Depressive disorder

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Major depressive disorder, also known as major depression, unipolar depression, unipolar disorder, 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, and 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 of the disorder 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. Statistically, major depression occurs more often in women than men, although men are at higher risk for suicide.

Both psychological and biological causes have been proposed, and the determination of whether there are two separate conditions or a continuum of a single disorder has been researched since the 1920s. Current classification has favored biological theories since the creation of the term major depressive disorder in 1980. The neurotransmitters serotonin and norepinephrine have been implicated, and most antidepressants work to increase their active levels in the brain. However, the precise role of neurotransmitter levels in depressive illness is not fully understood. Psychological factors have also been implicated, and forms of psychotherapy are used to address them. Hospitalization may be necessary in cases associated with self-neglect or a significant risk of suicide, and electroconvulsive therapy is used in severe cases.

Ideas about what causes and constitutes depression have evolved over the centuries, and they remain a source of discussion. The term depression is commonly used to describe a temporary depressed or sad mood. By contrast, major depression is 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, authorities such as Australian psychiatrist Gordon Parker have argued that it is overdiagnosed, and that current diagnostic standards have the effect of medicalizing sadness.

In Western countries, approximately 3.4% of people with major depression eventually commit suicide. Up to 60% of all people who commit suicide have depression or another mood disorder, and their risk may be higher if they feel a marked sense of hopelessness or have both depression and borderline personality disorder. Depressed individuals have a shortened life expectancy, being more susceptible to conditions such as heart disease than the non-depressed.

Signs and symptoms

Major depression is a serious condition that affects a person's work, family and school life, sleeping and eating habits, and general health.[1] The impact on functioning and well-being has been equated to that of chronic medical conditions such as congestive heart failure.[2]

A person suffering a major depressive episode usually experiences a pervasive low mood, or loss of interest or pleasure in favored activities. Depressed people may be preoccupied with feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness.[3] Other symptoms include poor concentration and memory, withdrawal from social situations and activities, reduced libido (sex drive), and thoughts of death or suicide. Insomnia is common: in the typical pattern, a person wakes very early and is unable to get back to sleep.[4] Hypersomnia, or oversleeping, is less common.[4] Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.[3] The person may report persistent physical symptoms such as fatigue, headaches, digestive problems, or chronic pain; this is a typical presentation in developing countries.[5] Family and friends may perceive that the person is either agitated or slowed down.[4] Older people with major depression are more likely than younger people to show cognitive symptoms such as forgetfulness and to show a more noticeable slowing of movements.[6][7] In severe cases, depressed people may experience psychotic symptoms such as delusions or, less commonly, hallucinations, usually of an unpleasant nature.[8][9]

Children may display an irritable rather than depressed mood,[3] and show different symptoms depending on age and situation.[10] Most exhibit a loss of interest in school and a decline in academic performance. Children with depression may be described as clingy, demanding, dependent, or insecure.[4] Those older than 12 years may begin abusing drugs or alcohol, or exhibit disruptive behavior.[11] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[3]


In the biopsychosocial model, both biological and psychological (including social) factors play a role in causing depression. There is overlap, and the precise causes vary depending on individual circumstances. The heritability of depression—the degree to which it is genetically determined—has been estimated to be approximately 40% for women and 30% for men.[12] From the evolutionary standpoint, major depression might be expected to reduce an individual's reproductive fitness. Some evolutionary explanations for the apparent contradiction between biopsychosocial, psychological and psychosocial hypotheses and the high heritability and prevalence of major depression are explained by the proposal that certain components of depression are adaptations.[13][14]

Biological causes

Most antidepressants increase synaptic levels of the monoamine neurotransmitter serotonin. Some also enhance the levels of two other neurotransmitters, norepinephrine and dopamine. This observation gave rise to the monoamine theory of depression. In its contemporary formulation, the monoamine theory postulates that a deficiency of certain neurotransmitters is responsible for the corresponding features of depression: "Norepinephrine may be related to alertness and energy as well as anxiety, attention, and interest in life; [lack of] serotonin to anxiety, obsessions, and compulsions; and dopamine to attention, motivation, pleasure, and reward, as well as interest in life." The proponents of this theory recommend choosing the antidepressant with the mechanism of action impacting the most prominent symptoms. Anxious and irritable patients should be treated with SSRIs or norepinephrine reuptake inhibitors, and those experiencing a loss of energy and enjoyment of life with norepinephrine and dopamine enhancing drugs.[15]

Psychological causes

Various aspects of personality and its development are integral in the occurrence and persistence of depression.[16] Although episodes are strongly correlated with adverse events, how a person copes with stress also plays a role.[16] Low self-esteem, learned helplessness, and self-defeating or distorted thinking are related to depression. Depression may also be connected to feelings of religious alienation.[17] It is unclear whether these are causes or effects, but in either case depressed persons who are able to make corrections in their thinking patterns often show improved mood and self-esteem.[18]

Cognitive psychology and cognitive behavioral therapy are based on the theory that depression arises from cognitive biases and distortions stemming from deficits in memory and information processing. According to psychologist Martin Seligman, depression in humans is similar to learned helplessness in laboratory animals, who remain in unpleasant situations from which they are able to escape, but over which they initially learned they had no control.[19] Learned helplessness and depression may be related to what psychologist Julian Rotter called an external locus of control, a tendency to attribute personal outcomes to external events seen as uncontrollable.[20] A related idea, Aaron T. Beck's cognitive triad, proposes that depression entails cognitive errors about oneself, one's world, and one's future.[21][22]

