TGI Friday! Our regular round-up of recently published ME/CFS research abstracts and other items | 26 April 2013

From Sleep Medicine Reviews, June 2013.

Clinical review

Sleep in the chronic fatigue syndrome

An N. Mariman(a), Dirk P. Vogelaers(a,b), Els Tobback(a), Liesbeth M. Delesie(a),, Ignace P. Hanoulle(a), Dirk A. Pevernagie (b,c)
(a) Ghent University Hospital, Department of Internal Diseases, Infectious Diseases and Psychosomatic Medicine, 185 De Pintelaan, 9000 Ghent, Belgium
(b) University of Ghent, Faculty of Medicine and Health Sciences Department of Internal Medicine, 25 Sint-Pietersnieuwstraat, 9000 Ghent, Belgium
© Kempenhaeghe Foundation Sleep Medicine Centre, P.O. Box 61, 5590 AB HEEZE, The Netherlands

Summary

Chronic fatigue syndrome (CFS) is a disabling condition characterized by severe fatigue lasting for more than six months and the presence of at least four out of eight minor criteria. Sleep disturbance presenting asunrefreshing or nonrestorative sleep is one of these criteria and is very common in CFS patients.

Biologically disturbed sleep is a known cause of fatigue and could play a role in the pathogenesis of CFS. However, the nature of presumed sleep impairment in CFS remains unclear. Whilst complaints of NRS persist over time, there is no demonstrable neurophysiological correlate to substantiatea basic deficit in sleep function in CFS.

Polysomnographic findings have not shown to be significantly different between subjects with CFS and normal controls. Discrepancies between subjectively poor and objectively normal sleep suggest a role for psychosocial factors negatively affecting perception of sleep quality.

Primary sleep disorders are often detected in patients who otherwise qualify for a CFS diagnosis. These disorders could contribute to the presence of daytime dysfunctioning.

There is currently insufficient evidence to indicate that treatment of primary sleep disorders sufficiently improves the fatigue associated with CFS. Therefore, primary sleep disorders may be a comorbid rather than an exclusionary condition with respect to CFS.


From the Journal of Psychosomatic Research, e-published on 25 March 2013.

Cognitive behavior therapy in patients with chronic fatigue syndrome: The role of illness acceptance and neuroticism.

Poppe C, Petrovic M, Vogelaers D, Crombez G.
Department of General Internal Medicine, Ghent University Hospital, Belgium.

Abstract

OBJECTIVE

Increasing the quality of life (QoL) of patients with chronic fatigue is challenging because recovery is seldom achieved. Therefore, it is important to identify processes that improve QoL. This study examined the extent of improvement related to cognitive behavior group therapy (CBT), and whether improvement is affected by initial levels of acceptance and neuroticism.

METHODS

Eighty CFS patients followed CBT, and self-reported (pre-post design) on mental and physical QoL (MQoL and PQoL), fatigue, acceptance, and neuroticism.

The extent of improvement was analyzed using t-tests, effect sizes, and clinically significant change criteria. Whether acceptance and neuroticism at baseline predicted changes was analyzed by means of correlation and regression analyses.

RESULTS

Significant improvement was found for all variables. The effect size for MQoL and PQoL was small; for acceptance and fatigue, effect size was moderate. About 20% (MQoL) to 40% (fatigue) of the participants clinically improved. Pre-treatment level of acceptance was negatively correlated with changes in MQoL, not with PQoL changes. Neuroticism pre-treatment was positively related with MQoL changes. Regression analysis showed an effect of acceptance on changes in MQoL beyond the effect of neuroticism.

CONCLUSIONS

Although CBT is an evidence-based treatment, the sizes of the effects are often small regarding QoL. Our study also revealed small effect sizes. Our study showed that patient characteristics at baseline were significantly associated with MQoL outcome; indicating that CFS patients with high neuroticism or with a low acceptance show more improvement in MQoL.

We propose to specifically target acceptance and neuroticism before treatment in order to maximize clinical relevance.


From Autoimmunity Highlights, April 2013.

Natural killer cells in patients with severe chronic fatigue syndrome

E. W. Brenu (1,2,5), S. L. Hardcastle (1,2), G. M. Atkinson (1,2), M. L. van Driel (3), S. Kreijkamp-Kaspers (4), K. J. Ashton (4), D. R. Staines (2,3), S. M. Marshall-Gradisnik (1,2).

1. Griffith Health Institute, School of Medical Science, Griffith University, Gold Coast, QLD, Australia
2. The National Centre for Neuroimmunology and Emerging Diseases, Griffith University, Gold Coast, QLD, Australia
3. Queensland Health, Gold Coast Public Health Unit, Robina, Gold Coast, QLD, Australia
4. Faculty of Health Sciences and Medicine, Bond University, Robina, QLD, Australia
5. Immunology Research Group, Centre for Medicine and Oral Health, Griffith University, GH1, Room 7.59, Southport, QLD, 4215, Australia

Abstract

Maintenance of health and physiological homeostasis is a synergistic process involving tight regulation of proteins, transcription factors and other molecular processes.

