Oh for fucks sake; stop writing this crapola and just solve fatigue! Oh, you don't have the brainpower to do that simple task? Then go back to playing in your sandbox and let the adults work at it!
Let's see how long everyone in stroke has been incompetent at this problem!
- post stroke fatigue
(58 posts to January 2018)
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 fire everyone involved with this lazy crapola!
Will your incompetent doctor, hospital and board of directors fail to deliver the action needed to solve this problem? NOT DOING SO IS COMPLETE FUCKING INCOMPETENCE!
Poststroke Fatigue: An Overlooked Barrier to Functional Recovery
Despite the significance of PSF, poststroke rehabilitation strategies continue to focus on conspicuous impairments, such as sensory, motor, cognitive, and speech deficits, while overlooking fatigue and its detrimental impact on recovery.5, 6 In this commentary, we assert that PSF must be recognized and prioritized as a core component of poststroke rehabilitation. To build this argument, we highlight emerging evidence on the impact of PSF on recovery, examine the reasons for its continued neglect, and advocate for its integration into rehabilitation frameworks as a crucial step toward improving functional recovery after stroke.
PSF HINDERS FUNCTIONAL CAPACITY AND RECOVERY AFTER STROKE
PSF is a multidimensional phenomenon2 that significantly impairs functional recovery after stroke.7 PSF reduces patient engagement in rehabilitation, which is essential for effective recovery.8 Individuals experiencing PSF are more likely to miss therapy sessions, exhibit reduced ability to actively participate in rehabilitation protocols,9 and report insufficient energy to complete home‐based exercises.10 PSF also increases the need for prolonged rest10 and reduces participation in cognitively, emotionally, or physically demanding tasks.11 As a result, PSF limits workforce reintegration,12 restricts social participation, and directly stalls functional gains, often leading to more frequent and prolonged hospitalizations.7
Even when individuals participate in rehabilitation, PSF affects physical and cognitive domains essential to the rehabilitation process.13 Fatigue impairs motor control by reducing movement accuracy, increasing force variability, and slowing reaction time.13, 14, 15, 16 For example, Hyngstrom et al. found that PSF diminishes hip flexor strength and gait stability,14 and other studies link PSF to impaired lower limb control15 and slower movement speed.13 These motor deficits translate into greater difficulty performing activities of daily living,17 which in turn hinder recovery and quality of life. Further, PSF can interfere with motor learning,11 the fundamental process underlying neurorehabilitation. Stroke rehabilitation relies on repeated, high‐quality practice to drive motor skill acquisition and memory consolidation.18 However, Branscheidt et al. demonstrated that physical fatigue impairs both processes in healthy adults, raising serious concerns about the impact of fatigue in clinical populations.11 Although the effect of PSF on motor learning after stroke has yet to be fully investigated, it is plausible that fatigue directly impairs learning or indirectly reduces training efficiency, thus diminishing functional recovery after stroke. Lastly, PSF reduces attention, planning, and capacity to retain the information, making it difficult to perform cognitive tasks, but also to integrate feedback and error monitoring during rehabilitation.19, 20
Taken together, PSF undermines recovery by limiting rehabilitation engagement and impairing both physical and cognitive function. Yet despite its profound impact, fatigue remains overlooked and underprioritized in rehabilitation. In the next section, we examine why this may be the case.
WHY PSF REMAINS UNDERPRIORITIZED IN STROKE REHABILITATION?
We argue that PSF remains underrecognized and undertreated in stroke rehabilitation due to its broad definition21 and poor operationalization,22, 23 its misinterpretation as a mere consequence of other psychiatric conditions2, 24 or the recovery process,2, 24 and the stigmatization of fatigue within rehabilitation settings.25
How we define and conceptualize fatigue remains a central obstacle to addressing it effectively. Clinically, PSF is evaluated exclusively via self‐reported measures that combine all aspects of fatigue into a single score23, 26; whereas scientifically, different operationalizations of fatigue are used interchangeably.3, 6 We posit that this lack of conceptual clarity leads to inconsistent results that prevent us from understanding the prevalence, behavioral presentation, mechanisms, and functional consequences of fatigue, ultimately hindering the development of effective clinical interventions.27, 28
In addition, fatigue is commonly interpreted as an inevitable consequence of the rehabilitation process itself10 or a simple byproduct of psychiatric conditions,29 such as depression, poor sleep, or anxiety. Yet accumulating evidence suggests that fatigue can be a distinct causal factor6 that independently contributes to poor functional performance and impairs recovery.3, 8, 11, 13, 14, 15, 16, 17, 30, 31, 32 For example, in major depressive disorders, fatigue is among the most reported symptoms,30 often precedes the onset of depressive episodes,31 and strongly predicts relapses after treatment.33 A similar scenario may hold for PSF, which could act as a prodromal symptom and an independent driver of functional decline. Supporting this, Ingles et al. found that fatigue impaired mobility after stroke, even after controlling for depression.32
Finally, the neglect of fatigue is compounded by the siloed nature of clinical care and scientific inquiry, where PSF is rarely integrated into rehabilitation frameworks.27 Historically, rehabilitation models have prioritized hemiparesis, cognitive decline, or aphasia. In contrast, fatigue is dismissed as a vague, subjective, and secondary complaint that should be endured rather than treated.34 This perception has led to stigma, making it difficult for patients to convey the severity of their fatigue and for clinicians to view it as anything other than inevitable or peripheral to recovery.10 Similarly, in research settings, fatigue is often dismissed as noise or a confound to be controlled for. Consequently, fatigue research has been segregated from traditional rehabilitation sciences, reinforcing the false belief that fatigue is unmeasurable, untreatable, and unworthy of investigation.3, 6
Taken together, these barriers contribute to a limited understanding of PSF and undermine efforts to address it as a distinct and treatable symptom of stroke survivors. To break this cycle, clinicians and researchers must redefine PSF as a core barrier to recovery that warrants clinical and scientific attention. Importantly, doing so requires greater conceptual clarity. Therefore, we must first establish what PSF is and, importantly, what it is not, to distinguish it from other comorbidities, identify its unique features, and target it more effectively in both clinical practice and research.
