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[WEB SITE] A reboot for chronic fatigue syndrome research

Research into this debilitating disease has a rocky past. Now scientists may finally be finding their footing.

Elizabeth Allen keeps careful records of the many treatments she has undergone to relieve the symptoms of chronic fatigue syndrome. Credit: Preston Gannaway for Nature

Name a remedy, and chances are that Elizabeth Allen has tried it: acupuncture, antibiotics, antivirals, Chinese herbs, cognitive behavioural therapy and at least two dozen more. She hates dabbling in so many treatments, but does so because she longs for the healthy days of her past. The 34-year-old lawyer was a competitive swimmer at an Ivy-league university when she first fell ill with chronic fatigue syndrome, 14 years ago. Her meticulous records demonstrate that this elusive malady is much worse than ordinary exhaustion. “Last year, I went to 117 doctor appointments and I paid $18,000 in out-of-pocket expenses,” she says.

Dumbfounded that physicians knew so little about chronic fatigue syndrome — also known as myalgic encephalomyelitis or ME/CFS — Allen resolved several years ago to take part in any study that would have her. In 2017, she got her chance: she entered a study assessing how women with ME/CFS respond to synthetic hormones.

After decades of pleading, people with the condition have finally caught the attention of mainstream science — and dozens of exploratory studies are now under way. Scientists entering the field are using the powerful tools of modern molecular biology to search for any genes, proteins, cells and possible infectious agents involved. They hope the work will yield a laboratory test to diagnose ME/CFS — which might have several different causes and manifestations — and they want to identify molecular pathways to target with drugs.

The US National Institutes of Health (NIH) in Bethesda, Maryland, bolstered the field last year by more than doubling spending for research into the condition, from around US$6 million in 2016 to $15 million in 2017. Included in that amount are funds for four ME/CFS research hubs in the United States that will between them receive $36 million over the next five years.

The stakes are high because the field’s scientific reputation has been marred by controversial research. A 2009 report1 that a retrovirus called XMRV could underlie the disease was greeted with fanfare only to be retracted two years later. And in 2011 and 2013, a British team reported that exercise and cognitive behavioural therapy relieved the symptoms of ME/CFS for many people in a large clinical study called the PACE trial2,3. US and UK health authorities had made recommendations based on the findings, but, starting around 2015, scientists and patient advocates began publicly criticizing the trial for what they saw as flaws in its design. The organizers of the trial deny that there were serious problems with it, but health officials in both countries have nevertheless been revising their guidelines.

Patients, meanwhile, are adrift in a vacuum of knowledge about the condition, says Jose Montoya, an infectious-disease specialist at Stanford Medical School in California and one of Allen’s physicians. “ME/CFS has suffered from scientists applying the usual approaches,” he says. He hopes that sophisticated analyses of genomics, proteomics, metabolomics and more will help to change that. “It wasn’t until the microscope became available that an Italian microbiologist could link cholera to the bacteria that caused it,” he says. “In the same sense, we have not had the equivalent to the microscope until now.”

Early days

In 1984 and 1985, an epidemic of persistent fatigue broke out in Lake Tahoe, Nevada. The US Centers for Disease Control and Prevention (CDC) tested people for Epstein–Barr virus, one cause of the fatigue-inducing illness called mononucleosis or glandular fever, but the results were inconclusive and the investigation was dropped. Around 1987, researchers coined the name chronic fatigue syndrome. But the media snidely called it ‘yuppie flu’. Doctors often told people their symptoms were caused by neuroses and depression.

But a small fraction of clinicians listened closely to patients — who insisted that their debilitating exhaustion was not just in their minds. And whereas a little exercise might temporarily uplift someone with depression, individuals with ME/CFS would be bedridden for days after exertion. Some people also struggle with chronic impairment, some with intestinal disorders, and others completely lose the ability to walk. Anthony Komaroff, a physician-scientist at Harvard Medical School in Boston, Massachusetts, began conducting studies on the disease in the mid-1980s despite being discouraged by his colleagues. “I was emboldened by the fact that when I asked my colleagues why they were sceptical, they could not articulate a reason,” he says.

In the 1990s, Leonard Jason, a psychology researcher at DePaul University in Chicago, Illinois, started questioning basic epidemiological information on ME/CFS. For one thing, the CDC described the syndrome as rare and predominantly affecting white women. But Jason reasoned that clinicians could be missing many cases. Those who were diagnosed were the ones most likely to return for a second, third or fourth medical opinion. And people who felt stigmatized, were confined to bed, were poor or had little social support might not go to such lengths to get a diagnosis.

So, Jason’s team called almost 30,000 random Chicago phone numbers to ask whether someone in the household had symptoms of the disorder. If they did, the team brought them into clinics for evaluation. As a result of the findings from this4 and other studies, the CDC removed the word ‘rare’ from its description of the syndrome. In 2015, a report5 from the US Institute of Medicine (IOM) estimated that 836,000 to 2.5 million Americans have the disorder. Another study6 estimated that more than 125,000 people in the United Kingdom are living with ME/CFS. And a report7 from Nigeria suggests that the prevalence of the disease might be even higher there, perhaps exacerbated by other infectious diseases and poor nutrition. But these tallies are fraught, owing to the different ways in which doctors diagnose the condition.

In many ways, people with ME/CFS remain invisible. Most have been dismissed by at least one physician. And society often ignores them, too. In the United States, financial pressures are common because health insurers might consider experimental treatments unnecessary, and employers might not feel that disability payments are justified. Even in countries where health care is a right, the situation has been dire. Many patient advocates say that UK government agencies have essentially treated ME/CFS as if it were a strictly psychological condition, a conclusion that they argue was bolstered by the PACE trial’s findings that exercise and cognitive behavioural therapy relieve symptoms. The National Health Service (NHS) recommended these interventions, even after many patients complained that exercise dramatically worsens their condition.

Epidemiologists have suggested8 that the anguish of contending with the disorder and society’s general dismissal of it contribute to an up to sevenfold increase in the rate of suicide for people with ME/CFS.

