is sickness behavior and Retrieved on 2008-10-17. antidepressants are analgesic". Med [46] Beck 1987, pp. 10–15 Hypotheses. 54: 126-130 PubMed [47] Beck 1987, p. 3 [37] Dantzer, R., O’Connor, J. C., Freund, G. G., Johnson, R. W. Kelley, K. W. (2008)


From Wikipedia, the free encyclopedia
[48] Seligman, M (1975). "Depression". Helplessness: On depression, development and death. San Francisco, CA, USA: WH Freeman. pp. 75–106. ISBN 0716707519. [49] ^ Barlow 2005, pp. 230–32 [50] Pinto A, Francis G (1993). "Cognitive correlates of depressive symptoms in hospitalized adolescents". Adolescence 28 (111): 661–72. PMID 8237551. [51] Bandura A (1998). "Self-Efficacy". in Friedman H. Encyclopedia of mental health. San Diego: Academic Press. ISBN 0122266765. mfp/BanEncy.html. Retrieved on 2008-08-17. [52] Brown GW, Harris TO (2001) [1978]. Social Origins of Depression: A Study of Psychiatric Disorder in Women. Routledge. ISBN 0-415-20268-X. [53] Hinrichsen GA, Emery EE (2006). "Interpersonal factors and late-life depression" (Subscription required). Clinical Psychology: Science and Practice 12 (3): 264–75. journal/118706655/ abstract?CRETRY=1&SRETRY=0. [54] ^ Carhart-Harris RL, Mayberg HS, Malizia AL, Nutt D (2008). "Mourning and melancholia revisited: Correspondences between principles of Freudian metapsychology and empirical findings in neuropsychiatry". Annals of General Psychiatry 7: 9. doi:10.1186/ 1744-859X-7-9. PMID 18652673. [55] ^ Freud, S (1984). "Mourning and Melancholia". in Richards A (ed.). 11.On Metapsychology: The Theory of Psycholoanalysis. Aylesbury, Bucks: Pelican. pp. 245–69. ISBN 0-14-021740-1. [56] ^ Radden, J (March 2003). "Is this dame melancholy? Equating today’s depression and past melancholia". Philosophy, Psychiatry, & Psychology 10 (1): 37–52. doi:10.1353/ppp.2003.0081. philosophy_psychiatry_and_psychology/ v010/10.1radden01.html. [57] Frankl VE (2000). Man’s search for ultimate meaning. New York, NY, USA: Basic Books. pp. 139–40. ISBN 0738203548. [58] Geppert CMA (May 2006). "Damage control". Psychiatric Times.

Major depressive disorder article/10168/51281. Retrieved on 2008-11-08. [59] May 1994, p. 133 [60] Boeree, CG (1998). "Abraham Maslow: Personality Theories" (PDF). Psychology Department, Shippensburg University. pt_maslow.pdf. Retrieved on 2008-10-27. [61] Maslow A (1971). The Farther Reaches of Human Nature. New York, NY, USA: Viking Books. pp. 318. ISBN 0670308536. [62] Heim C, Newport DJ, Mletzko T, Miller AH, Nemeroff CB (July 2008). "The link between childhood trauma and depression: insights from HPA axis studies in humans". Psychoneuroendocrinology 33 (6): 693–710. doi:10.1016/ j.psyneuen.2008.03.008. PMID 18602762. [63] Kessler, RC (1997). "The effects of stressful life events on depression". Annual revue of Psychology 48: 191–214. PMID 9046559. [64] Sadock 2002, p. 540 [65] Vilhjalmsson R (1993). "Life stress, social support and clinical depression: A reanalysis of the literature". Social Science & Medicine 37: 331–42. PMID 8356482. [66] Kim D. (2008) Blues from the Neighborhood? Neighborhood Characteristics and Depression. Epidemiol Rev Aug 27 PMID 18753674 [67] Bonde JP (July 2008). "Psychosocial factors at work and risk of depression: A systematic review of the epidemiological evidence". Journal of Occupational and Environmental Medicine 65: 438–45. doi:10.1136/oem.2007.038430. PMID 18417557. [68] Panksepp J, Moskal JR, Panksepp JB, Kroes RA (December 2002). "Comparative approaches in evolutionary psychology: Molecular neuroscience meets the mind" (PDF). Neuroendocrinology Letters 23 (Supplement 4): 105–15. PMID 12496741. 23s4/NEL231002R11_Panksepp_.pdf. [69] Sloman L, Gilbert P, Hasey G (April 2003). "Evolved mechanisms in depression: The role and interaction of


