EFFECTIVENESS OF ACETYLSALICYLIC ACID IN CORRECTION OF POST-STROKE FATIGUE DURING ACUTE CEREBROVASCULAR EVENTS

  • I.I. Delva Ukrainian Medical Stomatological Academy, Poltava, Ukraine
Keywords: stroke, fatigue, C-reactive protein, interleukin, acetylsalicylic acid.

Abstract

Post-stroke fatigue (PSF) is a common and often debilitating sequela of strokes that affects more than one third of stroke patients. Recent investigations revealed etiologic and pathogenetic heterogeneity of PSF depending on the time after acute cerebrovascular event (ACE). PSF that occur during acute stroke is associated predominantly with biological factors, including stroke-inducing immune and inflammatory reactions. In particular, we found significant associations between clinical features of PSF and certain regularities of C-reactive protein (CRP) and interleukin (IL)-1β levels in blood serum during the first 3 months after ACE occurrence. Given that there is not a clearly defined etiology for PSF, there are no rationally informed interventions. Іf dysregulation of the immune response isan important contributing factor to PSF, interventions that lessen inflammation would be appropriate treatment strategies. Іt would be reasonable to consider ASA, albeit at a higher dose than is normally used for secondary stroke prevention, as a treatment for PSF. Thus, it is advisable to study effects of ASA at the anti-inflammatory dose (300 mg a day) on markers of system inflammation an don PSF clinical course during the first 3 months after ACE occurrence. Objective: to study effectiveness of ASA at the anti-inflammatory dose (300 mg a day) on PSF clinical course and ASA effects on markers of system inflammation during the first 3 months after acute cerebrovascular event (ACE) occurrence. We recruited in the study 39 in hospital patients with ischemic strokes and transient ischemic attacks (TIA) who needed to take acetylsalicylic acid (ASA). All patients had been diagnosed with PSF within the first 3 days after ACE onset. PSF was diagnosed by use of questionnaire – Fatigue Assessment Scale (FAS). We formed two groups of patients. The first group (control PSF group) consisted of 24 patients who used ASA according to «Unified clinical protocol for medical care. Ischemic stroke (emergency, primary, secondary (specialized) medical aid, medical rehabilitation)» - after excluding hemorrhagic stroke by neuroimaging it was started ASA intake in the doses of 150-300 mg a day enterally during hospital stay with subsequent intake of 75-150 mg a day (prophylactic dose) continuously after hospital discharge. The second group (ASA PSF group) had 15 patients who started to use ASA just after excluding hemorrhagic stroke in the dosage of 300 mg a day for 3 months with subsequent dose reduction to 75-150 mg a day (prophylactic dosage) continuously. Diagnosis of PSF presence/absence, measurement of PSF severity and simultaneous measurement of systemic inflammatory markers in blood serum were carried out at the certain time points after ACE onset: at the first 3 days, at 1 month and at 3 months. Concentrations of СRP, IL-1β andIL-6 in blood serum were measured by enzyme-linked immunosorbent assay. The use of ASA in the dose of 300 mg a day during 3 months in patients who had been diagnosed with PSF within the first days after ACE occurrence is associated with significant decreasing of PSF intensity due to FAS in comparison with using of preventive ASA doses. The use of ASA in the dose of 300 mg a day during 3 months after ACE occurrence is associated with significant modification of post-stroke inflammatory response in form of CRP and IL-1β blood level changes.

