Journal of Stroke 2016;18(3):244-255

http://dx.doi.org/10.5853/jos.2016.01144

Review

Post-stroke Mood and Emotional Disturbances:

Pharmacological Therapy Based on Mechanisms
Jong S. Kim
Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, Korea

Post-stroke mood and emotional disturbances are frequent and diverse in their manifestations. Out
of the many post-stroke disturbances, post-stroke depression, post-stroke anxiety, post-stroke emotional incontinence, post-stroke anger proneness, and post-stroke fatigue are frequent and important
symptoms. These symptoms are distressing for both the patients and their caregivers, and negatively
influence the patients quality of life. Unfortunately, these emotional disturbances are not apparent
and are therefore often unnoticed by busy clinicians. Their phenomenology, predicting factors, and
pathophysiology have been under-studied, and are under-recognized. In addition, well-designed clinical trials regarding these symptoms are rare. Fortunately, these mood and emotional disturbances
may be treated or prevented by various methods, including pharmacological therapy. To administer
the appropriate therapy, we have to understand the phenomenology and the similarities and differences in the pathophysiological mechanisms associated with these emotional symptoms. This narrative review will describe some of the most common or relevant post-stroke mood and emotional disturbances. The phenomenology, factors or predictors, and relevant lesion locations will be described,
and pharmacological treatment of these emotional disturbances will be discussed based on presumable pathophysiological mechanisms.

Correspondence: Jong S. Kim

Stroke Center and Department of
Neurology, University of Ulsan College of
Medicine, Asan Medical Center,
88 Olympic-ro 43-gil, Songpa-gu,
Seoul 05505, Korea
Tel: +82-2-3010-3442
E-mail: jongskim@amc.seoul.kr
Received: August 18, 2016
Revised: September 7, 2016
Accepted: September 8, 2016
This study was supported by a grant from
the Ministry for Health, Welfare and Family
Affairs, Republic of Korea (HI14C1985).
The authors have no financial conflicts of
interest.

Keywords Stroke; Depression; Emotion; Serotonin; Treatment

Introduction
Mood and emotional disturbances are frequent symptoms in
stroke survivors.1 These symptoms are distressing for both the
patients and their caregivers, and negatively influence patient
quality of life.2,3 Important mood/emotional disturbances include
post-stroke depression (PSD), post-stroke anxiety, post-stroke
emotional incontinence (PSEI), post-stroke anger proneness
(PSAP), and post-stroke fatigue (PSF). Underlying factors and
predictors of these emotional disturbances partially overlap, but
are still different. The relationships between these phenomena
and lesion locations differ when considering the different emo-

tional symptoms. Thus, these diverse emotional disturbances are

pathophysiologically interrelated, but are different phenomena.
Studies have shown that these emotional disturbances have
negative impacts on patients clinical outcomes. PSD, for example, negatively influences later functional outcomes after
stroke,4-8 decreases quality of life,9 leads to less efficient use of
rehabilitation services,8 and increases mortality.10,11 Patients with
PSF are more often unemployed, change their jobs,12,13 and fail to
return to previous jobs13-16 than those without PSF. Although the
overall negative impacts of PSEI and PSAP are less marked than
those of PSD, they still lead to distress and embarrassment, impair certain domains of patients quality of life, and increase

Copyright 2016 Korean Stroke Society

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Vol. 18 / No. 3 / September 2016

caregiver burden.17
Fortunately, these mood and emotional disturbances can be
treated or prevented by various methods, including pharmacological therapy. In order to administer the proper therapy, we
have to understand the similarities and differences between the
phenomenologies and pathophysiological mechanisms associated with these symptoms. Regrettably, these important symptoms
have been underdiagnosed, neglected, and under-studied.
This narrative review will describe some of the most common
or relevant post-stroke mood and emotional disturbances. The
phenomenology, underlying factors or predictors, and relevant
lesion locations will be described. I will also discuss pharmacological treatments for these emotional disturbances based on
presumable pathophysiological mechanisms.