From Wikipedia, the free encyclopedia

Major depressive disorder

attachment and social rank in depressions". J Stud Alcohol Drugs 68 depression". Journal of Affective (6): 805–12. PMID 17960298. Disorders 74 (2): 107–21. doi:10.1016/ [77] Semple, David; Roger Smyth, Jonathan S0165-0327(02)00116-7. PMID Burns, Rajan Darjee, Andrew McIntosh 12706512. (2007) [2005]. "13". Oxford Handbook of Psychiatry. United Kingdom: Oxford pii/S0165032702001167. University Press. p. 540. ISBN [70] >Tooby, J, Cosmides, L (2005) (PDF). 0198527837. Conceptual foundations of evolutionary [78] Collier, Judith; Longmore, Murray psychology. In D. M. Buss (Ed.), The (2003). "4". in Scally, Peter. Oxford Handbook of Evolutionary Psychology. Handbook of Clinical Specialties (6 ed.). Hoboken, NJ: Wiley & Sons. pp. 5-67. Oxford University Press. p. 366. ISBN 978-0198525189. papers/bussconceptual05.pdf. [79] Ashton CH (March 1995). "Protracted [71] Carey TJ (2005). "Evolution, depression Withdrawal From Benzodiazepines: The and counselling". Counselling Psychology Post-Withdrawal Syndrome". Psychiatric Quarterly 18 (3): 215–22. doi:10.1080/ Annals ( 25 (3): 174–179. 09515070500304508. [80] Professor Heather Ashton (2004). routledg/ccpq/2005/00000018/00000003/ "Protracted Withdrawal Symptoms From art00005. Benzodiazepines". Comprehensive [72] Mashman, RC (1997). "An evolutionary Handbook of Drug & Alcohol Addiction. view of psychic misery". Journal of Social [81] Kaufmann IM (September 1, 1993). Behaviour & Personality 12: 979–99. "Rural psychiatric services. A ISSN 0886-1641. collaborative model". Canadian Family [73] Berber MJ (November 1999). "Pharmacological treatment of Physician 39: 1957–61. PMID 8219844. depression. Consulting with Dr Oscar" [82] "Call for action over Third World depression". BBC News (Health). British (PDF). Can Fam Physician 45: 2663–8. Broadcasting Corporation (BBC). PMID 10587774. PMC: 2328680. November 1, 1999. picrender.fcgi?artid=2328680&blobtype=pdf. 492941.stm. Retrieved on 2008-10-11. [74] Fergusson DM, Boden JM, Horwood LJ [83] ^ Sharp LK, Lipsky MS (September (March 2009). "Tests of causal links 2002). "Screening for depression across between alcohol abuse or dependence the lifespan: a review of measures for and major depression". Arch. Gen. use in primary care settings". American Psychiatry 66 (3): 260–6. doi:10.1001/ family physician 66 (6): 1001–8. PMID archgenpsychiatry.2008.543. PMID 12358212. 19255375. [84] Gilbody S, House AO, Sheldon TA (2005). cgi/ "Screening and case finding instruments pmidlookup?view=long&pmid=19255375. for depression". Cochrane Database of [75] Falk DE, Yi HY, Hilton ME (April 2008). Systematic Reviews (4). doi:10.1002/ "Age of onset and temporal sequencing 14651858.CD002792.pub2. of lifetime DSM-IV alcohol use disorders relative to comorbid mood and anxiety ab002792.html. disorders". Drug Alcohol Depend 94 [85] Dale J, Sorour E, Milner G (2008). "Do (1-3): 234–45. doi:10.1016/ psychiatrists perform appropriate j.drugalcdep.2007.11.022. PMID physical investigations for their patients? 18215474. A review of current practices in a general psychiatric inpatient and pii/S0376-8716(07)00499-1. outpatient setting". Journal of Mental [76] Schuckit MA, Smith TL, Danko GP, et al Health 17 (3): 293–98. doi:10.1080/ (November 2007). "A comparison of 09638230701498325. factors associated with substance[86] Orengo C, Fullerton G, Tan R (2004). induced versus independent "Male depression: A review of gender


From Wikipedia, the free encyclopedia
concerns and testosterone therapy". Geriatrics 59 (10): 24–30. PMID 15508552. [87] Reid LM, Maclullich AM (2006). "Subjective memory complaints and cognitive impairment in older people". Dementia and geriatric cognitive disorders 22 (5–6): 471–85. doi:10.1159/ 000096295. PMID 17047326. [88] Katz IR (1998). "Diagnosis and treatment of depression in patients with Alzheimer’s disease and other dementias". The Journal of clinical psychiatry 59 Suppl 9: 38–44. PMID 9720486. [89] Wright SL, Persad C (December 2007). "Distinguishing between depression and dementia in older persons: Neuropsychological and neuropathological correlates". Journal of geriatric psychiatry and neurology 20 (4): 189–98. doi:10.1177/ 0891988707308801. PMID 18004006. [90] Sadock 2002, p. 108 [91] Sadock 2002, p. 260 [92] "ICD-10:". icd/icd10online/?gf30.htm+f33. Retrieved on 2008-11-08. [93] Sadock 2002, p. 288 [94] American Psychiatric Association 2000a, p. xxix [95] American Psychiatric Association 2000a, p. 345 [96] "Mood (affective) disorders". ICD-10, Chapter V, Mental and behavioural disorders. World Health Organization (WHO). 2004. classifications/apps/icd/icd10online2005/ fr-icd.htm?gf30.htm. Retrieved on 2008-10-19. [97] American Psychiatric Association 2000a, p. 372 [98] Parker 1996, p. 173 [99] American Psychiatric Association 2000a, p. 352 [100] akefield JC, Schmitz MF, First MB, W Horwitz AV (April 2007). "Extending the bereavement exclusion for major depression to other losses: Evidence from the National Comorbidity Survey". Archives of General Psychiatry 64 (4): 433–40. doi:10.1001/archpsyc.64.4.433. PMID 17404120. Lay

Major depressive disorder
summary – The Washington Post (2007-04-03). [101] endler KS, Gardner CO (February 1, K 1998). "Boundaries of major depression: An evaluation of DSM-IV criteria". American Journal of Psychiatry 155 (2): 172–77. PMID 9464194. content/full/155/2/172. [102] Sadock 2002, p. 552 ^ [103] merican Psychiatric Association 2000a, A p. 778 [104] arta MG, Altamura AC, Hardoy MC, et C al. (2003). "Is recurrent brief depression an expression of mood spectrum disorders in young people?". European Archives of Psychiatry and Clinical Neuroscience 253 (3): 149–53. doi:10.1007/s00406-003-0418-5. [105] apaport MH, Judd LL, Schettler PJ, et R al. (2002). "A descriptive analysis of minor depression". American Journal of Psychiatry 159 (4): 637–43. doi:10.1176/ appi.ajp.159.4.637. PMID 11925303. [106] American Psychiatric Association ^ 2000a, p. 355 [107] merican Psychiatric Association 2000a, A pp. 419–20 [108] merican Psychiatric Association 2000a, A pp. 421–22 [109] merican Psychiatric Association 2000a, A pp. 417–18 [110]ICD-10:". " icd/icd10online/?gf50.htm+f530. Retrieved on 2008-11-06. [111] onacs, Ruta M (December 4, 2007). N "Postpartum depression". eMedicine. topic3408.htm. Retrieved on 2008-10-30. [112] merican Psychiatric Association 2000a, A p. 425 [113] kiskal HS, Benazzi F (May 2006). "The A DSM-IV and ICD-10 categories of recurrent [major] depressive and bipolar II disorders: Evidence that they lie on a dimensional spectrum". Journal of Affective Disorders 92 (1): 45–54. doi:10.1016/j.jad.2005.12.035. PMID 16488021. [114] atel V, Araya R, Bolton P et al. (April P 2004). "(fulltext) Editorial: Treating depression in the developing world" (Subscription required). Tropical Medicine & International Health 9 (5):


