Depression after stroke …

Adrian Marchidann MD

Stroke & Vascular Disorders

Updated 06.05.2024
Released 06.20.1997
Expires For CME 06.05.2027

Depression after stroke

Author: Adrian Marchidann MD

See Contributor Disclosures

Editor: Steven R Levine MD

Depression after stroke

In This Article

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Introduction

Overview

Depression occurs in approximately 33% of stroke survivors. It impairs rehabilitation and is associated with increased disability, cognitive impairment, and mortality. Both major depression and minor (dysthymic) depression may occur after a stroke. Major depression is mainly associated with lesions of the left frontal cortex and basal ganglia. Preexisting depression, cognitive impairment, anxiety, and stroke severity are the major predictors of depression after a stroke. The dysfunction of biogenic amines may explain poststroke depression. Poststroke depression may respond to antidepressant drugs.

Key points

	• Approximately one third of stroke survivors experience depression during the first year after stroke.
	• The cognitive dysfunction associated with depression impairs rehabilitation and burdens caregivers with additional stress.
	• Antidepressant medications may prevent depression after stroke.
	• Selective serotonin reuptake inhibitors are the mainstay of treatment of poststroke depression.
	• Well-designed clinical trials are needed to test the best strategies against depression across all stroke survivors.

Historical note and terminology

In 1904 Adolf Meyer reported the possibility of a relationship between traumatic insanities and specific locations and causes of brain injury (89). In 1914 Babinski reported a high prevalence of euphoria, indifference, and denial of illness in patients with right hemisphere lesions (11). Some years later, Bleuler noted that after stroke "melancholic moods lasting for months and sometimes longer appear frequently" (19), and Kraepelin recognized an association between manic-depressive insanity and cerebrovascular disease (71).

Clinical manifestations

Presentation and course

	• Stroke survivors experience both major and minor depression.
	• Only a minority of patients have depression symptoms without having major depression.

Up to 33% of stroke survivors experience depression at 3 months and 30% at 5 years (10). In a systematic review and meta-analysis of 77 studies of post-stroke depression, prevalence was 27%. Among those depressed at 3 months, 44% recovered, and 53% experienced persistent depression. The cumulative incidence at 1 year was 38% (79). By comparison, the 12-month prevalence of major depression in the United States is 6.7% (63). Both major and minor (dysthymic) depression occur after a stroke. The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders defines poststroke major depression as a "prominent and persistent period of depressed mood or markedly diminished interest or pleasure in all, or almost all, activities that predominate in the clinical picture." Table 1 shows the Diagnostic and Statistical Manual of Mental Disorders criteria for major depression.

The most specific symptoms of major depression after stroke include autonomic anxiety, morning depression, subjective anergia, worrying, brooding, loss of interest, hopelessness, and lack of self-confidence. Only 2% to 3% of stroke patients have symptoms without a depressed mood, suggesting “masked” depression (96). Depression interferes with rehabilitation by causing physical and cognitive function impairment (105; 113; 98). Older adults are more likely to mask depression with somatic rather than psychiatric symptoms (68).

Apathy occurs in more than 20% of first-ever stroke patients and may impair functional recovery (109). Although apathy and depression share some correlations, they may require different treatment approaches (86; 76). Mild to severe poststroke depression in the elderly is associated with increased mortality and may last for at least 7 years poststroke (91; 56). Other morbidities include dependency, risky behaviors, including drug and alcohol abuse, an increase in suicide rate, poor compliance with treatment, and self-care (61).

