UK MEGA project update on funding applications & patient advisory group

Posted on 03/30/2017 by wames

MEGA research blog post, by Sonya Chowdhury, 29 March 2017: Our latest funding application and Patient Advisory Group update

An update from the Scientific Team and Patient Advisory Group.

First the bad news: unfortunately our preliminary application to Wellcome, submitted at the start of the year, was turned down. No feedback was given so we don’t know why it was rejected.

The good news is that, in the last couple of weeks, the Scientific Team and the Patient Advisory Group have prepared a new outline application for further funding. With a short deadline it was tough going at times, but having had substantial input, the Patient Advisory Group are very pleased with the submission.

A very productive meeting between Prof Esther Crawley, Prof Julia Newton and the Patient Advisory Group was held early last week with some important points agreed:

  • Both the Scientific Team and the Patient Advisory Group agree that it is absolutely essential that we collect data from those most severely affected by M.E., and those affected long term. This will require home visits which are very expensive, and the financial limit of the current application will not cover this. However, it was confirmed at the meeting that we will submit an application to this current funding call with a full commitment that further applications will be made to include home visits. By establishing the MEGA bioresource and proving to funders that we can collect data from patients in clinic, the chances of us successfully accessing further funding are hugely increased.
  • Post-exertional malaise will be a prerequisite for inclusion in the bioresource. If successfully funded, a detailed definition of post-exertional malaise will be determined primarily by the Patient Advisory Group in conjunction with the ME/CFS specialists on the Scientific Team.
  • Those whose samples are collected for the bioresource will have their diagnoses and severity of illness confirmed and recorded at point of collection. Several case definitions will be used to categorise patients and it will be clear which case definition any given patient fits into. When analysing results of tests undertaken on samples from the bioresource, the Scientific Team will be clear which subset of patients the results specifically relate to (we will address this in more detail in a forthcoming blog post).

We have updated our Q&A page to highlight the points above.

Patient Advisory Group update

Three Patient Advisory Group members recently decided to leave the group. Their much valued contributions will be missed and their reasons for leaving have been taken on board.

Since their departure, valuable progress has been made and we are happy to report that, despite the initial rushed formation of the Patient Advisory Group and the pressure caused by tight application deadlines, things have really picked up and are beginning to fly. Enthusiasm among Patient Advisory Group members is high, the Scientific Team remains focused, and we all wait with fingers crossed for a positive outcome to this preliminary funding application.

As Prof Newton says, “MEGA represents the opportunity to develop the largest ME bioresource in the world. This will give researchers the material to address some of the big questions that are currently unanswered in ME, to not only help UK patients but the global patient community.”

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Patterns of control beliefs in CFS

Posted on 03/29/2017 by wames

Research abstract:

Patterns of control beliefs in chronic fatigue syndrome: results of a population-based survey, by Johanna M. Doerr, Daniela S. Jopp, Michael Chajewski, Urs M. Nater in BMC Psychology (open access), 6 March 2017

BACKGROUND:   Chronic fatigue syndrome (CFS) represents a unique clinical challenge for patients and health care providers due to unclear etiology and lack of specific treatment. Characteristic patterns of behavior and cognitions might be related to how CFS patients respond to management strategies.

METHODS:   This study investigates control beliefs in a population-based sample of 113 CFS patients, 264 individuals with insufficient symptoms or fatigue for CFS diagnosis (ISF), and 124 well individuals.

RESULTS:   Controlling for personality and coping, individuals with low confidence in their problem-solving capacity were almost 8 times more likely to be classified as ISF and 5 times more likely to be classified as CFS compared to being classified as well. However there was a wide distribution within groups and individuals with “low confidence” scores were found in 31.7% of Well individuals. Individuals with low levels of anxiety and who were more outgoing were less likely to be classified as ISF or CFS.

CONCLUSIONS:   These findings suggest that fostering control beliefs could be an important focus for developing behavioral management strategies in CFS and other chronic conditions.

 

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Expectations of recovery in severe ME could impose unreasonable, unrealistic, even fatal demands

Posted on 03/29/2017 by wames

Stonebird blog post, Mar 2017: 25% Group and Stonebird Response to BACME (British Association for ME/CFS), article on care provision for severe ME

Response to BACME Working Group on Severe CFS/ME Shared Clinical Practice Document Version 1

When you work with someone who has Severe ME you need to be more sensitive and aware than you can possibly imagine. Harm, even death for some, may follow poor treatment, care and ignorance. The frailty of someone with Severe/Very Severe ME cannot be exaggerated nor adequately described. You need to take the greatest of care.

