Volume 46 & Number 3 & June 2014 135

Screening, Diagnosis, and Treatment of

Post-Stroke Depression
Kimberly Dwyer Hollender

ABSTRACT
Depression is a common finding after an acute stroke and often interferes with the ability of the patient to
participate in the rehabilitation process. A literature review was conducted to investigate the potential
benefit of the early administration of antidepressant medication on the rate of depression after acute stroke.
Current practices for screening and diagnosing post-stroke depression (PSD) were also reviewed.
MEDLINE, CINAHL, Cochrane Library databases, and PsychInfo were searched for relevant articles
published in English up to August 2012. One of the challenges identified was that although several studies
suggest benefit to the addition of antidepressant medication, little consistency exists in the timing of the
intervention, particularly in regards to rehabilitation. Although patients reporting fewer depressive
symptoms have been shown to have higher levels of participation in post-stroke therapy, conclusions
regarding the benefit of early intervention cannot be made at this time. However, several studies do suggest
that, in addition to the benefit of treating PSD, different classes of antidepressant medication may actually
facilitate the neural mechanisms of recovery in patients with stroke. Overall, although the current available
research cannot recommend the routine administration of antidepressant medication for PSD, the current
research can support the administration of this pharmaceutical intervention on an individual basis. Future
research needs surrounding PSD are vast, and several questions need to be addressed before focusing on
the timing and benefit of early intervention including developing a universally validated screening tool,
developing a definitive definition, and establishing acceptable treatment recommendations. Once these topics
are further explored, the potential for antidepressants to improve neural mechanisms of recovery can also
be further investigated.

Keywords: antidepressants, depression, post-stoke depression, stroke

S
troke is currently one of the leading causes of
disability in the United States, leaving approx-
imately 15%Y30% of survivors permanently dis-
abled. Among post-stroke survivors, approximately 20%
will require institutional care at 3 months after stroke,
further contributing to the social isolation of the pa-
tient and increasing the healthcare burden (Creutzfeldt,
Holloway, & Walker, 2012). Complicating the rehabil-
itation from stroke, studies indicate that post-stroke
depression (PSD) may affect up to one third of stroke
survivors (Creutzfeldt et al., 2012). Therefore, early
intervention in this population would be ideal if anti-
depressants were effective in preventing or diminish-
ing the effects of depression. Although it is well known
that the incidence of depression increases with age and
Questions or comments about this article may be directed to
Kimberly Dwyer Hollender, MSN APN ACNP-BC CCRN, at kimk
.dwyer@gmail.com. She is a Stroke Nurse Practitioner at Robert
Wood Johnson University Hospital, New Brunswick, NJ.
At the time this article was written, the author was a Graduate
Nursing Student at the University of Medicine and Dentistry of
New Jersey, Stratford, NJ.
The author declares no conflicts of interest.
Copyright B 2014 American Association of Neuroscience Nurses
DOI: 10.1097/JNN.0000000000000047
disability, in stroke survivors, the risk of depression may
be almost doubled compared with the general popu-
lation (Ayerbe, Ayis, Rudd, Heuschmann, & Wolfe,
2011). In fact, Ayerbe et al. indicate that, although the
persistent frequency may be approximately 30%, as
many as half of post-stroke survivors may experience
depression at some point within a 5-year period. Al-
though this review found little evidence addressing the
timing of the intervention in regards to rehabilitation,
several questions were identified that will be essential
to further exploring this topic. These questions include
what effect PSD may have on stroke recovery, how to
best screen for PSD, and what treatment options exist
to address this common and debilitating obstacle for
post-stroke survivors.