PROPOSED FEATURE‐BASED FRAMEWORK TO CONCEPTUALIZE PSF
To move beyond the historical neglect of PSF, the field must establish a clear, shared definition of PSF and distinguish it from other comorbidities. Our central premise is that in response to the multidimensional nature of PSF, the field has collapsed distinct features of fatigue into a single, imprecise construct. As a consequence, clinically, fatigue is evaluated almost exclusively using self‐reported measures that combine multiple aspects of fatigue into a single score,23, 26 whereas, scientifically, different operationalizations of fatigue are often used interchangeably.3, 6 These approaches limit our ability to identify the neurobiological mechanisms that give rise to PSF and hinder the development of effective treatments. In an important step toward addressing this problem, Kluger et al. highlighted that fatigue comprises 2 main features, namely “perceptions of fatigue” and “performance fatigability,” and argued that these should not be used interchangeably.3 Although this framework has been highly informative, we argue that it remains incomplete.
Here, we propose to operationalize PSF along 4 distinguishable features that can co‐occur but need not covary16, 35 (Figure): (1) perceived effort (ie, how one perceives a previously exerted action; retrospective), (2) subjective feelings of tiredness (ie, how tired one feels), (3) reduced likelihood to exert effort (ie, an individual's decision to engage in effortful actions; prospective), and (4) decrements in performance (ie, fatigability3). Unlike traditional approaches, each feature should be assessed using dedicated tools. Ratings or ecological momentary assessment can capture perceived effort and subjective feelings of tiredness; effort‐based decision paradigms can quantify an individual's likelihood of exerting effort16, 36; and objective changes in accuracy, variability, or reaction time can index decrements in performance. Operationalizing fatigue through these features could help us move beyond descriptive accounts and toward mechanistic explanations of PSF.
We further encourage integrating these behavioral features with neurophysiological (eg, electromyography/electromyography/ECG/heart rate variability) and neuroimaging (eg, magnetic resonance imaging) measures to identify feature‐specific mechanisms and candidate biomarkers of PSF. Our working hypothesis is that each feature is supported by distinct neurobiological systems.16 Specifically, we hypothesize that (1) a sensorimotor network, involving the posterior insula, primary motor and sensory cortices, as well as the cerebellum, underpins perceived effort; (2) an affective network, involving the ventral anterior insula and other limbic regions, underpins subjective feelings of tiredness; (3) a decision‐making/valuation network, involving the ventral striatum and the ventromedial prefrontal cortex, underpins effort‐based decision‐making; and (4) task‐specific networks, in either the cognitive or physical domains, will underpin performance.
Within this framework, a critical unanswered question is how stroke interacts with the proposed feature‐specific mechanisms of fatigue. We posit that stroke can influence these systems via 2 complementary ways. First, the primary lesion may directly disrupt the neuroanatomical networks that support individual features.37 Damage to sensorimotor, affective, valuation, or task‐specific networks may disrupt the function of these networks, resulting in a maladaptive behavioral presentation of fatigue that is directly informed by the location of the lesion. Second, stroke may induce a broader allostatic response38, 39 in which lesion‐induced dyshomeostasis across neurophysiological systems drives persistent regulatory signaling.2 In this scenario, PSF may emerge not only from focal structural damage but also as a feedback signal arising from ongoing efforts to restore internal equilibrium and promote energy conservation, rest, and recovery. Importantly, these mechanisms are not mutually exclusive and may converge to produce similar behavioral manifestations of PSF. Future studies should therefore investigate whether PSF reflects direct neural disruption, systemic feedback signaling in response to homeostatic challenge, or a combination of both. Understanding how these mechanisms interact is essential for explaining why fatigue persists after stroke and why it remains a prominent barrier to recovery.
