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14-September-2008 18:02:35 - Major depressive disorder Redirected from Clinical depression Depression Classification and external resources Vincent van Gogh's 1890 painting On the Threshold of Eternity ICD-10 F32., F33. ICD-9 296 OMIM 608516 DiseasesDB 3589 MedlinePlus 003213 eMedicine med/532 Major depressive disorder, also known as major depression, unipolar depression, clinical depression, or simply depression, is a mental disorder characterized by a pervasive low mood and loss of interest or pleasure in usual activities. The diagnosis is made if a person has suffered one or more major depressive episodes. Diagnosis is based on the patient's self-reported experiences and observed behavior. There is no laboratory test for major depression, although physicians often test for physical conditions that may cause similar symptoms before arriving at a diagnosis. The course varies widely, from a one-off occurrence to a lifelong disorder with recurrent episodes. The most common time of onset is between the ages of 30 and 40, with a later peak between 50 and 60. The condition appears to be more common in women. Both psychological and biological causes have been proposed, and the question of whether there are two separate conditions, a biological and a reactive depression, or a continuum of a single entity, has been hotly debated since the 1920s. Current classification has favored the latter since the creation of the term major depressive disorder in 1980. The neurotransmitters serotonin and noradrenaline have been implicated, and most antidepressants work to increase the active levels of these in the brain. A host of psychological factors has also been implicated, and various forms of psychotherapy are used to address them. Electroconvulsive therapy is sometimes used in severe cases. Hospitalization may be necessary in cases with a significant risk of suicide or self-neglect. The term depression is commonly used to describe a temporary depressed mood, when a person may feel sad or down. Ideas about what causes and constitutes depression have evolved over the centuries. Major depression can be a serious and often disabling condition that can significantly affect a person's work, family and school life, sleeping and eating habits, and general health. However, it may be overdiagnosed, and current diagnostic standards arguably have the effect of medicalising sadness or misery. Around 3.4 percent of people with major depression commit suicide. Up to 60 percent of all people who commit suicide have a mood disorder, such as depression, and their risk may be especially high if they feel a marked sense of hopelessness or have both depression and borderline personality disorder. Depressed people have a shortened life expectancy, being more susceptible to and likely to die from conditions such as heart disease than the non-depressed. Contents 1 Signs and symptoms 1.1 Comorbidity 2 Diagnosis 2.1 Physical investigations 2.2 Clinical assessment 2.3 Rating scales 2.4 DSM IV-TR and ICD-10 criteria 2.4.1 Major depressive episode 2.4.2 Subtypes 2.5 Differential diagnoses 3 Causes 3.1 Psychological 3.2 Biological 4 Treatment 4.1 Psychotherapy 4.2 Medication 4.2.1 Augmentation 4.2.2 Efficacy of medication and psychotherapy 4.3 Electroconvulsive therapy 4.4 Other conventional methods of treatment 4.5 Alternative treatment methods 5 Prognosis 6 Epidemiology 7 History 7.1 Prehistory to antiquity 7.2 Medieval to Renaissance eras 7.3 17th to 19th centuries 7.4 20th century to the present day 8 Sociocultural aspects 9 References 9.1 Cited texts 10 External links Signs and symptoms A person suffering a major depressive episode almost always reports a pervasive low mood, and loss of interest or pleasure in favorite activities. They may ruminate over or be preoccupied with feelings of worthlessness, inappropriate or exaggerated guilt or regret, helplessness or hopelessness.1 Other symptoms include poor concentration and memory, withdrawal from social situations, family gatherings and activities with friends, reduced libido sex drive, and thoughts of death or suicide. Insomnia is a common symptom; the typical pattern is one of early morning wakening where the person reports waking up very early and being unable to get back to sleep.2 Hypersomnia, or oversleeping, is less common.2 Appetite is often decreased, with resulting weight loss, although increase and weight gain occasionally occurs.1 The patient may report persistent physical symptoms such as fatigue, headaches, digestive problems, or chronic pain, or describe feeling slowed down or sluggish. Family or friends may note the person appears agitated or slowed down.2 World map of suicide rates per 100,000. World map of suicide rates per 100,000. People are most likely to suffer their first depressive episode between the ages of 30 and 40.3 The risk is increased in the first year after childbirth post-natal depression, and after cardiovascular and neurological illnesses such as stroke,4 Parkinson's disease,4 and multiple sclerosis.4 Depressive episodes following a heart attack might even correspond with an increased risk of further cardiac complications, including death.5 There is a second, smaller peak of incidence later in life between the ages of 50 and 60;3 older people are more likely to present with cognitive symptoms such as forgetfulness and a more noticeable slowing of movements. The term pseudodementia was coined for this syndrome, due to its clinical resemblance to dementia.6 Diagnosis in children or adolescents may be delayed or missed as the symptoms are dismissed as normal moodiness. Their mood may be predominantly irritable rather than depressed.1 Children may show different symptoms depending on age and situation;7 most will exhibit a loss of interest in school and decline in academic performance.2 Those older than 12 years may also begin abusing drugs or alcohol, or exhibit disruptive behaviour. Thoughts or attempts of suicide are rare in children with major depression under 12 years of age. Comorbidity Major depression frequently co-occurs with other psychiatric problems; the National Comorbidity Survey US reports that 58% of those with major depression also suffer from lifetime anxiety. Even mild anxiety symptoms can have a major impact on the course of a depressive illness, and the commingling of any anxiety symptoms with the primary depression is important to consider. Psychiatrist Ellen Frank found that depressed patients with lifetime panic symptoms experienced significant delays in their remission, and had higher levels of residual impairment.8 Robert Sapolsky similarly argues that the relationship between stress, anxiety, and depression could be measured and demonstrated biologically.9 There are increased rates of alcohol and drug abuse and particularly dependence,10 and around a third of individuals diagnosed with attention-deficit hyperactivity disorder develop comorbid depression.11 Diagnosis Physical investigations Before a diagnosis of major depressive disorder is made, a physician generally performs a medical examination and selected investigations to rule out a medical illness as a cause of symptoms. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and full blood count including ESR to rule out a systemic infection or chronic disease.12 Testosterone levels may be used to diagnose hypogonadism, a cause of depression in men.13 Two commonly ordered investigations are EEG to exclude epilepsy, and a CT scan of the head to exclude brain lesions.14 Early dementia may present with depressive symptoms in older patients. No biological tests are used to confirm major depression as such.15 Investigations are not generally repeated for a subsequent episode unless there is a specific medical indication. These may include measuring serum sodium to rule out hyponatremia low sodium if the person presents with increased frequency of passing urine, a common side effect of selective serotonin reuptake inhibitor SSRI antidepressants.16 Clinical assessment If no medical cause is found, a psychiatric assessment may be done by the physician, or by referral to a psychiatrist or psychologist.17 Assessment is usually done on an outpatient basis; admission to an inpatient mental health unit is considered for patients who pose a risk to themselves or others. This will include a complete history of the person's current circumstances, biographical history and current symptoms, a discussion of alcohol and drug use, and a family medical history to see if other family members have suffered from a mood disorder. A mental state examination will include assessing the person's current mood and exploring thought content, in particular thoughts of hopelessness, self-harm or suicide.17 Rating scales Several rating scales are used in research or as screening tools, and have been widely promoted in primary healthcare to improve detection of depression. However, their benefit has been questioned,18 and there is strong evidence routine screening does little to improve detection rates.19 The Beck Depression Inventory is one of the most widely used diagnostic tools for self-diagnosis of depression, although its main purpose is not the diagnosis of depression, but determining the presence and severity of symptoms.20 Originally designed by psychiatrist Aaron T. Beck in 1961, it is a 21-question patient-completed survey that covers items related to the basic symptoms of depression, such as hopelessness and irritability, cognitions such as guilt or feelings of being punished, as well as physical symptoms such as fatigue, weight loss, and lack of interest in sex.21 Two Patient Health Questionnaires available are self-administered questionnaires. The PHQ-2 has only two questions that asks about the frequency of depressed mood and a loss of interest in doing things, with a positive to either question indicating the need for further testing.22 The PHQ-9 is a slightly more detailed nine question survey covering some of the major symptoms of depression and the frequency a person has experienced them. It is based directly on the diagnostic criteria listed in the DSM-IV and often used as a follow up to a positive PHQ-2 test.23 Other scales commonly used include the Geriatric Depression Scale in older populations, which is also valid in patients with mild to moderate dementia,24 the widely used Hamilton Depression Rating Scale HRSD-21 designed by psychiatrist Max Hamilton in 1960,25 and the Montgomery-Åsberg Depression Rating Scale MADRS.26 DSM IV-TR and ICD-10 criteria The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association's 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. The latter system is typically used in European countries, while the former is used in the USA and many other non-European nations,27 and are frequently referenced in research studies. Major depressive disorder is classified as a mood disorder in DSM IV-TR;28 the diagnosis hinges on the presence of a major depressive episode, which may be either single or recurrent.1 Further qualifiers are used to classify both the episode itself and the course of the disorder. There is also a category of Depressive Disorder Not Otherwise Specified. The ICD-10 system does not use the term Major depressive disorder, but lists similar criteria for the diagnosis of a Depressive episode mild, moderate or severe; multiple episodes without mania may be classed as Recurrent Depressive Disorder.29 Major depressive episode Main article: Major depressive episode A major depressive episode has been defined as a severely depressed mood that persists for at least two weeks.1 Episodes may be isolated or recurrent and categorized as mild few symptoms in excess of minimum criteria, moderate, or severe marked impact on social or occupational functioning; any