From Wikipedia, the free encyclopedia
539–41. doi:10.1111/ j.1365-3156.2004.01243.x. HTMLSTART?CRETRY=1&SRETRY=0 (fulltext). Retrieved on 2008-10-05. [115] hase, ME (1999). "When are T psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". Psychiatric Quarterly 70 (4): 333–46. doi:10.1023/ A:1022042316895. PMID 10587988. [116] ICE (2005). NICE guidelines: N Depression in children and adolescents. London: NICE. pp. 5. ISBN 1-84629-074-0. [117] ilson KC, Mottram PG, Vassilas CA W (January 2008). "Psychotherapeutic treatments for older depressed people". Cochrane Database of Systematic Reviews 23 (1): CD004853. PMID 18254062. [118] uijpers P, van Straten A, Smit F C (December 2006). "Psychological treatment of late-life depression: a metaanalysis of randomized controlled trials". International Journal of Geriatric Psychiatry 21 (12): 1139–49. PMID 16955421. [119] oth, Anthony; Fonagy, Peter (2005) R [1996]. What Works for Whom? Second Edition: A Critical Review of Psychotherapy Research. Guilford Press. pp. 78. ISBN 159385272X. [120] lein, Jesse (2008). "Review: Cognitive K behavioural therapy for adolescents with depression". Evidence-Based Mental Health 11: 76. content/full/11/3/76. Retrieved on 2008-11-27. [121] arrington R, Whittaker J, Shoebridge P, H Campbell F (May 1998). "Systematic review of efficacy of cognitive behaviour therapies in childhood and adolescent depressive disorder". BMJ 325 (7358): 229–30. doi:10.1136/bmj.325.7358.229. PMID 9596592. [122] oodyer I, Dubicka B, Wilkinson P, et al. G (July 2007). "Selective serotonin reuptake inhibitors (SSRIs) and routine specialist care with and without cognitive behaviour therapy in adolescents with major depression: Randomised controlled trial". BMJ 335 (7611): 142. doi:10.1136/ bmj.39224.494340.55. PMID 17556431.

Major depressive disorder
[123] oodyer IM, Dubicka B, Wilkinson P, et G al. (May 2008). "A randomised controlled trial of cognitive behaviour therapy in adolescents with major depression treated by selective serotonin reuptake inhibitors. The ADAPT trial". Health Technology Assessment 12 (14): 1–80. PMID 18462573. execsumm/summ1214.htm. [124] omino ME, Burns BJ, Silva SG, et al. D (May 2008). "Cost-effectiveness of treatments for adolescent depression: Results from TADS". American Journal of Psychiatry 165 (5): 588–96. doi:10.1176/ appi.ajp.2008.07101610. PMID 18413703. [125] eck 1987, p. 10 B [126] oelho HF, Canter PH, Ernst E C (December 2007). "Mindfulness-based cognitive therapy: Evaluating current evidence and informing future research". Journal of Consulting and Clinical Psychology 75 (6): 1000–05. doi:10.1037/ 0022-006X.75.6.1000. PMID 18085916. [127] eissman MM, Markowitz JC, Klerman W GL (2000). Comprehensive Guide to Interpersonal Psychotherapy. New York: Basic Books. ISBN 0-465-09566-6. (Page number needed) [128] woretzky J (1997). Psychology. Pacific D Grove, CA, USA: Brooks/Cole Pub. Co. pp. 602. ISBN 0-314-20412-1. [129] oidge N, Simon B, Lancee WJ, et al. D (2002). "Psychoanalytic patients in the US, Canada, and Australia: II. A DSM-IIIR validation study". Journal of the American Psychoanalytic Association 50 (2): 615–27. doi:10.1177/ 00030651020500021101. PMID 12206545. [130] arlow 2005, p. 20 B [131] e Maat S, Dekker J, Schoevers R, et al. d (June 2007). "Short Psychodynamic Supportive Psychotherapy, antidepressants, and their combination in the treatment of major depression: A mega-analysis based on three Randomized Clinical Trials". Depression and Anxiety 25: 565. doi:10.1002/ da.20305. PMID 17557313. [132] lair RG (October 2004). "Helping older B adolescents search for meaning in depression". Journal of Mental Health Counseling. articles/mi_hb1416/is_4_26/


From Wikipedia, the free encyclopedia

Major depressive disorder

ai_n29132028/pg_1?tag=artBody;col1. [141] apakostas GI, Thase ME, Fava M, P Retrieved on 2008-11-06. Nelson JC, Shelton RC (December 2007). [133] Karasu TB, Gelenberg A, Merriam A, ^ "Are antidepressant drugs that combine Wang P (April 2000). Practice Guideline serotonergic and noradrenergic for the Treatment of Patients With Major mechanisms of action more effective Depressive Disorder (Second Edition). than the selective serotonin reuptake American Psychiatric Association. pp. inhibitors in treating major depressive 1–78. doi:10.1176/ disorder? A meta-analysis of studies of appi.books.9780890423363.48690. newer agents". Biological Psychiatry 62 (11): 1217–27. doi:10.1016/ pracGuide/ j.biopsych.2007.03.027. PMID loadGuidelinePdf.aspx?file=MDD2e_05-15-06. 17588546. [134] ijeratne, Chanaka, Sachdev, Perminder W [142] rof Gordon Duff (31 May 2006.). "The P (2008). "Treatment-resistant depression: Medicines and Healthcare products Critique of current approaches". Regulatory Agency (MHRA)". Australian and New Zealand Journal of Psychiatry 42: 751–62. PMID 18696279. idcplg?IdcService=GET_FILE&dDocName=CON2023 [135] almer B, Gates J, Lader M (2003). P [143] Depression in children and young ^ "Causes and Management of people: Identification and management Hyponatremia". The Annals of in primary, community and secondary care. NHS National Institute for Health Pharmacotherapy 37 (11): 1694–702. and Clinical Excellence. September doi:10.1345/aph.1D105. PMID 2005. 14565794. [144] ayers AG, Baldwin DS (December M [136] Royal Pharmaceutical Society of Great ^ 2005). "Antidepressants and their effect Britain 2008, p. 204 on sleep". Human Psychopharmacology [137] hooley MA, Simon GE (2000). W "(abstract) Managing Depression in 20 (8): 533–59. doi:10.1002/hup.726. Medical Outpatients". New England PMID 16229049. [145]Lexapro Prescribing Information for the " Journal of Medicine 343: 1942–50. PMID U.S." (PDF). Forest Laboratories. March 11136266. 2009. content/short/343/26/1942 (abstract). lexapro_pi.pdf. Retrieved on 2009-04-09. Retrieved on 2008-11-11. [146] sapakis EM, Soldani F, Tondo L, T [138] isook S, Rush AJ, Haight BR, Clines DC, Z Baldessarini RJ (July 2008). "Efficacy of Rockett CB (2006). "Use of bupropion in antidepressants in juvenile depression: combination with serotonin reuptake meta-analysis". Br J Psychiatry 193 (1): inhibitors". Biological Psychiatry 59 (3): 10–7. doi:10.1192/bjp.bp.106.031088. 203–10. doi:10.1016/ PMID 18700212. j.biopsych.2005.06.027. PMID [147] uaiana G., Barbui C., Hotopf M. (July G 16165100. 2007). "Amitriptyline for depression.". [139] ush AJ, Trivedi MH, Wisniewski SR, et R al. (2006). "Bupropion-SR, sertraline, or Cochrane Database Syst Review 18 (3). venlafaxine-XR after failure of SSRIs for PMID 9597346. depression". New England Journal of [148] nderson IM (April 2000). "Selective A serotonin reuptake inhibitors versus Medicine 354 (12): 1231–42. tricyclic antidepressants: A meta-analysis doi:10.1056/NEJMoa052963. PMID of efficacy and tolerability". Journal of 16554525. [140] rivedi MH, Fava M, Wisniewski SR, T Affective Disorders 58 (1): 19–36. Thase ME, Quitkin F, Warden D, Ritz L, doi:10.1016/S0165-0327(99)00092-0. Nierenberg AA, Lebowitz BD, Biggs MM, PMID 10760555. Luther JF, Shores-Wilson K, Rush AJ (2006). "Medication augmentation after pii/S0165-0327(99)00092-0. the failure of SSRIs for depression". New [149] rishnan KR (2007). "Revisiting K monoamine oxidase inhibitors". Journal England Journal of Medicine 354 (12): 1243–52. doi:10.1056/NEJMoa052964. of Clinical Psychiatry 68 Suppl 8: 35–41. PMID 16554526. PMID 17640156.