Montoya will never forget one such tragedy. A decade ago, he opened an ME/CFS clinic for half a day each week at Stanford. One afternoon, he received a call from a crying woman whose 45-year-old daughter had returned home to California after falling ill with ME/CFS. The daughter had read about Montoya’s clinic online and wanted an appointment, but Montoya was booked for a couple of years. In her suicide note, he says, the daughter asked that her brain be donated to him for research. “I feel so guilty, since those were the years with hundreds of patients on the waiting list,” he says.

Immune system

Today, Montoya’s clinic is open five days a week. And in his research, he’s exploring several avenues. The hormone study in which Allen is participating is looking for changes in how the endocrine system is regulated among people with ME/CFS, a factor that might explain why the disorder is more common in women than in men. But Montoya’s leading hypothesis is that ME/CFS begins with an infection that throws the immune system out of whack.

Infections generally lead to inflammation when protein receptors on T cells, a kind of immune cell, recognize corresponding proteins carried by bacteria, parasites or viruses. The T cells multiply and catalyse an inflammatory attack that includes the replication of antibody-producing immune cells, called B cells. In the past few years, researchers have revealed hints of an unusual immune response in ME/CFS. Most recently, last June, Montoya and his colleagues revealed9 abnormalities in the levels of 17 immune-system proteins called cytokines in people with severe cases of the syndrome. What disrupts the inflammatory response, however, remains unknown. One possibility is that, as in some autoimmune disorders, T cells mistakenly become alarmed by one of the body’s own proteins, rather than by an invader, and B cells secrete self-reactive antibodies.

An accidental finding has lent support to this idea. In 2008, Øystein Fluge, an oncologist at Haukeland University Hospital in Bergen, Norway, treated a lymphoma patient with rituximab, an antibody therapy that kills B cells. The patient told him that the drug resolved their ME/CFS. Fluge and his colleagues then conducted a placebo-controlled trial with 30 people who had the condition (and not cancer), and found that rituximab improved their symptoms10. As word spread, Fluge was flooded with hundreds of e-mails from people asking to take part in his trials, and doctors around the world fielded desperate requests for the experimental therapy.

Yet any hopes that Fluge dared to have were dashed last October, as he assessed data from an as-yet unpublished 151-person clinical trial and found that rituximab proved no better than the placebo. Fluge says the finer details of the trial might yet reveal whether a small subset of participants benefited. Like many others, he suspects that ME/CFS might turn out to be several diseases, with different causes and underlying mechanisms. Therefore, what helps some people might not help others. This effect might not be discernible until researchers can tease out how patients differ from one another. Still, the trial’s overall failure suggests that autoimmunity is not the main cause of ME/CFS, says Derya Unutmaz, an immunologist at the Jackson Laboratory for Genomic Medicine in Farmington, Connecticut. Rather, he speculates that inflammation seen in ME/CFS might result from a problem on the regulatory side of a person’s immune system, which normally reins in the T-cell response to innocuous viruses, mould particles or other non-threatening stimuli. “Rituximab’s failure is very disappointing for patients, but the fact that such a trial was done is a very important thing in the field,” Unutmaz adds. “By ruling this out, we can focus on other directions.” This is the kind of scientific response that patient advocates have been fighting for since the 1990s.

Metabolic system and microbiome

Newsletters dating back decades document how activists have struggled to be recognized by scientists. In one column from 1998, the co-founder of an ME/CFS organization reports on a conference on the ailment in Boston. She notes that someone from ACT UP, a group known for driving research on HIV, was in attendance, “and may show us how to get more attention for the disease”.

Through the 2000s, advocates accused the NIH of favouring grant proposals focused on psychiatric and behavioural studies, as opposed to those exploring physiological pathways. A sea change occurred in 2015, however, with the IOM’s review5 of more than 9,000 scientific articles. “The primary message of this report,” concluded the IOM, “is that ME/CFS is a serious, chronic, complex and systemic disease.” Soon afterwards, NIH director Francis Collins said that the agency would support basic science to work out the mechanisms of the syndrome.

In September last year, the NIH announced the winners of new grants in support of research hubs looking into ME/CFS. Some of the projects sound as if they duplicate each other, but that’s by design. Walter Koroshetz, head of the NIH’s National Institute of Neurological Disorders and Stroke in Bethesda and chair of the Trans-NIH ME/CFS Working Group, explains that the NIH sees strength in replication. “There has not been a coordinated effort to follow up on publications and to figure out which findings are most important, which can be reproduced and which fall away when you look at a different patient population,” he says. For this reason, one of the NIH grants goes towards a centre at Research Triangle Institute in North Carolina that will merge ME/CFS data.

A $10-million, 5-year grant is also going to Unutmaz, who is studying the interplay between the immunological, metabolic and nervous systems of people with ME/CFS. As part of this, he will collaborate with microbiologists to assess the bacteria living in patients’ bodies, and to see how shifts in those populations alter metabolites, such as glucose, that may in turn affect inflammation. Unutmaz admits that his studies are at an early stage, and says the point is to generate data to form sharper hypotheses. “We don’t know what we don’t know in this disease,” he says. Researchers at Columbia University in New York City and Cornell University in Ithaca, New York, have won NIH grants to explore some of the same themes, and to delve into inflammation in the brain.

Some CFS researchers argue that the NIH’s contribution remains too lean. “A real problem is that funders want to see papers coming out in a short time period, but this is a complex disease that requires long-term studies that are expensive to conduct,” says Eleanor Riley, an immunologist at the University of Edinburgh, UK. Beginning in 2013, Riley helped to launch and maintain an NIH-supported biobank of ME/CFS samples at the London School of Hygiene and Tropical Medicine. But the bank has been limited by funding constraints.

Ronald Davis, a biochemist who directs Stanford’s Genome Technology Center, says that he too struggles to fund his lab’s work on ME/CFS. He points out that although HIV affects roughly the same number of people in the United States — about 1.2 million — it received 200 times as much funding from the NIH as ME/CFS did in 2017.

