Archive for category Fatigue

[VIDEO] Managing Fatigue After A Brain Injury – YouTube

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[BLOG POST] Five Reasons Fatigue Isn’t Like Normal Tiredness (Proving Most People Don’t Get It)

When you’re dealing with a chronic illness, there are a lot of things non-sick people say that are annoying. Things such as, “Aren’t you better yet?” Of course not. This is a chronic illness, not a you-have-it-for-a-week-and-then-it’s-over-with illness. You don’t say that, though. You smile and say, “unfortunately not.” Or friends and family might make a comment about how you’ve taken a lot of time off work lately, as if it was your life plan to become disabled. Or they might mention that you don’t go out much anymore…because clearly you prefer to stay in laid up in bed.

But the most jerkish thing people do is act like the fatigue you’re dealing with—the bone wearying, debilitating, sometimes disabling fatigue—is equivalent to how they felt when they ran a 10k that one time. “Just get more sleep,” they’ll tell you. Or, “You need to push through it. We all get tired.” If you weren’t so fatigued you’d punch the guy right in the face. But you are, so you smile and nod.

Even worse than thoughtless friends spouting this nonsense, is when you get the same thing from doctors. You’d think someone medically trained would be taught the difference between fatigue and normal tiredness, but they’re not. There aren’t even terms to differentiate the two, really. So for medical professionals and non-medical professionals alike, I’ve created a list of the top five reasons that fatigue and normal tiredness should not even be considered in the same sentence. (Other than that one, of course.) Feel free to share it with anyone who doesn’t get it.

5. Sleeping “cures” tiredness; it’s only mildly helpful for fatigue.

When you have chronic fatigue, the number one piece of advice you get from well-meaning non-sick people is to get more sleep. It makes sense. They reflect on their own life and think, “You know, when I feel tired, if I get a good night’s sleep I feel better. Sally should try that.” But that doesn’t work for Sally, and you know why? Because Sally has fucking lupus or Ehlers Danlos Syndrome or Rheumatoid Arthritis. Feeling tiredness in your muscles because you ran some extra errands today is resolved by getting a good eight hours of sleep, but do you know what is not cured by sleeping? Sjogren’s Syndrome. Multiple Sclerosis. Umm, cancer.

While it’s true that getting plenty of rest is good self-care that can reduce flares, it’s not a cure-all, and to suggest that it is is belittling. Especially considering that many people with chronic fatigue are often already sleeping much of the day. Some chronic illnesses sufferers can sleep for sixteen or twenty hours a day and still feel fatigued. Or even if they’re sleeping a normal eight hours, they may feel their worst in the morning, just when you’d predict they’d feel best if their issue was lack of sleep. And all of this ignores the fact that for some people…

4. Fatigue can actually keep you awake.

Sounds stupid, doesn’t it? After working hard all day, most people can lay their head on their pillow and be out within five minutes. Not the case with fatigue. I, myself, have a condition called lupus. It’s an autoimmune disorder, which means that my immune system literally attacks my body rather than outside invaders. It’s sort of like friendly fire in a war. My immune cells are like, “Sorry kidney! Didn’t mean to murder you when I was trying to take out that cold virus. My bad.”

So the fatigue I get stems from the fact that my body is working really hard against the onslaught from…my own body. This sort of fatigue can be so overwhelming that it’s uncomfortable. It’s almost like the tiredness equivalent of pain. It simply doesn’t feel the same as what you experience after doing a lot of cardio. It feels more like your entire life force has been sucked out of your body. It’s disconcerting.

You know that indescribable symptom you get when you have the flu? Not the runny nose or congestion. The feeling that you’re just “sick.” It’s like that feeling amplified. And that feeling is uncomfortable even if there’s not actual pain associated with it (which, with most chronic illnesses, there is anyway). This horrible feeling of fatigue can overcome you and actually make it difficult to fall asleep.

If this seems stupid and horribly counterproductive, you’re right! It feels that way to the sick person too. There’s nothing worse than being horribly fatigued, and yet not being able to fall asleep. That’s why a person with chronic fatigue will recoil at your advice to get more sleep. They’re trying and reminding them of their failure only makes them want to cut you.

3. Pushing through tiredness means you get extra work done; pushing through fatigue means you’re out of commission for a week.

This is probably the biggest pet peeve of the chronically ill: the suggestion that they should just suck it up and push through it. That is actually the worst single piece of advice you could give a chronically ill person, and this is why. People possessing average energy stores and bodies that aren’t falling apart can go for a day or week or even month where they’re not getting enough sleep. Sure they’ll feel crappy, but once they take a weekend to really rest, their body will be back to normal. For a healthy person, it might be totally reasonable to push through some tiredness to get extra work done.