episode with psychotic features is automatically rated as severe. If the patient has already had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead.30 Depression without periods of mania is sometimes referred to as unipolar depression because the mood remains at one emotional state or pole.31 The DSM excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if characteristic features develop.32 Subtypes Diagnosticians recognize several subtypes or course specifiers: Atypical depression is characterized by mood reactivity paradoxical anhedonia and positivity, significant weight gain or increased appetite comfort eating, excessive sleep or somnolence hypersomnia, an sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.33 Difficulties in measuring this subtype have led to questions of its validity and prevalence.34 Melancholic depression is characterized by a loss of pleasure anhedonia 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.35 Psychotic depression is the term for a major depressive episode, particularly of melancholic nature, where the patient experiences psychotic symptoms such as delusions or, less commonly, hallucinations. These are most commonly mood-congruent content coincident with depressive themes.36 Catatonic depression 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 immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia, a manic episode, or be due to neuroleptic malignant syndrome.37 Postpartum depression is listed as a course specifier in DSM-IV-TR; it refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10-15%, typically sets in within three months of labor, and lasts as long as three months.38 Seasonal affective disorder is a specifier. Some people have a seasonal pattern, with depressive episodes coming on in the autumn or winter, and resolving 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.39 Differential diagnoses In the process of differential diagnosis, alternative diagnoses are ruled out so that the applicable condition can be identified. Some potential diagnoses that may be considered before diagnosing MDD include the following: Dysthymia, which is a chronic, milder mood disturbance where a 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.40 Recurrent brief depression RBD, distinguished from Major Depressive Disorder primarily by differences in duration. People with RBD have depressive episodes about once per month, with individual episodes lasting less than two weeks and typically less than 2-3 days. Diagnosis of RBD requires that the episodes occur over the span of at least one year and, in female patients, independently of the menstrual cycle.41 People with clinical depression can develop RBD, and vice versa, and both illnesses have similar risks.42 Minor depression, which refers to a depression that does not meet full criteria for major depression but in which at least two symptoms are present for two weeks.43 Adjustment disorder with depressed mood, is a term given to a psychological response to identifiable event or stressor; the resulting emotional or behavioral symptoms, in this case low mood, are significant, but do not meet the criteria for a major depressive episode.44 Causes Current theories regarding the risk factors and causes of major depression fall into two categories, the psychological and the biological, although there is much overlap and integration. Debate has persisted for most of the twentieth century over whether a unitary or binary model of depression is a truer reflection of the syndrome;45 in the former, there is a continuum of depression ranked only by severity and the result of a psychobiological final common pathway,46 whereas the latter conceptualizes a distinction between biological and reactive depressive syndromes.47 The publishing of DSM-III has seen the unitarian model gain a more universal acceptance.45 Psychological Psychological factors include the complex development of personality and how a person has learned to cope with external environmental factors, such as stress.48 Events such as the death of a parent or loved one, issues with biological development, school related problems, abandonment or rejection, neglect, chronic illness, and physical, psychological, or sexual abuse increase the risk of depression later in life. Post-traumatic stress disorder PTSD and depression often co-occur, and both can result from childhood trauma.49 Stressful or traumatic life experiences or circumstances, including rape, assault, combat, or the death of a relative or friend, may trigger a depressive episode directly-although temporary grief-related depression is not considered a disorder. A depressive episode may also be triggered by other major changes such as unemployment, divorce, or a loss of religious faith.50 Ongoing issues, such as financial difficulties or poverty, major health problems, addictions such as problem gambling or drug addiction, marital or sexual difficulties, or work-related stress can also contribute to depression. According to sociologist George W. Brown and psychologist Tirril Harris,51 certain 'vulnerability factors'-namely early maternal loss, lack of a confiding relationship, greater than three children under the age of 14 at home and unemployment-can interact with 'provoking agents' to increase the risk of depression.52 Among these factors, confiding relationships appear to be especially important.52 Low self-esteem, learned helplessness, and self-defeating or distorted thinking are connected with depression. There is debate as to whether these are causes or effects of depression. In either case, it is known that depressed persons who are able to make corrections in their thinking patterns often show improved mood and self-esteem.53 Cognitive psychology and cognitive behavioural theory take the view that depression arises from deficits in memory and information processing which give rise to cognitive biases and distortions. According to psychologist Martin Seligman, depression in humans may be similar to learned helplessness in other animals, who remain in unpleasant situations from which they could escape, but over which they had initially had no control.54 Learned helplessness and depression may be related to what psychologist Julian Rotter called an external locus of control, a tendency to attribute outcomes to external events outside one's control.55 However, depressed people tend to blame themselves for negative events in particular, and to believe that the relevance of these events persists through time and pervades their entire lives and selfhoods.5657 This tendency is characteristic of a depressive attributional style, or pessimistic explanatory style, and the causal attributions made in such a style have been termed internal, stable, and global,56 or personal, permanent, and pervasive. According to psychologist Albert Bandura, people become depressed through a distorted self-concept and a lack of self-efficacy, in other words a habitual sense of inability to influence events and achieve personal goals.5859 A related idea, Aaron T. Beck's cognitive triad, is that depression entails cognitive errors about oneself, one's world, and one's future.56 Milder depression, however, has been associated with what has been called depressive realism, or the sadder-but-wiser effect, a view of the world that is relatively undistorted by positive biases.6061 From the psychoanalytic perspective, depression may be intertwined with self-criticism. In particular, wrote Sigmund Freud, the super-ego becomes over-severe, abuses the poor ego, humiliates it and ill-treats it, threatens it with the direst punishments.62 Freud also argued that objective loss, as occurs through death or a romantic break-up, could result in subjective loss as well, when the depressed subject had identified with the object of its affection through an unconscious but narcissistic process called the libidinal cathexis of the ego. Such loss results in a profoundly painful dejection, cessation of interest in the outside world, loss of the capacity to love, inhibition of all activity, and a lowering of self-regarding feelings that is more severe than mourning. In mourning 'it is the world that has become poor and empty; in depression it is the ego itself.'63 Rollo May and other existential psychologists have argued that depression can stem from an inadequate grasp of personal freedom and responsibility. Rollo May and other existential psychologists have argued that depression can stem from an inadequate grasp of personal freedom and responsibility. Existential psychologist Rollo May stated that depression is the inability to construct a future.64 From the existential perspective, in order to construct a future, people must become acutely aware of both their mortality and their freedom, and they must exercise the latter within the explicit framework of the former. This awareness and responsibility produce normal anxiety,65 whereas the lack of these things leads to neurotic anxiety,65 self-alienation,66 inauthentic living,67 and depression. Humanistic psychologists agree with many facets of existentialism, but argue that depression results from a specific incongruity between society and the individual's innate drive to self-actualize.68 Evolutionary psychology suggests that major depression can result from the overactivation or dysfunction of psychological mechanisms that are sensitive to certain kinds of material or social loss or defeat.697071 Some aspects of this approach have received empirical support and clinical application;7273 other components are still at a hypothetical stage. Biological Most experts believe that both biological and psychological factors play a role in causing depression. The heritability of depression-the degree to which it is genetically determined-has been estimated at around 40% for women and 30% for men.74 From the evolutionary standpoint, major depression might be expected to reduce the reproductive fitness of the individual suffering from it. Some evolutionary explanations for the apparent contradiction between this hypothesis and the high heritability and prevalence of major depression rest on the idea that some components of depression are adaptations.7571 Illustration of the major elements in a prototypical synapse. Synapses are gaps between nerve cells. These cells convert their electrical impulses into bursts of chemical relayers, called neurotransmitters, which travel across the synapses to receptors on adjacent cells, triggering electrical impulses to travel down the latter cells. Illustration of the major elements in a prototypical synapse. Synapses are gaps between nerve cells. These cells convert their electrical impulses into bursts of chemical relayers, called neurotransmitters, which travel across the synapses to receptors on adjacent cells, triggering electrical impulses to travel down the latter cells. Many modern antidepressant drugs change synaptic levels of certain neurotransmitters, especially serotonin and norepinephrine; this has implicated neurochemical factors. Serotonin in particular may regulate other neurotransmitter systems, and decreased serotonin activity may permit these systems to act in unusual and erratic ways. Facets of depression may be emergent properties of this dysregulation.76 However, the precise relationships between serotonin, Selective serotonin reuptake inhibitors, and depression are largely unknown, and tend to be greatly oversimplified when presented to the public.77 Many depressed individuals exhibit markedly higher levels of monoamine oxidase A MAO-A in the brain compared to people without depression.78 MAO-A is an enzyme that decreases the concentration of monoamines such as serotonin, norepinephrine and dopamine. There may be a link between depression and neurogenesis of the hippocampus,79 