Table 1. Criteria for Major Depressive Episode

(A) Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
	(1) Depressed mood most of the day, nearly every day, as indicated by either subjective report (eg, feels sad, empty, hopeless) or observation made by others (eg, appears tearful). Note: In children and adolescents, can be an irritable mood.
	(2) Markedly diminished interest or pleasure in most activities most of the day, nearly every day.
	(3) Significant unintentional weight loss or gain (more than 5% of body weight in a month) or decrease or increase in appetite nearly every day. In children, consider failure to gain the expected weight.
	(4) Insomnia or hypersomnia nearly every day.
	(5) Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
	(6) Fatigue or loss of energy nearly every day.
	(7) Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
	(8) Diminished ability to think or concentrate, or indecisiveness, nearly every day.
	(9) Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
(B) The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
(C) The episode is not attributable to the physiological effects of a substance or another medical condition.
Note: Criteria A to C represent a major depressive episode.
(D) The occurrence of the major depressive episode is not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic disorders.
(E) There has never been a manic episode or a hypomanic episode.
Note: Responses to a significant loss (eg, bereavement, financial ruin, losses from a natural disaster, a serious medical illness, or disability) may include feelings of intense sadness, rumination about the loss, insomnia, poor appetite, and weight loss noted in criterion A, which may resemble a depressive episode. Although such symptoms may be understandable or considered appropriate to the loss, the presence of a major depressive episode in addition to the normal response to a significant loss should also be carefully considered. This decision inevitably requires the exercise of clinical judgment based on the individual’s history and the cultural norms for the expression of distress in the context of loss.

Table 2. Criteria for Major Depressive Episode Due to Another Medical Condition*

(A) A prominent and persistent period of depressed mood or markedly diminished interest or pleasure in all, or almost all, activities that predominate in the clinical picture.

(B) There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiological consequence of another medical condition.

(C) The disturbance is not better explained by another mental disorder (eg, adjustment disorder, with depressed mood, in which the stressor is a serious medical condition).

(D) The disturbance does not occur exclusively during delirium.

(E) The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

A lesser form of depression, included in the Diagnostic and Statistical Manual of Mental Disorders, is minor depression. The "research criteria" for minor depression require depression or anhedonia with at least one, but fewer than four, additional symptoms of major depression or a diagnosis of mood disorder due to stroke with depressive features.

Another diagnostic category offered by the Diagnostic and Statistical Manual of Mental Disorders is dysthymia (Table 2). One limitation of this diagnosis is that it requires that the syndromic cluster of depressive symptoms be present most of the time for more than two years. Because waiting for 2 years to diagnose a poststroke dysthymic disorder is not clinically useful, most studies have used the symptom criteria for dysthymic disorder excluding the 2-year criterion.

Table 3. Diagnostic Criteria for Dysthymic Disorder *

	(A) Depressed mood for most of the day, for more days than not, as indicated either by subjective account or observation by others, for at least 2 years. (B) Presence, while depressed, of two (or more) of the following:
		(1) Poor appetite or overeating. (2) Insomnia or hypersomnia. (3) Low energy or fatigue. (4) Low self-esteem. (5) Poor concentration or difficulty making decisions. (6) Feelings of hopelessness.
* Adapted from the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (05).

Poststroke depression rating scale distinguishes two depression profiles: (1) an "endogenous" type, with higher scores on suicide and anhedonia; and (2) a "reactive" type, with higher scores on catastrophic reaction, hyperemotionalism, and diurnal mood variation (43). Both catastrophic reaction and hyperemotionalism (also known as "pathological affective display") were significantly associated with depression (103). However, the lack of these symptoms in many depressed stroke patients calls into question the "endogenous" and "reactive" categories.

A small study suggests that patients with poststroke depression exhibit no melancholia and have fewer cyclic and ideational disturbances, but they have more physical signs than those with primary depression (13). Early-onset major depression, within 3 to 6 months of stroke, was associated with a higher frequency of vegetative symptoms and larger lesion volume than late-onset (12 to 24 months later) major depression. At the same time, early-onset minor depression was associated with poorer social functioning and a higher frequency of melancholic, vegetative, and psychological symptoms of depression than late-onset minor depression (129).

Symptoms of depression are either masked by the patient’s cognitive impairment due to aphasia, agnosia, or memory loss or overlap with anxiety, emotional lability, abulia, apathy, fatigue, poor concentration, and disorders of sleep or appetite (37). Due to diagnostic challenges, depression after stroke is not easily identified by physicians who are not psychiatrists in 50% to 80% of cases (116), or, if diagnosed, depression is inadequately treated. Patients should be systematically screened by using a structured psychiatric interview, such as the Present State Exam or the Structured Clinical Interview.

