From the European Journal of Applied Physiology, 31 May 2014 [Epub ahead of print].
Dimensions of pure chronic fatigue: psychophysical, cognitive and biological correlates in the chronic fatigue syndrome.
Neu D, Mairesse O, Montana X, Gilson M, Corazza F, Lefevre N, Linkowski P, Le Bon O, Verbanck P.
Sleep Laboratory and Unit for Chronobiology U78, Department of Psychiatry, Brugmann University Hospital, Université Libre de Bruxelles (U.L.B), Arthur Van Gehuchten Square, 1020, Brussels, Belgium, firstname.lastname@example.org.
To investigate associated dimensions of fatigue regarding cognitive impairment, psychomotor performances, muscular effort power and circulating cytokine levels and their relations to symptom intensity in a sample of pure chronic fatigue syndrome (CFS) patients without overlapping objective sleepiness or sleep disorders.
16 CFS patients were compared to 14 matched controls. We assessed structured symptom-scales, polysomnography, multiple sleep latency tests, attention (Zazzo-Cancellation ZCT, digit-symbol-substitution DSST), psychomotor vigilance and speed (PVT, finger tapping test, FTT), dynamometer handgrip force (tonic and phasic trials) and circulating cytokines (IFN-γ, IL-1b, IL-6, IL-8, IL-10, TNF-α).
In addition to fatigue, CFS patients presented with higher affective symptom intensity and worse perceived sleep quality. Polysomnography showed more slow-wave sleep and microarousals in CFS but similar sleep time, efficiency and light-sleep durations than controls. Patients presented with impaired attention (DSST, ZCT), slower reaction times (PVT) but not with lower hit rates (FTT). Notwithstanding lower grip strength during tonic and phasic trials,
CFS also presented with higher fatigability during phasic trials. Cytokine levels were increased for IL-1b, IL-8, IL-10 and TNF-α and fatigue intensity was correlated to grip strength and IL-8.
In contrast to sleepiness, chronic fatigue is a more complex phenomenon that cannot be reduced to one single measured dimension (i.e., sleep propensity). Showing its relations to different measurements, our study reflects this multidimensionality, in a psychosomatic disorder such as CFS. To obtain objective information, routine assessments of fatigue should rule out sleepiness, combine aspects of mental and physical fatigue and focus on fatigability.
From the Sydney eScholarship Repository, 14 April 2014.
Do certain microbiological pathogens cause or have a role in the aetiology of the disease entity known as chronic fatigue syndrome?
Authors: Kelly, Thomas
Chronic Fatigue Syndrome (CFS) is a complex disorder with a common set of core symptoms and with many secondary symptoms. Underlying chronic infection has been advocated as a
contributing factor to CFS, yet its role and the extent of its impact are unconfirmed.
Blood samples were obtained from eighty-eight CFS patients and twenty nine controls. Evidence of infection by certain tick-borne and respiratory pathogens was tested for through the use of nested PCR, western blot, ELISA and IFA.
Of CFS participants, 19% had evidence of exposure to 3 out of 4 pathogen species compared to 3% of controls (p = 0.04). For tick-borne (TB) pathogens, 56% of CFS participants had exposure to at least one, compared to 14% of controls (p < 0.001). DISCUSSION The high prevalence of exposure to multiple pathogens within the test group suggests a relationship between CFS and infective agents. As hypothesised in previous studies, the results of this study could contribute towards the argument that chronic infections, as a result of contributing to immune dysregulation, may lead to fatiguing symptoms. More specific forms of investigation using methods that directly measure pathogen levels should be undertaken.
From Neurology and Neuophysiology, 30 April 2014.
Brain Derived Neurotrophic Factor is Decreased in Chronic Fatigue Syndrome and Multiple Sclerosis
Matthew Sorenson(1*), Leonard Jason(2), Jonna Peterson(3), Joshua Herrington(40, and Herbert Mathews(5)
1) School of Nursing, De Paul University, Chicago, USA
2) Department of Psychology, De Paul University, Chicago, USA
3) Rush University, Chicago, USA
4) Florida International University, Florida, USA
5) Loyola University Chicago, Chicago, USA
*Corresponding author: Matthew Sorenson, Associate Professor/Associate Director DePaul University School of Nursing, 990 West Fullerton Ave.,Suite 3000, Chicago, IL. 60614, USA, Tel: 773-325-1887; Fax: 773-325-7282; E-mail: email@example.com
This study examined the levels of a major regulator of neuronal survival, brain derived neurotrophic factor (BDNF) in two populations; individuals with multiple sclerosis and chronic fatigue syndrome.
BDNF is a protein involved in the maintenance and maturation of both peripheral and central neurons. In patients with multiple sclerosis, BDNF expression is often decreased and believed to reflect ineffective repair mechanisms. As a preliminary exploration, we examined the production of BDNF on the part of peripheral blood mononuclear cells in three groups: patients with Chronic Fatigue Syndrome (CFS [n=15]), patients with multiple sclerosis (n=57), and a set of putatively healthy controls (n=37).
Mononuclear cells were extracted from peripheral blood samples and cultured for 48 hours. Production of BDNF was evaluated from phyto-haemagglutinin (PHA) and phorbol-12-myristate-13-acetate (PMA) stimulated and unstimulated cells. BDNF levels were determined using a commercially available enzyme linked immune absorbent assay (sensitivity: 62.5-4,000 pg/mL).
Both CFS and MS samples displayed nearly identical levels of BDNF, levels that were 25 percent of that displayed by the healthy control sample. For unstimulated cells, the BDNF values were 404.71 pg/ml for the CFS sample, 573.33 pg/ml for the MS sample and ,114.15 pg/ml for the control sample. For stimulated cells, the BDNF values were 442.55 pg/ml for the CFS sample, 367.33 pg/ml for the stimulated MS sample, and 432.24 pg/ml for the stimulated control sample.
The deceased production of BDNF on the part of MS patients is consistent with the literature. However, the decreased production in those with CFS was unexpected and a novel finding. This finding could reflect a reduced ability to maintain neuronal structure and function in those with CFS. Future studies are needed to evaluate for neuronal damage in those with CFS.