Not so for chronically ill people. Being chronically ill is sort of like starting every day on three hours of sleep, regardless of how much sleep you’ve actually gotten. Strike that. It’s like starting the day on three hours of sleep plus you have the flu. A flu that might never go away or get better. (I’m a bundle of laughs at parties, let me tell you.) If a chronically ill person tries to “push through” their fatigue, they could actually make themselves substantively sicker. The immune system that was just sort of nibbling on their kidneys will now go on full attack, or the moderate pain they had in their joints will be turned up to eleven. And, as you can imagine, that increase of symptoms doesn’t just last during the period that they’re “pushing through” their fatigue. It can last for weeks because now they’ve actually made themselves sicker. Telling a chronically ill person to just suck it up and push through the fatigue is like telling a lung cancer patient to just have another five cigarettes. Go ahead! Suck that smoke through your throat hole. It won’t hurt you.

2. Tiredness is to fatigue as a pimple is to face herpes.

Hopefully this article has already made this clear, but fatigue is far far worse than being tired. Have you ever been so tired after a hard day’s work that you literally couldn’t talk? I haven’t, and I’ve worked very physical jobs. I used to set up stages and sound systems for concerts, lifting super heavy stuff in the heat for sixteen hours at a time. I’d be sore and I’d want to get in the hot tub at the end of the day, but I could always talk. Not so with lupus. Sometimes I am literally so fatigued that it is too much exertion to open my mouth and talk. If you knew me, you’d know what a personal tragedy this is. I am a talker. There is nothing I like more than shooting the shit. My husband wooed me by staying up until noon talking to me all night. On, like, fifteen occasions. That’s how much I love talking.

Recently I created a fatigue scale after I realized that doctors don’t have one. It is as follows:

Tiredness for me maxes out at around a 4. No matter how tired I am, I could always make myself run errands if I had to. When I’m fatigued, though, it’s not just that running errands is a bad idea (which it is). Sometimes I literally don’t have the strength, coordination, or mental capacity to do it. So for any non-sick person who’s never experienced fatigue beyond a four, your advice, while well meaning, is useless because you literally don’t get it.

1. Fatigue is a daily struggle; tiredness is a temporary inconvenience.

Finally, one of the worst things about struggling with chronic fatigue is that you don’t know if it’ll ever end. Most doctors don’t take complaints of fatigue seriously, and even when they do, there’s not much they can do for it anyway. We don’t have an opioid-equivalent fatigue reliever. We don’t even have a tylenol equivalent. When a non-sick person feels tired, they know that if they get a good night’s rest or take a vacation, they’ll feel better. There is no vacation from fatigue. You could fly to Aruba and you’d be just as debilitated.

That’s why the douchy “just get a good night’s sleep” comments sting so badly. If you had even half an understanding of what it’s like to live with this sort of fatigue, there’s no way you’d suggest that. Do you really think someone is this debilitated and they hadn’t even considered, umm, I don’t know, sleeping more. Of course they’ve tried sleeping more! They’re sick, not a moron.

So please. If you’re someone who’s lucky enough not to struggle with chronic fatigue, don’t be a douche. It’s really easy. Just treat the person you’re talking to with respect and assume they have as much common sense as you do.

 

via Five Reasons Fatigue Isn’t Like Normal Tiredness (Proving Most People Don’t Get It) — Miss•Treated

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[BLOG POST] Perfectly Imperfect For The Holidays – TBI Survivor Tips and Observations

By Bill Herrin

Living with a TBI is a reality all its own, and as I reiterate in many posts – it’s different for everyone, including how people around you act, react, overact, act up, or don’t react to you at all. With the Holidays now “officially” here, and Thanksgiving already passed – it’s the time of year that many people dread, and for many good reasons.

The way some people celebrate seems so perfectly “normal” from the outside – the whole family gets together, they have dinner together, or they open gifts, or they have a wonderful party…and that can happen, but from the outside it seems much more “perfect” than anything that we experience in our life. Why is that? Well, living with TBI overshadows a lot of our being, and it’s no wonder…it’s changed who we are in some ways.

It can change us immensely and visibly, or it can change us in a less obvious way – and sometimes, people don’t see what it’s done to a survivor at all. Either scenario can be very frustrating for the survivor of TBI, stroke, concussion, mild TBI, acquired brain injuries, etc.

Making The Holidays More Positive

On one hand, getting together with family and friends during the Holidays after TBI can be an annual test of wills due to lack of patience or empathy for one another, misread intentions, disagreements, or just a lack of understanding for each other.

On the other hand, all families, no matter how perfect things appear on the surface, can have similar issues. Yes, some actual families do get along great, and the Holidays are a positive experience for them – but don’t be dismayed, because (at the end of the day) we’re all perfectly imperfect people. Brain injury or no brain injury!

The point being made is plain and simple – although TBI survivors bear a load of issues in situations with people around, many times they still are left to shoulder the weight of inconsideration, improper actions, comments and more. Being the bigger person is hard to do (especially under the circumstances) but it’s worth the effort!

A Little Empathy Goes A Long Way…

Whether you’re reading this as a TBI Survivor, a caregiver, or as a friend or family member – it’s important to always work toward being empathetic toward each other.

As a survivor, knowing that everyone hasn’t experienced what you have been through is a good rule of thumb for overlooking things that could easily get under your skin. As a friend or family member, remember that you have no clue what it’s like to have a TBI is a good starting point, and overlooking things (that are said) can keep things on an even keel.