In December, the Open Medicine Foundation in Agoura Hills, California, a research charity that Davis advises, announced its support for an ME/CFS collaborative centre led by him. In one project, the team intends to finish analysing the complete genomes of 20 people severely ill with ME/CFS, along with the genomes of their family members, to look for a genetic predisposition to the disease. Another project involves the development of what could be the first diagnostic test for ME/CFS.

That test uses a small device containing 2,500 electrodes that measure electrical resistance in immune cells and plasma from blood. When Davis exposed blood samples from people with ME/CFS to a stressor — a splash of salt — the chip revealed that the blood did not recover as well as samples from healthy adults. Davis is holding out on pronouncements, however, until he has conducted a study large enough to show clear and statistically significant effects — including a difference between people with ME/CFS and those with other conditions. “With XMRV, the problem was that people jumped to conclusions,” Davis says. “I’ve learned that if it’s exciting, it’s probably wrong.”

A man prepares an IV tube

Researcher Ronald Davis prepares a treatment for his son, Whitney Dafoe, who has chronic fatigue syndrome and can no longer walk or speak.Credit: Veronica Weber/Palo Alto Weekly

Davis knows the pain of disappointment personally. He started studying ME/CFS in 2008, when his son, Whitney Dafoe, became incapacitated by the disease. Dafoe volunteered to be studied at his father’s centre. A member of the team, Laurel Crosby, recalls exchanging e-mails with Dafoe, discussing the research. But as Dafoe’s condition got worse, he stopped replying in sentences, and began answering text messages with just a ‘Y’ or an ‘N’. Then those, too, stopped coming. Dafoe, now 34 years old, can no longer speak. He communicates with his parents through small motions, such as ripping holes in the shape of hearts in paper towels.

A poster of Dafoe hangs in his father’s office. In it, he is standing on a beach in northern California with his arms raised towards the sky. Davis took the photo on one of the last days his son could walk. “Now he cannot talk, he can’t listen to music, he can’t write, he lays in bed all day, and there are thousands of patients like this, patients who are embarrassed to be told that nothing is wrong with them,” Davis says. So he is furiously testing the electrical device, as well as screening blood samples for proteins and genetic signatures that might reveal a biomarker for the disease. Not having clear criteria for a diagnosis has made clinical trials particularly challenging.

In 2015, David Tuller, a journalist turned ME/CFS advocate, published a critique of the PACE studies11. Weeks later, six researchers signed an open letter to the editor of The Lancet, which published the initial PACE results, requesting a reanalysis of the data. Last March, scientists and advocates did the same in a letter to Psychological Medicine — the journal that published the 2013 PACE results — requesting a retraction. A leading criticism was that the investigators had changed how they measured recovery during the course of the trial, making that outcome simpler to achieve. The PACE investigators have denied this charge and others on their website, writing that changes were made before they analysed the data, and wouldn’t have affected the results.

Patients and advocates disagree, and although the paper has not been retracted, the CDC subsequently abandoned the trial’s recommendations. In September last year, the NHS announced that it would also revise its recommendations. In a corresponding report12, a panel concluded that recent biological models based on measurable physiological abnormalities require greater consideration.

Despite the setbacks and the long delays, many argue that science is operating as it should — being self-critical and open to revision. In five years’ time, researchers should be able to pinpoint specific aberrations in the immune, metabolic, endocrine or nervous systems of people with ME/CFS, and perhaps find genetic predispositions to the condition. These indicators might yield diagnostic tests — and, further down the road, treatments.

Allen did not enrol in Montoya’s study with the expectation of a cure around the corner. She says she’ll be happy if — at the very least — a younger generation can avoid the complete bewilderment she felt when her body suddenly failed her. “I know how long science takes,” says Allen. “I am going to try and do whatever I can do to make it move forward as fast as possible.”

doi: 10.1038/d41586-017-08965-0

via A reboot for chronic fatigue syndrome research

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[Abstract] Cognitive behavior therapy to treat sleep disturbance and fatigue after traumatic brain injury – CNS

OBJECTIVE: To evaluate the efficacy of adapted cognitive behavioral therapy (CBT)
for sleep disturbance and fatigue in individuals with traumatic brain injury
(TBI).
DESIGN: Parallel 2-group randomized controlled trial.
SETTING: Outpatient therapy.
PARTICIPANTS: Adults (N=24) with history of TBI and clinically significant sleep
and/or fatigue complaints were randomly allocated to an 8-session adapted CBT
intervention or a treatment as usual (TAU) condition.
INTERVENTIONS: Cognitive behavior therapy.
MAIN OUTCOME MEASURES: The primary outcome was the Pittsburgh Sleep Quality Index
(PSQI) posttreatment and at 2-month follow-up. Secondary measures included the
Insomnia Severity Index, Fatigue Severity Scale, Brief Fatigue Inventory (BFI),
Epworth Sleepiness Scale, and Hospital Anxiety and Depression Scale.
RESULTS: At follow-up, CBT recipients reported better sleep quality than those
receiving TAU (PSQI mean difference, 4.85; 95% confidence interval [CI],
2.56-7.14). Daily fatigue levels were significantly reduced in the CBT group (BFI
difference, 1.54; 95% CI, 0.66-2.42). Secondary improvements were significant for
depression. Large within-group effect sizes were evident across measures (Hedges
g=1.14-1.93), with maintenance of gains 2 months after therapy cessation.
CONCLUSIONS: Adapted CBT produced greater and sustained improvements in sleep,
daily fatigue levels, and depression compared with TAU. These pilot findings
suggest that CBT is a promising treatment for sleep disturbance and fatigue after
TBI.

via Traumatic Brain Injury Resource Guide – Research Reports – Cognitive behavior therapy to treat sleep disturbance and fatigue after traumatic brain injury

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[ARTICLE] Fatigue and Cognitive Fatigability in Mild Traumatic Brain Injury are Correlated with Altered Neural Activity during Vigilance Test Performance – Full Text

Introduction: Fatigue is the most frequently reported persistent symptom following a mild traumatic brain injury (mTBI), but the explanations for the persisting fatigue symptoms in mTBI remain controversial. In this study, we investigated the change of cerebral blood flow during the performance of a psychomotor vigilance task (PVT) by using pseudo-continuous arterial spin labeling (PCASL) MRI technique to better understand the relationship between fatigability and brain activity in mTBI.