The term PSD is currently broadly defined and re-
fers to the development of depression after a stroke,
usually an acute ischemia stroke. At this time, diag-
nosis can be made by the measurement of depressive
symptoms measured with different screening tools
or be diagnosed specifically via interviews by trained
professionals (Koewenhoven, Kirkevold, Engedal, &
Kim, 2012). Although the specific definition and iden-
tification of PSD varies among the available research,
depression characterized by persistent low mood of
duration greater than 2 weeks is utilized here. This is

Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
136 Journal of Neuroscience Nursing
most similar to the Diagnostic and Statistical Manual
of Mental Disorders-Fourth Edition definition for minor
depression that requires the presence of two to four
depressive symptoms during a 2-week period and re-
quires one of these symptoms to be either depressed
mood or loss of interest in pleasure (Hackett, Anderson,
House, & Halteh, 2008). The pathophysiology of PSD
is multifactorial and may be influenced by location
and extent of brain injury, vascular comorbidities, and
reaction to new functional disability (Husseini et al.,
2012). Ultimately, depressive symptoms may be caused
by both the ischemic brain injury in addition to a psy-
chological reaction to the illness. The PSD may also
be difficult to differentiate from grief in post-stroke
survivors, as many will experience a grieving process
in the first weeks after stroke as survivors are coping
with the consequences of experiencing a potentially
life-threatening event. During this time, stroke survivors
may be recovering and coping from disabling conse-
quences of stroke, and their presentation and diagno-
sis of PSD may vary related to the time of evaluation
after initial insult (Hackett, Anderson, House, & Halteh,
2008). In Koewenhoven et al., having a stroke is de-
scribed as a ‘‘small death’’ or personal catastrophe that
may initiate both normal grieving processes and/or pro-
gression to depressive symptoms.
In the primary care setting, depression is a common
and often misunderstood condition that is frequently un-
derdiagnosed and undertreated (Gelenberg & Hopkins,
2007). Therefore, the additional burden of identifying
depression in the post-stroke population may further
complicate diagnosis and treatment. As mentioned, it
is important to differentiate depression from sadness
and from grief. Sadness has a cause, is a finite state,
and is often an emotion that is not experienced by those
with depression (Gelenberg & Hopkins, 2007). Al-
though grief may at times seem similar to depression,
a distinguishing factor is that grief does not blur one’s
sense of self. Most importantly, throughout this re-
view, sadness has not been directly related to lack of
motivation required to actively participate in the reha-
bilitation process. Furthermore, PSD has been shown
to reduce quality of life and has even been linked to
increased mortality (Ayerbe et al., 2011; Dennis,
O’Rourke, Lewis, Sharpe, & Warlow, 2000).
Several symptoms associated with PSD have been
associated with reduction in quality of life and have
been known to interfere with stroke recovery, includ-
ing alterations in weight and appetite, disturbed sleep
patterns, loss of energy, sense of worthlessness, sui-
cidal ideation, anhedonia, psychomotor retardation,
and/or agitation (Graven et al., 2011). Depression may
also reduce both the capacity and desire to participate
in rehabilitation as well as reduce the desire to social-
ize and ‘‘rejoin’’ society. Depression independent of
Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
Diagnosis and treatment of
depression, often underdiagnosed
and undertreated in primary
care settings, can be even more
complicated in individuals
who have experienced a stroke.
stroke is one of the top causes of disability globally, and
patients are among the highest utilizers of healthcare
and generally perform poorly in the work environ-
ment (Gelenberg & Hopkins, 2007). Furthermore,
depression increases mortality, worsens preexisting
medical conditions including cardiovascular disease
and diabetes, and ultimately, may lead to suicide
(Gelenberg & Hopkins, 2007). For this reason, all
patients with depression, whether they have experienced
stroke, should be asked directly about suicidal idea-
tions. Because no progress toward rehabilitation is made
because of lack of motivation caused by depressive
symptoms, lack of improvement and lack of sociali-
zation may further decrease this motivation, which often
continues a dangerous self-destructive cycle. This fur-
ther highlights why interventions to break this cycle
are an important element of post-stroke recovery.
Among stroke survivors diagnosed with PSD, de-
gree of physical disability, stroke severity, and cogni-
tive impairment were consistently associated with higher
rates of depression (Hackett & Anderson, 2005). Be-
cause almost 20% of post-stroke survivors require in-
stitutional care at 3 months after stroke, social isolation
may also contribute to PSD (Herrmann et al., 2011).
This is consistent with Herrmann et al.’s observation
that the most severe strokes often lead to greater func-
tional handicap, longer hospital stays, and an increased
need for institutional care contributing to greater inci-
dence of depression. In addition, a strong association
with severe stroke and depression may be because of
an association between cognitive impairment and de-
pression. This relationship is complex as both can be a
cause or an effect of each other (Ayerbe et al., 2011).
This potentially causal relationship will become a fac-
tor concerning future research topics and, possibly, fu-
ture treatment options.