Depression and depressive mood

Symptom characteristics and prevalence
The symptoms of post-stroke depression or depressive symptoms include depressed mood, anhedonia, loss of energy, decreased concentration, and psychic retardation. Although somatic symptoms, such as decreased appetite and insomnia are common, they may in part be attributed to the stroke itself, medications, or comorbid diseases. Guilty feelings and suicidal ideations
are less common than observed in primary depression.18
The Diagnostic and Statistical Manual of Mental Disorders,
Fifth Edition has been used for the diagnosis of PSD. It defines
depression as depressed mood or anhedonia (loss of interest or
pleasure) for 2 weeks or longer, in addition to the presence of at
least four of the following symptoms: substantial weight loss or
gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue or loss of energy, worthlessness or inappropriate
guilt, diminished concentration, and indecisiveness. However, it
remains controversial whether these criteria, validated in physically intact persons, can be used in stroke patients, especially in
the acute setting. Thus, other interviewer-administered or selfcompleted depression case-finding or screening instruments are
also used in the study of PSD. These include the nine-item Patient Health Questionnaire, The Center of Epidemiological Studies-Depression Scale, Hospital Anxiety and Depression Scale, the
Hamilton Depression Rating Scale, the Beck Depression Inventory, and the Montgomery-Asberg Depression Scale.19
The prevalence of PSD ranges from 5 to 67%.1,20-25 The wide
variability is due to different study settings, time since stroke,
and the different criteria/methods used to diagnose PSD.26 A
meta-analysis of 61 cohorts involving 25,488 patients published
in 2014 indicated that 31% of patients developed depression at
some time point up to 5 years following stroke.27
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Generally, the prevalence of major depression decreases over

time. In one study, PSD was present in 50% of the patients in the
acute phase, but only in 12% of the patients at a one-year follow-up.28 Another study reported the prevalence of depression as
30% at 3 months post-stroke. Of these patients, 60% were no
longer depressed one year later.29 In the authors recent study involving 478 patients with acute stroke, approximately 57% had
depression (Montgomery-Asberg Depression Scale > 8) at the
time of the stroke. This percentage rapidly decreased over time.30

Factors associated with PSD

Although various factors have been reported to be associated
with PSD, the results have been inconsistent. A recent systematic
review included 23 studies with 18,374 participants, and reported that demographic characteristics (age and sex) were not consistently associated with PSD.31 There was also no consistent association between hemisphere of stroke, lesion location, or pathological subtype, and depression. A history of depression before
stroke was associated with PSD in four of seven studies, while
cognitive impairment was associated with depression in two of
four studies.
Based on the literature, the most consistent factors associated
with PSD are severe stroke, and early or late physical disability. In
our recent study, changes in Montgomery-Asberg Depression
Scale scores were well-correlated with improvements in neurological impairment.30 It seems that patients acute depressive
symptoms are related to physical dysfunction, while PSD at the
chronic stage has an additional psychosocial component.21,32

Lesion location
Robinson emphasized the role of left frontal lesions in producing PSD.28 However, other studies have shown heterogeneous results,33-35 and one systematic review failed to find an association
between lesion location and PSD.36 We have shown that frontallenticulocapsular-brainstem base lesions are related to PSD.1 An
important confounding factor in these studies is the variability in
time since stroke.37 One study found that the association between left anterior cortical stroke and PSD was apparent at the
acute stage, but not the subacute or chronic stages.38 Higher lesion volumes, cerebral atrophy, silent infarcts, and white matter
lesions may also be associated with a higher risk of PSD.32,39-41

Pathophysiology
The close relationship between PSD and neurological deficits,1
and between changes in Montgomery-Asberg Depression Scale
scores and neurologic improvement,30 suggests that PSD may be
a psychological, reactive depressive symptom associated with
sudden functional deficits. When there are prolonged functional
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deficits, subsequent familial and social issues may perpetuate

PSD.42 The presence of PSD may also be dependent on the patients personality traits and environmental factors, such as social support, economic matters, job stability, etc.42
However, there still are patients whose depression is not readily explained by neurological changes. For instance, patients with
transient ischemic attacks or minor strokes can still have PSD.43
The possible role of anterior frontal lobe damage and the involvement of the frontal-basal ganglia brainstem pathway in
PSD development suggest alterations in neurotransmitter systems, such as serotonergic, adrenergic, and dopaminergic systems.1 It is generally likely that patients with PSD have symptoms due to mixed mechanisms.