Material and methods: Ten patients (mean age: 37.5 ± 11.2 years) with persistent complaints of fatigue after mTBI and 10 healthy controls (mean age 36.9 ± 11.0 years) were studied. Both groups completed a 20-min long PVT inside a clinical MRI scanner during simultaneous measurements of reaction time and regional cerebral blood flow (rCBF) with PCASL technique. Cognitive fatigability and neural activity during PVT were analyzed by dividing the performance and rCBF data into quintiles in addition to the assessment of self-rated fatigue before and after the PVT.

Results: The patients showed significant fatigability during the PVT while the controls had a stable performance. The variability in performance was also significantly higher among the patients, indicating monitoring difficulty. A three-way ANOVA, modeling of the rCBF data demonstrated that there was a significant interaction effect between the subject group and performance time during PVT in a mainly frontal/thalamic network, indicating that the pattern of rCBF change for the mTBI patients differed significantly from that of healthy controls. In the mTBI patients, fatigability at the end of the PVT was related to increased rCBF in the right middle frontal gyrus, while self-rated fatigue was related to increased rCBF in left medial frontal and anterior cingulate gyri and decreases of rCBF in a frontal/thalamic network during this period.

Discussion: This study demonstrates that PCASL is a useful technique to investigate neural correlates of fatigability and fatigue in mTBI patients. Patients suffering from fatigue after mTBI used different brain networks compared to healthy controls during a vigilance task and in mTBI, there was a distinction between rCBF changes related to fatigability vs. perceived fatigue. Whether networks for fatigability and self-rated fatigue are different, needs to be investigated in future studies.

Introduction

Fatigue is a frequently reported symptom after mild traumatic brain injury (mTBI) (13) and a major reason why patients fail to return to work (4). The subjective experience of fatigue may be concomitant with physiological fatigue or with deteriorating performance, but may also be a sole complaint (56). Research on the relationship between underlying neural correlates to fatigue in mTBI, and possible performance decrements is complicated by the fact that fatigue is still not a well-defined concept. It is multidimensional in its nature, involving both physiological and psychological components (79) and, therefore, a single explanatory mechanism is unlikely (310).

Kluger and coworkers (11) suggested distinguishing the self-rated fatigue measures from objective measures of fatigue by labeling the later as fatigability. Such distinction might encourage among others more focused correlational studies; such as fatigue in relation to the neural activity. Measuring performance during sustained cognitive process provides a method to evaluate fatigue/fatigability objectively (1214). For example, sustained attention during vigilance performance is a demanding cognitive task and performance induced fatigability has been demonstrated as increased error rate and reaction time (15). Our group has also found fatigability in mTBI on a higher order attention demanding task (16).

More recently, we studied the behavioral correlates of changes in resting-state functional connectivity before and after performing a 20-min psychomotor vigilance task (PVT) for mTBI patients with persistent post-concussion fatigue (17). Taking advantage of a quantitative data-driven analysis approach developed by us, we were able to demonstrate that there was a significant linear correlation between the self-rated fatigue and functional connectivity in the thalamus and middle frontal cortex. Furthermore, we found that the 20 min PVT was sufficiently sensitive to invoke significant mental fatigue and specific functional connectivity changes in mTBI patients. These findings indicate that resting-state functional MRI (fMRI) measurements before and after a 20 min PVT may serve as a useful method for objective assessment of fatigue level in the neural attention system. However, these measurements neither provide any information about the dynamic change of the neural activities in the involved functional networks during the performance of PVT nor can they answer whether other neural systems mediate the observed functional connectivity change in the attention network.

Arterial spin labeling (ASL) MRI technique has recently been used to examine the cerebral blood flow (CBF) in patients with amnestic mild cognitive impairment and cognitively normal healthy controls both at rest and during the active performance of a memory task (18). As compared to rest, CBF measurement during the task performance showed increased group difference between patients and healthy controls indicating that CBF measures during a cognitive task may increase the discriminatory ability and the sensitivity to detect subtle functional changes in neurological diseases. In another ASL MRI study, Lim et al. (19) investigated the neural correlates of cognitive fatigue effects in a group of healthy volunteers during a 20-min PVT (19). They observed progressively slower reaction times and significantly increased mental fatigue ratings after the task and reported that such persistent cognitive fatigue effect was significantly correlated with regional cerebral blood flow (rCBF) decline in the right fronto-parietal attention network in addition to the basal ganglia and sensorimotor cortices. They also found that the rCBF at rest in the thalamus and right middle frontal gyrus before the PVT task was predictive of subjects’ subsequent performance decline. Based on these findings, they claimed that the rCBF at rest in the attention network might be a useful indicator of performance potential and a marker of the level of fatigue in neural attention system. However, it remains to be clarified how the relationship between the neural activity in mTBI patients and their fatigability is dynamically influenced by the performance of a difficult cognitive task.