The problem with this BACME document is its underlying psychosocial values and attitudes. If you expect a person to get better, that will be your intention, that will be your goal, that is going to influence all your thoughts and actions in your caring role, especially if you set goals or limit care over time.

The care provided by someone with a biomedical understanding of Severe ME is going to be fundamentally different, however much the starting point of care might appear to be similar in this document, to the person who has a psychosocial approach to, because of the opposing underlying values and attitudes.

The most important aspect of caring for a person with Severe Myalgic Encephalomyelitis (ME) is the ‘how’ of caring; the basic core beliefs the carer has about caring and the person to be cared for. What the carer believes will subtly or overtly impact on how caring is provided and has a huge affect on the relationship, quality of care and health of the person receiving the care.

Great harm can be done by someone who is not fully aware that the person with Severe ME is seriously physically ill and that they are not going to be “made well” by changing their thoughts or increasing their activity in a graded way, as this dangerous document from BACME suggests.

The basic principles behind Severe ME-aware care are :

  1. Never define the person by their behaviour.
  2. Acknowledge the serious and severe physical illness underlying the person’s symptom experience.
  3. Adhere to a strictly defined definition of ME ( the ICC).
  4. Honour the WHO classification of ME as a neurological disease and respond appropriately and equally as in any other recognised neurological disease.
  5. Treat the person with respect on all levels; respect for the way interaction occurs, the physical and the cognitive limitations enforced on the person by their severely disabling multi-system dysfunction.
  6.  Honour what the person says regarding their physical and cognitive needs.
  7. Listen to the person and to only interact at the correct time in the correct way. We call this the MOMENT approach, honouring the severe illness the person has whilst maximising the opportunity to engage safely in order to help, not harm them, when undertaking all care needs. (Crowhurst 2015)
  8. Understand any hypersensitivity issues (chemical, drug, touch, noise, light, movement, motion, food); never ignore, undermine, negate or belittle them, recognising the danger of the ordinary environment as real, not just perceived.
  9. Understand and comprehend that the person with Severe ME is not experiencing the world the same way as a well person and cannot fit into the demands and obligations imposed on them by others, easily or at all. A flexible, knowledgeable, sensitive, compassionate, non-judgmental, person-centred not goal oriented approach at all times is critical. Being aware of the after impact of any interaction is essential; that even something once achieved cannot necessarily be achieved or tolerated again or regularly or increased.
  10. Recognise the irrelevance, unhelpful and dangerous nature of a psychosocial response and interpretation of Severe ME, a physical disease. Psychiatry has no right to first hand intervention in this disease which requires a biomedical response and care pathway .

It is vital to ensure that that you never put any overt or covert pressure, demand or expectation to improve, upon the person with Severe ME, nor any underlying belief that is in opposition to the truth and severity of the disease and very real lack of valid treatment and cure.

In ME when you push yourself you deteriorate, whether immediately or delayed, if you push too hard you may even enter worse illness experience than you have already experienced, beyond which you may not be able to recover from at all or only partly. The depth and level of physical and cognitive deterioration and harm that can follow is literally unimaginable before it occurs. The impact can be permanent or very long term.

There are many good observations and insights into the reality of Severe ME in this document; but its expectations of recovery that could impose unreasonable, unrealistic, even fatal demands, render it extremely dangerous.

Anyone who believes the message that people with Severe ME can do more than they physically can, by thought and activity, even if only over time, no matter how genuinely they believe it or how nice they are or how encouraging they are, can so easily do untold harm because they will exact subtle if not overt pressure, however kindly, upon the person to improve.

A carer following this guide, we fear, is unlikely to be able to separate care from treatment, to comprehend the importance of flowing with the person, just to help them cope, rather than set goals for “recovery” , however seemingly small from the well perspective nor appreciate the long term commitment just to improve quality of life and comfort rather than quality of thought and ability.

There is no place for complacency, mediocrity or carelessness in the life of someone with Severe ME. A carer’s interventions can cause serious harm to the person’s health. As the PACE and FINE Trials have shown, the psychosocial approach that this guide is constructed upon, is bound to fail and not just fail but cause real harm. (Vink 2017).

