Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, December 29, 2023

The role of clinical neurophysiology in the definition and assessment of fatigue and fatigability

Ask your doctor if anything in here will cure post stroke fatigue. The key word there is cure, NOT MANAGE OR ASSESS!

The role of clinical neurophysiology in the definition and assessment of fatigue and fatigability

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https://doi.org/10.1016/j.cnp.2023.12.004Get rights and content
Under a Creative Commons license
open access

Highlights

  • Though a common symptom, fatigue is difficult to define and investigate, and occurs in a wide variety of disorders, with differing pathological causes.

  • This review aims to guide clinicians in how to approach fatigue and to suggest that neurophysiological tests may allow an understanding of its origin and severity.

  • The effectiveness of neurophysiological tests as cost-effective objective biomarkers for the assessment of fatigue has been summarised.

Abstract

Though a common symptom, fatigue is difficult to define and investigate, occurs in a wide variety of neurological and systemic disorders, with differing pathological causes. It is also often accompanied by a psychological component. As a symptom of long-term COVID-19 it has gained more attention.

In this review, we begin by differentiating fatigue, a perception, from fatigability, quantifiable through biomarkers. Central and peripheral nervous system and muscle disorders associated with these are summarised. We provide a comprehensive and objective framework to help identify potential causes of fatigue and fatigability in a given disease condition. It also considers the effectiveness of neurophysiological tests as objective biomarkers for its assessment. Among these, twitch interpolation, motor cortex stimulation, electroencephalography and magnetencephalography, and readiness potentials will be described for the assessment of central fatigability, and surface and needle electromyography (EMG), single fibre EMG and nerve conduction studies for the assessment of peripheral fatigability.

The purpose of this review is to guide clinicians in how to approach fatigue, and fatigability, and to suggest that neurophysiological tests may allow an understanding of their origin and interactions. In this way, their differing types and origins, and hence their possible differing treatments, may also be defined more clearly.

Keywords

Fatigue
Fatigability
Neurophysiology
Electroencephalography
Transcranial magnetic stimulation
Electromyography
Evoked potentials
Covid-19
Myalgic encephalomyelitis/ Chronic fatigue syndrome

1. Introduction

Chronic, disruptive fatigue is a significant symptom in several chronic diseases, with a myriad of definitions. Since the turn of the century, there has been several attempts to delineate and differentiate different types of fatigue in pathophysiological terms (Chaudhuri and Behan, 2004, Kluger et al., 2013, Kuppuswamy, 2017). Some have focussed on symptoms reported by patients, which may be defined as ‘the state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli,’ (Dittner et al., 2004), ‘a reversible decrease or loss of abilities associated with a heightened sensation of physical or mental strain even without conspicuous effort, due to an overwhelming feeling of exhaustion, which leads to an inability to sustain or difficulty in sustaining even routine activities,’ (Staub and Bogousslavsky, 2001). Others have tried to capture the mechanisms of fatigue such as ‘difficulty in initiation of or sustaining voluntary activities,’ (Chaudhuri and Behan, 2004) and ‘a percept arising primarily from alterations within the activational systems that inform voluntary action,’ (Kuppuswamy, 2017).

These approaches have, at times, been confused by conflation of two distinct phenomena both described as fatigue; the ‘feeling’ or ‘perception’ which can only be described using self-reported measures such as questionnaires, and a reduction in performance over time, measurable by behavioural and neurological indices. This confusion has led to some proposing the use of the term ‘fatigue’ to refer only to the ‘feeling’ and not to performance changes, which are then referred to as ‘fatigability’ (Kluger et al., 2013). We will adopt this nomenclature. A further source of confusion arises from attributing fatigue and fatigability to different underlying neural systems. The terms ‘mental’ and ‘physical’ fatigue have been commonly interpreted as mental fatigue; perception involving higher order cognitive networks (fatigue in accordance with the new proposal); and physical fatigue; performance change related to reduced motor output (fatigability in accordance with the new proposal). However, it is important to note that both ‘fatigue’ and ‘fatigability’ may apply in both motor output and cognitive function.

The possible sites and mechanisms of fatigue are illustrated in Fig. 1.

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Fig. 1. Schematic diagram of the sites and possible mechanisms of fatigue. From Patikas et al. (2018).

Both fatigue and fatigability may also have ‘central’ and ‘peripheral’ origins within different systems. Within sensorimotor networks, changes seen in the neuromuscular junction and the muscular end organ are labelled as peripheral fatigability, while changes in neural networks proximal to the neuromuscular junction are labelled central fatigability. (Note: The dichotomisation into central and peripheral does not directly map on to fatigue and fatigability). Both central and peripheral changes are seen within the sensorimotor networks with repetition of activity, and therefore both central and peripheral factors contribute to performance fatigability (Gandevia et al., 1996, Gandevia et al., 1995b). Though the origins of fatigue are still debated, the general consensus is that it must be generated within the brain, and is possibly a result of poor integration between anticipated and real sensory input (Greenhouse-Tucknott et al., 2022, Kuppuswamy, 2022). Evidence from those with various diseases supports the idea that altered attention to a wide range of sensory inputs including proprioceptive, visual and auditory, (De Doncker et al., 2020), in the absence of explicit autonomic dysfunction, may lead to fatigue due to impaired sensory processing in this population.

The application of the concept of central and peripheral fatigue in cognitive systems is somewhat trickier, as the output of the cognitive system converges on the sensorimotor system, such as speech or movement. Metrics such as reaction time, movement speed and accuracy of movement capture the decline in cognitive function. Such motor metrics need to be relied upon as cognitive function does not have any independent effector organs. For purposes of this review, we will focus on fatigue and fatigability within the sensorimotor system.

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