Evidence-Based Reviews

Post-stroke depression: Rapid action helps restore lost function

Current Psychiatry. 2004 June;3(6):61-71

References

1. Heart and stroke statistical update. Dallas: American Heart Association, 2002.

2. Goldstein K. The organism:a holistic approach to biology derived from pathological data in man. New York: American Book Co, 1939.

3. Starkstein SE, Fedoroff JP, Price TR, et al. Catastrophic reaction after cerebrovascular lesions: frequency, correlates, and validation of a scale. J Neuropsychiatry Clin Neurosci 1993;5(2):189-94.

4. Robinson RG, Parikh RM, Lipsey JR, et al. Pathological laughing and crying following stroke: Validation of measurement scale and double-blind treatment study. Am J Psychiatry 1993;150:286-93.

5. Robinson RG, Kubos KL, Starr LB, et al. Mood changes in stroke patients: relationship to lesion location. Compr Psychiatry 1983;24(6):555-66.

6. Gainotti G, Azzoni A, Razzano C, et al. The Post-Stroke Depression Rating Scale: a test specifically devised to investigate affective disorders of stroke patients. J Clin Exp Neuropsychol 1997;19(3):340-56.

7. Carson AJ, MacHale S, Allen K, et al. Depression after stroke and lesion location: a systematic review. Lancet 2000;356(9224):122-6.

8. Narushima K, Kosier JT, Robinson RG. A reappraisal of poststroke depression, intra- and inter-hemispheric lesion location using meta-analysis. J Neuropsychiatry Clin Neurosci 2003;15(4):422-30.

9. Simons LA, McCallum J, Friedlander Y, Simons J. Risk factors for ischemic stroke: Dubbo Study of the elderly. Stroke 1998;29(7):1341-6.

10. Jonas BS, Mussolino ME. Symptoms of depression as a prospective risk factor for stroke. Psychosom Med 2000;62(4):463-71.

11. Cassidy EM, Walsh MT, O’Connor R, et al. Platelet surface glycoprotein expression in post-stroke depression: a preliminary study. Psychiatry Res 2003;118(2):175-81.

12. Pollock BG, Laghrissi-Thode F, Wagner WR. Evaluation of platelet activation in depressed patients with ischemic heart disease after paroxetine or nortriptyline treatment. J Clin Psychopharmacol 2000;20(2):137-40.

13. Everson SA, Roberts RE, Goldberg DE, Kaplan GA. Depressive symptoms and increased risk of stroke mortality over a 29-year period. Arch Intern Med 1998;158(10):1133-8.

14. Turner-Stokes L, Hassan N. Depression after stroke: a review of the evidence base to inform the development of an integrated care pathway. Part 2: Treatment alternatives. Clin Rehabil 2002;16(3):248-60.

15. Whyte EM, Mulsant BH. Post-stroke depression: epidemiology, pathophysiology, and biologic treatment. Biol Psychiatry 2002;52:253-64.

16. Currier M, Murray G, Welsh C. Electroconvulsive therapy for poststroke depressed geriatric patients. J Neuropsychiatry Clin Neurosci 1992;4(2):140-4.

17. Kemp BJ, Corgiat M, Gill C. Effects of brief cognitive behavioral group psychotherapy in older persons with and without disabling illness. Behav Health Ageing 1992;2:21-8.

18. Lincoln NB, Flannaghan T, Sutcliffe L, Rother L. Evaluation of cognitive behavioural treatment for depression after stroke: a pilot study. Clin Rehabil 1997;11(2):114-22.

19. Astrom M, Adolfsson R, Asplund K. Major depression in stroke patients: a 13-year longitudinal study. Stroke 1993;24:976-82.

20. Narushima K, Kosier JT, Robinson RG. Preventing poststroke depression: a 12-week double-blind randomized treatment trial and 21-month follow-up. J Nerv Ment Dis 2002;190(5):296-303.

21. Palomaki H, Kaste M, Berg A, et al. Prevention of poststroke depression: 1 year randomised placebo controlled double blind trial of mianserin with 6 month follow up after therapy. J Neurol Neurosurg Psychiatry 1999;66(4):490-4.