On the other hand, depressed individuals often blame themselves for negative events, and believe that the effect of these events persists through time and pervades their entire lives.[21][23] This tendency is characteristic of a depressive attributional, or pessimistic explanatory style.[21] According to psychologist Albert Bandura, individuals become depressed if they have a negative self-concept and lack a sense of self-efficacy; in other words they have a habitual sense of an inability to influence events and to achieve personal goals.[24][25] Milder depression 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.[26][27]

A large body of research has documented the importance of interpersonal factors, including strained or critical personal relationships, in the onset of depressive symptoms and major depression in young and middle-aged adults. Vulnerability factors—such as early maternal loss, lack of a confiding relationship, responsibility for the care of several young children at home, and unemployment—can interact with life stressors to increase the risk of depression.[28][29] For older adults, the factors are often health problems, changes in relationships with a spouse or adult children due to the transition to a care-giving or care-needing role, the death of a significant other, or a change in the availability or quality of social relationships with older friends because of their own health-related life changes.[30]

From the psychoanalytic perspective, depression may be intertwined with self-criticism. Sigmund Freud wrote that the "super-ego becomes over-severe, abuses the poor ego, humiliates it and ill-treats it, threatens it with the direst punishments".[31] Freud argued that objective loss, as occurs through death or a romantic break-up, could result in subjective loss as well, when the depressed subject has identified with the object of its affection through an unconscious, 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.'"[32]

Existential psychologist Rollo May stated that "depression is the inability to construct a future".[33] From the existential perspective, in order to construct a future, individuals must be acutely aware of both their mortality and their freedom to act, and they must exercise their freedom within the explicit framework of an acute awareness of their mortality. This awareness produces "normal" anxiety,[34] whereas the lack of awareness leads to neurotic anxiety,[34] self-alienation,[35] inauthentic living,[36] guilt,[36] and depression. Humanistic psychologists agree with many facets of existentialism,[37] but argue that depression can result from an incongruity between society and the individual's innate drive to self-actualize. Abraham Maslow believed that depression is especially likely to arise when the world precludes a sense of "richness" or "totality" for the self-actualizer.[38][39]

Evolutionary psychology suggests that major depression can result from overactivation of psychological mechanisms that evolved to produce adaptive responses to material or social loss or defeat.[14][40][41] Some aspects of this approach have received empirical support and clinical application;[42][43] other components are still at a hypothetical stage.

Social causes

Long-term risks for developing major depression include family disruption and low socioeconomic status in early childhood.[44] The risk is independent of later adult social status and is related to various social inequalities.[45] Childhood emotional, physical, sexual abuse, or neglect are also associated with increased risk of developing depressive disorders later in life.[46] Such events are more likely to occur in dysfunctional families, for example, one with an alcoholic parent.[47] Early adverse events and stressful conditions that persist through childhood and adolescence may be linked to the later development of depression.[48] Social rejection also predicts later depression,[49] and adolescents who are victimized by peers are more vulnerable to developing depressive symptoms if it impacts on the development of their identity, although family cohesion and emotional involvement are protective factors.[50]

In adulthood, a correlation between stressful life events and the onset of major depressive episodes has been found consistently and is likely causal, although the specific mechanisms are unclear. Negative events such as assault, divorce or separation, legal issues, major problems with work, finances, housing, health, or friends and confidants, have been found to precede episodes if they represent a long-term threat, particularly if the threat is of a loss or humiliation that devalues an individual in a core role.[51] The first episode of major depressive is more likely to be immediately preceded by stressful life events than are recurrent ones.[52] Social isolation has also been found to predict onset of a first episode.[53] There is evidence that neighborhood social disorder, for example, due to crime or illicit drugs, is a risk factor, and that a high neighborhood socioeconomic status, with better amenities, is a protective factor. There is some evidence of risk from psychosocial stressors in the workplace, such as working at a job that is demanding but involves little opportunity for decision-making.[54] There is mixed evidence regarding the role of social capital (features of social organization including interpersonal trust, civic engagement and cooperation for mutual benefit).[55]


Clinical assessment

A diagnostic assessment may be conducted by a general practitioner or by a psychiatrist or psychologist.[1] This includes 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 includes an assessment of the person's current mood and an exploration of thought content, in particular thoughts of hopelessness, self-harm or suicide.[1]

Before diagnosing a major depressive disorder, a doctor generally performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH to exclude hypo- or hyperthyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease.[56] Testosterone levels may be used to diagnose hypogonadism, a cause of depression in men.[57] Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimer's disease.[58] Depression is also a common initial symptom of dementia.[59] Conducted in older depressed people, screening tests such as the mini-mental state examination, or a more complete neuropsychological evaluation, can rule out cognitive impairment.[60] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[61] No biological tests confirm major depression.[62] Investigations are not generally repeated for a subsequent episode unless there is a specific medical indication, in which case serum sodium can 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.[63]

Specialist mental health services are rare in rural areas, and thus diagnosis and management is largely left to primary care clinicians.[64] This issue is even more marked in developing countries.[65]

Rating scales

Diagnostic screening programs have been advocated to improve detection of depression, but there is evidence that the use of screening instruments does little to improve detection rates.[66] A study in the U.K. concluded that screening alone is costly and does not improve the treatment or outcome of depression.[67]

