FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2005264225> ?p ?o ?g. }

• W2005264225 endingPage "2832" @default.
• W2005264225 startingPage "2829" @default.
• W2005264225 abstract "HomeStrokeVol. 43, No. 10Improving Recovery After Stroke Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBImproving Recovery After StrokeA Role for Antidepressant Medications? Harold P. AdamsJr, MD and Robert G. Robinson, MD Harold P. AdamsJrHarold P. AdamsJr From the Departments of Neurology (H.P.A.) and Psychiatry (R.G.R.), Carver College of Medicine, University of Iowa, Iowa City, IA. Search for more papers by this author and Robert G. RobinsonRobert G. Robinson From the Departments of Neurology (H.P.A.) and Psychiatry (R.G.R.), Carver College of Medicine, University of Iowa, Iowa City, IA. Search for more papers by this author Originally published2 Aug 2012https://doi.org/10.1161/STROKEAHA.111.640524Stroke. 2012;43:2829–2832Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 IntroductionAlthough stroke is a leading cause of death in the United States and around the world, many people fear this disease because of its nonfatal neurological impairments that lead to disability or dependency. Considerable research has focused on lessening the neurological effects of the acute brain injury. To date, success is limited. Despite these research efforts, only intravenous thrombolysis and endovascular interventions are accepted as effective in limiting the acute effects of ischemic stroke. Although these therapies are efficacious, only 3% to 5% of patients with stroke are receiving reperfusion-based therapies due to the very short time windows for treatment.1 No medical or surgical intervention is useful in improving outcomes after intracerebral hemorrhage.Annually, approximately 400 000 Americans need rehabilitation to help with recovery after stroke.2 Given the magnitude of the problem, effective new therapies are needed to augment the process of recovery. These therapies could be given as adjuncts to conventional rehabilitation to these patients who have potentially disabling residual neurological impairments. Because many more patients could be treated, an effective therapy that maximizes neurological recovery might have a much bigger societal impact than emergency reperfusion therapy alone.3,4 Unfortunately, relatively few clinical studies have tested interventions that might augment recovery. The basic science understandings of the process of recovery after stroke have advanced.5–10 It is now clear that the adult brain has a real capacity for physiological and anatomic modifications that lead to motor and cognitive recovery.11 This complex process is mediated by multiple mechanisms including enhanced regional metabolism and resolution of diaschisis. Cellular changes after stroke include proliferation of neural and glial cell precursors, activation of astrocytes and inflammatory cells, migration of blood vessels, increased axonal sprouting, increased branching of dendrites, and development of new synapses.12–14 Neurogenesis after stroke also includes production of progenitor cells in the subventricular zone, hippocampus, and other brain regions that migrate into areas of infarction. In experimental models, the maximal effects are seen within the first 2 to 3 weeks after stroke and may extend for 3 to 6 months.5Potential interventions to enhance restorative processes include administration of growth factors, use of marrow stromal cells or erythropoietin, robotic assistance, brain stimulation, and intralesional stem cell transplantation.15–18 Some of these interventions likely will be expensive and may require special expertise, resources, and technology that could limit their use. Another approach would be the adjunctive use of pharmacological therapies.19 Clinical studies of the potentially positive impact of medications have begun to emerge.20,21 Laboratory studies of medications that increase brain concentrations of brain amines (serotonin, dopamine, etc), including amphetamines, demonstrate a positive impact on outcomes.22 However, clinical trials have found conflicting results and some of these medications may not be optimal for treatment of patients with recent stroke.23Another promising approach is the use of antidepressants, particularly in management of patients who are not depressed. Depression is a common consequence of ischemic stroke; it occurs in approximately 25% to 30% of patients and it peaks within the first 3 to 6 months.24 When adjusting for age, severity of stroke, and other covariables, depression has major negative effects on cognitive and motor recovery and is associated with increased mortality and an increased risk of recurrent vascular events.24,25 However, there have been concerns about the safety of the antidepressants when given to elderly patients. In particular, the risk of bleeding may be increased because of potential interactions with antiplatelet agents. Some observational studies have reported an increased risk of either hemorrhagic or ischemic stroke among older patients taking antidepressant medications, whereas others have not found these associations.26–31 In addition, the use of antidepressants in preventing depression after stroke also has been debated. For example, a small randomized trial reported that early administration of sertraline reduced the incidence of depression (16.7% [8 of 48] versus 21.6% [11 of 51] for placebo, P=0.59).32 However, the nonsignificant results may be explained in part by the limited number of patients in the study. Based on a meta-analysis of randomized trials, Fournier et al33 concluded that the medications were effective in treating severe depression but of uncertain efficacy in less severely depressed patients. In a rebuttal, Isaccson and Adler34 noted that the scales used in the trials included in the meta-analysis were not sufficiently sensitive to detect treatment effects and, thus, the conclusions could not be sustained. This observation is supported by the findings of Hackett et al.35 In addition, a Cochrane systemic review found that antidepressant medications are effective in treating depression after stroke.36 Another meta-analysis performed by Yi et al37 found that fluoxetine is beneficial for prevention of poststroke depression although it did not reduce the severity of the depressive symptoms. Based on the available data, current American Heart Association guidelines recommend regular screening for depression for stroke and if depression is detected, antidepressants are advised.38 Given these recommendations, enrolling depressed patients into a randomized placebo-controlled trial testing the use of antidepressants in improving neurological outcomes would be problematic.Remission of depression is associated with improved outcomes with rehabilitation, which implies that the administration of antidepressant medications might potentially augment recovery.39–41 Recent data show that antidepressant medications also might be useful in fostering recovery in nondepressed patients.41,42 Because antidepressant medications are widely and safely used, they would be strong candidates to be used as adjunctive agents in the subacute phase of stroke. The selective serotonin reuptake inhibitors are of particular interest because of their safety profile in patients with heart disease and stroke.43,44 Laboratory research also supports the use of selective serotonin reuptake inhibitors as a tactic to maximize recovery after stroke.45–47Several clinical studies, testing different agents, have evaluated the potential use of the selective serotonin reuptake inhibitor medications in several settings after stroke. When compared with a control group that received placebo, Dam et al48 found that fluoxetine (20 mg/day) facilitated motor recovery among patients receiving physical therapy. Fruehwald et al49 initiated fluoxetine therapy (20 mg/day) within 2 weeks after stroke to 24 patients and