The same goes for a TBI survivor that fields negative comments or verbal jabs…working to focus on being together is the point! Enjoying each other’s company is a rarity and should be treated that way – as perfectly imperfect as any of us are.

Some Suggestions

Here are some suggestions to help make the Holidays less frustrating, and hopefully a better experience for a TBI Survivor (and their friends & family):

• Avoid alcoholic drinks (especially when using medications)

• Noise-canceling headphones or earplugs to bring noise levels down to a manageable level

• Bring someone with you that understands your needs when you go shopping, to a party, or for dinner at home (or elsewhere) with others

• Be careful to avoid sensory overload, and act accordingly at an event if necessary (retreat for a bit, leave early if needed, etc.)

• Be rested before any Holiday party, gathering, parade, etc. – if you know that a Holiday parade or program is going to be overwhelming, you may be better off skipping it altogether

• Do your Holiday shopping (along with a friend or family member, etc.) when crowds are at a minimum

• If blinking or bright holiday lights bother you, plan (in advance) to have sunglasses handy, or even a place that you can retreat to if necessary

• Unless you’re certain that a fireworks display is ok to attend, it may be best to skip it (New Year’s Eve, etc.)

• Movies, concerts, outdoor events with lots of lights can all cause issues for Survivors…base your decisions to go on previous experience when possible. If not, do you best to plan in advance on how you (with a friend or loved one) will have an action plan to deal with it

• Try to avoid situations that may overstimulate your senses. Noise, crowds, lights, etc. can trigger anxieties (fear, panic, etc.) and even fatigue – when your brain is overloaded by too many things going on at once

• Another good thing to keep in mind is to ask for assistance if you need it – taking on too much by yourself is asking for trouble, and if you have someone willing and able to help you, let them!

In closing…

In closing, if you’re a TBI Survivor – try to pace yourself during the holidays when there’s so much going on, and not get too overloaded with things to do, places to go, and people to see. As a friend, family member, or caregiver of a person with TBI – keep this in mind as well!

Helping advocate for a TBI Survivor is very important, and they will do much better with you as their “overload avoidance” point person (or team). Happy Holidays to all, and we’ll see you in 2020.

 

via Perfectly Imperfect For The Holidays – TBI Survivor Tips and Observations

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[ARTICLE] Follow-up after 5.5 years of treatment with methylphenidate for mental fatigue and cognitive function after a mild traumatic brain injury – Full Text

Objective: Prolonged mental fatigue and cognitive impairments are common after a mild traumatic brain injury (TBI). This sets limits for rehabilitation and for regaining the capacity for work and participation in social life.

Method: This follow-up study, over a period of approximately 5.5 years was designed to evaluate the effect and safety of methylphenidate treatment for mental fatigue after a mild TBI. A comparison was made between those who had continued, and those who had discontinued the treatment. The effect was also evaluated after a four-week treatment break.

Results: Significant improvement in mental fatigue, depression, and anxiety for the group treated with methylphenidate (p < .001) was found, while no significant change was found for the group without methylphenidate. The methylphenidate treatment group also improved their processing speed (p = .008). Withdrawal produced a pronounced and significant deterioration in mental fatigue, depression, and anxiety and a slower processing speed. This indicates that the methylphenidate effect is reversible if discontinued and that continued methylphenidate treatment can be a prerequisite for long-term improvement. The effect was found to be stable and safe over the years.

Conclusion: We suggest methylphenidate to be a possible treatment option for patients with post-TBI symptoms including mental fatigue and cognitive symptoms.

Introduction

Long-term mental fatigue and cognitive impairment are common after a mild, moderate or severe traumatic brain injury (TBI) and these can have a significant impact on work, well-being and quality of life (1). Fatigue and concentration deficits are acknowledged as being one of the most distressing and long-lasting symptoms following mild TBI (1). There is currently no approved treatment (2), although the most widely used research drug for cognitive impairments after TBI is methylphenidate (3). A few studies have used methylphenidate for mental fatigue after TBI with promising results including our own (4,5). Other clinical trials of drugs have reported improvements in mental fatigue ((−)-osu6162 (6)) or none ((−)-osu616, modafinil (79)).

In our feasibility study of methylphenidate (not placebo controlled) we reported decreased mental fatigue, improved processing speed and enhanced well-being with a “normal” dose of methylphenidate compared to no methylphenidate for people suffering from post-traumatic brain injury symptoms (4). We tested methylphenidate in two different dosages and found that the higher dose (20 mg three times/day) had the better effect compared to the lower dose. We also found methylphenidate to be well tolerated by 80% of the participants. Adverse events were reported as mild and the most commonly reported side-effects included restlessness, anxiety, headache, and increased heart rate; no dependence or misuse were detected (10). However, a careful monitoring for adverse effects is needed, as many patients with TBI are sensitive to psychotropic medications (11).

