Chronic fatigue syndrome patients had reduced activity in brain’s ‘reward center’

Chronic fatigue syndrome, a medical disorder characterized by extreme and ongoing fatigue with no other diagnosed cause, remains poorly understood despite decades of scientific study. Although researchers estimate that more than 1 million Americans are affected by this condition, the cause for chronic fatigue syndrome, a definitive way to diagnose it, and even its very existence remain in question. In a new study, researchers have found differing brain responses in people with this condition compared to healthy controls, suggesting an association between a biologic functional response and chronic fatigue syndrome.

The findings show that patients with chronic fatigue syndrome have decreased activation of an area of the brain known as the basal ganglia in response to reward. Additionally, the extent of this lowered activation was associated with each patient’s measured level of fatigue. The basal ganglia are at the base of the brain and are associated with a variety of functions, including motor activity and motivation. Diseases affecting basal ganglia are often associated with fatigue. These results shed more light on this mysterious condition, information that researchers hope may eventually lead to better treatments for chronic fatigue syndrome.

The study was conducted by Elizabeth R. Unger, James F. Jones, and Hao Tian of the Centers for Disease Control and Prevention (CDC), Andrew H. Miller and Daniel F. Drake of Emory University School of Medicine, and Giuseppe Pagnoni of the University of Modena and Reggio Emilia. An abstract of their study entitled, “Decreased Basal Ganglia Activation in Chronic Fatigue Syndrome Subjects is Associated with Increased Fatigue,” will be discussed at the meeting Experimental Biology 2012, being held April 21-25 at the San Diego Convention Center. The abstract is sponsored by the American Society for Investigative Pathology (ASIP), one of six scientific societies sponsoring the conference which last year attracted some 14,000 attendees.

More Fatigue, Less Activation

Dr. Unger says that she and her colleagues became curious about the role of the basal ganglia after previous studies by collaborators at Emory University showed that patients treated with interferon alpha, a common treatment for chronic hepatitis C and several other conditions, often experienced extreme fatigue. Further investigation into this phenomenon showed that basal ganglia activity decreased in patients who received this immune therapy. Since the fatigue induced by interferon alpha shares many characteristics with chronic fatigue syndrome, Unger and her colleagues decided to investigate whether the basal ganglia were also affected in this disorder.

The researchers recruited 18 patients with chronic fatigue syndrome, as well as 41 healthy volunteers with no symptoms of CFS. Each study participant underwent functional magnetic resonance imaging, a brain scan technique that measures activity in various parts of the brain by blood flow, while they played a simple card game meant to stimulate feelings of reward. The participants were each told that they’d win a small amount of money if they correctly guessed whether a preselected card was red or black. After making their choice, they were presented with the card while researchers measured blood flow to the basal ganglia during winning and losing hands.

The researchers showed that patients with chronic fatigue syndrome experienced significantly less change in basal ganglia blood flow between winning and losing than the healthy volunteers. When the researchers looked at scores for the Multidimensional Fatigue Inventory, a survey often used to document fatigue for chronic fatigue syndrome and various other conditions, they also found that the extent of a patient’s fatigue was tightly tied with the change in brain activity between winning and losing. Those with the most fatigue had the smallest change.

Results Suggest Role of Inflammation

Unger notes that the findings add to our understanding of biological factors that may play a role in chronic fatigue syndrome. “Many patients with chronic fatigue syndrome encounter a lot of skepticism about their illness,” she says. “They have difficulty getting their friends, colleagues, coworkers, and even some physicians to understand their illness. These results provide another clue into the biology of chronic fatigue syndrome.”

The study also suggests some areas of further research that could help scientists develop treatments for this condition in the future, she adds. Since the basal ganglia use the chemical dopamine as their major neurotransmitter, dopamine metabolism may play an important role in understanding and changing the course of this illness. Similarly, the difference in basal ganglia activation between the patients and healthy volunteers may be caused by inflammation, a factor now recognized as pivotal in a variety of conditions, ranging from heart disease to cancer.

Estimates from the CDC suggest that annual medical costs associated with chronic fatigue syndrome total about $14 billion in the United States. Annual losses to productivity because of lost work time range between $9 and $37 billion, with costs to individual households ranging between $8,000 and $20,000 per year.

