Major depressive disorderSynonymsClinical depression, major depression, unipolar depression, unipolar disorder, recurrent depression
Vincent van Gogh's 1890 painting
Sorrowing old man ('At Eternity's Gate')SpecialtyPsychiatrySymptoms
Low mood, low
self-esteem,
loss of interest in normally enjoyable activities, low energy,
pain without a clear cause
[1]ComplicationsSuicide[2]Usual onset20s–30s
[3][4]Duration> 2 weeks
[1]Causes
Genetic, environmental, and psychological factors
[1]Risk factorsFamily history, major life changes, certain medications,
chronic health problems,
substance abuse[1][3]Similar conditionsSadness[3]Treatment
Counseling,
antidepressant medication,
electroconvulsive therapy[1]Frequency216 million (2015)
[5]
Major depressive disorder (MDD), also known simply as depression, is a mental disorder characterized by at least two weeks of low mood that is present across most situations.[1] It is often accompanied by low self-esteem, loss of interest in normally enjoyable activities, low energy, and pain without a clear cause.[1] People may also occasionally have false beliefs or see or hear things that others cannot.[1] Some people have periods of depression separated by years in which they are normal while others nearly always have symptoms present.[3] Major depressive disorder can negatively affect a person's personal, work, or school life, as well as sleeping, eating habits, and general health.[1][3] Between 2–7% of adults with major depression die by suicide,[2]and up to 60% of people who die by suicide had depression or another mood disorder.[6]
The cause is believed to be a combination of genetic, environmental, and psychological factors.[1] Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance abuse.[1][3] About 40% of the risk appears to be related to genetics.[3] The diagnosis of major depressive disorder is based on the person's reported experiences and a mental status examination.[7] There is no laboratory test for major depression.[3] Testing, however, may be done to rule out physical conditions that can cause similar symptoms.[7] Major depression should be differentiated from sadnesswhich is a normal part of life and is less severe.[3] The United States Preventive Services Task Force (USPSTF) recommends screening for depression among those over the age 12,[8][9] while a prior Cochrane review found that the routine use of screening questionnaires have little effect on detection or treatment.[10]
Typically, people are treated with counseling and antidepressant medication.[1] Medication appears to be effective, but the effect may only be significant in the most severely depressed.[11][12] It is unclear whether medications affect the risk of suicide.[13]Types of counseling used include cognitive behavioral therapy (CBT) and interpersonal therapy.[1][14] If other measures are not effective electroconvulsive therapy (ECT) may be tried.[1] Hospitalization may be necessary in cases with a risk of harm to self and may occasionally occur against a person's wishes.[15]
Major depressive disorder affected approximately 216 million people (3% of the world's population) in 2015.[5] The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France.[4] Lifetime rates are higher in the developed world (15%) compared to the developing world (11%).[4] It causes the second most years lived with disability after low back pain.[16] The most common time of onset is in a person in their 20s and 30s. Females are affected about twice as often as males.[3][4] The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980.[17] It was a split of the previous depressive neurosis in the DSM-II which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood.[17] Those currently or previously affected may be stigmatized.[18]
Video explanation of depression
Signs and symptoms
An 1892 lithograph of a woman diagnosed with depression
Major depression significantly affects a person's family and personal relationships, work or school life, sleeping and eating habits, and general health.[19] Its impact on functioning and well-being has been compared to that of other chronic medical conditions such as diabetes.[20]
A person having a major depressive episode usually exhibits a very low mood, which pervades all aspects of life, and an inability to experience pleasure in activities that were formerly enjoyed. Depressed people may be preoccupied with, or ruminate over, thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness, hopelessness, and self-hatred.[21] In severe cases, depressed people may have symptoms of psychosis. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant.[22] Other symptoms of depression include poor concentration and memory (especially in those with melancholic or psychotic features),[23] withdrawal from social situations and activities, reduced sex drive, irritability,[24] and thoughts of death or suicide. Insomnia is common among the depressed. In the typical pattern, a person wakes very early and cannot get back to sleep.[25] Hypersomnia, or oversleeping, can also happen.[25] Some antidepressants may also cause insomnia due to their stimulating effect.[26]
A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organization's criteria for depression.[27] Appetite often decreases, with resulting weight loss, although increased appetite and weight gain occasionally occur.[21] Family and friends may notice that the person's behavior is either agitated or lethargic.[25] Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness,[23] and a more noticeable slowing of movements.[28] Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinson's disease, and chronic obstructive pulmonary disease.[29]
Depressed children may often display an irritable mood rather than a depressed mood,[21] and show varying symptoms depending on age and situation.[30] Most lose interest in school and show a decline in academic performance. They may be described as clingy, demanding, dependent, or insecure.[25] Diagnosis may be delayed or missed when symptoms are interpreted as normal moodiness.[21]
Associated conditions
Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reports that half of those with major depression also have lifetime anxiety and its associated disorders such as generalized anxiety disorder.[31] Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicide attempts.[32] There are increased rates of alcohol and drug abuse and particularly dependence,[33] and around a third of individuals diagnosed with ADHD develop comorbid depression.[34] Post-traumatic stress disorder and depression often co-occur.[19] Depression may also coexist with attention deficit hyperactivity disorder (ADHD), complicating the diagnosis and treatment of both.[35] Depression is also frequently comorbid with alcohol abuse and personality disorders.[36]
Depression and pain often co-occur. One or more pain symptoms are present in 65% of depressed patients, and anywhere from 5 to 85% of patients with pain will be suffering from depression, depending on the setting; there is a lower prevalence in general practice, and higher in specialty clinics. The diagnosis of depression is often delayed or missed, and the outcome worsens. The outcome can also worsen if the depression is noticed but completely misunderstood.[37]
Depression is also associated with a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders, which further increases their risk of medical complications.[38] In addition, cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care.[39]
Cause
The cause of major depressive disorder is unknown. The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression.[3][40]The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic,[41][42] implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood.[43]
Childhood abuse, either physical, sexual or psychological are all risk factors for depression, among other psychiatric issues that co-occur such as anxiety and drug abuse. Childhood trauma also correlates with severity of depression, lack of response to treatment and length of illness. However, some are more susceptible to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility.[44]
Genetics
The 5-HTTLPR, or serotonin transporter promoter gene's short allele has been associated with increased risk of depression. However, since the 1990s results have been inconsistent, with three recent reviews finding an effect and two finding none.[45][46][47][48][49] Other genes that have been linked to a GxE interaction include CRHR1, FKBP5 and BDNF, the first two of which are related to the stress reaction of the HPA axis, and the latter of which is involved in neurogenesis.
Other health problems
Depression may also come secondary to a chronic or terminal medical conditioned such as HIV/AIDS, or asthma and may be labeled "secondary depression".[50][51] It is unknown if the underlying diseases induce depression through effect on quality of life, of through shared etiologies (such as degeneration of the basal ganglia in parkinson's disease or immune dysregulation in asthma).[52] Depression may also be iatrogenic (the result of healthcare), such as drug induced depression. Therapies associated with depression include interferontherapy, beta-blockers, Isotretinoin, contraceptives,[53] cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents agents such as gonadotropin-releasing hormone agonist.[54] Drug abuse in early age is also associated with increased risk of developing depression later in life.[55] Depression that occurs as a result of pregnancy is called postpartum depression, and is though to be the result of hormonal changes associated with pregnancy.[56] Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is though to be the result of decreased sunlight.[57]
Pathophysiology
The pathophysiology of depression is not yet understood, but the current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA axisdysfunction and structural or functional abnormalities of emotional circuits.
The monoamine theory, derived from the efficacy of monoaminergic drugs in treating depression, was the dominant theory until recently. The theory postulates that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. Firstly, acute depletion of tryptophan, a necessary precursor of serotonin, a monoamine, can cause depression in those in remission or relatives of depressed patients; this suggests that decreased serotonergic neurotransmission is important in depression.[58] Secondly, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression.[59] Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum,[60] and polymorphism of dopamine receptor genes implicate dopamine in depression.[61][62] Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression.[63] However, this theory is inconsistent with the fact that serotonin depletion does not cause depression in healthy persons, the fact that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway.[64] One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants.[65] However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive that controls, the finding of increased jugular 5-HIAA in depressed patients that normalized with SSRI treatment, and the preference for carbohydrates in depressed patients.[66] Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public.[67]
Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behavior (which shares overlap with depression).[68][69][70]The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression,[71] and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.[72]
HPA axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in depressed patients. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%.[73][74] These stress-related abnormalities have been hypothesized to be the cause of hippocampal volume reductions seen in depressed patients.[75] Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors.[76] Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.[77]
Theories unifying neuroimaging findings have been proposed. The first model proposed is the "Limbic Cortical Model", which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing.[78] Another model, the "Corito-Striatal model", suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures results in depression.[79] Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies.[80]
DiagnosisClinical assessment
A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist,[19] who records the person's current circumstances, biographical history, current symptoms, and family history. The broad clinical aim is to formulate the relevant biological, psychological, and social factors that may be impacting on the individual's mood. The assessor may also discuss the person's current ways of regulating mood (healthy or otherwise) such as alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the person's current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harmor suicide, and an absence of positive thoughts or plans.[19] Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians.[81] This issue is even more marked in developing countries.[82] The mental health examination may include the use of a rating scale such as the Hamilton Rating Scale for Depression[83] or the Beck Depression Inventory[84] or the Suicide Behaviors Questionnaire-Revised.[85] The score on a rating scale alone is insufficient to diagnose depression to the satisfaction of the DSM or ICD, but it provides an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis.[86] Several rating scales are used for this purpose.[86]
Primary-care physicians and other non-psychiatrist physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatric physicians, in part because of the physical symptoms that often accompany depression, in addition to the many potential patient, provider, and system barriers that the authors describe. A review found that non-psychiatrist physicians miss about two-thirds of cases, though this has improved somewhat in more recent studies.[87]
Before diagnosing a major depressive disorder, in general a doctor performs a medical examination and selected investigations to rule out other causes of symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESRto rule out a systemic infection or chronic disease.[88] Adverse affective reactions to medications or alcohol misuse are often ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men.[89] Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression.[90]
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.[91][92] Cognitive testing and brain imaging can help distinguish depression from dementia.[93] A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms.[94] In general, investigations are not repeated for a subsequent episode unless there is a medical indication.
No biological tests confirm major depression.[95] Biomarkers of depression have been sought to provide an objective method of diagnosis. There are several potential biomarkers, including Brain-Derived Neurotrophic Factor and various functional MRI techniques. One study developed a decision tree model of interpreting a series of fMRI scans taken during various activities. In their subjects, the authors of that study were able to achieve a sensitivity of 80% and a specificity of 87%, corresponding to a negative predictive value of 98% and a positive predictive value of 32% (positive and negative likelihood ratios were 6.15, 0.23, respectively). However, much more research is needed before these tests could be used clinically.[96]
DSM-IV-TR and ICD-10 criteria
The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Association's revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), and the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10), which uses the name depressive episode for a single episode and recurrent depressive disorder for repeated episodes.[97] The latter system is typically used in European countries, while the former is used in the US and many other non-European nations,[98] and the authors of both have worked towards conforming one with the other.[99]
Both DSM-IV-TR and ICD-10 mark out typical (main) depressive symptoms.[100] ICD-10 defines three typical depressive symptoms (depressed mood, anhedonia, and reduced energy), two of which should be present to determine depressive disorder diagnosis.[101][102] According to DSM-IV-TR, there are two main depressive symptoms—depressed mood and anhedonia. At least one of these must be present to make a diagnosis of major depressive episode.[103]
Major depressive disorder is classified as a mood disorder in DSM-IV-TR.[104] The diagnosis hinges on the presence of single or recurrent major depressive episodes.[21] 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 very similar criteria for the diagnosis of a depressive episode (mild, moderate or severe); the term recurrent may be added if there have been multiple episodes without mania.[97]
Major depressive episode
A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks.[21] 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.[105] Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".[106]
DSM-IV-TR excludes cases where the symptoms are a result of bereavement, although it is possible for normal bereavement to evolve into a depressive episode if the mood persists and the characteristic features of a major depressive episode develop.[107] 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.[108] 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:[109] Excluded are a range of related diagnoses, including dysthymia, which involves a chronic but milder mood disturbance;[110] recurrent brief depression, consisting of briefer depressive episodes;[111][112] minor depressive disorder, whereby only some symptoms of major depression are present;[113] and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor.[114]
Subtypes
The DSM-IV-TR recognizes five further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features:
-
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.[115]
-
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.[116]
-
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 stuporous, 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.[117]
-
Postpartum depression, or mental and behavioral disorders associated with the puerperium, not elsewhere classified,[97] refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth. Postpartum depression has an incidence rate of 10–15% among new mothers. The DSM-IV mandates that, in order to qualify as postpartum depression, onset occur within one month of delivery. It has been said that postpartum depression can last as long as three months.[118]
-
Seasonal affective disorder (SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer.[119]
Screening
In 2016, the United States Preventive Services Task Force (USPSTF) recommended screening in the adult populations with evidence that it increases the detection of people with depression and with proper treatment improves outcomes.[8] They recommend screening in those between the age of 12 to 18 as well.[9]
A Cochrane review from 2005 found screening programs do not significantly improve detection rates, treatment, or outcome.[10]
Differential diagnoses
To confer major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a 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).[110]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.[114] Bipolar disorder, also 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.[120] Further differential diagnoses involve chronic fatigue syndrome.[121]
Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance abuse. Depression due to physical illness is diagnosed as a Mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, drug of abuse, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called Substance-induced mood disorder in the DSM-IV-TR).[3]
Prevention
Preventative efforts may result in decreases in rates of the condition of between 22 and 38%.[122] Eating large amounts of fish may also reduce the risk.[123]
Behavioral interventions, such as interpersonal therapy and cognitive-behavioral therapy, are effective at preventing new onset depression.[122][124][125] Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.[126]
However, an earlier meta-analysis found preventive programs with a competence-enhancing component to be superior to behavior-oriented programs overall, and found behavioral programs to be particularly unhelpful for older people, for whom social support programs were uniquely beneficial. In addition, the programs that best prevented depression comprised more than eight sessions, each lasting between 60 and 90 minutes, were provided by a combination of lay and professional workers, had a high-quality research design, reported attrition rates, and had a well-defined intervention.[127]
The Netherlands mental health care system provides preventive interventions, such as the "Coping with Depression" course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favorably to other psychotherapies.[124][128]
Management
The three most common treatments for depression are psychotherapy, medication, and electroconvulsive therapy. Psychotherapy is the treatment of choice (over medication) for people under 18. The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression, because the risk-benefit ratio is poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for:
- People with a history of moderate or severe depression
- Those with mild depression that has been present for a long period
- As a second line treatment for mild depression that persists after other interventions
- As a first line treatment for moderate or severe depression.
