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Questions and Answers
Depressed mood is a unique symptom of depressive disorders.
Depressed mood is a unique symptom of depressive disorders.
False
Depressive disorders always present with depressed mood as the most prominent symptom.
Depressive disorders always present with depressed mood as the most prominent symptom.
False
The clinical presentations of depressive states are uniform and consistent.
The clinical presentations of depressive states are uniform and consistent.
False
The concept of an 'episode' of clinical depression is universally agreed upon.
The concept of an 'episode' of clinical depression is universally agreed upon.
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The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders.
The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders.
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Reduced energy is not a central feature of depressive disorders.
Reduced energy is not a central feature of depressive disorders.
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Neurological disorders can cause depressed mood as a symptom of the disorder.
Neurological disorders can cause depressed mood as a symptom of the disorder.
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The mood of a patient with severe depressive episode is alleviated in circumstances where ordinary feelings of sadness would be alleviated, such as in pleasant company or after hearing good news.
The mood of a patient with severe depressive episode is alleviated in circumstances where ordinary feelings of sadness would be alleviated, such as in pleasant company or after hearing good news.
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Some patients with severe depressive episode maintain a smiling exterior despite deep feelings of depression.
Some patients with severe depressive episode maintain a smiling exterior despite deep feelings of depression.
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The gestalt of a patient with severe depressive episode is characterized by erect posture and an upright head.
The gestalt of a patient with severe depressive episode is characterized by erect posture and an upright head.
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Patients with severe depressive episode often experience a diurnal variation of mood, with their mood improving as the day wears on.
Patients with severe depressive episode often experience a diurnal variation of mood, with their mood improving as the day wears on.
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Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.
Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.
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Feelings of guilt in patients with severe depressive episode are always attached to specific past events.
Feelings of guilt in patients with severe depressive episode are always attached to specific past events.
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Lack of interest and enjoyment is a rare symptom in patients with severe depressive episode.
Lack of interest and enjoyment is a rare symptom in patients with severe depressive episode.
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In depression, psychomotor changes include increased energy and speed of thought.
In depression, psychomotor changes include increased energy and speed of thought.
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Anhedonia is not a key symptom of melancholic depression.
Anhedonia is not a key symptom of melancholic depression.
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Biological symptoms include decreased appetite and weight gain.
Biological symptoms include decreased appetite and weight gain.
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Depressed patients always experience sleep disturbance in the form of excessive sleeping.
Depressed patients always experience sleep disturbance in the form of excessive sleeping.
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Anxiety is a rare symptom in severe depression.
Anxiety is a rare symptom in severe depression.
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Irritability is never a core presenting feature in adolescents with depression.
Irritability is never a core presenting feature in adolescents with depression.
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Depressed patients never experience depersonalization or dissociative symptoms.
Depressed patients never experience depersonalization or dissociative symptoms.
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Depressive pseudodementia is a condition that is more common in younger individuals than in the elderly.
Depressive pseudodementia is a condition that is more common in younger individuals than in the elderly.
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In psychotic depression, there is no impairment of insight and patients are aware of their mistaken beliefs.
In psychotic depression, there is no impairment of insight and patients are aware of their mistaken beliefs.
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Delusions of severe depressive disorders are always mood-incongruent.
Delusions of severe depressive disorders are always mood-incongruent.
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Patients with a delusion of guilt may believe that they have done something good and will be rewarded.
Patients with a delusion of guilt may believe that they have done something good and will be rewarded.
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Cotard's syndrome is a mild depressive disorder characterized by a lack of energy.
Cotard's syndrome is a mild depressive disorder characterized by a lack of energy.
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Agitated depression is a condition that is seen more commonly among younger individuals than among middle-aged and elderly patients.
Agitated depression is a condition that is seen more commonly among younger individuals than among middle-aged and elderly patients.
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Retarded depression is a condition that is characterized by excessive motor activity.
Retarded depression is a condition that is characterized by excessive motor activity.
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Inattention to basic hygiene and nutrition is a common feature of mild depressive disorders.
Inattention to basic hygiene and nutrition is a common feature of mild depressive disorders.
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Depressive disorders are always characterized by a complete loss of function in social and occupational spheres.
Depressive disorders are always characterized by a complete loss of function in social and occupational spheres.
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Depressive stupor is a common occurrence in patients with severe depressive disorder.
Depressive stupor is a common occurrence in patients with severe depressive disorder.
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Patients in depressive stupor often exhibit aggressive behavior.
Patients in depressive stupor often exhibit aggressive behavior.
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Patients in depressive stupor always recall events that took place during the period of stupor.
Patients in depressive stupor always recall events that took place during the period of stupor.
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Atypical depression is a severe form of depressive disorder.
Atypical depression is a severe form of depressive disorder.
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Kraepelin's description of depressive stupor mentioned that patients often defend themselves from pinprick.
Kraepelin's description of depressive stupor mentioned that patients often defend themselves from pinprick.
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Patients in depressive stupor often feed themselves without assistance.
Patients in depressive stupor often feed themselves without assistance.
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Patients with atypical depression have a later onset of illness and a more acute course.
Patients with atypical depression have a later onset of illness and a more acute course.
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Depressive stupor is characterized by a high level of physical activity.
Depressive stupor is characterized by a high level of physical activity.
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Mixed depression is characterized by a complete lack of anxiety and agitation.
Mixed depression is characterized by a complete lack of anxiety and agitation.
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Mild depressive disorders are characterized by delusions and hallucinations.
Mild depressive disorders are characterized by delusions and hallucinations.
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Patients with mild depressive disorders often experience early-morning waking.
Patients with mild depressive disorders often experience early-morning waking.
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The diagnosis of atypical depression predicts a poor response to modern antidepressant drug treatment.
The diagnosis of atypical depression predicts a poor response to modern antidepressant drug treatment.
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Mixed depression is only seen in patients with bipolar disorder.
Mixed depression is only seen in patients with bipolar disorder.
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The ICD-10 classification provides a clear distinction between mild and severe depressive disorders.
The ICD-10 classification provides a clear distinction between mild and severe depressive disorders.
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In ICD-10, patients with minor anxiety– depressive disorder are diagnosed under the category of mood disorders.
In ICD-10, patients with minor anxiety– depressive disorder are diagnosed under the category of mood disorders.
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The DSM-5 includes a category of 'Mixed Anxiety and Depressive Disorder'.
The DSM-5 includes a category of 'Mixed Anxiety and Depressive Disorder'.
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Patients with minor anxiety– depressive disorders rarely present to primary care doctors with somatic symptoms.
Patients with minor anxiety– depressive disorders rarely present to primary care doctors with somatic symptoms.
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In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 1 year.
In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 1 year.
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Dysthymia is characterized by depressive symptoms that are severe enough to meet criteria for a depressive episode.
Dysthymia is characterized by depressive symptoms that are severe enough to meet criteria for a depressive episode.
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The diagnosis of minor anxiety– depressive disorder is clearly defined in both ICD-10 and DSM-5.
The diagnosis of minor anxiety– depressive disorder is clearly defined in both ICD-10 and DSM-5.
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Patients with minor anxiety– depressive disorders typically present with a uniform set of symptoms.
Patients with minor anxiety– depressive disorders typically present with a uniform set of symptoms.
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In most cultures, sadness, joylessness, anxiety, and lack of energy are uncommon symptoms of depression.
In most cultures, sadness, joylessness, anxiety, and lack of energy are uncommon symptoms of depression.
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Somatization of depression is more frequent and prominent in western cultures.
Somatization of depression is more frequent and prominent in western cultures.
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Particular cultures have no unique ways of dealing with painful emotions produced by loss.
Particular cultures have no unique ways of dealing with painful emotions produced by loss.
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The diagnosis of depression should not take cultural variations into account.
The diagnosis of depression should not take cultural variations into account.
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The term ‘minor’ accurately captures the serious consequences of affective disorders for an individual.
The term ‘minor’ accurately captures the serious consequences of affective disorders for an individual.
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Depression is overdiagnosed in primary care, particularly in most countries.
Depression is overdiagnosed in primary care, particularly in most countries.
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Somatic presentations of depression are rare in non-western cultures.
Somatic presentations of depression are rare in non-western cultures.
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Cultural stigmatization of mental illness has no impact on the presentation of depression.
Cultural stigmatization of mental illness has no impact on the presentation of depression.
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The use of somatic metaphors for emotional suffering is uncommon in non-western cultures.
The use of somatic metaphors for emotional suffering is uncommon in non-western cultures.
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The classification of depressive disorders based on presumed aetiology is widely accepted.
The classification of depressive disorders based on presumed aetiology is widely accepted.
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The symptomatic picture of melancholic depression is uniform and consistent across patients.
The symptomatic picture of melancholic depression is uniform and consistent across patients.
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The concept of reactive depression is no longer used in modern classification systems.
The concept of reactive depression is no longer used in modern classification systems.
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The distinction between severe and less severe depressive disorders is clearly defined in ICD-10.
The distinction between severe and less severe depressive disorders is clearly defined in ICD-10.
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Lewis (1934) suggested that every illness is solely the result of environmental factors.
Lewis (1934) suggested that every illness is solely the result of environmental factors.
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Aetiological factors are not considered in classifying depressive disorders.
Aetiological factors are not considered in classifying depressive disorders.
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Classification by symptomatic picture is a widely accepted method of classifying depressive disorders.
Classification by symptomatic picture is a widely accepted method of classifying depressive disorders.
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DSM-5 and ICD-10 have a unified approach to classifying depressive disorders.
DSM-5 and ICD-10 have a unified approach to classifying depressive disorders.
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According to the classification by symptom profile, melancholic depression is a type of non-major depressive episode.
According to the classification by symptom profile, melancholic depression is a type of non-major depressive episode.
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The presence of psychotic features in depression is always accompanied by melancholic symptoms.
The presence of psychotic features in depression is always accompanied by melancholic symptoms.
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Kraepelin's classification included a division into three groups: unipolar depression, bipolar disorder, and schizoaffective disorder.
Kraepelin's classification included a division into three groups: unipolar depression, bipolar disorder, and schizoaffective disorder.
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Atypical depression is a type of melancholic depression.
Atypical depression is a type of melancholic depression.
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Most patients with depressive disorders have melancholic symptoms of some kind.
Most patients with depressive disorders have melancholic symptoms of some kind.
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Neurobiological abnormalities are more commonly found in patients with non-melancholic depression.
Neurobiological abnormalities are more commonly found in patients with non-melancholic depression.
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The diagnosis of melancholic depression is not a distinct subtype of depression, but rather a point on a continuum of severity of depression.
The diagnosis of melancholic depression is not a distinct subtype of depression, but rather a point on a continuum of severity of depression.
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Tricyclic antidepressants are less effective in treating melancholic depression than selective serotonin reuptake inhibitors (SSRIs).
Tricyclic antidepressants are less effective in treating melancholic depression than selective serotonin reuptake inhibitors (SSRIs).
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DSM-5 and ICD-10 are entirely satisfactory classification systems.
DSM-5 and ICD-10 are entirely satisfactory classification systems.
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Comorbidity with anxiety disorders is a rare occurrence in depressive disorders.
Comorbidity with anxiety disorders is a rare occurrence in depressive disorders.
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In DSM-5, the term 'unipolar mania' is still used to describe a specific type of mania.
In DSM-5, the term 'unipolar mania' is still used to describe a specific type of mania.
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The 12-month prevalence of major depression in the community is around 10–20%
The 12-month prevalence of major depression in the community is around 10–20%
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The full diagnostic criteria for major depression are always met in adjustment disorders.
The full diagnostic criteria for major depression are always met in adjustment disorders.
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Rates of major depression are about three times as high in women as in men, across different cultures.
Rates of major depression are about three times as high in women as in men, across different cultures.
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Seasonal affective disorder is characterized by symptoms such as insomnia and decreased appetite.
Seasonal affective disorder is characterized by symptoms such as insomnia and decreased appetite.
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Dementia and depressive disorders can be easily distinguished based on cognitive impairment.
Dementia and depressive disorders can be easily distinguished based on cognitive impairment.
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Recurrent brief depression is a type of depression that is only seen in women and is linked to the menstrual cycle.
Recurrent brief depression is a type of depression that is only seen in women and is linked to the menstrual cycle.
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The epidemiology of depressive disorders is well-established and easily determinable.
The epidemiology of depressive disorders is well-established and easily determinable.
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The lifetime rates of major depression in different studies vary considerably, in the range 1–10%.
The lifetime rates of major depression in different studies vary considerably, in the range 1–10%.
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The mean age of onset of major depression is about 35 years.
The mean age of onset of major depression is about 35 years.
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In DSM-5, mood disorders secondary to a medical condition are classified as a separate category.
In DSM-5, mood disorders secondary to a medical condition are classified as a separate category.
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The distinction between depressive disorders and schizophrenia is always clear-cut.
The distinction between depressive disorders and schizophrenia is always clear-cut.
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Major depression has a low comorbidity with other disorders, particularly anxiety disorders and substance misuse.
Major depression has a low comorbidity with other disorders, particularly anxiety disorders and substance misuse.
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The ICD-10 classification provides a clear distinction between depressive disorders and anxiety disorders.
The ICD-10 classification provides a clear distinction between depressive disorders and anxiety disorders.
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ICD-10 and DSM-5 both classify depressive episodes based on the presence of psychotic features.
ICD-10 and DSM-5 both classify depressive episodes based on the presence of psychotic features.
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The lifetime risk for dysthymia is around 10%.
The lifetime risk for dysthymia is around 10%.
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For most clinical purposes, it is better to classify disorders rather than describe them systematically.
For most clinical purposes, it is better to classify disorders rather than describe them systematically.
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Atypical depression is a separate category in ICD-10, but is classified as a specifier in DSM-5.
Atypical depression is a separate category in ICD-10, but is classified as a specifier in DSM-5.
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The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders, but does not specify the exact criteria for the distinction.
The ICD-10 classification provides a clear distinction between severe and less severe depressive disorders, but does not specify the exact criteria for the distinction.
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The 1-week prevalence of mixed anxiety and depression in the community is around 5%.
The 1-week prevalence of mixed anxiety and depression in the community is around 5%.
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Recurrent brief depression is classified under the same heading in both ICD-10 and DSM-5.