Participants who experienced a positive effect with methylphenidate were allowed to continue the treatment. We have reported the long-term positive effects on mental fatigue and processing speed after 6 months (12) and 2 years (13). No serious adverse events were reported (13)(Figure 1). In a 30-week double-blind-randomized placebo-controlled trial, Zhang et al. reported that methylphenidate decreased mental fatigue and improved cognitive function in the participants who had suffered a TBI. Moreover, social and rehabilitation capacity and well-being were improved (5). Other studies evaluating methylphenidate treatment after TBI have focused only on cognitive function reporting improved cognitive function with faster information processing speed and enhanced working memory and attention span (1421). A single dose of methylphenidate improved cognitive function and brain functionality compared to placebo in participants suffering from post-TBI symptoms (22,23). Most of these have been short-term studies covering a period between 1 day and 6 weeks and included participants suffering from mild or more severe brain injuries.

This clinical follow-up study was designed to evaluate the long-term effect and safety of methylphenidate treatment. We also evaluated the effect after a four-week treatment break and compared the subjective and objective effects with and without methylphenidate. Patients who had discontinued methylphenidate during this long-term study were also included in this follow-up, as it was our intention to compare the long-term effects on mental fatigue in patients with and without methylphenidate treatment.

[…]

 

Continue —->  Follow-up after 5.5 years of treatment with methylphenidate for mental fatigue and cognitive function after a mild traumatic brain injury: Brain Injury: Vol 0, No 0

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[Review] Ketogenic Diet and Epilepsy – Full Text PDF

Abstract

Currently available pharmacological treatment of epilepsy has limited effectiveness.
In epileptic patients, pharmacological treatment with available anticonvulsants leads to seizure control in <70% of cases. Surgical intervention can lead to control in a selected subset of patients, but still leaves a significant number of patients with uncontrolled seizures. Therefore, in drug-resistant epilepsy, the ketogenic diet proves to be useful. The purpose of this review was to provide a comprehensive overview of what was published about the benefits of ketogenic diet treatment in patients with epilepsy. Clinical data on the benefits of ketogenic diet treatment in terms of clinical symptoms and adverse reactions in patients with epilepsy have been reviewed. Variables that could have influenced the interpretation of the data were also discussed (e.g., gut microbiota). The data in this review contributes to a better understanding of the potential benefits of a ketogenic diet in the treatment of epilepsy and informs scientists, clinicians, and patients—as well as their families and caregivers—about the possibilities of such treatment. Since 1990, the number of publications on attempts to treat drug-resistant epilepsy with a ketogenic diet has grown so rapidly that it has become a challenge to see the overall trajectory and major milestones achieved in this field. In this review, we hope to provide the latest data from randomized clinical trials, practice guidelines, and new research areas over the past 2 years.

[…]

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[Abstract] Poststroke Fatigue Is Related to Motor and Cognitive Performance

Abstract

Background and Purpose: Poststroke fatigue (PSF) is a common debilitating and persistent symptom after stroke. The relationship between PSF and motor and cognitive function remains inconclusive partly due to lack of control for effects of depression and use of insensitive measures. We examined the relationship between PSF and motor and cognitive performance using a comprehensive set of behavioral measures and excluding individuals with depression.

Methods: Fifty-three individuals poststroke (16 female) were included (median age: 63 years, median months poststroke: 20 months). Poststroke fatigue was quantified using the Fatigue Severity Scale (FSS) and cognitive performance was measured with the Montreal Cognitive Assessment, simple and choice reaction time (SRT and CRT) tasks. Lower extremity motor performance included Fugl-Meyer Motor Assessment, 5 times sit-to-stand test (5 × STS), Berg Balance Scale, Functional Ambulation Category, and gait speed. Upper extremity motor performance was indexed with Fugl-Meyer, grip strength, and Box and Block test. Spearman correlation and stepwise linear regression analyses were performed to examine relationships.

Results: Two motor performance measures, Berg Balance Scale and Functional Ambulation Category, were significantly correlated with FSS (ρ = −0.31 and −0.27, respectively) while all cognitive measures were significantly correlated with FSS (ρ = −0.28 for Montreal Cognitive Assessment, 0.29 for SRT, and 0.29 for CRT). Regression analysis showed that Berg Balance Scale was the only significant determinant for FSS (R2 = 0.11).

Discussion and Conclusions: Functional gait, balance, and cognitive performance are associated with PSF. Fatigue should be considered when planning and delivering interventions for individuals with stroke. Future studies are needed to explore the potential efficacy of balance and cognitive training in PSF management.

Video Abstract available for more insights from the authors (see Video, Supplemental Digital Content 1, available at: http://links.lww.com/JNPT/A287).

 

via Poststroke Fatigue Is Related to Motor and Cognitive Perform… : Journal of Neurologic Physical Therapy

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[Quotation] I Feel Like I’m Already Tired Tomorrow

Relationships Quotes Top 337 Relationship Quotes And Sayings 120

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[ARTICLE] Muscle fatigue assessment during robot-mediated movements – Full Text

Abstract

Background

Several neuromuscular disorders present muscle fatigue as a typical symptom. Therefore, a reliable method of fatigue assessment may be crucial for understanding how specific disease features evolve over time and for developing effective rehabilitation strategies. Unfortunately, despite its importance, a standardized, reliable and objective method for fatigue measurement is lacking in clinical practice and this work investigates a practical solution.

