Stroke is one of the most frequent causes of disability in the United States, with a high burden on patients and families. Poststroke depression complicates recovery and at its worst may contribute to mortality in the period following a stroke.
The following case reports the utilization of an effective tool to evaluate stroke patients for risk of poststroke depression during the acute phase of treatment to optimize patient recovery.
Case Report
P.S. is a 55-year-old right handed white woman with a past medical history of hypertension, hyperlipidemia, hypothyroidism and obesity who presented with acute onset of left-sided weakness and slurred speech.
She first noticed the symptoms approximately one week prior beginning with numbness to the fingertips of her left hand and a headache. The symptoms waxed and waned for the next week. The patient attributed the symptoms to “poor circulation.” P.S. self-treated with over the counter ibuprofen but did not seek treatment. Two days prior to presenting to the hospital, the numbness progressed to cover the entire left arm but P.S. did not discern any weakness and declined family request to go to the emergency room; instead seeking care from her primary care provider. It was while at the office of her primary care provider that she was noted to have weakness and slurred speech. She was transferred by ambulance to the Emergency Department (ED) of a nearby hospital and was subsequently transferred to a regional stroke center. The stroke team was called to evaluate the patient. She was evaluated by the stroke team NP, who noted deficits to cranial nerves II (left visual field cut), V (no sensation to left face), VII (left-sided facial drooping), XI (weakness to the left sternocleidomastoid and trapezius muscles) and XII (tongue protruding, mild deviation to the left).
Motor exam revealed flaccid left arm and mild weakness to left leg as well. She was not able to participate in coordination exam on the left due to weakness and also had dense sensory loss and neglect on the left side. The patient’s plantar response was up going on the left side. Based on the assessment, the NP suspected that P.S. had experienced a right middle cerebral artery (MCA) stroke and an MRI confirmed the diagnosis of a distribution stroke with severe reduction of blood flow at the distal right MCA.
P.S. was assigned a score of 14 on the National Institutes of Health Stroke Scale.1 Due to the weeklong course of symptoms, the stroke team determined that P.S. was not a candidate for thrombolytic therapy. She was admitted to the neurology service for evaluation and management of an acute ischemic stroke.
In addition to the usual evaluation of her stroke etiology, P.S. was screened for depression using the Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR) as part of the development of the treatment plan.² Her tabulated score was 15, which is consistent with moderate to severe depression. P.S. had not considered herself depressed and had no prior history of other mood disorders.
Given the potential for poststroke depression (PSD) to impact the patient’s recovery process, the stroke team decided that her treatment plan should include pharmacotherapy with the selective serotonin reuptake inhibitor (SSRI) fluoxetine for poststroke depression despite prior diagnosis with major depression.
Poststroke Depression
PSD is considered the most common neuropsychiatric disorder after stroke.³ It has a negative impact on quality of life among 1 in 3 patients who experience PSD, but more than half of all cases are neither diagnosed nor treated. Some form of depression occurs in at least one-quarter of patients in the first year after stroke, and the greatest risk is during the first few months after onset.4
SEE ALSO: Managing Acute Stroke and Preventing Secondary Stroke
The Diagnostic and Statistical Manual (DSM) 5 categorizes poststroke depression as “mood disorder due to a general medical condition (stroke) featuring depressive features and symptoms, major depressive-like episodes, manic features, or mixed features.”5
According to National Institute of Mental Health, 6.9% of all U.S. adults had at least one major depressive episode in 2012, whereas almost 33% of all stroke survivors experienced depression. Some observational studies noted a prevalence 25% to 50% in patients immediately after an acute stroke.5, 6
PSD affects both men and women but appears to be more prevalent in women. Women may experience PSD as much as twice the rate of men.7 With an estimated 800,000 strokes annually8 and approximately 130,000 resulting in death,9 this represents anywhere from 220,000 to 335,000 patients living with PSD.
Signs and symptoms of PSD can be the same as those of other depression diagnoses including depressed mood, suicidal thoughts, anxiety, increased emotionalism, sadness, anhedonia, apathy, hopelessness, guilt and insomnia.10
PSD is also associated with increased severity of stroke deficits, decreased and delayed recovery and increased mortality in the year following a stroke.6, 11, 12
Causes of PSD
The exact cause of PSD is not completely understood. Some cases may represent previously undiagnosed depression.