Recurrent brief depression is classified under the same heading in both ICD-10 and DSM-5.
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Rates of dysthymia are higher in men and in the unemployed.
Rates of dysthymia are higher in men and in the unemployed.
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The risk of depression in a first-degree relative of a proband is increased about twofold.
The risk of depression in a first-degree relative of a proband is increased about twofold.
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Investigators have employed only one main conceptual approach to elucidate the mechanisms of depression.
Investigators have employed only one main conceptual approach to elucidate the mechanisms of depression.
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The aetiology section in the current chapter is not structured to illustrate various ways of approaching research into the causation of psychiatric disorder.
The aetiology section in the current chapter is not structured to illustrate various ways of approaching research into the causation of psychiatric disorder.
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Family and twin studies have not found any correlation between depression and genetic factors.
Family and twin studies have not found any correlation between depression and genetic factors.
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The psychological and biological approaches to depression research represent the same level of enquiry.
The psychological and biological approaches to depression research represent the same level of enquiry.
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The current chapter does not provide any information about the role of current life difficulties and stresses in provoking depression.
The current chapter does not provide any information about the role of current life difficulties and stresses in provoking depression.
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The text does not mention anything about the predisposing factors of depression in adulthood.
The text does not mention anything about the predisposing factors of depression in adulthood.
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There is complete knowledge about the mechanisms involved in the translation of predisposing and provoking factors into clinical symptomatology.
There is complete knowledge about the mechanisms involved in the translation of predisposing and provoking factors into clinical symptomatology.
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The heritability of major depression is estimated to be higher than that of bipolar disorder or schizophrenia.
The heritability of major depression is estimated to be higher than that of bipolar disorder or schizophrenia.
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Twin studies have suggested that susceptibility to major depression and generalized anxiety disorder involves different genes and environmental risk factors.
Twin studies have suggested that susceptibility to major depression and generalized anxiety disorder involves different genes and environmental risk factors.
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The genetic liability to depression results from the combined action of a single gene of major effect.
The genetic liability to depression results from the combined action of a single gene of major effect.
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The gene coding for the serotonin transporter has a single allelic variant that influences the expression of transporter sites.
The gene coding for the serotonin transporter has a single allelic variant that influences the expression of transporter sites.
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GWAS studies in depression have reported several convincingly replicated loci.
GWAS studies in depression have reported several convincingly replicated loci.
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A recent whole genome sequencing study identified multiple genetic markers associated with depression.
A recent whole genome sequencing study identified multiple genetic markers associated with depression.
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The mode of inheritance of depression fits a simple Mendelian pattern.
The mode of inheritance of depression fits a simple Mendelian pattern.
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The heritability estimates for depression are consistently higher in men than in women.
The heritability estimates for depression are consistently higher in men than in women.
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The first approach to overcome the third problem of association is to separate events that are undoubtedly independent of illness from events that may have been secondary to the illness.
The first approach to overcome the third problem of association is to separate events that are undoubtedly independent of illness from events that may have been secondary to the illness.
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There is a sixfold excess of adverse life events in the months before the onset of depressive disorder, but only in established melancholic-type disorders.
There is a sixfold excess of adverse life events in the months before the onset of depressive disorder, but only in established melancholic-type disorders.
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Life events are important antecedents of all forms of depression, but are relatively more important in established melancholic-type disorders.
Life events are important antecedents of all forms of depression, but are relatively more important in established melancholic-type disorders.
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Neuroticism, as measured by the Eysenck Personality Questionnaire, is associated with decreased risk of depression after adverse life events.
Neuroticism, as measured by the Eysenck Personality Questionnaire, is associated with decreased risk of depression after adverse life events.
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Loss of a parent by death in childhood increases the risk of depressive disorder in adulthood.
Loss of a parent by death in childhood increases the risk of depressive disorder in adulthood.
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Remission from depression is often associated with 'threat' life events.
Remission from depression is often associated with 'threat' life events.
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Gross disruption of parent-child relationships, such as physical and sexual abuse, is a risk factor for anxiety disorders only.
Gross disruption of parent-child relationships, such as physical and sexual abuse, is a risk factor for anxiety disorders only.
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The importance of life events in the onset of a depressive episode increases as the number of episodes increases.
The importance of life events in the onset of a depressive episode increases as the number of episodes increases.
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Mothers with postnatal depression often manifest a rearing style that is characterized by overprotection and excessive care.
Mothers with postnatal depression often manifest a rearing style that is characterized by overprotection and excessive care.
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Vulnerability factors, such as poor social support, are not associated with an increased risk of depression.
Vulnerability factors, such as poor social support, are not associated with an increased risk of depression.
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The mechanism of the association between poor social support and depression is clear and well-established.
The mechanism of the association between poor social support and depression is clear and well-established.
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Stressful events are not a precipitating factor for depressive disorders.
Stressful events are not a precipitating factor for depressive disorders.
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Cognitive style characterized by sociotropy is associated with decreased risk of depression after adverse life events.
Cognitive style characterized by sociotropy is associated with decreased risk of depression after adverse life events.
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The events immediately preceding a depressive disorder are always the direct cause of the disorder.
The events immediately preceding a depressive disorder are always the direct cause of the disorder.
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Personality features have no influence on the way people respond to adverse circumstances and, thus, do not affect the likelihood of depressive disorders.
Personality features have no influence on the way people respond to adverse circumstances and, thus, do not affect the likelihood of depressive disorders.
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The genetic risk of depression is not influenced by inheritance of particular character traits and cognitive styles.
The genetic risk of depression is not influenced by inheritance of particular character traits and cognitive styles.
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The effects of physical illness can only lead to mood disorders in predisposed individuals.
The effects of physical illness can only lead to mood disorders in predisposed individuals.
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Endocrine disorders are a type of brain disease that can cause mood disorders.
Endocrine disorders are a type of brain disease that can cause mood disorders.
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Major depression occurs in all patients with Cushing’s disease.
Major depression occurs in all patients with Cushing’s disease.
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Organic mood disorders can never provide clues to aetiology.
Organic mood disorders can never provide clues to aetiology.
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The puerperium is a medical illness that can cause mood disorders.
The puerperium is a medical illness that can cause mood disorders.
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Cushing’s disease is the only medical condition that can cause mood disorders.
Cushing’s disease is the only medical condition that can cause mood disorders.
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Depressive disorders in patients with Cushing’s disease always remit after cortisol levels are restored to normal.
Depressive disorders in patients with Cushing’s disease always remit after cortisol levels are restored to normal.
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The distinction between organic and non-organic mood disorders is always clear-cut.
The distinction between organic and non-organic mood disorders is always clear-cut.
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Cognitive theories propose that depressive cognitions are a result of a primary disturbance of mood.
Cognitive theories propose that depressive cognitions are a result of a primary disturbance of mood.
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Patients with severe depressive episode often experience a diurnal variation of mood, with their mood worsening as the day wears on.
Patients with severe depressive episode often experience a diurnal variation of mood, with their mood worsening as the day wears on.
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Cognitive distortions include arbitrary inference, selective abstraction, and rationalization.
Cognitive distortions include arbitrary inference, selective abstraction, and rationalization.
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Beck's theory proposes that depressive cognitions are limited to feelings of worthlessness and pessimism.
Beck's theory proposes that depressive cognitions are limited to feelings of worthlessness and pessimism.
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Cognitive theories suggest that depressive disorders are a result of illogical ways of thinking, but do not specify what these ways are.
Cognitive theories suggest that depressive disorders are a result of illogical ways of thinking, but do not specify what these ways are.
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Most psychiatrists regard depressive cognitions as a primary cause of depressive disorders.
Most psychiatrists regard depressive cognitions as a primary cause of depressive disorders.
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Dysfunctional beliefs or schemas, such as 'No-one really likes me', are established in adulthood and affect the way a person responds to stress and adversity.
Dysfunctional beliefs or schemas, such as 'No-one really likes me', are established in adulthood and affect the way a person responds to stress and adversity.
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Abnormalities in information processing, such as negative biases in facial expression recognition, can only be demonstrated in depressed patients.
Abnormalities in information processing, such as negative biases in facial expression recognition, can only be demonstrated in depressed patients.
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The monoamine hypothesis suggests that depressive disorder is due to an abnormality in the release of a single neurotransmitter, serotonin, in the brain.
The monoamine hypothesis suggests that depressive disorder is due to an abnormality in the release of a single neurotransmitter, serotonin, in the brain.
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Structural and functional imaging techniques have not been used to elicit changes in the neural circuitry that underpins the expression of clinical affective symptomatology.
Structural and functional imaging techniques have not been used to elicit changes in the neural circuitry that underpins the expression of clinical affective symptomatology.
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Depressive disorders are not associated with distinct and persistent neuropathological changes in relevant brain regions.
Depressive disorders are not associated with distinct and persistent neuropathological changes in relevant brain regions.
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The prognosis of mood disorders improves as the number of episodes increases.
The prognosis of mood disorders improves as the number of episodes increases.
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Plasma tryptophan levels are increased in untreated depressed patients, particularly in those with melancholic depression.
Plasma tryptophan levels are increased in untreated depressed patients, particularly in those with melancholic depression.
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There is consistent evidence that depressed patients who have died, usually by suicide, have lowered brain concentrations of 5-HT or 5-HIAA.
There is consistent evidence that depressed patients who have died, usually by suicide, have lowered brain concentrations of 5-HT or 5-HIAA.
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Cerebrospinal fluid (CSF) studies have found a consistent reduction in CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in drug-free patients with major depression.
Cerebrospinal fluid (CSF) studies have found a consistent reduction in CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in drug-free patients with major depression.
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Neurochemical brain imaging studies have found a widespread increase in 5-HT1A receptor binding throughout the cortical and subcortical regions in depressed individuals.
Neurochemical brain imaging studies have found a widespread increase in 5-HT1A receptor binding throughout the cortical and subcortical regions in depressed individuals.
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The synthesis of 5-HT in the brain is independent of the availability of its precursor amino acid, l-tryptophan.
The synthesis of 5-HT in the brain is independent of the availability of its precursor amino acid, l-tryptophan.
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Decreases in plasma tryptophan levels are likely to be an important causal factor in the impairments of brain 5-HT function in depressed patients.
Decreases in plasma tryptophan levels are likely to be an important causal factor in the impairments of brain 5-HT function in depressed patients.
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Tryptophan depletion in healthy subjects with a family history of mood disorder produces significant clinical depressive symptomatology.
Tryptophan depletion in healthy subjects with a family history of mood disorder produces significant clinical depressive symptomatology.
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Noradrenaline receptors in the brain can be divided into only two subclasses.
Noradrenaline receptors in the brain can be divided into only two subclasses.
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Low brain 5-HT function is sufficient to cause depression.
Low brain 5-HT function is sufficient to cause depression.
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Increasing brain noradrenaline function decreases plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and growth hormone.
Increasing brain noradrenaline function decreases plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and growth hormone.
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The synthesis of brain 5-HT is dependent on the availability of its amino acid precursor, tyrosine.
The synthesis of brain 5-HT is dependent on the availability of its amino acid precursor, tyrosine.
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Unmedicated euthymic patients with a personal history of mood disorder do not undergo a rapid but temporary depressive relapse when exposed to tryptophan depletion.
Unmedicated euthymic patients with a personal history of mood disorder do not undergo a rapid but temporary depressive relapse when exposed to tryptophan depletion.
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GABA concentrations are higher in patients with panic disorder.
GABA concentrations are higher in patients with panic disorder.
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There is evidence for increased levels of glutamate in the anterior brain regions in depressed patients.
There is evidence for increased levels of glutamate in the anterior brain regions in depressed patients.
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The NMDA-receptor antagonist ketamine has no effect on patients with treatment-refractory depression.
The NMDA-receptor antagonist ketamine has no effect on patients with treatment-refractory depression.
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About 20% of patients with Cushing's syndrome suffer from major depression.
About 20% of patients with Cushing's syndrome suffer from major depression.
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Endocrine abnormalities are not found in depressive disorder.
Endocrine abnormalities are not found in depressive disorder.
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The hypothalamic-pituitary-adrenal axis is not affected in depressive disorders.
The hypothalamic-pituitary-adrenal axis is not affected in depressive disorders.
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Plasma cortisol secretion is decreased in about 50% of patients with depressive disorder.
Plasma cortisol secretion is decreased in about 50% of patients with depressive disorder.
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The adrenal gland is decreased in size in patients with depressive disorder.
The adrenal gland is decreased in size in patients with depressive disorder.
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Cortisol response to corticotropin (ACTH) challenge is decreased in patients with depressive disorder.
Cortisol response to corticotropin (ACTH) challenge is decreased in patients with depressive disorder.
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Glutamate levels are not being studied in mood disorders.
Glutamate levels are not being studied in mood disorders.
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Desipramine and clonidine stimulate the release of growth hormone in patients with melancholic depression.
Desipramine and clonidine stimulate the release of growth hormone in patients with melancholic depression.
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α-Methyl-para-tyrosine (AMPT) causes significant depressive symptoms in healthy subjects.
α-Methyl-para-tyrosine (AMPT) causes significant depressive symptoms in healthy subjects.
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Dopamine function is well studied and clearly understood in depression.
Dopamine function is well studied and clearly understood in depression.
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Low levels of homovanillic acid (HVA) are found only in patients with psychomotor retardation.
Low levels of homovanillic acid (HVA) are found only in patients with psychomotor retardation.
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Abnormalities in monoamine function are only found in unmedicated depressed patients.
Abnormalities in monoamine function are only found in unmedicated depressed patients.
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Lowering 5-HT and dopamine function is sufficient to cause clinical depression in anyone, regardless of prior illness.
Lowering 5-HT and dopamine function is sufficient to cause clinical depression in anyone, regardless of prior illness.
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Decreased levels of free thyroxine are commonly found in depressed patients.
Decreased levels of free thyroxine are commonly found in depressed patients.
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Administration of CRH to animals produces changes in neuroendocrine regulation, sleep, and appetite that are opposite to those found in depressed patients.
Administration of CRH to animals produces changes in neuroendocrine regulation, sleep, and appetite that are opposite to those found in depressed patients.
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Childhood trauma does not affect HPA axis regulation.