Methods

40 healthy young adults performed a haptic reaching task, while holding a robotic manipulandum. Subjects were required to perform wrist flexion and extension movements in a resistive visco-elastic force field, as many times as possible, until the measured muscles (mainly flexor and extensor carpi radialis) exhibited signs of fatigue. In order to analyze the behavior and the characteristics of the two muscles, subjects were divided into two groups: in the first group, the resistive force was applied by the robot only during flexion movements, whereas, in the second group, the force was applied only during extension movements. Surface electromyographic signals (sEMG) of both flexor and extensor carpi radialis were acquired. A novel indicator to define the Onset of Fatigue (OF) was proposed and evaluated from the Mean Frequency of the sEMG signal. Furthermore, as measure of the subjects’ effort throughout the task, the energy consumption was estimated.

Results

From the beginning to the end of the task, as expected, all the subjects showed a decrement in Mean Frequency of the muscle involved in movements resisting the force. For the OF indicator, subjects were consistent in terms of timing of fatigue; moreover, extensor and flexor muscles presented similar OF times. The metabolic analysis showed a very low level of energy consumption and, from the behavioral point of view, the test was well tolerated by the subjects.

Conclusion

The robot-aided assessment test proposed in this study, proved to be an easy to administer, fast and reliable method for objectively measuring muscular fatigue in a healthy population. This work developed a framework for an evaluation that can be deployed in a clinical practice with patients presenting neuromuscular disorders. Considering the low metabolic demand, the requested effort would likely be well tolerated by clinical populations.

Background

Muscle fatigue has been defined as “the failure to maintain a required or expected force” [1] and it is a complex phenomenon experienced in everyday life that has reached great interest in the areas of sports, medicine and ergonomics [2]. Muscle fatigue can affect task performance, posture-movement coordination [3], position sense [4] and it can be a highly debilitating symptom in several pathologies [5]. For many patients with neuromuscular impairments, taking into account muscle fatigue is of crucial importance in the design of correct rehabilitation protocols [6] and fatigue assessment can provide crucial information about skeletal muscle function. Specifically, several neuromuscular diseases (e.g. Duchenne, Becker Muscular Dystrophies, and spinal muscular atrophy) present muscle fatigue as a typical symptom [7], and fatigue itself accounts for a significant portion of the disease burden. A systematic approach to assess muscle fatigue might provide important cues on the disability itself, on its progression and on the efficacy of adopted therapies. In particular, therapeutic strategies are now under deep investigation and a lot of effort has been devoted to accelerate the development of drugs targeting these disorders [8]. Therefore, the need for an objective tool to measure muscle fatigue is impelling and of great relevance.

Currently, in clinical practice muscle fatigue is evaluated by means of qualitative rating scales like the 6-min walk test (6MWT) [9] or through subjective questionnaires administered to the patient (e.g. the Multidimensional Fatigue Inventory (MFI), the Fatigue Severity Scale (FSS), and the Visual Analog Scale (VAS)) [10]. During the 6MWT patients have to walk, as fast as possible, along a 25 meters linear course and repeat it as often as they can for 6 min: ‘fatigue’ is then defined as the difference between the distance covered in the sixth minute compared to the first. Obviously, such a measure is only applicable to ambulant patients and this is a strong limitation to clinical investigation because a patient may lose ambulatory ability during a clinical trial, resulting in lost ability to perform the primary clinical endpoint [11]. It should also be considered that neuromuscular patients, e.g. subjects with Duchenne Muscular Dystrophy, generally lose ambulation before 15 years of age [12], excluding a large part of the population from the measurement of fatigue through the 6MWT. Since neuromuscular patients often experience a progressive weakness also in the upper limb, reporting of muscle fatigue in this region is common. A fatigue assessment for upper limb muscles could be used to monitor patients across different stages of the disease. As for the questionnaires, the MFI is a 20 items scale designed to evaluate five dimensions of fatigue (general fatigue, physical fatigue, reduced motivation, reduced activity, and mental fatigue) [13]. Similarly, the FSS questionnaire contains nine statements that rate the severity of fatigue symptoms and the patient has to agree or disagree with them [14]. The VAS is even more general: the patient has to indicate on a 10 cm line ranging from “no fatigue” to “severe fatigue” the point that best describes his/her level of fatigue [15]. Despite the ease to administer, such subjective assessments of fatigue may not correlate with the actual severity or characteristics of fatigue, and may provide just qualitative information with low resolution, reliability and objectivity. Considering various levels of efficacy among the methods currently used in clinical practice, research should focus on the development of an assessment tool for muscle fatigue, that is easy and fast to administer, even to patients with a high level of impairment. Such a tool, should provide clear results, be easy to read and understand by a clinician, be reliable and objectively correlated with the physiology of the phenomenon.