The guidelines further note that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.[129]
American Psychiatric Association treatment guidelines recommend that initial treatment should be individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and patient preference. Options may include pharmacotherapy, psychotherapy, exercise, electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS) or light therapy. Antidepressant medication is recommended as an initial treatment choice in people with mild, moderate, or severe major depression, and should be given to all patients with severe depression unless ECT is planned.[130]
Treatment options are much more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition.[131] A 2014 Cochrane review found insufficient evidence to determine the effectiveness of psychological versus medical therapy in children.[132]
Lifestyle
Physical exercise is recommended for management of mild depression,[133] and has a moderate effect on symptoms.[134] Exercise has also been found to be effective for (unipolar) major depression.[135] It is equivalent to the use of medications or psychological therapies in most people.[134] In older people it does appear to decrease depression.[136] Exercise may be recommended to people who are willing, motivated, and physically healthy enough to participate in an exercise program as treatment.[135]
There is a small amount of evidence that skipping a night's sleep may improve depressive symptoms, with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of mania or hypomania.[137]
In observational studies smoking cessation has benefits in depression as large as or larger than those of medications.[138]
Besides exercise, sleep and diet may play a role in depression, and interventions in these areas may be an effective add on to conventional methods.[139]
Counseling
Psychotherapy can be delivered, to individuals, groups, or families by mental health professionals. A 2015 review found that cognitive behavioral therapy appears to be similar to antidepressant medication in terms of effect.[140] A 2012 review found psychotherapy to be better than no treatment but not other treatments.[141] With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used.[142][143] A 2014 Cochrane review found that work-directed interventions combined with clinical interventions helped to reduce sick days taken by people with depression.[144]
Psychotherapy has been shown to be effective in older people.[145][146] Successful psychotherapy appears to reduce the recurrence of depression even after it has been terminated or replaced by occasional booster sessions.
Cognitive behavioral therapy
Cognitive behavioral therapy (CBT) currently has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression.[147] In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy.[148] Cognitive behavioral therapy has also been shown to reduce the number of sick days taken by people with depression, when used in conjunction with primary care.[144]
The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. Research beginning in the mid-1990s suggested that CBT could perform as well as or better than antidepressants in patients with moderate to severe depression.[149][150] CBT may be effective in depressed adolescents,[151] although its effects on severe episodes are not definitively known.[152] Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions.[153] CBT is particularly beneficial in preventing relapse.[154][155]
Cognitive behavioral therapy and occupational programs (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression.[156]
Variants
Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy,[157] and mindfulness-based cognitive therapy.[158] Mindfulness based stress reduction programs may reduce depression symptoms.[159][160] Mindfulness programs also appear to be a promising intervention in youth.[161]
Psychoanalysis
Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts.[162] Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression.[163] A more widely practiced therapy, called psychodynamic psychotherapy, is in the tradition of psychoanalysis but less intensive, meeting once or twice a week. It also tends to focus more on the person's immediate problems, and has an additional social and interpersonal focus.[164] In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression.[165]
Antidepressants
Sertraline (Zoloft) is used primarily to treat major depression in adults.
Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. Stronger evidence supports the usefulness of antidepressants in the treatment of depression that is chronic (dysthymia) or severe.
While small benefits were found, researchers Irving Kirsch and Thomas Moore state they may be due to issues with the trials rather than a true effect of the medication.[166] In a later publication, Kirsch concluded that the overall effect of new-generation antidepressant medication is below recommended criteria for clinical significance.[12] Similar results were obtained in a meta analysis by Fornier.[11]
A review commissioned by the National Institute for Health and Care Excellence concluded that there is strong evidence that SSRIs have greater efficacy than placebo on achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression.[167] Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo.[168]
In 2014 the U.S. FDA published a systematic review of all antidepressant maintenance trials submitted to the agency between 1985 and 2012. The authors concluded that maintenance treatment reduced the risk of relapse by 52% compared to placebo, and that this effect was primarily due to recurrent depression in the placebo group rather than a drug withdrawal effect.[11]
To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50–75%, and it can take at least six to eight weeks from the start of medication to remission.[169]Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence,[169] and even up to one year of continuation is recommended.[170] People with chronic depression may need to take medication indefinitely to avoid relapse.[19]
Selective serotonin reuptake inhibitors (SSRIs) are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants.[171] People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases.[172] Another option is to switch to the atypical antidepressant bupropion.[173] Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs.[174]However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits,[175] and it is specifically discouraged in children and adolescents.[176][177]
For child and adolescent depression, fluoxetine is recommended if medication are used.[178] Fluoxetine; however, appears to have only slight benefit in children,[178][179] while other antidepressants have not been shown to be effective.[180] There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia.[181] Any antidepressant can cause low serum sodium levels (also called hyponatremia);[182] nevertheless, it has been reported more often with SSRIs.[171] It is not uncommon for SSRIs to cause or worsen insomnia; the sedating antidepressant mirtazapine can be used in such cases.[183][184]
Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed.[185] The safety profile is different with reversible monoamine oxidase inhibitors such as moclobemide where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.[186]
For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs.[187][188] For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection;[189] another an increased risk;[190] and a third no risk in those 25–65 years old and a decrease risk in those more than 65.[191] A black box warning was introduced in the United States in 2007 on SSRI and other antidepressant medications due to increased risk of suicide in patients younger than 24 years old.[192] Similar precautionary notice revisions were implemented by the Japanese Ministry of Health.[193]
Other medications
There is some evidence that omega-3 fatty acids fish oil supplements containing high levels of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) are effective in the treatment of, but not the prevention of major depression.[194] However, a Cochrane review determined there was insufficient high quality evidence to suggest Omega-3 fatty acids were effective in depression.[195] There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D deficient.[196] There is some preliminary evidence that COX-2 inhibitors have a beneficial effect on major depression.[197] Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population.[198] There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed.[199] Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication.[200] Limited evidence suggests stimulants such as amphetamine and modafinil may be effective in the short term, or as add on therapy.[201][202]
Electroconvulsive therapy
Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in patients to provide relief from psychiatric illnesses.[203]:1880 ECT is used with informed consent[204] as a last line of intervention for major depressive disorder.[205]
A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar.[206] Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months.[207]
Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.[208]:259 Immediately following treatment, the most common adverse effects are confusion and memory loss.[205][209] ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.[210]
A usual course of ECT involves multiple administrations, typically given two or three times per week until the patient is no longer suffering symptoms. ECT is administered under anesthetic with a muscle relaxant.[211] Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some patients receive maintenance ECT.[205]
ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe.[212]
Transcranial magnetic stimulation
Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain.[213] TMS was approved by the FDA for treatment-resistant major depressive disorder in 2008[214] and as of 2014 evidence supports that it is probably effective.[215] The American Psychiatric Association[216]the Canadian Network for Mood and Anxiety Disorders,[217] and the Royal Australia and New Zealand College of Psychiatrists have endorsed rTMS for trMDD.[218]
Other
Bright light therapy reduces depression symptom severity, with benefit was found for both seasonal affective disorder and for nonseasonal depression, and an effect similar to those for conventional antidepressants. For non-seasonal depression, adding light therapy to the standard antidepressant treatment was not effective.[219] For non-seasonal depression where light was used mostly in combination with antidepressants or wake therapy a moderate effect was found, with response better than control treatment in high-quality studies, in studies that applied morning light treatment, and with people who respond to total or partial sleep deprivation.[220] Both analyses noted poor quality, short duration, and small size of most of the reviewed studies. There is insufficient evidence for Reiki[221] and dance movement therapy in depression.[222]
Prognosis
Major depressive episodes often resolve over time whether or not they are treated. Outpatients on a waiting list show a 10–15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder.[223] The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months.[224]
Studies have shown that 80% of those suffering from their first major depressive episode will suffer from at least 1 more during their life,[225] with a lifetime average of 4 episodes.[226]Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence.[227] 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.[228][229]
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.[230]
Those people experiencing repeated episodes of depression require ongoing treatment in order to prevent more severe, long-term depression. In some cases, people must take medications for long periods of time or for the rest of their lives.[231]
Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms that may include psychosis, early age of onset, more previous episodes, incomplete recovery after 1 year, pre-existing severe mental or medical disorder, and family dysfunction as well.[232]
Depressed individuals have a shorter life expectancy than those without depression, in part because depressed patients are at risk of dying by suicide.[233] However, they also have a higher rate of dying from other causes,[234] being more susceptible to medical conditions such as heart disease.[235] Up to 60% of people who die by suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder.[236] The lifetime risk of suicide associated with a diagnosis of major depression in the US is estimated at 3.4%, which averages two highly disparate figures of almost 7% for men and 1% for women[237] (although suicide attempts are more frequent in women).[238] The estimate is substantially lower than a previously accepted figure of 15%, which had been derived from older studies of hospitalized patients.[239]
Depression is often associated with unemployment and poverty.[240] Major depression is currently the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the World Health Organization.[241] Delay or failure in seeking treatment after relapse, and the failure of health professionals to provide treatment, are two barriers to reducing disability.[242]
Epidemiology
Disability-adjusted life year for unipolar depressive disorders per 100,000 inhabitants in 2004.
[243]
no data
<700
700–775
775–850
850–925
925–1000
1000–1075
1075–1150
1150–1225
1225–1300
1300–1375
1375–1450
>1450
Major depressive disorder affects approximately 216 million people in 2015 (3% of the global population).[5] The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France.[4] In most countries the number of people who have depression during their lives falls within an 8–18% range.[4] In North America, the probability of having a major depressive episode within a year-long period is 3–5% for males and 8–10% for females.[244][245] Major depression to be about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this.[246] The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors.[246] Depression is a major cause of disability worldwide.[247]
People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60.[248] The risk of major depression is increased with neurological conditions such as stroke, Parkinson's disease, or multiple sclerosis, and during the first year after childbirth.[249] It is also more common after cardiovascular illnesses, and is related more to a poor outcome than to a better one.[235][250] Studies conflict on the prevalence of depression in the elderly, but most data suggest there is a reduction in this age group.[251] Depressive disorders are more common to observe in urban than in rural population and the prevalence is in groups with stronger socioeconomic factors i.e. homelessness.[252]
History
Diagnoses of depression go back at least as far as
Hippocrates
The Ancient Greek physician Hippocrates described a syndrome of melancholia as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment.[253] It was a similar but far broader concept than today's depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included.[254]
The term depression itself was derived from the Latin verb deprimere, "to press down".[255] From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Baker's Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753.[256] The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function.[257] 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.[254]
A historical caricature of a man with an approaching depression
Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states.[258]
Sigmund Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised.[259] The patient's decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness.[260] He also emphasized early life experiences as a predisposing factor.[254] Adolf 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.[261] The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.[262]
In the mid-20th century, researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms.[263] The chemical imbalance theory has never been proven.[264]
The term "unipolar" (along with the related term "bipolar") was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.[265]
The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria),[266] and was incorporated into the DSM-III in 1980.[267] 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.[100][267] The ancient idea of melancholia still survives in the notion of a melancholic subtype.