Childhood trauma does not affect HPA axis regulation.
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CRH has a neurotransmitter role in cortical regions of the brain.
CRH has a neurotransmitter role in cortical regions of the brain.
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About 50% of depressed patients have a blunted TSH response to intravenous TRH.
About 50% of depressed patients have a blunted TSH response to intravenous TRH.
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Cytokines can induce expression of the tryptophan-metabolizing enzyme indoleamine 2, 3-dioxygenase, which increases tryptophan levels.
Cytokines can induce expression of the tryptophan-metabolizing enzyme indoleamine 2, 3-dioxygenase, which increases tryptophan levels.
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HPA axis changes in depressed patients are always state abnormalities that remit when the patient recovers.
HPA axis changes in depressed patients are always state abnormalities that remit when the patient recovers.
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About 80% of depressed inpatients do not show the normal suppression of cortisol secretion induced by administering 1 mg of the synthetic corticosteroid dexamethasone.
About 80% of depressed inpatients do not show the normal suppression of cortisol secretion induced by administering 1 mg of the synthetic corticosteroid dexamethasone.
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In experimental animal studies, early adverse experiences do not produce longstanding changes in HPA axis regulation.
In experimental animal studies, early adverse experiences do not produce longstanding changes in HPA axis regulation.
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Dexamethasone non-suppression is more common in depressed patients with anxiety.
Dexamethasone non-suppression is more common in depressed patients with anxiety.
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Abnormalities in the dexamethasone suppression test are confined to mood disorders.
Abnormalities in the dexamethasone suppression test are confined to mood disorders.
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The glucocorticoid receptor hypothesis of depression suggests that dysfunction of the HPA axis and the resulting depressive syndrome are linked to genetic or acquired defects of serotonin receptors.
The glucocorticoid receptor hypothesis of depression suggests that dysfunction of the HPA axis and the resulting depressive syndrome are linked to genetic or acquired defects of serotonin receptors.
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Animal experimental studies have found that antidepressant medication decreases expression of glucocorticoid receptors.
Animal experimental studies have found that antidepressant medication decreases expression of glucocorticoid receptors.
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The dexamethasone suppression test is a diagnostic marker of melancholic depression.
The dexamethasone suppression test is a diagnostic marker of melancholic depression.
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The dexamethasone suppression test is a specific test for mood disorders.
The dexamethasone suppression test is a specific test for mood disorders.
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The dexamethasone suppression test is a highly sensitive test for diagnosing depression.
The dexamethasone suppression test is a highly sensitive test for diagnosing depression.
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Abnormalities in functional brain imaging in depression support a single structure model of mood disorders.
Abnormalities in functional brain imaging in depression support a single structure model of mood disorders.
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The default mode network becomes active during task-based activity.
The default mode network becomes active during task-based activity.
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Deficits in executive function are not prominent in patients with depression.
Deficits in executive function are not prominent in patients with depression.
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Cognitive impairments in patients with depression persist even after the mood disorder remits.
Cognitive impairments in patients with depression persist even after the mood disorder remits.
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The neural circuitry that underpins emotional processing in depression is characterized by decreased limbic processing of aversive material.
The neural circuitry that underpins emotional processing in depression is characterized by decreased limbic processing of aversive material.
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Adverse early experiences such as parental conflict or abuse do not play a part in shaping features of personality that determine vulnerability to depression.
Adverse early experiences such as parental conflict or abuse do not play a part in shaping features of personality that determine vulnerability to depression.
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The predisposition to develop depressive disorders has no genetic contribution.
The predisposition to develop depressive disorders has no genetic contribution.
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Neuropsychological changes in mood disorders are limited to attention and learning.
Neuropsychological changes in mood disorders are limited to attention and learning.
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Recordings of the sleep EEG have shown a decrease in deep sleep in patients with major depression.
Recordings of the sleep EEG have shown a decrease in deep sleep in patients with major depression.
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Selective REM sleep deprivation can produce a temporary worsening of mood in depressed patients.
Selective REM sleep deprivation can produce a temporary worsening of mood in depressed patients.
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Enlarged lateral ventricles are typically seen in younger subjects with early-onset depression.
Enlarged lateral ventricles are typically seen in younger subjects with early-onset depression.
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The neurotrophic hypothesis of depression suggests that stress can lead to an increase in neurons and upregulation of adult neurogenesis, particularly in the hippocampus.
The neurotrophic hypothesis of depression suggests that stress can lead to an increase in neurons and upregulation of adult neurogenesis, particularly in the hippocampus.
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In major depression, decreased deep white matter hyperintensities are associated with late onset of depressive disorder.
In major depression, decreased deep white matter hyperintensities are associated with late onset of depressive disorder.
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Cerebral blood flow and metabolism are negatively correlated.
Cerebral blood flow and metabolism are negatively correlated.
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Decreased REM sleep latency is not a characteristic of sleep changes in depression.
Decreased REM sleep latency is not a characteristic of sleep changes in depression.
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Many effective antidepressant drugs increase REM sleep time and the latency to its onset.
Many effective antidepressant drugs increase REM sleep time and the latency to its onset.
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The neural basis of emotional processing is not closely related to the pathophysiology of depressive disorders.
The neural basis of emotional processing is not closely related to the pathophysiology of depressive disorders.
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Monoamine neurotransmission is not capable of altering emotional processing at both a behavioural and neural level.
Monoamine neurotransmission is not capable of altering emotional processing at both a behavioural and neural level.
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Adverse childhood experiences do not play a significant role in the risk of subsequent depression.
Adverse childhood experiences do not play a significant role in the risk of subsequent depression.
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Genetic factors do not interact with environmental and interpersonal factors in a complex manner to contribute to the development of depressive disorders.
Genetic factors do not interact with environmental and interpersonal factors in a complex manner to contribute to the development of depressive disorders.
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Recent stressful life events and difficulties are not significant risk factors for the development of depressive disorders.
Recent stressful life events and difficulties are not significant risk factors for the development of depressive disorders.
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Neurobiological and psychological mechanisms of depressive disorders are mutually exclusive.
Neurobiological and psychological mechanisms of depressive disorders are mutually exclusive.
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The impact of genetic factors on the risk of depression is not partially mediated through an increased risk of early adverse experiences.
The impact of genetic factors on the risk of depression is not partially mediated through an increased risk of early adverse experiences.
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Major depression is not a disorder with important genetic, environmental, and interpersonal determinants.
Major depression is not a disorder with important genetic, environmental, and interpersonal determinants.
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About 75% of patients with recurrent depression achieve a period of 5 years of clinical stability with good social and occupational performance.
About 75% of patients with recurrent depression achieve a period of 5 years of clinical stability with good social and occupational performance.
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About 5% of patients who present with a depressive disorder will eventually have a manic illness.
About 5% of patients who present with a depressive disorder will eventually have a manic illness.
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Dysthymia is a chronic disorder that lasts for less than a year.
Dysthymia is a chronic disorder that lasts for less than a year.
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The development of mania is a common occurrence in patients with dysthymia.
The development of mania is a common occurrence in patients with dysthymia.
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The average length of a depressive episode is about 1 year.
The average length of a depressive episode is about 1 year.
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Patients with minor depressive disorders have a higher recurrence rate than those with major depression.
Patients with minor depressive disorders have a higher recurrence rate than those with major depression.
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Around 50% of patients with major depression will experience further episodes.
Around 50% of patients with major depression will experience further episodes.
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Mortality is decreased in patients with depression due to lower rates of suicide.
Mortality is decreased in patients with depression due to lower rates of suicide.
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Patients with recurrent major depression experience on average about 2 further episodes over a 25-year follow-up.
Patients with recurrent major depression experience on average about 2 further episodes over a 25-year follow-up.
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Treatment of depression has no impact on mortality rates.
Treatment of depression has no impact on mortality rates.
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About 20% of depressed patients do not achieve complete symptom remission between episodes.
About 20% of depressed patients do not achieve complete symptom remission between episodes.
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The risk of suicide is higher in bipolar disorder than in unipolar disorder.
The risk of suicide is higher in bipolar disorder than in unipolar disorder.
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The age of onset of major depression typically occurs after the age of 21.
The age of onset of major depression typically occurs after the age of 21.
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The interval between episodes of major depression becomes progressively longer.
The interval between episodes of major depression becomes progressively longer.
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Duloxetine fatalities have been reported after consumption of as little as 500 mg.
Duloxetine fatalities have been reported after consumption of as little as 500 mg.
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MAOIs are recommended as first-line antidepressant drugs.
MAOIs are recommended as first-line antidepressant drugs.
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Moclobemide is more effective than conventional MAOIs for patients with resistant depression.
Moclobemide is more effective than conventional MAOIs for patients with resistant depression.
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Reboxetine is a sedating antidepressant drug.
Reboxetine is a sedating antidepressant drug.
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Lithium has established efficacy as a sole treatment for unipolar depression.
Lithium has established efficacy as a sole treatment for unipolar depression.
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Lithium augmentation can produce a rapid amelioration of the depressed state within 48 hours.
Lithium augmentation can produce a rapid amelioration of the depressed state within 48 hours.
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The effects of lithium augmentation are restricted to patients taking tricyclic antidepressants.
The effects of lithium augmentation are restricted to patients taking tricyclic antidepressants.
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Agomelatine may have a different mechanism of action, involving the activation of serotonin receptors.
Agomelatine may have a different mechanism of action, involving the activation of serotonin receptors.
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Trazodone and mirtazapine are safer than tricyclic antidepressants in overdose.
Trazodone and mirtazapine are safer than tricyclic antidepressants in overdose.
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Antidepressant drugs have similar clinical response rates in patients with dysthymia and major depression.
Antidepressant drugs have similar clinical response rates in patients with dysthymia and major depression.
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Tricyclic antidepressants are more effective than SSRIs in the treatment of moderate depression.
Tricyclic antidepressants are more effective than SSRIs in the treatment of moderate depression.
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Antidepressants are effective in the treatment of minor depression.
Antidepressants are effective in the treatment of minor depression.
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Lofepramine is a tricyclic antidepressant that is particularly hazardous in overdose.
Lofepramine is a tricyclic antidepressant that is particularly hazardous in overdose.
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Venlafaxine is an SSRI that is more effective than tricyclic antidepressants in patients with more severe depressive states.
Venlafaxine is an SSRI that is more effective than tricyclic antidepressants in patients with more severe depressive states.
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Duloxetine is an SNRI that is more effective than SSRIs in the treatment of depression.
Duloxetine is an SNRI that is more effective than SSRIs in the treatment of depression.
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Tricyclic antidepressants have a higher dropout rate due to side effects compared to SSRIs in short-term clinical trials.
Tricyclic antidepressants have a higher dropout rate due to side effects compared to SSRIs in short-term clinical trials.
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Anticonvulsants such as carbamazepine, valproate, and lamotrigine are not useful in the management of bipolar disorder.
Anticonvulsants such as carbamazepine, valproate, and lamotrigine are not useful in the management of bipolar disorder.
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Lamotrigine has not been shown to have antidepressant effects in placebo-controlled trials in bipolar depressed patients.
Lamotrigine has not been shown to have antidepressant effects in placebo-controlled trials in bipolar depressed patients.
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Atypical antipsychotic agents, used at low doses, are not of benefit when combined with antidepressants in non-psychotically depressed patients who have failed to respond to antidepressant treatment alone.
Atypical antipsychotic agents, used at low doses, are not of benefit when combined with antidepressants in non-psychotically depressed patients who have failed to respond to antidepressant treatment alone.
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The addition of atypical antipsychotic drugs to ineffective SSRI treatment does not result in clinical remission.
The addition of atypical antipsychotic drugs to ineffective SSRI treatment does not result in clinical remission.
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Electroconvulsive therapy is not described in Chapter 25.
Electroconvulsive therapy is not described in Chapter 25.
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Antipsychotic drugs are not combined with antidepressant drugs in the treatment of patients with depressive psychosis.
Antipsychotic drugs are not combined with antidepressant drugs in the treatment of patients with depressive psychosis.
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The addition of olanzapine to antidepressant treatment does not result in clinical remission.
The addition of olanzapine to antidepressant treatment does not result in clinical remission.
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Cognitive behaviour therapy is superior to a waiting list control in relieving depressive symptomatology, but it is not generally superior to other structured psychological treatments.
Cognitive behaviour therapy is superior to a waiting list control in relieving depressive symptomatology, but it is not generally superior to other structured psychological treatments.
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Supportive psychotherapy is a type of therapy that focuses on the identification and resolution of current life difficulties, and it is less effective than problem-solving therapy in moderately depressed patients in primary care.
Supportive psychotherapy is a type of therapy that focuses on the identification and resolution of current life difficulties, and it is less effective than problem-solving therapy in moderately depressed patients in primary care.
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Randomized trials suggest that problem-solving treatment is as effective as drug treatment in moderately depressed patients in primary care.
Randomized trials suggest that problem-solving treatment is as effective as drug treatment in moderately depressed patients in primary care.
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Cognitive behaviour therapy is not effective as a sole treatment for patients with severe depression, and this view is supported by trial evidence.
Cognitive behaviour therapy is not effective as a sole treatment for patients with severe depression, and this view is supported by trial evidence.
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Behavioural activation is a type of therapy that uses the principles of operant conditioning to track the links between actions and emotional outcomes, and it is less effective than cognitive behaviour therapy in depression.
Behavioural activation is a type of therapy that uses the principles of operant conditioning to track the links between actions and emotional outcomes, and it is less effective than cognitive behaviour therapy in depression.
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Interpersonal therapy is less effective than antidepressant medication in depressed patients.
Interpersonal therapy is less effective than antidepressant medication in depressed patients.
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The National Institute for Health and Clinical Excellence concluded that cognitive behaviour therapy is superior to drug treatment in moderately depressed outpatients.
The National Institute for Health and Clinical Excellence concluded that cognitive behaviour therapy is superior to drug treatment in moderately depressed outpatients.
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In severely depressed inpatients, ECT is probably inferior to antidepressant drug treatment in the short term.
In severely depressed inpatients, ECT is probably inferior to antidepressant drug treatment in the short term.
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Delusions are not a feature that distinguishes patients who respond to full ECT from those who respond to placebo.