From Wikipedia, the free encyclopedia
[150] alenstein M, McCarthy JF, Austin KL, V Greden JF, Young EA, Blow FC (2006). "What happened to lithium? Antidepressant augmentation in clinical settings". American Journal of Psychiatry 163 (7): 1219–25. doi:10.1176/ appi.ajp.163.7.1219. PMID 16816227. [151] schor T, Bauer M (2006). "Efficacy and B mechanisms of action of lithium augmentation in refractory major depression". Current Pharmaceudical Design 12 (23): 2985-92. PMID 16918427. [152] uzzetta F, Tondo L, Centorrino F, G Baldessarini RJ (March 2007). "Lithium treatment reduces suicide risk in recurrent major depressive disorder". Journal of Clinical Psychiatry 68 (3): 380–83. PMID 17388706. [153] ierenberg AA, Fava M, Trivedi MH, N Wisniewski SR, Thase ME, McGrath PJ, Alpert JE, Warden D, Luther JF, Niederehe G, Lebowitz B, Shores-Wilson K, Rush AJ (2006). "A comparison of lithium and T(3) augmentation following two failed medication treatments for depression: A STAR*D report". American Journal of Psychiatry 163 (9): 1519–30. doi:10.1176/appi.ajp.163.9.1519. PMID 16946176. [154] ender KJ (2008-02-01). "Evidence B Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times". Psychiatric Times. article/10168/1147436. Retrieved on 2008-08-06. [155] irsch I, Deacon BJ, Huedo-Medina TB, K Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial severity and antidepressant benefits: A meta-analysis of data submitted to the Food and Drug Administration". PLoS Med. 5 (2): e45. doi:10.1371/journal.pmed.0050045. PMID 18303940. PMC: 2253608. ?request=get-document&doi=10.1371/ journal.pmed.0050045&ct=1. [156] urner EH, Matthews AM, Linardatos E, T Tell RA, Rosenthal R (January 2008). "Selective publication of antidepressant trials and its influence on apparent efficacy". New England Journal of Medicine 358 (3): 252–60. doi:10.1056/ NEJMsa065779. PMID 18199864.

Major depressive disorder 358/3/252. [157]FDA Proposes New Warnings About " Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications" (htm). FDA. 2007-05-02. 2007/NEW01624.html. Retrieved on 2008-05-29. [158] American Psychiatric Association ^ (April 2000b). "Practice guideline for the treatment of patients with major depressive disorder". American Journal of Psychiatry 157 (Supp 4): 1–45. PMID 10767867. summary/ summary.aspx?doc_id=2605#s23. [159] K ECT Review Group (March 2003). U "Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis". Lancet 361 (9360): 799–808. doi:10.1016/S0140-6736(03)12705-5. PMID 12642045. [160] rudic J, Olfson M, Marcus SC, Fuller P RB, Sackeim HA (2004). "Effectiveness of electroconvulsive therapy in community settings". Biological Psychiatry 55 (3): 301–12. doi:10.1016/ j.biopsych.2003.09.015. PMID 14744473. [161] ourgon LN, Kellner CH (March 2000). B "Relapse of depression after ECT: a review". The journal of ECT 16 (1): 19–31. PMID 10735328. template-journal/lwwgateway/media/ landingpage.htm?issn=1095-0680&volume=16&issu [162] ackeim HA, Haskett RF, Mulsant BH, et S al. (March 2001). "Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: A randomized controlled trial". JAMA: Journal of the American Medical Association 285 (10): 1299–307. doi:10.1001/jama.285.10.1299. PMID 11255384. content/full/285/10/1299. [163] ew JD, Mulsant BH, Haskett RF, Joan P, T Begley AE, Sackeim HA (2007). "Relapse during continuation pharmacotherapy after acute response to ECT: A comparison of usual care versus protocolized treatment". Annals of Clinical Psychiatry 19 (1): 1–4.