The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia.[268][269] There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s.[270]
Society and culture
Terminology
The term "depression" is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or simply to a low mood. 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."[272] There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or is an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle.[273][274]
The diagnosis is less common in some countries, such as China. It has been argued that the Chinese traditionally deny or somatizeemotional depression (although since the early 1980s, the Chinese denial of depression may have modified).[275] Alternatively, it may be that Western cultures reframe and elevate some expressions of human distress to disorder status. Australian professor Gordon Parker and others have argued that the Western concept of depression "medicalizes" sadness or misery.[276][277] Similarly, Hungarian-American psychiatrist Thomas Szasz and others argue that depression is a metaphorical illness that is inappropriately regarded as an actual disease.[278] There has also been concern that the DSM, as well as the field of descriptive psychiatry that employs it, tends to reify abstract phenomena such as depression, which may in fact be social constructs.[279] American archetypal psychologist James Hillman writes that depression can be healthy for the soul, insofar as "it brings refuge, limitation, focus, gravity, weight, and humble powerlessness."[280] Hillman argues that therapeutic attempts to eliminate depression echo the Christian theme of resurrection, but have the unfortunate effect of demonizing a soulful state of being.
Stigma
Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley,[281] American-British writer Henry James,[282] and American president Abraham Lincoln.[283] Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen[284] and American playwright and novelist Tennessee Williams.[285] Some pioneering psychologists, such as Americans William James[286][287] and John B. Watson,[288] dealt with their own depression.
There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times.[289][290]British literature gives many examples of reflections on depression.[291] English philosopher John Stuart Mill experienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridge's "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear."[292][293] English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression,[294] and it was subsequently popularized by depression sufferer former British Prime Minister Sir Winston Churchill.[294]
Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly.[295] In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996;[296] a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment.[297]
Research
Trials are looking at the effects of botulinum toxins on depression. The idea is that the drug is used to make the person look less frowning and that this stops the negative facial feedback from the face.[298] In 2015 it turned out, however, that the partly positive effects that had been observed until then could have been placebo effects.[299]
MDD has been studied by taking MRI scans of patients with depression have revealed a number of differences in brain structure compared to those who are not depressed. Meta-analyses of neuroimaging studies in major depression reported that, compared to controls, depressed patients had increased volume of the lateral ventricles and adrenal gland and smaller volumes of the basal ganglia, thalamus, hippocampus, and frontal lobe (including the orbitofrontal cortex and gyrus rectus).[300][301] Hyperintensities have been associated with patients with a late age of onset, and have led to the development of the theory of vascular depression.[302]
Elderly
Depression is especially common among those over 65 years of age and increases in frequency with age beyond this age.[303] In addition the risk of depression increases in relation to the age and frailty of the individual.[303] Depression is one the most important factors which negatively impact quality of life in adults as well as the elderly.[303] Both symptoms and treatment among the elderly differ from those of the rest of the adult populations.[303]
As with many other diseases it is common among the elderly not to present classical depressive symptoms.[303] Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases.[303] Treatment differs in that studies of SSRI-drugs have shown lesser and often inadequate effect among the elderly, while other drugs with more clear effects have adverse effects which can be especially difficult to handle among the elderly.[303] Duloxetineis an SNRI-drug with documented effect on recurring depression among the elderly, but has adverse effects in form of dizziness, dryness of the mouth, diarrhea, and constipation.[303]
Problem solving therapy was as of 2015 the only psychological therapy with proven effect, and can be likened to a simpler form of cognitive behavioral therapy.[303] However, elderly with depression are seldom offered any psychological treatment, and the evidence surrounding which other treatments are effective is incomplete.[303] Electroconvulsive therapy(ECT or electric-shock therapy) has been used as treatment of the elderly, and register-studies suggest it is effective although less so among the elderly than among the rest of the adult population.[303]
The risks involved with treatment of depression among the elderly as opposed to benefits is not entirely clear.[303] Awaiting more evidence on how depression-treatment among the elderly is best designed it is important to follow up treatment results, and to reconsider changing treatments if it does not help.[303]
Other animals
Models of depression in animals for the purpose of study include iatrogenic depression models (such as drug induced), forced swim tests, tail suspension test, and learned helplessness models. Criteria frequently used to assess depression in animals include expression of despair, neurovegetative changes, and anhedonia, as many other depressive criteria are untestable in animals such as guilt and suicidality.[304]
References
- ^ Jump up to:a b c d e f g h i j k l m n "Depression". NIMH. May 2016. Retrieved 31 July 2016.
- ^ Jump up to:a b Richards, C. Steven; O'Hara, Michael W. (2014). The Oxford Handbook of Depression and Comorbidity. Oxford University Press. p. 254. ISBN 9780199797042.
- ^ Jump up to:a b c d e f g h i j k l American Psychiatric Association (2013), Diagnostic and Statistical Manual of Mental Disorders (5th ed.), Arlington: American Psychiatric Publishing, pp. 160–168, ISBN 978-0-89042-555-8, retrieved 22 July 2016
- ^ Jump up to:a b c d e f Kessler, RC; Bromet, EJ (2013). "The epidemiology of depression across cultures.". Annual Review of Public Health. 34: 119–38. PMC 4100461 . PMID 23514317. doi:10.1146/annurev-publhealth-031912-114409.
- ^ Jump up to:a b c GBD 2015 Disease and Injury Incidence and Prevalence, Collaborators. (8 October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015.". Lancet. 388 (10053): 1545–1602. PMC 5055577 . PMID 27733282. doi:10.1016/S0140-6736(16)31678-6.
-
Jump up^ Lynch, Virginia A.; Duval, Janet Barber (2010). Forensic Nursing Science. Elsevier Health Sciences. p. 453. ISBN 0323066380.
- ^ Jump up to:a b Patton, Lauren L. (2015). The ADA Practical Guide to Patients with Medical Conditions (2 ed.). John Wiley & Sons. p. 339. ISBN 9781118929285.
- ^ Jump up to:a b Siu, AL; US Preventive Services Task Force, (USPSTF); Bibbins-Domingo, K; Grossman, DC; Baumann, LC; Davidson, KW; Ebell, M; García, FA; Gillman, M; Herzstein, J; Kemper, AR; Krist, AH; Kurth, AE; Owens, DK; Phillips, WR; Phipps, MG; Pignone, MP (26 January 2016). "Screening for Depression in Adults: US Preventive Services Task Force Recommendation Statement.". JAMA. 315 (4): 380–7. PMID 26813211. doi:10.1001/jama.2015.18392.
- ^ Jump up to:a b Siu, AL; U.S. Preventive Services Task, Force (1 March 2016). "Screening for Depression in Children and Adolescents: U.S. Preventive Services Task Force Recommendation Statement.". Annals of Internal Medicine. 164 (5): 360–6. PMID 26858097. doi:10.7326/M15-2957.
- ^ Jump up to:a b Gilbody S, House AO, Sheldon TA (2005). "Screening and case finding instruments for depression". Cochrane Database of Systematic Reviews (4): CD002792. PMID 16235301. doi:10.1002/14651858.CD002792.pub2.
- ^ Jump up to:a b c Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J (January 2010). "Antidepressant drug effects and depression severity: a patient-level meta-analysis". JAMA. 303 (1): 47–53. PMC 3712503 . PMID 20051569. doi:10.1001/jama.2009.1943.
- ^ Jump up to: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. PMC 2253608 . PMID 18303940. doi:10.1371/journal.pmed.0050045.
-
Jump up^ Braun, C; Bschor, T; Franklin, J; Baethge, C (2016). "Suicides and Suicide Attempts during Long-Term Treatment with Antidepressants: A Meta-Analysis of 29 Placebo-Controlled Studies Including 6,934 Patients with Major Depressive Disorder.". Psychotherapy and psychosomatics. 85 (3): 171–9. PMID 27043848. doi:10.1159/000442293.
-
Jump up^ Driessen Ellen; Hollon Steven D (2010). "Cognitive Behavioral Therapy for Mood Disorders: Efficacy, Moderators and Mediators". Psychiatric Clinics of North America. 33(3): 537–55. PMC 2933381 . PMID 20599132. doi:10.1016/j.psc.2010.04.005.
-
Jump up^ Association, American Psychiatric. American Psychiatric Association Practice Guidelines for the Treatment of Psychiatric Disorders: Compendium 2006. American Psychiatric Pub. p. 780. ISBN 9780890423851.
-
Jump up^ Global Burden of Disease Study 2013, Collaborators (22 August 2015). "Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet. 386 (9995): 743–800. PMC 4561509 . PMID 26063472. doi:10.1016/S0140-6736(15)60692-4.
- ^ Jump up to:a b Hersen, Michel; Rosqvist, Johan (2008). Handbook of Psychological Assessment, Case Conceptualization, and Treatment, Volume 1: Adults. John Wiley & Sons. p. 32. ISBN 9780470173565.
-
Jump up^ Strakowski, Stephen M.; Nelson, Erik. "Introduction". Major Depressive Disorder. Oxford University Press. p. Chapter 1. ISBN 9780190206185.
- ^ Jump up to:a b c d e Depression (PDF). National Institute of Mental Health (NIMH). Archived from the original on 27 July 2011. Retrieved 7 September 2008.
-
Jump up^ Hays RD, Wells KB, Sherbourne CD, Rogers W, Spritzer K (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. doi:10.1001/archpsyc.1995.03950130011002.
- ^ Jump up to:a b c d e f American Psychiatric Association 2000a, p. 349
-
Jump up^ American Psychiatric Association 2000a, p. 412
- ^ Jump up to:a b Delgado PL, Schillerstrom J (2009). "Cognitive Difficulties Associated With Depression: What Are the Implications for Treatment?". Psychiatric Times. 26 (3).
-
Jump up^ Judd, LL; Schettler, PJ; Coryell, W; Akiskal, HS; Fiedorowicz, JG (2013). "Overt irritability/anger in unipolar major depressive episodes: past and current characteristics and implications for long-term course". JAMA Psychiatry. 70 (11): 1171–80. PMID 24026579. doi:10.1001/jamapsychiatry.2013.1957.
- ^ Jump up to:a b c d American Psychiatric Association 2000a, p. 350
-
Jump up^ "Insomnia: Assessment and Management in Primary Care". American Family Physician. 59 (11): 3029–38. 1999. Retrieved 12 November 2014.
-
Jump up^ Patel V, Abas M, Broadhead J (2001). "Depression in developing countries: Lessons from Zimbabwe". BMJ. 322 (7284): 482–84. doi:10.1136/bmj.322.7284.482.
-
Jump up^ Faculty of Psychiatry of Old Age, NSW Branch, RANZCP; Kitching D Raphael B (2001). Consensus Guidelines for Assessment and Management of Depression in the Elderly(PDF). North Sydney, New South Wales: NSW Health Department. p. 2. ISBN 0-7347-3341-0.
-
Jump up^ Yohannes AM, Baldwin RC (2008). "Medical Comorbidities in Late-Life Depression". Psychiatric Times. 25 (14).
-
Jump up^ American Psychiatric Association 2000a, p. 354
-
Jump up^ Kessler RC, Nelson CB, McGonagle KA, Liu J, Swartz M, Blazer DG (1996). "Comorbidity of DSM-III-R major depressive disorder in the general population: results from the US National Comorbidity Survey". British Journal of Psychiatry. 168 (suppl 30): 17–30. PMID 8864145.
-
Jump up^ Hirschfeld RM (2001). "The Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care". Primary Care Companion to the Journal of Clinical Psychiatry. 3 (6): 244–254. PMC 181193 . PMID 15014592.
-
Jump up^ 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. doi:10.1016/0899-3289(95)90017-9.
-
Jump up^ 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.
-
Jump up^ Brunsvold GL, Oepen G (2008). "Comorbid Depression in ADHD: Children and Adolescents". Psychiatric Times. 25 (10).
-
Jump up^ Melartin, Tarja K.; Rytsälä, Heikki J.; Leskelä, Ulla S.; Lestelä-Mielonen, Paula S.; Sokero, T. Petteri; Isometsä, Erkki T. (1 February 2002). "Current comorbidity of psychiatric disorders among DSM-IV major depressive disorder patients in psychiatric care in the Vantaa Depression Study". The Journal of Clinical Psychiatry. 63 (2): 126–134. PMID 11874213. doi:10.4088/jcp.v63n0207.
-
Jump up^ Bair MJ, Robinson RL, Katon W, Kroenke K (2003). "Depression and Pain Comorbidity: A Literature Review". Archives of Internal Medicine. 163 (20): 2433–45. PMID 14609780. doi:10.1001/archinte.163.20.2433.
-
Jump up^ Swardfager W, Herrmann N, Marzolini S, Saleem M, Farber SB, Kiss A, Oh PI, Lanctôt KL (2011). "Major depressive disorder predicts completion, adherence, and outcomes in cardiac rehabilitation: a prospective cohort study of 195 patients with coronary artery disease.". Journal of Clinical Psychiatry. 72 (9): 1181–8. PMID 21208573. doi:10.4088/jcp.09m05810blu.