It must be Viewed within its psychosocial context, this document cannot possibly be recommended for anyone with WHO G93.3 defined Myalgic Encephalomyelitis.

References:

Crowhurst G (2016) The MOMENT Approach

BACME Working Group on Severe CFS/ME Shared Clinical Practice Document Version 1 (2017)

Vink M (2017) Assessment of Individual PACE Trial Data: in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome, Cognitive Behavioral and Graded Exercise Therapy are Ineffective, Do Not Lead to Actual Recovery and Negative Outcomes may be Higher than Reported. J Neurol Neurobiol 3(1)

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The problem of bias in behavioural intervention studies: lessons from the PACE trial

Posted on 03/29/2017 by wames

Abstract:

The problem of bias in behavioural intervention studies: Lessons from the PACE trial, by Carolyn Wilshire in Journal of Health Psychology [Preprint 23 March 2017]

Geraghty’s recent editorial on the PACE trial for chronic fatigue syndrome has stimulated a lively discussion. Here, I consider whether the published claims are justified by the data. I also discuss wider issues concerning trial procedures, researcher allegiance and participant reporting bias.

Cognitive behavioural therapy and graded exercise therapy had modest, time-limited effects on self-report measures, but little effect on more objective measures such as fitness and employment status.

Given that the trial was non-blinded, and the favoured treatments were promoted to participants as ‘highly effective’, these effects may reflect participant response bias. In non-blinded trials, the issue of reporting biases deserves greater attention in future.

Read the full article

 

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The role of autonomic function in exercise-induced analgesia in ME/CFS

Posted on 03/28/2017 by wames

Research abstract:

The Role of Autonomic Function in Exercise-induced Endogenous Analgesia: A Case-control Study in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Healthy People by Jo Nijs, Lieven Danneels, Luc Lambrecht, Greta Moorkens, Mira Meeus, Lorna Paul, Jessica Van Oosterwijck, Uros Marusic, and Inge De Wandele in Pain Physician 2017; 20:E389-E399

BACKGROUND: Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) are unable to activate brain-orchestrated endogenous analgesia (or descending inhibition) in response to exercise. This physiological impairment is currently regarded as one factor explaining post-exertional malaise in these patients. Autonomic dysfunction is also a feature of ME/CFS.

OBJECTIVES: This study aims to examine the role of the autonomic nervous system in exercise-induced analgesia in healthy people and those with ME/CFS, by studying the recovery of autonomic parameters following aerobic exercise and the relation to changes in self-reported pain intensity.

STUDY DESIGN: A controlled experimental study.

SETTING: The study was conducted at the Human Physiology lab of a University.

METHODS: Twenty women with ME/CFS- and 20 healthy, sedentary controls performed a submaximal bicycle exercise test known as the Aerobic Power Index with continuous cardiorespiratory monitoring. Before and after the exercise, measures of autonomic function (i.e., heart rate variability, blood pressure, and respiration rate) were performed continuously for 10 minutes and self-reported pain levels were registered. The relation between autonomous parameters and self-reported pain parameters was examined using correlation analysis.

RESULTS: Some relationships of moderate strength between autonomic and pain measures were found. The change (post-exercise minus pre-exercise score) in pain severity was correlated (r = .580, P = .007) with the change in diastolic blood pressure in the healthy group. In the ME/CFS group, positive correlations between the changes in pain severity and low frequency (r = .552, P = .014), and between the changes in bodily pain and diastolic blood pressure (r = .472, P = .036), were seen. In addition, in ME/CHFS the change in headache severity was inversely correlated (r = -.480, P = .038) with the change in high frequency heart rate variability.

LIMITATIONS: Based on the cross-sectional design of the study, no firm conclusions can be drawn on the causality of the relations.

CONCLUSIONS: Reduced parasympathetic reactivation during recovery from exercise is associated with the dysfunctional exercise-induced analgesia in ME/CFS. Poor recovery of diastolic blood pressure in response to exercise, with blood pressure remaining elevated, is associated with reductions of pain following exercise in ME/CFS, suggesting a role for the arterial baroreceptors in explaining dysfunctional exercise-induced analgesia in ME/CFS patients.

Comment by Dr Charles Shepherd:

One of the most consistent neurological abnormalities to be reported in ME/CFS involves what is called the autonomic nervous system (ANS).