Pseudo-Continuous Arterial Spin Labeling (PCASL) can provide quantitative rCBF measurements with whole-brain coverage and high signal-to-noise ratio. Furthermore, it is non-invasive and repetitive experiments can be carried out. It has been shown that fMRI experiments based on PCASL perfusion measurements may have higher sensitivity than experimental designs based on blood oxygenation level-dependent (BOLD) fMRI, particularly when studying slow neural activity changes within a subject (2022) and useful as a biomarker of brain function (18). To shed light on the questions discussed above, in this study we used PCASL MRI technique to measure the rCBF changes during a 20 min PVT in a group of mTBI patients with chronic fatigue and matched healthy control subjects. The aims of the present study are the following: (1) evaluate the PVT induced fatigability over time by dividing the performance data (error rate and reaction time) into quintiles to verify if the change of fatigability for mTBI patients follows the same pattern as that for healthy controls; (2) estimate the dynamic change of neural activity during PVT in terms of rCBF measurements in each quintile to reveal brain activities significantly associated with the change of fatigability. (3) Voxel-wise assessment of the rCBF values pre- and post-PVT to detect brain activity associated with changes in self-rated fatigue level. […]

Continue —> Frontiers | Fatigue and Cognitive Fatigability in Mild Traumatic Brain Injury are Correlated with Altered Neural Activity during Vigilance Test Performance | Neurology

Figure 4. Summary of the F-score results from the three-way ANOVA modeling of the regional cerebral blood flow data acquired during a 20-min psychomotor vigilance task (PVT) performance to illustrate the brain regions of statistically significant differences (family-wise error rate, p ≤ 0.05) in neural activity associated with the two fixed factors (the PVT performance time and subject group) and their interaction. (A) The effect of PVT performance time; (B) the interaction effect between the PVT performance time and subject groups. The color bar indicates the F-score of the three-way ANOVA results.

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[BLOG POST] Tired After a Stroke? Understanding Post-Stroke Fatigue | Saebo

Feeling tired is a normal part of life. Whether you didn’t get a good night of sleep or wore yourself out with a busy day or an exerting activity, your body can only handle so much before you start to feel the physical effects of being tired. In cases like these, all you need to do is rest in order to feel re-charged and rejuvenated. But for individuals who have suffered from a stroke, it’s not that easy.

Fatigue after a stroke is common, and it’s different from simply feeling tired. Post-stroke fatigue can make somebody feel like they completely lack energy or strength, with a persistent feeling of being tired or weary. Unlike typical tiredness, a nap or sleeping longer at night won’t solve things. If you are experiencing post-stroke fatigue, it is important to consult with your doctor so you can take the proper steps to start feeling better and more energized.

 

What is Post-Stroke Fatigue?

Post-stroke fatigue can occur after a mild or severe stroke, and roughly 40 to 70 percent of stroke patients experience this “invisible symptom.” It’s a particularly frustrating side effect of a stroke because it can make you feel completely exhausted and off your game, which in turn makes recovering from the stroke seem even more difficult.

Those who experience post-stroke fatigue can feel like they are not in control of their recovery, as it’s hard for them to muster the energy to participate in their rehab activities or normal day-to-day functions. Many individuals with post-stroke fatigue initially confuse it with “being tired,” but post-stroke fatigue is not the same thing as just being tired. It can come out of nowhere, without warning, and rest isn’t always the solution.

Post-stroke fatigue is draining both physically and emotionally/mentally, and the severity of the stroke does not seem to correlate to the severity of the fatigue. Even a mild stroke can result in extreme post-stroke fatigue, and even if you suffered a stroke some time ago and feel as if you’ve made a full recovery, post-stroke fatigue can still impact you.

 

What Causes Post-Stroke Fatigue?

 

Experts aren’t entirely sure what causes post-stroke fatigue because there has been limited research on the subject.Medical conditions like diabetes and heart disease can play a role, as can any pre-existing fatigue issues an individual had before suffering from a stroke. In addition to fatigue, sleep apnea is another issue reported by stroke survivors, so it’s possible there is some sort of link between the two, though nothing has been proven.

Survivors often feel stressed or depressed about the stroke afterwards, from worrying about the recovery process to being concerned with their symptoms. Stress and the mental demands that come with it can lead to fatigue. There are a lot of unknowns about the cause of post-stress fatigue, but one thing is certain: a stroke takes a big toll on a person’s body, and many stroke survivors feel severe fatigue as a result.

 

How Do You Tell if You Have Post-Stroke Fatigue?

Remember that there’s a difference between feeling tired and having post-stroke fatigue. The latter will give you afeeling of complete exhaustion; you will lack all energy and feel extremely weary. You will probably feel like you have to rest every day, or even multiple times a day. This can make it difficult to accomplish things, whether it’s something as simple as spending time with family, running errands, or even attending your post-stroke therapy sessions.

Until you feel the type of exhaustion that comes with post-stroke fatigue it’s difficult to explain, so don’t feel frustrated if your friends and family don’t understand why you’re struggling. If you think you have post-stroke fatigue, don’t hesitate to consult with your doctor.

 

Tips to Increase Your Energy

The first step in combating post-stroke fatigue is to discuss it with your doctor. Let them know what you’ve been feeling. Your doctor will probably start the process by making sure you’ve had an up-to-date physical. With that information, your doctor can rule out other potential causes for your fatigue or determine if your fatigue might stem from your medication.

It goes without saying, but try to take naps if time allows. Naps won’t cure you of your fatigue long term, but resting when you feel run down can help you feel more refreshed, even if only for a short while.

Do your best to relax. Don’t let your post-stroke fatigue, or any other side effects of your stroke, get you down. Stay positive! Being stressed or tense will only sap you of more energy. A positive attitude goes a long way in feeling upbeat and energetic. Try to get back into the swing of things by returning to your pre-stroke routines. Simple things like staying active and involved with friends and family can yield big benefits.

Yes, it will seem overwhelming at times. Suffering from a stroke, dealing with the aftermath, and having no energy on top of it can be tough, but celebrate your successes. Take baby steps, and be proud of the progress you’ve made. Focus on what you’ve accomplished during your recovery so far, rather than dread what’s left to be done.

 

Tired of Being Tired

Post-stroke fatigue is a daunting condition, and many people who are recovering from a stroke might not even realize they have it, instead thinking they are simply tired. If you’ve had a stroke and find yourself feeling sapped of your energy on a consistent basis, talk to your doctor. There’s a chance you have post-stroke fatigue. You’re not alone; 40 to 70 percent of stroke survivors experience this kind of exhaustion.