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.8081 Similar relationships have been observed between depression and an area of the anterior cingulate cortex implicated in the modulation of emotional behavior.82 One of the neurotrophins responsible for neurogenesis is the brain-derived neurotrophic factor BDNF. The level of BDNF in the blood plasma of depressed subjects is drastically, more than threefold, reduced as compared to the norm. Antidepressant treatment increases the blood level of BDNF. Although the decreased plasma BDNF levels have been found in many other disorders, there are indications of BDNF involvement in the causes of depression and the mechanism of the action of antidepressants.83 Depression may also be caused in part by an overactive hypothalamic-pituitary-adrenal axis HPA axis that resembles the neuro-endocrine response to stress. These HPA axis abnormalities participate in the development of depressive symptoms, and antidepressants serve to regulate HPA axis function.84 Depression may be affected by variations in the circadian rhythm. The REM stage of sleep, in which dreaming occurs, tends to be especially quick to arrive, and especially intense, for depressed people. Although the precise relationship between sleep and depression is mysterious, the relationship appears to be particularly strong among those whose depressive episodes are not precipitated by unusual stress. In such cases, clients may be especially unaffected by therapeutic intervention.85 Treatment Main article: Treatment for depression The three most commonly indicated 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 in severe cases or in emergencies. The term refractory- or treatment-resistant depression is used to describe cases that do not respond to adequate courses of least two antidepressants.86 Psychotherapy Main article: Psychotherapy Albert Ellis invented Rational Emotive Behavior Therapy, the earliest form of Cognitive Behavioral Therapy. Albert Ellis invented Rational Emotive Behavior Therapy, the earliest form of Cognitive Behavioral Therapy. There are a number of different psychotherapies for depression, which may be provided to individuals or groups. Psychotherapy can be delivered by a variety of mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and psychiatric nurses. With more complex and chronic forms of depression the most effective treatment is often considered to be a combination of medication and psychotherapy.87 Psychotherapy is the treatment of choice in people under 18; medication is offered only in conjunction with the former and generally not as a first line agent. 88 The most studied form of psychotherapy for depression is Cognitive behavioral therapy CBT, thought to work by teaching clients to learn a set of cognitive and behavioral skills, which they can employ on their own. Earlier research suggested that cognitive-behavioral therapy was not as effective as antidepressant medication in the treatment of depression; however, more recent research suggests that it can perform as well as antidepressants in treating patients with moderate to severe depression.89 For the treatment of adolescent depression, CBT performed no better than placebo, and significantly worse than the antidepressant fluoxetine.90 Combining fluoxetine with CBT appeared to bring no additional benefit9192 or, at the most, only marginal benefit.93 Two randomized, controlled trials of mindfulness-based cognitive therapy MBCT, which includes elements of mation, have been reviewed. MBCT was significantly more effective than usual care for the prevention of recurrent depression in patients who had had three or more depressive episodes. According to the review, the usual care did not include antidepressant treatment or any psychotherapy, and the improvement observed may have reflected the non-specific or placebo effects.94 Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment for depression. Here, the therapy takes a structured course with a set number of weekly sessions often 12 as in the case of CBT, however the focus is on relationships with others. Therapy can be used to help a person develop or improve interpersonal skills in order to allow him or her to communicate more effectively and reduce stress.95 Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,96 is used by its practitioners to treat clients presenting with major depression.97 A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.98 In a meta-analysis of three controlled trials, psychodynamic psychotherapy was found to be as effective as medication for mild to moderate depression.99 Medication Main article: Antidepressant To find the most effective pharmaceutical treatment, the dosages of medications must often be adjusted, different combinations of antidepressants tried, or antidepressant changed. Response rates to the first agent administered may be as low as 50%.100 It may take anywhere from three to eight weeks after the start of medication before its therapeutic effects can be fully discovered. Patients are generally advised not to stop taking an antidepressant suddenly and to continue its use for at least four months to prevent the chance of recurrence. People with chronic depression need to take the medication for the rest of their lives.17 Isoniazid, the first compound called antidepressant Isoniazid, the first compound called antidepressant Selective serotonin reuptake inhibitors SSRIs, such as sertraline Zoloft, escitalopram Lexapro, fluoxetine Prozac, paroxetine, and citalopram are the primary medications considered, due to their relatively mild side effects and broad effect on the symptoms of depression and anxiety. Those who do not respond to the first SSRI tried can be switched to another; such a switch results in improvement in almost 50% of cases.101 Another popular option is to switch to the atypical antidepressant bupropion Wellbutrin or to add bupropion to the existing therapy;102 this strategy is possibly more effective.103104 It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine Zispin, Remeron can be used in such cases.105106107 Venlafaxine Effexor may be moderately more effective than SSRIs;108 however, it is not recommended as a first-line treatment because of the higher rate of side effects,109 and its use is specifically discouraged in children and adolescents.110 Fluoxetine is the only antidepressant recommended for people under the age of 18.111 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.112113 A different class of antidepressants, the monoamine oxidase inhibitors, have historically been plagued by questionable efficacy and life-threatening adverse effects. They are still used only rarely, although newer agents of this class, with a better side effect profile, have been developed.114 Augmentation Physicians often add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance; a 2002 large community study of 244,859 depressed Veterans Administration patients found that 22% had received a second agent, most commonly a second antidepressant.115 Lithium has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.116 Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.117 Addition of atypical antipsychotics when the patient has not responded to an antidepressant is also known to increase the effectiveness of antidepressant drugs, albeit at the cost of more frequent side effects.118 There is some evidence for the addition of a thyroid hormone, triiodothyronine, in patients with normal thyroid function.119 Efficacy of medication and psychotherapy Two recent meta-analyses of clinical trial results submitted to the FDA concluded that antidepressants are statistically superior to placebo but their overall effect is low-to-moderate. In that respect they often did not exceed the National Institute for Health and Clinical Excellence criteria for a clinically significant effect. In particular, the effect size was very small for moderate depression but increased with severity reaching clinical significance for very severe depression.120121 These result were consistent with the earlier clinical studies in which only patients with severe depression benefited from either psychotherapy or treatment with an antidepressant, imipramine, more than from the placebo treatment.122123124 Despite obtaining similar results, the authors argued about their interpretation. One author concluded that there seems little evidence to support the prescription of antidepressant medication to any but the most severely depressed patients, unless alternative treatments have failed to provide benefit.120 The other author agreed that antidepressant 'glass' is far from full but disagreed that it is completely empty. He pointed out that the first-line alternative to medication is psychotherapy, which does not have superior efficacy.125 Antidepressants in general are as effective as psychotherapy for major depression, and this conclusion holds true for both severe and mild forms of MDD.126127 In contrast, medication gives better results for dysthymia.126127 The subgroup of SSRIs may be slightly more efficacious than psychotherapy. On the other hand, significantly more patients drop off from the antidepressant treatment than from psychotherapy, likely because of the side effects of antidepressants.126 Successful psychotherapy appears to prevent the recurrence of depression even after it has been terminated or replaced by occasional booster sessions. The same degree of prevention can be achieved by continuing antidepressant treatment.127 Electroconvulsive therapy Main article: Electroconvulsive therapy Electroconvulsive therapy ECT is a treatment where seizures are electrically induced in anesthetized patients for therapeutic effect. ECT is most often used as a last resort intervention for severe major depression which has not responded to other treatment.128 It is also works more quickly than antidepressant therapy, and is thus the treatment of choice in emergencies such as catatonic depression where the patient has ceased oral intake of fluid or nutrients, or severe suicidality.128 Strong evidence suggests it is the most effective treatment for depression129 and results in improved quality of life in both the short- and long-term.130 Antidepressant therapy is generally continued after treatment, although some patients require maintenance monthly ECT to remain well. Short-term memory loss, disorientation, and headache are common side effects. Long-term memory loss may occur in some instances.131 The American Psychiatric Association and the National Institute for Health and Clinical Excellence have concluded that the procedure does not cause brain damage.132133 Other conventional methods of treatment St John's wort extract is used extensively in Europe to treat mild and moderate depression. It is a prescription antidepressant in several European countries but is classified as herbal supplement and sold over the counter in the US. Opinions on its efficacy for major depression differ. A systematic meta-analysis of 37 trials conducted by Cochrane Collaboration indicated statistically significant weak-to-moderate effect as compared to placebo. The same meta-analysis found that St John's wort efficacy for major depression is not different from prescription antidepressants.134 NCCAM and other NIH-affiliated organizations hold that St John's wort has minimal or no effects beyond placebo in the treatment of major depression, based primarily on one study with negative outcome conducted by NCCAM.135136 S-Adenosyl methionine SAM-e is available as a prescription antidepressant in Europe and an over-the-counter dietary supplement in the US. Fairly strong evidence from 16 clinical trials suggests it to be more effective than placebo and as effective as standard antidepressant medication for the treatment of major