Several rating scales are used in research or as screening tools. The Beck Depression Inventory is a widely used tool in the diagnosis of depression, although its main purpose is not diagnosis, but determining the presence and severity of symptoms.[68][69] Originally designed by psychiatrist Aaron T. Beck in 1961, it is a 21-question self-report inventory that covers symptoms such as irritability, fatigue, weight loss, lack of interest in sex and thoughts including feelings of guilt, hopelessness or of being punished.[70] Other scales include the Geriatric Depression Scale in older populations, which is also valid in patients with mild to moderate dementia;[71][59] the Hamilton Depression Rating Scale (HRSD-21) designed by psychiatrist Max Hamilton in 1960;[72][73] and the Montgomery-Ã…sberg Depression Rating Scale (MADRS).[74][75] The Patient Health Questionnaires are two self-administered questionnaires for use in primary care. The PHQ-2 has two screening questions about the frequency of depressed mood and a loss of interest in activities; a positive to either question indicates further testing is required.[76] The PHQ-9 is a slightly more detailed nine-question survey for assessing symptoms of major depressive disorder in greater detail, and is often used to follow up a positive PHQ-2 test.[77]

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.[78]

Major depressive disorder is classified as a mood disorder in DSM IV-TR.[79] The diagnosis hinges on the presence of a single or recurrent major depressive episode.[3] Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Depressive Disorder Not Otherwise Specified is diagnosed if the depressive episode's manifestation does not meet the criteria for a major depressive episode. The ICD-10 system does not use the term Major depressive disorder, but lists similar criteria for the diagnosis of a Depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.[80]

Major depressive episode

A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[3] Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe. If the patient has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead.[81] Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[82]

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 the mood persists and the characteristic features of a major depressive episode develop.[83] The criteria have been criticized because they do not take into account any other aspects of the personal and social context in which depression can occur.[84][85] In addition, some studies have found little empirical support for the DSM-IV cut-off criteria, indicating they are a diagnostic convention imposed on a continuum of depressive symptoms of varying severity and duration:[86] excluded are a range of related diagnoses, including dysthymia which involves a chronic but milder mood disturbance,[87] Recurrent brief depression which involves briefer depressive episodes,[88][89] Minor depressive disorder which involves only some of the symptoms of major depression,[90] and Adjustment disorder with depressed mood which involves low mood resulting from a psychological response to an identifiable event or stressor.[91]


Diagnosticians recognize several subtypes, which are sometimes called "course specifiers":

  • Melancholic depression is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.[92]
  • Atypical depression is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.[93]
  • 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 remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome.[94]
  • Postpartum depression refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression, which has incidence rate of 10–15% among new mothers, typically sets in within three months of labor, and lasts as long as three months.[95]
  • Seasonal affective disorder is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.[96]

Differential diagnoses

In order to diagnose MDD, several other potential diagnoses must be ruled out, including the following:

  • Dysthymia is a chronic, milder mood disturbance in which 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).[87]
  • Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.[91]
  • Bipolar disorder, previously known as manic-depressive disorder, is a condition in which depressive phases alternate with periods of mania or hypomania. Although depression is currently categorized as a separate disorder, there is ongoing debate because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a mood disorder continuum.[97]
  • Loneliness and depression have enough features in common that loneliness may be viewed as a differential diagnosis.[98] In general, depression is likely to coexist with loneliness if the loneliness is chronic rather than transient. If the individual has global concerns that do not focus strictly on interpersonal relationships, feels a high degree of guilt, or is particularly vegetative, then the person is likely to be depressed; if these conditions are not met, he or she may be lonely instead.


The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice for people under 18, while electroconvulsive therapy is only used as a last resort. Care is usually given on an outpatient basis, while treatment in an inpatient unit is considered if there is a significant risk to self or others.

Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy are often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.[99]


Psychotherapy can be delivered, to individuals or groups, 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.[100] In people under 18, medication is usually offered only in conjunction with psychotherapy, not as a first line treatment.[101]

The most studied form of psychotherapy for depression is cognitive behavioral therapy (CBT), thought to work by teaching clients to learn a set of useful cognitive and behavioral skills. Earlier research suggested that cognitive-behavioral therapy was not as effective as antidepressant medication; however, more recent research suggests that it can perform as well as antidepressants in patients with moderate to severe depression.[102] Overall, systematic review reveals CBT to be an effective treatment in depressed adolescents,[103] although possibly not for severe episodes.[104] Combining fluoxetine with CBT appeared to bring no additional benefit[105][106] or, at the most, only marginal benefit.[107]

Two randomized, controlled trials of mindfulness-based cognitive therapy (MBCT), which includes elements of meditation, 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.[108]

Interpersonal psychotherapy focuses on the social and interpersonal triggers that may cause depression. There is evidence that it is an effective treatment. 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.[109]

Psychoanalysis, a school of thought founded by Sigmund Freud that emphasizes the resolution of unconscious mental conflicts,[110] is used by its practitioners to treat clients presenting with major depression.[111] A more widely practiced, eclectic technique, called psychodynamic psychotherapy, is loosely based on psychoanalysis and has an additional social and interpersonal focus.[112] In a meta-analysis of three controlled trials, Short Psychodynamic Supportive Psychotherapy (SPSP) was found to be as effective as medication for mild to moderate depression.[113]