Several depression scales, such as the Hamilton Depression Scale and the Center for Epidemiological Studies Scale for Depression are used for screening and assessing the severity of depression. However, the diagnosis of depression should always be based on the clinical interview. In clinical trials involving patients with stroke, the secondary outcomes are often studied by using the several tools listed below.

Depression
	Hamilton Depression Rating Scale (50) Montgomery Esberg Depression Rating Scale (90) Geriatric Depression Scale (47) Beck Depression Inventory (15) Hospital Anxiety and Depression Scale (140)
Anxiety
	Hamilton Anxiety Scale Beck Anxiety Inventory Hospital Anxiety and Depression Scale (140)
Psychological distress
	Scales such as the General Health Questionnaire (45)
General health
	Nottingham Health Profile (57)
Cognition
	Mini-Mental State Examination (41)
Social activities
	Frenchay Activities Index (135)
Activities of daily living
	Barthel Index (83)
Disability
	Hemispheric Stroke Scale (02)
Dependence in self-care activities of daily living
	Modified Rankin Scale (101)
Health-related quality of life
	36-item short questionnaire (SF-36) (137)

In a cross-sectional study of the Rasch analysis of the Beck Depression Inventory-II (BDI-II) in stroke survivors, a shorter, 16-item version of the BDI-II may be more appropriate for use as a unidimensional measure of depression in patients following the first stroke (75).

Beck Depression Inventory, Hamilton Rating Scale for Depression, and Clinical Global Impression assessment by professionals, in addition to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Revised Diagnosis, are useful in assessing depression. However, none of these instruments stood apart from the others. Proxy ratings should be used with caution, and the use of the Visual Analogue Mood Scale among patients with aphasia and other cognitive impairments cannot be recommended (16).

Proxies tended to score the patients as more severely affected than the patients scored themselves (139; 53).

Comorbidities and psychiatric distress associated with aging complicate the diagnosis and treatment of depression. Moreover, depression causes additional stress on caregivers (06).

Prognosis and complications

Major depression is diagnosed in 60% of patients 1 year after stroke but resolves by the 2-year evaluation (104). Of those with dysthymia, 60% were still depressed at the 2-year evaluation. However, most patients with minor depression were not depressed 3 to 6 months after the acute event (54). During the first year after stroke, there was an increasing frequency of major depression and a decreasing frequency of minor depression. Patients with aphasia were more severely affected (62). Depression following cortical stroke appears to last longer than after subcortical stroke (124). Patients who recovered from depression had improved cognitive recovery and overall function (67; 26).

Independent outcomes of depression after stroke include lower quality of life, disability, and mortality (10).

Psychological well-being, social functioning, and quality of life are adversely affected by depression (30; 80; 24).

Depression correlates with recovery, functional outcome, and handicap (98; 52; 100).

Cognitive dysfunction, as measured by the Mini-Mental Status Examination, often follows stroke (60). This dysfunction may impair recovery (105; 124). Cognition seemed to be affected more by left-side lesions. The domains most affected are verbal memory, language, visuo-constructional ability, executive motor functions, and frontal lobe-related tasks (21). Cognitive impairment due to major depression after left-side stroke may persist up to 1 year after the stroke (34).

Depression not only follows stroke but also predicts it (94). The relationship between depressive symptoms and stroke mortality was confirmed in a prospective study of behavioral, social, and psychological factors related to health and mortality in a community sample (38). However, it is the persistently high level of depression that is associated with an increased risk of stroke, not just depression, that improves over time (115).

Mood symptoms on a self-reported rating scale were associated with death at 12 and 24 months after stroke (56). Moreover, at a 10-year follow-up, depression increased mortality by 3.4 times (91). This may be due to decreased medication compliance (130).

Suicidal thoughts can occur in the acute phase of stroke, mostly in patients with a lower educational level or a preexistent mood disorder (110).

The Fatigue Severity Scale was significantly higher in the suicidality group and remained a significant predictor, with an odds ratio of 1.5 (128). Other risk factors are low income, living alone, male sex, young age, and severe stroke. The patients born outside Europe had a lower risk of suicide compared to those of European descent. The risk was highest during the first 2 years after stroke (36). The increased vulnerability of these patients underscores the importance of psychiatric evaluation.