By speaking with the proper medical professionals, making it a point to rest as often as possible, and having a positive mindset, you can combat the constant drowsiness and work on returning to your pre-stroke energy levels.

Source: Tired After a Stroke? Understanding Post-Stroke Fatigue | Saebo

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[ARTICLE] Cognitive fatigue in individuals with traumatic brain injury is associated with caudate activation – Full Text

Abstract

We investigated differences in brain activation associated with cognitive fatigue between persons with traumatic brain injury (TBI) and healthy controls (HCs). Twenty-two participants with moderate-severe TBI and 20 HCs performed four blocks of a difficult working memory task and four blocks of a control task during fMRI imaging. Cognitive fatigue, assessed before and after each block, was used as a covariate to assess fatigue-related brain activation. The TBI group reported more fatigue than the HCs, though their performance was comparable. Regarding brain activation, the TBI group showed a Task X Fatigue interaction in the caudate tail resulting from a positive correlation between fatigue and brain activation for the difficult task and a negative relationship for the control task. The HC group showed the same Task X Fatigue interaction in the caudate head. Because we had prior hypotheses about the caudate, we performed a confirmatory analysis of a separate dataset in which the same subjects performed a processing speed task. A relationship between Fatigue and brain activation was evident in the caudate for this task as well. These results underscore the importance of the caudate nucleus in relation to cognitive fatigue.

Continue —> Cognitive fatigue in individuals with traumatic brain injury is associated with caudate activation | Scientific Reports

The interaction of Group, Task and Fatigue in Experiment 1 in the caudate head (indicated by blue arrow). The plots on the left are included only to show the slopes of the regression lines. For the HC group, there was a negative correlation between fatigue and activation for the 0-back task (top left), and a positive correlation for the 2-back task (top right). For the TBI group, the correlations between fatigue and activation in both tasks were very weak (lower plots). In all cases, the vertical axis is the percent signal change in the caudate head and the horizontal axis is the normalized fatigue score. On the right is a 3-dimensional rendering of the activation in the caudate head for Experiment 1.

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[WEB SITE] Cognitive fatigue after TBI linked with caudate activation

Individuals with neurological damage often report difficulties with cognitive fatigue, a subjective lack of mental energy that is perceived to interfere with daily activities. Because of poor correlation between self-reports of cognitive fatigue and tests of cognitive performance, scientists are looking at more objective measures, such as correlations with neuroimaging findings. In the Kessler study, brain activation patterns were compared in 22 individuals with moderate to severe TBI and 20 healthy controls. Both groups performed tasks of working memory during functional MRI imaging of the brain; the TBI group reported more fatigue, although performance was comparable between the groups. The results showed that the experience of self-reported fatigue is associated with activation changes in the caudate nucleus of the basal ganglia.

“These results are consistent with findings in our related research in the multiple sclerosis (MS) population,” said Dr. Wylie, the lead author, “which suggests that the TBI and MS populations share a mechanism for cognitive fatigue.” This has important implications for the development of effective treatments. “This study points to the caudate nucleus as a likely target for clinical interventions to alleviate fatigue,” explained Dr. Wylie, who is associate director of Neuroscience Research and the Rocco Ortenzio Neuroimaging Center at Kessler Foundation.

Story Source:

Materials provided by Kessler Foundation. Note: Content may be edited for style and length.


Journal Reference:

  1. G. R. Wylie, E. Dobryakova, J. DeLuca, N. Chiaravalloti, K. Essad, H. Genova. Cognitive fatigue in individuals with traumatic brain injury is associated with caudate activation. Scientific Reports, 2017; 7 (1) DOI: 10.1038/s41598-017-08846-6

Source: Cognitive fatigue after TBI linked with activation of caudate: Findings underscore the role of the caudate nucleus in the mechanism of cognitive fatigue in traumatic brain injury — ScienceDaily

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[WEB SITE] Managing fatigue after a brain injury – Synapse

Fatigue is a common and very disabling symptom experienced by people with a brain injury.

It may be a continual sense of mental fatigue or it can happen when a person is trying to do too much and the brain is overloaded, often resulting in mind-numbing fatigue that can last for several days.

Brain disorders such as traumatic brain injury can be likened to a highway when one of three lanes is closed down. If traffic is light, there will be no difference but once the traffic reaches a critical point, the cars barely move and it can take ages for the traffic jam to clear.

It is important to avoid fatigue as much as possible, as any other problems are worsened as well, such as:

  • Vision problems
  • Slurred speech
  • Difficulty finding words
  • Poor concentration
  • Cramps or weak muscles
  • Poor coordination or balance.

Fatigue can occur for no apparent reason or after physical activity, but is quite likely to occur from too much mental activity. Examples include planning the week’s errands, organizing a work schedule or simply reading.

Fatigue can be managed with good planning and rest periods, but carers and the family member must realize fatigue is a very real problem.

Symptoms of fatigue

The following symptoms may all suggest fatigue:

  • Withdrawal, short answers, dull tone of voice
  • Loss of appetite
  • Shortness of breath
  • Slower movement and speech
  • Irritability, anxiety, crying episodes
  • Increased forgetfulness
  • Lack of motivation and interest.

What are the triggers of fatigue?

Work out what triggers it and what factors make the symptoms worse, such as long conversations, noisy shopping centres, movies with complicated plots, or talking with two or more people at once.

In some cases, fatigue could be a side-effect of certain medications, in which case you should discuss options with your doctor.

Be aware of the first signs of fatigue and immediately stop and rest – overloading your brain can easily result in several days of extreme tiredness. Make a note of how long you can do certain activities before fatigue starts e.g. if fatigue starts after 30 minutes of reading, only read for 20 minutes in future.

Managing fatigue

Contingency plans: Fatigue may occur at the least convenient times – on public transport or during a meeting. You need to negotiate ways of coping when this happens. You can use specific strategies or call in extra support. Work out contingency plans with your family member. Your rehab team, occupational therapist or physiotherapist can help with suggestions.