Finally, our central premise is that the proposed feature‐based approach will enable clinicians and researchers to more precisely characterize how PSF manifests, distinguish it from other comorbidities, and target it as a primary outcome of rehabilitation. For example, disproportionate increases in perceived effort and reduced willingness to exert effort despite preserved motor performance would be consistent with a central regulatory signal rather than primary neuromuscular weakness. In contrast, isolated decrements in performance accompanied by stable effort ratings and preserved willingness to exert effort would point toward neuromuscular fatigability or weakness. By assessing PSF at the level of its constituent features, an apparently intangible symptom can be transformed into a set of quantifiable, mechanistically interpretable components that can be meaningfully integrated into both clinical practice and research.
CALL TO ACTION: INTEGRATING PSF INTO STROKE REHABILITATION
Given its profound impact on recovery, PSF must be systematically addressed as a core component of stroke rehabilitation. To achieve this, we propose 3 key priorities. First, we should reframe PSF as a primary, persistent symptom that warrants direct clinical and scientific attention. We should no longer dismiss it as a secondary complaint or an inevitable byproduct of rehabilitation. Clinicians should proactively educate patients and caregivers about the prevalence, consequences, and management of PSF. This shared understanding could help align expectations, incorporate fatigue into rehabilitation goals, and guide the development of personalized fatigue management strategies. Similarly, rehabilitation scientists must directly integrate PSF into core research questions rather than treating it as a confound that must be controlled for. More research is needed to clarify how fatigue manifests after stroke, as well as its effects on motor and cognitive function. Experimental and clinical studies that explicitly target fatigue might enable the identification of mechanistic pathways, improve the design of therapeutic interventions, and generate evidence‐based strategies for addressing PSF in rehabilitation settings. We propose that only by simultaneously advancing both the clinical and scientific approaches to PSF can we fully understand and address the barriers that fatigue imposes on poststroke recovery.
Second, rather than collapsing fatigue into a single self‐reported score, PSF could, and we argue should, be measured with a multidimensional battery that separately captures its different features. When feasible, these behavioral indices can be paired with physiological recordings to identify candidate biomarkers of PSF. The development and use of this strategy could result in feature‐based subscores that (1) track trajectories across subacute and chronic phases, (2) reveal individual differences of relative prominence for each feature, and (3) support patient stratification into actionable phenotypes (eg, effort sensitive, fatigability dominant, tiredness dominant, or mixed). Crucially, each phenotype could imply distinct intervention strategies. For example, sensorimotor recalibration and feedback optimization for elevated perceived effort, autonomic regulation strategies for pronounced tiredness, contingency‐based scheduling for effort‐averse decision profiles, and targeted strengthening/aerobic conditioning for predominant fatigability. Characterizing PSF in this way may not only advance science but also transform clinical practice, ensuring fatigue is no longer overlooked but systematically measured, targeted, and followed as a core outcome of recovery after stroke.
Lastly, we may not accomplish these priorities without a multidisciplinary approach to PSF. Collaboration among neurologists, rehabilitation specialists, psychologists, researchers, and, importantly, patients will accelerate understanding, facilitate the development of validated assessment tools, and lead to the establishment of effective, evidence‐based treatments. We propose that such a coordinated approach is essential to shift the current paradigm of stroke care to a more holistic model that addresses inconspicuous yet debilitating symptoms like fatigue. By prioritizing awareness, measurement, and collaboration, we can meaningfully integrate PSF into rehabilitation frameworks and improve long‐term recovery outcomes and quality of life for stroke survivors.
CONCLUSIONS
PSF is not just a vague, secondary symptom that must be pushed through—it is a measurable, mechanistically driven, and clinically significant barrier to recovery after stroke. Yet, continuing to overlook it perpetuates poor quality of life, stalls functional gains, and undermines the central goals of rehabilitation. The scientific understanding and tools to address PSF are already within reach; what remains missing is widespread recognition and coordinated action. By redefining how we conceptualize, measure, and manage fatigue, we can establish PSF as a core target of stroke rehabilitation, at par with motor, cognitive, and speech impairments. To us, the path forward is clear: it is time to stop dismissing fatigue and start treating it as an integral component of stroke recovery.
Sources of Funding
This work was supported by the National Institutes of Health (K01AG070327 to Neha Lodha) and (R00NS133961 to Agostina Casamento‐Moran).
Footnotes
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
This article was sent to Jose R. Romero, MD, Associate Editor, for review by expert referees, editorial decision, and final disposition.
For Sources of Funding and Disclosures, see page 5.
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