Clinical vignette

A 52-year-old married man suffered a heart attack while playing basketball. Two days later, he had a large stroke resulting in left hemiparesis and sensory deficit. Within a few days after the stroke, he experienced depression with anxiety, sadness, tension, restlessness, worry, low energy, and loss of interest in activities that he previously enjoyed, such as eating out and shopping. He also complained of insomnia and loss of appetite. This syndrome lasted for 3 months. Administration of nortriptyline improved his mood progressively, and he became euthymic after 3 weeks.

Biological basis

	• Dysfunction of biogenic amines may play a role in post-stroke depression.
	• There is no clear relationship between the location of the stroke and depression.
	• Left hemisphere lesions are associated with depression in the acute inpatient phase, whereas right hemisphere lesions are associated with chronic depression.
	• Other risk factors for poststroke depression are preexisting depression, family history of mental illness, anxiety, preexisting cerebral atrophy, cognitive dysfunction, and severity of stroke.

Etiology and pathogenesis

The pathophysiology of post-stroke depression is multifactorial, with biological and psychological components. This is more than just a reaction to the disability, as it may occur in animal models, in patients with anosognosia, and after a transient ischemic attack or small stroke.

The main triggers of depression after a stroke studied include genetic predisposition, location of the stroke, and disruption of cortico-striato-pallido-thalamic-cortical projections. Multiple humoral factors are associated with depression following stroke causing increased inflammation, alteration of the neurotrophic factors, and disruption of the serotonergic, noradrenergic, and dopaminergic pathways.

According to a systematic review and meta-analysis of 50 observational studies including 20,293 participants, preexisting depression, cognitive impairment, stroke severity, and anxiety are the major predictors of depression after stroke (10). A cohort study of 1221 patients showed that persistent depression was also associated with being married or partnered (RR = 3.94, 95% CI: 2.42–6.41). The higher risk of depression in Australia and New Zealand compared to Vietnam suggests a cultural component (04). In a cross-sectional study, health literacy is associated with less depression, higher perceived participation, and recovery of walking 1 year after stroke (40).

Multiple observational studies found an effect of lesion location on depression (122; 08; 92; 14; 84; 95; 125; 134). However, the correlation between depression and lesion location has not been confirmed (55; 25).

Nevertheless, a systematic review found that patients with left hemisphere lesions are depressed in the acute inpatient phase, whereas those with right-side lesions are more depressed in the chronic outpatient phase (18). Voxel-based lesion behavior mapping (VLBM) is a novel approach to mapping brain lesions and their functional consequences. An analysis of 270 patients has revealed that stroke in the right basal ganglia increases the risk of depression at 6 months follow-up (69).

Perhaps more important than the lesion location is the nature of the deficit. Dysphagia after stroke significantly impairs psycho-social functioning and is an independent risk factor for depression (59).

Neuroimaging studies suggest an association between white matter hyperintensities and both motor and neuropsychological poststroke deficits (27). Preexisting subcortical atrophy and a family or personal history of psychiatric disorder are risk factors for poststroke depression (123; 121). The severity of deep white matter hyperintensities is associated with delayed depression and anxiety after ischemic stroke and unfavorable outcomes at 3 months, despite treatment of anxiety (66). Lobar cerebral microbleeds may also play a role (127).

Poststroke depression has been associated with decreased levels of serotonin, noradrenaline, and dopamine (72). Positron emission tomography has shown that right hemisphere lesions may result in compensatory upregulation of serotonin receptors, which is lacking after left hemisphere lesions, leading to depression (87). Genetic factors related to serotonin transmission confer increased susceptibility to depression after stroke (70; 39; 64).

Neurogenesis may play an important role in recovery from ischemia and depression (74). Neurotrophins are molecules that promote the development and survival of neurons. One of these molecules, brain-derived neurotrophic factor, has an antidepressant role and confers resilience to chronic stress. It not only protects against ischemic injury and hypoglycemia in cultured neurons but also plays a central role in hippocampal neurogenesis and functional recovery after stroke (81).