depression.137138 Repetitive transcranial magnetic stimulation rTMS, used in treatment-resistant depression, is supported by multiple controlled studies; it has been approved for this indication in Europe, Canada and Australia, but not in the US.139 A 2008 meta-analysis based on 32 trials found a robust effect of this method on depression, and it appeared similarly effective for both uncomplicated depression and depression resistant to medication.140 However, it was inferior to ECT in a side-by-side randomized trial.141 Vagus nerve stimulation VNS is an approved therapy for treatment-resistant depression and is used as an adjunct to existing antidepressant treatment. The support for this method comes mainly from open-label trials, which indicate that several months may be required to see a benefit.139 The only large double-blind trial conducted lasted only 10 weeks and yielded inconclusive results; VNS failed to show superiority over a sham treatment on the primary efficacy outcome, but the results were more favorable for the secondary outcome.142 Alternative treatment methods Bright light therapy is sometimes used to treat depression, especially in its seasonal form. Bright light therapy is sometimes used to treat depression, especially in its seasonal form. A meta-analysis of bright light therapy commissioned by the American Psychiatric Association found it to be more effective than placebo-usually, dim light-for both seasonal affective disorder and for nonseasonal depression, with effect sizes similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective.143 A meta-analysis of light therapy for non-seasonal depression conducted by Cochrane Collaboration studied a different set of trials, in which light was used mostly as an addition to medication or sleep deprivation. A moderate statistically significant effect of light therapy was found; however, it disappeared if a different statistical technique was used.144 Both analyses noted poor quality of most studies and their small size and urged caution in the interpretation of their results. The short duration 1-2 weeks of most trials makes it unclear whether the effect of light therapy could be sustained in the longer term. A 2004 Cochrane Review concluded that there was insufficient evidence to judge the efficacy of acupuncture in the management of depression. Although acupuncture showed no difference in the improvement of depression compared with conventional medication, the methodological quality of the evidence base was found to be poor.145 Exercise, when used in conjunction with medication by non-suicidal patients, can have beneficial effects in preventing the return of depression. Patients who completed 30 minutes of brisk exercise at least three times a week were found to have a significantly lower incidence of relapse.146 The support for the use of deep brain stimulation in treatment-resistant depression comes from a handful of case studies, and this treatment is still in a very early investigational stage.139 Tryptophan and 5-hydroxytryptophan may be more effective than placebo in alleviating depression according to the Cochrane Collaboration meta-analysis. However, only two out of 108 trials were of sufficient quality to be included in this analysis.147 Omega-3 fatty acids have been studied in clinical trials for major depression primarily as an adjunctive to antidepressant therapy. A meta-analysis of eight such trials indicated a statistically significant superiority of combinations with omega-3 fatty acids over single antidepressants; however, the authors warned that, due to multiple problems with these trials, a reliable conclusion is difficult to achieve.148 Dehydroepiandrosterone DHEA, available as a supplement in the US, has been shown to be more effective than placebo for major depression in two small double-blind trials: in one as an adjunctive to antidepressant treatment149, and in another as monotherapy.150 Chromium picolinate was found to be equivalent to placebo for atypical depression overall but possibly efficacious in the sub-group of patients with severe carbohydrate craving.151 Zinc supplementation was found in a small study to augment the effect of antidepressants.152 Cranial electrotherapy stimulation CES, electrosleep devices currently on the market have been granted marketing authorization by the FDA based on the legacy waver, that is because a sufficiently similar device had been marketed before 1976, when the new regulations requiring controlled testing were introduced.153 The FDA considers them to be the class III devices-devices for which insufficient information exists to ... provide reasonable assurance of safety and effectiveness154 The effects of CES on depression were inconclusive or negative in multiple double-blind studies of psychiatric patients.155156157158156159 In one of them, four out of six clinically depressed patients dropped out of the study because of the massive worsening of depressive symptoms, with two of them becoming actively suicidal.159 One of the authors of the latter study cautioned that CES should not be used as a treatment of choice for the patients with the primary diagnosis of depression, and should be used with caution if this diagnosis is suspected.160 Nevertheless, the CES practitioners continue to employ it as a treatment of choice for depression.161162 Prognosis Major depressive episodes often tend to resolve over time whether they are treated or not. Outpatients on a waiting list show a 10-15% decrease in symptoms over a few months, and around 20% will no longer meet full criteria.163 The median duration of an episode has been estimated to be at least 23 weeks, with the highest rate of recovery in the first three months.164 Studies recruiting from the general population indicate around half those who have a major depressive episode whether treated or not do not have any further episodes, but around half have at least one more and a minority experience chronic recurrence.165 Studies recruiting from selective inpatient sources suggest low recovery and high chronicity, but studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Recurrence occurs in 40% to 70% within several years, however, and overall about one tenth have poor, one third have intermediate, and one half have favorable outcomes. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.166167 There is a higher-than-average suicide risk in major depression. Articles and textbooks have often quoted a suicide rate of 15%, based on reviews of more severely depressed hospitalized patients. However, this was generalized to all people with major depression, both in and out of hospital. A reexamination indicated an approximate figure of 3.4%, with differing rates of around 7% for men and 1% for women.168169 Up to 60% of people who commit suicide have a mood disorder such as major depression, and their risk is especially high if they feel a marked sense of hopelessness or have both depression and borderline personality disorder.170 Depressed people also have a higher rate of dying from other causes.171 Major depression can be a serious and disabling condition that can significantly affect a person's work, family and school life, sleeping and eating habits, and general health.17 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. Combined evidence from many randomized controlled trials indicates that 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. Thus in a significant minority of patients depression recurs despite the prolonged treatment with antidepressants.172 The reason for recurrence in these cases is poorly understood and could be a true pharmacologic failure or a worsening of the disease, a relapse that overrides medication. Because of the difficulties of carrying out controlled clinical trials of longer duration, the approval of most antidepressants for the prevention of recurrence is based on trials that lasted up to a year.173 Epidemiology The National Comorbidity Survey Replication NCS-R, conducted from 2001 through 2002, found that 16.2% of people had suffered a major depressive episode in their lives.174 Lifetime prevalence estimates in community epidemiological surveys carried out by the World Health Organization in ten countries varied widely, from 3% in Japan to 16.9% in the US, with the majority between 8% to 12%.175 North American population studies have shown that 3-5% of males and 8-10% of females are suffering from a major depressive episode over a 12 month period.176177 Overall, major depression annually affects about 8.2% of the Canadian population and about 8.7% of the US population. Researchers who compared epidemiological factors in Canada and the US found the rate of major depression to be twice as high for Americans without medical insurance than either for Americans with insurance or for Canadians-for whom health care is publicly funded-in general.178 Population studies have consistently shown major depression to be more common in women, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.179 Major depression is currently the leading cause of disease burden in North America and high-income countries, and 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.180 History See also: History of mental disorders and Classification of mental disorders Prehistory to antiquity Notes in the Ancient Egyptian document known as the Ebers papyrus appear to refer to emotional distress of the heart or mind, which has been interpreted as sadness or depression.181 Passages of the Hebrew Bible Old Testament, composed and compiled between the 12th and 2nd centuries BC, have been interpreted as describing mood disorders in figures such as Job, King Saul and in the psalms of David.182 The four temperaments clockwise from top right; choleric; melancholic; sanguine; phlegmatic, according to an ancient theory of mental states The four temperaments clockwise from top right; choleric; melancholic; sanguine; phlegmatic, according to an ancient theory of mental states The modern idea of depression appears similar in some ways to the much older concept of melancholia, which derives its name from the Greek theory of the four humours: disease being caused by an imbalance in the four basic bodily fluids, or humors. Personality types were similarly thought to be determined by the dominant humor in a particular person. The theory was first put forward by Greek scholar Empedocles 490-430 BC, and was influentially adopted by Hippocrates 460-377 BC. Melancholia was thought to be caused by an excess of black bile; derived literally from the Ancient Greek μέλας, melas, black, + χολή, kholé, bile;183 a person whose constitution tended to have a preponderance of black bile was thought to have a melancholic disposition. Melancholia was described as a distinct disease with particular mental and physical symptoms by Hippocrates in his Aphorisms, where he characterized all fears and despondencies, if they last a long time as being symptomatic of melancholia.184 Between 150-200 AD, Aretaeus of Cappadocia noted that sufferers were dull or stern; dejected or unreasonably torpid, without any manifest cause. Although humoral theory fell out of favor in some quarters, it was later revived in Greece and the Roman Empire when Galen AD 129-ca. 200 proposed that melancholy was caused by animal spirits. Such accounts show similarities to more modern concepts that developed from the 19th century. Prominence was given to a clustering of sadness, dejection, and despondency symptoms, but also often included fear, anger, delusions and obsessions.185 Medieval to Renaissance eras Influenced by Greek and Roman texts, physicians in the Persian and then the Muslim empire developed ideas about melancholia during the Islamic Golden Age. Ishaq ibn Imran d. 908, known as Isaac in the West, combined the concepts of