Treatment
In 2008, two Cochrane reviews were published regarding the
prevention44 and treatment45 of PSD. The authors identified 14
prevention trials involving 1,515 people, and reported a small effect for psychological intervention. However, there was no evidence of an effect due to antidepressant drugs. Nevertheless, a
few trials of antidepressant drugs46,47 published afterwards have
shown some benefit of antidepressant drug use. The Cochrane
review of treatment trials identified 16 trials involving 1,655
subjects. Although antidepressant drugs (13 trials) produced improvements in depressive symptoms, it is uncertain whether they
lead to higher rates of remission for depression. The use of antidepressants increases gastrointestinal and central nervous system side effects. There was no evidence for effectiveness of psychological therapies alone for the treatment of PSD.
Therefore, although antidepressants seem to be effective for
the treatment of PSD, the evidence is not robust. Nevertheless,
European48 and American49 guidelines recommend pharmaceutical treatment, such as selective serotonin-reuptake inhibitors
(SSRI) or tricyclic antidepressant drugs for patients with PSD,
along with monitoring for effectiveness and side effects. It is
recommended that treatment be continued for at least 6 months
after initial recovery.

Post-stroke anxiety

and insomnia. Beck Anxiety Inventory, Hamilton Anxiety and Depression Scale, Hospital Anxiety and Depression Scale, and the
General Health Questionnaire-30 have also been used for the
study of post-stroke anxiety.50,51
The prevalence of post-stroke anxiety, with or without PSD, is
higher in hospital settings (acute stroke patients: 28, 1517, and
313%, respectively; stroke survivors: 24, 617, and 311%, respectively) than in community studies (11, 8, and 12%, respectively).26 While one study showed that the prevalence of poststroke anxiety decreased over time (33% at 3 months, 18% at 2
years),22 another study reported no such changes over 3 years
after stroke.52 Post-stroke anxiety tends to last longer when it is
associated with PSD.52 A recent systematic review53 involving 39
cohorts and 4,706 patients showed that 24% of patients with
stroke had anxiety symptoms and 18% had an anxiety disorder
in the first 5 years after stroke.
Because early-onset anxiety is more often associated with
previous psychiatric disorders than late-onset anxiety, it has
been proposed that early-onset anxiety may be a recurrence/exacerbation of a pre-stroke generalized anxiety disorder.51
Although post-stroke anxiety by itself does not influence
functional or cognitive recovery, it is associated with worse social functioning and quality of life. In a systematic review,53 the
quality of life was negatively correlated with anxiety in four of
five cohorts. Patients with post-stroke anxiety and PSD were
worse in activities of daily living at 1- and 2-year follow-ups
than patients with post-stroke anxiety alone.54

Factors associated with post-stroke anxiety

Post-stroke anxiety is closely associated with PSD.53 Early
studies proposed that following left hemispheric strokes, poststroke anxiety with PSD is associated with cortical infarcts. On
the other hand, following right hemispheric strokes, post-stroke
anxiety without PSD is associated with posterior infarcts.55 However, a recent meta-analysis showed that there is no association
between post-stroke anxiety and lesion location.53 Furthermore,
no associations were observed with age and sex. Thus, the factors associated with anxiety in patients with stroke without PSD
remain unknown.

Prevalence and characteristics

Treatment

Post-stroke anxiety disorders have received relatively little attention compared to PSD. The core symptoms of post-stroke
anxiety are excessive anxiousness or worry, and difficulty in controlling worries. Criteria from The Diagnostic and Statistical
Manual of Mental Disorders, Fifth Edition require three or more
of the following in addition to the above symptoms: restlessness,
decreased energy, poor concentration, irritation, nervous tension,

Antidepressant/antianxiety drugs alone or with psycho-behavioral therapy may reduce anxiety symptoms. However, because
there are no randomized, placebo-controlled trials, there is not
enough evidence regarding the management of post-stroke anxiety.56