continued treatment for 12 weeks; they found sustained benefits from treatment at 18 months when compared with a group of patients treated with a placebo. In a study using functional MRI, Pariete el al50 reported that a single dose of fluoxetine (20 mg) led to hyperactivation of the ipsilesional insular and lateral motor51 cortex at 5 hours when compared with placebo; they also found that fluoxetine improved finger-tapping speed as well as strength of the paretic arm. In a crossover study of 8 patients with chronic stroke, Zittel et al52 reported that a single (40 mg) dose of citalopram improved motor performance on a peg board when compared with the responses among patients receiving placebo. In another study, Acler et al53 gave citalopram (10 mg/day) for 1 month to 10 patients with stroke and reported greater improvements in the National Institutes of Health Stroke Scale when compared with 10 patients treated with placebo. Bilge et al39 treated patients with poststroke depression with citalopram (20 mg/day) for 6 months and found improvements in the scores of the Scandinavian Stroke Scale, modified Rankin Scale, and Barthel Index at 12 months; the results paralleled improvement in the depression. Another trial found that paroxetine improved motor outcomes after stroke.54 A crossover study that included functional MRI reported that reboxetine increased grip strength and finger dexterity and was associated with a reduction in cortical hyperactivity.51The 2 largest studies were conducted by Chollet et al44 and our group.42 In the former study, 57 patients were treated with fluoxetine (20 mg/day) and 56 patients received placebo for 3 months beginning within 10 days of stroke. All patients needed rehabilitation and the mean baseline National Institutes of Health Stroke Scale scores were approximately 13 in both groups. At 3 months, improvements in the Fugl-Meyer motor scores were significantly higher with fluoxetine (34 points; 95% CI, 29.7–38.4) than with placebo (24 points; 95% CI, 19.9–28.7.) Similarly, modified Rankin Scale scores of 0 to 2 were achieved in 26% of fluoxetine-treated patients and 9% of control subjects. In a 3-arm trial that enrolled patients within 3 months of stroke and treated for 3 months, we compared 32 patients treated with fluoxetine (40 mg/day), 22 patients treated with nortriptyline (100 mg/day), or 29 patients administered placebo. After controlling for age, depression, rehabilitation intensity, and baseline severity of stroke, improvements in the modified Rankin Scale were significantly greater at 12 months with treatment (t[156]=3.17, P=0.002.)42 Furthermore, follow-up of this group found that 70% of the patients treated with antidepressants had survived 7 years compared with 36% of those given placebo (P=0.001.)42 In another multicenter, randomized, placebo-controlled trial, we demonstrated that escitalopram (10 mg/day) given for 1 year prevents development of poststroke depression and was associated with improved short- and long-term memory recovery, even after controlling for age, sex, and baseline cognitive function.43,55 These findings are buttressed by the results of the project of Simis and Nitrin56 who reported that citalopram was associated with improved memory and attention.Although these studies are relatively small, they demonstrate the potentially positive impact of the adjunctive use of selective serotonin reuptake inhibitor medications in treatment of nondepressed patients with recent stroke.3 Interest in the potential efficacy of antidepressants in improving outcomes after stroke, especially in nondepressed patients, is considerable. The selective serotonin reuptake inhibitors appear to augment motor and cognitive recovery. The medications seem to be relatively safe in patients with stroke.43,44,55 Because the prices of the medications are relatively inexpensive (for example, US $4 per month for fluoxetine), the cost-effectiveness of these agents could be considerable. Although the