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 one SSRI can be switched to another; such a switch results in improvement in almost 50% of cases.[114] Another popular option is to switch to the atypical antidepressant bupropion (Wellbutrin) or to add bupropion to the existing therapy;[115] this strategy is possibly more effective.[116][117] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine (Zispin, Remeron) can be used in such cases.[118][119][120] Venlafaxine (Effexor), a serotonin-norepinephrine reuptake inhibitor, may be moderately more effective than SSRIs;[121] however, it is not recommended as a first-line treatment because of the higher rate of side effects,[122] and its use is specifically discouraged in children and adolescents.[123] Fluoxetine is the only antidepressant recommended for people under the age of 18.[123]

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.[124][125] 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.[126]

To find the most effective treatment, the dosages of antidepressants must often be adjusted, or different medications and combinations tried. Response rates to the first agent administered may be as low as 50%.[127] It may take anywhere from three to eight weeks after the start of medication before the therapeutic effects are fully revealed. Patients are 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 usually need to take medication for the rest of their lives.[1] The term refractory- or treatment-resistant depression is used to describe cases that do not respond to adequate courses of least two antidepressants.[128]

A doctor may add a medication with a different mode of action to bolster the effect of an antidepressant in cases of treatment resistance.[129] Lithium has been used to augment antidepressant therapy in those who have failed to respond to antidepressants alone.[130] Furthermore, lithium dramatically decreases the suicide risk in recurrent depression.[131] Addition of a thyroid hormone, triiodothyronine may work as well as lithium, even in patients with normal thyroid function.[132] 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.[133]

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; 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 although did increase with severity and reach clinical significance for very severe depression.[134][135] These results 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.[136][137][138] 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".[134] The other author agreed that the "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.[139]

Antidepressants in general are as effective as psychotherapy for major depression, and this conclusion holds true for both severe and mild forms of MDD.[140][141] In contrast, medication gives better results for dysthymia.[140][141] 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.[140] 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.[141]

Electroconvulsive therapy

Electroconvulsive therapy (ECT) is a procedure in which seizures are electrically induced in anesthetized patients. ECT is most often used as a last resort (from the perspective of hospital psychiatrists) for severe major depression which has not responded to trials of antidepressant or, less often, psychotherapy or supportive interventions.[142] It has a quicker effect than antidepressant therapy, and thus may be the treatment of choice in emergencies such as catatonic depression where the patient has ceased oral intake of fluid or nutrients, or where there is severe suicidality.[142] Some evidence suggests it is the most effective treatment for depression in the short-term[143] and one study without a comparison group or assessment of additional treatments given, suggested remission is related to improved self-rated quality of life in both the short-term (correlated with the degree of amnesia) and after six months.[144] However, ECT has been found to have much lower remission rates in real-world practice[145] and on its own does not have a sustained benefit as nearly everyone relapses.[146] The relapse rate in the first six months may be reduced by the use of psychiatric medications or further ECT (although some authorities, such as NICE, do not recommend the latter), but remains high.[147][148] Common initial adverse effects include short-term memory loss, disorientation, headache; long-term memory[149] and other cognitive deficits may persist. According to the American Psychiatric Association and the National Institute for Health and Clinical Excellence, available evidence suggests that the procedure, when administered according to their standards and without complications, does not cause brain damage in adults.[150][151]

Other methods of treatment

Two products, St John's wort and S-Adenosyl methionine, are available as prescription antidepressants in several European countries, but in the US are classified as herbal supplements and sold over-the-counter. There is inconsistent evidence on the effect of St John's wort extract on major depression. The pharmaceutical quality of the extract has an effect on the safety and efficacy for the treatment of any type of depression.[152][153] Clinical trials of S-Adenosyl methionine (SAM-e) have shown that it is equivalent to tricyclic antidepressants in effectiveness, although the safety and efficacy of over-the-counter versions is unknown.[154][155] Other supplements such as omega-3 fatty acids,[156] tryptophan, and 5-hydroxytryptophan (5-HTP),[157] have shown no effect beyond those of placebo.

Repetitive transcranial magnetic stimulation (rTMS) utilizes powerful magnetic fields which applied to the brain from outside the head. Multiple controlled studies support the use of this method in treatment-resistant depression; it has been approved for this indication in Europe, Canada and Australia, but not in the US.[158][159] It was inferior to ECT in a side-by-side randomized trial.[160]

Other therapeutic approaches have been used to treat depression. Bright light therapy has been found to be an effective treatment for the winter depression produced by seasonal affective disorder. There has been some conflicting evidence as to its effectiveness for non-seasonal depression.[161][162] Exercise has not been shown to reduce the symptoms of depression.[163]


Major depressive episodes often resolve over time whether they are treated or not. Outpatients on a waiting list show a 10–15% reduction in symptoms over a few months, and around 20% will no longer meet full criteria.[164] The median duration of an episode has been estimated at least 23 weeks, with the highest rate of recovery in the first three months.[165]

General population studies indicate around half those who have a major depressive episode (whether treated or not) recover and remain well, while 35% will have at least one more, and around 15% experience chronic recurrence.[166] Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence.[167][168]

Recurrence is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use. Thus, depression recurs despite the prolonged antidepressant treatment in a significant minority of patients;[169] 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.[170]