-
Jump up^ Schulman J, Shapiro BA (2008). "Depression and Cardiovascular Disease: What Is the Correlation?". Psychiatric Times. 25 (9).
-
Jump up^ Department of Health and Human Services (1999). "The fundamentals of mental health and mental illness" (PDF). Mental Health: A Report of the Surgeon General. Retrieved 11 November 2008.
-
Jump up^ Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H, McClay J, Mill J, Martin J, Braithwaite A, Poulton R (July 2003). "Influence of life stress on depression: Moderation by a polymorphism in the 5-HTT gene". Science. 301 (5631): 386–89. Bibcode:2003Sci...301..386C. PMID 12869766. doi:10.1126/science.1083968.
-
Jump up^ Haeffel GJ, Getchell M, Koposov RA, Yrigollen CM, Deyoung CG, Klinteberg BA, Oreland L, Ruchkin VV, Grigorenko EL (2008). "Association between polymorphisms in the dopamine transporter gene and depression: evidence for a gene-environment interaction in a sample of juvenile detainees" (PDF). Psychol Sci. 19 (1): 62–9. PMID 18181793. doi:10.1111/j.1467-9280.2008.02047.x.
-
Jump up^ Slavich GM (2004). "Deconstructing depression: A diathesis-stress perspective (Opinion)". APS Observer. Retrieved 11 November 2008.
-
Jump up^ Saveanu, Radu V.; Nemeroff, Charles B. (1 March 2012). "Etiology of Depression: Genetic and Environmental Factors". Psychiatric Clinics of North America. 35 (1): 51–71. doi:10.1016/j.psc.2011.12.001.
-
Jump up^ Caspi, A.; Sugden, K.; Moffitt, T. E.; Taylor, A.; Craig, I. W.; Harrington, H.; McClay, J.; Mill, J.; Martin, J.; Braithwaite, A.; Poulton, R. (2003). "Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene". Science. 301 (5631): 386–389. Bibcode:2003Sci...301..386C. PMID 12869766. doi:10.1126/science.1083968.
-
Jump up^ Kendler, K.; Kuhn, J.; Vittum, J.; Prescott, C.; Riley, B. (2005). "The interaction of stressful life events and a serotonin transporter polymorphism in the prediction of episodes of major depression: a replication". Archives of General Psychiatry. 62 (5): 529–535. PMID 15867106. doi:10.1001/archpsyc.62.5.529.
-
Jump up^ Risch, N.; Herrell, R.; Lehner, T.; Liang, K.; Eaves, L.; Hoh, J.; Griem, A.; Kovacs, M.; Ott, J.; Merikangas, K. R. (2009). "Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis". Journal of the American Medical Association. 301 (23): 2462–2471. PMC 2938776 . PMID 19531786. doi:10.1001/jama.2009.878.
-
Jump up^ Munafo, M.; Durrant, C.; Lewis, G.; Flint, J. (2009). "Gene × Environment Interactions at the Serotonin Transporter Locus". Biological Psychiatry. 65 (3): 211–219. PMID 18691701. doi:10.1016/j.biopsych.2008.06.009.
-
Jump up^ Katja Karg; Margit Burmeister; Kerby Shedden; Srijan Sen (2011). "The serotonin transporter promoter variant (5-HTTLPR), stress, and depression meta-analysis revisited: evidence of genetic moderation.". Archives of General Psychiatry. 68 (5): 444–454. PMID 21199959. doi:10.1001/archgenpsychiatry.2010.189.
-
Jump up^ Simon, Gregory E (9 January 2017). "Treating depression in patients with chronic disease". Western Journal of Medicine. 175 (5): 292–293. PMC 1071593 . PMID 11694462.
-
Jump up^ Clayton, P. J.; Lewis, C. E. (1 March 1981). "The significance of secondary depression". Journal of Affective Disorders. 3 (1): 25–35. PMID 6455456. doi:10.1016/0165-0327(81)90016-1.
-
Jump up^ Kewalramani, Anupama; Bollinger, Mary E.; Postolache, Teodor T. (1 January 2008). "Asthma and Mood Disorders". International journal of child health and human development : IJCHD. 1 (2): 115–123. PMC 2631932 . PMID 19180246.
-
Jump up^ Rogers, Donald; Pies, Ronald (9 January 2017). "General Medical Drugs Associated with Depression". Psychiatry (Edgmont). 5 (12): 28–41. PMC 2729620 . PMID 19724774.
-
Jump up^ Botts, S; Ryan, M. Drug-Induced Diseases Section IV: Drug-Induced Psychiatric Diseases Chapter 18: Depression. pp. 1–23.
-
Jump up^ Brook, David W.; Brook, Judith S.; Zhang, Chenshu; Cohen, Patricia; Whiteman, Martin (1 November 2002). "Drug Use and the Risk of Major Depressive Disorder, Alcohol Dependence, and Substance Use Disorders". Archives of General Psychiatry. 59 (11): 1039. doi:10.1001/archpsyc.59.11.1039.
-
Jump up^ Meltzer-Brody, Samantha (9 January 2017). "New insights into perinatal depression: pathogenesis and treatment during pregnancy and postpartum". Dialogues in Clinical Neuroscience. 13 (1): 89–100. PMC 3181972 . PMID 21485749.
-
Jump up^ Melrose, Sherri (1 January 2015). "Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches". Depression Research and Treatment. 2015: 1–6. PMC 4673349 . PMID 26688752. doi:10.1155/2015/178564.
-
Jump up^ Ruhe, HG; Mason, NS; Schene, AH (2007). "Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies". Molecular Psychiatry. 12: 331–359. PMID 17389902. doi:10.1038/sj.mp.4001949.
-
Jump up^ Delgado PL, Moreno FA (2000). "Role of norepinephrine in depression". J Clin Psychiatry. 61 Suppl 1: 5–12. PMID 10703757.
-
Jump up^ Savitz, Jonathan; Drevets, Wayne (2013). "Neuroreceptor imaging in depression". Neurobiology of Disease. 52: 49–65. PMID 22691454. doi:10.1016/j.nbd.2012.06.001.
-
Jump up^ HASLER, GREGOR (4 December 2016). "PATHOPHYSIOLOGY OF DEPRESSION: DO WE HAVE ANY SOLID EVIDENCEOF INTEREST TO CLINICIANS?". World Psychiatry. 9(3): 155–161. PMC 2950973 . PMID 20975857.
-
Jump up^ Dunlop, Boadie W.; Nemeroff, Charles B. (1 April 2007). "The Role of Dopamine in the Pathophysiology of Depression". Archives of General Psychiatry. 64 (3): 327–37. PMID 17339521. doi:10.1001/archpsyc.64.3.327.
-
Jump up^ 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". Archives of General Psychiatry. 63 (11): 1209–16. PMID 17088501. doi:10.1001/archpsyc.63.11.1209.
-
Jump up^ al.], editors, Kenneth L. Davis; et al. (2002). Neuropsychopharmacology : the fifth generation of progress : an official publication of the American College of Neuropsychopharmacology (5th ed.). Philadelphia, Pa.: Lippincott Williams & Wilkins. pp. 1139–1163. ISBN 9780781728379.
-
Jump up^ Adell, Albert (1 April 2015). "Revisiting the role of raphe and serotonin in neuropsychiatric disorders". The Journal of General Physiology. 145 (4): 257–259. doi:10.1085/jgp.201511389.
-
Jump up^ Andrews, Paul W.; Bharwani, Aadil; Lee, Kyuwon R.; Fox, Molly; Thomson, J. Anderson. "Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response". Neuroscience & Biobehavioral Reviews. 51: 164–188. PMID 25625874. doi:10.1016/j.neubiorev.2015.01.018.
-
Jump up^ Lacasse, Jeffrey R.; Leo, Jonathan (8 November 2005). "Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature". PLoS Medicine. 2(12): e392. PMC 1277931 . PMID 16268734. doi:10.1371/journal.pmed.0020392.
-
Jump up^ Krishnadas, Rajeev; Cavanagh, Jonathan (1 May 2012). "Depression: an inflammatory illness?". Journal of Neurology, Neurosurgery, and Psychiatry. 83 (5): 495–502. PMID 22423117. doi:10.1136/jnnp-2011-301779.
-
Jump up^ Patel, Amisha (1 September 2013). "Review: the role of inflammation in depression". Psychiatria Danubina. 25 Suppl 2: S216–223. PMID 23995180.
-
Jump up^ Dowlati, Yekta; Herrmann, Nathan; Swardfager, Walter; Liu, Helena; Sham, Lauren; Reim, Elyse K.; Lanctôt, Krista L. (1 March 2010). "A meta-analysis of cytokines in major depression". Biological Psychiatry. 67 (5): 446–457. PMID 20015486. doi:10.1016/j.biopsych.2009.09.033.
-
Jump up^ Köhler, Ole; Benros, Michael E.; Nordentoft, Merete; Farkouh, Michael E.; Iyengar, Rupa L.; Mors, Ole; Krogh, Jesper (1 December 2014). "Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects: a systematic review and meta-analysis of randomized clinical trials". JAMA psychiatry. 71 (12): 1381–1391. PMID 25322082. doi:10.1001/jamapsychiatry.2014.1611.
-
Jump up^ Raedler, Thomas J. (1 November 2011). "Inflammatory mechanisms in major depressive disorder". Current Opinion in Psychiatry. 24 (6): 519–525. PMID 21897249. doi:10.1097/YCO.0b013e32834b9db6.
-
Jump up^ Arana, George W. (1 December 1985). "The Dexamethasone Suppression Test for Diagnosis and Prognosis in Psychiatry". Archives of General Psychiatry. 42 (12): 1193–204. PMID 3000317. doi:10.1001/archpsyc.1985.01790350067012.
-
Jump up^ Arana, G. W.; Baldessarini, R. J.; Ornsteen, M. (1 December 1985). "The dexamethasone suppression test for diagnosis and prognosis in psychiatry. Commentary and review". Archives of General Psychiatry. 42 (12): 1193–1204. PMID 3000317. doi:10.1001/archpsyc.1985.01790350067012.
-
Jump up^ Varghese, Femina P.; Brown, E. Sherwood (1 January 2001). "The Hypothalamic-Pituitary-Adrenal Axis in Major Depressive Disorder: A Brief Primer for Primary Care Physicians". Primary Care Companion to The Journal of Clinical Psychiatry. 3 (4): 151–155. PMC 181180 . PMID 15014598. doi:10.4088/pcc.v03n0401.
-
Jump up^ Lopez-Duran, Nestor L.; Kovacs, Maria; George, Charles J. (9 January 2017). "Hypothalamic-Pituitary-Adrenal Axis Dysregulation in Depressed Children and Adolescents: A Meta-Analysis". Psychoneuroendocrinology. 34 (9): 1272–1283. PMC 2796553 . PMID 19406581. doi:10.1016/j.psyneuen.2009.03.016.
-
Jump up^ Dedovic, Katarina; Ngiam, Janice (14 May 2015). "The cortisol awakening response and major depression: examining the evidence". Neuropsychiatric Disease and Treatment. 11: 1181–1189. PMC 4437603 . PMID 25999722. doi:10.2147/NDT.S62289.
-
Jump up^ "Limbic-cortical dysregulation: a proposed model of depression". The Journal of Neuropsychiatry and Clinical Neurosciences. 9 (3): 471–481. 1 August 1997. doi:10.1176/jnp.9.3.471.
-
Jump up^ Graham, Julia; Salimi-Khorshidi, Gholamreza; Hagan, Cindy; Walsh, Nicholas; Goodyer, Ian; Lennox, Belinda; Suckling, John (1 November 2013). "Meta-analytic evidence for neuroimaging models of depression: State or trait?". Journal of Affective Disorders. 151(2): 423–431. doi:10.1016/j.jad.2013.07.002.
-
Jump up^ Hamilton, J. Paul; Etkin, Amit; Furman, Daniella J.; Lemus, Maria G.; Johnson, Rebecca F.; Gotlib, Ian H. (1 July 2012). "Functional neuroimaging of major depressive disorder: a meta-analysis and new integration of base line activation and neural response data". The American Journal of Psychiatry. 169 (7): 693–703. PMID 22535198. doi:10.1176/appi.ajp.2012.11071105.
-
Jump up^ Kaufmann IM (1 September 1993). "Rural psychiatric services. A collaborative model". Canadian Family Physician. 39: 1957–61. PMC 2379905 . PMID 8219844.
-
Jump up^ "Call for action over Third World depression". BBC News (Health). British Broadcasting Corporation (BBC). 1 November 1999. Retrieved 11 October 2008.
-
Jump up^ Zimmerman M, Chelminski I, Posternak M (September 2004). "A Review of Studies of the Hamilton Depression Rating Scale in Healthy Controls: Implications for the Definition of Remission in Treatment Studies Of Depression". J Nerv Ment Dis. 192 (9): 595–601. PMID 15348975. doi:10.1097/01.nmd.0000138226.22761.39.