preliminary data are promising, they are not definitive. A recommendation for widespread use of antidepressants in the management of patients with recent stroke is premature. Larger trials are needed to test the use of antidepressants in a broad range of patients with recent stroke. If these trials replicate the results of the recent studies, the overall impact of adjunctive antidepressant therapy could represent a major advance in the care of persons surviving stroke.DisclosuresDr Adams is a consultant (member of adjudication panel) for Merck <$10 000; a consultant (member of safety panel) for Medtronic <$10 000; and has received grant support from the National Institutes of Neurological Disorders and Stroke >$10 000. Dr Robinson is a consultant for Avanir <$10 000 and an expert witness <$10 000.FootnotesCorrespondence to Harold P. Adams, Jr, MD, Department of Neurology, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242-1053. E-mail [email protected]eduReferences1. Kleindorfer D, Xu Y, Moomaw CJ, Khatri P, Adeoye O, Hornung R. US geographic distribution of rtPA utilization by hospital for acute ischemic stroke. Stroke. 2009; 40:3580–3584.LinkGoogle Scholar2. National Institute of Neurological Disorders and Stroke. Post-Stroke Rehabilitation Fact Sheet. NIH Publication 80-4846. Bethesda, MD: National Institute of Neurological Disorders and Stroke; 2008.Google Scholar3. Robinson RG, Adams HP. Selective serotonin-reuptake inhibitors and recovery after stroke. Lancet Neurol. 2011; 10:110–111.CrossrefMedlineGoogle Scholar4. Cramer SC. Listening to fluoxetine: a hot message from the FLAME trial of poststroke motor recovery. Int J Stroke. 2011; 6:315–316.CrossrefMedlineGoogle Scholar5. Cramer SC. Reparing the human brain after stroke: I. Mechanisms of spontaneous recovery. Ann Neurol. 2008; 63:272–287.CrossrefMedlineGoogle Scholar6. Cramer SC. Repairing the human brain after stroke. II. Restorative therapies. Ann Neurol. 2008; 63:549–560.CrossrefMedlineGoogle Scholar7. Cramer SC. Brain repair after stroke. N Engl J Med. 2010; 362:1827–1829.CrossrefMedlineGoogle Scholar8. Johansson BB. Environmental effects on functional outcome after stroke. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:47–55.CrossrefGoogle Scholar9. Carmichael ST. Molecular mechanisms of neural repair after stroke. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:11–21.CrossrefGoogle Scholar10. Chopp M, Li Y, Zhang ZG. Mechanisms underlying improved recovery of neurological function after stroke in the rodent after treatment with neurorestorative cell-based therapies. Stroke. 2009; 40:S143–S145.LinkGoogle Scholar11. Rossini PM, Calautti C, Pauri F, Baron JC. Post-stroke plastic reorganisation in the adult brain. Lancet Neurol. 2003; 2:493–502.CrossrefMedlineGoogle Scholar12. Jones T, Allred R, Adkins D, Hsu JE, O'Bryant A, Maldonado M. Remodeling the brain with behavioral experience after stroke. Stroke. 2009; 40:S136–S138.LinkGoogle Scholar13. Jones TA, Adkins DL. Behavioral influence on neuronal events after stroke. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:23–33.CrossrefGoogle Scholar14. Marti-Fabregas J, Romaguera-Ros M, Gomez-Pinedo U, Martinez-Ramirez S, Jimenez-Xarrie E, Marin R , et al. Proliferation in the human ipsilateral subventricular zone after ischemic stroke. Neurology. 2010; 74:357–365.CrossrefMedlineGoogle Scholar15. Teskey GC, Kolb B. Post-stroke recovery therapies in animals. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:35–45.CrossrefGoogle Scholar16. Fisher M, Finkelstein S. Pharmacological approaches to stroke recovery. Cerebrovasc Dis. 1999; 9(suppl 5):29–32.CrossrefMedlineGoogle Scholar17. Zhang ZG, Chopp M. Neurorestorative therapies for stroke: underlying mechanisms and translation to the clinic. Lancet Neurol. 2009; 8:491–500.CrossrefMedlineGoogle Scholar18. Caplan LR, Arenillas J, Cramer SC, Joutel A, Lo EH, Meschia J , et al. Stroke-related translational research. Arch Neurol. 