  1. 1.0 1.1 1.2 1.3 Mayo Clinic Staff (2006-03-06). Depression (PDF). National Institute of Mental Health (NIMH). Retrieved on 2008-09-07.
  2. Hays RD, Wells KB, Sherbourne CD, et al. (1995). "Functioning and well-being outcomes of patients with depression compared with chronic general medical illnesses". Archives of General Psychiatry 52 (1): 11–19. PMID 7811158.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 American Psychiatric Association 2000, p. 349
  4. 4.0 4.1 4.2 4.3 American Psychiatric Association 2000, p. 350
  5. Patel V, Abas M, Broadhead J et al. (February 2001). "(fulltext) Depression in developing countries: Lessons from Zimbabwe". British Medical Journal 322 (7284): 482–84. doi:10.1136/bmj.322.7284.482. Retrieved on 2008-10-05.
  6. Kiloh LG (1961). "Pseudodementia". Acta Psychiatrica Scandinavica 37: 336–51. PMID 14455934.
  7. Faculty of Psychiatry of Old Age, NSW Branch, RANZCP; Kitching, David & Raphael, Beverley (2001). Consensus Guidelines for Assessment and Management of Depression in the Elderly. North Sydney, New South Wales: NSW Health Department, p. 2. ISBN 0-7347-33410. 
  8. American Psychiatric Association 2000, p. 412
  9. Sadock 2002, p. 555
  10. American Psychiatric Association 2000, p. 354
  11. Wiener, Jerry M.; Dulcan, Mina K. (2004). Textbook of Child and Adolescent Psychiatry. Arlington, VA: American Psychiatric Publishing, p. 413. ISBN 1585620572. 
  12. 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.
  13. 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.
  14. 14.0 14.1 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.
  15. Nutt DJ (2008). "Relationship of neurotransmitters to the symptoms of major depressive disorder". Journal of Clinical Psychiatry 69 Suppl E1: 4–7. PMID 18494537.
  16. 16.0 16.1 Sadock 2002, p. 541
  17. Exline JJ, Yali AM, Sanderson WC (December 2000). "Guilt, discord, and alienation: the role of religious strain in depression and suicidality". Journal of clinical psychology 56 (12): 1481–96. <1481::AID-1>3.0.CO;2-A doi:10.1002/1097-4679(200012)56:12<1481::AID-1>3.0.CO;2-A. PMID 11132565.
  18. Warman DM, Beck AT (June 2003). About treatment and supports: Cognitive behavioral therapy. National Alliance on Mental Illness (NAMI) website. Retrieved on 2008-10-17.
  19. Seligman, Martin (1975). Helplessness: On depression, development and death. San Francisco, CA, USA: WH Freeman. ISBN 0716707519. 
  20. 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.
  21. 21.0 21.1 21.2 Barlow 2005, pp. 230–32
  22. Allen, Joseph P. (2003). "An Overview of Beck's Cognitive Theory of Depression in Contemporary Literature". Personality Papers. Retrieved on 2008-10-30.
  23. Pinto A, Francis G (1993). "Cognitive correlates of depressive symptoms in hospitalized adolescents". Adolescence 28 (111): 661–72. PMID 8237551.
  24. Kanfer, R; Zeiss A (1983). "Depression, Interpersonal Standard Setting". Journal of Abnormal Psychology 92 (3): 319–29. PMID 6619407.
  25. Bandura A (1998). "Self-Efficacy", in Friedman H: Encyclopedia of mental health. San Diego: Academic Press. Retrieved on 2008-08-17. 
  26. Alloy LB, Abramson LY (1979). "Judgment of contingency in depressed and nondepressed students: Sadder but wiser?". Journal of Experimental Psychology: General 108: 441–85. PMID 528910.
  27. Taylor, Shelley E. (1991). Positive Illusions: Creative Self-deception and the Healthy Mind. New York, NY, USA: Basic Books. ISBN 0465060536. 
  28. Brown GW, Harris TO [1978] (2001). Social origins of Depression: A Study of psychiatric disorder in women. Routledge. ISBN 0-415-20268-X. 
  29. 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.
  30. Hinrichsen GA, Emery EE (2006). "Interpersonal Factors and Late-Life Depression". Clinical Psychology: Science and Practice 12 (3): 264–75.
  31. Freud S (Strachey J, Trans.) (1953–74). The standard edition of the complete psychological works of Sigmund Freud22, p. 61. 
  32. Carhart-Harris RL, Mayberg HS, Malizia AL, Nutt D (2008). "Mourning and melancholia revisited: Correspondences between principles of Freudian metapsychology and empirical findings in neuropsychiatry". Annals of General Psychiatry 7: 9. doi:10.1186/1744-859X-7-9. PMID 18652673.
  33. Geppert, Cynthia A. (May 2006). "Biologic, Syndromic, Social, and Personal Damage". Psychiatric Times 23 (6): 979–99.
  34. 34.0 34.1 May R (1996). The meaning Of anxiety. New York: W. W. Norton and Company. ISBN 0-393-31456-1. 
  35. Fromm Erich (1941). Escape from Freedom. New York: Holt, Rinehart, & Winston. 
  36. 36.0 36.1 Heidegger Martin (1927). Being and time. Halle, Germany: Niemeyer. 
  37. Hergenhahn 2005, pp. 546–47
  38. Boeree, Dr. C. George (1998). Abraham Maslow: Personality Theories (PDF). Psychology Department, Shippensburg University. Retrieved on 2008-10-27.
  39. Maslow A (1971). The farther reaches of human nature, 318. 
  40. Mashman, RC (1997). "An evolutionary view of psychic misery". Journal of Social Behaviour & Personality 12: 979–99.
  41. Nesse RM (January 2000). "Is depression an adaptation?". Archives of General Psychiatry 57 (1): 14–20. PMID 10632228.
  42. Gilbert P (2000). Overcoming Depression: A Self-Help Guide Using Cognitive Behavioral Techniques (2nd rev. ed.). London: Robinson Publishing. ISBN 1841191256. 
  43. Carey TJ (2005). "Evolution, depression and counselling". Counselling Psychology Quarterly 18 (3): 215–22.