As mentioned, the complexity and lack of knowl-
edge differentiating the normal grieving process from
PSD contributes to the challenge of early identifica-
tion. In addition, other obstacles exist including lack
of consistency of screening tools, common distur-
bances of language and cognition after stroke, change

in emotional and behavioral cues related to infarct lo-
cation, lack of knowledge of care providers, and social
stigma associated with depression (Hackett, Anderson,
House, & Xia, 2008). According to Herrmann et al.
(2011), ‘‘in the absence of active screening, depression
in acute stroke patients is underrecognized and under-
treated’’ (p. 1198). Because pressure exists to reduce
length of stays in hospitals, many patients with stroke
are also being discharged before the diagnosis of PSD.
Interestingly, patients with stroke were more likely to
be diagnosed with depression and receive a psychiatric
consultation and an antidepressant if they were treated
on a specialized stroke unit. More importantly, Hackett
and Anderson (2005) state that current tools to identify
depression after stroke are not accurate as they have
not been rigorously developed and validated. Many
studies also exclude patients with communication prob-
lems, cognitive loss, or previous psychiatric illness be-
cause of difficulty in completing a validated screening
tool. Hackett, Anderson, House, and Xia (2008) de-
scribe that, as most patients after stroke are at increased
age and frequently experience neurological impair-
ments, including aphasia, the fact that up to half of all
survivors of stoke are excluded limits the external valid-
ity of results in many studies. Furthermore, in addition
to disturbances of language and cognition, behavioral
cues such as slowness, reduced appetite, and loss of
facial expression may be misleading in the diagnoses
of abnormal mood. In their review of trials addressing
interventions to prevent depression after stroke, Hackett,
Anderson, House, and Halteh (2008) identified that
the Hamilton Depression Scale is the most commonly
used screening tool. However, in the 14 trials reviewed,
12 different assessment scales were used to diagnose
depression.
Before determining if early invention in this pop-
ulation is indicated, there must first be a validated
screening tool to establish early risk or diagnosis. Al-
though several different studies utilized different screen-
ing tools, Ginkel et al. (2012) specifically looked at the
nine-item patient health questionnaire (PHQ-9) and the
two-item patient health questionnaire (PHQ-2). These
two screening tools were compared with the Compos-
ite International Diagnostic Interview, which has shown
to have good diagnostic reliability in the diagnosis of
depression. Ultimately, the researchers report that the
PHQ-9 and PHQ-2 had acceptable diagnostic value;
however, the greatest flaw with this screening tool is
that it relies heavily on good verbal communication.
The authors recommend that all patients with stroke
receive screening via the PHQ-2 followed by the PHQ-9,
if results are positive. The PHQ-2 specifically ad-
dresses mood and anhedonia. In a larger study con-
ducted in 2009, investigators looked at three different
scales including the Beck Depression Inventory (BDI),
Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
Volume 46 & Number 3 & June 2014 137
the Hamilton Rating Scale for Depression, and the
Clinical Global Impression assessment by professionals
(Berg, Psych, Lonnqvist, Palomaki, & Kaste, 2009).
Overall, the authors noted there to be little variability
in the feasibility of the different scales. Interestingly,
professionals using the CBI tool often over scored pa-
tients as depressed (Berg et al., 2009). The study also
revealed that the BDI had better sensitivity, whereas
the Hamilton Rating Scale for Depression had a higher
specificity. Of the BDI items, ‘‘discouraged about the
future’’ was the best discriminator of depression (Berg
et al., 2009). The other items in the BDI correlated
with the timing of the screening. At the 3-month
screening, ‘‘feeling like a failure,’’ ‘‘feeling guilty,’’ and
‘‘looking unattractive’’ were the most important discrim-
inators (Berg et al., 2009). Whereas at the 18-month
screening, ‘‘sadness,’’ ‘‘dissatisfaction,’’ ‘‘feeling dis-
appointed,’’ and ‘‘loss of interest in people’’ all cor-
related best with a diagnosis of depression (Berg et al.,
2009). Finally, the researchers also looked at the
Visual Analogue Mood Scale among patients with apha-
sia and other cognitive impairments and ultimately found
that Visual Analogue Mood Scale was not a reliable
tool in screening for depression (Berg et al., 2009).