2011; 68:1110–1123.CrossrefMedlineGoogle Scholar19. Loubinoux I, Chollet F. Neuropharmacology in stroke recovery. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:183–193.CrossrefGoogle Scholar20. Rosser N, Floel A. Pharmacological enhancement of motor recovery in subacute and chronic stroke. Neurorehabilitation. 2008; 23:95–103.MedlineGoogle Scholar21. Liepert J. Pharmacotherapy in restorative neurology. Curr Opin Neurol. 2008; 21:639–643.CrossrefMedlineGoogle Scholar22. Lokk J, Roghani RS, Delbari A. Effect of methylphenidate and/or levodopa coupled with physiotherapy on functional and motor recovery after stroke—a randomized, double-blind, placebo-controlled trial. Acta Neurol Scand. 2010; 123:266–273.CrossrefGoogle Scholar23. Zorowitz RD, Smout RJ, Gassaway JA, Horn SD. Neurostimulant medication usage during stroke rehabilitation: the Post-Stroke Rehabilitation Outcomes Project (PSROP). Top Stroke Rehabil. 2005; 12:28–36.CrossrefMedlineGoogle Scholar24. Paolucci S, Gandolfo C, Provinciali L, Torta R, Toso V, DESTRO Study Group. The Italian multicenter observational study on post-stroke depression (DESTRO). J Neurol. 2006; 253:556–562.CrossrefMedlineGoogle Scholar25. Platz T. Depression and its effects after stroke. In: , Cramer SC, Nudo RJ, eds. Brain Repair After Stroke. Cambridge, UK: Cambridge University Press; 2010:145–161.CrossrefGoogle Scholar26. Smoller JW, Allison M, Cochrane BB, Curb JD, Perlis RH, Robinson JG , et al. Antidepressant use and risk of incident cardiovascular morbidity and mortality among postmenopausal women in the Women's Health Initiative Study. Arch Intern Med. 2009; 169:2128–2139.CrossrefMedlineGoogle Scholar27. Coupland C, Dhiman P, Morriss R, Arthur A, Barton G, Hippisley-Cox J. Antidepressant use and risk of adverse outcomes in older people: population based cohort study. BMJ. 2011; 343:d4551.CrossrefMedlineGoogle Scholar28. Wu C-S, Wang S-C, Cheng YC, Gau SS. Association of cerebrovascular events with antidepressant use: a case-crossover study. Am J Psychiatry. 2011; 168:511–521.CrossrefMedlineGoogle Scholar29. Douglas IJ, Smeeth L, Irvine D. The use of antidepressants and the risk of haemorrhagic stroke: a nested case control study. Br J Clin Pharmacol. 2011; 71:116–120.CrossrefMedlineGoogle Scholar30. Trifiro G, Dieleman J, Sen EF, Gambassi G, Stukenboom MC. Risk of ischemic stroke associated with antidepressant drug use in elderly persons. J Clin Psychopharmacol. 2010; 30:252–258.CrossrefMedlineGoogle Scholar31. Almeida OP, Alfonso H, Hankey GJ, Flicker L. Depression, antidepressant use and mortality in later life: the Health in Men Study. PLoS One. 2010;e11266.CrossrefMedlineGoogle Scholar32. Almeida OP, Waterreus A, Hankey GJ. Preventing depression after stroke: results from a randomized placebo-controlled trial. J Clin Psychiatry. 2006; 67:1104–1109.CrossrefMedlineGoogle Scholar33. Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC , et al. Antidepressant drug effects and depression severity. JAMA. 2011; 303:47–53.CrossrefGoogle Scholar34. Isacsson G, Adler M. Randomized clinical trials underestimate the efficacy of antidepressants in less severe depression. Acta Psychiatr Scand. 2012; 125:423–424.CrossrefMedlineGoogle Scholar35. Hackett ML, Hill KM, Hewison J, Anderson CS, House AO; on behalf of the Auckland Regional Community Stroke. Stroke survivors who score below threshold on standard depression measures may still have negative cognitions of concern. Stroke. 2010; 41:478–481.LinkGoogle Scholar36. Hackett ML, Anderson CS, House A, Xia J. Interventions for treating depression after stroke. Cochrane Database Syst Rev. 2008; 4:CD003437.Google Scholar37. Yi ZM, Liu F, Zhai SD. Fluoxetine for the prophylaxis of poststroke depression in patients with stroke: a meta-analysis. Int J Clin Pract. 2010; 64:1310–1317.CrossrefMedlineGoogle Scholar38. Miller EL, Murray L, Richards L, Zorowitz RD, Bakas T, Clark P , et al. Comprehensive overview of nursing and interdisciplinary rehabilitation care of the stroke patient. Stroke. 