Delusions are not a feature that distinguishes patients who respond to full ECT from those who respond to placebo.
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Relapse rates are low in depressed patients who have not responded to full trials of medication and are treated with ECT.
Relapse rates are low in depressed patients who have not responded to full trials of medication and are treated with ECT.
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In major depression, psychotherapies have been extensively evaluated and are proven to be more effective than antidepressant medication.
In major depression, psychotherapies have been extensively evaluated and are proven to be more effective than antidepressant medication.
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The overall response rate is about 30% for ECT and 20% for simulated treatment.
The overall response rate is about 30% for ECT and 20% for simulated treatment.
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Cognitive behaviour therapy is superior to other structured therapies such as interpersonal therapy in the management of mild to moderate depression.
Cognitive behaviour therapy is superior to other structured therapies such as interpersonal therapy in the management of mild to moderate depression.
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ECT is considered to be a relatively ineffective treatment for depressive disorders with marked weight loss, early-morning waking, retardation, and delusions.
ECT is considered to be a relatively ineffective treatment for depressive disorders with marked weight loss, early-morning waking, retardation, and delusions.
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Couple therapy is not significantly more effective than a waiting list control.
Couple therapy is not significantly more effective than a waiting list control.
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Dynamic psychotherapy aims to resolve underlying developmental conflicts and attendant life difficulties that are believed to be causing or maintaining the depressive disorder.
Dynamic psychotherapy aims to resolve underlying developmental conflicts and attendant life difficulties that are believed to be causing or maintaining the depressive disorder.
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More recent meta-analyses have shown that short-term psychodynamic therapy is less effective than cognitive behaviour therapy in depressed patients.
More recent meta-analyses have shown that short-term psychodynamic therapy is less effective than cognitive behaviour therapy in depressed patients.
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The antidepressant effect of sleep deprivation is permanent and does not disappear after the next night’s sleep.
The antidepressant effect of sleep deprivation is permanent and does not disappear after the next night’s sleep.
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Bright light treatment is usually given for a few minutes in the morning.
Bright light treatment is usually given for a few minutes in the morning.
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Patients with ‘atypical’ depressive features such as overeating and oversleeping respond poorly to bright light treatment.
Patients with ‘atypical’ depressive features such as overeating and oversleeping respond poorly to bright light treatment.
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The usual onset of the antidepressant effect of bright light is within 2–5 months.
The usual onset of the antidepressant effect of bright light is within 2–5 months.
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Lieverse et al. (2011) showed that bright light treatment is not effective in non-seasonal depression.
Lieverse et al. (2011) showed that bright light treatment is not effective in non-seasonal depression.
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The duration of exposure to bright light usually needs to be less than an hour.
The duration of exposure to bright light usually needs to be less than an hour.
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In patients with recurrent depression, maintenance antidepressant treatment for 1–2 years has been shown to lower the relapse rate from 78% to 18%.
In patients with recurrent depression, maintenance antidepressant treatment for 1–2 years has been shown to lower the relapse rate from 78% to 18%.
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Cognitive therapy given during an acute phase of depression has been shown to lead to a less sustained improvement in depressive symptomatology compared to antidepressant drug treatment.
Cognitive therapy given during an acute phase of depression has been shown to lead to a less sustained improvement in depressive symptomatology compared to antidepressant drug treatment.
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Lithium carbonate has been shown to be highly effective in the prevention of recurrent unipolar depression.
Lithium carbonate has been shown to be highly effective in the prevention of recurrent unipolar depression.
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Maintenance treatment with cognitive therapy has been shown to be less effective in preventing relapse compared to maintenance medication.
Maintenance treatment with cognitive therapy has been shown to be less effective in preventing relapse compared to maintenance medication.
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Mindfulness-based cognitive therapy (MBCT) has been shown to be less effective in lowering the risk of relapse in patients with recurrent depression compared to maintenance antidepressant treatment.
Mindfulness-based cognitive therapy (MBCT) has been shown to be less effective in lowering the risk of relapse in patients with recurrent depression compared to maintenance antidepressant treatment.
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Combining interpersonal therapy with medication in the treatment of the acute episode has been shown to increase relapse rates over the following 12 months.
Combining interpersonal therapy with medication in the treatment of the acute episode has been shown to increase relapse rates over the following 12 months.
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In patients who achieve remission from depression with interpersonal therapy as a sole treatment, continuation therapy has been shown to be unhelpful in preventing recurrence.
In patients who achieve remission from depression with interpersonal therapy as a sole treatment, continuation therapy has been shown to be unhelpful in preventing recurrence.
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Stopping antidepressants soon after a treatment response has been obtained is associated with a low risk of relapse.
Stopping antidepressants soon after a treatment response has been obtained is associated with a low risk of relapse.
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Continuing antidepressant treatment for 6 months past the point of remission doubles the relapse rate.
Continuing antidepressant treatment for 6 months past the point of remission doubles the relapse rate.
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Relapse refers to the worsening of symptoms after a period of complete recovery from a single episode of mood disorder.
Relapse refers to the worsening of symptoms after a period of complete recovery from a single episode of mood disorder.
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Treatment to prevent relapse should be called prophylactic or maintenance treatment.
Treatment to prevent relapse should be called prophylactic or maintenance treatment.
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About two-thirds of patients who are withdrawn from medication will relapse during the next year.
About two-thirds of patients who are withdrawn from medication will relapse during the next year.
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Involvement of the family in the management of depressive disorders is unlikely to improve the outcome.
Involvement of the family in the management of depressive disorders is unlikely to improve the outcome.
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The majority of relapses occur in the last 6 months of the first year after medication withdrawal.
The majority of relapses occur in the last 6 months of the first year after medication withdrawal.
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Antidepressant drug treatment is indicated for patients with mild depressive conditions.
Antidepressant drug treatment is indicated for patients with mild depressive conditions.
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Placebo-controlled studies have reached the conclusion that continuing antidepressant treatment for less than 6 months halves the relapse rate.
Placebo-controlled studies have reached the conclusion that continuing antidepressant treatment for less than 6 months halves the relapse rate.
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Patients with severe depressive disorders can be treated at home if they have a supportive family.
Patients with severe depressive disorders can be treated at home if they have a supportive family.
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Work can provide a valuable distraction from depressive thoughts for patients with severe depression.
Work can provide a valuable distraction from depressive thoughts for patients with severe depression.
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Inpatient treatment is necessary for patients who live alone or whose families cannot care for them during the day.
Inpatient treatment is necessary for patients who live alone or whose families cannot care for them during the day.
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The risk of suicide is a key factor in determining the level of care and supervision required for a patient with a depressive disorder.
The risk of suicide is a key factor in determining the level of care and supervision required for a patient with a depressive disorder.
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Dysthymia is not an indication for antidepressant medication.
Dysthymia is not an indication for antidepressant medication.
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Guidelines for a stepped-care approach to the management of depression have not been developed by the National Institute for Health and Clinical Excellence.
Guidelines for a stepped-care approach to the management of depression have not been developed by the National Institute for Health and Clinical Excellence.
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Patients with a depressive disorder of moderate or greater severity may not require any treatment if they have a supportive family.
Patients with a depressive disorder of moderate or greater severity may not require any treatment if they have a supportive family.
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A depressive disorder can be diagnosed simply based on the presence of prominent depressive symptoms.
A depressive disorder can be diagnosed simply based on the presence of prominent depressive symptoms.
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A patient's social resources are not an important consideration in the diagnosis of depressive disorder.
A patient's social resources are not an important consideration in the diagnosis of depressive disorder.
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The effects of the disorder on other people, such as family members, are not a significant consideration in the diagnosis of depressive disorder.
The effects of the disorder on other people, such as family members, are not a significant consideration in the diagnosis of depressive disorder.
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A patient's history of previous mood disturbance is not an important factor in assessing the current disorder.
A patient's history of previous mood disturbance is not an important factor in assessing the current disorder.
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The severity of a depressive disorder is solely determined by the presence of biological symptoms.
The severity of a depressive disorder is solely determined by the presence of biological symptoms.
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Aetiology is not an important consideration in the diagnosis of depressive disorder.
Aetiology is not an important consideration in the diagnosis of depressive disorder.
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The risk of suicide is not a significant consideration in the diagnosis of depressive disorder.
The risk of suicide is not a significant consideration in the diagnosis of depressive disorder.
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SSRIs are never used as a first-choice treatment for depression.
SSRIs are never used as a first-choice treatment for depression.
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Lofepramine is a sedating compound.
Lofepramine is a sedating compound.
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Tricyclic antidepressants are commonly used as first-choice agents for patients with severe depression.
Tricyclic antidepressants are commonly used as first-choice agents for patients with severe depression.
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Mirtazapine is used to treat patients who require concomitant sedation.
Mirtazapine is used to treat patients who require concomitant sedation.
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Concomitant treatment with nonsteroidal anti-inflammatory drugs increases the risk of bleeding with SSRIs.
Concomitant treatment with nonsteroidal anti-inflammatory drugs increases the risk of bleeding with SSRIs.
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The dosage and precautions for antidepressant drugs are described in Chapter 25.
The dosage and precautions for antidepressant drugs are described in Chapter 25.
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Amitriptyline is a commonly used first-choice agent for treating depression.
Amitriptyline is a commonly used first-choice agent for treating depression.
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The choice of antidepressant drug should be made without considering the patient's medical history and potential side effects.
The choice of antidepressant drug should be made without considering the patient's medical history and potential side effects.
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In patients with moderate to severe depression, adding cognitive behaviour therapy to antidepressant medication is unhelpful.
In patients with moderate to severe depression, adding cognitive behaviour therapy to antidepressant medication is unhelpful.
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If a depressive disorder does not respond within a reasonable time to a chosen combination of antidepressant drugs, graded activity, and psychological treatment, switching to a different antidepressant is the first step.
If a depressive disorder does not respond within a reasonable time to a chosen combination of antidepressant drugs, graded activity, and psychological treatment, switching to a different antidepressant is the first step.
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SSRIs have a clear dose–response relationship.
SSRIs have a clear dose–response relationship.
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Switching from an SSRI to a different class of drug has been shown to be significantly better in terms of remission rate than switching to a second SSRI.
Switching from an SSRI to a different class of drug has been shown to be significantly better in terms of remission rate than switching to a second SSRI.
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If a patient does not respond to one antidepressant, the next step is to increase the dose of the same medication.
If a patient does not respond to one antidepressant, the next step is to increase the dose of the same medication.
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Couple therapy is not a helpful addition in depressed patients where problems with a partner are playing a role in maintaining the disorder.
Couple therapy is not a helpful addition in depressed patients where problems with a partner are playing a role in maintaining the disorder.
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Therapy directed towards self-examination is particularly helpful in patients with severe depression.
Therapy directed towards self-examination is particularly helpful in patients with severe depression.
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In patients with recurrent depressive disorders, therapy directed towards self-examination may be offered during acute episodes.
In patients with recurrent depressive disorders, therapy directed towards self-examination may be offered during acute episodes.
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ECT is usually considered as a first-line treatment of depression.
ECT is usually considered as a first-line treatment of depression.
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The therapeutic effect of antidepressant drugs is usually faster than that of ECT.
The therapeutic effect of antidepressant drugs is usually faster than that of ECT.
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Patients who refuse to drink enough fluid to maintain an adequate output of urine are candidates for ECT.
Patients who refuse to drink enough fluid to maintain an adequate output of urine are candidates for ECT.
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Patients with depressive psychosis respond better to ECT than to a combination of an antidepressant drug and an antipsychotic drug.
Patients with depressive psychosis respond better to ECT than to a combination of an antidepressant drug and an antipsychotic drug.
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The patient should be encouraged to engage in activities that they are likely to fail at due to slowness or poor concentration.
The patient should be encouraged to engage in activities that they are likely to fail at due to slowness or poor concentration.
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Psychotherapy can be used as the sole therapy for patients with severe depression with melancholic features.
Psychotherapy can be used as the sole therapy for patients with severe depression with melancholic features.
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The therapeutic response to psychotherapy is usually faster than that to antidepressant drugs.
The therapeutic response to psychotherapy is usually faster than that to antidepressant drugs.
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The more structured therapies such as interpersonal therapy and cognitive behaviour therapy have a weaker evidence base with regard to the treatment of moderate to severe depression.
The more structured therapies such as interpersonal therapy and cognitive behaviour therapy have a weaker evidence base with regard to the treatment of moderate to severe depression.
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Aripiprazole is more likely to cause metabolic side effects than other atypical antipsychotics.
Aripiprazole is more likely to cause metabolic side effects than other atypical antipsychotics.
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The combination of lithium with SSRIs is contraindicated due to the risk of 5-HT neurotoxicity.
The combination of lithium with SSRIs is contraindicated due to the risk of 5-HT neurotoxicity.
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The aim of lithium augmentation is to obtain a lithium concentration within the range of 1.0-1.5 mmol/l.
The aim of lithium augmentation is to obtain a lithium concentration within the range of 1.0-1.5 mmol/l.
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Risperidone is less likely to cause weight gain compared to olanzapine and quetiapine.
Risperidone is less likely to cause weight gain compared to olanzapine and quetiapine.
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Lithium augmentation is usually not well tolerated in depressed patients.
Lithium augmentation is usually not well tolerated in depressed patients.
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About 20% of depressed patients will show a useful response to lithium augmentation over 1-3 weeks.
About 20% of depressed patients will show a useful response to lithium augmentation over 1-3 weeks.
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The discontinuation rate due to adverse effects is significantly lower with atypical antipsychotics than with placebo.
The discontinuation rate due to adverse effects is significantly lower with atypical antipsychotics than with placebo.
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The combination of lithium with MAOIs or clomipramine is not effective in depressed patients who are otherwise refractory to treatment.
The combination of lithium with MAOIs or clomipramine is not effective in depressed patients who are otherwise refractory to treatment.
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SSRIs are usually combined with serotonergic agents like bupropion in combination treatment.
SSRIs are usually combined with serotonergic agents like bupropion in combination treatment.
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When switching between agents with different pharmacological properties, cross-tapering can be employed.
When switching between agents with different pharmacological properties, cross-tapering can be employed.
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Amitriptyline is slightly less effective than SSRIs in patients with severe depression.