-
Jump up^ McPherson A, Martin CR (February 2010). "A Narrative Review of the Beck Depression Inventory (BDI) and Implications for its Use in an Alcohol-Dependent Population". J Psychiatr Ment Health Nurs. 17 (1): 19–30. PMID 20100303. doi:10.1111/j.1365-2850.2009.01469.x.
-
Jump up^ Osman, A.; Bagge, C. L.; Gutierrez, P. M.; Konick, L. C.; Kopper, B. A.; Barrios, F. X. (1 December 2001). "The Suicidal Behaviors Questionnaire-Revised (SBQ-R):Validation with Clinical and Nonclinical Samples". Assessment. 8 (4): 443–454. PMID 11785588. doi:10.1177/107319110100800409.
- ^ Jump up to:a b Sharp LK, Lipsky MS (2002). "Screening for depression across the lifespan: a review of measures for use in primary care settings". American Family Physician. 66 (6): 1001–8. PMID 12358212.
-
Jump up^ Cepoiu M, McCusker J, Cole MG, Sewitch M, Belzile E, Ciampi A (2008). "Recognition of depression by non-psychiatric physicians—a systematic literature review and meta-analysis". J Gen Intern Med. 23 (1): 25–36. PMC 2173927 . PMID 17968628. doi:10.1007/s11606-007-0428-5.
-
Jump up^ 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.
-
Jump up^ Orengo CA, Fullerton G, Tan R (2004). "Male depression: A review of gender concerns and testosterone therapy". Geriatrics. 59 (10): 24–30. PMID 15508552.
-
Jump up^ Parker, GB; Brotchie, H; Graham, RK (15 January 2017). "Vitamin D and depression.". Journal of Affective Disorders. 208: 56–61. PMID 27750060. doi:10.1016/j.jad.2016.08.082.
-
Jump up^ Reid LM, Maclullich AM (2006). "Subjective memory complaints and cognitive impairment in older people". Dementia and geriatric cognitive disorders. 22 (5–6): 471–85. PMID 17047326. doi:10.1159/000096295.
-
Jump up^ 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.
-
Jump up^ Wright SL, Persad C (2007). "Distinguishing between depression and dementia in older persons: Neuropsychological and neuropathological correlates". Journal of Geriatric Psychiatry and Neurology. 20 (4): 189–98. PMID 18004006. doi:10.1177/0891988707308801.
-
Jump up^ Sadock 2002, p. 108
-
Jump up^ Sadock 2002, p. 260
-
Jump up^ Hahn, Tim; Marquand, Andre F.; Ehlis, Ann-Christine; Dresler, Thomas; Kittel-Schneider, Sarah; Jarczok, Tomasz A.; Lesch, Klaus-Peter; Jakob, Peter M.; Mourao-Miranda, Janaina; Brammer, Michael J.; Fallgatter, Andreas J. (April 2011). "Integrating Neurobiological Markers of Depression" (PDF). JAMA Psychiatry. 68 (4): 361–368. doi:10.1001/archgenpsychiatry.2010.178. Retrieved August 4, 2017.
- ^ Jump up to:a b c "Mental and behavioural disorders: Mood [affective] disorders". World Health Organization. 2010. Retrieved 8 November 2008.
-
Jump up^ Sadock 2002, p. 288
-
Jump up^ American Psychiatric Association 2000a, p. xxix
- ^ Jump up to:a b Gruenberg, A.M., Goldstein, R.D., Pincus, H.A. (2005). "Classification of Depression: Research and Diagnostic Criteria: DSM-IV and ICD-10" (PDF). Biology of Depression: From Novel Insights to Therapeutic Strategies (eds J. Licinio and M.-L. Wong). Wiley-VCH Verlag GmbH. doi:10.1002/9783527619672.ch1. Retrieved 30 October 2008.
-
Jump up^ "The ICD-10 Classification of Mental and Behavioural Disorders: Clinical descriptions and diagnostic guidelines" (PDF). World Health Organization. 2010. Retrieved 12 November2014.
-
Jump up^ The ICD-10 classification of mental and behavioral disorders. Clinical description and diagnostic guideline. Geneva: World Health Organization, 1992
-
Jump up^ American Psychiatric Association 2000a
-
Jump up^ American Psychiatric Association 2000a, p. 345
-
Jump up^ American Psychiatric Association 2000a, p. 372
-
Jump up^ Parker 1996, p. 173
-
Jump up^ American Psychiatric Association 2000a, p. 352
-
Jump up^ Wakefield JC, Schmitz MF, First MB, Horwitz AV (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. PMID 17404120. doi:10.1001/archpsyc.64.4.433. Lay summary – The Washington Post (3 April 2007).
-
Jump up^ Kendler KS, Gardner CO (1 February 1998). "Boundaries of major depression: An evaluation of DSM-IV criteria". American Journal of Psychiatry. 155 (2): 172–77. PMID 9464194.
- ^ Jump up to:a b Sadock 2002, p. 552
-
Jump up^ American Psychiatric Association 2000a, p. 778
-
Jump up^ Carta MG, Altamura AC, Hardoy MC, Pinna F, Medda S, Dell'Osso L, Carpiniello B, Angst J (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. PMID 12904979. doi:10.1007/s00406-003-0418-5.
-
Jump up^ 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. PMID 11925303. doi:10.1176/appi.ajp.159.4.637.
- ^ Jump up to:a b American Psychiatric Association 2000a, p. 355
-
Jump up^ American Psychiatric Association 2000a, pp. 419–20
-
Jump up^ American Psychiatric Association 2000a, pp. 421–22
-
Jump up^ American Psychiatric Association 2000a, pp. 417–18
-
Jump up^ Nonacs, Ruta M (4 December 2007). "Postpartum depression". eMedicine. Retrieved 30 October 2008.
-
Jump up^ American Psychiatric Association 2000a, p. 425
-
Jump up^ Akiskal HS, Benazzi F (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. PMID 16488021. doi:10.1016/j.jad.2005.12.035.
-
Jump up^ Hawk, Caroline; Jason, Leonard A.; Torres-Harding, Susan (1 January 2006). "Differential diagnosis of chronic fatigue syndrome and major depressive disorder". International Journal of Behavioral Medicine. 13 (3): 244–251. PMID 17078775. doi:10.1207/s15327558ijbm1303_8.
- ^ Jump up to:a b Cuijpers P, van Straten A, Smit F, Mihalopoulos C, Beekman A (2008). "Preventing the onset of depressive disorders: a meta-analytic review of psychological interventions". Am J Psychiatry. 165 (10): 1272–80. PMID 18765483. doi:10.1176/appi.ajp.2008.07091422.
-
Jump up^ Li, F; Liu, X; Zhang, D (10 September 2015). "Fish consumption and risk of depression: a meta-analysis.". Journal of epidemiology and community health. 70: jech–2015–206278. PMID 26359502. doi:10.1136/jech-2015-206278.
- ^ Jump up to:a b Muñoz RF, Beardslee WR, Leykin Y (May–June 2012). "Major depression can be prevented". The American Psychologist. 67 (4): 285–95. PMC 4533896 . PMID 22583342. doi:10.1037/a0027666.
-
Jump up^ Cuijpers, P (20 September 2012). Prevention and early treatment of mental ill-health(PDF). PSYCHOLOGY FOR HEALTH: Contributions to Policy Making, Brussels.
-
Jump up^ Griffiths, K.M.; Farrer, L.; Christensen, H. (2010). "The efficacy of internet interventions for depression and anxiety disorders: a review of randomised controlled trials" (PDF). Medical Journal of Australia. 192 (11): 4–11. Retrieved 12 November 2014.
-
Jump up^ Jané-Llopis E, Hosman C, Jenkins R, Anderson P (2003). "Predictors of efficacy in depression prevention programmes" (PDF). British Journal of Psychiatry. Retrieved 2 April 2009.
-
Jump up^ Cuijpers P, Muñoz RF, Clarke GN, Lewinsohn PM (2009). "Psychoeducational treatment and prevention of depression: the "Coping with Depression" course thirty years later". Clinical Psychology Review. 29 (5): 449–458. PMID 19450912. doi:10.1016/j.cpr.2009.04.005.
-
Jump up^ "Depression". National Institute for Health and Care Excellence. December 2004. Archived from the original on 15 November 2008. Retrieved 20 March 2013.
-
Jump up^ "PsychiatryOnline | APA Practice Guidelines | Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition".[permanent dead link]
-
Jump up^ Patel V, Araya R, Bolton P (2004). "Editorial: Treating depression in the developing world". Tropical Medicine & International Health. 9 (5): 539–41. PMID 15117296. doi:10.1111/j.1365-3156.2004.01243.x. (Subscription required (help)).
-
Jump up^ Cox GR, Callahan P, Churchill R, Hunot V, Merry SN, Parker AG, Hetrick SE (30 November 2014). "Psychological therapies versus antidepressant medication, alone and in combination for depression in children and adolescents.". The Cochrane database of systematic reviews. 11: CD008324. PMID 25433518. doi:10.1002/14651858.CD008324.pub3.
-
Jump up^ "Management of depression in primary and secondary care" (PDF). National Clinical Practice Guideline Number 23. National Institute for Health and Clinical Excellence. 2007. Retrieved 4 November 2008.
- ^ Jump up to:a b Cooney GM, Dwan K, Greig CA, Lawlor DA, Rimer J, Waugh FR, McMurdo M, Mead GE (12 September 2013). Mead, Gillian E, ed. "Exercise for depression". Cochrane Database of Systematic Reviews. 9: CD004366. PMID 24026850. doi:10.1002/14651858.CD004366.pub6.
- ^ Jump up to:a b Josefsson, T.; Lindwall, M.; Archer, T. (2014). "Physical exercise intervention in depressive disorders: Meta-analysis and systematic review". Scandinavian Journal of Medicine & Science in Sports. 24 (2): 259–272. PMID 23362828. doi:10.1111/sms.12050.
-
Jump up^ Bridle C, Spanjers K, Patel S, Atherton NM, Lamb SE (September 2012). "Effect of exercise on depression severity in older people: systematic review and meta-analysis of randomised controlled trials". Br J Psychiatry. 201 (3): 180–5. PMID 22945926. doi:10.1192/bjp.bp.111.095174.
-
Jump up^ Giedke H, Schwärzler F (2002). "Therapeutic use of sleep deprivation in depression". Sleep Medicine Reviews. 6 (5): 361–77. PMID 12531127. doi:10.1053/smrv.2002.0235.
-
Jump up^ Taylor G, McNeill A, Girling A, Farley A, Lindson-Hawley N, Aveyard P (13 February 2014). "Change in mental health after smoking cessation: systematic review and meta-analysis". BMJ. 348 (feb13 1): g1151–g1151. PMC 3923980 . PMID 24524926. doi:10.1136/bmj.g1151.
-
Jump up^ Lopresti; Hood; Drummond (1 January 2006). "3) A review of lifestyle factors that contribute to important pathways associated with major depression: Diet, sleep and exercise." (PDF). Journal of Affective Disorders. 148 (1): 12–27.
-
Jump up^ Amick, HR; Gartlehner, G; Gaynes, BN; Forneris, C; Asher, GN; Morgan, LC; Coker-Schwimmer, E; Boland, E; Lux, LJ; Gaylord, S; Bann, C; Pierl, CB; Lohr, KN (8 December 2015). "Comparative benefits and harms of second generation antidepressants and cognitive behavioral therapies in initial treatment of major depressive disorder: systematic review and meta-analysis.". BMJ (Clinical research ed.). 351: h6019. PMC 4673103 . PMID 26645251.
-
Jump up^ Khan A, Faucett J, Lichtenberg P, Kirsch I, Brown WA (30 July 2012). "A Systematic Review of Comparative Efficacy of Treatments and Controls for Depression". PLOS ONE. 7 (7): e41778. PMC 3408478 . PMID 22860015. doi:10.1371/journal.pone.0041778.
-
Jump up^ Thase ME (1999). "When are psychotherapy and pharmacotherapy combinations the treatment of choice for major depressive disorder?". Psychiatric Quarterly. 70 (4): 333–46. PMID 10587988. doi:10.1023/A:1022042316895.
-
Jump up^ Cordes, J. (2013). "Depression". Encyclopedia of Sciences and Religions. p. 610. ISBN 978-1-4020-8264-1. doi:10.1007/978-1-4020-8265-8_301.
- ^ Jump up to:a b Nieuwenhuijsen, Karen; Faber, Babs; Verbeek, Jos H.; Neumeyer-Gromen, Angela; Hees, Hiske L.; Verhoeven, Arco C.; van der Feltz-Cornelis, Christina M.; Bültmann, Ute (2014). "Interventions to improve return to work in depressed people". The Cochrane Database of Systematic Reviews. 12: CD006237. PMID 25470301. doi:10.1002/14651858.CD006237.pub3.