2010; 41:2402–2448.LinkGoogle Scholar39. Bilge C, Kocer E, Kocer A, Turk Boru U. Depression and functional outcome after stroke: the effect of antidepressant therapy on functional recovery. Eur J Phys Rehabil Med. 2008; 44:13–18.MedlineGoogle Scholar40. Narushima K, Robinson RG. The effect of early versus late antidepressant treatment on physical impairment associated with poststroke depression. Is there a time-related therapeutic window?J Nerv Ment Dis. 2003; 191:645–652.CrossrefMedlineGoogle Scholar41. Tallelli P, Werring DJ. Pharmacological augmentation of motor recovery after stroke: antidepressants for non-depressed patients?J Neurol. 2009; 256:1159–1160.CrossrefMedlineGoogle Scholar42. Mikami K, Jorge RE, Adams HP, Davis PH, Leira EC, Jang M, Robinson RG. Effect of antidepressants on the course of disability following stroke. Am J Geriatr Psychiatry. 2011; 19:1007–1015.CrossrefMedlineGoogle Scholar43. Robinson RG, Jorge RE, Moser DJ, Acion L, Solodkin A, Small SL , et al. Escitalopram and problem-solving therapy for prevention of poststroke depression: a randomized controlled trial. JAMA. 2008; 299:2391–2400.CrossrefMedlineGoogle Scholar44. Chollet F, Tardy J, Albucher J-F, Thalamas C, Berard E, Lamy C , et al. Fluoxetine for motor recovery after acute ischaemic stroke (FLAME): a randomised placebo-controlled trial. Lancet Neurol. 2011; 10:123–130.CrossrefMedlineGoogle Scholar45. Lim CM, Kim SW, Park JY, Kim C, Yoon SH, Lee JK. Fluoxetine affords robust neuroprotection in the postischemic brain via its anti-inflammatory effect. J Neurosci Res. 2009; 87:1037–1045.CrossrefMedlineGoogle Scholar46. Malberg J, Schechter E. Increasing hippocampal neurogenesis: a novel mechanism for antidepressant drugs. Curr Pharm Des. 2005; 11:145–155.CrossrefMedlineGoogle Scholar47. Newton SS, Duman RS. Neurogenic actions of atypical antipsychotic drugs and therapeutic implications. CNS Drugs. 2007; 21:715–725.CrossrefMedlineGoogle Scholar48. Dam M, Tonin P, De Boni A, Pizzolato G, Casson S, Ermani M , et al. Effects of fluoxetine and maprotiline on functional recovery in poststroke hemiplegic patients undergoing rehabilitation therapy. Stroke. 2009; 27:1211–1214.CrossrefGoogle Scholar49. Fruehwald S, Gatterbauer E, Rehak P, Baumhackl U. Early fluoxetine treatment of post-stroke depression—a three-month double-blind placebo-controlled study with an open-label long-term follow up. J Neurol. 2009; 250:347–351.CrossrefGoogle Scholar50. Pariente J, Loubinoux I, Carel C, Albucher J-F, Leger A, Manelfe C , et al. Fluoxetine modulates motor performance and cerebral activation of patients recovering from stroke. Ann Neurol. 2001; 50:718–729.CrossrefMedlineGoogle Scholar51. Wang LE, Fink GR, Diekhoff S, Rehme AK, Eickhoff SB, Grefkes C. Noradrenergic enhancement improves motor network connectivity in stroke patients. Ann Neurol. 2011; 69:375–378.CrossrefMedlineGoogle Scholar52. Zittel S, Weiller C, Liepert J. Citalopram improves dexterity in chronic stroke patients. Neurorehabil Neural Repair. 2009; 22:311–314.CrossrefGoogle Scholar53. Acler M, Robol E, Fiaschi A, Manganotti P. 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.CrossrefMedlineGoogle Scholar54. Loubinoux I, Pariente J, Boulanouar K, Carel C, Anelfe C, Ascol O , et al. A single dose of the serotonin neurotransmission agonist paroxetine enhances motor output: double-blind, placebo-controlled, MRI study in healthy subjects. Neuroimage. 2009; 15:26–36.CrossrefGoogle Scholar55. Jorge RE, Acion L, Moser D, Adams HP, Robinson RG. Escitalopram and enhancement of cognitive recovery following stroke. Arch Gen Psychiatry. 2010; 67:187–196.CrossrefMedlineGoogle Scholar56. Simis S, Nitrini R. Cognitive improvement after treatment of depressive symptoms in the acute phase of stroke. Arq Neuropsiquiatr. 