Inflammatory Signaling in Post-Stroke Fatigue and Depression

Wen, Hongmei; Weymann, Kris; Wood, Lisa J.; Wang, Qing Mei

doi:10.1159/000494988

Cited by 60 publications

(52 citation statements)

References 122 publications

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“…Etiology of the PSD is considered multifactorial, a combination of biological and environmental factors; in this sense one of the most supported biological hypotheses currently is related with the participation of inflammatory mediators. 22 In this sense it has been shown that the proinflammatory environment increases the activation of the KP in the CNS. 23,24 However, the neurobiological relevance of this route lies mainly in that there is evidence that some of its intermediate metabolites have redox and neuroactive properties, modulating glutamatergic, cholinergic, and dopaminergic neurotransmission.…”

Section: Discussionmentioning

confidence: 99%

Serum Kynurenines Correlate With Depressive Symptoms and Disability in Poststroke Patients: A Cross-sectional Study

Carrillo‐Mora

Cruz

Estrada-Cortés

et al. 2020

Neurorehabil Neural Repair

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Background Poststroke depression (PSD) is related to adverse functional and cognitive prognosis in stroke patients. The participation of kynurenine pathway metabolites in depression has been previously proposed; however, there are few studies on its role in PSD and disability in stroke. Objective To investigate if there is a correlation between serum kynurenines levels with poststroke anxiety and depression symptoms and disability scales. Methods A cross-sectional case-control study was conducted in patients with first stroke, of >1 month and <1 year of evolution, with no history of previous psychiatric or neurological disorders; the Hospital Anxiety and Depression Scale (HADS), Montreal Cognitive Assessment (MoCA), functional evaluations (Barthel index, Functional Independence Measure [FIM]) were applied and serum kynurenines (Kyns) were determined. Results Sixty patients were included; significant depressive symptoms were found in 63% of the cases; a significant and positive correlation was obtained between levels of 3-hydroxykynurenine (3-HK) with HADS-T ( r = 0.30, P = .025) and HADS-D ( r = 0.28, P = .039). Depressed patients showed significantly higher levels of 3HK ( P = .048) and KYNA ( P = .0271) than nondepressed patients; the 3HK levels were inversely correlated with functional scales: Barthel index ( r = −0.31, P = .02), FIM ( r = −0.40, P = .01); in addition, serum 3HK levels were significantly higher in patients with poor sleep quality ( P = .0190). Conclusions Serum Kyns show correlation with the presence and severity of depressive symptoms and with the disability and sleep quality. Kyns may be a potential marker of depression risk and disability in stroke in future.

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Section: Discussionmentioning

confidence: 99%

Serum Kynurenines Correlate With Depressive Symptoms and Disability in Poststroke Patients: A Cross-sectional Study

Carrillo‐Mora

Cruz

Estrada-Cortés

et al. 2020

Neurorehabil Neural Repair

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“…Post-stroke fatigue (PSF) is a common and lasting sequela after stroke. Of the patients with a first stroke, up to 75% will suffer PSF in the first year following stroke [1]. PSF has a detrimental impact on the recovery of neurological function, quality of life and rehabilitation of stroke survivors [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Elevated plasma high‐sensitivity C‐reactive protein at admission predicts the occurrence of post‐stroke fatigue at 6 months after ischaemic stroke

Liu

Wang

et al. 2020

Euro J of Neurology

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Background and purpose Post‐stroke fatigue (PSF) is a common neuropsychiatric affective symptom occurring after stroke. Evidence indicates activated inflammatory pathways are involved in modulating the stroke and fatigue. High‐sensitivity C‐reactive protein (hs‐CRP) is one of the most sensitive indicators of inflammation. Our aim was to estimate the association between plasma hs‐CRP and PSF after acute ischaemic stroke. Methods In all, 212 acute ischaemic stroke patients were consecutively recruited within the first 14 days after stroke onset and followed up for 6 months. Plasma hs‐CRP levels were assayed by enzyme linked immunosorbent assay. Fatigue severity was assessed using the Fatigue Scale for Motor and Cognitive Functions. A score ≥ 43 is defined as PSF. Results Sixty‐eight stroke patients (32.1%) were diagnosed with PSF at 6 months’ follow‐up. In the patients with PSF, plasma hs‐CRP levels were significantly higher compared with those in non‐PSF patients (t = −8.524, P ≤ 0.001). In multivariate analyses, plasma levels of hs‐CRP were independently associated with PSF at 6 months (odds ratio 3.435, 95% confidence interval 2.222–5.309; P ≤ 0.001) after adjusting other recorded variables. Based on the receiver operating characteristic curve, the optimal cut‐off value of plasma hs‐CRP levels as an indicator for the prediction of PSF was projected to be 0.52 mg/dl, which yielded a sensitivity of 77.9% and a specificity of 74.3%, with the area under the curve 0.794 (95% confidence interval 0.725–0.864; P ≤ 0.001). Conclusion Elevated plasma hs‐CRP levels at admission were associated with PSF 6 months after stroke, suggesting that these alterations might predict the development of PSF in stroke patients.

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“…Increasing evidence points to systemic inflammatory responses and sickness behaviour induced by pro-inflammatory cytokines as important factors in post-stroke fatigue. 37 To date, there are no human studies on the role of HMGB1 in post-stroke fatigue. However, in an experimental animal stroke model, it was observed that the release of HMGB1 and signalling through RAGE contributed to brain injury–induced sickness behaviour.…”

Section: Discussionmentioning

confidence: 99%

Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn’s disease

et al. 2021

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Fatigue is common in all chronic inflammatory and autoimmune diseases. A conceptual model for understanding the biological basis of fatigue describes it as being a part of the sickness behaviour response generated by pro-inflammatory cytokines and other mediators. We hypothesised that the pro-inflammatory high mobility group box 1 (HMGB1) protein is a fatigue-inducing molecule and that auto-Abs against HMGB1 reduce fatigue. We measured Abs against disulphide (ds) HMGB1 and fully reduced (fr) HMGB1 in plasma from 57 patients with Crohn’s disease. Fatigue was rated using the fatigue visual analogue scale (fVAS) and disease activity with faecal calprotectin, C-reactive protein and the Simple Endoscopic Score for Crohn’s disease. Multivariable regression models identified anti-dsHMGB1 and anti-frHMGB1 Abs as the strongest contributing factors for fVAS scores ( B = −29.10 ( P = 0.01), R2 = 0.17, and B = −17.77 ( P = 0.01), R2 = 0.17, respectively). Results indicate that anti-HMGB1 auto-Abs alleviate fatigue possibly by down-regulating HMGB1-induced sickness behaviour.

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Inflammatory Signaling in Post-Stroke Fatigue and Depression

Cited by 60 publications

References 122 publications

Serum Kynurenines Correlate With Depressive Symptoms and Disability in Poststroke Patients: A Cross-sectional Study

Serum Kynurenines Correlate With Depressive Symptoms and Disability in Poststroke Patients: A Cross-sectional Study

Elevated plasma high‐sensitivity C‐reactive protein at admission predicts the occurrence of post‐stroke fatigue at 6 months after ischaemic stroke

Anti-HMGB1 auto-Abs influence fatigue in patients with Crohn’s disease

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