-
Jump up^ Wilson KC, Mottram PG, Vassilas CA (2008). "Psychotherapeutic treatments for older depressed people". Cochrane Database of Systematic Reviews. 23 (1): CD004853. PMID 18254062. doi:10.1002/14651858.CD004853.pub2.
-
Jump up^ Cuijpers P, van Straten A, Smit F (2006). "Psychological treatment of late-life depression: a meta-analysis of randomized controlled trials". International Journal of Geriatric Psychiatry. 21 (12): 1139–49. PMID 16955421. doi:10.1002/gps.1620. hdl:1871/16894.
-
Jump up^ Childhood Depression. abct.org. Last updated: 30 July 2010
-
Jump up^ NICE (2005). NICE guidelines: Depression in children and adolescents. London: NICE. p. 5. ISBN 1-84629-074-0. Retrieved 16 August 2008.
-
Jump up^ Dobson KS (1989). "A meta-analysis of the efficacy of cognitive therapy for depression". J Consult Clin Psychol. 57 (3): 414–9. PMID 2738214. doi:10.1037/0022-006X.57.3.414.
-
Jump up^ Roth, Anthony; Fonagy, Peter (2005) [1996]. What Works for Whom? Second Edition: A Critical Review of Psychotherapy Research. Guilford Press. p. 78. ISBN 1-59385-272-X.
-
Jump up^ Weersing VR, Walker PN (2008). "Review: Cognitive behavioural therapy for adolescents with depression". Evidence-Based Mental Health. 11 (3): 76. PMID 18669678. doi:10.1136/ebmh.11.3.76. Retrieved 27 November 2008.
-
Jump up^ Harrington R, Whittaker J, Shoebridge P, Campbell F (1998). "Systematic review of efficacy of cognitive behaviour therapies in childhood and adolescent depressive disorder". BMJ. 316 (7144): 1559–63. PMC 28555 . PMID 9596592. doi:10.1136/bmj.316.7144.1559.
-
Jump up^ Becker SJ (2008). "Cognitive-Behavioral Therapy for Adolescent Depression: Processes of Cognitive Change". Psychiatric Times. 25 (14).
-
Jump up^ Almeida AM, Lotufo Neto F (2003). "Cognitive-behavioral therapy in prevention of depression relapses and recurrences: a review". Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999). 25 (4): 239–44. PMID 15328551.
-
Jump up^ Paykel ES (2007). "Cognitive therapy in relapse prevention in depression". The International Journal of Neuropsychopharmacology. 10 (1): 131–6. PMID 16787553. doi:10.1017/S1461145706006912.
-
Jump up^ Nieuwenhuijsen K, Faber B, Verbeek JH, Neumeyer-Gromen A, Hees HL, Verhoeven AC, van der Feltz-Cornelis CM, Bültmann U (2014). "Interventions to improve return to work in depressed people". The Cochrane Database of Systematic Reviews. 12: CD006237. PMID 25470301. doi:10.1002/14651858.CD006237.pub3.
-
Jump up^ Beck 1987, p. 10
-
Jump up^ Coelho HF, Canter PH, Ernst E (2007). "Mindfulness-based cognitive therapy: Evaluating current evidence and informing future research". Journal of Consulting and Clinical Psychology. 75 (6): 1000–05. PMID 18085916. doi:10.1037/0022-006X.75.6.1000.
-
Jump up^ Khoury B, Lecomte T, Fortin G, Masse M, Therien P, Bouchard V, Chapleau MA, Paquin K, Hofmann SG (August 2013). "Mindfulness-based therapy: a comprehensive meta-analysis". Clin Psychol Rev. 33 (6): 763–71. PMID 23796855. doi:10.1016/j.cpr.2013.05.005.
-
Jump up^ Jain FA, Walsh RN, Eisendrath SJ, et al. (2014). "Critical Analysis of the Efficacy of Meditation Therapies for Acute and Subacute Phase Treatment of Depressive Disorders: A systematic Review". Psychosomatics. 56: 297–302. doi:10.1016/j.psym.2014.10.007.
-
Jump up^ Simkin DR, Black NB (July 2014). "Meditation and mindfulness in clinical practice.". Child and adolescent psychiatric clinics of North America. 23 (3): 487–534. PMID 24975623. doi:10.1016/j.chc.2014.03.002.
-
Jump up^ Dworetzky J (1997). Psychology. Pacific Grove, CA, USA: Brooks/Cole Pub. Co. p. 602. ISBN 0-314-20412-1.
-
Jump up^ Doidge N, Simon B, Lancee WJ, First M, Brunshaw J, Brauer L, Grant DC, Stevens A, Oldham JM, Mosher P (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. doi:10.1177/00030651020500021101.
-
Jump up^ Barlow 2005, p. 20
-
Jump up^ de Maat S, Dekker J, Schoevers R, van Aalst G, Gijsbers-van Wijk C, Hendriksen M, Kool S, Peen J, Van R, de Jonghe F (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 (7): 565–74. PMID 17557313. doi:10.1002/da.20305.
-
Jump up^ Kirsch I, Moore TJ, Scoboria A, Nicholls SS (2002). "The emperor's new drugs: An analysis of antidepressant medication data submitted to the U.S. Food and Drug Administration". Prevention & Treatment. 5. doi:10.1037/1522-3736.5.1.523a.
-
Jump up^ "The treatment and management of depression in adults" (PDF). NICE. October 2009. Retrieved 12 November 2014.
-
Jump up^ Leucht C, Huhn M, Leucht S (2012). Leucht, C, ed. "Amitriptyline versus placebo for major depressive disorder". Cochrane Database of Systematic Reviews. 12: CD009138. PMID 23235671. doi:10.1002/14651858.CD009138.pub2.
- ^ Jump up to:a b Karasu TB, Gelenberg A, Merriam A, Wang P (April 2000). "Practice Guideline for the Treatment of Patients With Major Depressive Disorder (Second Edition)". Am J Psychiatry. 157 (4 Suppl): 1–45. PMID 10767867.; Third edition doi:10.1176/appi.books.9780890423363.48690
-
Jump up^ Thase ME (2006). "Preventing relapse and recurrence of depression: a brief review of therapeutic options". CNS spectrums. 11 (12 Suppl 15): 12–21. PMID 17146414.
- ^ Jump up to:a b Royal Pharmaceutical Society of Great Britain 2008, p. 204
-
Jump up^ Whooley MA, Simon GE (2000). "Managing Depression in Medical Outpatients". New England Journal of Medicine. 343 (26): 1942–50. PMID 11136266. doi:10.1056/NEJM200012283432607. Retrieved 11 November 2008.
-
Jump up^ 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. PMID 16165100. doi:10.1016/j.biopsych.2005.06.027.
-
Jump up^ Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC (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. PMID 17588546. doi:10.1016/j.biopsych.2007.03.027.
-
Jump up^ Gordon Duff (31 May 2006). "Updated prescribing advice for venlafaxine (Efexor/Efexor XL)". Medicines and Healthcare products Regulatory Agency (MHRA). Archived from the original on 13 November 2008.
-
Jump up^ "Depression in children and young people: Identification and management in primary, community and secondary care" (PDF). NHS National Institute for Health and Clinical Excellence. 2005. Retrieved 12 November 2014.
-
Jump up^ Mayers AG, Baldwin DS (2005). "Antidepressants and their effect on sleep". Human Psychopharmacology. 20 (8): 533–59. PMID 16229049. doi:10.1002/hup.726.
- ^ Jump up to:a b Cipriani, A; Zhou, X; Del Giovane, C; Hetrick, SE; Qin, B; Whittington, C; Coghill, D; Zhang, Y; Hazell, P; Leucht, S; Cuijpers, P; Pu, J; Cohen, D; Ravindran, AV; Liu, Y; Michael, KD; Yang, L; Liu, L; Xie, P (27 August 2016). "Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis.". Lancet. 388 (10047): 881–90. PMID 27289172. doi:10.1016/S0140-6736(16)30385-3.
-
Jump up^ Tsapakis EM, Soldani F, Tondo L, Baldessarini RJ (2008). "Efficacy of antidepressants in juvenile depression: meta-analysis". Br J Psychiatry. 193 (1): 10–7. PMID 18700212. doi:10.1192/bjp.bp.106.031088.
-
Jump up^ Cipriani A, Zhou X, Del Giovane C, Hetrick SE, Qin B, Whittington C, Coghill D, Zhang Y, Hazell P, Leucht S, Cuijpers P, Pu J, Cohen D, Ravindran AV, Liu Y, Michael KD, Yang L, Liu L, Xie P (8 June 2016). "Comparative efficacy and tolerability of antidepressants for major depressive disorder in children and adolescents: a network meta-analysis". Lancet. 388: 881–90. PMID 27289172. doi:10.1016/S0140-6736(16)30385-3.
-
Jump up^ Nelson JC, Devanand DP (April 2011). "A systematic review and meta-analysis of placebo-controlled antidepressant studies in people with depression and dementia". Journal of the American Geriatrics Society. 59 (4): 577–85. PMID 21453380. doi:10.1111/j.1532-5415.2011.03355.x.
-
Jump up^ Palmer BF, Gates JR, Lader M (2003). "Causes and Management of Hyponatremia". Annals of Pharmacotherapy. 37 (11): 1694–702. PMID 14565794. doi:10.1345/aph.1D105.
-
Jump up^ Guaiana G, Barbui C, Hotopf M (2007). "Amitriptyline for depression". Cochrane Database of Systematic Reviews. 18 (3): 11–7. PMID 17636748. doi:10.1002/14651858.CD004186.pub2.
-
Jump up^ Anderson IM (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. doi:10.1016/S0165-0327(99)00092-0.
-
Jump up^ Krishnan KR (2007). "Revisiting monoamine oxidase inhibitors". Journal of Clinical Psychiatry. 68 Suppl 8: 35–41. PMID 17640156.
-
Jump up^ Bonnet U (2003). "Moclobemide: therapeutic use and clinical studies". CNS Drug Rev. 9(1): 97–140. PMID 12595913. doi:10.1111/j.1527-3458.2003.tb00245.x.
-
Jump up^ Hammad TA (16 August 2004). "Review and evaluation of clinical data. Relationship between psychiatric drugs and pediatric suicidality" (PDF). FDA. pp. 42; 115. Retrieved 29 May 2008.
-
Jump up^ Hetrick, SE; McKenzie, JE; Cox, GR; Simmons, MB; Merry, SN (14 November 2012). "Newer generation antidepressants for depressive disorders in children and adolescents.". The Cochrane database of systematic reviews. 11: CD004851. PMID 23152227. doi:10.1002/14651858.CD004851.pub3.
-
Jump up^ Gunnell D, Saperia J, Ashby D (2005). "Selective serotonin reuptake inhibitors (SSRIs) and suicide in adults: meta-analysis of drug company data from placebo controlled, randomised controlled trials submitted to the MHRA's safety review". BMJ. 330 (7488): 385. PMC 549105 . PMID 15718537. doi:10.1136/bmj.330.7488.385.
-
Jump up^ Fergusson D, Doucette S, Glass KC, Shapiro S, Healy D, Hebert P, Hutton B (2005). "Association between suicide attempts and selective serotonin reuptake inhibitors: systematic review of randomised controlled trials". BMJ. 330 (7488): 396. PMC 549110 . PMID 15718539. doi:10.1136/bmj.330.7488.396.
-
Jump up^ Stone M, Laughren T, Jones ML, Levenson M, Holland PC, Hughes A, Hammad TA, Temple R, Rochester G (11 August 2009). "Risk of suicidality in clinical trials of antidepressants in adults: analysis of proprietary data submitted to US Food and Drug Administration". BMJ (Clinical research ed.). 339: b2880. PMC 2725270 . PMID 19671933. doi:10.1136/bmj.b2880.
-
Jump up^ "FDA Proposes New Warnings About Suicidal Thinking, Behavior in Young Adults Who Take Antidepressant Medications". FDA. 2 May 2007. Retrieved 29 May 2008.
-
Jump up^ Medics and Foods Department. Pharmaceuticals and Medical Devices Safety Information (PDF) (Report). 261 (in Japanese). Ministry of Health, Labour and Welfare (Japan).
-
Jump up^ Hallahan B, Ryan T, Hibbeln JR, Murray IT, Glynn S, Ramsden CE, SanGiovanni JP, Davis JM (2016). "Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression". Br J Psychiatry. 209 (3): 192–201. PMID 27103682. doi:10.1192/bjp.bp.114.160242.
-
Jump up^ Appleton, Katherine M; Sallis, Hannah M; Perry, Rachel; Ness, Andrew R; Churchill, Rachel (4 November 2015). "Omega-3 fatty acids for depression in adults". Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd (11): CD004692. PMID 26537796. doi:10.1002/14651858.cd004692.pub4.
-
Jump up^ Parker GB, Brotchie H, Graham RK (2017). "Vitamin D and depression". J Affect Disord. 208: 56–61. PMID 27750060. doi:10.1016/j.jad.2016.08.082.