This is a part of the nervous system that has its control centres in the brain. The regulatory centres then send messages, which are not under conscious control, via the sympathetic and parasympathetic nerves, to regulate the heart rate and blood pressure, the bowels and bladder, and blood flow to muscle and other key parts of the body – including the brain.

The ANS can either speed up or slow down activities in the heart, bowels and bladder – so overactivity will speed up the pulse rate and can also cause irritable bowel and irritable bladder type symptoms.

It also appears that the ANS has a role in pain production and post-exertional symptomatology.

This is why the MEA Ramsay Research Fund is keen to fund more research into the role of the ANS – including a large study that researchers in Brussels and Glasgow have been carrying out for us.

The results in this paper relate to a study that examined the role of the ANS in exercise induced-analgesia (more information on this normal physiological response below) in people with ME/CFS, and in healthy controls, following an exercise challenge and in relation to self-reporting of pain severity.

Measurements of ANS activity (i.e. pulse rate, blood pressure, respiratory rate) were carried out before and after exercise along with self reporting of pain levels.

The study concluded that there is dysfunctional exercise-induced analgesia in people with ME/CFS.

This is an important new finding that helps to increase our understanding of why pain occurs in ME/CFS and something that could lead to more effective methods of both prevention and treatment of pain in ME/CFS

Dr Charles Shepherd
Hon Medical Adviser, ME Association
29 March 2017

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How living with CFS/ME impacts upon people’s identity

Posted on 03/28/2017 by wames

Thesis abstract:

A life lived differently: an exploration of how living with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) impacts upon people’s identity, by Rebecca E. Murray. University of Huddersfield Doctoral thesis 2017 [Published online March 13, 2017]

Existing literature provides an insight into CFS/ME, but it is fractured, in that it does little to serve understanding, empathy or  coping. Moreover the experiences of people with CFS/ME are under theorised.

The literature demonstrates that issues of identity appear central to the lived experience of chronic illness, yet the mechanisms underpinning identity are not fully explored.  Consequently there is  little understanding of the crisis of identity in CFS/ME. Therefore, the aims and objectives of the current research endeavoured to examine identity within the context of the lived experience of CFS/ME.

Drawing upon Wenger’s (1998) ‘Communities of Practice’ theory (CoP), the current research aimed to make transparent the mechanism of identity by exploring the lived experience of identity in chronic illness; specifically CFS/ME. It is argued throughout, that a millennia of meaning underpins the crisis of identity in CFS/ME and that CoP, whilst predominantly a social theory of learning, was re-conceptualised here to illuminate the crisis of identity in chronic illness.

Data were gathered via a closed Facebook group; cfsid, which was created for the purpose of the current research. Participants (n. 37) contributed over time and in depth and in so doing revealed the complex foundation of their shifting identities. The data was analysed using a theoretical thematic analysis (Braun and Clarke, 2006).

Aligned with CoP, the key findings indicate that the mechanism underpinning the crisis of identity in CFS/ME is the changing nature of participation. The history of CFS/ME is one defined by scepticism and as such the controversy surrounding CFS/ME interacted with the lived experience of the illness for participants. The lived experience of CFS/ME for participants was reliably defined by their inability to participate in either life or self. Lives and selves were unrecognisable, but all was not lost as acceptance and adjustment allowed participants to negotiate ways in which they could participate despite their CFS/ME.

Participants’ experiences of participation emerged within the analysis as a journey to finding a new way to be in the world. On looking to the future, if people with CFS/ME are to be better supported and enabled within their lived experience of chronic illness, the burdening history of CFS/ME needs to be replaced by legitimacy, and the importance of the negotiation of participation in chronic illness needs to be illuminated further.

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Genes, mitochondria, autoimmunity & CFS: Prof Alan Light’s research

Posted on 03/27/2017 by wames

Health rising blog post, by Cort Johnson, 23 Feb 2017: Genes, Mitochondria, Autoimmunity and Chronic Fatigue Syndrome: The Alan Light Talk

Dr. Light has said that he wants to do for fatigue what researchers have done for pain; that is uncover the molecular pathways that cause fatigue.  Some time ago Light presented one of the most spectacular graphs of ME/CFS ever done. I still remember the gasp that filtered through the IACFS/ME conference when Dr. Light showed the slide below . It showed the levels of molecular receptors associated with fatigue and pain skyrocketing after exercise in white blood cells.