Amitriptyline is slightly less effective than SSRIs in patients with severe depression.
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The evidence for combination treatment with antidepressants is abundant and well-documented.
The evidence for combination treatment with antidepressants is abundant and well-documented.
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Combination of a tricyclic antidepressant with SSRIs is a recommended approach.
Combination of a tricyclic antidepressant with SSRIs is a recommended approach.
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Antipsychotic drugs are not useful in non-psychotic resistant depression except at high doses.
Antipsychotic drugs are not useful in non-psychotic resistant depression except at high doses.
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Atypical antipsychotic drugs are used in high doses to augment SSRIs in nonpsychotic depression.
Atypical antipsychotic drugs are used in high doses to augment SSRIs in nonpsychotic depression.
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In patients with psychotic depression, it is usually best to prescribe a combination treatment of antidepressant and antipsychotic medication.
In patients with psychotic depression, it is usually best to prescribe a combination treatment of antidepressant and antipsychotic medication.
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The addition of tri-iodothyronine (T3) to ineffective tricyclic antidepressant treatment has consistently shown to be highly effective in all studies.
The addition of tri-iodothyronine (T3) to ineffective tricyclic antidepressant treatment has consistently shown to be highly effective in all studies.
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Tri-iodothyronine (T3) is typically started at a dose of 20 μg daily and increased to 40 μg after 1 week if tolerance is good.
Tri-iodothyronine (T3) is typically started at a dose of 20 μg daily and increased to 40 μg after 1 week if tolerance is good.
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The use of ECT is contraindicated in patients with evidence of cardiovascular disease.
The use of ECT is contraindicated in patients with evidence of cardiovascular disease.
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The response to ECT is not affected by medication resistance.
The response to ECT is not affected by medication resistance.
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Tri-iodothyronine (T3) augmentation is only effective in treating depressive disorders with underlying thyroid activity.
Tri-iodothyronine (T3) augmentation is only effective in treating depressive disorders with underlying thyroid activity.
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The addition of tri-iodothyronine (T3) to antidepressant treatment is always associated with severe side effects.
The addition of tri-iodothyronine (T3) to antidepressant treatment is always associated with severe side effects.
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ECT is only beneficial in patients who have not responded to antidepressant drugs and have no psychotic features.
ECT is only beneficial in patients who have not responded to antidepressant drugs and have no psychotic features.
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The efficacy of tri-iodothyronine (T3) augmentation is established for all types of antidepressant drugs.
The efficacy of tri-iodothyronine (T3) augmentation is established for all types of antidepressant drugs.
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Among patients who have had three episodes of major depression, the likelihood of another episode is 80%.
Among patients who have had three episodes of major depression, the likelihood of another episode is 80%.
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Lithium is a first choice medication for long-term maintenance treatment of recurrent depression in most patients.
Lithium is a first choice medication for long-term maintenance treatment of recurrent depression in most patients.
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In patients with prolonged depression, it is particularly important to watch carefully for suicidal intentions.
In patients with prolonged depression, it is particularly important to watch carefully for suicidal intentions.
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Maintenance treatment should be considered if a patient has had one previous episode of depression within a 5-year period.
Maintenance treatment should be considered if a patient has had one previous episode of depression within a 5-year period.
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Cognitive behaviour therapy is only effective in lowering the risk of relapse in patients with no residual depressive symptomatology.
Cognitive behaviour therapy is only effective in lowering the risk of relapse in patients with no residual depressive symptomatology.
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A study found that cognitive behaviour therapy was less effective than treatment as usual in bringing about a therapeutic response.
A study found that cognitive behaviour therapy was less effective than treatment as usual in bringing about a therapeutic response.
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General practitioners do not play a key role in the long-term monitoring of patients with depressive disorders.
General practitioners do not play a key role in the long-term monitoring of patients with depressive disorders.
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Annual monitoring of body weight, blood pressure, glucose, and lipids is not recommended for patients with depressive disorders.
Annual monitoring of body weight, blood pressure, glucose, and lipids is not recommended for patients with depressive disorders.
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The relapse rate in the year after ECT may be as low as 20%.
The relapse rate in the year after ECT may be as low as 20%.
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A randomized study found post-ECT prophylaxis with a combination of lithium and nortriptyline to be less effective than maintenance ECT in sustaining remission.
A randomized study found post-ECT prophylaxis with a combination of lithium and nortriptyline to be less effective than maintenance ECT in sustaining remission.
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The choice of antidepressant medication is not influenced by the patient's response in the acute or continuation phase of treatment.
The choice of antidepressant medication is not influenced by the patient's response in the acute or continuation phase of treatment.
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After recovery, the patient should be followed up for several weeks by the psychiatric team or general practitioner.
After recovery, the patient should be followed up for several weeks by the psychiatric team or general practitioner.
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Lithium does not have a specific effect on lowering the risk of suicidal behaviour in patients with mood disorders.
Lithium does not have a specific effect on lowering the risk of suicidal behaviour in patients with mood disorders.
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If residual symptoms are still present, it is safer to withdraw medication.
If residual symptoms are still present, it is safer to withdraw medication.
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Psychotherapy is not helpful in readjusting lifestyle to reduce the risk of further depressive episodes.
Psychotherapy is not helpful in readjusting lifestyle to reduce the risk of further depressive episodes.
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Community nurses and nurse therapists do not play a valuable role in delivering treatment for depressive disorders.
Community nurses and nurse therapists do not play a valuable role in delivering treatment for depressive disorders.
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Newer antidepressant drugs are not better tolerated in the longer term than older antidepressant drugs.
Newer antidepressant drugs are not better tolerated in the longer term than older antidepressant drugs.
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A mild depressive episode requires at least three symptoms of A and two symptoms of B.
A mild depressive episode requires at least three symptoms of A and two symptoms of B.
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The severity of symptoms and degree of functional impairment are not considered in the classification of depressive episodes.
The severity of symptoms and degree of functional impairment are not considered in the classification of depressive episodes.
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All three symptoms of A are required for a severe depressive episode, but only three symptoms of B are required.
All three symptoms of A are required for a severe depressive episode, but only three symptoms of B are required.
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Reduced concentration is a symptom of A in the ICD-10 classification.
Reduced concentration is a symptom of A in the ICD-10 classification.
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The ICD-10 classification provides a clear distinction between moderate and mild depressive episodes.
The ICD-10 classification provides a clear distinction between moderate and mild depressive episodes.
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According to the ICD-10, at least three of the symptoms listed are required to make a diagnosis of depression 'with somatic features'
According to the ICD-10, at least three of the symptoms listed are required to make a diagnosis of depression 'with somatic features'
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In DSM-5, the diagnosis of depression 'with melancholic features' requires either 'loss of interest' or 'lack of emotional reactivity' to be present
In DSM-5, the diagnosis of depression 'with melancholic features' requires either 'loss of interest' or 'lack of emotional reactivity' to be present
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Weight loss of 3% or more of body weight in the last month is a diagnostic criterion for depression 'with somatic features' in ICD-10
Weight loss of 3% or more of body weight in the last month is a diagnostic criterion for depression 'with somatic features' in ICD-10
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Early-morning waking (2 hours or more before usual time) is a diagnostic criterion for depression 'with melancholic features' in DSM-5
Early-morning waking (2 hours or more before usual time) is a diagnostic criterion for depression 'with melancholic features' in DSM-5
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Marked loss of appetite is a diagnostic criterion for depression 'with melancholic features' in both ICD-10 and DSM-5
Marked loss of appetite is a diagnostic criterion for depression 'with melancholic features' in both ICD-10 and DSM-5
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What is the classification term used for a depressive episode that is characterized by a lack of energy and depression?
What is the classification term used for a depressive episode that is characterized by a lack of energy and depression?
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What is the DSM-5 classification term used for a depressive disorder that is characterized by persistent depressive symptoms that have persisted for at least 1 year?
What is the DSM-5 classification term used for a depressive disorder that is characterized by persistent depressive symptoms that have persisted for at least 1 year?
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What is the ICD-10 classification term used for a depressive disorder that is characterized by recurrent episodes of depression?
What is the ICD-10 classification term used for a depressive disorder that is characterized by recurrent episodes of depression?
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What is the classification term used for a depressive disorder that is characterized by brief episodes of depression?
What is the classification term used for a depressive disorder that is characterized by brief episodes of depression?
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What is the ICD-10 classification term used for a depressive disorder that is characterized by mild depressive symptoms?
What is the ICD-10 classification term used for a depressive disorder that is characterized by mild depressive symptoms?
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The DSM-5 includes a specifier 'with peripartum onset' for depressive disorders.
The DSM-5 includes a specifier 'with peripartum onset' for depressive disorders.
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The ICD-10 classification provides a clear distinction between mild and moderate depressive disorders.
The ICD-10 classification provides a clear distinction between mild and moderate depressive disorders.
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Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.
Depressive cognitions in patients with severe depressive episode are limited to feelings of worthlessness and pessimism.
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Agitated depression is a condition that is seen more commonly among middle-aged and elderly patients than among younger individuals.
Agitated depression is a condition that is seen more commonly among middle-aged and elderly patients than among younger individuals.
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In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 2 years.
In DSM-5, Persistent Depressive Disorder (Dysthymia) requires symptoms to have persisted for at least 2 years.
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The hypothalamic-pituitary-adrenal axis is studied in the context of genetic epidemiology.
The hypothalamic-pituitary-adrenal axis is studied in the context of genetic epidemiology.
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Neurogenesis, neurotropins, and synaptic plasticity are related to neuropsychology and brain imaging.
Neurogenesis, neurotropins, and synaptic plasticity are related to neuropsychology and brain imaging.
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Cognitive style is investigated in the context of early environment.
Cognitive style is investigated in the context of early environment.
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Monoamines are related to psychological investigations.
Monoamines are related to psychological investigations.
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Personality is investigated in the context of genetic epidemiology.
Personality is investigated in the context of genetic epidemiology.
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What is the primary genetic contribution to mood disorders?
What is the primary genetic contribution to mood disorders?
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How do adverse early life experiences affect development?
How do adverse early life experiences affect development?
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What triggers depressive disorders in people who lack social support?
What triggers depressive disorders in people who lack social support?
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What is associated with changes in the activity of monoamine neurons and the HPA axis?
What is associated with changes in the activity of monoamine neurons and the HPA axis?
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What may involve a loss of synaptic plasticity and dendrite formation?
What may involve a loss of synaptic plasticity and dendrite formation?
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What suggests persistent biological vulnerability in mood disorders?
What suggests persistent biological vulnerability in mood disorders?
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Freud suggested that melancholia results from the loss of a loved one through death.
Freud suggested that melancholia results from the loss of a loved one through death.
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Depressed patients often appear to be critical of others, according to Freud's theory.
Depressed patients often appear to be critical of others, according to Freud's theory.
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Freud's theory proposes that depression occurs when feelings of love and hostility are present at the same time, but not simultaneously.
Freud's theory proposes that depression occurs when feelings of love and hostility are present at the same time, but not simultaneously.
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Melanie Klein believed that weaning represents a significant symbolic gain for the infant.
Melanie Klein believed that weaning represents a significant symbolic gain for the infant.
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According to Melanie Klein, 'depressive anxiety' leads to attempts at revenge and hatred towards others.
According to Melanie Klein, 'depressive anxiety' leads to attempts at revenge and hatred towards others.
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Freud's theory of depression is based on the idea that the patient's feelings of love are redirected against themselves as self-reproach.
Freud's theory of depression is based on the idea that the patient's feelings of love are redirected against themselves as self-reproach.
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Freud's paper 'Mourning and melancholia' was published in 1915.
Freud's paper 'Mourning and melancholia' was published in 1915.
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Freud's theory of depression suggests that the patient's feelings of hostility are redirected against the loved one as self-reproach.
Freud's theory of depression suggests that the patient's feelings of hostility are redirected against the loved one as self-reproach.
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Melanie Klein's theory is based on the idea that the infant's feelings of love and hostility are present at the same time.
Melanie Klein's theory is based on the idea that the infant's feelings of love and hostility are present at the same time.
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Freud's theory of depression proposes that the patient's feelings of love are redirected against the therapist as transference.
Freud's theory of depression proposes that the patient's feelings of love are redirected against the therapist as transference.
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Decreased plasma tryptophan is a evidence of abnormalities in noradrenaline activity in depression
Decreased plasma tryptophan is a evidence of abnormalities in noradrenaline activity in depression
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Decreased brain 5-HT reuptake sites are only detected by PET
Decreased brain 5-HT reuptake sites are only detected by PET
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Clinical relapse after α-methyl-para-tyrosine (AMPT) is a evidence of abnormalities in dopamine activity in depression
Clinical relapse after α-methyl-para-tyrosine (AMPT) is a evidence of abnormalities in dopamine activity in depression
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Decreased homovanillic acid (HVA) levels in cerebrospinal fluid is a evidence of abnormalities in 5-HT activity in depression
Decreased homovanillic acid (HVA) levels in cerebrospinal fluid is a evidence of abnormalities in 5-HT activity in depression
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Blunted 5-HT neuroendocrine responses is a evidence of abnormalities in noradrenaline activity in depression
Blunted 5-HT neuroendocrine responses is a evidence of abnormalities in noradrenaline activity in depression
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Immune changes in depression include increased natural killer cell activity.
Immune changes in depression include increased natural killer cell activity.
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Induction of indoleamine 2,3-dioxygenase is an immune change associated with depression.
Induction of indoleamine 2,3-dioxygenase is an immune change associated with depression.
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Increases in positive acute phase proteins are a characteristic of depression.
Increases in positive acute phase proteins are a characteristic of depression.
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Decreased inflammatory cytokine levels, such as IL-6 and TNFα, are associated with depression.
Decreased inflammatory cytokine levels, such as IL-6 and TNFα, are associated with depression.
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Lowered proliferative responses of lymphocytes to mitogens are a characteristic of depression.
Lowered proliferative responses of lymphocytes to mitogens are a characteristic of depression.
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Dorsolateral and dorsomedial prefrontal cortex are associated with impaired voluntary regulation of emotion in depressed patients.
Dorsolateral and dorsomedial prefrontal cortex are associated with impaired voluntary regulation of emotion in depressed patients.