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Emotional incontinence
Prevalence and characteristics
Since Wilson described patients with uncontrollable outbursts
of involuntary laughing or crying as having pathologic laughing
and crying,57 these abnormal emotional displays have been described using a variety of terminologies: pseudobulbar affect,
emotionalism, lability of mood, emotional incontinence, and involuntary emotional expression disorder.58
Typically, patients show excessive and inappropriate crying or
laughing without apparent motivating stimuli, or in response to
stimuli that would not normally evoke such responses. The episodes are sudden, episodic, and uncontrollable. Although early
reports emphasized the importance of these incongruent or contradictory emotional stimuli, and the unheralded, uncontrollable nature of symptoms,59 recent studies have found that symptoms are more often triggered by appropriate and congruent
stimuli.1,60 Although some authors have distinguished strict
pathological laughing and crying from milder emotional lability,59
more recent studies61,62 have reported that these two conditions
differ in a quantitative rather than a qualitative way. With this
consideration, we will use the broad term post-stroke emotional
incontinence (PSEI) in this article.
The most frequently used diagnostic criteria are those of
House,60 followed by those from Kim.1 In the acute/subacute
stage of stroke, PSEI prevalence has been reported to vary from
6% to 34%.1,60,63-70 The heterogeneous results are due to different diagnostic criteria, the timing of assessment, and characteristics of study populations. There have been few studies that examined the longitudinal course of PSEI. One report indicates that
the prevalence of PSEI is 15% one month post-stroke, 21% at
six months post-stroke, and 11% at twelve months post-stroke.60

Factors and lesion locations associated with PSEI

Severe motor1 and neurologic dysfunction,67,69 lesion location,1,63,70 and the presence of depression1,60,65 are reported to be
related to PSEI. We reported that lesion location (subcortical
area) is the only factor associated with PSEI at the time of admission, whereas functional status, serotonin polymorphisms,
and low social support were related to PSEI at three months
post-stroke.70
Studies using computed tomography and magnetic resonance
imaging have shown that lenticulocapsular71,72 and brainstem lesions72 are closely related to PSEI. We studied 148 patients with
unilateral strokes who were identified using computed tomography and magnetic resonance imaging and found that the anterior cortex-internal capsule/basal ganglia-ventral brainstem circuitry is closely related to PSEI.1 Patients with lesions in the thalhttp://dx.doi.org/10.5853/jos.2016.01144

amus or cerebellum also occasionally exhibited PSEI. Although

this lesion location is similar to that producing PSD, PSEI seems
to be more closely related to subcortical (basal ganglia and pontine) lesions.1

Pathogenesis
Wilson proposed that pathological crying and laughing is
caused by the release (or disinhibition) of a brainstem fasciorespiratory control center for emotional expression secondary to lesions of descending regulatory pathways.57 Previous studies have
described patients presenting with PSEI due to lesions of the
ponto-cerebellar pathway, and hypothesized that the cerebellum
may play a modulatory role and adjust the execution of laughing
or crying to cognitive and situational contexts.73-78 Rabins and
Archinegas79 suggested that a complex cortico-limbic subcortical-thalamic-ponto-cerebellar system contributes to the expression of emotions, and any deficit in this system may lead to PSEI.
Neuroanatomical lesion studies suggest the involvement of
serotonergic fibers,66,80,81 that ascends from the brainstem raphe
nuclei to limbic forebrain structures and then project through
the basal ganglia to the frontal cortex. Furthermore, serotonin
transporter binding ratios in the midbrain and pons regions are
lower in patients with stroke with PSEI than in those without
PSEI.82 Finally, serotonin gene polymorphisms were found to be
related to the development of PSEI.69,70
Other neurotransmitters that may also be involved include dopamine and glutamine, which may have roles in regulating the
influence of the motor cortex on the brainstem laughing/crying
centers.79,83-85 The balance between glutamatergic excitation and
inhibition is in turn modulated by other neurotransmitter systems, such as dopamine, serotonin, acetylcholine, and sigma receptor systems.79 Non-competitive glutamate receptor antagonists, such as dextromethorphan stabilize glutamatergic neurotransmission,86 and have been found to be effective in the treatment of pathological laughing and crying in amyotrophic lateral
sclerosis85 and multiple sclerosis,87 perhaps due to their effect on
sigma-1 receptors. As activation of sigma-1 receptor agonists
increases the serotonergic function of the dorsal raphe nucleus,88
dextromethorphan may also modulate the serotonergic system.

Treatment
A recent Cochran review confirmed that SSRIs are effective in
reducing the frequency and severity of PSEI.89 In five randomized
controlled trials,90-94 SSRI administration was effective in alleviating PSEI. In addition, two randomized controlled trials have
shown that tricyclic antidepressants are effective in treating
PSEI.95,96 In the authors view, SSRIs should be the first option for
PSEI treatment, because they are better tolerated in stroke pahttp://j-stroke.org

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tients and more promptly reduce PSEI symptoms than tricyclic

antidepressants.
There have been small studies that have used the selective adrenergic receptor inhibitors reboxetine,97 venlafaxine,98 mirtazapine,99 and lamotrigine.100 The mechanisms of action of these
agents may involve the direct or indirect augmentation of serotonergic function. As discussed earlier, levodopa and amantadine
may be effective in treating PSEI. Due to limited data, these selective adrenergic receptor inhibitors and dopaminergic drugs
are currently reserved for patients who fail to respond to SSRIs.99
Dextromethorphan/quinidine (Nuedexta, Avanir) is another potentially useful drug for the treatment of PSEI.85,87 Dextromethorphan is a sigma-1 receptor agonist, and adding quinidine sulfate increases the bioavailability of dextromethorphan.