 

Source: Federation of American Societies for Experimental Biology (FASEB). (2012, April 24). Chronic fatigue syndrome patients had reduced activity in brain’s ‘reward center’. ScienceDaily. Retrieved March 4, 2017 from https://www.sciencedaily.com/releases/2012/04/120424142109.htm

 

Visual stress could be a symptom of Chronic Fatigue Syndrome, research suggests

University of Leicester research team discovers vision-related abnormalities that could help in diagnosis of illness

People suffering from Chronic Fatigue Syndrome (CFS) could experience higher levels of visual stress than those without the condition, according to new research from the University of Leicester.

CFS, also known as Myalgic Encephalomyelitis (ME), is a condition that causes persistent exhaustion that affects everyday life and doesn’t go away with sleep or rest. Diagnosis of the condition is difficult as its symptoms are similar to other illnesses.

A research team from the University of Leicester led by Dr Claire Hutchinson from the Department of Neuroscience, Psychology and Behaviour has examined patients with and without CFS and has found that those suffering from the condition are more vulnerable to pattern-related visual stress, which causes discomfort and exhaustion when viewing repetitive striped patterns, such as when reading text.

The results of the study, which is published in the journal Perception, could help in the diagnosis of CFS, as the findings suggest that there are visual system abnormalities in people with ME/CFS that may represent an identifiable and easily measurable behavioural marker of the condition.

Dr Hutchinson explained: “Diagnosis of ME/CFS is controversial. With the exception of disabling fatigue, there are few definitive clinical features of the condition and its core symptoms, overlap with those often prevalent in other conditions. As a result, ME/CFS is often a diagnosis of exclusion, being made as a last resort and possibly after a patient has experienced a series of inappropriate treatments of misdiagnosed disorders.

“It is imperative therefore that research focuses on identifying significant clinical features of CFS/ME with a view to elucidating its underlying pathology and delineating it from other illnesses. Doing so will help researchers and healthcare professionals gain important insights into the condition, aid diagnosis and, in the longer term, inform evidence-based therapeutic interventions.”

The study assessed vulnerability of ME/CFS patients to pattern-related visual stress using a standardised test called the pattern glare test, in which people report the number of visual distortions they experience when looking at three repetitive striped patterns of different levels of detail.

During the study twenty patients with CFS and twenty patients without the condition were recruited.

Participants viewed 3 patterns, the spatial frequencies (SF) of which were either 0.3 (low-SF), 2.3 (mid-SF) and 9.4 (high-SF) cycles per degree (c/deg). They then reported the number of distortions they experienced when viewing each pattern.

Patients with ME/CFS reported more distortions on the intermediate striped pattern (Pattern 2) than people without the condition.

Dr Hutchinson added: “The existence of pattern-related visual stress in ME/CFS may represent an identifiable and easily measurable behavioural marker of ME. This could, in conjunction with other diagnostic tests, help delineate it from other conditions.”

The work was funded by ME Research UK who provided funding for a 1-year MPhil studentship, awarded to Rachel Wilson, who was supervised by Drs Claire Hutchinson and Kevin Paterson from the University of Leicester’s Department of Neuroscience, Psychology and Behaviour.

Dr Neil Abbot, Research & Operations Director at ME Research UK, added: “Around three-quarters of people with ME/CFS report a range of eye and vision-related symptoms that interfere with their everyday lives, yet there has been very little scientific investigation of the problem.

“Dr Claire Hutchinson and her team have previously confirmed the existence of eye movement difficulties in ME/CFS patients, and that symptoms, including eye pain, can be severe. Her new report in Perception extends these findings and raises the possibility that vision anomalies, including pattern-related visual stress, may have a diagnostic role in the disease.”

The study ‘Increased vulnerability to pattern-related visual stress in Myalgic Encephalomyelitis’ was published in the journal Perception.

Journal Reference: Rachel L. Wilson, Kevin B. Paterson and Claire V. Hutchinson. Increased Vulnerability to Pattern-Related Visual Stress in Myalgic Encephalomyelitis. Perception, November 2015 DOI: 10.1177/0301006615614467

 

Source: University of Leicester. (2015, November 24). Visual stress could be a symptom of Chronic Fatigue Syndrome, research suggests. ScienceDaily. Retrieved March 4, 2017 from https://www.sciencedaily.com/releases/2015/11/151124082235.htm

 

Chronic Fatigue Syndrome Linked To Stomach Virus

Chronic fatigue syndrome, also known as ME (myalgic encephalitis), is linked to a stomach virus, suggests research published ahead of print in Journal of Clinical Pathology.