  44. Gilman, Stephen E; Kawachi I, Fitzmaurice GM, Buka SL (May 2003). "Family disruption in childhood and risk of adult depression". American Journal of Psychiatry 160: 939–46. PMID 12727699.
  45. Gilman, Stephen E; Kawachi I, Fitzmaurice GM, Buka SL (April 2002). "Socioeconomic status in childhood and the lifetime risk of major depression". International Journal of Epidemiology 31: 359-67. PMID 11980797.
  46. Chapman DP, Whitfield CL, Felitti VJ, Dube SR, Edwards VJ, Anda RF (October 2004). "Adverse childhood experiences and the risk of depressive disorders in adulthood". Journal of Affective Disorders 82: 217–25. PMID 15488250.
  47. Anda RF, Whitfield CL, Felitti VJ, Chapman D, Edwards VJ, Dube SR, Williamson DF (August 2002). "Adverse childhood experiences, alcoholic parents, and later risk of alcoholism and depression". Psychiatric Services 53: 1001–09. Retrieved on 2008-10-02.
  48. Hazel NA, Hammen C, Brennan PA, Najman J (April 2008). "Early childhood adversity and adolescent depression: The mediating role of continued stress". Psychological Medicine 38: 581–89. PMID 18261247.
  49. Nolan SA, Flynn C, Garber J (October 2003). "Prospective relations between rejection and depression in young adolescents". Journal of Personality and Social Psychology 85: 745–55. PMID 14561127.
  50. van Hoof A, Quinten A, Raaijmakers AW, van Beek Y, Hale WW (III), Aleva L (October 2007). "A Multi-mediation Model on the Relations of Bullying, Victimization, Identity, and Family with Adolescent Depressive Symptoms". Journal of Youth and Adolescence 37: 772–82. doi:10.1007/s10964-007-9261-8. Retrieved on 2008-10-01.
  51. Kendler KS, Hettema JM, Butera F, Gardner CO, Prescott CA (August 2003). "Life event dimensions of loss, humiliation, entrapment, and danger in the prediction of onsets of major depression and generalized anxiety". Archives of General Psychiatry 60: 789–96. PMID 12912762.
  52. Stroud CB, Davila J, Moyer A (2008). "The relationship between stress and depression in first onsets versus recurrences: A meta-analytic review". Archives of General Psychiatry 117: 206–13. PMID 18266498.
  53. Bruce ML, Hoff RA (July 1994). "Social and physical health risk factors for first-onset major depressive disorder in a community sample". Social Psychiatry and Psychiatric Epidemiology 29: 165–71. PMID 7939965.
  54. Bonde JP (July 2008). "Psychosocial factors at work and risk of depression: A systematic review of the epidemiological evidence". Journal of Occupational and Environmental Medicine 65: 438–45. PMID 18417557.
  55. Kim D (August 2008). "Blues from the Neighborhood? Neighborhood Characteristics and Depression". Epidemiologic Reviews. doi:10.1093/epirev/mxn009. PMID 18753674.
  56. 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.
  57. Orengo C, Fullerton G, Tan R (2004). "Male depression: A review of gender concerns and testosterone therapy". Geriatrics 59 (10): 24–30. PMID 15508552.
  58. Reid LM, Maclullich AM (2006). "Subjective memory complaints and cognitive impairment in older people". Dementia and geriatric cognitive disorders 22 (5-6): 471–85. doi:10.1159/000096295. PMID 17047326.
  59. 59.0 59.1 Katz IR (1998). "Diagnosis and treatment of depression in patients with Alzheimer's disease and other dementias". The Journal of clinical psychiatry 59 Suppl 9: 38–44. PMID 9720486.
  60. Wright SL, Persad C (December 2007). "Distinguishing between depression and dementia in older persons: neuropsychological and neuropathological correlates". Journal of geriatric psychiatry and neurology 20 (4): 189–98. doi:10.1177/0891988707308801. PMID 18004006.
  61. Sadock 2002, p. 108
  62. Sadock 2002, p. 260
  63. 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.
  64. Kaufmann IM (1993). "(link to fulltext) Rural psychiatric services. A collaborative model". Canadian Family Physician 39: 1957–61. Retrieved on 2008-10-11.
  65. Call for action over Third World depression. BBC News (Health). British Broadcasting Corporation (BBC) (November 1, 1999). Retrieved on 2008-10-11.
  66. 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.
  67. 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.
  68. Beck Depression Inventory - 2nd Edition. Nova Southeastern University Center for Center for Psychological Studies. Retrieved on 2008-10-17.
  69. Goodwin FK, Jamison KR (1990). Manic-Depressive Illness. New York: Oxford University Press, pp. 361–62. ISBN 0-19-503934-3. 
  70. Beck AT (1972). Depression: Causes and treatment. Philadelphia: University of Pennsylvania Press, p. 333. ISBN 0-8122-1032-8. 
  71. Yesavage JA (1988). "Geriatric Depression Scale". Psychopharmacology Bulletin 24 (4): 709–11.
  72. Hamilton M (1960). "A rating scale for depression". Journal of Neurology, Neurosurgery and Psychiatry 23: 56–62. PMID 14399272.
  73. Bagby RM, Ryder AG, Schuller DR, Marshall MB (2004). "The Hamilton Depression Rating Scale: has the gold standard become a lead weight?". American Journal of Psychiatry 161 (12): 2163–77. PMID 15569884.
  74. Montgomery SA, Asberg M (April 1979). "A new depression scale designed to be sensitive to change". British Journal of Psychiatry 134: 382–9. PMID 444788.
  75. Demyttenaere K, De Fruyt J (2003). "Getting what you ask for: on the selectivity of depression rating scales". Psychotherapy and psychosomatics 72: 61–70. PMID 12601223.
  76. 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.
  77. Resources for clinicians: Patient health questionnaire. The MacArthur Initiative on Depression Primary Care. Dartmouth College & Duke University (2006). Retrieved on 2008-09-02.