In general, muscle fatigue can manifest from either central and/or peripheral mechanisms. Under controlled conditions, surface electromyography (sEMG) is a non-invasive and widely used technique to evaluate muscle fatigue [16]. Certain characteristics of the sEMG signal can be indicators of muscle fatigue. For example during sub-maximal tasks, muscle fatigue will present with decreases in muscle fiber conduction velocity and frequency and increases in amplitude of the sEMG signal [16]. The trend and rate of change will depend on the intensity of the task: generally, sEMG amplitude has been observed to increase during sub-maximal efforts and decrease during maximal efforts; further it has been reported that there is a significantly greater decline in the frequency content of the signal during maximal efforts compared to sub-maximal [17]. Accordingly, spectral (i.e. mean frequency) and amplitude parameters (i.e. Root Mean Square (RMS)) of the signals, can be used to measure muscle fatigue as extensively discussed in many widely acknowledged studies [161819], however, context of contraction type and intensity must be specified for proper interpretation. A significant problem with the majority of existing protocols is that they rely on quantifying maximal voluntary force loss, maximum voluntary muscle contraction (MVC) [182021] or high fatiguing dynamic tasks [1922] that cannot be reliably performed in clinical practice, especially in the case of pediatric subjects. Actually, previous works pointed out that not only the capacity to maintain MVC can be limited by a lack of cooperation [2324], but also, that sustaining a maximal force in isometric conditions longer than 30 s reduces subject’s motivation leading to unreliable results [25]. Besides, neuromuscular patients might have a high level of impairment and low residual muscular function thus making even more difficult, as well as dangerous for their muscles, sustaining high levels of effort or the execution of a true MVC. In order to overcome this issue, maximal muscle contractions can be elicited by magnetic [10] or electrical stimulation [26]. Although such procedures allow to bypass the problem mentioned above, these involve involuntary muscle activation and not physiological recruitment of motor units [24]; moreover, they can be uncomfortable for patients and can require advanced training, which makes them difficult to be included in clinical fatigue assessment protocols. As for the above mentioned problem with children motivation, work by Naughton et al. [27] showed that the test-retest coefficient of variation of fatigue index during a Wing-Gate test, significantly decreased when using a computerized feedback game linked to pedal cadence, suggesting that game-based procedures may ensure more consistent results in children assessment.

In recent years, the assessment of sensorimotor function has been deepened thanks to the introduction of innovative protocols administered through robotic devices [28293031]. These methods have the ambition to add meaningful information to the existing clinical scales and can be exploited as a basis for the implementation of a muscle fatigue assessment protocol. In order to fill the gap between the need of a quantitative clinical measurement protocol of muscle fatigue and the lack of an objective method which does not demand a high level of muscle activity, we propose a new method based on a robotic test, which is fast and easy to administer. Further, we decided to address the analysis of muscle fatigue on the upper limb as to provide a test suitable to assess patients from the beginning to the late stages of the disease, regardless of walking ability. Moreover, we focused on an isolated wrist flexion/extension tasks to assess wrist muscle fatigue. This ensured repeatability of the tests and prevented the adoption of compensatory movements or poor postures that may occur in multi-segmental tasks, involving the shoulder-elbow complex. In the present work, we tested the method on healthy subjects with the specific goal to evaluate when during the test the first meaningful symptoms of fatigue appaered and not how much subjects are fatigued at the end of the test. The most relevant and novel features of the proposed test include the ability to perform the test regardless of the subjects’ capability and strength, the objectivity and repeatability of the data it provides, and the simplicity and minimal time required to administer.[…]

 

Continue —->  Muscle fatigue assessment during robot-mediated movements | Journal of NeuroEngineering and Rehabilitation | Full Text

Fig. 1

Fig. 1 Experimental setup. Participant sitting on a chair with the forearm secured to the WRISTBOT while performing the wrist rotation reaching task. The visual targets of the reaching task are shown on a dedicated screen

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[ARTICLE] Effort and Fatigue-Related Functional Connectivity in Mild Traumatic Brain Injury – Full Text

Mental fatigue in healthy individuals is typically observed under conditions of high cognitive demand, particularly when effort is required to perform a task for a long period of time—thus the concepts of fatigue and effort are closely related. In brain injured individuals, mental fatigue can be a persistent and debilitating symptom. Presence of fatigue after brain injury is prognostic for return to work/school and engagement in activities of daily life. As such, it should be a high priority for treatment in this population, but because there is little understanding of its behavioral and neural underpinnings, the target for such treatment is unknown. Here, the neural underpinnings of fatigue and effort are investigated in active duty military service members with mild traumatic brain injury (mTBI) and demographically-matched orthopedic controls. Participants performed a Constant Effort task for which they were to hold a pre-defined effort level constant for long durations during fMRI scanning. The task allowed for investigation of the neural systems underlying fatigue and their relationship with sense of effort. While brain activation associated with effort and fatigue did not differentiate the mTBI and controls, functional connectivity amongst active brain regions did. The mTBI group demonstrated immediate hyper-connectivity that increased with effort level but diminished quickly when there was a need to maintain effort. Controls, in contrast, demonstrated a similar pattern of hyper-connectivity, but only when maintaining effort over time. Connectivity, particularly between the left anterior insula, rostral anterior cingulate cortex, and right-sided inferior frontal regions, correlated with effort-level and state fatigue in mTBI participants. These connections also correlated with effort level in the Control group, but only the connection between the left insula and superior medial frontal gyrus correlated with fatigue, suggesting a differing pattern of connectivity. These findings align, in part, with the dopamine imbalance, and neural efficiency hypotheses that pose key roles for medial frontal connections with insular or striatal regions in motivating or optimizing performance. Sense of effort and fatigue are closely related. As people fatigue, sense of effort increases systematically. The data propose a complex link between sense of effort, fatigue, and mTBI that is centered in what may be an inefficient neural system due to brain trauma that warrants further investigation.