The most famous graph in ME/CFS history
The healthy controls are on top and the ME/CFS patients are below. It was even worse than it seemed. In a 2011 Bateman Horne Center video, Dr. Light explained that the differences were so extreme that he had to transform the data into log scale format in order to fit the graph on the page.  The expression of some genes was 10 times greater in the ME/CFS patients as in the healthy controls.

Even 48 hours later – still well within the post-exertional malaise (PEM) period for many with ME/CFS/FM – the gene expression was still incredibly high relative to the controls.

Light has found, by the way, that many people with ME/CFS (70%) fit the criteria for FM.  When Light compared ME/CFS patients with FM vs ME/CFS without FM he found only a few differences. When he looked at FM patients without fatigue, though, they looked exactly like the healthy controls. That indicated that the Lights were really zeroing in on how fatigue is produced.

A key distinction between FM patients without fatigue and ME/CFS and FM patients with fatigue emerged when the Lights looked at the baseline findings. It turned out that ME/CFS patients looked like healthy controls at baseline but the “pure” FM patients without fatigue looked very different.  The expression of three genes were dramatically elevated – so dramatically, in fact, that Light suggested that they might not be able to get any higher during exercise.

The fact that the rest of the genes were unaffected by exercise could explain why studies suggest that exercise seems to work so much better in FM than in ME/CFS. FM patients with ME/CFS characteristics do get knocked out by exercise, but the “pure” FM patients – which make up a considerable portion of the FM population – don’t.

Light did, however, find a startlingly different subgroup hidden within the ME/CFS population. After putting them on the bike this rather large group (40% of the study) looked exactly like the healthy controls with the exception of one gene called the alpha 2A receptor (AD2A).

This ubiquitous receptor causes the blood vessels to constrict in order to keep blood from pooling in our legs when we stand. The expression of that gene plummeted in the ME/CFS subgroup. That suggested that when those ME/CFS patients most needed their blood vessels to constrict in order to pound more blood into their muscles, the gene that did that pooped out. Not surprisingly, 70% of the people with this gene expression signature have orthostatic intolerance.

(Talk about from bench to bedside or vice versa. Dr. Light found this group when Dr. Bateman told him about a young man she could not figure out at all. Looking at the gene expression data, Light found zero increase in his ADR2A gene expression. Light then went back and specifically looked at this gene and found this major group characterized by orthostatic intolerance (OI). Unfortunately most OI drugs do not work on these patients; midodrine works for a short period but has side effects.  What a nice example of a physician and researcher working together to break new ground.)

It’s important to note that the Lights were not looking at the cause of chronic fatigue syndrome (ME/CFS) – they were looking at the effects of the cause. Something, they believed – probably in the immune system – was causing the gene expression of their immune cells to go bonkers during exercise.  It could be a virus, it could be an autoimmune process, it could be toxins, it could be any number of things.

The search for the cause came next…. read more

The Gist

  • in 2011 the Light’s found that the gene expression of receptors on white blood cells which responded to muscle metabolites skyrocketed during and after exercise
  • Their findings suggested a large and unusual immune response occurred during and after exercise in ME/CFS/FM
  • One subset of ME/CFS/FM patients with orthostatic intolerance had a very different response
  • Six years later in a small study the Light’s found evidence of acquired mitochondrial mutations that could be impacting the energy levels of these immune cells
  • They also found widespread evidence of mutations in some genes associated with autoimmunity
  • They suggest that the low energy state in the immune cells of ME/CFS/FM patients results in the increased production autoantibodies
  • They believe these autoantibodies may be targeting processes vital to producing energy and the ability to exercise
  • A large NIH grant will allow them to greatly expand their study
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CBT for CFS/ME in children is different from CBT for depression

Posted on 03/27/2017 by wames

Discussion paper abstract:

BACKGROUND:   Approximately one in three children and young people with chronic fatigue syndrome (CFS/ME) also have probable depression. Cognitive behaviour therapy (CBT) has a growing evidence base as an effective treatment approach for CFS/ME and for depression in this population.

AIMS:   Given the high degree of co-morbidity, this discussion paper aims to compare and contrast CBT for CFS/ME and CBT for depression in children and young people.

METHOD:    The existing literature on CBT for depression and CBT for CFS/ME, in relation to children and young people was reviewed.

RESULTS:   Whilst there are commonalities to both treatments, the cognitive behavioural model of CFS/ME maintenance includes different factors and has a different emphasis to the cognitive behavioural model of depression, resulting in different intervention targets and strategies in a different sequence.