As stated, one of the greatest challenges of screen-
ing for depression in the post-stroke population are the
common communication problems present after the
event. In fact, aphasia may affect between 20% and 38%
of stroke survivors (Townend, Brady, & McLaughlan,
2007). Aphasia is usually associated with left-hemisphere
damage and may include difficulty understanding lan-
guage, producing language, reading, writing, and
performing numerical skills (Townend et al., 2007).
Patients with left-hemisphere damage are more likely
to retain emotional awareness and therefore are likely
at greatest risk of extreme emotional reactions, includ-
ing depression (Townend et al., 2007). Because com-
pleting a screening tool based on traditional language
would be a challenge, many studies have utilized adap-
tive methods. These have included using informants,
clinical observation, modifying questions, and modi-
fying timing of interviews or using visual analogue
scales (Townend et al., 2007). Of these adaptive tech-
niques, the use of informants including family, nurses,
and adjunct staff was the most common followed by
clinical observation. At this time, there is very little in-
formation regarding the validity and reliability of these
techniques. Many studies failed to identify the actual
procedure used to modify the existing screening tool
and failed to describe how informants or clinicians were
trained in the screening process.
Factors influencing undertreatment of depression
in the general U.S. population include racial and eth-
nic disparities in the use of psychiatric resources,
financial stress, lack of health insurance coverage,
138 Journal of Neuroscience Nursing
and the presence of concurrent medical conditions
(Husseini et al., 2012). In their study of the frequency
of antidepressant use for PSD, Husseini et al. deter-
mined that only a minority of patients with depression
taking antidepressants continued to have depressive
symptoms (G2%). Interestingly, the study also revealed
that there was no association between lack of antide-
pressant use and age, gender, race, living situation, med-
ication insurance status, and follow-up care (Husseini
et al., 2012). On the other hand, persistent depression
at 12 months was associated with younger age, poor
functional outcome, female gender, non-White race,
and inability to work. Overall, the study found that over
two thirds of patients with transient ischemic attack
and stroke with PSD were not treated.
After reviewing much of the available literature,
the two most commonly studied pharmacological in-
terventions to treat PSD were either selective serotonin
reuptake inhibitors (SSRIs) or tricyclic antidepressants
(TCAs). The SSRIs have been found to be the most
tolerated antidepressants in the general population,
and they selectively block serotonin reuptake at the
presynaptic nerve terminal; however, each SSRI may
differ in their pharmacokinetics (Khawam, Laurencic,
& Malone, 2006). Before reporting their research find-
ings in 2005, Murray et al. found that only a few short-
term randomized control trials existed for the use of
antidepressants in patients with stroke. These small
trials included short-term trials of nortriptyline, citalo-
pram, and fluoxetine that showed conflicting findings.
In their 28-week study, Murray et al. assessed the ef-
fects of sertraline, an SSRI, on patients 18 years old or
older who developed depression within 12 months of
stroke. Although all patients initially had to present
to an acute care facility, depression was assessed
on an outpatient basis and was confirmed using the
MontgomeryYAsberg Depression Rating Scale. In
fact, only 15% of the included patients in the trial were
still in the hospital and begun treatment at a mean of
17 days after stroke. Because the other 85% of par-
ticipants had a mean interval of treatment intervention
at 147 days, conclusions regarding ‘‘early’’ interven-
tion cannot be made from this study (Murray et al.,
2005). The study was conducted in four different
stroke centers throughout Sweden, and participants
received either sertraline 50 mg or placebo once a day
for 4 weeks and then were increased to two capsules
after the fourth week. To continue the trial, the par-
ticipants then had to have a decrease of at least 20%
from the baseline MontgomeryYAsberg Depression
Rating Scale score. Whereas the antidepressant out-
come did not differ between the sertraline and placebo
group at the end of 26 weeks, quality-of-life scores
were significantly higher in the sertraline group and
a decrease in emotionalism and hostility was noted
Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
(Murray et al., 2005). Interestingly, the outcome for
sertraline was numerically better but not statistically
different from the placebo (p G .1) at the 26th week
of the trial (Murray et al., 2005). However, the quality-
of-life scores as measured by the Visual Analog Scale
Technique was statistically better than the placebo
group (p G .05) and correlated with the Emotional
Distress Scale (Murray et al., 2005). Performance in
activities of daily living (ADLs) and improvements
in neurological deficit were measured but showed no
statistical improvement in this study.