Introduction

A signature injury of service members deployed during the conflicts in Iraq and Afghanistan is traumatic brain injury (TBI). Of the approximately 360,000 service members who suffer from TBI, 70% are classified as mild injuries (mTBI; DVBIC Quarterly Reports). At least 19% of the service members with mTBI have persistent symptoms that contribute to difficulty engaging in social and work activities. The consequences of persistent fatigue in mTBI pose a real challenge to rehabilitation (1). High levels of mental fatigue commonly persist and relate to failure to return to work and loss of productivity (23). In fact, presence of fatigue is the strongest predictive factor of poor outcomes following TBI (1). Despite the prevalence of fatigue in TBI, our understanding of its behavioral and neural underpinnings is lacking.

Mental fatigue is a complex process that is operationally defined by time on task and increased mental effort. When performance suffers (reaction time, accuracy, etc.) over time, presumably from fatigue, there tends to be fairly diffusely increased brain activity (4). Simultaneously, there may also be decreased motivation under high effort (5). According to Kahneman’s “resource capacity theory,” the amount of effort needed to perform a task is related to the complexity of the task and an individual’s limited general capacity to perform mental work [i.e., resource capacity, (67)]. When a task is difficult, the demand for resources is high, and performance suffers when resources near depletion. When a person recognizes that performance is suffering, tasks are perceived as more difficult, and require greater effort, which Kahneman equates with the experience of mental fatigue.

Brain imaging in mTBI indicates an increase in brain activity with increased time on task regardless of the type or demand requirements of the task (8). In contrast, healthy individuals have decreased activation over time without a serious decrement in performance, and without reporting significant fatigue. This brain response in TBI may suggest a perception of higher levels of effort when the task is long, or that individuals with TBI inefficiently regulate cognitive control and exert more mental effort to maintain a high-level of performance, resulting in fatigue.

While there is a plethora of literature reporting that task demand causes degradation of performance in mTBI, few have investigated whether task demand results in fatigue more so than in healthy controls, or how this fatigue manifests in behavior or in neural function. The few available studies have small sample sizes [e.g., (9)] limiting their generalizability. The brain networks implicated in effort and fatigue include frontostriatal circuitry, or the ventromedial prefrontal cortex more specifically. Damage to these brain regions is thought to diminish resource capacity and impair allocation of resources, resulting in an increased perception of expended effort (1012). Additionally, fatigue related to lack of motivation to engage and maintain performance on a task, or to predict and manage change in performance based on feedback about performance, is associated with the integrity of the ventromedial prefrontal cortical. That is, individuals with larger lesions of this brain region report more fatigue and apathy (1314). The frontostriatal network is involved in coding the incentive value for an expected outcome (15), and is mediated by dopaminergic frontostriatal networks (131619). Breakdowns in ventromedial prefrontal cortex-related network connectivity may disrupt the ability to appropriately detect, monitor, and self-correct errors or to adequately motivate behavior (2021). For example, the anterior cingulate cortex is associated with monitoring and detecting errors, the pre-supplementary motor area with engaging in task, and the connectivity amongst these two regions is related to fatigue (22).

One gap in the existing literature on fatigue is that paradigms infer “probable” fatigue [exception is Wylie et al. (22)], rather than directly measuring it. In the present study, we investigate brain activity and network connectivity in mTBI participants while they perform a task explicitly designed to study the relationship between task-related effort and fatigue. We assess fatigue with a questionnaire about fatigue over the week prior to scanning (trait) as well as with task manipulation during brain imaging [state, Constant Effort Task [CE]]. For Constant Effort, subjects are asked to squeeze a bulb to a prescribed effort level and hold it constant for a discrete period of time. The task is considered a general index of central fatigue as it is not specific to motor system engagement (2324). Varying effort levels result in predictable changes in the ability to maintain pressure on the bulb such that the time it takes to fatigue is slower at low effort levels than at higher effort levels. Performance on the CE task during functional fMRI allowed for identification of the neural systems underlying effort and fatigue as well as the differences in these systems in mTBI relative to control. We hypothesize that fatigue in mTBI arises when there is an altered perception of the amount of effort needed to perform the task, either because there is a failure to:

a) update the amount of effort given to the task based on internal feedback about performance, which is assessed by contrasting performance across effort levels,

b) sustain a given effort level, which is assessed via time on task, or

c) both.