From Wikipedia, the free encyclopedia

Major depressive disorder

doi:10.1080/10401230601163360. PMID (4): CD004366. doi:10.1002/ 17453654. 14651858.CD004366.pub3. PMID [164] rederikse M, Petrides G, Kellner C F 18843656. (March 2006). "Continuation and [172]St. John’s Wort and Depression". " maintenance electroconvulsive therapy NCCAM Health Information. Archived for the treatment of depressive illness: a from the original on 2007-10-11. response to the National Institute for Clinical Excellence report". The journal 20071011030548/ health/stjohnswort/sjwataglance.htm. of ECT 22 (1): 13–7. PMID 16633200. Retrieved on 2008-10-13. [173] inde K, Mulrow CD, Berner M, Egger M L template-journal/lwwgateway/media/ (2005). "St John’s wort for depression". landingpage.htm?an=00124509-200603000-00003. Cochrane Database Systematic Reviews [165] ational Institute for Clinical Excellence N (2): CD000448. doi:10.1002/ (2003) (PDF). Guidance on the use of 14651858.CD000448.pub2. PMID electroconvulsive therapy. London: 15846605. National Institute for Health and Clinical [174] arino LV, Dang KH, Dianat N, et al S Excellence. ISBN 1-84257-282-2. (2007). "Drug interaction between oral contraceptives and St. John’s Wort: 59ectfullguidance.pdf. appropriateness of advice received from [166] ellner CH, Knapp RG, Petrides G, et al. K community pharmacists and health food (December 2006). "Continuation store clerks". J Am Pharm Assoc (2003) electroconvulsive therapy vs pharmacotherapy for relapse prevention 47 (1): 42–7. PMID 17338474. in major depression: A multisite study [175] ichardson AJ (February 2008). "n-3 R from the Consortium for Research in Fatty acids and mood: the devil is in the Electroconvulsive Therapy (CORE)". detail". Br. J. Nutr. 99 (2): 221–3. Archives of General Psychiatry 63 (12): doi:10.1017/S0007114507824123. PMID 1337–44. doi:10.1001/ 17919344. archpsyc.63.12.1337. PMID 17146008. [176] reeman MP, Hibbeln JR, Wisner KL, F Davis JM, Mischoulon D, Peet M, Keck full/63/12/1337. PE, Marangell LB, Richardson AJ, Lake J, [167] arlow 2005, p. 239 B Stoll AL (2006). "Omega-3 fatty acids: [168]ngram A, Saling MM, Schweitzer I I evidence basis for treatment and future (March 2008). "Cognitive Side Effects of research in psychiatry". Journal of Brief Pulse Electroconvulsive Therapy: A Clinical Psychiatry 67 (12): 1954–67. Review". Journal of ECT 24 (1): 3–9. PMID 17194275. PMID 18379328. [177] oss BM, Seguin J, Sieswerda LE (2007). R [169] eisner AD (December 2003). "The R "Omega-3 fatty acids as treatments for electroconvulsive therapy controversy: mental illness: which disorder and which evidence and ethics" (PDF). fatty acid?". Lipids Health Dis 6: 21. Neuropsychology review 13 (4): doi:10.1186/1476-511X-6-21. PMID 199–219. PMID 15000226. 17877810. PMC: 2071911. art.pdf?issn=1040-7308&volume=13&page=199. 6//21. [170]Management of depression in primary " [178] ppleton KM, Hayward RC, Gunnell D, et A and secondary care" (PDF). National al (December 2006). "Effects of n-3 longClinical Practice Guideline Number 23. chain polyunsaturated fatty acids on National Institute for Health and Clinical depressed mood: systematic review of Excellence. 2007. published trials". Am. J. Clin. Nutr. 84 (6): 1308–16. PMID 17158410. CG023fullguideline.pdf. Retrieved on 2008-11-04. pmidlookup?view=long&pmid=17158410. [171] ead GE, Morley W, Campbell P, Greig M [179] ogers PJ, Appleton KM, Kessler D, et al R CA, McMurdo M, Lawlor DA (2008). (February 2008). "No effect of n-3 long"Exercise for depression". Cochrane chain polyunsaturated fatty acid (EPA database of systematic reviews (Online) and DHA) supplementation on depressed


From Wikipedia, the free encyclopedia
mood and cognitive function: a randomised controlled trial". Br. J. Nutr. 99 (2): 421–31. doi:10.1017/ S0007114507801097. PMID 17956647. [180] illiams AL, Girard C, Jui D, Sabina A, W Katz DL (2005). "S-adenosylmethionine (SAMe) as treatment for depression: a systematic review" (PDF). Clin Invest Med 28 (3): 132–9. PMID 16021987. cim_jun2005.pdf. Retrieved on 2008-12-04. [181] haw K, Turner J, Del Mar C (2002). S "Tryptophan and 5-hydroxytryptophan for depression". Cochrane Database of Systematic Reviews (1): CD003198. doi:10.1002/14651858.CD003198. PMID 11869656. [182] arangell LB, Martinez M, Jurdi RA, M Zboyan H (September 2007). "Neurostimulation therapies in depression: A review of new modalities". Acta Psychiatrica Scandinavica 116 (3): 174–81. doi:10.1111/ j.1600-0447.2007.01033.x. PMID 17655558. [183] Schutter DJ (April 2008). ^ "Antidepressant efficacy of highfrequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind shamcontrolled designs: A meta-analysis". Psychological Medicine: 1–11. doi:10.1017/S0033291708003462. PMID 18447962. [184] eNoon, Daniel J. (October 8, 2008). D "FDA OKs TMS Depression Device: Brain-Stimulating Device Cleared for Depression Treatment After 1 Drug Failure". WebMD. WebMD. news/20081008/fda-oks-tms-depressiondevice. Retrieved on 10 November 2008. [185] ranti S, Mogg A, Pluck G, et al (January E 2007). "A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression". Am J Psychiatry 164 (1): 73–81. doi:10.1176/appi.ajp.164.1.73. PMID 17202547. [186]New Device Approval: VNS Therapy " System - P970003s050" (htm). FDA. 2005-08-12. mda/docs/p970003s050.html. Retrieved on 2008-11-11.