-
Jump up^ Müller N, Myint AM, Schwarz MJ (February 2011). "Inflammatory biomarkers and depression". Neurotox Res. 19 (2): 308–18. PMID 20658274. doi:10.1007/s12640-010-9210-2.
-
Jump up^ Cipriani A, Hawton K, Stockton S, Geddes JR (27 June 2013). "Lithium in the prevention of suicide in mood disorders: updated systematic review and meta-analysis". BMJ. 346(jun27 4): f3646–f3646. PMID 23814104. doi:10.1136/bmj.f3646.
-
Jump up^ Nolen-Hoeksema, Susan. (2014) "Treatment of Mood Disorders". In (6th ed.) Abnormal Psychology p. 196. New York: McGraw-Hill. ISBN 978-0-07-803538-8.
-
Jump up^ Gelenberg, Alan J.; Freeman, Marlene P.; Markowitz, John C. "Practice Guideline for the Treatment of Patients with Major Depressive Disorder. 3rd edition." (PDF). American Psychiatric Association (APA). Retrieved 3 November 2014.
-
Jump up^ Corp, Stephanie A.; Gitlin, Michael J.; Altshuler, Lori L. (1 September 2014). "A review of the use of stimulants and stimulant alternatives in treating bipolar depression and major depressive disorder". The Journal of Clinical Psychiatry. 75 (9): 1010–1018. PMID 25295426. doi:10.4088/JCP.13r08851.
-
Jump up^ Malhi, Gin S.; Byrow, Yulisha; Bassett, Darryl; Boyce, Philip; Hopwood, Malcolm; Lyndon, William; Mulder, Roger; Porter, Richard; Singh, Ajeet; Murray, Greg (1 March 2016). "Stimulants for depression: On the up and up?". The Australian and New Zealand Journal of Psychiatry. 50 (3): 203–207. PMID 26906078. doi:10.1177/0004867416634208.
-
Jump up^ Rudorfer, MV, Henry, ME, Sackeim, HA (2003). "Electroconvulsive therapy". In A Tasman, J Kay, JA Lieberman (eds) Psychiatry, Second Edition. Chichester: John Wiley & Sons Ltd, 1865–1901.
-
Jump up^ Beloucif S (2013). "Informed consent for special procedures: electroconvulsive therapy and psychosurgery". Curr Opin Anaesthesiol. 26 (2): 182–5. PMID 23385317. doi:10.1097/ACO.0b013e32835e7380.
- ^ Jump up to:a b c FDA. FDA Executive Summary. Prepared for the 27–28 January 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT). Quote, p38: "Three major practice guidelines have been published on ECT. These guidelines include: APA Task Force on ECT (2001); Third report of the Royal College of Psychiatrists' Special Committee on ECT (2004); National Institute for Health and Clinical Excellence (NICE 2003; NICE 2009). There is significant agreement between the three sets of recommendations."
-
Jump up^ Dierckx B, Heijnen WT, van den Broek WW, Birkenhäger TK; Heijnen, WT; Van Den Broek, WW; Birkenhäger, TK (2012). "Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression: A meta-analysis". Bipolar Disorders. 14 (2): 146–150. PMID 22420590. doi:10.1111/j.1399-5618.2012.00997.x.
-
Jump up^ Jelovac A, et al. (Nov 2013). "Relapse following successful electroconvulsive therapy for major depression: a meta-analysis". Neuropsychopharmacology. 38 (12): 2467–74. PMC 3799066 . PMID 23774532. doi:10.1038/npp.2013.149.
-
Jump up^ Surgeon General (1999). Mental Health: A Report of the Surgeon General, chapter 4.
-
Jump up^ American Psychiatric Association; Committee on Electroconvulsive Therapy; Richard D. Weiner (chairperson); et al. (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging (2nd ed.). Washington, DC: American Psychiatric Publishing. ISBN 978-0-89042-206-9.
-
Jump up^ Pompili M, et al. (Dec 2014). "Electroconvulsive treatment during pregnancy: a systematic review". Expert Rev Neurother. 14 (12): 1377–90. PMID 25346216. doi:10.1586/14737175.2014.972373.
-
Jump up^ "5 Outdated Beliefs About ECT". Psych Central.com.
-
Jump up^ Abbott, C. C.; Gallegos, P.; Rediske, N.; Lemke, N. T.; Quinn, D. K. (2013). "A Review of Longitudinal Electroconvulsive Therapy: Neuroimaging Investigations". Journal of Geriatric Psychiatry and Neurology. 27 (1): 33–46. PMID 24381234. doi:10.1177/0891988713516542.
-
Jump up^ "NiCE. January 2014 Transcranial magnetic stimulation for treating and preventing migraine". Archived from the original on 4 October 2015.
-
Jump up^ "Melkerson, MN (2008-12-16). "Special Premarket 510(k) Notification for NeuroStar® TMS Therapy System for Major Depressive Disorder" (pdf). Food and Drug Administration. Retrieved 2010-07-16." (PDF).
-
Jump up^ Lefaucheur, JP; André-Obadia, N (November 2014). "Evidence-based guidelines on the therapeutic use of repetitive transcranial magnetic stimulation (rTMS).". Clinical Neurophysiology. 125 (11): 2150–206. PMID 25034472. doi:10.1016/j.clinph.2014.05.021.
-
Jump up^ "American Psychiatric Association (2010). (eds: Gelenberg, AJ, Freeman, MP, Markowitz, JC, Rosenbaum, JF, Thase, ME, Trivedi, MH, Van Rhoads, RS). Practice Guidelines for the Treatment of Patients with Major Depressive Disorder, 3rd Edition" (PDF).
-
Jump up^ "Journal of Affective Disorders" (PDF). 2009. pp. S1–S64. Archived from the original(PDF) on 23 August 2015.
-
Jump up^ Rush, A. John; Marangell, Lauren B.; Sackeim, Harold A.; George, Mark S.; Brannan, Stephen K.; Davis, Sonia M.; Howland, Robert; Kling, Mitchel A.; Rittberg, Barry R.; Burke, William J.; Rapaport, Mark H.; Zajecka, John; Nierenberg, Andrew A.; Husain, Mustafa M.; Ginsberg, David; Cooke, Robert G. (2005). "The Royal Australian and New Zealand College of Psychiatrists. (2013) Position Statement 79. Repetitive Transcranial Magnetic Stimulation. Practice and Partnerships Committee". Biological Psychiatry. 58 (5): 347–54. PMID 16139580. doi:10.1016/j.biopsych.2005.05.025.
-
Jump up^ Golden RN, Gaynes BN, Ekstrom RD, Hamer RM, Jacobsen FM, Suppes T, Wisner KL, Nemeroff CB (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. PMID 15800134. doi:10.1176/appi.ajp.162.4.656.
-
Jump up^ Tuunainen A, Kripke DF, Endo T (2004). Tuunainen, Arja, ed. "Light therapy for non-seasonal depression". Cochrane Database Syst Rev (2): CD004050. PMID 15106233. doi:10.1002/14651858.CD004050.pub2.
-
Jump up^ Joyce, Janine; Herbison, G Peter (3 April 2015). "Reiki for depression and anxiety". Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd. doi:10.1002/14651858.cd006833.pub2.
-
Jump up^ Meekums, Bonnie; Karkou, Vicky; Nelson, E Andrea (19 February 2015). "Dance movement therapy for depression". Cochrane Database of Systematic Reviews. John Wiley & Sons, Ltd. doi:10.1002/14651858.cd009895.pub2.
-
Jump up^ 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. doi:10.1016/S0165-0327(00)00304-9.
-
Jump up^ 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. doi:10.1097/01.nmd.0000217820.33841.53.
-
Jump up^ Fava GA, Park SK, Sonino N (2006). "Treatment of recurrent depression.". Expert Review of Neurotherapeutics. 6 (11): 1735–1740. PMID 17144786. doi:10.1586/14737175.6.11.1735.
-
Jump up^ Limosin F, Mekaoui L, Hautecouverture S (2007). "Stratégies thérapeutiques prophylactiques dans la dépression unipolaire [Prophylactic treatment for recurrent major depression]". La Presse Médicale. 36 (11–C2): 1627–1633. PMID 17555914. doi:10.1016/j.lpm.2007.03.032.
-
Jump up^ Eaton WW, Shao H, Nestadt G, Lee HB, Lee BH, Bienvenu OJ, Zandi P (2008). "Population-based study of first onset and chronicity in major depressive disorder". Archives of General Psychiatry. 65 (5): 513–20. PMC 2761826 . PMID 18458203. doi:10.1001/archpsyc.65.5.513.
-
Jump up^ Holma KM, Holma IA, Melartin TK, Rytsälä HJ, Isometsä ET (2008). "Long-term outcome of major depressive disorder in psychiatric patients is variable". Journal of Clinical Psychiatry. 69 (2): 196–205. PMID 18251627. doi:10.4088/JCP.v69n0205.
-
Jump up^ Kanai T, Takeuchi H, Furukawa TA, Yoshimura R, Imaizumi T, Kitamura T, Takahashi K (2003). "Time to recurrence after recovery from major depressive episodes and its predictors". Psychological Medicine. 33 (5): 839–45. PMID 12877398. doi:10.1017/S0033291703007827.
-
Jump up^ Geddes JR, Carney SM, Davies C, Furukawa TA, Kupfer DJ, Frank E, Goodwin GM (2003). "Relapse prevention with antidepressant drug treatment in depressive disorders: A systematic review". Lancet. 361 (9358): 653–61. PMID 12606176. doi:10.1016/S0140-6736(03)12599-8.
-
Jump up^ "Major Depression". MedlinePlus. 10 March 2014. Retrieved 16 July 2010.
-
Jump up^ "Depression, Major: Prognosis". MDGuidlines. Guardian Life Insurance Company of America. Retrieved 16 July 2010.
-
Jump up^ Cassano P, Fava M (2002). "Depression and public health: an overview". J Psychosom Res. 53 (4): 849–57. PMID 12377293. doi:10.1016/S0022-3999(02)00304-5.
-
Jump up^ Rush AJ (2007). "The varied clinical presentations of major depressive disorder". The Journal of Clinical Psychiatry. 68 (Supplement 8): 4–10. PMID 17640152.
- ^ Jump up to:a b Alboni P, Favaron E, Paparella N, Sciammarella M, Pedaci M (2008). "Is there an association between depression and cardiovascular mortality or sudden death?". Journal of cardiovascular medicine (Hagerstown, Md.). 9 (4): 356–62. PMID 18334889. doi:10.2459/JCM.0b013e3282785240.
-
Jump up^ Barlow DH; Durand VM (2005). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA, USA: Thomson Wadsworth. pp. 248–49. ISBN 0-534-63356-0.
-
Jump up^ 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. doi:10.1046/j.1440-1614.2001.00895.x.
-
Jump up^ Oquendo MA, Bongiovi-Garcia ME, Galfalvy H, Goldberg PH, Grunebaum MF, Burke AK, Mann JJ (2007). "Sex differences in clinical predictors of suicidal acts after major depression: a prospective study". The American Journal of Psychiatry. 164 (1): 134–41. PMC 3785095 . PMID 17202555. doi:10.1176/ajp.2007.164.1.134.
-
Jump up^ Bostwick JM, Pankratz VS (2000). "Affective disorders and suicide risk: A reexamination". American Journal of Psychiatry. 157 (12): 1925–32. PMID 11097952. doi:10.1176/appi.ajp.157.12.1925.
-
Jump up^ Weich S, Lewis G (1998). "Poverty, unemployment, and common mental disorders: Population based cohort study". BMJ. 317 (7151): 115–19. PMC 28602 . PMID 9657786. doi:10.1136/bmj.317.7151.115. Retrieved 16 September 2008.
-
Jump up^ Mathers CD, Loncar D (2006). "Projections of global mortality and burden of disease from 2002 to 2030". PLoS Med. 3 (11): e442. PMC 1664601 . PMID 17132052. doi:10.1371/journal.pmed.0030442.
-
Jump up^ Andrews G (2008). "In Review: Reducing the Burden of Depression". Canadian Journal of Psychiatry. 53 (7): 420–27. PMID 18674396.
-
Jump up^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.
-
Jump up^ 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): 593–602. PMID 15939837. doi:10.1001/archpsyc.62.6.593.
-
Jump up^ 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. PMID 10711905. doi:10.1001/archpsyc.57.3.209.
- ^ Jump up to:a b Kuehner C (2003). "Gender differences in unipolar depression: An update of epidemiological findings and possible explanations". Acta Psychiatrica Scandinavica. 108(3): 163–74. PMID 12890270. doi:10.1034/j.1600-0447.2003.00204.x.
-
Jump up^ "The world health report 2001 – Mental Health: New Understanding, New Hope". WHO website. World Health Organization. 2001. Retrieved 19 October 2008.
-
Jump up^ 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(11): 993–99. PMID 9366655. doi:10.1001/archpsyc.1997.01830230023003.