melancholia and phrenitis.186 In The Canon of Medicine 1020s, Avicenna described melancholia as a depressive type of mood disorder in which the person may become suspicious and develop certain types of phobias.187 The Canon of Medicine became the standard of medical science in Europe for centuries, together with works of Hippocrates and Galen.188 Galen's ideas about medicine dominated Western medical thinking from the medieval era until the Renaissance, in part because the Catholic church supported them. In addition to viewing mental illness through the lens of Galen's four humors, medieval Europeans viewed mental illness as the entry of demons or evil spirits into the body189 and either a punishment for sin or a test of faith and character.190 The Franciscan monk Bartholomeus Anglicus ca. 1203-1272 described a condition which resembles depression in his encyclopedia, De Proprietatibis Rerum, and he suggested that music would help people with this condition. In Christian settings, a spiritual malaise called acedia sloth or absence of caring was described, involving low spirits and lethargy, especially related to isolation. It was viewed as a spiritual disease, vice, or undesirable trait of character.191190 17th to 19th centuries The seminal scholarly work of the 17th century was Robert Burton's The Anatomy of Melancholy, drawing on numerous theories and the author's own experiences. Burton suggested that melancholy could be combated with a healthy diet, sufficient sleep, music, and meaningful work, along with talking about the problem with a friend.192193 Shakespeare's plays, such as Hamlet and King Lear, described characters with deep melancholy. There was increasing medical dissatisfaction with the concept of melancholia. During the 18th century its connections to humoral theory were increasingly challenged by mechanical and electrical explanations; references to dark and gloomy states gave way to ideas of slowed circulation and depleted energy.194 The German physician Johann Christian Heinroth 1773-1843, however, argued that melancholia was a disturbance of the soul due to moral conflict within the patient. Eventually various authors proposed up to 30 different subtypes of melancholia, and alternative terms were suggested and discarded. Hypochondria came to be seen as a separate disorder. Melancholia and Melancholy had been used interchangeably until the 19th century, but the former came to refer to a pathological condition and the latter to a temperament.185 The term depression was derived from the Latin verb deprimere, to press down.195 From the 14th century, to depress meant to subjugate or to bring down in spirits. An early published instance of a psychological usage of the noun was in 1665 in Richard Baker's Chronicle, referring to someone having a great depression of spirit, and Samuel Johnson used the term in a similar sense in 1753.196 The term also came in to use in physiology and economics. One of the earliest uses to refer to a psychiatric symptom was by Louis Delasiauve in 1856; by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.197 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.185 Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and by the end of the century it had become a synonym of melancholia; the German psychiatrist Emil Kraepelin 1855-1926 may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.182 English psychiatrist Henry Maudsley proposed an overarching category of affective disorder.198 20th century to the present day Emil Kraepelin helped to distinguish mood disorders from psychoses. Emil Kraepelin helped to distinguish mood disorders from psychoses. The influential system put forward by Emil Kraepelin unified nearly all types of mood disorder into manic-depressive insanity, with a separate category of Dementia praecox now known as schizophrenia. Kraepelin worked from an assumption of underlying brain pathology, but also promoted a distinction between endogenous and exogenous types.182 Kurt Schneider honed the terms and coined endogenous depression, commonly associated with prominent psychomotor slowing and seen in inpatients, and reactive depression, more usually seen in outpatients, in 1920.47 The latter was so named for reactivity in mood and not reaction to outside events and was frequently misinterpreted. This view was challenged in 1926 by British psychiatrist Edward Mapother, who found a continuum of severity, and noted no clear differences in cause, prognosis or treatment response.199 The unitarian view became more popular in the United Kingdom, while the binary view held sway in the US, influenced by the work of Adolf Meyer and before him Sigmund Freud.200 Freud had emphasized early life experiences and conflicting psychological drives; he associated melancholia with psychological loss and self-criticism.185 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.198 The 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, as well as including a depressive type of manic-depressive psychosis within Major affective disorders.201 The depressive reaction of the 1950s was distinguished from endogenous depression, purportedly a rare biological condition, which borrowed as a synonym the longstanding term, melancholic.202 In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in transmitters 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.203 During the 1960s and 70s, manic-depression came to refer to just one type of mood disorder now most commonly known as bipolar disorder which was distinguished from unipolar depression. The terms unipolar and bipolar had been coined by Karl Kleist.182 The term Major depressive disorder was introduced by a group of US psychiatrists 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, and was incorporated in to the DSM-III in 1980.204 In order 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.204205 The ancient idea of melancholia still survives in the notion of a melancholic subtype. The new definitions of depression were widely accepted, although there have been conflicting findings and views on the validity of imposing such categorical cut-offs on a continuum,206 and of not incorporating any evaluation of the personal and social context except for grief in which it occurs.207208 Debate has also continued about whether a categorical distinction between unipolar and bipolar distinction best reflects the evidence.209 There are also some continuing empirical arguments for a return to the diagnosis of melancholia.210211 Many causes for depression have been proposed.212 Biological psychiatrists, for example, explored the biological substrates of depression; psychiatrist David Healy wrote about the growth of the diagnosis, along with perspectives on the development and promotion of antidepressants and the biological model since the late 1950s.213 Sociocultural aspects 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.214 There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or an indicator of the need to address social problems, structural determinants of powerlessness, and emotional struggle.215216 The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatize emotional depression, or alternatively that Western cultures reframe and elevate some expressions of human distress to disorder status.217 Australian psychiatrist Gordon Parker and others have argued that the Western concept of depression medicalizes sadness or misery.202218 The influential psychologist William James was nearly driven to suicide during his depression. His choice to believe in free will was instrumental in helping him to overcome this condition. The influential psychologist William James was nearly driven to suicide during his depression. His choice to believe in free will was instrumental in helping him to overcome this condition.219 Evolutionary theorists view depression as an adaptation to regulate relationships or resources, although it may be unwanted or disordered in modern environments.220 From this perspective, depression can be seen 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.73 Like an ageing hunter in our foraging past, an alienated member of today's society may feel and act in ways that 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.69 These insights may be helpful in counselling therapy.73221 There is ongoing debate about the extent to which depression and mental illness in general may be linked to creativity in arts.222 The relationship between depression and creativity appears to be especially strong among female poets.223224 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 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.225 English essayist and wit Samuel Johnson used the term the black dog in 1780s to describe his own depression.226 Subsequently popularised by depression sufferer former British Prime Minister Sir Winston Churchill,226 the term lives on in the Black Dog Institute, an Australian facility for research and education into mood disorders such as major depression and bipolar disorder.227 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 the British writer Henry James228 and American president Abraham Lincoln.229230 Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen231 and American playwright and novelist Tennessee Williams.232 Even some pioneering psychologists, such as William James219233 and John B. Watson,234 dealt with depression in their adulthoods. For more information on historical and contemporary public figures who faced depression, see the List of people with depression. References ^ a b c d e American Psychiatric Association 2000, p. 349 ^ a b c d American Psychiatric Association 2000, p. 350 ^ a b Eaton WW, Anthony JC, Gallo J, Cai G, Tien A, Romanoski A, Lyketsos C, Chen LS 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. ^ a b c Rickards H 2005. Depression in 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. ^ Huffman JC, Smith FA, Blais MA, Taylor AM, Januzzi JL, Fricchione GL 2008. Pre-existing major depression predicts in-hospital cardiac complications after acute myocardial infarction. Psychosomatics 49 4: 309-16. PMID 18621936. ^ Kiloh LG 1961. Pseudodementia. Acta Psychiatrica Scandinavica 37: 336-51. PMID 14455934. ^ American Psychiatric Association 2000, p. 354 ^ Frank E, Prien RF, Jarrett RB, Keller MB, Kupfer DJ, Lavori PW, Rush AJ, Weissman MM 1991. Conceptualization and rationale for consensus definitions of terms in major depressive disorder. Remission, recovery, relapse, and recurrence. Archives of General Psychiatry 48 9: 851-55. doi:10.1001/archpsyc.48.9.851. PMID 1929776. ^ Sapolsky, Robert M., Ph.D. 2004. Why Zebras Don't Get Ulcers. Henry Holt and Company, LLC, 291-98. ISBN 0-8050-7369-8. ^ Grant BF 1995. Comorbidity between DSM-IV drug use disorders and major depression: results of a national survey of adults. Journal of Substance Abuse 7 4: 481-87. PMID 8838629. ^ Hallowell EM Ratey JJ 2005. Delivered from Distraction: Getting the Most out of Life with Attention Deficit Disorder. New York: Ballantine Books, pp. 253-55. ISBN 0-345-44231-8. ^ Dale J Sorour E, Milner G 2008. Do psychiatrists perform appropriate physical investigations for their patients? A review of current practices in a general psychiatric inpatient and outpatient setting. Journal of Mental Health 17 3: 293-98. doi:10.1080/09638230701498325. ^ Orengo C, Fullerton G, Tan R 2004. Male depression: A review of gender concerns and testosterone therapy. Geriatrics 59 10: 24-30. PMID 15508552. ^ Sadock 2002, p. 108 ^ Sadock 2002, p. 260 ^ Palmer B, Gates J Lader M 2003. Causes and Management of Hyponatremia. The Annals of Pharmacotherapy 37 11: 1694-702. doi:10.1345/aph.1D105. ^ a b c d Mayo Clinic Staff 2006-03-06. Depression PDF. National Institute of Mental Health NIMH. Retrieved on 2008-09-07. ^ Gilbody S, Sheldon