The researchers base their findings on 165 patients with ME, all of whom were subjected to endoscopy because of longstanding gut complaints.

Endoscopy involves the threading of a long tube with a camera on the tip through the gullet into the stomach.

Specimens of stomach tissue were also taken to search for viral proteins and compared with specimens taken from healthy people and patients with other gut diseases none of whom had been diagnosed with ME.

Patients with ME often have intermittent or persistent gut problems, including indigestion and irritable bowel syndrome.

And viral infections, such as Epstein Barr virus (glandular fever), cytomegalovirus, and parvovirus, among others, produce many of the symptoms associated with chronic fatigue syndrome.

Enteroviruses, which infect the bowel, cause severe but short lasting respiratory and gut infections.

There are more than 70 different types, and they head for the central nervous system, heart and muscles.

Most of the biopsy specimens from patients with gut problems showed evidence of mild long term inflammation, although few were infected with Helicobacter pylori, a common bacterial infection associated with inflammation.

But more than 80% of the specimens from the ME patients tested positive for enteroviral particles compared with only seven of the 34 specimens from healthy people.

In a significant proportion of patients, the initial infection had occurred many years earlier.

 

Source: BMJ Specialty Journals. (2007, September 17). Chronic Fatigue Syndrome Linked To Stomach Virus. ScienceDaily. Retrieved March 4, 2017 from  https://www.sciencedaily.com/releases/2007/09/070913132933.htm

 

Chronic Fatigue Patients Show Lower Response To Placebos

Contrary to conventional wisdom, patients with chronic fatigue syndrome respond to placebos at a lower rate than people with many other illnesses, according to the first systematic review of the topic.

According to the new analysis by Dr. Hyong Jin Cho of King’s College London and colleagues, 19.6 percent of patients with chronic fatigue syndrome improved after receiving inactive treatments, compared with a widely accepted figure of about 30 percent for other conditions.

Because the placebo effect seems to be strongest in diseases with highly subjective symptoms, some medical professionals believed it could be as high as 50 percent among CFS patients.

The review, reported in the current issue of Psychosomatic Medicine, pooled data from 29 studies in which 1,016 people with CFS received various placebos.

CFS is a complex illness that has no known cause or cure. Myriad symptoms include severe malaise, muscle and joint pain, sleep and mood disturbances and headache. The symptoms continue for at least six months and cannot be explained by any other medical conditions. The Centers for Disease Control and Prevention estimate that as many as 500,000 Americans may have CFS or related conditions.

With so many mysteries surrounding CFS, a great deal of controversy exists among both doctors and patients as to whether its origins are primarily psychological or physiological. Current evidence suggests that emotional or social stresses such as bereavement or problems at work, combined with other triggers such as common viral infections, contribute to the disorder. Additional factors, such as avoidance of physical activity, may cause the symptoms to become chronic, says Cho.

The authors propose several possible explanations for the surprisingly low placebo response revealed in the analysis. Perhaps patients have low expectations due to the reality that CFS is very difficult to treat and often persists for many years. Alternatively, disconnects between how patients and doctors view the illness “may impede development of a collaborative therapeutic relationship,” reviewers suggest.

The study also showed that the placebo response is 24 percent for medical interventions but only 14 percent for psychiatric/psychological treatments. The authors say the reason may be that many CFS sufferers seen in specialist settings or self-help groups “have a firm conviction that their illness is of physical origin” and thus would have little faith in psychiatric/psychological treatments. This finding supports the idea that the placebo response is greatly influenced by patients’ expectations of improvement.

According to the review, behavioral therapy and graded exercise therapy have benefits, and if patients were more aware of them, says Cho, they might be “more open, more optimistic, and more collaborative with the professionals, and the overall outcome of the treatments could be enhanced.”

Dr. Lucinda Bateman, an internist who specializes in CFS and fibromyalgia and serves on the board of the American Association for Chronic Fatigue Syndrome, has worked with about 500 CFS patients over the past 15 years.