Because sertraline was found to improve emotion-
alism and feelings of hostility after stroke, fluoxetine,
another SSRI, was also found to have similar results
in a study by Choi-Kwon et al. In this study, it was
found that, although fluoxetine did not significantly
improve symptoms of PSD, fluoxetine did improve
symptoms of post-stroke emotional incontinence and
anger proneness in the treatment group. Two other
measures including excessive inappropriate laughing
and excessive inappropriate crying were also assessed,
and the treatment group was found to have an im-
provement in inappropriate laughing (p = .089) at the
3-month mark (Choi-Kwon et al., 2006). Because
improvement of these symptoms may correlate with
improved quality of life, this is an important finding.
Furthermore, as these symptoms were significantly re-
lieved by an SSRI, this suggests that these emotional
disturbances are related to serotonergic dysfunction,
whereas PSD may not necessarily be caused from the
same dysfunction (Choi-Kwon et al., 2006). Again,
although this study presents important findings regard-
ing treatment options of PSD, the intervention began
in an average of 14 months after the onset of stroke
and, therefore, cannot necessarily be analyzed for an
early intervention potential (Choi-Kwon et al., 2006).
Finally, as identified by Ried et al. (2011) in a study
of both prestroke and PSD, whereas PSD was asso-
ciated with earlier mortality, post-stroke SSRI treat-
ment was associated with longer survival. The most
important takeaway from this study, however, was that
SSRIs must be resumed after stroke if the patient had
been managed for depression with this medication.
Because these previous studies were unable to prove
a strong correlation between SSRIs and treatment of
PSD specifically, another antidepressant option of
consideration is noradrenaline reuptake inhibitors.
In a study of the noradrenaline reuptake inhibitor,
reboxetine, authors specifically focused on a subset
of patients with PSD classified as ‘‘retarded’’ de-
pressed (Rampello et al., 2005). Essentially a retarded
depression is a state of clinical depression in which
the individual is lethargic rather than anxious and char-
acterized by restlessness. The authors report that a
reduction in the BDI and Hamilton Depression Scale

was observed in both the treatment and placebo
groups; however, the reduction in the group treated
with reboxetine was the only statistically significant
change (Rampello et al., 2005). Furthermore, a statis-
tically significant variation was noted in the reboxetine
group with respect to improvement in the synoptic
table and the ‘‘retarded’’ symptomatological cluster
(Rampello et al., 2005). Importantly, although these
findings may have future treatment implications, au-
thors note that, currently, there is no reliable biological
marker to differentiate between anxious and retarded
depression, and this distinction is largely dependent on
the practitioner. In relation to timing of the interven-
tion, participants were again assessed on an outpatient
basis and were required to have had a stroke within
12 months. Therefore, generalization to an acute in-
patient population and assessment of early interven-
tion to rehabilitation could not be determined.
Because all pharmacological interventions carry dif-
ferent risks of potential serious adverse reactions, it is
important to explore nonpharmacological interventions.
For treatment of depression independent of stroke, a
combination of psychotherapy and antidepressants has
been found to be superior to either treatment option
independently (Gelenberg & Hopkins, 2007). In 2007,
a group of authors explored whether motivational in-
terviewing could help build a patient’s motivation to
adjust and adapt to having had a stroke and its residual
deficits. Motivational interviewing is a specific talk-
based therapy originally designed to help with addic-
tions; however, it has recently been adapted to target
health problems related to poor motivation (Watkins
et al., 2007). The authors identified that patients with
depression may lack motivation to participate in reha-
bilitation and therefore could potentially benefit from
this intervention. Interestingly, although they were
unable to prove a correlation between the effect of
motivational interviewing on either function or expec-
tations of recovery, they did prove that motivational
interviewing has a beneficial effect on patient’s mood
(p = .03) and a protective effect against depression
(p = .03; Watkins et al., 2007). This improvement
was made after four sessions of motivational inter-
viewing, and authors suggest that other healthcare
providers under supervision may integrate this type
of therapy into ‘‘normal’’ conversation (Watkins et al.,
2007). This study was conducted in an acute post-
stroke population, and patients typically started the
intervention between 2 and 4 weeks after stroke. Al-
though this study did not find this intervention to im-
prove function, this intervention does warrant further
investigation as it could potentially be used as a pre-
vention method for the development of depression.