Post-stroke aggression and anger

proneness
Symptom characteristics and prevalence
Stroke patients may show aggressive behaviors including hitting or hurting others, kicking, biting, grabbing, pushing, throwing objects, etc. Their verbal behavior also includes cursing,
screaming, making noises, hostile muttering, etc. This overt aggression is observed usually during the acute stage in patients.
However, simple anger-proneness or inability to control anger
and aggression is a much more commonly observed symptom.
Patients become more irritable, impulsive, hostile, and less tolerable. They easily anger at their spouses and other family members regarding trivial matters.101 Therefore, these symptoms may
be described as post-stroke anger proneness (PSAP).94
The PSAP has been studied using various tools, such as the
Spielberger Trait Anger Scale, Present State Examination, NEO
Personality Inventory Revised, and the Emotional Behavior Index.101-104 PSAP is found to be present in 15-35% of patients
during the acute stage,102,103,105,106 and in 32% of patients in the
subacute stage.101 Although these results are not comparable
due to different study settings and the different diagnostic tools
used, we can at least conclude that anger proneness or aggressiveness is fairly common during both the acute and the subacute stages of stroke.

Associated factors, lesion locations, and

pathophysiology
Studies have shown that motor dysfunction, dysarthria, high
National Institute of Health Stroke Scale scores, previous stroke,
premorbid neuroticism personality trait, history of depression, and
low monoamine oxidase A activity are related to PSAP.101,103,104,106
Kim et al.101 emphasized that PSAP is more closely associated with
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PSEI than PSD and that the distribution of lesion locations associated with PSAP is similar to that of lesions associated with
PSEI (fronto-lenticulocapsular-pontine base area).
Therefore, similar to PSEI, serotonergic dysfunction seems to
play a role in the development of PSAP. Because PSAP is also associated with severe neurologic dysfunction, depression, and a
previous history of stroke, some of the patients anger may be a
manifestation of depression or frustration. Thus, PSAP may be a
multi-factorial phenomenon related to reactive behavioral
changes associated with functional deficits and repeated strokes,
serotonergic dysfunction due to brain damage, or genetic polymorphisms involving monoamine oxidase A.101

Treatment
SSRIs such as fluoxetine107 and citalopram108 are of benefit in
the treatment of aggressive behavior in patients with personality
disorder or dementia. Beta adrenergic antagonists109 and lithium110 may reduce aggressiveness in patients with brain injury.
However, clinical trials in patients with stroke are very rare. In
our double-blinded study, anger scores were significantly reduced after fluoxetine therapy in patients with subacute stroke.94
In the authors more recent study involving 478 patients, escitalopram was effective in the prevention of anger-proneness when
administered during the acute stage.30

Post-stroke fatigue
Symptom characteristics and prevalence
Staub and Bogousslavsky111 defined fatigue in stroke patients
as a feeling of early exhaustion developing during mental activity, with weariness, lack of energy, and aversion to effort. Fatigue
can be further distinguished by its onset: fatigue during the
acute stage vs. chronic, persistent fatigue. It can also be classified based on different constructs: exertion vs. mental fatigue.112
Although there is no fatigue scale that fully considers the
complex nature of PSF, several instruments have been developed
to measure PSF: the Fatigue Assessment Scale,113 the Fatigue Impact Scale,114 the Checklist of Individual Strength,115 the Visual
Analogue Scale,116,117 the Chalder fatigue scale,118 the Multidimensional Fatigue Symptom Inventory,119 and the Fatigue Severity Scale.12,116,117,120-122
The prevalence of PSF ranges from 23% to 75%.112 This wide
range is attributable to differences in the definition of PSF, the
time elapsed since stroke, and the characteristics of patients. In
a systematic review of nine longitudinal cohort studies, the authors reported that the prevalence of fatigue decreased with
time after stroke in seven studies, but increased in two studies.123