The immune system consists of innate and adaptive immune cells that are required to sustain immunity. The presence of pathogens and tumour cells activates innate immune cells, in particular Natural Killer (NK) cells.

Stochastic expression of NK receptors activates either inhibitory or activating signals and results in cytokine production and activation of pathways that result in apoptosis of target cells. Thus, NK cells are a necessary component of the immunological process and aberrations in their functional processes, including equivocal levels of NK cells and cytotoxic activity pre-empts recurrent viral infections, autoimmune diseases and altered inflammatory responses.

NK cells are implicated in a number of diseases including chronic fatigue syndrome (CFS). The purpose of this review is to highlight the different profiles of NK cells reported in CFS patients and to determine the extent of NK immune dysfunction in subtypes of CFS patients based on severity in symptoms.


From the Journal of Psychosomatic Research, e-published 5 March 2013.

Moderators of the treatment response to guided self-instruction for chronic fatigue syndrome.

Tummers M, Knoop H, van Dam A, Bleijenberg G.
Expert Centre for Chronic Fatigue, Radboud University Nijmegen Medical
Centre, Nijmegen, The Netherlands.

Abstract

OBJECTIVE

The efficiency and efficacy of guided self-instruction for chronic fatigue syndrome (CFS) can be enhanced if it is known which patients will benefit from the intervention. This study aimed to identify moderators of treatment response.

METHODS

This study is a secondary analysis of two randomized controlled trials evaluating the efficacy of guided self-instruction for CFS. A sample of 261 patients fulfilling US Center for Disease Control and Prevention criteria for CFS was randomly allocated to guided self-instruction or a wait list.

The following potential treatment moderators were selected from the literature: age, fatigue severity, level of physical functioning, pain, level of depressive symptoms, self-efficacy with respect to fatigue, somatic attributions, avoidance of activity, and focus on bodily symptoms.

Logistic and linear regression analyses were used with interaction term between treatment response and the potential moderator.

RESULTS

Age, level of depression, and avoidance of activity moderated the response to guided self-instruction.

Patients who were young, had low levels of depressive symptoms, and who had a low tendency to avoid activity benefited more from the intervention than older patients and patients with high levels of depressive symptoms and a strong tendency to avoid activity.

CONCLUSION

Guided self-instruction is exclusively aimed at cognitions and behaviours that perpetuate fatigue. Patients with severe depressive symptom may need more specific interventions aimed at the reduction of depressive symptoms to profit from the intervention. Therefore we suggest that patients with substantial depressive symptoms be directly referred to regular cognitive behaviour therapy.


From Antioxidants and Redox Signalling. [Epub ahead of print on 22 April, 2013]

Could mitochondrial dysfunction be a differentiating marker between Chronic Fatigue Syndrome and Fibromyalgia?

Castro-Marrero J, Cordero MD, Saez-Francas N, Jimenez-Gutiérrez C, Aguilar-Montilla FJ, Aliste L, Alegre-Martin J.
Vall de Hebron Univ Hospital Research Institute, CFS Unit, BARCELONA, Barcelona, Spain; jesus.castro@vhir.org.

Abstract

Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are complex and serious illnesses. It is estimated to affects up to 2.5% and 5% of the general population worldwide, respectively. The aetiology is unknown; however, recent studies suggest that mitochondrial dysfunction has been involved in the pathophysiology of both conditions.

We have investigated the possible association between mitochondrial biogenesis and oxidative stress in patients with CFS and FM. We studied 23 CFS patients, 20 FM patients and 15 healthy controls. Peripheral blood mononuclear cells (PBMC) showed decreased levels of CoQ10 from CFS patients (p<0.001 compared to controls) and FM subjects (p<0.001 compared to controls) and ATP levels for CFS patients (p<0.001 compared to controls) and for FM subjects (p<0.001 compared to controls). On the contrary, CFS/FM patients had significantly increased levels of lipid peroxidation, respectively (p<0.001 for both CFS and FM patients respect to controls) indicative of oxidative stress-induced damage. Mitochondrial citrate synthase activity was significantly lower in FM patients (p<0.001) and however, in CFS resulted in similar levels than controls. Mitochondrial DNA content (mtDNA/gDNA ratio) was normal in CFS and reduced in FM patients vs. healthy controls, respectively (p<0.001). Expression levels of PGC-1α and TFAM by immunoblotting showed significantly lower in FM patients (p<0.001) and were normal in CFS subjects compared to healthy controls. These data lead to the hypothesis that mitochondrial dysfunction-dependent events could be a marker of differentiation between CFS and FM indicating the mitochondria as a new potential therapeutic target for these conditions.


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