These observations—plus the fact that depression is a common sequela of stroke—suggest that stroke and depression may result from a common pathophysiology. Some evidence suggests that depression is a cerebrovascular disease. For example, stroke and depression are both associated with increased platelet reactivity (stickiness). However, platelet reactivity does not appear greater in patients who develop depression after a stroke than in those who do not.¹¹

Table 2

Diagnostic criteria for mood disorder due to stroke*

A prominent and persistent disturbance in mood predominates in the clinical picture and is characterized by either (or both) of the following: depressed mood or markedly diminished interest or pleasure in all or most all activities elevated, expansive, or irritable mood There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of the stroke. The disturbance is not better accounted for by another mental disorder (such as adjustment disorder with depressed mood in response to the stress of having had a stroke). The disturbance does not occur exclusively during the course of a delirium. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
Specify type:
With depressive features: if the predominant mood is depressed but the full criteria are not met for a major depressive episode.
With major-depressive-like episode: if the full criteria are met (except criterion D) for a major depressive episode.
*DSM-IV-TR diagnostic criteria for mood disorder due to a general medical condition
Source: Adapted and reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, text revision. Copyright 2000. American Psychiatric Association.

A study of antidepressants’ effects on platelet dysfunction found that the selective serotonin reuptake inhibitors (SSRIs) paroxetine and sertraline may reverse platelet abnormalities, whereas the tricyclic nortriptyline does not.¹²

Summary. A biopsychosocial model helps explain the pathogenesis PSD, which may present as:

a syndrome similar to MDD
a relatively minor depression similar to dysthymic disorder
a discrete phenomenon such as catastrophic reaction and emotional lability.

Evaluating patients for PSD

In the absence of PSD diagnostic guidelines, Table 1 provides a clinically useful approach. A comprehensive workup may suggest whether an individual’s depressive symptoms are endogenous or reactive, although this distinction may be subtle. Gathering information from other physicians, the patient, family, and caregivers may require more than one session.

Diagnostic criteria. Consult DSM-IV criteria for “mood disorder due to general medical condition” as they pertain to patients “with depressive features” (minor depression) or “with major depression-like episodes” (Table 2). In the initial evaluation, do not rely exclusively on instruments such as the Hamilton Depression Rating Scale for measuring depression, as patients with emotional lability may not meet the cut-off scores for depression. These scales may help monitor progress later during therapy.

Risk factors. Interview the patient, family, and caregivers to determine if the patient has possible risk factors for PSD:

history of stroke
personal or family history of depression
loss of social activities
major life event within 6 months of stroke
cognitive impairment 1 month post-stroke.

Determine whether the patient’s stroke was precipitated by cocaine or other drug abuse. If so, address the cause.

Medical comorbidities. Consider the effect of medical comorbidities such as Parkinson’s disease, heart disease, or diabetes on the patient’s mood. Also rule out other metabolic causes of depression such as thyroid abnormalities, medication side effects, and vitamin B₁₂ deficiency.

Table 3

Treating post-stroke depression with antidepressants

	TCAs	SSRIs
Efficacy	Proven in double-blind, placebo-controlled trials One study found nortriptyline more effective than fluoxetine	Greater anxiolytic effect than TCAs (?) Overall less efficacious than TCAs (?)
Side effects	Alpha-adrenergic blockade, anticholinergic, antihistaminic, and cardiac effects	Drug interactions related to cytochrome P-450 isoenzyme inhibition Fluoxetine may prolong bleeding time
Overdose risk	Potentially fatal	Safe in overdose
Onset of action	Slower than SSRIs (?)	More rapid than TCAs (?)
Cost	Less expensive than SSRIs	More expensive than TCAs
(?) Not supported by controlled clinical trials
TCAs: Tricyclic antidepressants
SSRIs: Selective serotonin reuptake inhibitors

Cognitive changes. Quantify any cognitive deficits with neuropsychological testing, such as the Mini-Mental State Examination. Also learn all you can about the patient’s premorbid personality for comparison with post-stroke behavior. Ask the nursing or rehabilitation staff about inpatients’ motivation and participation in care.

Social support. Determine if caregivers can provide transportation, medication monitoring, and other social support.

Treatment options

PSD calls for rapid, comprehensive treatment with antidepressants, psychotherapy, and help reintegrating into the community. Untreated PSD is associated with increased morbidity and mortality, whereas effective treatment improves functional outcomes.¹³

Antidepressants. Tricyclic antidepressants (desipramine, imipramine, and nortriptyline), SSRIs (citalopram and fluoxetine), and trazodone have been used to treat depression in stroke patients (Table 3) ¹⁴ Controlled studies suggest that:

>60% of patients with PSD respond to medication
they tolerate antidepressants well
no antidepressant class has a distinct therapeutic advantage over others.