“In my clinical experience, I have found that CFS is among the most difficult conditions to improve at all, with either physical or psychological interventions.” This is true in part, she says, because there is a great deal of variation among patients diagnosed with CFS, and Bateman believes that ultimately CFS may be found to involve more than one disease.

In the absence of a cure, Bateman has found that the most effective treatment for CFS combines improving symptoms with medication, helping patients retain physical conditioning when possible and using psychological and psychiatric interventions to help patients adapt to living with chronic illness.

She doesn’t discount the placebo effect, however. “When you say to people, ‘I believe you, I will help you manage your symptoms, I will advocate for you,’ that hope and feeling of control over their disease could be considered placebo effect, but it’s an important part of delivering medical care.”‘

 

Source: Center For The Advancement Of Health. “Chronic Fatigue Patients Show Lower Response To Placebos.” ScienceDaily. ScienceDaily, 22 March 2005. https://www.sciencedaily.com/releases/2005/03/050322120639.htm

 

Hit-and-run Injury To The Brain: New Evidence On Chronic Fatigue Causation

Press Release: A seven-year tracking study has prompted scientists to suggest that chronic fatigue syndrome could be the result of brain injuries inflicted during the early stages of glandular fever.

Australian researchers have put the suggestion in this week’s Journal of Infectious Diseases, which reveals new findings from the ‘Dubbo Infection Outcomes Study’. Since 1999, a team led by UNSW Professor Andrew Lloyd have been tracking the long-term health of individuals infected with Epstein-Barr virus (EBV), Ross River virus (RRV) or Q fever infection. Their goal is to discover whether the post-infection fatigue syndrome that may affect up to 100,000 Australians is caused by the persistence of EBV, a weakened immune system, psychological vulnerability, or some combination of these.

Glandular fever — sometimes called ‘the kissing disease’ — is caused by Epstein-Barr virus (EBV). Transmitted via saliva, its acute symptoms include fever, sore throat, tiredness, and swollen lymph glands. Most patients recover within several weeks but one in ten young people will suffer prolonged symptoms, marked by fatigue. When these symptoms persist in disabling degree for six months or more, the illness may be diagnosed as chronic fatigue syndrome (CFS).

The researchers followed the course of illness among 39 people diagnosed with acute glandular fever. Eight patients developed a ‘post-infective fatigue syndrome’ lasting six months or longer, while the remaining 31 recovered uneventfully. Detailed studies of the activity of the Epstein-Barr virus in the blood and the immune response against the virus were conducted on blood samples collected from each individual over 12 months.

Commenting on the findings, Professor Lloyd says: “Our findings reveal that neither the virus nor an abnormal immune response explain the post-infective fatigue syndrome. We now suspect it’s more like a hit and run injury to the brain.

“We believe that the parts of the brain that control perception of fatigue and pain get damaged during the acute infection phase of glandular fever. If you’re still sick several weeks after infection, it seems that the symptoms aren’t being driven by the activity of the virus in body, it’s happening in the brain.”

The research team comprising scientists from the University of New South Wales, the University of Sydney and the Queensland Institute of Medical Research plan to test their ‘brain injury’ hypothesis by doing neurological tests on the study participants.

###

About the Dubbo Infection Outcomes Study: this is a major prospective cohort study following individuals from the time of onset of documented infection with Epstein-Barr virus (the cause of glandular fever), Ross River virus (the mosquito-borne infection which causes rash and joint pain) and Q fever (an infection common in meatworkers and those exposed to livestock).

Research Paper:
‘Prolonged illness after infectious mononucleosis is associated with altered immunity but not with increased viral load’, The Journal of Infectious Diseases, vol. 193 (2006), pp 664-671. Authors: Barbara Cameron, Mandvi Bharadwaj, Jacqueline Burrows, Chrysa Fazou, Denis Wakefield, Ian Hickie, Rosemary French, Rajiv Khanna, Andrew Lloyd.

Funding: The Dubbo Infection Outcomes Study is 82 per cent funded by the US Centers for Disease Control. It also receives funding from the National Health and Medical Research Council of Australia.

 

Source: University of New South Wales. “Hit-and-run Injury To The Brain: New Evidence On Chronic Fatigue Causation.” ScienceDaily. ScienceDaily, 1 March 2006. https://www.sciencedaily.com/releases/2006/03/060301092926.htm

 

New Therapy For Chronic Fatigue Syndrome To Be Tested

Press Release: A preliminary study suggests there may be hope in the offing for some sufferers of chronic fatigue syndrome with a new therapy being tested by researchers at the Stanford University School of Medicine.