Major depressive disorder
[187] ush AJ, Marangell LB, Sackeim HA, et R al. (September 2005). "Vagus nerve stimulation for treatment-resistant depression: A randomized, controlled acute phase trial". Biological Psychiatry 58 (5): 347–54. doi:10.1016/ j.biopsych.2005.05.025. PMID 16139580. [188] aban C, Martinez-Aran A, Cruz N, Vieta D E (September 2008). "Safety and efficacy of Vagus Nerve Stimulation in treatmentresistant depression. A systematic review". J Affect Disord 110 (1-2): 1–15. doi:10.1016/j.jad.2008.02.012. PMID 18374988. pii/S0165-0327(08)00095-5. [189] enton D, Donohoe RT (September B 1999). "The effects of nutrients on mood". Public Health Nutr 2 (3A): 403–9. PMID 10610080. abstract_S1368980099000555. [190] uijpers P, van Straten A, Smit F, C Mihalopoulos C, Beekman A (October 2008). "Preventing the onset of depressive disorders: a meta-analytic review of psychological interventions". Am J Psychiatry 165 (10): 1272–80. doi:10.1176/appi.ajp.2008.07091422. PMID 18765483. [191] hristensen H; Griffiths KM. (2002). C "The prevention of depression using the Internet" (PDF). Medical Journal of Australia. issues/177_07_071002/chr10370_fm.pdf. Retrieved on 2009-04-02. [192]ané-Llopis E; Hosman C; Jenkins R; J Anderson P. (2003). "Predictors of efficacy in depression prevention programmes" (PDF). British Journal of Psychiatry. reprint/183/5/384.pdf. Retrieved on 2009-04-02. [193] osternak MA, Miller I (2001). P "Untreated short-term course of major depression: A meta-analysis of outcomes from studies using wait-list control groups". Journal of Affective Disorders 66 (2–3): 139–46. doi:10.1016/ S0165-0327(00)00304-9. PMID 11578666. [194] osternak MA, Solomon DA, Leon AC, et P al. (2006). "The naturalistic course of unipolar major depression in the absence of somatic therapy". Journal of Nervous


From Wikipedia, the free encyclopedia
and Mental Disease 194 (5): 324–29. doi:10.1097/ 01.nmd.0000217820.33841.53. PMID 16699380. [195] aton WW, Shao H, Nestadt G, et al. E (May 2008). "Population-based study of first onset and chronicity in major depressive disorder". Archives of General Psychiatry 65 (5): 513–20. doi:10.1001/ archpsyc.65.5.513. PMID 18458203. [196] olma KM, Holma IA, Melartin TK, et al. H (February 2008). "Long-term outcome of major depressive disorder in psychiatric patients is variable". Journal of Clinical Psychiatry 69 (2): 196–205. PMID 18251627. [197] anai T, Takeuchi H, Furukawa TA, et al. K (July 2003). "Time to recurrence after recovery from major depressive episodes and its predictors". Psychological Medicine 33 (5): 839–45. doi:10.1017/ S0033291703007827. PMID 12877398. [198] eddes JR, Carney SM, Davies C, et al. G (February 2003). "Relapse prevention with antidepressant drug treatment in depressive disorders: A systematic review". Lancet 361 (9358): 653–61. doi:10.1016/S0140-6736(03)12599-8. PMID 12606176. [199] assano P, Fava M (October 2002). C "Depression and public health: an overview". J Psychosom Res 53 (4): 849–57. PMID 12377293. pii/S0022399902003045. [200] ush AJ (2007). "The varied clinical R presentations of major depressive disorder". The Journal of clinical psychiatry 68 (Supplement 8): 4–10. PMID 17640152. [201] Alboni P, Favaron E, Paparella N, ^ Sciammarella M, Pedaci M (April 2008). "Is there an association between depression and cardiovascular mortality or sudden death?". Journal of cardiovascular medicine (Hagerstown, Md.) 9 (4): 356–62. doi:10.2459/ JCM.0b013e3282785240. PMID 18334889. [202] arlow 2005, pp. 248–49 B [203] lair-West GW, Mellsop GW (2001). B "Major depression: Does a gender-based down-rating of suicide risk challenge its diagnostic validity?". Australian and New Zealand Journal of Psychiatry 35 (3): 322–28. doi:10.1046/

Major depressive disorder
j.1440-1614.2001.00895.x. PMID 11437805. [204] quendo MA, Bongiovi-Garcia ME, O Galfalvy H, et al (January 2007). "Sex differences in clinical predictors of suicidal acts after major depression: a prospective study". The American journal of psychiatry 164 (1): 134–41. doi:10.1176/appi.ajp.164.1.134. PMID 17202555. [205] ostwick, JM; Pankratz VS (2000). B "Affective disorders and suicide risk: A reexamination". American Journal of Psychiatry 157 (12): 1925–32. doi:10.1176/appi.ajp.157.12.1925. PMID 11097952. content/full/157/12/1925. [206]The world health report 2001 - Mental " Health: New Understanding, New Hope". WHO website. World Health Organization. 2001. whr/2001/en/index.html. Retrieved on 2008-10-19. [207] ndrade L, Caraveo-Anduaga JJ, A Berglund P, et al. (2003). "The epidemiology of major depressive episodes: Results from the International Consortium of Psychiatric Epidemiology (ICPE) Surveys". Int J Methods Psychiatr Res 12 (1): 3–21. doi:10.1002/mpr.138. PMID 12830306. [208] essler RC, Berglund P, Demler O, et al. K (2003). "The epidemiology of major depressive disorder: Results from the National Comorbidity Survey Replication (NCS-R)". JAMA 289 (203): 3095–105. doi:10.1001/jama.289.23.3095. PMID 12813115. [209] essler RC, Berglund P, Demler O, Jin R, K Merikangas KR, Walters EE (2005). "Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication". Archives of General Psychiatry 62 (6): 617–27. doi:10.1001/ archpsyc.62.6.593. PMID 15939837. [210] urphy JM, Laird NM, Monson RR, M Sobol AM, Leighton AH (2000). "A 40-year perspective on the prevalence of depression: The Stirling County Study". Archives of General Psychiatry 57 (3): 209–15. doi:10.1001/archpsyc.57.3.209. PMID 10711905. [211] Kuehner, C (2003). "Gender ^ differences in unipolar depression: An