In a 2008 systemic review, Hackett, Anderson,
House, and Xia noted that, in the 12 antidepressant
Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
Volume 46 & Number 3 & June 2014 139
interventions reviewed, there was evidence of bene-
ficial effect of antidepressants on reduction in mood
scores and no evidence that antidepressants improved
cognitive function. Furthermore, these authors con-
cluded that, in the reviewed studies, there was no evi-
dence that pharmacotherapy improved ADLs or reduced
disability (Hackett, Anderson, House, & Xia, 2008).
An important point noted in their review was that, in
most pharmacotherapy trials, a therapeutic dose of the
antidepressant medication was not always given for
an adequate period. Therefore, a common flaw was
that maximal or sustained responses to antidepressant
medication for PSD could not be assessed (Hackett,
Anderson, House, & Xia, 2008). In addition to a re-
view of pharmacotherapy interventions, this same study
also reviewed available trials regarding psychotherapy
to treat PSD. Consistent with the findings from Watkins
et al. (2007), no significant findings exist in the current
research to support the use of psychotherapy to treat
PSD. The authors recommend that future psychother-
apy trials should focus on adherence to a therapeutic
model and therapist’s characteristics. Finally, Hackett,
Anderson, House, and Xia (2008) express concern
that, in their review of trials for the prevention of PSD,
randomization of patients ranged from several days to
7 months, and after 6 months, interventions could
hardly be considered preventive. These authors also
point out that patients in the acute phase and patients
who survive long term will likely present with different
psychological challenges.
Although several studies have looked at antide-
pressants solely for the treatment of PSD, some re-
searchers suspect that antidepressants may also improve
outcomes of stroke itself (Burns & Greenberg, 2010).
Potentially, three different mechanisms including pro-
tection against acute ischemic neuronal injury, increased
ischemia-induced neurogenesis, and enhanced brain
repair may influence stroke outcomes (Burns &
Greenberg, 2010). Although the mechanisms remain
undetermined, both TCAs and SSRIs have reduced
ischemic injuries when given before forced cerebral
ischemia in animal studies (Burns & Greenberg, 2010).
Other animal studies have indicated that treatment of
depression with both nonpharmacological and phar-
macological agents has contributed to neurogenesis in
the hippocampus of rodents (Burns & Greenberg, 2010).
Finally, rodent studies with fluoxetine showed improve-
ments in vision after being exposed to monocular vi-
sual deprivation, potentially indicating a function of
neurorepair (Burns & Greenberg, 2010). Supporting
this hypothesis that antidepressants may influence
stroke recovery independent of depression, Mikami
et al. (2011) found that fluoxetine or nortriptyline
significantly improved Modified Rankin Scale (MRS)
scores. The MRS measures functional disability after
140 Journal of Neuroscience Nursing
stroke. These findings have important implications for
future research in the use of antidepressant medica-
tion in the stroke population beyond the treatment of
depression.
Side effects of antidepressants are vast and differ
greatly between the different classes available. In a
study conducted in 2007, researchers surveyed both
patients and practitioners regarding the most impor-
tant factors regarding selection of an antidepressant
(Gardner, MacKinnon, Langille, & Andreou, 2007).
As expected, the most important differentiating factor
was common medication side effects (Gardner et al.,
2007). The remaining top ranked factors included pre-
cautions, physician experience, and problems with
discontinuing the medication (Gardner et al., 2007).
Most interestingly, physicians ranked cost as the sec-
ond most important factor, whereas patients ranked
this factor at number 12. As mentioned, SSRIs have
had the greatest levels of tolerability in the general pop-
ulation and most often are associated with nausea and
mild headache (Gelenberg & Hopkins, 2007). De-
creased libido and difficulty achieving orgasm have
also been noted to be persistent problems. However,
depression may also affect sexual desire and perfor-
mance, and differentiation may be difficult (Khawam
et al., 2006). Most importantly, however, SSRIs may
increase the risk of bleeding in the elderly population
and may cause hyponatremia (Gelenberg & Hopkins,
2007). This is because of SSRIs inhibiting platelet
function and disorders may range from bruising to
gastrointestinal bleeding (Khawam et al., 2006). There-
fore, caution should be used with regard to hemorrhagic
strokes. Other potential side effects include anorexia
early in treatment, gastrointestinal disturbances (nau-
sea, vomiting, and diarrhea), sedation or insomnia, and
serotonin syndrome (Khawam et al., 2006). The TCAs
also have many potentially dangerous side effects in-
cluding anticholinergic side effects, sedation, cardiac
effects, and weight gain. Furthermore, TCAs have many
significant potential drug interactions including phe-
nytoin, valproic acid, and carbamazepine (Khawam
et al., 2006). Because most strokes occur in the elderly
population, special considerations should be made be-
fore initiating antidepressant therapy. Because of phys-
iological changes, medication doses may need to be
adjusted, and extreme caution should be used with
polypharmacy (Khawam et al., 2006). If TCAs are to
be administered, low doses should be started first be-
cause of increased potential for orthostatic hypoten-
sion and fall incidence. Finally, all antidepressants
may increase the risk of suicidal thoughts, particularly
in the adolescent population.