-
Jump up^ Rickards H (2005). "Depression in neurological disorders: Parkinson's disease, multiple sclerosis, and stroke". Journal of Neurology Neurosurgery and Psychiatry. 76: i48–i52. PMC 1765679 . PMID 15718222. doi:10.1136/jnnp.2004.060426.
-
Jump up^ Strik JJ, Honig A, Maes M (2001). "Depression and myocardial infarction: relationship between heart and mind". Progress in neuro-psychopharmacology & biological psychiatry. 25 (4): 879–92. PMID 11383983. doi:10.1016/S0278-5846(01)00150-6.
-
Jump up^ Jorm AF (2000). "Does old age reduce the risk of anxiety and depression? A review of epidemiological studies across the adult life span". Psychological Medicine. 30 (1): 11–22. PMID 10722172. doi:10.1017/S0033291799001452.
-
Jump up^ Gelder, M., Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp105.
-
Jump up^ Hippocrates, Aphorisms, Section 6.23
- ^ Jump up to:a b c Radden, J (2003). "Is this dame melancholy? Equating today's depression and past melancholia". Philosophy, Psychiatry, & Psychology. 10 (1): 37–52. doi:10.1353/ppp.2003.0081.
-
Jump up^ depress. (n.d.). Online Etymology Dictionary. Retrieved 30 June 2008, from Dictionary.com
-
Jump up^ Wolpert, L (1999). "Malignant Sadness: The Anatomy of Depression". The New York Times. Retrieved 30 October 2008.
-
Jump up^ Berrios GE (1988). "Melancholia and depression during the 19th century: A conceptual history". British Journal of Psychiatry. 153 (3): 298–304. PMID 3074848. doi:10.1192/bjp.153.3.298.
-
Jump up^ Davison, K (2006). "Historical aspects of mood disorders". Psychiatry. 5 (4): 115–18. doi:10.1383/psyt.2006.5.4.115.
-
Jump up^ 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. PMC 2515304 . PMID 18652673. doi:10.1186/1744-859X-7-9.
-
Jump up^ Freud, S (1984). "Mourning and Melancholia". In Richards A. 11.On Metapsychology: The Theory of Psycholoanalysis. Aylesbury, Bucks: Pelican. pp. 245–69. ISBN 0-14-021740-1.
-
Jump up^ Lewis, AJ (1934). "Melancholia: A historical review". Journal of Mental Science. 80 (328): 1–42. doi:10.1192/bjp.80.328.1.
-
Jump up^ American Psychiatric Association (1968). "Schizophrenia". Diagnostic and statistical manual of mental disorders: DSM-II (PDF). Washington, DC: American Psychiatric Publishing, Inc. pp. 36–37, 40. Retrieved 3 August 2008.
-
Jump up^ Schildkraut JJ (1965). "The catecholamine hypothesis of affective disorders: A review of supporting evidence". American Journal of Psychiatry. 122 (5): 509–22. PMID 5319766. doi:10.1176/ajp.122.5.509.
-
Jump up^ Paris J (2014). "The mistreatment of major depressive disorder.". Can J Psychiatry(Review). 59 (3): 148–51. PMC 4079242 . PMID 24881163. doi:10.1177/070674371405900306.
-
Jump up^ Angst J. Terminology, history and definition of bipolar spectrum. In: Maj M, Akiskal HS, López-Ibor JJ, Sartorius N (eds.), Bipolar disorders. Chichester: Wiley & Sons, LTD; 2002. pp. 53–55.
-
Jump up^ Spitzer RL, Endicott J, Robins E (1975). "The development of diagnostic criteria in psychiatry" (PDF). Retrieved 8 November 2008.
- ^ Jump up to: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. PMID 1829000. doi:10.1007/BF02189537.
-
Jump up^ Bolwig, Tom G.; Shorter, Edward (2007). "Melancholia: Beyond DSM, beyond neurotransmitters. Proceedings of a conference, May 2006, Copenhagen, Denmark". Acta Psychiatrica Scandinavica Suppl. 115 (433): 4–183. PMID 17280564. doi:10.1111/j.1600-0447.2007.00956.x.
-
Jump up^ Fink M, Bolwig TG, Parker G, Shorter E (2007). "Melancholia: Restoration in psychiatric classification recommended". Acta Psychiatrica Scandinavica. 115 (2): 89–92. PMC 3712974 . PMID 17244171. doi:10.1111/j.1600-0447.2006.00943.x.
-
Jump up^ Healy, David (1999). The Antidepressant Era. Cambridge, MA: Harvard University Press. p. 42. ISBN 0-674-03958-0.
-
Jump up^ Wolf, Joshua "Lincoln's Great Depression", The Atlantic, October 2005, Retrieved 10 October 2009
-
Jump up^ Maloney F (3 November 2005). "The Depression Wars: Would Honest Abe Have Written the Gettysburg Address on Prozac?". Slate magazine. Washington Post. Retrieved 3 October 2008.
-
Jump up^ Karasz A (2005). "Cultural differences in conceptual models of depression". Social Science in Medicine. 60 (7): 1625–35. PMID 15652693. doi:10.1016/j.socscimed.2004.08.011.
-
Jump up^ 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. 13 (1): 54–64. doi:10.5172/hesr.13.1.54.
-
Jump up^ 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. doi:10.1176/appi.ajp.158.6.857.
-
Jump up^ Parker G (2007). "Is depression overdiagnosed? Yes". BMJ. 335 (7615): 328. PMC 1949440 . PMID 17703040. doi:10.1136/bmj.39268.475799.AD.
-
Jump up^ 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. doi:10.1080/09638239917580.
-
Jump up^ Steibel W (Producer) (1998). "Is depression a disease?". Debatesdebates. Retrieved 16 November 2008.
-
Jump up^ Blazer DG (2005). The age of melancholy: "Major depression" and its social origins. New York, NY, USA: Routledge. ISBN 978-0-415-95188-3.
-
Jump up^ Hillman J (T Moore, Ed.) (1989). A blue fire: Selected writings by James Hillman. New York, NY, USA: Harper & Row. pp. 152–53. ISBN 0-06-016132-9.
-
Jump up^ Seymour, Miranda (2002). Mary Shelley. Grove Press. pp. 560–61. ISBN 0-8021-3948-5.
-
Jump up^ "Biography of Henry James". pbs.org. Retrieved 19 August 2008.
-
Jump up^ Burlingame, Michael (1997). The Inner World of Abraham Lincoln. Urbana: University of Illinois Press. pp. xvii, 92–113. ISBN 0-252-06667-7.
-
Jump up^ Pita E (26 September 2001). "An Intimate Conversation with...Leonard Cohen". Retrieved 3 October 2008.
-
Jump up^ Jeste ND, Palmer BW, Jeste DV (2004). "Tennessee Williams". American Journal of Geriatric Psychiatry. 12 (4): 370–75. PMID 15249274. doi:10.1097/00019442-200407000-00004.
-
Jump up^ James H (Ed.) (1920). Letters of William James (Vols. 1 and 2). Montana USA: Kessinger Publishing Co. pp. 147–48. ISBN 978-0-7661-7566-2.
-
Jump up^ Hergenhahn 2005, p. 311
-
Jump up^ Cohen D (1979). J. B. Watson: The Founder of Behaviourism. London, UK: Routledge & Kegan Paul. p. 7. ISBN 0-7100-0054-5.
-
Jump up^ Andreasen NC (2008). "The relationship between creativity and mood disorders". Dialogues in clinical neuroscience. 10 (2): 251–5. PMC 3181877 . PMID 18689294.
-
Jump up^ Simonton, DK (2005). "Are genius and madness related? Contemporary answers to an ancient question". Psychiatric Times. 22 (7).
-
Jump up^ Heffernan CF (1996). The melancholy muse: Chaucer, Shakespeare and early medicine. Pittsburgh, PA, USA: Duquesne University Press. ISBN 0-8207-0262-5.
-
Jump up^ Mill JS (2003). "A crisis in my mental history: One stage onward". Autobiography (txt). Project Gutenberg EBook. pp. 1826–32. ISBN 1-4212-4200-1. Retrieved 9 August 2008.
-
Jump up^ Sterba R (1947). "The 'Mental Crisis' of John Stuart Mill". Psychoanalytic Quarterly. 16(2): 271–72. Retrieved 5 November 2008.
- ^ Jump up to: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. 2005. Retrieved 18 August 2008.
-
Jump up^ Jorm AF, Angermeyer M, Katschnig H (2000). "Public knowledge of and attitudes to mental disorders: a limiting factor in the optimal use of treatment services". In Andrews G, Henderson S. Unmet Need in Psychiatry:Problems, Resources, Responses. Cambridge University Press. p. 409. ISBN 0-521-66229-X.
-
Jump up^ Paykel ES, Tylee A, Wright A, Priest RG, Rix S, Hart D (1997). "The Defeat Depression Campaign: psychiatry in the public arena". American Journal of Psychiatry. 154 (6 Suppl): 59–65. PMID 9167546. doi:10.1176/ajp.154.6.59.
-
Jump up^ Paykel ES, Hart D, Priest RG (1998). "Changes in public attitudes to depression during the Defeat Depression Campaign". British Journal of Psychiatry. 173 (6): 519–22. PMID 9926082. doi:10.1192/bjp.173.6.519.
-
Jump up^ Kruger TH, Wollmer MA (2015). "Depression – An emerging indication for botulinum toxin treatment". Toxicon. 107 (Pt A): 154–7. PMID 26415901. doi:10.1016/j.toxicon.2015.09.035.
-
Jump up^ Milev, R (2015). "Response of Depression to Botulinum Toxin Treatment: Agitation as a Predictor". Frontiers in Psychiatry. 6: 55. PMC 4403301 . PMID 25941497. doi:10.3389/fpsyt.2015.00055..
-
Jump up^ Kempton MJ, Salvador Z, Munafò MR, Geddes JR, Simmons A, Frangou S, Williams SC (2011). "Structural Neuroimaging Studies in Major Depressive Disorder: Meta-analysis and Comparison With Bipolar Disorder". Arch Gen Psychiatry. 68 (7): 675–90. PMID 21727252. doi:10.1001/archgenpsychiatry.2011.60. see also MRI database at www.depressiondatabase.org
-
Jump up^ Arnone D, McIntosh AM, Ebmeier KP, Munafò MR, Anderson IM (July 2011). "Magnetic resonance imaging studies in unipolar depression: Systematic review and meta-regression analyses". Eur Neuropsychopharmacol. 22 (1): 1–16. PMID 21723712. doi:10.1016/j.euroneuro.2011.05.003.
-
Jump up^ Herrmann LL, Le Masurier M, Ebmeier KP (2008). "White matter hyperintensities in late life depression: a systematic review". Journal of Neurology, Neurosurgery, and Psychiatry. 79 (6): 619–24. PMID 17717021. doi:10.1136/jnnp.2007.124651.
- ^ Jump up to:a b c d e f g h i j k l m Services, Swedish Council on Health Technology Assessmentl. "Depression treatment for the elderly". www.sbu.se. Retrieved 16 June 2016.
-
Jump up^ Krishnan, Vaishnav; Nestler, Eric J. (1 January 2011). "Animal Models of Depression: Molecular Perspectives". Current Topics in Behavioral Neurosciences. 7: 121–147. PMC 3270071 . PMID 21225412. doi:10.1007/7854_2010_108.
Cited works
- American Psychiatric Association (2000a). Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc. ISBN 0-89042-025-4.
- Barlow DH; Durand VM (2005). Abnormal psychology: An integrative approach (5th ed.). Belmont, CA, USA: Thomson Wadsworth. ISBN 0-534-63356-0.
- Beck AT, Rush J, Shaw BF, Emery G (1987) [1979]. Cognitive Therapy of depression. New York, NY, USA: Guilford Press. ISBN 0-89862-919-5.
- Hergenhahn BR (2005). An Introduction to the History of Psychology (5th ed.). Belmont, CA, USA: Thomson Wadsworth. ISBN 0-534-55401-6.
- May R (1994). The discovery of being: Writings in existential psychology. New York, NY, USA: W. W. Norton & Company. ISBN 0-393-31240-2.
- Hadzi-Pavlovic, Dusan; Parker, Gordon (1996). Melancholia: a disorder of movement and mood: a phenomenological and neurobiological review. Cambridge, UK: Cambridge University Press. ISBN 0-521-47275-X.
- Royal Pharmaceutical Society of Great Britain (2008). British National Formulary (BNF 56). UK: BMJ Group and RPS Publishing. ISBN 978-0-85369-778-7.
- Sadock, Virginia A.; Sadock, Benjamin J.; Kaplan, Harold I. (2003). Kaplan & Sadock's synopsis of psychiatry: behavioral sciences/clinical psychiatry. Philadelphia: Lippincott Williams & Wilkins. ISBN 0-7817-3183-6.
External linksClassification
External resources
This audio file was created from a revision of the "Major depressive disorder" article dated 2014-10-06, and does not reflect subsequent edits to the article. (
Audio help)