Because estimating and maintaining effort are likely a result of a complex network of interacting brain regions, we examined not only brain activation during task performance, but also functional connectivity (FC) amongst the regions active during the task. We predict that mTBI participants will demonstrate increased pre-frontal and anterior cingulate cortex activation, as well as increased connectivity of these regions to ventral-striatal regions relative to Control participants.[…]

 

Continue —> Frontiers | Effort and Fatigue-Related Functional Connectivity in Mild Traumatic Brain Injury | Neurology

Figure 1. Effort and Fatigue in the Constant Effort task demonstrated differing regional effects with effort associated with caudal, medial prefrontal cortex (red) while fatigue was associated with rostral prefrontal cortex as well as postcentral and posterior cingulate cortex (blue). Controls demonstrated significantly higher activity than mTBI in a small area of the right medial prefrontal cortex (green) while mTBI had more activity in the posterior occipital cortex, but there were no other significant group effects. When these regions were used in computing functional connectivity, it was only the connectivity amongst the regions of the effort effect (red) that demonstrated group differences in connection strength. For example, the connection between the left insula (A) and the right inferior frontal gyrus (B, pars orbitalis) was significantly stronger in the TBI group for time on task at 75% effort.

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[BLOG POST] Antidepressants help us understand why we get fatigued during exercise

In general, the term ‘fatigue’ is used to describe any exercise-induced decline in the ability of a muscle to generate force. To identify the causes of fatigue, it is common to examine two divisions of the body that might be affected during exercise. The central component of fatigue includes the many nerves that travel throughout the brain to the spinal cord. The peripheral component predominantly reflects elements in the muscle itself. If there is a problem with either of these components, the ability to contract a muscle might be compromised. For many years, there has been suggestion that central fatigue is heavily influenced by neurotransmitters that get released in the central nervous system (such as dopamine and serotonin). However, little research has been performed in this area.

Serotonin is a chemical that can improve mood, and increasing the amount of serotonin that circulates in the brain is a common therapy for depression. However, serotonin also plays a vital role in activating neurons in the spinal cord which tell the muscle to contract. With the correct amount of serotonin release, a muscle will activate efficiently. However, if too much serotonin is released, there is a possibility that the muscle will rapidly fatigue. Recent animal studies indicate that moderate amounts of serotonin release, which are common during exercise, can promote muscle contractions (Cotel et al. 2013). However, massive serotonin release, which may occur with very large bouts of exercise, could further exacerbate the already fatigued muscle (Perrier et al. 2018).

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. These medications keep serotonin levels high in the central nervous system by stopping the chemical from being reabsorbed by nerves (reuptake inhibition). Instead of using SSRIs to relieve symptoms of depression, we used them in our recent study (Kavanagh et al. 2019) to elevate serotonin in the central nervous system, and then determine if characteristics of fatigue are enhanced when serotonin is elevated. We performed three experiments that used maximal voluntary contractions of the biceps muscle to cause fatigue in healthy young individuals. Our main goal was to determine if excessive serotonin limits the amount of exercise that can be performed, and then determine which central or peripheral component was compromised by excessive serotonin.

WHAT DID WE FIND?

Given that SSRIs influence neurotransmitters in the central nervous system, it was not surprising that peripheral fatigue was unaltered by the medication. However, central fatigue was influenced with enhanced serotonin. The time that a maximum voluntary contraction could be held was reduced with enhanced serotonin, whereby the ability of the central nervous system to drive the muscle was compromised by 2-5%. We further explored the location of dysfunction and found that the neurons in the spinal cord that activate the muscle were 4-18% less excitable when fatiguing contractions were performed in the presence of enhanced serotonin.

SIGNIFICANCE AND IMPLICATIONS

The central nervous system is diverse, and the fatigue that is experienced during exercise is not just restricted to the brain. Instead, the spinal cord plays an integral role in activating muscles, and mechanisms of fatigue also occur in these lower, often overlooked, neural circuits. This is the first study to provide evidence that serotonin released onto the motoneurones contributes to central fatigue in humans.

PUBLICATION REFERENCE

Kavanagh JJ, McFarland AJ, Taylor JL. Enhanced availability of serotonin increases activation of unfatigued muscle but exacerbates central fatigue during prolonged sustained contractions. J Physiol. 597:319-332, 2019.

If you cannot access the paper, please click here to request a copy.

KEY REFERENCES

Cotel F, Exley R, Cragg SJ, Perrier JF. Serotonin spillover onto the axon initial segment of motoneurons induces central fatigue by inhibiting action potential initiation. Proc Natl Acad Sci U S A. 110:4774-4779, 2013.

Perrier JF, Rasmussen HB, Jørgensen LK, Berg RW. Intense activity of the raphe spinal pathway depresses motor activity via a serotonin dependent mechanism. Front Neural Circuits. 11:111, 2018.

AUTHOR BIO

Associate Professor Justin Kavanagh is a researcher and lecturer at Griffith University. His team explores how the central nervous system controls voluntary and involuntary movement, and he has particular interests in understanding how medications can be used to study mechanisms of human movement.

via Antidepressants help us understand why we get fatigued during exercise – Motor Impairment

 

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