  78. Sadock 2002, p. 288
  79. American Psychiatric Association 2000, p. 345
  80. Mood (affective) disorders. ICD-10, Chapter V, Mental and behavioural disorders. World Health Organization (WHO) (2004). Retrieved on 2008-10-19.
  81. American Psychiatric Association 2000, p. 372
  82. Parker 1996, p. 173
  83. American Psychiatric Association 2000, p. 352
  84. 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.
  85. Vedantam S (April 3, 2007). Criteria for depression are too broad, researchers say: Guidelines may encompass many who are just sad. Washington Post (online) P.A02. Washington Post. Retrieved on 2008-10-10.
  86. 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.
  87. 87.0 87.1 Sadock 2002, p. 552
  88. American Psychiatric Association 2000, p. 778
  89. Carta MG, Altamura AC, Hardoy MC, 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.
  90. Rapaport MH, Judd LL, Schettler PJ, et al. (2002). "A descriptive analysis of minor depression". American Journal of Psychiatry 159 (4): 637–43. doi:10.1176/appi.ajp.159.4.637. PMID 11925303.
  91. 91.0 91.1 American Psychiatric Association 2000, p. 355
  92. American Psychiatric Association 2000, pp. 419–20
  93. American Psychiatric Association 2000, p. 421–22
  94. American Psychiatric Association 2000, pp. 417–18
  95. Nonacs, Ruta M (December 4, 2007). Postpartum depression. eMedicine. Retrieved on 2008-10-30.
  96. American Psychiatric Association 2000, p. 425
  97. 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.
  98. Loneliness as a Component of Psychiatric Disorders: The Relationship Between Loneliness and Depression (subscription required). Medscape. Retrieved on 2008-10-30.
  99. Patel V, Araya R, Bolton P et al. (April 2004). "(fulltext) Editorial: Treating depression in the developing world". Tropical Medicine & International Health 9 (5): 539–41. doi:10.1111/j.1365-3156.2004.01243.x. Retrieved on 2008-10-05.
  100. 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.
  101. NICE (2005). NICE guidelines: Depression in children and adolescents. London: NICE, p. 5. ISBN 1-84629-074-0. Retrieved on 2008-08-16. 
  102. Roth, Anthony; Fonagy, Peter [1996] (2005). What Works for Whom? Second Edition: A Critical Review of Psychotherapy Research. Guilford Press, p. 78. ISBN 159385272X. 
  103. Reinecke MA, Ryan NE, DuBois DL (1997). "Cognitive-behavioral therapy of depression and depressive symptoms during adolescence: A review and meta-analysis". Journal of the American Academy of Child and Adolescent Psychiatry 37 (1): 26–34. PMID 9444896.
  104. Harrington R, Whittaker J, Shoebridge P, Campbell F (May 1998). "Systematic review of efficacy of cognitive behaviour therapies in childhood and adolescent depressive disorder". British Medical Journal 325 (7358): 229–30. PMID 9596592.
  105. 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.
  106. 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 Technology Assessment 12 (14): 1–80. PMID 18462573.
  107. 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.
  108. 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.
  109. Weissman MM, Markowitz JC, Klerman GL (2000). Comprehensive Guide to Interpersonal Psychotherapy. New York: Basic Books. ISBN 0-465-09566-6. 
  110. Dworetzky J (1997). Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co, 602. ISBN 0-314-20412-1. 
  111. 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.
  112. Durand VM, Barlow D (1999). Abnormal psychology: An integrative approach. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. ISBN 0-534-34742-8. 
  113. 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.
  114. 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.
  115. 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.
  116. Rush AJ, Trivedi MH, Wisniewski SR, et al. (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.
  117. 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.
  118. 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.
  119. 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.
  120. Lawrence RW (August 2004). "Effect of mirtazapine versus fluoxetine on "sleep quality"". Journal of Clinical Psychiatry 65 (8): 1149–50. PMID 15323610.
  121. 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.
  122. Cipriani A, Geddes JR, Barbui C (2007). "Venlafaxine for major depression". British Medical Journal 334: 215 (editorial). doi:10.1136/bmj.39098.457720.BE. Retrieved on 2008-09-13.
  123. 123.0 123.1 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.
  124. 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.
  125. 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.
  126. Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". Journal of Clinical Psychiatry 68 Suppl 8: 35–41. PMID 17640156.
  127. 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.
  128. Wijeratne, Chanaka, Sachdev, Perminder (2008). "Treatment-resistant depression: Critique of current approaches". Australian and New Zealand Journal of Psychiatry 42: 751–62. PMID 18696279.
  129. 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.
  130. 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.
  131. Guzzetta F, Tondo L, Centorrino F, Baldessarini RJ (March 2007). "Lithium treatment reduces suicide risk in recurrent major depressive disorder". Journal of Clinical Psychiatry 68 (3): 380–83. PMID 17388706.