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The anterior cingulate is associated with abnormal emotional processing in depressed patients.
The anterior cingulate is associated with abnormal emotional processing in depressed patients.
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The ventral striatum is associated with impaired incentive behavior in depressed patients.
The ventral striatum is associated with impaired incentive behavior in depressed patients.
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The amygdala is associated with impaired attentional processes in depressed patients.
The amygdala is associated with impaired attentional processes in depressed patients.
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Psychomotor disturbances are associated with dorsolateral and dorsomedial prefrontal cortex in depressed patients.
Psychomotor disturbances are associated with dorsolateral and dorsomedial prefrontal cortex in depressed patients.
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Amitriptyline is an antidepressant drug that is known to have no anticholinergic effects.
Amitriptyline is an antidepressant drug that is known to have no anticholinergic effects.
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All SSRIs have a similar toxicity profile in overdose.
All SSRIs have a similar toxicity profile in overdose.
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Mirtazapine is an antidepressant drug that is known to cause marked sedation and weight gain.
Mirtazapine is an antidepressant drug that is known to cause marked sedation and weight gain.
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Reboxetine is an antidepressant drug that is known to cause no anticholinergic effects and no sedation.
Reboxetine is an antidepressant drug that is known to cause no anticholinergic effects and no sedation.
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Venlafaxine is an antidepressant drug that has a low toxicity profile in overdose.
Venlafaxine is an antidepressant drug that has a low toxicity profile in overdose.
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What is an important aspect of improving the outcome of depression treatment?
What is an important aspect of improving the outcome of depression treatment?
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What is a common question asked by patients with a first episode of moderate to severe depression?
What is a common question asked by patients with a first episode of moderate to severe depression?
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What is a key aspect of depression that patients and families often want to know?
What is a key aspect of depression that patients and families often want to know?
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What is a common feeling experienced by patients with depression?
What is a common feeling experienced by patients with depression?
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What is a consideration in the management of depression?
What is a consideration in the management of depression?
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What has been developed by the National Institute for Health and Clinical Excellence (2009a)?
What has been developed by the National Institute for Health and Clinical Excellence (2009a)?
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What is recommended for patients with persistent mild depressive symptoms that do not respond to exercise programmes and sleep hygiene?
What is recommended for patients with persistent mild depressive symptoms that do not respond to exercise programmes and sleep hygiene?
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What is the recommended treatment for patients who present with moderate or severe depression?
What is the recommended treatment for patients who present with moderate or severe depression?
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How long should patients who respond to antidepressant medication continue treatment?
How long should patients who respond to antidepressant medication continue treatment?
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What is recommended for patients who have relapsed despite antidepressant treatment?
What is recommended for patients who have relapsed despite antidepressant treatment?
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What should patients at high risk of relapse be advised to do?
What should patients at high risk of relapse be advised to do?
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What should be considered for patients who are well but who have experienced three or more previous episodes of depression?
What should be considered for patients who are well but who have experienced three or more previous episodes of depression?
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What is the primary focus of the treatment plan for depression?
What is the primary focus of the treatment plan for depression?
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Who should be involved in discussions about the nature of depression and treatment plan?
Who should be involved in discussions about the nature of depression and treatment plan?
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What is the aim of involving the family in discussions about depression and treatment plan?
What is the aim of involving the family in discussions about depression and treatment plan?
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What is recommended for patients with short-lived mild depression who may recover quickly without treatment?
What is recommended for patients with short-lived mild depression who may recover quickly without treatment?
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What is not recommended for the treatment of mild depression?
What is not recommended for the treatment of mild depression?
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What is recommended for patients with persistent mild depression?
What is recommended for patients with persistent mild depression?
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In treating resistant depression, adding an atypical antipsychotic drug to an SSRI is a recommended treatment option.
In treating resistant depression, adding an atypical antipsychotic drug to an SSRI is a recommended treatment option.
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MAOIs are not effective in combination with lithium.
MAOIs are not effective in combination with lithium.
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ECT is a pharmacological treatment option for resistant depression.
ECT is a pharmacological treatment option for resistant depression.
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Adding mirtazapine to an SSRI is an example of an antidepressant combination.
Adding mirtazapine to an SSRI is an example of an antidepressant combination.
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Increasing the dose of an antidepressant is only recommended if the patient has depressive psychosis.
Increasing the dose of an antidepressant is only recommended if the patient has depressive psychosis.
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Study Notes
Depressive Disorders
- Depressive disorders are a group of psychiatric syndromes characterized by depressed mood, negative thinking, lack of enjoyment, reduced energy, and slowness.
- The central features of depressive disorders are:
- Depressed mood
- Negative thinking
- Lack of enjoyment
- Reduced energy
- Slowness
- Depressed mood is usually the most prominent symptom, but not always.
Clinical Features of Severe Depression
- A severe depressive episode is characterized by:
- Low mood
- Lack of enjoyment (anhedonia)
- Negative thinking
- Reduced energy
- Decreased social and occupational functioning
- Appearance:
- Neglected dress and grooming
- Facial features: downturned mouth corners, vertical furrowing of the brow
- Reduced blinking rate
- Bent shoulders, inclined head, and downward gaze
- Reduced gestures and movements
- Mood:
- Pervasive misery
- Unimproved by pleasant circumstances
- Experienced as different from ordinary sadness
- Often worse in the morning, improving as the day progresses (diurnal variation of mood)
- Depressive cognitions:
- Negative thoughts (worthlessness, pessimism, guilt)
- Feelings of guilt often take the form of unreasonable self-blame
- Pessimistic thoughts concern future prospects
- Gloomy preoccupations may progress to thoughts of suicide
- Lack of interest and enjoyment (anhedonia):
- No enthusiasm for activities and hobbies
- No pleasure in everyday things
- Withdrawal from social encounters
- Reduced energy:
- Lethargic, find everything an effort, leaving tasks unfinished
- Attribution to physical illness
- Psychomotor changes:
- Psychomotor retardation: slow walking, acting, and speaking
- Agitation: restlessness, inability to relax, pacing
- Biological symptoms:
- Sleep disturbance (early-morning waking, delay in falling asleep, waking during the night)
- Loss of appetite, weight, and libido
- Constipation, loss of interest in activities
- Amenorrhoea in women
- Other features:
- Depersonalization
- Obsessional symptoms
- Panic attacks
- Dissociative symptoms (rare)
- Complaints of poor memory, which can be severe
Psychotic Depression
- Psychotic depression is a severe depressive disorder characterized by:
- Delusions and hallucinations
- Complete loss of function in social and occupational spheres
- Inattention to basic hygiene and nutrition
- Impaired insight
- Delusions of worthlessness, guilt, ill health, and poverty
- Hallucinations may be mood-congruent or mood-incongruent
Clinical Variants of Depressive Disorders
- Agitated depression:
- Prominent agitation
- More common among middle-aged and elderly patients
- Retarded depression:
- Prominent psychomotor retardation
- No evidence that it represents a separate syndrome
- May predict a good response to electroconvulsive therapy (ECT)
Depressive Stupor
- In severe depressive disorder, patients may exhibit depressive stupor, characterized by extreme slowing of movement and poverty of speech.
- Patients may become motionless and mute, with impaired recall of events during the stupor state.
- Kraepelin described patients in depressive stupor as lying mute in bed, giving no answers, and showing no defensive response to pinprick.
- Today, it is believed that patients can recall nearly all events that took place during the period of stupor upon recovery.
- Depressive stupor may be accompanied by catatonic motor disturbances.
Atypical Depression
- Atypical depression is characterized by variably depressed mood with mood reactivity to positive events.
- Additional symptoms include overeating and oversleeping, extreme fatigue and heaviness in the limbs, and pronounced anxiety.
- Patients often have a lifelong tendency to react exaggeratedly to perceived or real rejection.
- Atypical depression typically has an earlier onset of illness and a more chronic course.
- Recognition of atypical depression is important, as patients may be mismanaged due to their interpersonal sensitivity.
- Historically, atypical depression has been associated with poor response to tricylic antidepressants, but better response to monoamine oxidase inhibitors (MAOIs).
Mixed Depression
- Mixed depression is characterized by symptoms of depression, accompanied by symptoms typically seen in mania.
- Common symptoms include irritable mood, mood lability, distractibility, agitation, and impulsivity.
- Mixed depression is more common in patients with a family history of bipolar disorder.
- Patients with mixed depression are more likely to develop bipolar disorder in the future.
Mild Depressive States
- Mild depressive disorders present with similar symptoms to severe depression, but with less intensity.
- Additional symptoms may include anxiety, phobias, obsessional symptoms, and dissociative symptoms.
- Mild depressive disorders often involve sleep disturbances, but not early-morning waking, and may include difficulty falling asleep or waking during the night.
- Biological features like poor appetite, weight loss, and low libido are typically absent.
- Mild depressive disorders can be challenging to classify and may merge into minor mood disorders.
Minor Anxiety–Depressive Disorders
- Minor anxiety–depressive disorders involve a mix of anxiety and depressive symptoms that do not meet criteria for a specific disorder.
- Symptoms may include fatigue, anxiety, depression, irritability, poor concentration, insomnia, somatic symptoms, and bodily preoccupation.
- These disorders are common in primary care and may cause significant distress and impairment.
- Cultural variations in the clinical presentation of depressive states exist, but sadness, joylessness, anxiety, and lack of energy are common symptoms across cultures.
Classification of Depressive Disorders
- There is no general agreement on the best method of classifying depressive disorders.
- Approaches have been tried based on:
- Presumed aetiology (causes)
- Symptomatic picture (symptoms)
- Course (development and progression)
Classification by Presumed Aetiology
- Historical distinction between endogenous depression (caused by internal factors) and reactive depression (caused by external factors) is no longer used.
- Neither ICD-10 nor DSM-5 contains categories of reactive or endogenous depression.
Classification by Symptomatic Picture
- Melancholic depression:
- Characterized by "biological" symptoms such as loss of appetite, psychomotor changes, weight loss, constipation, reduced libido, amenorrhoea, and early-morning waking.
- Associated with:
- More severe symptomatology
- Family history of depression
- Poor response to placebo medication
- Possibly better response to tricyclic antidepressants than selective serotonin reuptake inhibitors (SSRIs)
- More evidence of neurobiological abnormalities
- Psychotic depression:
- Characterized by severe depression with psychotic features.
- Requires treatment with antidepressant medication and antipsychotic drugs.
- Non-melancholic depression:
- Includes mild depressive episodes and atypical depression.
- Characterized by:
- Anxiety
- Hostility
- Phobias
- Obsessional symptoms
Classification by Course
- Unipolar and bipolar disorders:
- Mood disorders are characteristically recurrent.
- Kraepelin's classification of manic-depressive psychosis is no longer used.
- Seasonal affective disorder:
- Characterized by depressive episodes that occur at the same time every year.
- Associated with:
- Hypersomnia
- Increased appetite
- Afternoon slump in energy levels
- Treatment includes exposure to bright artificial light.
Recurrent Brief Depression
- Characterized by:
- Recurrent depressive episodes of short duration (typically 2-7 days)
- No apparent link to the menstrual cycle in female sufferers
- Associated with:
- Suicidal behavior
- Personal distress
- Social and occupational impairment
- Treatment is often with antidepressant medication, but its value is questionable.
Classification in DSM-5 and ICD-10
- Both systems contain categories for:
- Single episodes of mood disorder
- Recurrent episodes
- Milder but persistent depressive states (dysthymia)
- Differences between DSM-5 and ICD-10:
- DSM-5 includes mood disorders secondary to a medical condition
- ICD-10 classifies these conditions as mood disorders under "Organic Mental Disorders"
- Both systems allow for the diagnosis of:
- Recurrent brief depression
- Atypical depression
Aetiology of Depression
- The aetiology of depression is a complex phenomenon, with multiple approaches to understanding its causes, including genetic, environmental, and psychological factors.
- Family and twin studies have shown that depression tends to run in families, with a threefold increased risk in first-degree relatives.
- Environmental influences, such as childhood experiences and current life difficulties, also play a significant role in the development of depression.
Genetic Causes
- Twin studies have found that the concordance rate for depressive disorders is higher in monozygotic twins (45%) than in dizygotic twins (20%).
- The heritability of major depression is estimated to be around 37%, which is lower than that of bipolar disorder or schizophrenia.
- Genetic factors may interact with environmental factors to contribute to the development of depression.
- The mode of inheritance of depression is likely to be polygenic, involving the combined action of multiple genes with small effects.
Molecular Genetics
- The monoamine theory of depression suggests that allelic variations in genes involved in monoamine synthesis or metabolism may contribute to the risk of mood disorders.
- Association studies have identified several candidate genes, including the serotonin transporter gene, but the results have been inconsistent.
- Genome-wide association studies (GWAS) have not yet identified any convincingly replicated loci for depression.
- A recent whole genome sequencing study identified two replicated genetic markers for severe recurrent depression in a Han Chinese population.
Personality
- Certain personality traits, such as high levels of premorbid anxiety, may be associated with an increased risk of depression.
- Aspects of personality, such as cognitive style, may influence the way people respond to adverse circumstances, making them more likely to develop depressive disorders.
- Neuroticism, as measured by the Eysenck Personality Questionnaire, is associated with an increased risk of depression, and may share common genes with major depression.
Early Environment
- Parental deprivation, particularly parental separation, may be a risk factor for depression in later life.
- Gross disruption of parent-child relationships, such as physical or sexual abuse, is also a risk factor for depression.
- Subtle differences in parental style, such as non-caring or overprotective parenting, may also contribute to the development of depression.
- Mothers with postnatal depression may manifest a rearing style that is characterized by neglect and emotional indifference, which may increase the risk of depression in their children.
Precipitating Factors
- Recent life events, such as adverse life events, may precipitate depression in susceptible individuals.
- The association between life events and depression is not coincidental, and is not specific to depression.
- Methodologically reliable research has shown that there is a sixfold excess of adverse life events in the months before the onset of depressive disorder.
- Life events are important antecedents of all forms of depression, but appear to be relatively less important in established melancholic-type disorders and where there is a strong family history of depression.
Vulnerability Factors and Life Difficulties
- Poor social support, measured as lack of intimacy or social integration, is associated with an increased risk of depression.