2009; 64:412–417.CrossrefGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Williams-Cooke C, Watts E, Bonnett J, Alshehri M and Siengsukon C (2021) Association Between Sleep Duration and Functional Disability in Inpatient Stroke Rehabilitation: A Pilot Observational Study, Archives of Rehabilitation Research and Clinical Translation, 10.1016/j.arrct.2021.100150, 3:3, (100150), Online publication date: 1-Sep-2021. Mead G, Legg L, Tilney R, Hsieh C, Wu S, Lundström E, Rudberg A, Kutlubaev M, Dennis M, Soleimani B, Barugh A, Hackett M and Hankey G (2019) Fluoxetine for stroke recovery: Meta-analysis of randomized controlled trials, International Journal of Stroke, 10.1177/1747493019879655, 15:4, (365-376), Online publication date: 1-Jun-2020. Gu S and Wang C (2018) Early Selective Serotonin Reuptake Inhibitors for Recovery after Stroke: A Meta-Analysis and Trial Sequential Analysis, Journal of Stroke and Cerebrovascular Diseases, 10.1016/j.jstrokecerebrovasdis.2017.11.031, 27:5, (1178-1189), Online publication date: 1-May-2018. Mortensen J and Andersen G (2018) Potential Role of Selective Serotonin Reuptake Inhibitors in Improving Functional Outcome after Stroke, CNS Drugs, 10.1007/s40263-018-0573-x, 32:10, (895-903), Online publication date: 1-Oct-2018. van der Kemp J, Dorresteijn M, Ten Brink A, Nijboer T and Visser-Meily J (2017) Pharmacological Treatment of Visuospatial Neglect: A Systematic Review, Journal of Stroke and Cerebrovascular Diseases, 10.1016/j.jstrokecerebrovasdis.2017.02.012, 26:4, (686-700), Online publication date: 1-Apr-2017. Rundek T and Sacco R (2016) Prognosis after Stroke Stroke, 10.1016/B978-0-323-29544-4.00016-5, (234-252.e10), . Cramer S (2016) Marrow-Derived Mesenchymal Stromal Cells in the Treatment of Stroke Translational Neuroscience, 10.1007/978-1-4899-7654-3_17, (317-334), . Howland R (2016) Hey Mister Tambourine Man, Play a Drug for Me: Music as Medication, Journal of Psychosocial Nursing and Mental Health Services, 10.3928/02793695-20161208-05, 54:12, (23-27), Online publication date: 1-Dec-2016. Adams H, Chollet F and Thijs V (2015) Measuring Autonomy and Functional Recovery after Stroke, Journal of Stroke and Cerebrovascular Diseases, 10.1016/j.jstrokecerebrovasdis.2015.08.017, 24:11, (2429-2433), Online publication date: 1-Nov-2015. Flaster M, Sharma A and Rao M (2015) Poststroke Depression: A Review Emphasizing the Role of Prophylactic Treatment and Synergy with Treatment for Motor Recovery, Topics in Stroke Rehabilitation, 10.1310/tsr2002-139, 20:2, (139-150), Online publication date: 1-Mar-2013. Adams H and Nudo R (2013) Management of patients with stroke: Is it time to expand treatment options?, Annals of Neurology, 10.1002/ana.23948, 74:1, (4-10), Online publication date: 1-Jul-2013. October 2012Vol 43, Issue 10 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.111.640524PMID: 22858725 Manuscript receivedDecember 1, 2011Manuscript acceptedMarch 22, 2012Originally publishedAugust 2, 2012Manuscript revisedFebruary 22, 2012 Keywordsselective serotonin reuptake inhibitorsantidepressant medicationsstroke recoveryPDF download Advertisement SubjectsTreatment" @default.
• W2005264225 created "2016-06-24" @default.
• W2005264225 creator A5029167216 @default.
• W2005264225 creator A5066461508 @default.
• W2005264225 date "2012-10-01" @default.
• W2005264225 modified "2023-10-16" @default.
• W2005264225 title "Improving Recovery After Stroke" @default.
• W2005264225 cites W1467291425 @default.
• W2005264225 cites W1491167098 @default.
• W2005264225 cites W1512855441 @default.
• W2005264225 cites W1532732682 @default.
• W2005264225 cites W1557314957 @default.
• W2005264225 cites W159314493 @default.
• W2005264225 cites W1814473376 @default.
• W2005264225 cites W1967239173 @default.
• W2005264225 cites W1974737100 @default.
• W2005264225 cites W1977120596 @default.
• W2005264225 cites W1981323743 @default.
• W2005264225 cites W1983596415 @default.
• W2005264225 cites W1995292121 @default.
• W2005264225 cites W1995558035 @default.
• W2005264225 cites W2004762037 @default.
• W2005264225 cites W2007498774 @default.
• W2005264225 cites W2021700369 @default.
