Journal of Neuroscience Nursing:
Screening, Diagnosis, and Treatment of Post-Stroke Depression
Dwyer Hollender, Kimberly
Questions or comments about this article may be directed to Kimberly Dwyer Hollender, MSN APN ACNP-BC CCRN, at firstname.lastname@example.org. 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.
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.
Stroke is currently one of the leading causes of disability in the United States, leaving approximately 15%–30% of survivors permanently disabled. Among post-stroke survivors, approximately 20% will require institutional care at 3 months after stroke, further contributing to the social isolation of the patient and increasing the healthcare burden (Creutzfeldt, Holloway, & Walker, 2012). Complicating the rehabilitation 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 antidepressants were effective in preventing or diminishing the effects of depression. Although it is well known that the incidence of depression increases with age and disability, in stroke survivors, the risk of depression may be almost doubled compared with the general population (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. Although 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 refers to the development of depression after a stroke, usually an acute ischemia stroke. At this time, diagnosis 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 identification of PSD varies among the available research, depression characterized by persistent low mood of duration greater than 2 weeks is utilized here. This is 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 requires 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 psychological 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 consequences of stroke, and their presentation and diagnosis 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 described as a “small death” or personal catastrophe that may initiate both normal grieving processes and/or progression to depressive symptoms.
In the primary care setting, depression is a common and often misunderstood condition that is frequently underdiagnosed 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). Although 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 review, sadness has not been directly related to lack of motivation required to actively participate in the rehabilitation 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, including alterations in weight and appetite, disturbed sleep patterns, loss of energy, sense of worthlessness, suicidal 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 socialize and “rejoin” society. Depression independent of 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 environment (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 ideations. Because no progress toward rehabilitation is made because of lack of motivation caused by depressive symptoms, lack of improvement and lack of socialization may further decrease this motivation, which often continues a dangerous self-destructive cycle. This further highlights why interventions to break this cycle are an important element of post-stroke recovery.
Among stroke survivors diagnosed with PSD, degree of physical disability, stroke severity, and cognitive impairment were consistently associated with higher rates of depression (Hackett & Anderson, 2005). Because almost 20% of post-stroke survivors require institutional 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 functional handicap, longer hospital stays, and an increased need for institutional care contributing to greater incidence of depression. In addition, a strong association with severe stroke and depression may be because of an association between cognitive impairment and depression. 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 factor concerning future research topics and, possibly, future treatment options.
As mentioned, the complexity and lack of knowledge differentiating the normal grieving process from PSD contributes to the challenge of early identification. In addition, other obstacles exist including lack of consistency of screening tools, common disturbances of language and cognition after stroke, change in emotional and behavioral cues related to infarct location, 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 undertreated” (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 problems, cognitive loss, or previous psychiatric illness because of difficulty in completing a validated screening tool. Hackett, Anderson, House, and Xia (2008) describe that, as most patients after stroke are at increased age and frequently experience neurological impairments, including aphasia, the fact that up to half of all survivors of stoke are excluded limits the external validity 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 population is indicated, there must first be a validated screening tool to establish early risk or diagnosis. Although several different studies utilized different screening 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 Composite 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 addresses mood and anhedonia. In a larger study conducted in 2009, investigators looked at three different scales including the Beck Depression Inventory (BDI), 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 patients 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 discriminators (Berg et al., 2009). Whereas at the 18-month screening, “sadness,” “dissatisfaction,” “feeling disappointed,” and “loss of interest in people” all correlated best with a diagnosis of depression (Berg et al., 2009). Finally, the researchers also looked at the Visual Analogue Mood Scale among patients with aphasia 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 screening 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 language, 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, including depression (Townend et al., 2007). Because completing a screening tool based on traditional language would be a challenge, many studies have utilized adaptive methods. These have included using informants, clinical observation, modifying questions, and modifying timing of interviews or using visual analogue scales (Townend et al., 2007). Of these adaptive techniques, 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 information 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 ethnic disparities in the use of psychiatric resources, financial stress, lack of health insurance coverage, 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. determined that only a minority of patients with depression taking antidepressants continued to have depressive symptoms (<2%). Interestingly, the study also revealed that there was no association between lack of antidepressant use and age, gender, race, living situation, medication 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 interventions 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 findings 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, citalopram, and fluoxetine that showed conflicting findings. In their 28-week study, Murray et al. assessed the effects 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 Montgomery–Asberg 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 participants had a mean interval of treatment intervention at 147 days, conclusions regarding “early” intervention 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 participants then had to have a decrease of at least 20% from the baseline Montgomery–Asberg Depression Rating Scale score. Whereas the antidepressant outcome 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 (Murray et al., 2005). Interestingly, the outcome for sertraline was numerically better but not statistically different from the placebo (p < .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 < .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 emotionalism 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 improvement 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 relieved 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 regarding 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 associated with earlier mortality, post-stroke SSRI treatment 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” depressed (Rampello et al., 2005). Essentially a retarded depression is a state of clinical depression in which the individual is lethargic rather than anxious and characterized 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 statistically 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, authors 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 intervention, participants were again assessed on an outpatient basis and were required to have had a stroke within 12 months. Therefore, generalization to an acute inpatient population and assessment of early intervention to rehabilitation could not be determined.