José Montoya, MD, associate professor of medicine (infectious diseases), and postdoctoral scholar Andreas Kogelnik, MD, PhD, have used the drug valganciclovir – an antiviral often used in treating diseases caused by human herpes viruses – to treat a small number of CFS patients.

The researchers said they treated 25 patients during the last three years, 21 of whom responded with significant improvement that was sustained even after going off the medication at the end of the treatment regimen, which usually lasts six months. The first patient has now been off the drug for almost three years and has had no relapses. A paper describing the first dozen patients Montoya and Kogelnik treated with the drug was published in the December issue of Journal of Clinical Virology.

“This study is small and preliminary, but potentially very important,” said Anthony Komaroff, MD, professor of medicine at Harvard Medical School, who was not involved in the study. “If a randomized trial confirmed the value of this therapy for patients like the ones studied here, it would be an important landmark in the treatment of this illness.”

Montoya has received a $1.3 million grant from Roche Pharmaceutical, which manufactures the drug under the brand name Valcyte, to conduct a randomized, placebo-controlled, double-blind study set to begin this quarter at Stanford. The study will assess the effectiveness of the drug in treating a subset of CFS patients.

Montoya is speaking about his efforts at the biannual meeting of the International Association for Chronic Fatigue Syndrome in Fort Lauderdale on Jan. 11 and 12.

Chronic fatigue syndrome has baffled doctors and researchers for decades, because aside from debilitating fatigue, it lacks consistent symptoms. Although many genetic, infectious, psychiatric and environmental factors have been proposed as possible causes, none has been nailed down. It was often derided as “yuppie flu,” since it seemed to occur frequently in young professionals, though the Centers for Disease Control and Prevention says it’s most common in the middle-aged. But to those suffering from it, CFS is all too real and its effects are devastating, reducing once-vigorous individuals to the ranks of the bedridden, with an all-encompassing, painful and sleep-depriving fatigue.

More than 1 million Americans suffer from the disorder, according to the CDC. The disease often begins with what appears to be routine flulike symptoms, but then fails to subside completely – resulting in chronic, waxing and waning debilitation for years.

Valganciclovir is normally used against diseases caused by viruses in the herpes family, including cytomegalovirus, Epstein-Barr virus and human herpes virus-6. These diseases usually affect patients whose immune systems are severely weakened, such as transplant and cancer patients. Montoya, who had used the drug in treating such patients for years, decided to try using it on a CFS patient who came to him in early 2004 with extremely high levels of antibodies for three of the herpes family viruses in her blood. At the time, she had been suffering from CFS for five years.

When a virus infects someone, the levels of antibodies cranked out by the immune system in response typically increase until the virus is overcome, then slowly diminish over time. But Montoya’s patient had persistently high antibodies for the three viruses. In addition, the lymph nodes in her neck were significantly enlarged, some up to eight times their normal size, suggesting her immune system was fighting some kind of infection, even though a comprehensive evaluation had failed to point to any infectious cause.

Concerned about the unusual elevations in antibody levels as well as the swelling of her lymph nodes, Montoya decided to prescribe valganciclovir. “I thought by giving an antiviral that was effective against herpes viruses for a relatively long period of time, perhaps we could impact somehow the inflammation that she had in her lymph nodes,” said Montoya.

Within four weeks, the patient’s lymph nodes began shrinking. Six weeks later she phoned Montoya from her home in South America, describing how she was now exercising, bicycling and going back to work at the company she ran before her illness. “We were really shocked by this,” recalled Montoya.

Of the two dozen patients Montoya and Kogelnik have since treated, the 20 that responded all had developed CFS after an initial flulike illness, while the non-responders had suffered no initial flu.

Some of the patients take the drug for more than six months, such as Michael Manson, whose battle with CFS has lasted more than 18 years. The former triathlete was stricken with a viral infection a year after his marriage. After trying unsuccessfully to overcome what he thought were lingering effects of the flu, he had no choice but to drastically curtail all his activities and eventually stop working.