From Wikipedia, the free encyclopedia
update of epidemiological findings and possible explanations". Acta Psychiatrica Scandinavica 108 (3): 163–74. doi:10.1034/j.1600-0447.2003.00204.x. PMID 12890270. [212] aton WW, Anthony JC, Gallo J, et al. E (1997). "Natural history of diagnostic interview schedule/DSM-IV major depression. The Baltimore Epidemiologic Catchment Area follow-up". Archives of General Psychiatry 54: 993–99. PMID 9366655. [213] ickards H (2005). "Depression in R neurological disorders: Parkinson’s disease, multiple sclerosis, and stroke". Journal of Neurology Neurosurgery and Psychiatry 76: i48–i52. doi:10.1136/ jnnp.2004.060426. PMID 15718222. PMC: 1765679. content/full/76/suppl_1/i48. [214] trik JJ, Honig A, Maes M (May 2001). S "Depression and myocardial infarction: relationship between heart and mind". Progress in neuro-psychopharmacology & biological psychiatry 25 (4): 879–92. PMID 11383983. pii/S0278-5846(01)00150-6. [215]orm AF (January 2000). "Does old age J reduce the risk of anxiety and depression? A review of epidemiological studies across the adult life span". Psychological Medicine 30 (1): 11–22. PMID 10722172. [216] eich S, Lewis G (1998). "(fulltext) W Poverty, unemployment, and common mental disorders: Population based cohort study". BMJ 317: 115–19. PMID 9657786. content/full/317/7151/115 (fulltext). Retrieved on 2008-09-16. [217] athers CD, Loncar D (November 2006). M "Projections of global mortality and burden of disease from 2002 to 2030". PLoS Med. 3 (11): e442. doi:10.1371/ journal.pmed.0030442. PMID 17132052. [218] ndrews G (July 2008). "(fulltext) In A Review: Reducing the Burden of Depression". Canadian Journal of Psychiatry 53 (7): 420–27. PMID 18674396. (fulltext). Retrieved on 08-11-10. [219] orld Health Organization (WHO) W (2004). "The global burden of disease: 2004 update, Part 3, Disease incidence,

Major depressive disorder
prevalence and disability" (PDF). global_burden_disease/ GBD_report_2004update_part3.pdf. Retrieved on 2009-01-30. [220] essler RC, Nelson C, McGonagle KA, et K al. (1996). "Comorbidity of DSM-III-R major depressive disorder in the general population: results from the US National Comorbidity Survey". British Journal of Psychiatry 168 (suppl 30): 17–30. PMID 8864145. [221] irschfeld RMA (2001). "The H Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care". Primary Care Companion to the Journal of Clinical Psychiatry 3 (6): 244–254. PMID 15014592. [222] apolsky Robert M (2004). Why zebras S don’t get ulcers. Henry Holt and Company, LLC. pp. 291–98. ISBN 0-8050-7369-8. [223] rant BF (1995). "Comorbidity between G DSM-IV drug use disorders and major depression: Results of a national survey of adults". Journal of Substance Abuse 7 (4): 481–87. doi:10.1016/ 0899-3289(95)90017-9. PMID 8838629. [224] allowell EM, Ratey JJ (2005). Delivered H from distraction: Getting the most out of life with Attention Deficit Disorder. New York: Ballantine Books. pp. 253–55. ISBN 0-345-44231-8. [225] air MJ, Robinson RL, Katon W et al. B (2003). "(fulltext) Depression and Pain Comorbidity: A Literature Review". Archives of Internal Medicine 163 (20): 2433–45. cgi/content/full/163/20/2433 (fulltext). Retrieved on 08-11-11. [226] ippocrates, Aphorisms, Section 6.23 H [227] epress. (n.d.). Online Etymology d Dictionary. Retrieved June 30, 2008, from [228] olpert, L. "Malignant Sadness: The W Anatomy of Depression". The New York Times. first/w/wolpert-sadness.html. Retrieved on 2008-10-30. [229] errios GE (September 1988). B "Melancholia and depression during the 19th century: A conceptual history". British Journal of Psychiatry 153: 298–304. doi:10.1192/bjp.153.3.298. PMID 3074848.


From Wikipedia, the free encyclopedia
[230] avison, K (2006). "Historical aspects of D mood disorders". Psychiatry 5 (4): 115–18. retrieve/pii/S1476179306700246. [231] ewis, AJ (1934). "Melancholia: A L historical review". Journal of Mental Science 80: 1–42. doi:10.1192/ bjp.80.328.1. [232] merican Psychiatric Association (1968). A "Schizophrenia" (PDF). Diagnostic and statistical manual of mental disorders: DSM-II. Washington, DC: American Psychiatric Publishing, Inc.. DSMPDF/dsm-ii.pdf. Retrieved on 2008-08-03. [233] childkraut, JJ (1965). "The S catecholamine hypothesis of affective disorders: A review of supporting evidence". American Journal of Psychiatry 122 (5): 509–22. PMID 5319766. [234] pitzer RL, Endicott J, Robins E (1975). S "The development of diagnostic criteria in psychiatry" (PDF). classics1989/A1989U309700001.pdf. Retrieved on 2008-11-08. [235] Philipp M, Maier W, Delmo CD (1991). ^ "The concept of major depression. I. Descriptive comparison of six competing operational definitions including ICD-10 and DSM-III-R". European Archives of Psychiatry and Clinical Neuroscience 240 (4–5): 258–65. doi:10.1007/ BF02189537. PMID 1829000. y2460650rm747035/. [236] ruenberg, A.M., Goldstein, R.D., Pincus, G H.A. (2005) Classification of Depression: Research and Diagnostic Criteria: DSMIV and ICD-10 (PDF). Retrieved on October 30, 2008. [237] olwig, Tom G. (2007). "Melancholia: B Beyond DSM, beyond neurotransmitters. Proceedings of a conference, May 2006, Copenhagen, Denmark". Acta Psychiatrica Scandinavica Suppl 115 (433): 4–183. doi:10.1111/ j.1600-0447.2007.00956.x. PMID 17280564. journal/118538120/issue. [238] ink M, Bolwig TG, Parker G, Shorter E F (2007). "Melancholia: Restoration in psychiatric classification recommended".

Major depressive disorder
Acta Psychiatrica Scandinavica 115 (2): 89–92. doi:10.1111/ j.1600-0447.2006.00943.x. PMID 17244171. [239] ealy, David (1999). The Antidepressant H Era. Cambridge, MA: Harvard University Press. pp. 42. ISBN 0-674-03958-0. [240] aloney F (November 3, 2005). "The M Depression Wars: Would Honest Abe Have Written the Gettysburg Address on Prozac?". Slate magazine. Washington Post. Retrieved on 2008-10-03. [241] arasz A (April 2005). "Cultural K differences in conceptual models of depression". Social Science in Medicine 60 (7): 1625–35. doi:10.1016/ j.socscimed.2004.08.011. PMID 15652693. [242] ilbury, F; Rapley M (2004). "There are T orphans in Africa still looking for my hands’: African women refugees and the sources of emotional distress". Health Sociology Review 13 (1): 54–64. doi:10.5555/hesr.2004.13.1.54 (inactive 2008-10-31). hesr.2004.13.1.54. Retrieved on 2008-10-03. [243] arker, G; Gladstone G, Chee KT (2001). P "Depression in the planet’s largest ethnic group: The Chinese". American Journal of Psychiatry 158 (6): 857–64. PMID 11384889. [244] arker, G (2007). "Is depression P overdiagnosed? Yes". BMJ 335 (7615): 328. doi:10.1136/bmj.39268.475799.AD. PMID 17703040. cgi/content/full/335/7615/328. [245] ilgrim D, Bentall R (1999). "The P medicalisation of misery: A critical realist analysis of the concept of depression". Journal of Mental Health 8 (3): 261–74. doi:10.1080/ 09638239917580. apl/cjmh/1999/00000008/00000003/ art00007. [246] teibel W (Producer) (March 1998). "Is S depression a disease?". Debatesdebates. isdepressionadiseasetranscript.html. Retrieved on 2008-11-16.


