The point is to solve the fatigue problem! HOW EXACTLY ARE YOU GOING TO ACCOMPLISH THAT?
Survivors don't want to 'cope' 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
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.(WHOM is doing the followup to solve the fatigue problem? Specific names only!
Introduction
Post-stroke
fatigue (PSF) is a significant symptom for stroke survivors with few
effective, evidence-based interventions currently available. The lack of
evidence-based interventions is largely a result of poor understanding
of the phenomenon, with little agreement on its definition and
measurement. Fatigue is a complex phenomenon with multiple driving
factors, which requires a systematic deconstruction of the phenomenon to
propel advances in the field. This aim was pursued following the recent
Stroke Recovery and Rehabilitation Roundtable (SRRR) consensus process
involving experts in the field, which has produced a comprehensive
definition and guidelines for measurement of PSF alongside a brief
exposition on the possible mechanisms of fatigue and available
interventions.1
In
this companion SRRR paper we have put forward a clear definition of
fatigue that incorporated both expert consensus and personal experience
of stroke survivors. PSF is not mere tiredness, but a “feeling of
exhaustion, weariness or lack of energy that can be overwhelming, and
which can involve physical, emotional, cognitive and perceptual
contributors, which is not relieved by rest and affects a person’s daily
life.” Previous studies of PSF have frequently been confounded by other
conditions such as depression, anxiety, and sleep disorders which often
associate with fatigue.2
While these conditions might contribute to the feeling of fatigue, they
are dissociable and need to be identified at the time of diagnosis. For
example, Fluoxetine relieves depression but not fatigue.3
The consensus view of our SRRR working group was that the Fatigue
Severity Scale-7 (FSS-7) represented the most commonly used fatigue
measure. Despite its wide usage, this scale has several drawbacks as it
does not distinguish between different domains and does not measure
fatigue severity or the impact of fatigue on communication ability. It
primarily captures impact and interference of fatigue in daily life. For
research purposes nuanced interpretations of findings will require the
use of domain specific scores from other elaborate fatigue scales
summarized in the main paper.1
Clinically, in order to ensure that PSF does not continue to be an
invisible symptom, it is important that it is detected as soon as
possible following stroke. We have recommended that the Stroke Fatigue
Clinical Assessment Tool (SF-CAT) best meets this need. The SF-CAT can
be administered via interview and should be part of clinical follow up
for all stroke survivors.
The primary goal of
the current current paper is to elaborate on mechanisms of PSF briefly
discussed in a companion SRRR paper on PSF.1
Here, we present a more comprehensive description of the potential
processes that drive PSF in order to guide future research into the
biological mechanisms of PSF and ultimately the development of new
therapeutic interventions. We draw from the literature both in stroke
and other diseases where fatigue is a significant symptom and put
forward a model of PSF that further highlights promising avenues of
future research.
We begin by presenting the
idea of PSF as a cluster of disorders with potentially dissociable
mechanisms. We then discuss evidence that supports inflammation and
immune dysregulation as a potential process that could underpin both
acute PSF and long-term PSF. Next, we discuss how dopamine (DA), a
neuromodulator with diverse functions including effort perception,
motivation, and memory, could be implicated in PSF, with evidence
supporting dopaminergic pathways as a potential therapeutic target.
Finally, we discuss whole brain neural network changes and exercise
induced multi-system dynamics in the context of PSF, both
mechanistically and therapeutically. Furthermore, throughout the
manuscript, we present evidence from other human diseases where fatigue
is a significant symptom, to identify possible overlapping mechanisms
with PSF. This is based on the premise that fatigue, in the chronic
stages of a disease is delinked from the primary etiopathology of the
disease and commonalities in the experience of chronic fatigue indicate a
common disease-independent mechanism. Finally, we present a single
framework (Figure 1) that links the available evidence and identifies the gaps in our knowledge about PSF.
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