From Psychological Medicine, 7 October 2013.
Review Article
Childhood stressors in the development of fatigue syndromes: a review of the past 20 years of research
A. Borsini(a1), N. Hepgul9(a1), V. Mondelli)a1), T. Chalder(a2) and C. M. Pariante(a1)
a1) Section of Stress, Psychiatry and Immunology and Perinatal Psychiatry, Department of Psychological Medicine, Institute of Psychiatry, King's College London, UK
a2) Department of Psychological Medicine, Institute of Psychiatry, King's College London, UK
Abstract
BACKGROUND
Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both highly prevalent conditions associated with extreme disability and with the development of co-morbid psychiatric disorders, such as depression and anxiety. Childhood stressors have been shown to induce persistent changes in the function of biological systems potentially relevant to the pathogenesis of both CFS and FM, such as the inflammatory system and the hypothalamic–pituitary–adrenal (HPA) axis. In this review, we examined whether multiple forms of childhood stressors are contributing factors to the development of these disorders, and of the associated psychiatric symptoms.
METHOD
Using PubMed, we identified 31 papers relevant to this narrative review. We included cohort studies and case-control studies, without any exclusion in terms of age and gender. No study characteristics or publication date restrictions were imposed.
RESULTS
Most studies across the literature consistently show that there is a strong association between experiences of childhood stressors and the presence of CFS and FM, with rates of CFS/FM being two- to three-fold higher in exposed than in unexposed subjects. We also found evidence for an increased risk for the development of additional symptoms, such as depression, anxiety and pain, in individuals with CFS and FM with a previous history of childhood stressors, compared with individuals with CFS/FM and no such history.
CONCLUSIONS
Our review confirms that exposure to childhood stressors is associated with the subsequent development of fatigue syndromes such as CFS and FM, and related symptoms. Further studies are needed to identify the mechanisms underlying these associations.
From Fatigue: Biomedicine, Health & Behavior, published 2 October 2014.
Post-exertion malaise in chronic fatigue syndrome: symptoms and gene expression
Jacob D. Meyer(a.b), Alan R. Light©, Sanjay K. Shukla(d), Derek Clevidence(e), Steven Yale(d), Aaron J. Stegner(b) & Dane B. Cook(a,b*)
a) William S. Middleton Memorial Veterans Hospital, Madison, USA
b) Department of Kinesiology, University of Wisconsin – Madison, Madison, USA
c) Departments of Anesthesiology and Neurobiology and Anatomy, University of Utah, Salt Lake City, USA
d) Clinical Research Center, Marshfield Clinic Research Foundation,
Marshfield, USA
e) Meriter Clinic, Monona, USA
Abstract
BACKGROUND
A primary complaint of chronic fatigue syndrome (CFS) patients is post-exertion malaise, which is a worsening of symptoms following activities such as exercise.
PURPOSE
To examine the link between gene expression for metabolite, adrenergic, immune, and glucocorticoid receptors on leukocytes and symptoms (pain, fatigue, and mood) following a maximal exercise test.
METHODS
Thirteen CFS patients and 11 healthy participants matched on age and fitness underwent blood draws and completed questionnaires immediately before, and 15 minutes, 48 hours, and 72 hours following, maximal exercise.
Symptom and genetic measures collected before and after exercise were compared using a doubly multivariate repeated-measures analysis of variance. Results: This comparison of CFS and healthy participants resulted in a significant multivariate main effect for Group (p < 0.05). Univariate analyses indicated group differences for adrenergic α-2A and glucocorticoid (NR3C1) receptor messenger ribonucleic acid and symptoms of fatigue and confusion. Changes in gene expression were significantly correlated with symptoms.CONCLUSIONSResults suggest that increased glucocorticoid sensitivity may contribute to the symptoms of post-exertion malaise in CFS. As NR3C1 interacts with other transcription factors, investigating the resulting cascades maylead to greater understanding of the biological mechanism of post-exertion malaise. This finding, if confirmed, could lead to novel approaches to prevent symptom exacerbation in CFS.
From Clinical Autonomic Research, 3 September 2013. Click on link for full text.
What is brain fog? An evaluation of the symptom in postural tachycardia syndrome
Amanda J. Ross, Marvin S. Medow, Peter C. Rowe, Julian M. Stewart
A. J. Ross Department of Behavioral Biology, Johns Hopkins University,
Baltimore, MD, USA
M. S. Medow J. M. Stewart Departments of Physiology and Pediatrics,
New York Medical College, Valhalla, NY, USA
P. C. Rowe Department of Pediatrics, Johns Hopkins University School
of Medicine, Baltimore, MD, USA
J. M. Stewart New York Medical College, Center for Hypotension, 19
Bradhurst Ave. Suite 1600S, Hawthorne, NY 10532, USA
Abstract
PURPOSE
Adolescents with postural tachycardia syndrome (POTS) often experience ill-defined cognitive impairment referred to by patients a ‘‘brain fog.’’ The objective of this study was to evaluate the symptom of brain fog as a means of gaining further insight into its etiology and potential palliative interventions.
METHODS
Eligible subjects who reported having been diagnosed with POTS were recruited from social media web sites. Subjects were asked
to complete a 38-item questionnaire designed for this study, and the Wood mental fatigue inventory (WMFI).
RESULTS
Responses were received from 138 subjects with POTS (88 % female), ranging in age from 14 to 29 years; 132 subjects reported brain fog. WMFI scores correlated with brain fog frequency and severity (P\0.001). The top ranked descriptors of brain fog were
‘‘forgetful,’’ ‘‘cloudy,’’ and ‘‘difficulty focusing, thinking and communicating.’’ The most frequently reported brain fog triggers were fatigue (91 %), lack of sleep (90 %), prolonged standing (87 %), dehydration (86 %), and feeling faint (85 %). Although aggravated by upright posture, brain fog was reported to persist after assuming a recumbent posture. The most frequently reported interventions for the treatment of brain fog were intravenous saline (77 %), stimulant medications (67 %), salt tablets (54 %), intra-muscular vitamin B-12 injections (48 %), and midodrine (45 %).
CONCLUSIONS
Descriptors for ‘‘brain fog’’ are most consistent with it being a cognitive complaint. Factors other than upright posture may play a role in the persistence of this symptom. Subjects reported a number of therapeutic interventions for brain fog not typically used in the treatment of POTS that may warrant further investigation.