CONCLUSIONS:   A collaborative, formulation-driven approach to intervention should inform the intervention targets and treatment strategies.

Same, Same But Different? Cognitive Behavioural Treatment Approaches for Paediatric CFS/ME and Depression, by ME Loades & T Chalder in Behav Cogn Psychother. 2017 Mar 9:1-16 [Epub ahead of print]

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ME/CFS & Gulf War patients exhibit increased humoral responses to the enzyme dUTPase

Posted on 03/27/2017 by wames

Research abstract:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) are debilitating diseases with overlapping symptomology and there are currently no validated tests for definitive diagnosis of either syndrome.

While there is evidence supporting the premise that some herpesviruses may act as possible triggers of ME/CFS, the involvement of herpesviruses in the pathophysiology of GWI has not been studied in spite of a higher prevalence of ME/CFS in these patients.

We have previously demonstrated that the deoxyuridine triphosphate nucleotidohydrolases (dUTPase) encoded by Epstein-Barr virus (EBV), human herpesvirus-6 (HHV-6), and varicella-zoster virus (VZV) possess novel functions in innate and adaptive immunity.

The results of this study demonstrate that a significant percentage of patients with ME/CFS (30.91-52.7%) and GWI (29.34%) are simultaneously producing antibodies against multiple human herpesviruses-encoded dUTPases and/or the human dUTPase when compared to controls (17.21%).

GWI patients exhibited significantly higher levels of antibodies [i.e.humoral response] to the HHV-6 and human dUTPases than controls (p = 0.0053 and p = 0.0036, respectively), while the ME/CFS cohort had higher anti-EBV-dUTPase antibodies than in both GWI patients (p = 0.0008) and controls (p <0.0001) as well as significantly higher anti-human dUTPase antibodies than in controls (p = 0.0241).

These results suggest that screening of patients’ sera for the presence of various combinations of anti-dUTPase antibodies could be used as potential biomarkers to help identify/distinguish patients with these syndromes and better direct treatment.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Gulf War Illness patients exhibit increased humoral responses to the Herpesviruses-encoded dUTPase: Implications in disease pathophysiology, by Peter Halpin, Marshall Vance Williams, Nancy G Klimas, Mary Ann Fletcher, Zachary Barnes, Maria Eugenia Ariza in Journal of Medical Virology   [Preprint March 17, 2017]

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Neurobiological & spinal fluid abnormalities in CFS are not influenced by psychiatric status

Posted on 03/24/2017 by wames

Research highlights:

  • Patients have higher brain ventricular lactate, more abnormal spinal fluids, lower brain GSH, and reduced cerebral blood flow than controls
  • Psychiatric comorbidity does not influence any of these potential biological markers of CFS
  • 50% of the patients had more than one of these abnormalities
  • The subgroup of patients with brain abnormalities may have an underlying encephalopathy producing their illness

Research abstract:

The purpose of this study was to investigate whether CFS patients without comorbid psychiatric diagnoses differ from CFS patients with comorbid psychiatric diagnoses and healthy control subjects in neuropsychological performance, the proportion with elevated spinal fluid protein or white cell counts, cerebral blood flow (CBF), brain ventricular lactate and cortical glutathione (GSH).

The results of the study did not show any differences in any of the outcome measures between CFS patients with and without psychiatric comorbidity, thus indicating that psychiatric status may not be an exacerbating factor in CFS. Importantly, significant differences were found between the pooled samples of CFS compared to controls. These included lower GSH and CBF and higher ventricular lactate and rates of spinal fluid abnormalities in CFS patients compared to healthy controls.

Thirteen of 26 patients had abnormal values on two or more of these 4 brain-related variables. These findings, which replicate the results of several of our prior studies, support the presence of a number of neurobiological and spinal fluid abnormalities in CFS.

These results will lead to further investigation into objective biomarkers of the disorder to advance the understanding of CFS.

Multimodal and simultaneous assessments of brain and spinal fluid abnormalities in chronic fatigue syndrome and the effects of psychiatric comorbidity by BH Natelson, X Mao, AJ Stegner, G Lange, D Vu, M Blate, G Kang, E Soto, T Kapusuz, DC Shungu in J Neurol Sci. 2017 Apr 15;375:411-416 [Epub 2017 Feb 22]

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