A systematic review and meta-analysis of 12 studies with 3230 patients revealed that the baseline levels of high-sensitivity C-reactive protein and homocysteine are elevated in patients with post-stroke depression compared to those without depression (58). The inflammatory response following stroke may disrupt the hypothalamic-pituitary axis, with increased glucocorticoid levels and decreased production of neurotrophic factor (93). Although most inflammatory markers are weakly associated with post-stroke depression, they have little prediction value, underscoring the need for other markers (77).

Epidemiology

	• Almost a third of patients develop depression after stroke, but more patients may have depressive symptoms without meeting the criteria for depression.
	• Chronic disability, female sex, lack of support, and advanced age are the main risk factors.
	• Young patients are also susceptible to depression due to increased stress related to family and early career demands.
	• Anxiety and depression may occur at the same time.
	• The suicide risk is twice that of the general population.

Approximately a third of stroke survivors experience depression during the first year of stroke (49). Half of these suffer from major depression. The number of patients with depressive symptoms but without major or minor depression is also high. Depression after stroke is associated with long-lasting disability, female sex, living alone, and age over 70 years (51).

The prevalence of depression ranges from 40% to 50% in the acute phase of stroke, between 49% and 54% in rehabilitation centers, and around 23% in the community (22). A Finnish study found major depression in 26% and minor depression in 14% of a consecutive series of 486 patients with ischemic stroke (99). In an 18-month follow-up study of 100 stroke patients, 46% of patients who were depressed during the first two months were also depressed at 12 and 18 months poststroke (17). Data from the South London Stroke Register including 3689 patients found a frequency of depression of 30% at 5 years after stroke. Although some patients recovered from depression, new ones were diagnosed, suggesting the need for regular screening for depression after stroke (09).

Women tend to have a higher prevalence of post-stroke major depression as compared to men (52; 97). Their quality of life is worse up to 12 months after stroke in the dimensions of mobility, pain, discomfort, anxiety, and depression (23). Preexisting psychiatric disorders and severe cognitive impairment correlate with severe depression (97).

Not only the elderly are vulnerable to poststroke depression but the younger patients too, mostly due to concerns related to career and family (82).

Anxiety after stroke is almost as common as depression, and additional patients became anxious or depressed at each time point. Prevalence of anxiety ranges between 22% and 25%, whereas depression is between 24% and 30%. Some 11% and 7% of those initially not anxious become anxious at 4 and 6 months after stroke, respectively. Depression evolution shows a similar pattern (33).

Neuroticism, the tendency to experience negative mood states, is another predictor of post-stroke depression (01).

The rate of suicide attempts and completed suicides after stroke is double compared to the general population (36). In a systematic review of 21 studies that included 17,189 patients with stroke, 12.2% of them experienced suicide ideation (28).

Differential diagnosis

Poststroke depression should be differentiated from poststroke apathy, catastrophic reaction, and emotional lability (pathological laughing and crying).

Apathy manifests as a lack of feeling, emotion, interest, or concern. Apathy may occur independently or be associated with depression. Patients with apathy (without depression) showed a significantly higher frequency of lesions involving the posterior limb of the internal capsule as compared to patients with no apathy (118).

The catastrophic reaction is expressed as anxiety, tears, aggressive behavior, swearing, displacement, refusal, renouncement, and compensatory boasting (46). This reaction was seen in 19% of patients with acute stroke lesions, and 66% of patients with the catastrophic reaction also had major depression (119).

Emotional lability is characterized by sudden, easily provoked episodes of crying or laughing, which may or may not be appropriate to the context. No significant correlations were found between emotional lability and depression, social functioning, activities of daily living, and cognitive level, suggesting that poststroke depression and pathological emotions may be independent phenomena (106). A prospective study of 148 patients with single unilateral stroke found depression in 18% of the patients and emotional lability in 34% (65). Anterior cortical lesion location was significantly associated with depression, whereas lenticulo-capsular strokes were significantly associated with emotional lability.

Severe fatigue occurred in about half of the stroke patients, as compared to 16% of the healthy controls (132).

Psychological factors like helplessness and passive coping revealed an increased association with depression, whereas acceptance revealed a decreased association with depression (133).

