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Identifying and Treating Depression After Stroke: Pulling Together the Evidence

Disclosure: Dr. Silver has nothing to disclose.
Pub Date: Thursday, Dec. 8, 2016
Author: Brian Silver, MD, FAHA, FAAN
Affiliation: Rhode Island Hospital/Alpert Medical School of Brown University

Citation

Towfighi A, Ovbiagele B, El Husseini N, Hackett ML, Jorge RE, Kissela BM, Mitchell PH, Skolarus LE, Whooley MA, Williams LS; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; and Council on Quality of Care and Outcomes Research. Poststroke depression: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association [published online ahead of print December 8, 2016]. Stroke. doi: 10.1161/STR.0000000000000113.

Article Text

Providers who treat patients with stroke are familiar with the issue of poststroke depression (PSD). Not only does it affect patient mood, but it can also affect ability to participate in rehabilitation activities because of the vegetative symptoms such as inattention, fatigue, decreased energy, and lack of interest in activities.1 It is also common, affecting 1/3 of stroke survivors, and typically is most frequent within the first year after stroke. Between 10 and 25% of patients with stroke contemplate suicide2-5 and 0.6-1.3% of people with a history of stroke attempt suicide.5,6

 

In the Scientific Statement, “Poststroke Depression,” Dr. Amytis Towfighi and colleagues evaluated scientific research in the area of PSD and asked the following questions: How common is it? What is the natural history? Why do people get PSD? What makes it more likely that someone will have PSD? What is the relationship between PSD and a patient’s motor function, quality of life, use of the health care system, and risk of death? How should health care providers screen for PSD? How should PSD be treated and how can it be prevented? As expected, there was not a clear answer to every question, and more research into many of these questions is needed.7

The key findings in the Statement are that 1) PSD is common; 2) PSD is complex and likely involves biological (i.e. changes in brain neurotransmitters) and psychosocial factors; 3) PSD is predicted by physical disability, stroke severity, history of depression, and cognitive impairment; 4) PSD is associated with worse functional outcomes after stroke, and that treatment with fluoxetine, which modulates the serotonin system, improved motor recovery in one randomized trial; 5) the relationship between quality of life and utilization after healthcare with poststroke depression requires more study; 6) PSD is associated with a higher risk of death after stroke; 7) screening for poststroke depression with the PHQ-9 is pragmatic and highly sensitive; 8) antidepressants may be effective for treating PSD; and 9) psychosocial therapies may prevent the development of PSD.7

Progress has been made in determining the biological processes that are associated with PSD.1 These include genetic factors such as 5-HTTLPR and the STin2 VNTR polymorphisms of the serotonin transporter gene (SERT) which are more prevalent in stroke survivors with PSD,8 hypothalamic-pituitary-adrenal (HPA) axis abnormalities,9 an increase in proinflammatory cytokines,10 alteration in monoamine systems,11 and elevation of glutamate levels.12 These abnormalities provide potential targets for treatment.

The serotonin system has been of particular interest in targeting therapies for poststroke depression. The first randomized trial using a medication that partially activated the serotonin system, nortriptyline, found a benefit to treatment.13 Since then, treatment with medications that increase serotonin in the central nervous system have been associated with reduced disability14 and mortality.15 A multicenter randomized controlled trial in Denmark of the efficacy of citalopram to reduce disability and cardiovascular mortality following stroke (The Efficacy of Citalopram Treatment in Acute Stroke [TALOS] study) is ongoing.16

Non-pharmacological approaches that have been used successfully include psychosocial-behavioral interventions.17 A follow-up study comparing in-person versus telephone counseling versus standard care has just completed (PSD2).18

It is likely that improved detection and treatment of PSD will occur over the next decade because of better screening tools and understanding of mechanism. Not only is there a possibility of improving emotional outcomes but also function and survival after stroke.

References

  1. Robinson RG, Jorge RE. Post-Stroke Depression: A Review. Am J Psychiatry 2016;173:221-31.
  2. Santos CO, Caeiro L, Ferro JM, Figueira ML. A study of suicidal thoughts in acute stroke patients. J Stroke Cerebrovasc Dis 2012;21:749-54.
  3. Fuller-Thomson E, Tulipano MJ, Song M. The association between depression, suicidal ideation, and stroke in a population-based sample. Int J Stroke 2012;7:188-94.
  4. Dou J, Tang J, Lu CH, Jiang ES, Wang PX. A study of suicidal ideation in acute ischemic stroke patients. Health Qual Life Outcomes 2015;13:7.
  5. Chung JH, Kim JB, Kim JH. Suicidal ideation and attempts in patients with stroke: a population-based study. J Neurol 2016.
  6. Eriksson M, Glader EL, Norrving B, Asplund K. Poststroke suicide attempts and completed suicides: a socioeconomic and nationwide perspective. Neurology 2015;84:1732-8.
  7. Towfighi A, Ovbiagele B, El Husseini N, Hackett ML, Jorge RE, Kissela BM, Mitchell PH, Skolarus LE, Whooley MA, Williams LS; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; and Council on Quality of Care and Outcomes Research. Poststroke depression: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association [published online ahead of print December 8, 2016]. Stroke. doi: 10.1161/STR.0000000000000113.
  8. Kohen R, Cain KC, Mitchell PH, et al. Association of serotonin transporter gene polymorphisms with poststroke depression. 2008;65:1296-302.
  9. Astrom M, Olsson T, Asplund K. Different linkage of depression to hypercortisolism early versus late after stroke. A 3-year longitudinal study. Stroke 1993;24:52-7.
  10. Jiao JT, Cheng C, Ma YJ, et al. Association between inflammatory cytokines and the risk of post-stroke depression, and the effect of depression on outcomes of patients with ischemic stroke in a 2-year prospective study. Exp Ther Med 2016;12:1591-8.
  11. Ji XW, Wu CL, Wang XC, Liu J, Bi JZ, Wang DY. Monoamine neurotransmitters and fibroblast growth factor-2 in the brains of rats with post-stroke depression. Exp Ther Med 2014;8:159-64.
  12. Cheng SY, Zhao YD, Li J, Chen XY, Wang RD, Zeng JW. Plasma levels of glutamate during stroke is associated with development of post-stroke depression. Psychoneuroendocrinology 2014;47:126-35.
  13. Lipsey JR, Robinson RG, Pearlson GD, Rao K, Price TR. Nortriptyline treatment of post-stroke depression: a double-blind study. Lancet 1984;1:297-300.
  14. Chollet F, Tardy J, Albucher JF, et al. Fluoxetine for motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-controlled trial. Lancet Neurol 2011;10:123-30.
  15. Jorge RE, Robinson RG, Arndt S, Starkstein S. Mortality and poststroke depression: a placebo-controlled trial of antidepressants. Am J Psychiatry 2003;160:1823-9.
  16. The Efficacy of Citalopram Treatment in Acute Stroke (TALOS). (Accessed September 25, 2016, at https://clinicaltrials.gov/ct2/show/NCT01937182 )
  17. Mitchell PH, Veith RC, Becker KJ, et al. Brief psychosocial-behavioral intervention with antidepressant reduces poststroke depression significantly more than usual care with antidepressant: living well with stroke: randomized, controlled trial. Stroke 2009;40:3073-8.
  18. Living Well With Stroke (PSD2). (Accessed September 25, 2016, at https://clinicaltrials.gov/ct2/show/NCT01133106.)

-- The opinions expressed in this commentary are not necessarily those of the editors or of the American Heart Association --