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Published on: May 22, 2019
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Poststroke fatigue: hints to a biological mechanism
Kyra Becker1, Ruth Kohen2, Richard Lee1
1Department of Neurology, University of Washington School of Medicine, Seattle, Washington.
Summary
Poststroke fatigue (PSF) may be linked to immune system genes. Specific gene variations in IL1RN and TLR4 were associated with fatigue levels after ischemic stroke, suggesting immune dysregulation plays a role.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Poststroke fatigue (PSF) is a prevalent condition with an unclear biological basis.
- This study investigated the potential link between PSF and systemic inflammation.
- Immune response gene polymorphisms were examined as a potential factor in PSF.
Purpose of the Study:
- To explore the relationship between genetic variations in immune response genes and the occurrence of poststroke fatigue.
- To investigate the role of specific single nucleotide polymorphisms (SNPs) in IL1RN and TLR4 genes in PSF.
Main Methods:
- A substudy of a larger trial involving patients with ischemic stroke.
- Fatigue was assessed using the Fatigue Assessment Scale at multiple time points post-stroke (30, 90, 180, 365 days).
- Genotyping was performed for one SNP in IL1RN (rs4251961) and two SNPs in TLR4 (rs4986790, rs4986791).
Main Results:
- Over half (56%) of the 39 participants reported fatigue, which remained consistent over time.
- The C allele of the IL1RN rs4251961 SNP was significantly associated with increased self-reported fatigue (P = .03).
- Polymorphisms in the TLR4 gene were associated with reduced levels of fatigue (P = .04).
Conclusions:
- Single nucleotide polymorphisms in genes with opposing effects on immune responses were differentially associated with PSF.
- These findings suggest a direct association between immune signaling dysregulation and the development of poststroke fatigue.
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