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Factors associated with post-stroke fatigue

Neurologic deficit is one of the most important factors related
to PSF.12,13,119,124,125 However, the association may at least in part
be attributed to associated depression. Studies have shown that
the significant association between disability and PSF in the
subacute state is lost after controlling for the effects of depression during the chronic stage.14,126 Medical co-morbidities such
as hypertension,127 medications such as sedative drugs128 or antidepressants,129,130 decreased appetite,12 and sleep disturbances,122,125,131-136 may result in PSF. In addition, post-stroke pain,133,137,138
and pre-stroke fatigue have been found to be associated with
PSF.12,122,124,128,130,139
Although patients with PSF are often depressed,12,111,114,121,122,132,140
many PSF patients do not have depression.12,13,111,114,115,118,124 Although one study reported an association between PSF and suicidality,141 PSF patients rarely express worthlessness and hopelessness. The impact of depression on PSF may differ according
to the stage of stroke. While neurologic disability leads to exertional fatigue during the early stage of stroke,14 depression seems
to play a more important role in chronic and mental fatigue.142,143
Thus, depression may be a factor in prolonged fatigue.134 Impairments in some domains of cognition, such as attention deficits,14
slow mental processing,15,144,145 and memory dysfunction,15 seems
to be associated with mental fatigue.
Studies have shown that PSF is related to damage to the medial prefrontal cortex,146 basal ganglia,121 and the brainstem/thalamic reticular formation.111,147,148 This suggests that alterations in
neurotransmitters such as dopamine or adrenaline may lead to
PSF.147,148 However, more recent MRI-based studies have found
no association between PSF and lesion location.12,114,115,119,143,149
Chronic inflammation and altered immune responses after stroke
may also be involved in PSF.150

Treatment
A double-blinded placebo-controlled trial involving 83 patients with PSF showed that fluoxetine was not effective in improving PSF.116 Another study showed that duloxetine, citalopram, and sertraline did not relieve PSF.151 Thus, SSRIs may not
be effective for PSF. Modafinil, a drug originally used for patients
with hypersomnia or narcolepsy, was used in a recent randomized, placebo-controlled trial.152 Forty-one patients were treated
with either 400 mg modafinil or placebo. There was no difference in the primary outcomes or Multidimensional Fatigue Inventory-20 general fatigue scores 90 days post-stroke. However,
modafinil improved PSF, as measured by the Fatigue Severity
Score, a secondary outcome (P = 0.02). Thus, more studies are
needed to confirm the efficacy of modafinil as a treatment for
PSF. The neurobiochemical effects of modafinil remain unclear. It
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may affect dopamine and norepinephrine transporters. It is also

known to have some effects on the serotonin, glutamate, orexin,
and histamine systems.153

Summary
Post-stroke mood and emotional disturbances are common
and manifest in diverse manners. The phenomenology, predicting
factors, pathophysiology, and response to pharmacological treatments are different, although there are also factors that are in
common. PSD appears to be associated with complex pathophysiological mechanisms involving both psychological/psychiatric problems associated with patients functional deficits and
neurochemical changes secondary to brain damage. Therefore,
although antidepressants, and especially SSRIs, are considered to
be the management options of choice, their benefits are not robust. It remains uncertain whether pharmacological treatment in
stroke patients is needed to prevent PSD or perhaps to improve
neurological outcomes.
PSEI is more closely associated with lesion location and consequent alterations in neurotransmitters, notably serotonin. Thus,
PSEI tends to respond more to SSRIs compared to PSD. Although
PSAP is also a complex phenomenon, it seems to have better responsiveness to SSRIs than PSD. PSF is a common and disabling
symptom. Although PSF is closely associated with PSD, it is also
causally related to multiple factors, including functional impairment, co-morbid diseases, and perhaps, multiple neurotransmitter changes. Thus, the benefits of pharmacological therapy are
unproven, and treatment may have to be individualized according to the causative factors present in each patient. Adrenergic/
dopaminergic drugs such as modafinil may be used in some patients.
Recognizing these emotional disturbances is important because they are often treatable. Proper management may improve
patients quality of life in a prolonged manner, even after the
cessation of treatment.154 Undoubtedly, more research is needed
to improve the management of post-stroke mood and emotional
disturbances.

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