Management

	• Poststroke depression may be treated with a combination of pharmacological, psychosocial, and stroke-focused treatments.
	• Selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors (SNRIs) have been successfully used to treat depression.
	• Although effective, tricyclic antidepressants have more side effects.
	• The role of cognitive behavioral therapy is not clear yet.
	• Initial studies of neuromodulation with transcranial magnetic stimulation have shown promising results.

Several studies have shown that poststroke depression may be adequately treated with antidepressant drugs.

Nortriptyline, trazodone, fluoxetine, citalopram, and venlafaxine have been studied in patients with depression after stroke (78; 102; 32; 138; 07; 107; 42). Delirium, confusion, drowsiness, and agitation occurred in some patients.

A Cochrane review found a small potential benefit of pharmacotherapy in treating depression and reducing depressive symptoms, at the cost of a significant increase in adverse events (03).

Psychosocial therapies have also been explored for the management of depression after stroke. A meta-analysis found inconclusive effects of cognitive behavioral therapy (136). Family support significantly increased the social activities and quality of life for carers but without significant effects on patients (85). In a small study of 60 patients with subacute aphasia, intensive social interaction had a small-to-medium effect in reducing depression severity (117).

Task-specific treadmill training designed to improve gait speed may potentially provide secondary benefits by positively impacting depression, mobility, and social participation for people after stroke (114). A meta-analysis of 13 studies found only short-term benefits of exercise against depression (35).

Sexuality is an important issue in post-stroke rehabilitation. Because preferences for the timing of this counseling vary, an ongoing exploration of the need for such counseling is important (126).

Very early mobilization may reduce depressive symptoms in stroke patients at 7 days poststroke (31). However, very early high-dose rehabilitation therapy is associated with a worse outcome (73).

Transcranial direct current stimulation has shown promise in the treatment of poststroke depression (131). A meta-analysis including 22 randomized controlled studies of repetitive transcranial magnetic stimulation suggests a beneficial effect on poststroke depression. However, because of the heterogeneity and potential biases found, the result should be treated with caution (111). A Cochrane systematic review found little or no effect on the prevalence of depression (03).

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All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Adrian Marchidann MD

Dr. Marchidann of Kings County Hospital has no relevant financial relationships to disclose.
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Steven R Levine MD

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
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Former Authors

Robert G Robinson MD
Tiffany W Chow MD
Maria Laura Garau MD
Sergio E Starkstein MD
Tarakad S Ramachandran MD
Arun Ramachandran MD

Patient Profile

Age range of presentation: 13 to 65+ years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

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Depression after stroke

Associated Disorders

Binswanger disease
Cortical lesions
Dysthymic depression
Multi-infarct dementia
Parietal lesions
- Subcortical lesions
- Thromboembolism

Differential Diagnosis

poststroke apathy
catastrophic reaction
pathological laughing and crying
emotional lability
severe fatigue

Depression after stroke …

Depression after stroke

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Criteria for Major Depressive Episode

Table 2. Criteria for Major Depressive Episode Due to Another Medical Condition*

Table 3. Diagnostic Criteria for Dysthymic Disorder *

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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to access the full version.

Questions or Comment?

Also in This Category

Wilson disease

Anti-LGI1 encephalitis

Fatal familial insomnia

Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

Atrial myxoma

Anterior cerebral artery stroke syndromes

	• Because of high post-stroke depression prevalence, it is reasonable to attempt preventive measures.
	• Despite several studies that have demonstrated the prevention of depression after stroke with antidepressant medications, the level of certainty is very low.

	• Most cases of depression after stroke are not diagnosed by physicians who are not specialized in psychiatry.
	• Patients with stroke should be screened for depression.

Depression after stroke

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Criteria for Major Depressive Episode

Table 2. Criteria for Major Depressive Episode Due to Another Medical Condition*

Table 3. Diagnostic Criteria for Dysthymic Disorder *

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Wilson disease

Anti-LGI1 encephalitis

Fatal familial insomnia

Vein of Galen malformations

Patent foramen ovale

Neuroimaging in acute stroke

Atrial myxoma

Anterior cerebral artery stroke syndromes

This is an article preview.
Start a Free Account
to access the full version.