Because all pharmacological interventions carry different 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 interviewing 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 addictions; 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 rehabilitation 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 expectations 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 interviewing, 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. Although this study did not find this intervention to improve function, this intervention does warrant further investigation as it could potentially be used as a prevention method for the development of depression.
In a 2008 systemic review, Hackett, Anderson, House, and Xia noted that, in the 12 antidepressant interventions reviewed, there was evidence of beneficial effect of antidepressants on reduction in mood scores and no evidence that antidepressants improved cognitive function. Furthermore, these authors concluded that, in the reviewed studies, there was no evidence 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 review 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 psychotherapy 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 antidepressants solely for the treatment of PSD, some researchers suspect that antidepressants may also improve outcomes of stroke itself (Burns & Greenberg, 2010). Potentially, three different mechanisms including protection 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 pharmacological agents has contributed to neurogenesis in the hippocampus of rodents (Burns & Greenberg, 2010). Finally, rodent studies with fluoxetine showed improvements in vision after being exposed to monocular visual 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 stroke. These findings have important implications for future research in the use of antidepressant medication 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 important 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 precautions, physician experience, and problems with discontinuing the medication (Gardner et al., 2007). Most interestingly, physicians ranked cost as the second most important factor, whereas patients ranked this factor at number 12. As mentioned, SSRIs have had the greatest levels of tolerability in the general population and most often are associated with nausea and mild headache (Gelenberg & Hopkins, 2007). Decreased libido and difficulty achieving orgasm have also been noted to be persistent problems. However, depression may also affect sexual desire and performance, 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). Therefore, caution should be used with regard to hemorrhagic strokes. Other potential side effects include anorexia early in treatment, gastrointestinal disturbances (nausea, vomiting, and diarrhea), sedation or insomnia, and serotonin syndrome (Khawam et al., 2006). The TCAs also have many potentially dangerous side effects including anticholinergic side effects, sedation, cardiac effects, and weight gain. Furthermore, TCAs have many significant potential drug interactions including phenytoin, valproic acid, and carbamazepine (Khawam et al., 2006). Because most strokes occur in the elderly population, special considerations should be made before initiating antidepressant therapy. Because of physiological 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 because of increased potential for orthostatic hypotension 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 diagnosis and treatment of PSD as mentioned above. In addition to the obvious limitations associated with the 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 participants, 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 options. Hackett, Anderson, House, and Xia (2008) also identified that, in psychotherapy trials, one of the greatest challenges was adequate training of professionals in the delivery of the intervention and consistency of this delivery. Furthermore, another challenge in comparing 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 contribute 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 undertreated, few facilities have implemented screening programs, and the gold standard of treatment remains largely undetermined. The first step in improving identification 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 therapists often interact with post-stroke patients to evaluate both swallowing and communication difficulties, these professionals should be involved in the development of screening in aphasic patients. Until an accurate screening tool is identified, it would be difficult to promote the need for bedside evaluation among nursing and care providers. Once a best practice screening method is identified, focus may fully take place on treatment options. Because this literature review initially sought to investigate the benefit of early intervention 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 research 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 improves 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 population with depression, a combination of both psychotherapy and pharmacotherapy has been recommended over one intervention independently. Although no studies were identified at this time that assessed the combination 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 understand and further intervene to treat this debilitating consequence of stroke.
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antidepressants; depression; post-stoke depression; stroke
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