From Wikipedia, the free encyclopedia
[247] lazer DG (2005). The age of B melancholy: "Major depression" and its social origins. New York, NY, USA: Routledge. ISBN 978-0415951883. [248] illman J (T Moore, Ed.) (1989). A blue H fire: Selected writings by James Hillman. New York, NY, USA: Harper & Row. pp. 152–53. ISBN 0060161329. [249] urlingame, Michael (1997). The Inner B World of Abraham Lincoln. Urbana: University of Illinois Press. ISBN 0-252-06667-7. [250] eymour, Miranda (2002). Mary Shelley. S Grove Press. pp. 560–61. ISBN 0802139485. [251]Biography of Henry James". " americancollection/american/genius/ henry_bio.html. Retrieved on 2008-08-19. [252] urlingame, Michael (1997). The Inner B World of Abraham Lincoln. Urbana: University of Illinois Press. ISBN 0-252-06667-7. [253] ita E (2001-09-26). "An Intimate P Conversation with...Leonard Cohen". press/elmunmag.htm. Retrieved on 2008-10-03. [254]este ND, Palmer BW, Jeste DV (2004). J "Tennessee Williams". American Journal of Geriatric Psychiatry 12 (4): 370–75. doi:10.1176/appi.ajgp.12.4.370. PMID 15249274. [255]ames H (Ed.). Letters of William James J (Vols. 1 and 2). Montana USA: Kessinger Publishing Co. pp. 147–48. ISBN 978-0766175662. [256] ergenhahn 2005, p. 311 H [257] ohen D (1979). J. B. Watson: The C Founder of Behaviourism. London, UK: Routledge & Kegan Paul. pp. 7. ISBN 0710000545. [258] ndreasen NC (2008). "The relationship A between creativity and mood disorders". Dialogues in clinical neuroscience 10 (2): 251–5. PMID 18689294. [259] imonton, DK (June 2005). "Are genius S and madness related? Contemporary answers to an ancient question". Psychiatric Times 22 (7). article/10168/52456?pageNumber=1. [260] effernan CF (1996). The melancholy H muse: Chaucer, Shakespeare and early medicine. Pittsburgh, PA, USA:

Major depressive disorder
Duquesne University Press. ISBN 0820702625. [261] ill JS. "A crisis in my mental history: M One stage onward" (txt). Autobiography. Project Gutenberg EBook. pp. 1826–32. ISBN 1421242001. 10378-8.txt. Retrieved on 2008-08-09. [262] terba R (1947). "The ’Mental Crisis’ of S John Stuart Mill". Psychoanalytic Quarterly 16 (2): 271–72. document.php?id=PAQ.016.0271C. Retrieved on 2008-11-05. [263] "Churchill’s Black Dog?: The History of ^ the ‘Black Dog’ as a Metaphor for Depression" (PDF). Black Dog Institute website. Black Dog Institute. January 2005. docs/McKinlay.pdf. Retrieved on 2008-08-18. [264]orm AF, Angermeyer M, Katschnig H J (2000). "Public knowledge of and attitudes to mental disorders: a limiting factor in the optimal use of treatment services". in Andrews G, Henderson S (eds). Unmet Need in Psychiatry:Problems, Resources, Responses. Cambridge University Press. pp. 409. ISBN 0-521-66229-X. [265] aykel ES, Tylee A, Wright A, Priest RG, P Rix S, Hart D (1997). "The Defeat Depression Campaign: psychiatry in the public arena". American Journal of Psychiatry 154: 59–65. PMID 9167546. [266] aykel ES, Hart D, Priest RG (1998). P "Changes in public attitudes to depression during the Defeat Depression Campaign". British Journal of Psychiatry 173: 519–22. PMID 9926082.

Cited texts
• American Psychiatric Association (2000a). Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc.. ISBN 0890420254. • Barlow DH; Durand VM (2005). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA, USA: Thomson Wadsworth. ISBN 0534633560. • Beck, Aaron T.; Rush J, Shaw BF, Emery G (1987) [1979]. Cognitive Therapy of


From Wikipedia, the free encyclopedia
depression. New York, NY, USA: Guilford Press. ISBN 0898629195. Freeman, Arthur; Epstein, Norman & Simon, Karen M. (1987). Depression in the Family. Haworth Press. ISBN 0866566244. Hergenhahn BR (2005). An Introduction to the History of Psychology (5th edition ed.). Belmont, CA, USA: Thomson Wadsworth. ISBN 0534554016. May R (1994). The discovery of being: Writings in existential psychology. New York, NY, USA: W. W. Norton & Company. ISBN 0393312402. Parker, Gordon; Dusan Hadzi-Pavlovic, Kerrie Eyers (1996). Melancholia: A disorder of movement and mood: A phenomenological and neurobiological review. Cambridge: Cambridge University Press. ISBN 052147275X. Royal Pharmaceutical Society of Great Britain (September 2008). British National

Major depressive disorder
Formulary (BNF 56). UK: BMJ Group and RPS Publishing. ISBN 9780853697787. • Sadock, Benjamin J.; Sadock, Virginia A. (2002). Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry (9th ed.). Lippincott Williams & Wilkins. ISBN 0781731836.




External links
• DSM-IV diagnostic criteria for major depressive disorder – DSM-IV-TR text from • Depression at the Open Directory Project • National Alliance on Mental Illness – National Alliance on Mental Illness • Depression, out of the shadows – Public Broadcasting Service, a USA television program broadcast in May 2008



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