Assess best hours: Some people function best in the mornings, so complete demanding tasks then. Others function better in the afternoon or the evening. Organize your routine accordingly. Don’t drive when you are tired.

Assess your environment: Provide an uncluttered environment that is easy to move around and work in. Think about how and where things are stored; bench heights, entrances, types of furnishing and lighting. For example, some people may find fluorescent lighting or dim lighting more tiring.

Schedule rest periods: Make a daily or weekly schedule, and include regular rest periods. “Rest” means do nothing at all. If you have a nap, don’t oversleep in case this affects your normal sleep cycle.

Use aids: Use mechanical aids to conserve energy for when it really counts. One man spared his legs extra effort by using his wheelchair to get from his house to the car, then from the car to the church, before walking his daughter, the bride, down the aisle.

Break it down: Break down activities into a series of smaller tasks. This provides opportunities to rest while allowing the person to complete the task. Encourage sensible shortcuts.

Set priorities: Focus on things that must be done and let the others go.

Medication highs and lows: Be aware of changes throughout the day that relate to medication. Is the person better or worse immediately after their tablets? Plan their activities around these times.

Weather: Hot weather can also increase fatigue. Plan around this.

Seek support: Ask for advice. In particular, an occupational therapist can visit your home and advise on an energy-conserving plan. For more information, talk to your doctor or condition-specific support organization.

Healthy lifestyle

AS with virtually every aspect of a traumatic brain injury and similar brain disorders, fatigue will be less of a problem if you focus on a healthy lifestyle:

  • Sleep well
  • Get regular exercise
  • Avoid alcohol or limit your intake
  • Eat a healthy diet and watch your weight
  • Learn stress management techniques
  • Maintain contact with friends and family.

Source: Managing fatigue after a brain injury – Synapse – reconnecting lives

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[Abstract+References] Cognitive Behavior Therapy to Treat Sleep Disturbance and Fatigue After Traumatic Brain Injury: A Pilot Randomized Controlled Trial – Conference Paper

Abstract

Objective

To evaluate the efficacy of adapted cognitive behavioral therapy (CBT) for sleep disturbance and fatigue in individuals with traumatic brain injury (TBI).

Design

Parallel 2-group randomized controlled trial.

Setting

Outpatient therapy.

Participants

Adults (N=24) with history of TBI and clinically significant sleep and/or fatigue complaints were randomly allocated to an 8-session adapted CBT intervention or a treatment as usual (TAU) condition.

Interventions

Cognitive behavior therapy.

Main Outcome Measures

The primary outcome was the Pittsburgh Sleep Quality Index (PSQI) posttreatment and at 2-month follow-up. Secondary measures included the Insomnia Severity Index, Fatigue Severity Scale, Brief Fatigue Inventory (BFI), Epworth Sleepiness Scale, and Hospital Anxiety and Depression Scale.

Results

At follow-up, CBT recipients reported better sleep quality than those receiving TAU (PSQI mean difference, 4.85; 95% confidence interval [CI], 2.56–7.14). Daily fatigue levels were significantly reduced in the CBT group (BFI difference, 1.54; 95% CI, 0.66–2.42). Secondary improvements were significant for depression. Large within-group effect sizes were evident across measures (Hedges g=1.14–1.93), with maintenance of gains 2 months after therapy cessation.

Conclusions

Adapted CBT produced greater and sustained improvements in sleep, daily fatigue levels, and depression compared with TAU. These pilot findings suggest that CBT is a promising treatment for sleep disturbance and fatigue after TBI.

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Source: Cognitive Behavior Therapy to Treat Sleep Disturbance and Fatigue After Traumatic Brain Injury: A Pilot Randomized Controlled Trial – Archives of Physical Medicine and Rehabilitation

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[WEB SITE] Mental Fatigue – University of Gothenburg, Sweden

Mental fatigue or brain fatigue

Mental fatigue can be a disabling consequence of traumatic brain injury, stroke, infection or inflammation in the Central Nervous System (CNS). The condition is characterized by pronounced mental fatigue after moderate mental activity. Pronounced fatigue can appear very rapidly and, when it does, it is not possible for the affected person to continue the activity. Typical for this kind of fatigue is a profound, long recovery time to get one’s mental energy back. Attention cannot be maintained for more than short periods. Other common associated symptoms are: irritability, tearfulness, sound and light sensitivity as well as headaches.

Read more under About Mental Fatigue.

Measure mental fatigue with an app.  Androids and Windows. Coming soon for iPhone.

Android

Windows 10

Contact information

Lars Rönnbäck, professor and senior physician in neurology

Birgitta Johansson, Ph.D., specialist in neuropsychology

Institute of neuroscience and physiology
Department of clinical neuroscience and rehabilitation
Sahlgrenska Academy
University of Gothenburg Sweden

mf@gu.se

Source: Mental Fatigue – Mental Fatigue, University of Gothenburg, Sweden

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[Systematic Review] Does Tai Chi relieve fatigue? A systematic review and meta-analysis of randomized controlled trials – Full Text

Abstract

Background

Fatigue is not only a familiar symptom in our daily lives, but also a common ailment that affects all of our bodily systems. Several randomized controlled trials (RCTs) have proven Tai Chi to be beneficial for patients suffering from fatigue, however conclusive evidence is still lacking. A systematic review and meta-analysis was performed on all RCTs reporting the effects of Tai Chi for fatigue.

Methods

In the end of April 2016, seven electronic databases were searched for RCTs involving Tai Chi for fatigue. The search terms mainly included Tai Chi, Tai-ji, Taiji, fatigue, tiredness, weary, weak, and the search was conducted without language restrictions. Methodological quality was assessed using the Cochrane Risk of Bias tool. RevMan 5.3 software was used for meta-analysis. Publication bias was estimated with a funnel plot and Egger’s test. We also assessed the quality of evidence with the GRADE system.