During his longest period of extreme fatigue, 13 1/2 weeks, Manson said, “My wife literally thought I was passing away. I could hear the emotion in her voice as she tried to wake me, but I couldn’t wake up to console her. That was just maddening.”

Now in his seventh month of treatment, Manson is able to go backpacking with his children with no ill after-effects. Prior to starting the treatment, Manson’s three children, ages 9 to 14, had never seen him healthy.

Montoya and Kogelnik emphasized that even if their new clinical trial validates the use of valganciclovir in treating some CFS patients, the drug may not be effective in all cases. In fact, the trial will assess the effectiveness of the medication among a specific subset of CFS patients; namely, those who have viral-induced dysfunction of the central nervous system.

“This could be a solution for a subset of patients, but that subset could be quite large,” said Kristin Loomis, executive director of the HHV-6 Foundation, which has helped fund a significant portion of the preparatory work for the clinical trial. “These viruses have been suspected in CFS for decades, but researchers couldn’t prove it because they are so difficult to detect in the blood. If Montoya’s results are confirmed, he will have made a real breakthrough.”

“What is desperately needed is the completion of the randomized, double-blind, placebo-controlled clinical trial that we are about to embark on,” Montoya said.

 

Source: Stanford University Medical Center. “New Therapy For Chronic Fatigue Syndrome To Be Tested.” ScienceDaily. ScienceDaily, 9 January 2007. https://www.sciencedaily.com/releases/2007/01/070108191506.htm

 

New Hypothesis Proposed For Cause Of Chronic Fatigue Syndrome

Press Release: COLUMBUS, Ohio — Researchers here have proposed a new theory for the cause of chronic fatigue syndrome (CFS) — one that blames the illness both on a low-level viral infection and on the body’s own immune response to that virus.

If true, it would offer an explanation for why virologists so far haven’t found evidence of a common virus when looking at a population of CFS patients. The hypothesis was included in a paper published in the current issue of the American Journal of Medicine.

The new theory, proposed by Ronald Glaser, professor of medical microbiology and immunology, and Janice Kiecolt-Glaser, professor of psychology and psychiatry at Ohio State University, is the latest work in more than two decades of their research on the effects of stress on the human immune system.

“Our data suggests that stress may be causing the expression of certain viral proteins and that these proteins may be modulating the body’s immune response, turning it on or off,”Glaser said.

CFS was first characterized by researchers in the mid-1980s who described it as a combination of symptoms including low-grade fevers, body aches, malaise, and depression among other signs. The condition seems more prevalent among young adult women. Those diagnosed with CFS often experience stress and depression.

Symptoms routinely linger for six months or more and may continue for years. The federal Centers for Disease Control and Prevention estimate that CFS may affect anywhere from four to 10 of every 100,000 people in the United States.

Other researchers have reported higher-than-normal titers of antibodies to various latent viruses — Epstein-Barr virus, cytomegalovirus, human herpes virus 6, for example — in the blood of patients diagnosed as having CFS. But no one viral infection was present in all patients — evidence that would be needed to prove a viral cause of the illness.

The Ohio State researchers’ new theory poses several mechanisms that might be linked to CFS.

Once a person is infected, these viruses can remain latent in the body for long periods of time. Glaser proposes that the viruses could be partially reactivated, that is, viral proteins could be produced at levels high enough to cause a low-grade infection but too low to be seen using current laboratory assays.

Glaser and Kiecolt-Glaser suggest that CFS patients may experience an ongoing, low-grade viral infection — more like a smoldering fire rather than a three-alarm blaze — which could stimulate parts of the immune response without raising antibody titers to typically high levels.

That low-grade infection would be enough to increase production of various cytokines — chemical mediators for the immune system — and begin the immune response.

“A lot of the symptoms that you find in chronic fatigue syndrome are the same ones induced by cytokines during our normal immune response,” Glaser said.

He admits that studies of patients have yet to show a pattern of abnormal cytokine behavior that would substantiate their theory but he has an explanation for that.

“We haven’t discovered all the cytokines involved in immunity. We may not have found the right one, yet,” he said, adding that new cytokines are steadily being identified.

Stress and depression may be playing a related role as well, Kiecolt-Glaser said. Earlier research has repeatedly shown that increased stress and depression can reactivate latent viruses, decrease the body’s immune response, and stimulate the production of certain cytokines linked to some CFS-like symptoms.