  132. 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 T(3) augmentation following two failed medication treatments for depression: A STAR*D report". American Journal of Psychiatry 163 (9): 1519–30. doi:10.1176/appi.ajp.163.9.1519. PMID 16946176.
  133. Bender KJ. "Evidence Grows for Value of Antipsychotics as Antidepressant Adjuncts - Psychiatric Times", Psychiatric Times, 2008-02-01. Retrieved on 2008-08-06. 
  134. 134.0 134.1 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.
  135. 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.
  136. 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.
  137. 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.
  138. 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.
  139. Turner EH, Rosenthal R (March 2008). "Efficacy of antidepressants". British Medical Journal 336 (7643): 516–17. doi:10.1136/bmj.39510.531597.80. PMID 18319297.
  140. 140.0 140.1 140.2 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.
  141. 141.0 141.1 141.2 Imel ZE, Malterer MB, McKay KM, Wampold BE (October 2008). "A meta-analysis of psychotherapy and medication in unipolar depression and dysthymia". Journal of Affective Disorders 110 (3): 197–206. doi:10.1016/j.jad.2008.03.018. PMID 18456340.
  142. 142.0 142.1 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.
  143. 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.
  144. 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.
  145. Prudic J, Olfson M, Marcus SC, Fuller RB, Sackeim HA (2004). "Effectiveness of electroconvulsive therapy in community settings". Biological Psychiatry 55 (3): 301–12. doi:10.1016/j.biopsych.2003.09.015. PMID 14744473.
  146. Sackeim HA, Haskett RF, Mulsant BH, et al. (March 2001). "Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: A randomized controlled trial". JAMA: Journal of the American Medical Association 285 (10): 1299–307. PMID 11255384.
  147. Tew JD, Mulsant BH, Haskett RF, Joan P, Begley AE, Sackeim HA (2007). "Relapse during continuation pharmacotherapy after acute response to ECT: A comparison of usual care versus protocolized treatment". Annals of Clinical Psychiatry 19 (1): 1–4. doi:10.1080/10401230601163360. PMID 17453654.
  148. Kellner CH, Knapp RG, Petrides G, et al. (December 2006). "Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: A multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE)". Archives of General Psychiatry 63 (12): 1337–44. doi:10.1001/archpsyc.63.12.1337. PMID 17146008.
  149. Barlow 2005, p. 239
  150. American Psychiatric Association. Electroconvulsive Therapy (ECT). Retrieved on 2007-12-29.
  151. 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. 
  152. Linde K, Mulrow CD, Berner M, Egger M (2005). "St John's wort for depression". Cochrane Database Systematic Reviews (2): CD000448. doi:10.1002/14651858.CD000448.pub2. PMID 15846605.
  153. St. John's Wort and Depression. NCCAM Health Information. Retrieved on 2008-10-13.
  154. 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.
  155. Bressa GM (1994). "S-adenosyl-l-methionine (SAMe) as antidepressant: Meta-analysis of clinical studies". Acta Neurologica Scandinavica, Suppl. 154: 7–14. PMID 7941964.
  156. 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". The American journal of clinical nutrition 84 (6): 1308–16. PMID 17158410.
  157. 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.
  158. 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.
  159. 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.
  160. 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.
  161. 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.
  162. 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.
  163. Mead GE, Morley W, Campbell P, Greig CA, McMurdo M, Lawlor DA (2008). "Exercise for depression". Cochrane database of systematic reviews (Online) (4): CD004366. doi:10.1002/14651858.CD004366.pub3. PMID 18843656.
  164. 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.
  165. Posternak MA, Solomon DA, Leon AC, et al. (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.
  166. Eaton WW, Shao H, Nestadt G, et al. (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.
  167. Holma KM, Holma IA, Melartin TK, et al. (February 2008). "Long-term outcome of major depressive disorder in psychiatric patients is variable". Journal of Clinical Psychiatry 69 (2): 196–205. PMID 18251627.
  168. 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.
  169. 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/S0140-6736(03)12599-8. PMID 12606176.
  170. Frank C (March/April 1999). "Skirmish or Siege? Is depression primarily a recurring disease? Can you ever really be cured?". Psychology Today Magazine. Retrieved on 2008-10-30.

Cited texts

  • American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc., 943. ISBN 0890420254. 
  • Barlow; Durand VM (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 (2005). An Introduction to the History of Psychology, 5th edition, Belmont, CA, USA: Thomson Wadsworth. ISBN 0534554016. 
  • Parker, Gordon; Dusan Hadzi-Pavlovic, Kerrie Eyers (1996). Melancholia: A disorder of movement and mood: A phenomenological and neurobiological review. Cambridge: Cambridge University Press. ISBN 052147275X. 
  • Sadock, Benjamin J.; Sadock, Virginia A. (2002). Kaplan and Sadock's Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 9th, Lippincott Williams & Wilkins. ISBN 0781731836. 

External links


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