Many practitioners and researchers have focused on the psychosocial aspects of stroke, such as accepting the limits of new disability, illness, loss of income related to hospitalization, decreased roles and uncertainty of the future limited support systems, loss of independence as the most important contributing factors to developing PSD.11
In seminal research into a possible biological cause of PSD, Robinson and colleagues hypothesized disruption in the serotonin and norepinephrine pathways in the basal ganglia and frontal lobes.13
Carson et al. reported that area of the lesion alone did not effectively predict the likelihood of PSD as it is often seen in patients whose infarcts occurred in regions not known to affect mood and personality. Other studies have also pointed to changes to the basal ganglia and limbic regions post stroke.14
Recently investigators in China, Hong Kong and Australia observed cerebral microbleeds on the MRI scans of post-ischemic stroke patients and hypothesized that microbleeds to the regions of the brain responsible for regulation of moods, emotions including the limbic system, brain stem, frontal regions and those regulated by the neurotransmitters serotonin, norepinephrine and dopamine may be affected by previously unobserved, and therefore undiagnosed, microbleeds.15
Additionally, the pathophysiology of PSD is not completely understood. However, as research continues into the biological processes involved in the development of PSD it is hoped a better understanding will emerge.
Diagnosis
Timely diagnosis is important in facilitating early access to treatment and improving prognosis. Clinical guidelines recommend that stroke survivors be routinely screened for mood disorders using a validated tool.16
The same diagnostic criteria are appropriate to diagnose PSD.12 The QIDS-SR16 is an assessment tool that can be used to assess depressive symptoms in acute stroke patients.2 The 16-question tool was developed to aid a clinician in quickly diagnosing a depressive disorder while still utilizing accepted diagnostic criteria.
Research has shown that the QIDS- SR16 is both valid and reliable, as well as generalizable to the spectrum of depressive disorders included in the DSM.17 The short questionnaire may be beneficial to evaluate patients who are ill, since it can be completed quickly. This may be useful with patients with limited energy; fatigue is often present in acute ischemic stroke.
Treatment
Several studies historically have examined the pharmacologic treatment of PSD.18-26 SSRIs have been evaluated as both prophylaxis early in the course of PSD or later with the development of worsening symptom that interfere with rehabilitation and recovery.
SSRIs may have an important role in improving neuropsychiatric outcomes in patients who have had a recent stroke, including lower risk of new-onset depression, better motor recovery, fewer cognitive deficits, improved levels of functioning and reduced long-term disability.27
Fluoxetine has been studied extensively. This research shows that it is well tolerated, decreases depressive symptoms and may be associated with increased survival. This is possibly due to increased adherence to vascular disease-preventing regimens with improvement in depressive symptoms, and it may have an effect on serotonin mediated platelet activation.18
It is important to consider potential side effects that may exacerbate poststroke deficits including sedation, lowering of the seizure threshold, falls and bleeding. Fluoxetine has few adverse events and has the benefit of being affordable, which may be an important determinant for a patient facing financial burdens associated with hospitalization due to acute ischemic stroke and subsequent rehabilitation needs.
Patient Outcome
P.S. was admitted to the stroke unit and underwent evaluation to identify the possible causes of her right MCA stroke including a CT scan of the brain, transthoracic echocardiogram (TTE) and cardiac MRI in addition to the initial MRI of the brain.
MRI of the brain showed evidence of right MCA stroke, a sizable infarct in the right frontoparietal areas and several punctate infarcts in the right parietal lobe with severe reduction of blood flow at the distal right MCA.
Involvement of the frontal lobe had the potential to contribute to PSD symptoms in P.S. Repeat CT scan demonstrated evolution of the stroke with mild mass effect. TTE and showed evidence of a 1.2 cm mobile echodensity potentially along the intraatrial septum in the left atrium. Cardiac MRI was performed, but it did not demonstrate any intraatrial source of the stroke, including vegetations or thrombus. The most likely etiology of her stroke was artery-to-artery embolism.
Once stabilized and able to participate in rehabilitation activities, P.S. was discharged to a rehabilitation center for short-term placement to aid in amelioration of her stroke deficits. Research shows that rehabilitation is helpful in the prevention or reductions of depression in stroke patients.