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References

1. Delva II, Lytvynenko NV, Delva MY. Post-stroke fatigue and its dimensions within first 3 months after stroke. Wiadomosci lekarskie (Warsaw, Poland: 1960). 2017;70(1):43-46.
2. Delva M, Lytvynenko N, Delva I. Factors associated with the time-based phenomenology of post-stroke fatigue over the first year after stroke occurrence. Georgian medical news. 2018;6(279):92–97.
3. Chen K, Marsh EB. Chronic post-stroke fatigue: It may no longer be about the stroke itself. Clinical neurology and neurosurgery. 2018;174:192-197.
4. Wu S., Mead G, Macleod M. Chalder T, Model of understanding fatigue after stroke, Stroke. 2015;46:893–898.
5. McKechnie F, Lewis S, Mead G. A pilot observation al study of the association between fatigue after stroke and C-reactive protein. The journal of the Royal College of Physicians of Edinburgh. 2010;40(1):9-12.
6. Ormstad H, Aass HC, Amthor KF, Lund-Sorensen N, Sandvik L. Serum cytokine and glucose levels as predictors of poststroke fatigue in acute ischemic stroke patients. J Neurol. 2011;258:670–676.
7. Ormstad H, Aass HC, Amthor KF, Lund-Sorensen N, Sandvik L. Serum levels of cytokines, glucose, and hemoglobin as possible predictors of poststroke depression, and association with poststroke fatigue. Int J Neurosci. 2012;122:682–690.
8. McGeough E, Pollock A, Smith LN, Dennis M, Sharpe M, Lewis S, at all. Interventions forpost-stroke fatigue. Cochrane Database Syst Rev. 2009:p.CD007030.
9. Becker KJ. Inflammation and the silent sequelae of stroke. Neurotherapeutics. 2016;13(4):801-810.
10. Wingerchuk DM, Benarroch EE, O’Brien PC, Keegan BM, Lucchinetti CF,Noseworthy JH, et al. A randomized controlled crossover trial of aspirin forfatigue in multiple sclerosis. Neurology. 2005;64:1267–1269.
11. Shaygannejad V, Janghorbani M, Ashtari F, Zakeri H. Comparison of the effect of aspirin and amantadine for the treatment of fatigue in multiplesclerosis: a randomized, blinded, crossover study. Neurol Res. 2012;34:854–858.
12. Gaglia MA Jr, Clavijo L. Cardiovascular pharmacology core reviews: aspirin. J Cardiovasc Pharmacol Ther. 2013;18:505-513.
13. Gao XR, Adhikari CM, PengLY, et al. Efficacy of differen doses of aspirin in decreasing blood levels of inflammatory markers in patients with cardiovascular metabolic syndrome. JPharm Pharmacol.2009;61:1505-1510.
14. Ikonomidis I, Andreotti F, Economou E, et al. Increased proinflammatory cytokines in patients with chronic stable angina and their reduction by aspirin. Circulation.1999;100:793-798.
15. Michielsen HJ, De Vries J, Van Heck GL. Psychometric qualities of a brief self-rated fatigue measure: The Fatigue Assessment Scale (FAS). J Psychosom Res.2003;54:345–352.
16. Delva M, Lytvynenko N, Delva I. Factors associated with the time-based phenomenology of post-stroke fatigue over the first year after stroke occurrence. Georgian Med News. 2018;279:92-97.
17. Miller AH, Haroon E, Raison CL, Felger JC. Cytokine targets in the brain: impact on neurotransmitters and neurocircuits. Depress Anxiety. 2013;30(4):297–306.
18. Malynn S, Campos-Torres A, Moynagh P, Haase J. The pro-inflammatory cytokine TNF-alpha regulates the activity and expression of the serotonin transporter (SERT) in astrocytes. Neurochem Res. 2013;38(4):694–704.
19. Ronnback L, Hansson E. On the potential role of glutamate transport in mental fatigue. J Neuroinflammation.2004;1:22.
20. Karshikoff B, Sundelin T,Lasselin J.Role of inflammation in human fatigue: relevance of multidimensional assessments and potential neuronal mechanisms. Frontiers in immunology. 2017;8:21.
Published
2019-04-12
How to Cite
Delva, I. (2019). EFFECTIVENESS OF ACETYLSALICYLIC ACID IN CORRECTION OF POST-STROKE FATIGUE DURING ACUTE CEREBROVASCULAR EVENTS. The Medical and Ecological Problems, 23(1-2), 8-12. https://doi.org/10.31718/mep.2019.23.1-2.02