“Part of this is a chicken-and-egg problem,” Kiecolt-Glaser said. “People diagnosed with CFS often are depressed since they’re unable to carry out normal, daily activities. What we don’t know is whether the depression followed the diagnosis of CFS or if CFS contributed to it.

“We do know, however, that this kind of depression can weaken our immune response.”

Glaser said researchers need to reconsider past work on CFS.

“We need to look for immune system changes that are much more subtle and specific than those we’ve been using as benchmarks,” he said.

 

Source: Ohio State University. “New Hypothesis Proposed For Cause Of Chronic Fatigue Syndrome.” ScienceDaily. ScienceDaily, 3 November 1998. https://www.sciencedaily.com/releases/1998/10/981031180910.htm

Chronic Fatigue Syndrome Impairs A Person’s Slow Wave Activity During Sleep

Press Release: Chronic fatigue syndrome (CFS) has been associated with altered amounts of slow wave sleep, which could reflect reduced electroencephalograph (EEG) activity and impaired sleep regulation. A study published in the journal SLEEP finds that CFS is also associated with a blunted slow wave activity (SWA) response to sleep challenge, suggesting an impairment of the basic sleep drive and homeostatic response.

The study, authored by Roseanna Armitage, PhD, and colleagues at the University of Michigan, focused on 13 pairs of identical twins discordant for CFS. Analyses, which were restricted to the first four non-REM periods each night in order to show comparability, revealed that SWA, or other sleep EEG measures, did not differ between the CFS and healthy twins during a regular night’s sleep. According to Armitage, it was only after a “challenge” to sleep regulation was introduced (keeping them awake an extra four hours) that the CFS twins exhibited significantly less SWA power in the first non-REM period of recovery sleep and accumulated a smaller percentage of SWA in the first non-REM period than their twin counterparts.

“CFS shares symptoms with depression, and some experts have suggested that it is not a distinctly different disorder,” said Armitage. “We have also conducted studies of SWA response to sleep challenge in depression, and the results are very different. Depressed women did not show a blunted SWA response to sleep challenge. The present CFS study included only women, and none had current depression. Therefore, our results cannot be explained on the basis of depression.”

Experts recommend that adults get between seven and eight hours of sleep each night to maintain good health and optimum performance. Persons who think they might have a sleep disorder are urged to consult with their primary care physician, who will refer them to a sleep specialist.

Article: “The Impact of a Four-Hour Sleep Delay on Slow Wave Activity in Twins Discordant for Chronic Fatigue Syndrome”, Sleep, May 1, 2007.

 

Source: American Academy of Sleep Medicine. “Chronic Fatigue Syndrome Impairs A Person’s Slow Wave Activity During Sleep.” ScienceDaily. ScienceDaily, 7 May 2007. www.sciencedaily.com/releases/2007/05/070501075253.htm

Research Provides More Evidence That Chronic Fatigue Syndrome Is A Legitimate Medical Condition

Press Release: Researchers at Georgetown University Medical Center have found that chronic fatigue syndrome (CFS) may be rooted in distinct neurological abnormalities that can be medically tested. Although the sample studied was small, this research provides objective, physiological evidence that the controversial disorder can be considered a legitimate medical condition.

Chronic fatigue syndrome defines a range of illnesses including fibromyalgia and Gulf War syndrome, all of which have fatigue as a major symptom. Even among medical professionals, there is a disagreement about the causes, diagnosis and treatment of CFS because so much about the disorder remains unknown. One reason CFS is difficult to diagnose is because it shares symptoms with many other diseases, including multiple sclerosis and lupus. Even when other illnesses are ruled out and a CFS diagnosis is given, there is not a standardized course of treatment and it’s difficult for doctors to measure patient improvement. Estimates are that two to four times as many women as men are diagnosed with CFS.

The Georgetown study, published in the November edition of the BMC Neurology Journal, an online publication, reveals that patients diagnosed with CFS and its family of illnesses have a set of proteins in their spinal cord fluid that were not detected in healthy individuals. These proteins might give insight into the causes of CFS and could someday be used as markers to diagnose patients with the disorder.