T, Wessely S 2006. Should we screen for depression?. British Medical Journal 332: 1027-30. doi:10.1136/bmj.332.7548.1027. ^ Gilbody S, House AO, Sheldon TA 2005. Screening and case finding instruments for depression. Cochrane Database of Systematic Reviews 4. doi:10.1002/14651858.CD002792.pub2. ^ Beck Depression Inventory - 2nd ion. Nova Southeastern University Center for Center for Psychological Studies. ^ Beck AT 1972. Depression: Causes and Treatment. Philadelphia: University of Pennsylvania Press. ISBN 0-8122-1032-8. ^ Spitzer RL, Kroenke K, Williams JB November 1999. Validation and utility of a self-report version of PRIME-MD: The PHQ primary care study. Primary Care Evaluation of Mental Disorders. Patient Health Questionnaire. Journal of the American Medical Association 282 18: 1737-44. PMID 10568646. ^ Resources for Clinicians: Patient Health Questionnaire. The MacArthur Initiative on Depression Primary Care. Dartmouth College Duke University 2006. Retrieved on 2008-09-02. ^ Yesavage JA 1988. Geriatric Depression Scale. Psychopharmacology Bulletin 24 4: 709-11. ^ Hamilton M 1960. A rating scale for depression. Journal of Neurology, Neurosurgery and Psychiatry 23: 56-62. PMID 14399272. ^ Montgomery SA, Asberg M April 1979. A new depression scale designed to be sensitive to change. British Journal of Psychiatry 134: 382-89. PMID 444788. ^ Sadock 2002, p. 288 ^ American Psychiatric Association 2000, p. 345 ^ World Health Organization Mood affective disorders ICD-10, Chapter V, Mental and behavioural disorders ^ American Psychiatric Association 2000, p. 372 ^ Parker 1996, p. 173 ^ American Psychiatric Association 2000, p. 352 ^ American Psychiatric Association 2000, p. 421-22 ^ Sadock 2002, p. 548 ^ American Psychiatric Association 2000, p. 419-20 ^ American Psychiatric Association 2000, p. 412 ^ American Psychiatric Association 2000, p. 417-18 ^ Ruta M Nonacs. eMedicine - Postpartum Depression ^ American Psychiatric Association 2000, p. 425 ^ Sadock 2002, p. 552 ^ American Psychiatric Association 2000, p. 778 ^ Carta, Mauro Giovanni; Altamura, Alberto Carlo; Hardoy, Maria Carolina et 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. ^ Rapaport MH, Judd LL, Schettler PJ, Yonkers KA, Thase ME, Kupfer DJ, Frank E, Plewes JM, Tollefson GD, Rush AJ 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. ^ American Psychiatric Association 2000, p. 355 ^ a b Parker G 2000. abstract Classifying depression: Should paradigms lost be regained?. American Journal of Psychiatry 157: 1195-1203. doi:10.1176/appi.ajp.157.8.1195. ^ Akiskal HS, McKinney WT 1975. Overview of recent research in depression: Integration of ten conceptual models into a comprehensive clnical frame. Archives of General Psychiatry 32: 285-305. PMID 1092281. ^ a b Schneider, K 1920. Zeitschrift für die gesante. Neurol Psychiatr 59: 281-86. ^ Rabasca, L. 2000. Personality styles may predict susceptibility to depression. American Psychological Association APA website. American Psychological Association. Retrieved on 2008-09-12. ^ Vranceanu A-M, Hobfoll SE, Johnson RJ 2007. Child multi-type maltreatment and associated depression and PTSD symptoms: The role of social support and stress. Child Abuse Neglect 31: 71-84. doi:10.1016/j.chiabu.2006.04.010. PMID 1839899. ^ N. J. C. Andreasen April 1972. The role of religion in depression. Journal of Religion and Health 11 2: 153-66. Springer. doi:10.1007/BF01533217. ^ Brown GW, Harris TO 1978 2001. Social Origins of Depression: A Study of Psychiatric Disorder in Women. Routledge. ISBN 0-415-20268-X. ^ a b Patten, SB December 1991. Are the Brown and Harris vulnerability factors risk factors for depression?. Journal of Psychiatry Neuroscience 16 5: 267-71. PMID 1188364. ^ Warman, Debbie M., Beck, Aaron T. june 2003. About Treatment and Supports: Cognitive Behavioral Therapy. National Alliance on Mental Illness NAMI website. ^ Seligman MEP 1975. Helplessness: On Depression, Development and Death. San Francisco, CA, USA: WH Freeman. ISBN 0716707519. ^ Benassi, V; Sweeney PD Dufour C 1988. Is there a relation between locus of control orientation and depression?. Journal of Abnormal Psychology 97 3: 357-67. doi:10.1037/0021-843X.97.3.357. ^ a b c Barlow 2005, p. 230-32 ^ Pinto, A; Francis G 1993. Cognitive correlates of depressive symptoms in hospitalized adolescents. Adolescence 28 111: 661-72. PMID 8237551. ^ Kanfer, R; Zeiss A 1983. Depression, Interpersonal Standard Setting. Journal of Abnormal Psychology 92 3: 319-29. PMID 6619407. ^ Bandura, A 1998. Self-Efficacy, in Friedman H: Encyclopedia of Mental Health. San Diego: Academic Press. Retrieved on 2008-08-17. ^ Alloy LB, Abramson LY 1979. Judgment of contingency in depressed and nondepressed students: Sadder but wiser?. Journal of Experimental Psychology: General 108: 441-85. ^ Taylor SE 1991. Positive illusions: Creative self-deception and the healthy mind. New York, NY, USA: Basic Books. ISBN 0465060536. ^ Freud S Strachey J, Trans. 1953-74. The standard ion of the complete psychological works of Sigmund Freud 22, p. 61. ^ 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. Ann Gen Psychiatry 7: 9. doi:10.1186/1744-859X-7-9. PMID 18652673. PMC:2515304. ^ Biologic, Syndromic, Social, and Personal Damage - Psychiatric Times ^ a b May R 1996. The Meaning Of Anxiety. New York, NY, USA: W. W. Norton and Company. ISBN 0-393-31456-1. ^ Fromm, Erich 1941. Escape from Freedom. New York, NY, USA: Holt, Rinehart, Winston. ^ Heidegger, Martin 1927. Being and Time. Halle, Germany: Niemeyer. ^ Hergenhahn 2005, p. 546-47 ^ a b Mashman, RC 1997. An evolutionary view of psychic misery. Journal of Social Behaviour Personality 12: 979-99. ^ Nesse RM January 2000. Is depression an adaptation?. Archives of General Psychiatry 57 1: 14-20. PMID 10632228. ^ a b Sloman L, Gilbert P, Hasey G April 2003. Evolved mechanisms in depression: the role and interaction of attachment and social rank in depression. Journal of Affective Disorders 74 2: 107-21. PMID 12706512. ^ Gilbert P 2000. Overcoming Depression: A Self-Help Guide Using Cognitive Behavioral Techniques 2nd rev. ed.. London, UK: Robinson Publishing. ISBN 1841191256. ^ a b c Carey TJ 2005. Evolution, depression and counselling. Counselling Psychology Quarterly 18 3: 215-22. ^ 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. ^ 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. ^ Mandell AJ, Knapp S 1979. Asymmetry and mood, emergent properties of serotonin regulation: A proposed mechanism of action of lithium. Archives of General Psychiatry 36 8: 909-16. PMID 454111. ^ Lacasse JR, Leo J December 2005. Serotonin and depression: A disconnect between the advertisements and the scientific literature PDF. PLoS Medicine website. PLoS medicine. ^ Meyer JH, Ginovart N, Boovariwala A, et al. November 2006. Elevated monoamine oxidase a levels in the brain: An explanation for the monoamine imbalance of major depression. Arch Gen Psychiatry 63 11: 1209-16. doi:10.1001/archpsyc.63.11.1209. PMID 17088501. ^ Mayberg, Helen July 6, 2007. Brain Pathway May Underlie Depression. Scientific American 17 4: pp. 26-31. Retrieved on 2008-09-13. ^ Sheline YI, Gado MH, Kraemer HC 2003. Untreated depression and hippocampal volume loss. American Journal of Psychiatry 160: 1516-18. PMID 12900317. ^ Duman RS, Heninger GR, Nestler EJ 1997. A molecular and cellular theory of depression. Archives of General Psychiatry 54 7: 597-606. PMID 9236543. ^ Drevets WC, Savitz J, Trimble M August 2008. The subgenual anterior cingulate cortex in mood disorders. CNS Spectrums 13 8: 663-81. PMID 18704022. ^ Sen S, Duman R, Sanacora G September 2008. Serum brain-derived neurotrophic factor, depression, and antidepressant medications: meta-analyses and implications. Biological Psychiatry 64 6: 527-32. doi:10.1016/j.biopsych.2008.05.005. PMID 18571629. ^ Carmine M. Pariante, Institute of Psychiatry, King's College London Depression, stress and the adrenal axis. The British Society for Neuroendocrinology, 2003. ^ Barlow 2005, p. 227-28 ^ Wijeratne, Chanaka, Sachdev, Perminder 2008. Treatment-resistant depression: critique of current approaches.. Australian and New Zealand Journal of Psychiatry 42: 751-62. PMID 18696279. ^ Thase, ME 1999. When are 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. ^ NICE 2005. NICE guidelines: Depression in children and adolescents. London: NICE, p. 5. ISBN 1-84629-074-0. Retrieved on 2008-08-16. ^ Roth, Anthony; Fonagy, Peter 1996 2005. What Works for Whom? Second ion: A Critical Review of Psychotherapy Research. Guilford Press, p. 78. ISBN 159385272X. ^ March J, Silva S, Petrycki S, et al. August 2004. Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study TADS randomized controlled trial. JAMA 292 7: 807-20. doi:10.1001/jama.292.7.807. PMID 15315995. ^ Goodyer I, Dubicka B, Wilkinson P, et al. 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. British Medical Journal 335 7611: 142. doi:10.1136/bmj.39224.494340.55. PMID 17556431. ^ Goodyer IM, Dubicka B, Wilkinson P, et 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 Technol Assess 12 14: 1-80. PMID 18462573. ^ Domino ME, Burns BJ, Silva SG, et al. 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. ^ Coelho HF, Canter PH, Ernst E 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. ^ Weissman MM, Markowitz JC, Klerman GL 2000. Comprehensive Guide to Interpersonal Psychotherapy. New York: Basic Books. ISBN 0-465-09566-6. ^ Dworetzky J 1997. Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co, 602. ISBN 0-314-20412-1. ^ Doidge N, Simon B, Lancee WJ, et al. 2002. Psychoanalytic patients in the US, Canada, and Australia: II. A DSM-III-R validation study. Journal of the American Psychoanalytic Association 50 2: 615-27. PMID 12206545. ^ Durand VM, Barlow D 1999. Abnormal psychology: An integrative approach. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. ISBN 0-534-34742-8. ^ de Maat S, Dekker J, Schoevers R, et al. 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. ^ Depression Guideline Panel. Depression in primary care. Vol. 2. Treatment of major depression. Clinical practice guideline. No. 5. Rockville, MD: Agency for Health Care Policy and Research, 1999. ^ Sutherland JE, Sutherland SJ, Hoehns JD March 2003. Achieving the best outcome in treatment of depression. Journal of Family Practice 52 3: 201-09. PMID 12620174. ^ Zisook S, Rush AJ, Haight BR, Clines DC, Rockett CB 2006. Use of bupropion in combination with serotonin reuptake inhibitors. Biological Psychiatry 59 3: 203-10. doi:10.1016/j.biopsych.2005.06.027. PMID 16165100. ^ Rush AJ, Trivedi MH, Wisniewski SR, Stewart JW, Nierenberg AA, Thase ME, Ritz L, Biggs MM, Warden D, Luther JF, Shores-Wilson K, Niederehe G, Fava M 2006. Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression. New England Journal of Medicine 354 12: 1231-42. doi:10.1056/NEJMoa052963. PMID 16554525. ^ Trivedi MH, Fava M, Wisniewski SR, Thase ME, Quitkin F, Warden D, Ritz L, Nierenberg AA, Lebowitz BD, Biggs MM, Luther JF, Shores-Wilson K, Rush AJ 2006. Medication augmentation after the failure of SSRIs for depression. New England Journal of Medicine 354 12: 1243-52. doi:10.1056/NEJMoa052964. PMID 16554526. ^ Mayers AG, Baldwin DS December 2005. Antidepressants and their effect on sleep. Human Psychopharmacology 20 8: 533-59. doi:10.1002/hup.726. PMID 16229049. ^ Winokur A, DeMartinis NA, McNally DP, Gary EM, Cormier JL, Gary KA October 2003. Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia. Journal of Clinical Psychiatry 64 10: 1224-29. PMID 14658972. ^ Lawrence RW August 2004. Effect of mirtazapine versus fluoxetine on sleep quality. Journal of Clinical Psychiatry 65 8: 1149-50. PMID 15323610. ^ Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC December 2007. Are antidepressant drugs that combine serotonergic and noradrenergic mechanisms of action more effective than the selective serotonin reuptake inhibitors in treating major depressive disorder? A meta-analysis of studies of newer agents. Biological Psychiatry 62 11: 1217-27. doi:10.1016/j.biopsych.2007.03.027. PMID 17588546. ^ Cipriani A, Geddes JR, Barbui C 2007. Venlafaxine for major depression. British Medical Journal 334: p. 215 orial. doi:10.1136/bmj.39098.457720.BE. Retrieved on 2008-09-13. ^ Depression in children and young people: identification and management in primary, community and secondary care. NHS National Institute for Health and Clinical Excellence September 2005. Retrieved on 2008-08-17. ^ Depression in children and young people: identification and management in primary, community and secondary care. NHS National Institute for Health and Clinical Excellence September 2005. Retrieved on 2008-08-17. ^ Anderson IM 1998. SSRIS versus tricyclic antidepressants in depressed inpatients: A meta-analysis of efficacy and tolerability. Depression and Anxiety 7 Suppl 1: 11-17. PMID 9597346. ^ Anderson IM April 2000. Selective serotonin reuptake inhibitors versus tricyclic antidepressants: A meta-analysis of efficacy and tolerability. Journal of Affective Disorders 58 1: 19-36. PMID 10760555. ^ Krishnan KR 2007. Revisiting monoamine oxidase inhibitors. Journal of Clinical Psychiatry 68 Suppl 8: 35-41. PMID 17640156. ^ Valenstein M, McCarthy JF, Austin KL, 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. ^ Bauer M, Dopfmer S 1999. Lithium augmentation in treatment-resistant depression: Meta-analysis of placebo-controlled studies. Journal of Clinical Psychopharmacology 19 5: 427-34. doi:10.1097/00004714-199910000-00006. PMID 10505584. ^ Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ March 2007. Lithium treatment reduces suicide risk in recurrent major depressive disorder. J Clin Psychiatry 68 3: 380-83. PMID 17388706. ^ Bender KJ 2008-02-01. Evidence Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times htm. Psychiatric Times. Retrieved on 2008-08-06. ^ Nierenberg AA, Fava M, Trivedi MH, 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 T3 augmentation following two failed medication treatments for depression: A STARD report. American Journal of Psychiatry 163 9: 1519-30. doi:10.1176/appi.ajp.163.9.1519. PMID 16946176. ^ a b Kirsch I, Deacon BJ, Huedo-Medina TB, 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. ^ Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R January 2008. Selective publication of antidepressant trials and its influence on apparent efficacy. N. Engl. J. Med. 358 3: 252-60. doi:10.1056/NEJMsa065779. PMID 18199864. ^ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP 1989. National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments. Archives of General Psychiatry 46 11: 971-82; discussion 983. PMID 2684085. ^ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D 1995. Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program. Journal of Consulting and Clinical Psychology 63 5: 841-47. PMID 7593878. ^ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J 1991. Patient predictors of response to psychotherapy and pharmacotherapy: Findings in the NIMH Treatment of Depression Collaborative Research Program. American Journal of Psychiatry 148 8: 997-1008. PMID 1853989. ^ Turner EH, Rosenthal R March 2008. Efficacy of antidepressants. BMJ 336 7643: 516-7. doi:10.1136/bmj.39510.531597.80. PMID 18319297. ^ a b c Cuijpers P, van Straten A, van Oppen P, Andersson G August 2008. Are Psychological and Pharmacologic Interventions Equally Effective in the Treatment of Adult Depressive Disorders? A Meta-Analysis of Comparative Studies. Journal of Clinical Psychiatry: e1-e11. ^ a b c Imel ZE, Malterer MB, McKay KM, Wampold BE October 2008. A meta-analysis of psychotherapy and medication in unipolar depression and dysthymia. J Affect Disord 110 3: 197-206. doi:10.1016/j.jad.2008.03.018. PMID 18456340. ^ a b American Psychiatric Association April 2000. Practice guideline for the treatment of patients with major depressive disorder. American Journal of Psychiatry 157 Supp 4: 1-45. PMID 10767867. ^ The UK ECT Review Group 2003. Efficacy and safety of electroconvulsive therapy in depressive disorders: A systematic review and meta-analysis. The Lancet 361 9360: 799-808. ^ McCall WV, Prudic J, Olfson M, Sackeim H February 2006. Health-related quality of life following ECT in a large community sample. Journal of Affective Disorders 90 2-3: 69-74. PMID 16412519. ^ Barlow 2005, p. 239 ^ American Psychiatric Association. Electroconvulsive Therapy ECT. Retrieved on 2007-12-29. ^ National Institute for Clinical Excellence 2003. Guidance on the use of electroconvulsive therapy PDF, London: National Institute for Health and Clinical Excellence. ISBN 1-84257-282-2. ^ Linde K, Mulrow CD, Berner M, Egger M 2005. St John's wort for depression. Cochrane Database Syst Rev 2: CD000448. doi:10.1002/14651858.CD000448.pub2. PMID 15846605. ^ St. John's Wort and Depression National Center for Complementary and Alternative Medicine. NCCAM Publication No. D005. Updated December 2007. Retrieved on 2008-09-03. ^ How is depression detected and treated? NIMH on depression, including a section on St John's wort ^ Mischoulon D, Fava M November 2002. Role of S-adenosyl-L-methionine in the treatment of depression: A review of the evidence. American Journal of Clinical Nutrition 76 5: 1158S-61S. PMID 12420702. ^ Bressa GM 1994. S-adenosyl-l-methionine SAMe as antidepressant: Meta-analysis of clinical studies. Acta Neurologica Scandinavica, Suppl. 154: 7-14. PMID 7941964. ^ a b c Marangell LB, Martinez M, Jurdi RA, 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. ^ Schutter DJ April 2008. Antidepressant efficacy of high-frequency transcranial magnetic stimulation over the left dorsolateral prefrontal cortex in double-blind sham-controlled designs: A meta-analysis. Psychological Medicine: 1-11. doi:10.1017/S0033291708003462. PMID 18447962. ^ Eranti S, Mogg A, Pluck G, et al. January 2007. A randomized, controlled trial with 6-month follow-up of repetitive transcranial magnetic stimulation and electroconvulsive therapy for severe depression. American Journal of Psychiatry 164 1: 73-81. doi:10.1176/appi.ajp.164.1.73. PMID 17202547. ^ Rush AJ, Marangell LB, Sackeim HA, et 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. ^ Golden RN, Gaynes BN, Ekstrom RD, et al. April 2005. The efficacy of light therapy in the treatment of mood disorders: A review and meta-analysis of the evidence. American Journal of Psychiatry 162 4: 656-62. doi:10.1176/appi.ajp.162.4.656. PMID 15800134. ^ Tuunainen A, Kripke DF, Endo T 2004. Light therapy for non-seasonal depression. Cochrane Database Syst Rev 2: CD004050. doi:10.1002/14651858.CD004050.pub2. PMID 15106233. ^ Smith, CA; PPJ Hay 2005. Acupuncture for Depression. Cochrane Database of Systematic Reviews 2005 2: CD004046. doi:10.1002/14651858.CD004046.pub2. ^ Merritt, R 2000-09-22. Study: Exercise has long-lasting effect on depression. Duke University News. Retrieved on 2008-09-07. ^ Shaw K, Turner J, Del Mar C 2002. Tryptophan and 5-hydroxytryptophan for depression. Cochrane Database of Systematic Reviews 1: CD003198. doi:10.1002/14651858.CD003198. PMID 11869656. ^ Appleton KM, Hayward RC, Gunnell D, et al. December 2006. Effects of n-3 long-chain polyunsaturated fatty acids on depressed mood: Systematic review of published trials. American Journal of Clinical Nutrition 84 6: 1308-16. PMID 17158410. ^ Wolkowitz OM, Reus VI, Keebler A, et al. April 1999. Double-blind treatment of major depression with dehydroepiandrosterone. American Journal of Psychiatry 156 4: 646-49. PMID 10200751. ^ Schmidt PJ, Daly RC, Bloch M, et al. February 2005. Dehydroepiandrosterone monotherapy in midlife-onset major and minor depression. Archives of General Psychiatry 62 2: 154-62. doi:10.1001/archpsyc.62.2.154. PMID 15699292. ^ Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR September 2005. A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression: Effect on carbohydrate craving. Journal of Psychiatric Practice 11 5: 302-14. PMID 16184071. ^ Nowak G, Siwek M, Dudek D, Zieba A, Pilc A 2003. Effect of zinc supplementation on antidepressant therapy in unipolar depression: A preliminary placebo-controlled study PDF. Polish Journal of Pharmacology 55 6: 1143-47. PMID 14730113. ^ FDA CDRH CFR Title 21 Database Search ^ FDA 515i Reclassification Letter to Manufacturers ^ Levitt EA, James NM, Flavell P December 1975. A clinical trial of electrosleep therapy with a psychiatric inpatient sample. Australian and New Zealand Journal of Psychiatry 9 4: 287-90. PMID 769773. ^ a b Passini FG, Watson CG, Herder J October 1976. The effects of cerebral electric therapy electrosleep on anxiety, depression, and hostility in psychiatric patients. Journal of Nervous and Mental Disorders 163 4: 263-66. PMID 972328. ^ Philip P, Demotes-Mainard J, Bourgeois M, Vincent JD March 1991. Efficiency of transcranial electrostimulation on anxiety and insomnia symptoms during a washout period in depressed patients. A double-blind study. Biological Psychiatry 29 5: 451-56. PMID 2018818. ^ Moore JA, Mellor CS, Standage KF, Strong H 1975. A double-blind study of electrosleep for anxiety and insomnia. Biological Psychiatry 10 1: 59-63. PMID 1091305. ^ a b Feighner JP, Brown SL, Olivier JE 1973. Electrosleep therapy. A controlled double blind study. Journal of Nervous and Mental Disorders 157 2: 121-28. PMID 4724809. ^ Feighner JP 1971. Electrosleep therapy: Current usage in psychiatry. California Medicine 115 3: 44. PMID 18730592. ^ Shealy CN October 2003. Transcutaneous electrical nerve stimulation: The treatment of choice for pain and depression. Journal of Alternative and Complementary Medicine 9 5: 619-23. doi:10.1089/107555303322524463. PMID 14629839. ^ Shealy CN, Thomlinson P 2008. Safe effective nondrug treatment of chronic depression: A review of research on low-voltage cranial electrical stimulation and other adjunctive therapies. Complementary Health Practice Review 13 2: 92-99. doi:10.1177/1533210108317232. ^ Posternak MA, Miller I 2001. 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. PMID 11578666. ^ Posternak MA, Solomon DA, Leon AC, Mueller TI, Shea MT, Endicott J, Keller MB 2006. The naturalistic course of unipolar major depression in the absence of somatic therapy. Journal of Nervous and Mental Disease 194 5: 324-29. PMID 16699380. ^ Eaton WW, Shao H, Nestadt G, Lee BH, Bienvenu OJ, Zandi P 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. ^ Holma KM, Holma IA, Melartin TK, Rytsälä HJ, Isometsä ET February 2008. Long-term outcome of major depressive disorder in psychiatric patients is variable. Journal of Clinical Psychiatry 69 2: 196-205. PMID 18251627. ^ Kanai T, Takeuchi H, Furukawa TA, et al. July 2003. Time to recurrence after recovery from major depressive episodes and its predictors. Psychological Medicine 33 5: 839-45. PMID 12877398. ^ Bostwick, JM; Pankratz VS 2000. Affective disorders and suicide risk: A reexamination. American Journal of Psychiatry 157 12: 1925-32. PMID 11097952. ^ Blair-West GW, Mellsop GW 2001. 