Results

Ten trials (n = 689) were included, and there was a high risk of bias in the blinding. Two trials were determined to have had low methodological quality. Tai Chi was found to have improved fatigue more than conventional therapy (standardized mean difference (SMD): -0.45, 95% confidence interval (CI): -0.70, -0.20) overall, and have positive effects in cancer-related fatigue (SMD:-0.38, 95% CI: -0.65, -0.11). Tai Chi was also more effective on vitality (SMD: 0.63, 95% CI: 0.20, 1.07), sleep (SMD: -0.32, 95% CI: -0.61, -0.04) and depression (SMD: -0.58, 95% CI: -1.04, -0.11). However, no significant difference was found in multiple sclerosis-related fatigue (SMD: -0.77, 95% CI: -1.76, 0.22) and age-related fatigue (SMD: -0.77, 95% CI: -1.78, 0.24). No adverse events were reported among the included studies. The quality of evidence was moderate in the GRADE system.

Conclusions

The results suggest that Tai Chi could be an effective alternative and /or complementary approach to existing therapies for people with fatigue. However, the quality of the evidence was only moderate and may have the potential for bias. There is still absence of adverse events data to evaluate the safety of Tai Chi. Further multi-center RCTs with large sample sizes and high methodological quality, especially carefully blinded design, should be conducted in future research.

Background

Although no one can exactly quantify or document fatigue [1], fatigue is a common symptom not only deeply related to most acute and chronic diseases, but also to everyday life. It is not only common, but problematic, for people with conditions such as cancer, multiple sclerosis, and rheumatoid arthritis [2]. The National Comprehensive Cancer Network (NCCN) defined cancer related fatigue as ‘an persistent, unusual, subjective feeling of tiredness correlated with cancer or cancer treatment that obstruct to normal functioning’ [3]. Definition of fatigue was also described as “a subjective feeling of lacking mental and/or physical energy, which was perceived by the caregiver or individuals interfering with usual and desired activities” [4]. Because of its subjective nature, fatigue can only be gauged by self-reported or caregiver-reported questionnaires [5]. Fatigue generally lasts longer than somnolence [6]. Tiredness is a state of temporary decreasing in strength and energy, which may be experienced as a partial of fatigue [7]. Some authors simply divided fatigue into acute and chronic fatigue [2]. Acute fatigue occurs in healthy populations, with a rapid onset and short duration. After a period of rest and exercise, it is generally relieved. Chronic fatigue mainly affects clinically disordered individuals and is onset gradually, persists and develops over time. It usually can’t be alleviated by usual recovery techniques [6]. As a symptom, fatigue is a common complaint among most people, and many ailments are accompanied by fatigue. However, it is often ignored, under-diagnosed, and seen as a natural result of physical deterioration [8].

A previous study had shown that 10.6% of women and 10.2% of men complained of fatigue for ≥ 1 month in the South London general practice attenders [9]. The prevalence rate of chronic fatigue was 10.7% in general Chinese population [10]. Among older adults with myocardial infarction, fatigue is frequently reported to be one of the most serious barriers to physical activity [11]. Fatigue occurs in 50%-83% of patients with multiple sclerosis [12]. Among breast cancer patients 58%-94% undergoing treatment and 56%-95% who are post-chemotherapy experience fatigue [13]. Although the methods, standards, and results of these studies are not always consistent, it is undeniable that fatigue is a common symptom from which many patients suffer.

The mechanisms behind fatigue are unclear [5], however they may be related to a patient’s physical condition. There is no panacea for fatigue other than treating the symptoms [5]. Evidence has shown that exercise including walking, running, jogging, swimming, resistance (strengthening) training, stretching, aerobic exercise can counter fatigue among sufferers of chronic fatigue syndrome [14], multiple sclerosis [15], fibromyalgia [16] and among cancer survivors [17,18]. So we supposes that Tai Chi, a traditional Chinese martial art, may be an effective treatment for patients suffering from fatigue.

Tai Chi has popular in China for several centuries. Many different types of Tai Chi exist, but most consist of movement, meditation and breathing, while concentrating on the mind and maintaining low intensity [1920], and further modulate various aspects of the body including the physical, the psychological, mood and spirit [21]. In the theory of Chinese medicine (CM), Tai Chi can maintain the harmony between qi and the blood, keep yin and yang in balance and also enhance immunity [2223]. These properties are both important in relieving fatigue and maintaining energy. Qi, the energy which promotes the body’s movement, can circulate around the entire body freely if yin and yang are kept in balance [23].

Tai Chi may relieve fatigue via different mechanisms of action. Firstly, through slow movement and weight shifting, Tai Chi may relieve stress, make people more happy [24] and promote relaxation [25]. Secondly, the proven efficacy of Tai Chi to enhance aerobic capacity and immune function [26] and to improve pain [27], depression and psychological well-being [28] may be beneficial to relieve fatigue.

An advantage of Tai Chi is that it is easy to learn, teach, and popularize, and more reports on evidence of its effects should lead to it becoming even more popular. As a low impact exercise, Tai Chi may be ideal for people with fatigue, lack of exercise or who do not have active lifestyles [19]. Several studies have reported that Tai Chi plays a critical role in fighting fatigue [2932]. However, there not been explicit studies to reach a conclusion on Tai Chi’s effects on fatigue. Others have shown no difference between Tai Chi groups and control groups [33,34]. In addition, most of the studies focus on only one ailment [32,35,36]. As far as we know, the majority of the literature on Tai Chi intervention for fatigue is empirical, and uses small sample sizes. Few of the existing studies have explored fatigue as the primary outcome. To date, there have been no systematic reviews nor meta-analyses to evaluate the effects of Tai Chi for fatigue, but single RCTs based on a specific population in a certain place. This systematic review evaluates the effects and safety of Tai Chi for fatigue, and provides an overall understanding of the current situation, as well as problems in this field.

Continue —> Does Tai Chi relieve fatigue? A systematic review and meta-analysis of randomized controlled trials

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