On discharge the patient was continued on fluoxetine 20 mg daily, lisinopril/hydrochlorothiazide 10/12.5 mg daily, aspirin 325 mg daily, heparin 5,000 units twice daily, atorvastatin 80 mg daily, Omega 3 ethyl esters 2 g daily (as a triglyceride-lowering agent), levothyroxine 125 mcg daily, sulfamethoxazole and trimethoprim 800/160 mg twice daily for a total of 7 days.
At the time of discharge, P.S. was tolerating a mechanical soft diet with thin liquids. She received physical therapy and occupational therapy to improve strength and function in the left arm and leg, and speech therapy to improve dysphagia. After the initial period of acceptance of her stroke diagnosis, P.S. remained euthymic. She tolerated fluoxetine without side effects. Continued follow up was scheduled on an outpatient basis after discharge from the rehabilitation facility.
References
1. National Institute of Health. National Institute of Neurological Disorders and Stroke. Stroke Scale. http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf.
2. Rush AJ, et al. The 16-item Quick Inventory of Depressive Symptomatology (QIDS) Clinician Rating (QIDS-C) and Self-Report (QIDS-SR): A psychometric evaluation in patients with chronic major depression. Biological Psychiatry. 2003;54:573-583.
3. Jiang X, et al. Correlative study on risk factors of depression among acute stroke patients. Eur Rev Med Pharmacol Sci. 2014;18(9):1315-1323.
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13. Robinson RG, et al. Current research in affective disorders following stroke. J Neuropsych Clin Neurosci. 1990;2:1-14.
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15. Tang WK, et al. Pontine microbleeds and depression in stroke. J Geriatr Psychiatry Neurol. 2014;27(3):159-164. doi: 10.1177/0891988714522699
16. Burton LJ, et al. Screening for mood disorders after stroke: a systematic review of psychometric properties and clinical utility. Psychol Med. 2014;1-21. doi:10.1017/S0033291714000336
17. Rush AJ, et al. The 16-item quick inventory of depressive symptomatology (QIDS), clinician rating (QIDS-C), and self-report (QIDS-SR): A psychometric evaluation in patients with chronic major depression. Biol Psychiatry. 2003;54(5):573-583.
18. Jorge RE, et al. Mortality and poststroke depression: a placebo-controlled trial of antidepressants. Am J Psychiatry. 2003;160:1823-1829.
19. Dam M, et al. Effects of fluoxetine and maprotiline on functional recovery in poststroke hemiplegic patients undergoing rehabilitation therapy. Stroke. 1996;27:1211-1214.
20. Miyai I, et al. Effects of antidepressants on functional recovery following stroke: a double-blind study. J. Neurol. Rehabilitation. 1998;12:5-13.
21. Narushima K, et al. Effect of antidepressant therapy on executive function after stroke. Br J Psychiatry 2007;190:260-265.
22. Jorge RE, et al. Mortality and poststroke depression: a placebo-controlled trial of antidepressants. Am J Psychiatry. 2003;160:1823-1829.
23. Zittel S, et al. Citalopram improves dexterity in chronic stroke patients. Neurorehabil Neural Repair. 2008;22:311-314.
24. Acler M, et al. A double blind placebo RCT to investigate the effects of serotonergic modulation on brain excitability and motor recovery in stroke patients. J Neurol. 2009;256:1152-1158.
25. Jorge RE, et al. Escitalopram and enhancement of cognitive recovery following stroke. Arch Gen Psychiatry. 2010;67:187-196.
26. Laska AC, et al. Long-term antidepressant treatment with moclobemide for aphasia in acute stroke patients: a randomised, double-blind, placebo-controlled study. Cerebrovasc. Dis. 2005;19:125-132.
27. Sathyanarayana Rao TS, et al. Exploring new frontiers in neuropsychopharmacology: SSRIs for stroke. Indian J Psychiatry. 2011;53(4):283-286. doi: 10.4103/0019-5545.91899.
Susan Alex is an adult nurse practitioner who practices in the stroke service at University of Texas Southwestern Medical Center in Dallas. Michelle Drew is an adjunct professor in the DNP program at Texas Woman’s University.