Several limitations have been identified in the diag-
nosis and treatment of PSD as mentioned above. In
addition to the obvious limitations associated with the
Copyright © 2014 American Association of Neuroscience Nurses. Unauthorized reproduction of this article is prohibited.
potential deficits after stroke, many limitations exist
throughout the available research. As identified by
Hackett, Anderson, House, and Xia (2008) and Hackett,
Anderson, House, and Halteh (2008) many studies
of the use of pharmacotherapy include short duration
of many interventions, variations in types of partic-
ipants, differences in the methods used to diagnosis
PSD, lack of measureable end points, poor design, and
poor interpretation of results. Many trials that were
identified were also small and lacked the ability to be
generalized to a wider population. Dropout rates and
lack of true randomization of trials also weaken the
available research. Whereas potential side effects of
pharmacotherapy have been reviewed here, few studies
reported adverse events making it difficult to fully
assess the benefits and risks of pharmacotherapy op-
tions. Hackett, Anderson, House, and Xia (2008) also
identified that, in psychotherapy trials, one of the
greatest challenges was adequate training of profes-
sionals in the delivery of the intervention and consistency
of this delivery. Furthermore, another challenge in com-
paring various studies is that there is large variety in the
timing of the screening and intervention as described.
Finally, although a wide range of different screening
tools are utilized in the available research, differences
in the definition and diagnosis of PSD are vast.
Because stroke and depression independently con-
tribute greatly to disability worldwide, it is fair to state
that depression after stroke compounds this burden to
the patient, community, and population. Although it is
known that PSD is largely underdiagnosed and under-
treated, few facilities have implemented screening pro-
grams, and the gold standard of treatment remains
largely undetermined. The first step in improving iden-
tification and diagnosis would be the agreement of a
specific and universal definition of PSD, followed by
the identification of the best screening tool. Because
communication difficulties after stroke are common
and contribute to the risk of PSD, focus must also be
made to create a valid and specific tool for screening
in this population. Because speech and swallow thera-
pists often interact with post-stroke patients to evalu-
ate both swallowing and communication difficulties,
these professionals should be involved in the devel-
opment of screening in aphasic patients. Until an ac-
curate screening tool is identified, it would be difficult
to promote the need for bedside evaluation among
nursing and care providers. Once a best practice screen-
ing method is identified, focus may fully take place on
treatment options. Because this literature review ini-
tially sought to investigate the benefit of early inter-
vention on PSD in relation to rehabilitation, no studies
were found that specifically addressed this topic, and
few studies focused on early intervention in the acute
care patient population. Instead, focus turned to the

best potential treatment options for PSD available in
the current research. Although SSRIs seem to have the
greatest potential in the treatment of PSD, further re-
search needs to focus on the risk to benefit ratio of this
intervention. Although several studies have suggested
that antidepressants may improve mood, mixed evidence
exists to affirm that treatment with antidepressants im-
proves participation in rehabilitation and improvement
in ADLs. Further exploration of other antidepressants
remains largely open. Timing of therapy, duration of
therapy, and contraindications to therapy will all be
needed areas of further research. In the general popu-
lation with depression, a combination of both psycho-
therapy and pharmacotherapy has been recommended
over one intervention independently. Although no stud-
ies were identified at this time that assessed the com-
bination of these therapies, it is likely that a combination
approach may also benefit this population. As evident
throughout this review, vast opportunities exist for
future research regarding PSD to adequately under-
stand and further intervene to treat this debilitating
consequence of stroke.
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