• W2005264225 cites W2022805748 @default.
• W2005264225 cites W2039226845 @default.
• W2005264225 cites W2040868194 @default.
• W2005264225 cites W2041690448 @default.
• W2005264225 cites W2044170764 @default.
• W2005264225 cites W204476827 @default.
• W2005264225 cites W2048235983 @default.
• W2005264225 cites W2053342374 @default.
• W2005264225 cites W2054423368 @default.
• W2005264225 cites W2054524438 @default.
• W2005264225 cites W2054930100 @default.
• W2005264225 cites W2066553255 @default.
• W2005264225 cites W2067131879 @default.
• W2005264225 cites W2068557183 @default.
• W2005264225 cites W2071031270 @default.
• W2005264225 cites W2072717324 @default.
• W2005264225 cites W2074125037 @default.
• W2005264225 cites W2075545935 @default.
• W2005264225 cites W2077699169 @default.
• W2005264225 cites W2078932584 @default.
• W2005264225 cites W2104721829 @default.
• W2005264225 cites W2108025392 @default.
• W2005264225 cites W2108029338 @default.
• W2005264225 cites W2112867635 @default.
• W2005264225 cites W2112923399 @default.
• W2005264225 cites W2117179240 @default.
• W2005264225 cites W2121567769 @default.
• W2005264225 cites W2127537047 @default.
• W2005264225 cites W2136546676 @default.
• W2005264225 cites W2140658948 @default.
• W2005264225 cites W2146408281 @default.
• W2005264225 cites W2163801252 @default.
• W2005264225 cites W2164156963 @default.
• W2005264225 cites W2343701004 @default.
• W2005264225 cites W2499347101 @default.
• W2005264225 cites W71638793 @default.
• W2005264225 doi "https://doi.org/10.1161/strokeaha.111.640524" @default.
• W2005264225 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22858725" @default.
• W2005264225 hasPublicationYear "2012" @default.
• W2005264225 type Work @default.
• W2005264225 sameAs 2005264225 @default.
• W2005264225 citedByCount "14" @default.
• W2005264225 countsByYear W20052642252013 @default.
• W2005264225 countsByYear W20052642252014 @default.
• W2005264225 countsByYear W20052642252015 @default.
• W2005264225 countsByYear W20052642252016 @default.
• W2005264225 countsByYear W20052642252017 @default.
• W2005264225 countsByYear W20052642252018 @default.
• W2005264225 countsByYear W20052642252019 @default.
• W2005264225 countsByYear W20052642252021 @default.
• W2005264225 crossrefType "journal-article" @default.
• W2005264225 hasAuthorship W2005264225A5029167216 @default.
• W2005264225 hasAuthorship W2005264225A5066461508 @default.
• W2005264225 hasBestOaLocation W20052642251 @default.
• W2005264225 hasConcept C126322002 @default.
• W2005264225 hasConcept C127413603 @default.
• W2005264225 hasConcept C1862650 @default.
• W2005264225 hasConcept C2776361831 @default.
• W2005264225 hasConcept C2778818304 @default.
• W2005264225 hasConcept C2780645631 @default.
• W2005264225 hasConcept C71924100 @default.
• W2005264225 hasConcept C78519656 @default.
• W2005264225 hasConceptScore W2005264225C126322002 @default.
• W2005264225 hasConceptScore W2005264225C127413603 @default.
• W2005264225 hasConceptScore W2005264225C1862650 @default.
• W2005264225 hasConceptScore W2005264225C2776361831 @default.
• W2005264225 hasConceptScore W2005264225C2778818304 @default.
• W2005264225 hasConceptScore W2005264225C2780645631 @default.
• W2005264225 hasConceptScore W2005264225C71924100 @default.
• W2005264225 hasConceptScore W2005264225C78519656 @default.
• W2005264225 hasIssue "10" @default.
• W2005264225 hasLocation W20052642251 @default.
• W2005264225 hasLocation W20052642252 @default.
• W2005264225 hasOpenAccess W2005264225 @default.

• next