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. PMID 11437805. ^ Barlow 2005, p. 248-49 ^ Rush AJ 2007. The varied clinical presentations of major depressive disorder. The Journal of clinical psychiatry 68 Supplement 8: 4-10. PMID 17640152. ^ Geddes JR, Carney SM, Davies C, et al. February 2003. Relapse prevention with antidepressant drug treatment in depressive disorders: A systematic review. Lancet 361 9358: 653-61. doi:10.1016/S0140-67360312599-8. PMID 12606176. ^ Skirmish or Siege? Is depression primarily a recurring disease? Can you ever really be cured? Psychology Today ^ Kessler RC, Berglund P, Demler O, Jin R, Koretz D, Merikangas KR, Rush AJ, Walters EE, Wang PS 2003. The epidemiology of major depressive disorder: Results from the National Comorbidity Survey Replication NCS-R. JAMA 289 203: 3095-105. PMID 12813115. ^ Andrade L, Caraveo-Anduaga JJ, 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. PMID 12830306. ^ Kessler RC, Berglund P, Demler O, Jin R, 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. ^ Murphy JM, Laird NM, Monson RR, 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. ^ Vasiliadis H-M, Lesage A, Adair C, Wang PS, Kessler RC January 2007. Do Canada and the United States differ in prevalence of depression and utilization of services?. Psychiatric Services 58 1: 63-71. PMID 17215414. ^ Kuehner, C 2003. Gender differences in unipolar depression: An 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. ^ Mathers CD, Loncar D November 2006. 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. ^ Nasser, M. 1987 Psychiatry in Ancient Egypt PDF. Bulletin Of The Royal College Of Psychiatrists, Vol 11, December. ^ a b c d Davison, K 2006. Historical aspects of mood disorders. Psychiatry 5 4: 115-18. ^ Liddell, Henry George and Robert Scott 1980. A Greek-English Lexicon Abridged ion. United Kingdom: Oxford University Press. ISBN 0-19-910207-4. ^ Hippocrates, Aphorisms, Section 6.23 ^ a b c d Radden, J March 2003. Is this dame melancholy? Equating today's depression and past melancholia. Philosophy, Psychiatry, Psychology 10 1: 37-52. ^ Jacquart, D, The Influence of Arabic Medicine in the Medieval West, pp. 980 in Morrison Rashed 1996, pp. 963-84 ^ Amber Haque 2004, Psychology from Islamic perspective: Contributions of early Muslim scholars and challenges to contemporary Muslim psychologists, Journal of Religion and Health 43 4: 357-377 366. ^ S Safavi-Abbasi, LBC Brasiliense, RK Workman 2007, The fate of medical knowledge and the neurosciences during the time of Genghis Khan and the Mongolian Empire, Neurosurgical Focus 23 1, E13, p. 3. ^ Kent 2003, p. 34 ^ a b Merkel, L. 2003 The History of Psychiatry PGY II Lecture Website of the University of Virginia Health System. Retrieved on 2008-08-04 ^ Daly, RW 2007. Before depression: The medieval vice of acedia. Psychiatry: Interpersonal Biological Processes 70 1: 30-51. doi:10.1521/psyc.2007.70.1.30. ^ Kent 2003, p. 55 ^ http://www.gutenberg.org/files/10800/10800-8.txt ^ Jackson SW July 1983. Melancholia and mechanical explanation in eighteenth-century medicine. Journal of the History of Medical and Allied Sciences 38 3: 298-319. PMID 6350428. ^ depress. n.d.. Online Etymology Dictionary. Retrieved June 30, 2008, from Dictionary.com ^ Wolpert, L. 2001 Malignant Sadness: The Anatomy of Depression. Faber and Faber. New ion, introduction. ISBN 0571207278 ^ Berrios GE September 1988. Melancholia and depression during the 19th century: A conceptual history. British Journal of Psychiatry 153: 298-304. PMID 3074848. ^ a b Lewis, AJ 1934. Melancholia: A historical review. Journal of Mental Science 80: 1-42. doi:10.1192/bjp.80.328.1. ^ Mapother, E 1926. Discussion of manic-depressive psychosis. British Medical Journal 2: 872-79. ^ Parker 1996, p. 11 ^ American Psychiatric Association 1968. Schizophrenia, Diagnostic and statistical manual of mental disorders: DSM-II PDF, Washington, DC: American Psychiatric Publishing, Inc.. Retrieved on 2008-08-03. ^ a b Parker, G 2007. Is depression overdiagnosed? Yes. British Medical Journal 335 7615: 328. doi:10.1136/bmj.39268.475799.AD. PMID 17703040. ^ Schildkraut, JJ 1965. The catecholamine hypothesis of affective disorders: A review of supporting evidence. American Journal of Psychiatry 122 5: 509-22. ^ a b 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. ^ Gruenberg, A.M., Goldstein, R.D., Pincus, H.A. 2005 Classification of Depression: Research and Diagnostic Criteria: DSM-IV and ICD-10 PDF. ^ Kendler KS, Gardner CO February 1998. Boundaries of major depression: An evaluation of DSM-IV criteria. American Journal of Psychiatry 155 2: 172-77. PMID 9464194. ^ Wakefield JC, Schmitz MF, First MB, 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. ^ Vedantam, S. 2007 Criteria for depression are too broad, researchers say: Guidelines may encompass many who are just sad Washington Post, April 3, P.A02 ^ Akiskal HS, Benazzi F May 2006. The 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. ^ Melancholia: Beyond DSM, beyond neurotransmitters. Proceedings of a conference, May 2006, Copenhagen, Denmark 2007. Acta Psychiatrica Scandinavica Suppl 115 433: 4-183. doi:10.1111/j.1600-0447.2007.00956.x. PMID 17280564. ^ Fink M, Bolwig TG, Parker G, Shorter E 2007. Melancholia: Restoration in psychiatric classification recommended. Acta Psychiatrica Scandinavica 115 2: 89-92. doi:10.1111/j.1600-0447.2006.00943.x. ^ Castrén, E 2005. Is mood chemistry?. Nature Reviews Neuroscience 6 3: 241-46. PMID 15738959. ^ Healy, David. 1999. The Antidepressant Era, Paperback ion, Harvard University Press. ISBN 0-674-03958-0 ^ Maloney, F. 2005 The Depression Wars: Would Honest Abe have written the Gettysburg Address on Prozac? Slate, Culturebox, Nov 3rd. ^ Karasz A April 2005. Cultural differences in conceptual models of depression. Social Science in Medicine 60 7: 1625-35. doi:10.1016/j.socscimed.2004.08.011. PMID 15652693. ^ Tilbury, F., Rapley, M. 2004 'There are orphans in Africa still looking for my hands': African women refugees and the sources of emotional distress Health Sociology Review. Vol 13, Issue 1, 54-64 ^ Parker, G; Gladstone G, Chee KT 2001. Depression in the planet's largest ethnic group: The Chinese. American Journal of Psychiatry 158 6: 857-64. PMID 11384889. ^ Pilgrim D, Bentall R 1999. The medicalisation of misery: A critical realist analysis of the concept of depression. Journal of Mental Health 8 3: 261-74. ^ a b James H Ed. 1920. Letters of William James Vols. 1 and 2. Boston, MA, USA: Atlantic Monthly Press, 147-48. ^ Klein, J.M. 2007 The mind, as it evolves. Los Angeles Times, Health, February 12. ^ Geoghegan T Thursday, 28 February 2008, Is depression good for you?, http://news.bbc.co.uk/1/hi/magazine/7268496.stm ^ Simonton, DK June 2005. Are genius and madness related? Contemporary answers to an ancient question. Psychiatric Times 22 7. ^ Kaufman, JC 2001. The Sylvia Plath effect: Mental illness in eminent creative writers. Journal of Creative Behavior 35 1: 37-50. ^ Bailey, DS 2003. Considering Creativity: The 'Sylvia Plath' effect. Journal of Creative Behavior 34 10: 42. ^ Mill JS 1873. A crisis in my mental history: One stage onward, Autobiography txt, Project Gutenberg EBook, 1826-32. Retrieved on 2008-08-09. ^ a b 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. Retrieved on 2008-08-18. ^ Overview. Black Dog Institute website. Black Dog Institute November 2007. Retrieved on 2008-08-18. ^ Henry James. pbs.org. Retrieved on 2008-08-19. ^ Burlingame, Michael. The inner world of Abraham Lincoln ISBN 0-252-06667-7 ^ http://info.epmhmr.org/poc/view_doc.php?id=2941type=bookcn=5 ^ Pita, Elena An Intimate Conversation with...Leonard Cohen, El Mundo September 26, 2001 translated from Spanish ^ Jeste ND, Palmer BW, Jeste DV 2004. Tennessee Williams. American Journal of Geriatric Psychiatry 12 4: 370-75. doi:10.1176/appi.ajgp.12.4.370. PMID 15249274. ^ Hergenhahn 2005, p. 311 ^ Cohen D 1979. J. B. Watson: The Founder of Behaviourism. London, UK: Routledge Kegan Paul, 7. ISBN 0710000545. Cited texts American Psychiatric Association 2000, Diagnostic and statistical manual of mental disorders, Fourth ion, Text Revision: DSM-IV-TR, Washington, DC: American Psychiatric Publishing, Inc., pp. 943, ISBN 0890420254 Barlow, DH 2005, Abnormal psychology: An integrative approach 5th ed., Belmont, CA, USA: Thomson Wadsworth, ISBN 0534633560 Kent, Deborah 2003, Snake Pits, Talking Cures Magic Bullets: A History of Mental Illness, Twenty-First Century Books, ISBN 0761327045 Hergenhahn, BR 2005, An Introduction to the History of Psychology 5th ion ed., Belmont, CA, USA: Thomson Wadsworth, ISBN 0534554016 Parker, Gordon 1996, Melancholia: A disorder of movement and mood: a phenomenological and neurobiological review, Cambridge: Cambridge University Press, ISBN 052147275X Sadock, Benjamin J. 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 mindsite.com Depression at Epocrates Online Black Dog Institute - Depression and Bipolar Disorder Information Australia Depression at the Open Directory Project National Alliance on Mental Illness - Depression support, advocacy, and education National Depressive and Manic Depressive Association - National Depressive and Manic Depressive Association v d e WHO ICD-10 mental and behavioral disorders F · 290-319 Neurological/symptomatic Dementia Alzheimer's disease, multi-infarct dementia, Pick's disease, Creutzfeldt-Jakob disease, Huntington's disease, Parkinson's disease, AIDS dementia complex, Frontotemporal dementia, Elopement, Sundowning, Wandering · Delirium · Post-concussion syndrome · Organic brain syndrome Psychoactive substance alcohol drunkenness, alcohol dependence, alcoholic hallucinosis, Alcohol withdrawal, delirium tremens, Korsakoff's syndrome, alcohol abuse · opioids opioid dependency · sedative/hypnotic benzodiazepine withdrawal · cocaine cocaine dependence · general Intoxication, Drug abuse, Physical dependence, Withdrawal Psychotic disorder Schizophrenia disorganized schizophrenia · Schizophreniform disorder · Schizotypal personality disorder · Delusional disorder · Folie à deux · Schizoaffective disorder Mood affective Mania · Bipolar disorder · Clinical depression · Cyclothymia · Dysthymia Neurotic, stress-related and somatoform Anxiety disorder Agoraphobia, Panic disorder, Panic attack, Generalized anxiety disorder, Social anxiety, Social phobia · OCD · Acute stress reaction · PTSD · Adjustment disorder · Conversion disorder Ganser syndrome · Somatoform disorder Somatization disorder, Body dysmorphic disorder, Hypochondriasis, Nosophobia, Da Costa's syndrome, Psychalgia · Neurasthenia Physiological/physical behavioral Eating disorder: Anorexia nervosa · Bulimia nervosa Sleep disorder: Dyssomnia Hypersomnia, Insomnia · Parasomnia REM behavior disorder, Night terror · Nightmare Sexual dysfunction: Erectile dysfunction · Premature ejaculation · Vaginismus · Dyspareunia · Hypersexuality · Female sexual arousal disorder Postpartum depression · Postnatal psychosis Adult personality and behavior Personality disorder · Passive-aggressive behavior · Kleptomania · Trichotillomania · Voyeurism · Factitious disorder · Munchausen syndrome · Ego-dystonic sexual orientation · Fetishism Mental retardation Mental retardation Psychological development developmental disorder Specific: speech and language expressive language disorder, aphasia, expressive aphasia, receptive aphasia, Landau-Kleffner syndrome, lisp · Scholastic skills dyslexia, dysgraphia, Gerstmann syndrome · Motor function developmental dyspraxia Pervasive: Autism · Rett syndrome · Asperger syndrome Behavioral and emotional, childhood and adolescence onset ADHD · Conduct disorder · Oppositional defiant disorder · Separation anxiety disorder · Selective mutism · Reactive attachment disorder · Tic disorder · Tourette syndrome · Speech stuttering · cluttering Retrieved from http://en..org/wiki/Major_depressive_disorder Categories: Mood disorders | Abnormal psychology Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Afrikaans العربية Bosanski Català Česky Dansk Deutsch Eesti Ελληνικά Español Esperanto Français 한국어 Hrvatski Bahasa Indonesia Italiano עברית Kurdî / كوردی Latina Lietuvių Lingála Magyar Bahasa Melayu Nederlands Nedersaksisch 日本語 ‪Norsk bokmål‬ ‪Norsk nynorsk‬ Occitan O'zbek Polski Português Română Ру�?�?кий Simple English Sloven�?ina Срп�?ки / Srpski Suomi Svenska Tiếng Việt Türkçe Україн�?ька ייִדיש 中文 This page was last modified on 13 September 2008, at 13:2

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