Mechanisms of Post-Stroke Fatigue: A Follow-Up From the Third Stroke Recovery and Rehabilitation Roundtable

 The point is to solve the fatigue problem! HOW EXACTLY ARE YOU GOING TO ACCOMPLISH THAT? 

Survivors don't want to wait for more research. They want to have fatigue cured! GET THERE!

Well, post stroke fatigue has been proven for years! Don't you keep up-to-date on research? 

 This post stroke fatigue has been known forever. SOLVE THE FUCKING PROBLEM!

At least half of all stroke survivors experience fatigue Known since March 2017

Or is it 70%? Known since March 2015

Or is it 40%? Known since September 2017

I'd have you all fired for incompetence for not solving the problem of fatigue! Telling us it exists does nothing for survivor recovery!

The latest here:

Mechanisms of Post-Stroke Fatigue: A Follow-Up From the Third Stroke Recovery and Rehabilitation Roundtable

Annapoorna Kuppuswamy, PhD https://orcid.org/0000-0002-4288-0814 a.kuppuswamy@ucl.ac.uk, Sandra Billinger, PhD, […], and Dale Corbett, PhD https://orcid.org/0000-0003-0217-4576+8View all authors and affiliations

Volume 38, Issue 1

https://doi.org/10.1177/15459683231219266

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• • Abstract
  • Introduction
  • PSF: Single or Multiple Disorders?
  • Precipitating Factors of PSF
  • Exercise as a Possible Intervention for PSF
  • A Unifying Model of Fatigue
  • Conclusion
  • Acknowledgments
  • Declaration of Conflicting Interests
  • Funding
  • ORCID iDs
  • Footnote
  • References
• PDF / ePub
• • Cite article
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Abstract

Background

Post-stroke fatigue (PSF) is a significant and highly prevalent symptom, whose mechanisms are poorly understood. The third Stroke Recovery and Rehabilitation Roundtable paper on PSF focussed primarily on defining and measuring PSF while mechanisms were briefly discussed. This companion paper to the main paper is aimed at elaborating possible mechanisms of PSF.

Methods

This paper reviews the available evidence that potentially explains the pathophysiology of PSF and draws parallels from fatigue literature in other conditions. We start by proposing a case for phenotyping PSF based on structural, functional, and behavioral characteristics of PSF. This is followed by discussion of a potentially significant role of early inflammation in the development of fatigue, specifically the impact of low-grade inflammation and its long-term systemic effects resulting in PSF. Of the many neurotransmitter systems in the brain, the dopaminergic systems have the most evidence for a role in PSF, along with a role in sensorimotor processing. Sensorimotor neural network dynamics are compromised as highlighted by evidence from both neurostimulation and neuromodulation studies. The double-edged sword effect of exercise on PSF provides further insight into how PSF might emerge and the importance of carefully titrating interventional paradigms.

Conclusion

The paper concludes by synthesizing the presented evidence into a unifying model of fatigue which distinguishes between factors that pre-dispose, precipitate, and perpetuate PSF. This framework will help guide new research into the biological mechanisms of PSF which is a necessary prerequisite for developing treatments to mitigate the debilitating effects of post-stroke fatigue.