- The mechanism of this association is unclear, and may be due to a lack of opportunities to confide, distorted perception of intimacy, or other factors.
- The effects of physical illness, such as Cushing's disease, can also contribute to the development of depression.
- Organic mood disorders, such as those caused by brain disease or certain infections, may provide clues to the aetiology of depression.
Psychological Approaches to Aetiology
- Cognitive theories propose that depressive disorders are caused by negative views of the self, the world, and the future, which are maintained by illogical ways of thinking, such as:
- Arbitrary inference
- Selective abstraction
- Overgeneralization
- Personalization
- These negative views are often established early in life, usually through childhood adversity, and affect how a person responds to stress and adversity
- Schemas can become activated by matching life experiences, increasing the risk of depression
Neurobiological Approaches to Aetiology
- Depressive disorders must ultimately be mediated through changes in brain neurochemistry and circuitry involved in emotional regulation
- Monoamine neurotransmitters, particularly noradrenaline and 5-hydroxytryptamine (5-HT), play an important role in the actions of effective antidepressant drugs
- Monoamine pathways innervate cortical and subcortical brain regions involved in mood regulation
- Recent studies have used structural and functional imaging techniques to identify changes in neural circuitry associated with depressive disorders
- Mood disorders are associated with distinct and persistent neuropathological changes in relevant brain regions
The Monoamine Hypothesis
- The monoamine hypothesis suggests that depressive disorder is due to an abnormality in a monoamine neurotransmitter system at one or more sites in the brain
- Three monoamine transmitters have been implicated: serotonin (5-HT), noradrenaline, and dopamine
- The hypothesis has been tested through the study of:
- Biochemistry of neurotransmitters in patients with mood disorders
- Effects of selective drugs on measurable indices of monoamine system function
- Pharmacological properties shared by antidepressant drugs
5-HT Function
- Plasma tryptophan levels are decreased in untreated depressed patients, particularly in those with melancholic depression
- Studies of cerebrospinal fluid (CSF) have found inconsistent evidence of a consistent reduction in CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA) in depressed patients
- Post-mortem brain studies have found little consistent evidence of lowered brain concentrations of 5-HT or 5-HIAA in depressed patients
- Neurochemical brain imaging studies have found evidence of decreased 5-HT1A receptor binding throughout cortical and subcortical regions
- Neuroendocrine tests have found blunted 5-HT-mediated endocrine responses in depressed patients
- Tryptophan depletion studies have found that lowering brain 5-HT function can induce depressive symptoms in vulnerable individuals
Noradrenaline Function
- There is no consistent evidence of changes in brain or CSF concentrations of noradrenaline or its major metabolite, 3-methoxy-4-hydroxy-phenylethylene glycol (MHPG), in depressed patients
- Neuroendocrine tests have found blunted growth hormone responses to clonidine in depressed patients
- Catecholamine depletion studies have found that lowering brain catecholamine function can induce depressive symptoms in vulnerable individuals
Dopamine Function
- Dopamine neurons in the mesolimbic system play a key role in incentive behavior and reward
- Abnormalities in dopamine function may be involved in the pathophysiology of depression
- CSF levels of homovanillic acid (HVA) are consistently low in depressed patients
- Some brain imaging studies have found increased binding of dopamine D2/D3 receptors in striatal regions
- Regional reductions in dopamine D1 receptors have been reported in some studies
Dexamethasone Suppression Test
- The dexamethasone suppression test is used to study depressed patients, suppressing cortisol levels by inhibiting ACTH release at the pituitary level.
- About 50% of depressed inpatients do not show normal suppression of cortisol secretion after administering 1 mg of dexamethasone.
- Dexamethasone non-suppression is more common in depressed patients with melancholia.
- Abnormalities in the dexamethasone suppression test are not exclusive to mood disorders, also reported in mania, chronic schizophrenia, and dementia.
Glucocorticoid Receptor Hypothesis
- The glucocorticoid receptor hypothesis suggests that dysfunction of the HPA axis and depressive syndrome are linked to genetic or acquired defects of glucocorticoid receptors.
- Antidepressant medication increases expression of glucocorticoid receptors, which may be a therapeutic mechanism to normalize excessive HPA axis activity.
- HPA axis changes in depressed patients are generally regarded as state abnormalities, remitting when the patient recovers.
Corticotropin-Releasing Hormone (CRH) and Depression
- CRH has a neurotransmitter role in limbic regions, regulating biochemical and behavioral responses to stress.
- Administration of CRH to animals produces changes in neuroendocrine regulation, sleep, and appetite similar to those found in depressed patients.
- CRH levels may be increased in the CSF of depressed patients, suggesting a possible role in the pathophysiology of depression.
- Non-peptide antagonists of CRH receptors may have value as antidepressant agents.
Thyroid Function and Depression
- Circulating plasma levels of free thyroxine are normal in depressed patients, but levels of free triiodothyronine may be decreased.
- About 25% of depressed patients have a blunted thyrotropin-stimulating hormone (TSH) response to intravenous thyrotropin-releasing hormone (TRH).
- Abnormalities in thyroid function are not specific to depression, also found in alcoholism and panic disorder.
Depression and the Immune System
- Patients with depression manifest various disturbances of immune function, including decreased cellular immune responses and immune activation.
- Changes in immune regulation may play a role in HPA axis dysfunction in depression.
- Cytokines can induce expression of the tryptophan-metabolizing enzyme indoleamine 2,3-dioxygenase, which lowers tryptophan levels and puts vulnerable individuals at risk of depression.
Sleep Changes in Depression
- Disturbed sleep is characteristic of depression, with abnormalities in sleep architecture, including impaired sleep continuity and duration, decreased deep sleep, and increased REM sleep.
- Decreased REM sleep latency may persist in recovered depressed patients, indicating a vulnerability to relapse.
- Many effective antidepressant drugs decrease REM sleep time and latency, and both total sleep deprivation and selective REM sleep deprivation can produce temporary alleviation of mood in depressed patients.
Brain Imaging in Mood Disorders
- Structural brain imaging studies have found abnormalities in patients with depression, including enlarged lateral ventricles, decreased hippocampal volume, and decreased grey matter volume in anterior brain areas.
- The neurotrophic hypothesis of depression suggests that stress and cortisol hypersecretion can lead to atrophy and death of neurons and downregulation of adult neurogenesis.
- Functional brain imaging studies have shown abnormalities in cerebral blood flow and metabolism, supporting a circuitry model of mood disorders.
Neuropsychological Changes in Mood Disorders
- Patients with acute depression and mania show poor performance on various measures of neuropsychological function, including attention, learning, memory, and executive function.
- Cognitive impairments resolve as the mood disorder remits, but may persist in euthymic patients with recurrent depression.
- Depression is clinically associated with negative biases in the processing of emotional information, which can be reversed by antidepressant medication.
Conclusions
- The predisposition to develop depressive disorders has a significant genetic contribution.
- Adverse early experiences, such as parental conflict or abuse, may play a part in shaping features of personality that determine vulnerability to depression.
- The precipitating causes of mood disorders include stressful life events and certain physical illnesses, which can be modified by background factors, such as personality, early life experiences, and genetic inheritance.
- Two kinds of pathophysiological mechanisms have been proposed to explain how precipitating events lead to depressive disorders: psychological and neurobiological mechanisms.
Major Depression
- 10% of patients who present with a depressive disorder will eventually have a manic illness, and these patients are more likely to have a family history of mania or to show brief, mild manic mood swings during antidepressant treatment.
- The age of onset of major depression varies widely and can occur at any point in the lifespan, with about half of all cases occurring before the age of 21.
- The average length of a depressive episode is about 6 months, but around 25% of patients have episodes that last for more than 1 year, and around 10–20% develop a chronic unremitting course.
- About 80% of patients with major depression will experience further episodes, and over a 25-year follow-up, patients with recurrent major depression experience on average about four further episodes.
- The interval between episodes becomes progressively shorter, and about 50% of depressed patients do not achieve complete symptom remission between episodes, experiencing continuing subsyndromal depressive symptomatology of fluctuating severity.
Dysthymia
- Dysthymia is a chronic disorder that lasts for many years, but about 50% of outpatients may be expected to show a clinical recovery over a 5-year follow-up.
- Some patients with dysthymia develop major depression (so-called double depression), while some patients who originally present with major depression subside into dysthymia.
Minor Depressive Disorders
- Minor depressive disorders are depressive disorders that do not meet threshold criteria for major depression, even of mild severity.
- These conditions show a recurrence rate similar to that of major depression, and patients who meet the criteria for minor depression at one point in follow-up may then subsequently be diagnosed as suffering from major depression, and vice versa.
Mortality of Depressive Disorders
- Mortality is significantly increased in patients with depression, largely due to suicide, accidents, cardiovascular disease, and comorbid substance misuse.
- The standardized mortality ratio in mood disorders is about twice that found in the general population, and there is now compelling evidence that depressive disorders increase the risk of general medical conditions such as diabetes and cardiovascular disease.
- Treatment lowers the mortality in patients with depression, and rates of suicide in patients with depression are at least 15 times higher than those in the general population.
Prognostic Factors
- The best predictor of the future course is the history of previous episodes, and the risk of recurrence is much higher in individuals with a history of several previous episodes.
- Other factors that predict a higher risk of future episodes include incomplete symptomatic remission, early age of onset, poor social support, poor physical health, comorbid substance misuse, and comorbid personality disorder.
The Acute Treatment of Depression
- Antidepressant drugs are effective in the acute treatment of major depression, with the largest effects relative to placebo seen in patients with major depression whose symptoms are of at least moderate severity.
- Short-term response rates in controlled trials are about 50% for patients on active treatment, and about 30% for those on placebo, with the number needed to treat (NNT) being between 5 and 7.
- In terms of efficacy, there is little to choose between the various antidepressants, although some are better than others in certain defined situations.
Tricyclic Antidepressants
- Tricyclic antidepressants have been extensively compared with placebo in both inpatients and outpatients with major depression, and are clearly more effective than placebo in all but the most severely depressed patients.
- There is little evidence that tricyclic antidepressant drugs differ from one another in clinical efficacy, but they do differ in terms of their side effect profile.
Selective Serotonin Reuptake Inhibitors and Serotonin and Noradrenaline Reuptake Inhibitors
- SSRIs have undergone extensive trials both against placebo and against comparator antidepressants, and are as effective as tricyclic antidepressants in the broad range of depressed patients.
- Venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRI), appears to be slightly more effective than SSRIs in patients with more severe depressive states.
Monoamine Oxidase Inhibitors
- MAOIs are effective antidepressants and of equal therapeutic activity to tricyclic antidepressants for moderate to severe depressive disorders, particularly with melancholic features.
- However, MAOIs are liable to cause dangerous reactions with other drugs and some foods, and for this reason they are not recommended as first-line antidepressant drugs.
Anticonvulsants in Bipolar Disorder
- Anticonvulsants such as carbamazepine, valproate, and lamotrigine are useful in managing bipolar disorder and can prevent episodes of major depression.
- Lamotrigine has shown antidepressant effects in placebo-controlled trials in bipolar depressed patients, particularly those with higher levels of symptomatology.
Atypical Antipsychotic Drugs
- Atypical antipsychotic agents, used at relatively low doses, can be beneficial when combined with antidepressants in non-psychotically depressed patients who have failed to respond to antidepressant treatment alone.
- A meta-analysis of trials involving 3500 patients found that the addition of drugs such as aripiprazole, quetiapine, and risperidone to ineffective SSRI treatment resulted in clinical remission (NNT = 9).
Electroconvulsive Therapy (ECT)
- ECT is more effective than simulated ECT in patients with major depression, with a response rate of about 70% for ECT and 40% for simulated treatment (NNT = 3–4).
- ECT is probably superior to antidepressant drug treatment in severely depressed inpatients, at least in the short term.
- Delusions and retardation are features that distinguish patients who respond to full ECT from those who respond to placebo.
Psychological Treatments
- Psychotherapies can be employed as alternatives to antidepressant medication or as adjuncts.
- Specific psychotherapies are somewhat more effective than treatment as usual in the management of mild to moderate depression, particularly in primary care.
- Structured treatments such as cognitive behavior therapy do not appear to be superior to other structured therapies such as interpersonal therapy.
Supportive Psychotherapy and Problem-Solving
- Supportive psychotherapy focuses on identifying and resolving current life difficulties, and using the patient's strengths and available coping resources.
- Problem-solving treatment is better than treatment as usual in moderately depressed patients in primary care.
Cognitive Behavior Therapy (CBT)
- CBT aims to help patients modify their ways of thinking and acting in relation to life situations and depressive symptoms.
- CBT is superior to a waiting list control in relieving depressive symptomatology, and is as effective as pharmacological treatment in moderately depressed outpatients.
- Combined CBT and pharmacological treatment is better than pharmacological treatment alone.
Behavioral Activation
- Behavioral activation uses the principles of operant conditioning to assist patients in engaging in behaviors that will lead to a positive effect on mood.
- A recent meta-analysis of 26 randomized trials of behavioral activation in depression showed that the technique was superior to control procedures.
Interpersonal Psychotherapy
- Interpersonal therapy is a systematic and standardized treatment approach to personal relationships and life problems.
- It is more effective than placebo with clinical management and GP treatment as usual, and is as effective as antidepressant medication.
Couple Therapy
- Couple therapy aims to understand the nature of interactions between the patient and their partner and modify them to make the relationship more mutually supportive.
- It is significantly more effective than a waiting list control and as effective as cognitive behavior therapy.
Dynamic Psychotherapy
- Dynamic psychotherapy aims to resolve underlying developmental conflicts and attendant life difficulties that are believed to be causing or maintaining the depressive disorder.
- It has been shown to have equivalent benefit in depressed patients for short-term psychodynamic therapy compared to other psychotherapies.
Other Treatments
- Sleep deprivation can bring about rapid short-term changes in mood, but the alleviation of depressed mood is nearly always temporary.
- Bright light treatment has been shown to be effective in treating winter depression, with an onset of antidepressant effect within 2–5 days.
- Bright light treatment may also be effective in non-seasonal depression, particularly in elderly people with depression.