“For years, patients with chronic fatigue syndrome have suffered from painful symptoms for which there is no blood test, diagnosable physical condition or any method for doctors to measure improvement,” said James Baraniuk, MD, assistant professor of medicine at Georgetown University Medical Center and first author on the study. “Our research provides initial evidence that chronic fatigue syndrome and its family of illnesses may be legitimate, neurological diseases and that at least part of the pathology involves the central nervous system.”

The disorder is characterized by profound fatigue that is not improved by bed rest and that may get worse with physical or mental activity, according to the Centers for Disease Control and Prevention. Persons with CFS usually function at a lower level of activity than they were capable of before the onset of illness, feeling too tired to perform normal activities or easily exhausted with no apparent reason. Patients also report various nonspecific symptoms, including weakness, muscle pain, impaired memory and/or mental concentration, insomnia and post-exertional fatigue lasting more than 24 hours.

The study looked at 50 individuals suffering from at least two disorders related to CFS, including fibromyalgia and Gulf War syndrome. By examining spinal cord fluid in patients with CFS and in healthy individuals, the researchers found that CFS patients have 16 proteins that healthy individuals do not. Five of these 16 proteins are found in all patients with the illnesses but in none of the controls. The results indicate that those 16 proteins could possibly serve as a “biosignature” for the disease and could someday be used to diagnose CFS.

“Although this is a small study and more research on the subject is necessary, these results indicate it might be possible to develop a simple laboratory test to diagnose these disorders in the future,” Baraniuk said.

Other co-authors on the paper include Begona Casada, PhD, and Hilda Maibach, MS, of Georgetown University Medical Center; Daniel J. Clauw, MD, of the University of Michigan; and Lewis K. Pannell, PhD, of the University of South Carolina; and Sonya Hess, PhD, of the National Institute of Diabetes and Digestive and Kidney Diseases.

 

Source: Georgetown University Medical Center. “Research Provides More Evidence That Chronic Fatigue Syndrome Is A Legitimate Medical Condition.” ScienceDaily. ScienceDaily, 10 January 2006. www.sciencedaily.com/releases/2006/01/060110013424.htm

Chronic Fatigue: Clues In The Blood

Press Release: University of New South Wales, July 8, 2007. Researchers at UNSW believe that blood may hold vital insights into what is happening in the brain of patients with chronic fatigue syndrome (CFS).

In a study unparalleled in its scope, a team led by UNSW Professor Andrew Lloyd of the Centre for Infection and Inflammation Research, has studied the differences in gene expression patterns in the blood of people who either recover promptly after acute glandular fever or develop the prolonged illness called post-infective syndrome.

The researchers examined six million pieces of gene expression information for analysis in the project, known as the Dubbo Infection Outcomes Study. The study is named after the NSW town in which the work was conducted. The team studied the expression of 30,000 genes in the blood, testing each of the 15 individuals between four and five times over a 12-month period.

The team was able to narrow its findings to the expression of just 35 genes whose pattern of expression correlated closely with the key symptoms of the illness when examined from onset through to recovery. Gene expression is significant because it is the process by which a gene’s DNA sequence is converted into the proteins which ultimately determine the manifestations of disease.

Since 1999, the team has been tracking the long-term health of individuals infected with Ross River virus (RRV), Q fever infection and Epstein-Barr virus, which causes glandular fever.

“These [35] genes might point to the nature of the disease process that underlies CFS, which is currently unknown,” said Professor Lloyd, who is based in the School of Medical Sciences at UNSW. “None of them are ones that I would have predicted, except for those relating to neurotransmitters,” he concedes. “Some of them relate to transport of zinc and other metal ions within the cell, which may suggest a fundamental disturbance in cellular function.”

The researchers now hope to narrow the focus of research onto the expression of these 35 genes in the blood of a much larger group of subjects from the Dubbo Infection Outcomes Study, with varied patterns of illness and recovery.

“There are very few complex diseases which have been comprehensively analysed, with large scale and longitudinal studies, like this,” said Professor Lloyd. “It sets a standard for highly sophisticated, comprehensive gene expression studies in the blood of all sorts of human diseases from rheumatoid arthritis and multiple sclerosis through to schizophrenia.”

The research paper has been published in the Journal of Infectious Diseases.

 

Source: University of New South Wales. “Chronic Fatigue: Clues In The Blood.” ScienceDaily. ScienceDaily, 8 July 2007. https://www.sciencedaily.com/releases/2007/07/070706090020.htm