Relapse and Recurrence of Mood Disorders
- Mood disorders often recur, and if left untreated, have a poor long-term prognosis
- There is an increasing emphasis on long-term management, including prevention of relapse and recurrence
- Relapse refers to the worsening of symptoms after an initial improvement during treatment, whereas recurrence refers to a new episode after a period of complete recovery
Prevention of Relapse and Recurrence
- Treatment to prevent relapse is called continuation treatment, and treatment to prevent recurrence is called prophylactic or maintenance treatment
- Continuation therapy for 6 months past the point of remission halves the relapse rate
- Treatment should be at the originally effective dose of medication if possible
- Continuation of antidepressant treatment for longer than 6 months confers little extra benefit, except in the elderly, where continuation therapy for 12 months is more appropriate
Maintenance Treatment
- Maintenance antidepressant treatment can substantially reduce relapse rates
- Lithium carbonate has also been used in the prevention of recurrent unipolar depression, but the overall evidence for its efficacy is less robust
- Maintaining the dose of medication at the level that was required to achieve remission appears most effective in prophylaxis if tolerability permits
- Lithium together with the antidepressant appears worthwhile in some patients
Cognitive Therapy
- Cognitive therapy given during an acute phase of depression leads to a more sustained improvement in depressive symptomatology and lessens the risk of subsequent relapse compared to antidepressant drug treatment
- Cognitive behavioural therapy continued (or started) after remission prevents relapse, perhaps to a greater extent than maintenance medication
- Mindfulness-based cognitive therapy (MBCT) integrates cognitive behaviour therapy with meditation techniques and is as effective as maintenance antidepressant treatment in preventing relapse
Interpersonal Therapy
- Combining interpersonal therapy with medication in the treatment of the acute episode appears to decrease relapse rates over the following 12 months
- The effect of continuation treatment with combined interpersonal therapy and medication has also been studied in older depressed patients
- Continuation therapy with interpersonal therapy as a sole treatment prevents recurrence
Assessment of Depressive Disorders
- The aims of assessment are to decide whether the diagnosis is depressive disorder, judge the severity of the disorder, form an opinion about the causes, assess the patient's social resources, and gauge the effect of the disorder on other people
- Diagnosis depends on thorough history-taking and examination of the physical and mental state
- Particular care should be taken not to overlook a depressive disorder in patients who do not complain spontaneously of being depressed ('masked depression')
Management of Depressive Disorders
- The first question concerns the level of care and supervision that may be required, which depends on the severity of the disorder and the quality of the patient's social resources
- Patients who live alone, or whose families cannot care for them during the day, may need intensive community treatment or day-patient care
- Involvement of the family wherever possible is likely to improve the outcome
- The need for antidepressant drug treatment should be considered, particularly for patients with a major depressive syndrome of at least moderate severity
Choice and Use of Antidepressant Drugs
- SSRIs are the usual first choice for antidepressant treatment, unless the patient has done well previously with a different agent.
- Lofepramine, a tricyclic antidepressant, is another option with a different side effect profile.
- Mirtazapine may be considered if the patient needs concomitant sedation or if there are relative contraindications to the use of SSRIs.
Dosage and Precautions
- The dosage of antidepressant drugs should be as prescribed, and the patient should be warned about the effects of taking alcohol.
- Patients should be advised about driving, particularly that they should not drive while experiencing sedative side effects or any other effects that might impair their performance in an emergency.
Electroconvulsive Therapy (ECT)
- ECT is rarely part of first-line treatment of depression and is usually considered only for patients who have already been admitted to hospital.
- ECT is indicated for patients who refuse to drink enough fluid to maintain adequate urine output, those who present a highly dangerous suicidal risk, or those suffering extreme distress.
Activity
- Suitable activity should be considered for every patient to prevent social withdrawal and deprivation of social stimulation and rewarding experiences.
- The type and amount of activity should be tailored to the individual patient and adjusted as the illness runs its course.
Psychotherapy
- The appropriate kind of psychological treatment should be decided in each case, taking into account the patient's preferences and the availability of suitably trained therapists.
- Cognitive behaviour therapy (CBT) and interpersonal therapy are evidence-based treatments for moderate to severe depression.
- CBT can be added to antidepressant medication to enhance therapeutic response.
Failure to Respond to Initial Treatment
- If a depressive disorder does not respond to initial treatment, the plan should be reviewed, and the patient's medication adherence and diagnosis should be reassessed.
- The treatment plan can be adjusted by increasing the dose of antidepressant medication, switching to a different medication, or adding another medication.
Switching Antidepressant Medications
- If a patient does not respond to one antidepressant, the first step is usually to stop the first medication and try another.
- Switching to a different class of drug (e.g., from SSRI to mirtazapine or venlafaxine) may be marginally better than switching to a second SSRI.
Combination Treatment
- Combination strategies aim to supplement the antidepressant effect of an ineffective or partially effective medication with another antidepressant agent.
- The evidence for combination treatment is limited, but it is endorsed in case series and expert reviews.
Augmentation of Antidepressant Drug Treatment
- Augmentation therapy involves adding a second compound to the antidepressant to enhance therapeutic response.
- Antipsychotic drugs, lithium, and other agents can be used for augmentation therapy.
- The evidence for augmentation therapy is limited, and the approach should be used with caution due to the increased risk of adverse effects.
Lithium Augmentation
- Lithium can be effective in the treatment of resistant depression, and about 50% of depressed patients will show a useful response over 1–3 weeks.
- Lithium can be added to any primary antidepressant medication with good effect, although combination with SSRIs and venlafaxine should be undertaken with caution.
Tri-iodothyronine (T3) Augmentation
- T3 can be added to ineffective tricyclic antidepressant treatment to bring about a clinical response, even in patients with normal thyroid activity
- Dose of 20-40 μg daily, starting with 10 μg and increasing to 20 μg after 1 week if tolerated
- Mild side effects, including tremor and sweating, but not recommended for patients with cardiovascular disease
Electroconvulsive Therapy (ECT)
- Considered for severe depression that persists despite antidepressant treatment
- ECT is more effective than drugs in severe depressions, particularly when psychotic features are present
- Meta-analysis suggests that medication resistance lowers the response rate to ECT (48% vs 65%)
- Relapse rate in the year after ECT can be as high as 50% if patients continue on the same antidepressant medication
Post-ECT Prophylaxis
- Combination of lithium and nortriptyline or maintenance ECT can be effective in sustaining remission
- However, relapse rate is still high, with around 50% of patients relapsing in 6 months
Continuing Support and Other Measures
- Continuing support is essential for patients who do not respond to treatment
- Reassurance and discussion of problems contributing to depression can be helpful
- Structured psychotherapies, such as cognitive behaviour therapy, can be effective in bringing about a therapeutic response
- Watching for suicidal intentions is important, particularly in patients with prolonged depression
- Other treatment approaches, such as deep brain stimulation and neurosurgery, can be considered for severe symptoms and longstanding refractory illness
Prevention of Relapse and Recurrence
- Following recovery, patients should be followed up for several months by the psychiatric team or general practitioner
- Antidepressant medication should usually be continued for about 6 months and then gradually withdrawn over several weeks
- Watching for signs of discontinuation reactions or relapse is important
- Involving relatives in the plan can be helpful
- Maintenance treatment should be considered for patients with a history of recurrence, particularly if there is a family history of recurrent major depression
Maintenance Treatment
- Long-term maintenance treatment may be necessary due to the high recurrence rate of major depression (90% in patients with three previous episodes)
- Factors to consider include the likely impact of recurrence, previous response to drug treatment, and the patient's view of long-term drug treatment
- Choice of medication depends on response in the acute or continuation phase of treatment
- Lithium can be effective for long-term maintenance treatment of recurrent depression, particularly in patients with a history of manic episodes
Criteria for Depressive Episode in ICD-10
- A Depressed Mood is a necessary criterion for a depressive episode
- Loss of Interest and Enjoyment is another essential criterion for a depressive episode
- Reduced Energy and Decreased Activity is the third criterion for a depressive episode
Additional Criteria
- Reduced Concentration is a symptom of a depressive episode
- Reduced Self-Esteem and Confidence is a symptom of a depressive episode
- Ideas of Guilt and Unworthiness are a symptom of a depressive episode
- Pessimistic Thoughts are a symptom of a depressive episode
- Ideas of Self-Harm are a symptom of a depressive episode
- Disturbed Sleep is a symptom of a depressive episode
- Diminished Appetite is a symptom of a depressive episode
Classification of Depressive Episodes
- Mild Depressive Episode: at least two symptoms from A and at least two symptoms from B
- Moderate Depressive Episode: at least two symptoms from A and at least three symptoms from B
- Severe Depressive Episode: all three symptoms from A and at least four symptoms from B
- Severity of symptoms and degree of functional impairment also guide classification of depressive episodes
Multifactorial Origin of Mood Disorders
- Mood disorders have a multifactorial origin, involving genetic, environmental, and psychological factors.
- Multiple genes with small individual effects contribute to mood disorders.
- Genetic contributions can affect mood disorders directly through cortical circuitry modification or indirectly through personality and psychological coping mechanisms.
Early Life Experiences and Mood Disorders
- Adverse early life experiences shape personality and limit subsequent attachment behavior and social support access.
- Early life experiences can affect the development of the hypothalamic–pituitary–adrenal (HPA) axis and neurobiological responses to stress in adulthood.
Triggering Factors and Vulnerability
- Depressive disorders are often triggered by current life events, particularly in individuals lacking social support.
- The impact of life events is modified by early life experience, personality, and genetic inheritance.
- The interaction of these factors determines an individual's resilience or vulnerability to a life event and subsequent risk of clinical mood disturbance.
Neurobiology of Depression
- The neurobiology of depression episodes is associated with changes in monoamine neurons and HPA axis activity.
- These changes modify the activity of neural circuitry involved in emotional regulation.
- At a cellular level, depression may involve a loss of synaptic plasticity and dendrite formation.
Brain Abnormalities in Mood Disorders
- Structural and functional brain abnormalities in mood disorders suggest persistent biological vulnerability.
- This vulnerability is likely produced by genetic inheritance or early developmental factors.
Psychoanalytical Theory of Depression
- Sigmund Freud's paper "Mourning and Melancholia" (1917) highlights the similarities between mourning and depressive disorders, suggesting a common cause.
- Freud proposes that melancholia results from a loss of an "object" (an internal representation or abstraction), not just a physical loss, due to the absence of actual loss in some depressed patients.
- Depressed patients often exhibit self-criticism, which Freud believes is a disguised accusation of someone else they feel affection for, indicating ambivalence (love and hostility simultaneously).
Object Relations and Depression
- Melanie Klein develops Freud's ideas, suggesting that weaning (loss of the breast) represents a significant symbolic loss for the infant, leading to feelings of remorse and guilt.
- In normal development, this "depressive anxiety" motivates attempts at reparation and concern for others.
- Failure to navigate this process can result in depressive reactions to future losses.
Attachment Theory and Depression
- John Bowlby's work shows that the main caregiver's rearing abilities play a crucial role in shaping the infant's secure emotional attachment.
- Secure attachment is essential for developing satisfactory interpersonal relationships, and insecure attachments can increase the risk of adult psychopathology, including depression.
Abnormalities in Monoamine Activity in Depression
- 5-HT (Serotonin) shows decreased plasma tryptophan levels in individuals with depression
- Blunted 5-HT neuroendocrine responses are observed in depressed individuals
- Decreased brain 5-HT1A receptor binding is evident in Positron Emission Tomography (PET) scans
- Decreased brain 5-HT reuptake sites are seen in Single Photon Emission Computed Tomography (SPET) and PET scans
- Clinical relapse occurs after tryptophan depletion, suggesting a link between 5-HT and depression
Noradrenaline Abnormalities in Depression
- Blunted noradrenaline-mediated growth hormone release is observed in depressed individuals
- Clinical relapse occurs after administration of α-methyl-para-tyrosine (AMPT), indicating noradrenaline's role in depression
Dopamine Abnormalities in Depression
- Decreased homovanillic acid (HVA) levels are seen in cerebrospinal fluid of depressed individuals
- Clinical relapse occurs after administration of α-methyl-para-tyrosine (AMPT), suggesting dopamine's involvement in depression
Immune Changes in Depression
- Lymphocytes exhibit lowered proliferative responses to mitogens
- Natural killer cell activity is decreased
- Levels of positive acute phase proteins are increased
- Inflammatory cytokine levels are elevated, including:
- IL-6 (interleukin 6)
- TNFα (tumor necrosis factor alpha)
- Indoleamine 2,3-dioxygenase is induced
Neuropsychological Correlates of Depression
- Dorsolateral prefrontal cortex: Altered cerebral perfusion and metabolism are associated with cognitive dysfunction, particularly executive dysfunction, in depressed patients.
- Dorsomedial prefrontal cortex: Impaired voluntary regulation of emotion is linked to altered cerebral perfusion and metabolism in this region.
- Medial prefrontal cortex: Abnormal emotional processing is correlated with altered cerebral perfusion and metabolism in this region.
- Anterior cingulate: Impaired attentional processes and altered emotional salience are associated with altered cerebral perfusion and metabolism in this region.
- Amygdala: Abnormal emotional processing is linked to altered cerebral perfusion and metabolism in this region.
- Ventral striatum: Impaired incentive behavior and psychomotor disturbances are correlated with altered cerebral perfusion and metabolism in this region.
Pharmacological Treatments for Resistant Depression
- Maximizing antidepressant dosage to the highest tolerable level is a treatment option.
- Adding an antipsychotic drug is recommended for patients with depressive psychosis.
- Switching to a different class of antidepressant, such as venlafaxine or tricyclic antidepressants, may be effective.
- Combining antidepressants, such as an SSRI with mirtazapine, or venlafaxine with mirtazapine, is a potential treatment strategy.
- Adding an atypical antipsychotic drug to an SSRI or venlafaxine may improve treatment outcomes.
- Lithium can be added to antidepressant drug treatment to enhance its effectiveness.
- Monoamine oxidase inhibitors (MAOIs) can be used in combination with lithium to treat resistant depression.
- Electroconvulsive therapy (ECT) is a treatment option for severe cases of resistant depression.
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Description
This chapter focuses on depressive disorders, distinguishing them from normal feelings of unhappiness and symptoms of other disorders. Learn about the central features of these syndromes.