From the Medical-Surgical Journal, Society of Physicians and Naturalists Iasi – Romania, July-September 2014
Main neuroendocrine features, diagnosis and therapeutic possibilities in the chronic fatigue syndrome, an underdiagnosed entity.
Amihăesei IC, Cojocaru E.
Abstract
Chronic fatigue syndrome is characterized by severe, persistent fatigue which is not relieved by rest and is not associated to other medical conditions. Other common symptoms are including concentration and memory impairment, muscle and multiple joints pain, extreme exhaustion after physical or mental exertions, irritable bowel syndrome-like symptoms and depression, anxiety, mood swings and panic attacks.
Etiology of the syndrome is not yet clear, post-viral and stress hypotheses were not verified. Diagnosis is confirmed in case of new onset of severe fatigue, for six consecutive months or more; fatigue is leading to significant reduction of the activity levels and is accompanied by other four or more of the specific associated symptoms, which are also lasting for six months or longer.
The management of the disease is based on cognitive behavioral therapy, graded exercise therapy and pacing; medication plays a minor role in therapy. The occupational status is severely affected, more than half of the cases being unable to work. Full recovery rate is in average of about 5%.
From Radiology, October 2014.
Original Research
Neuroradiology
Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome
See the editorial on this feature by Radiology editor Dr. Herbert Kressel and Dr. Leonard Berlin in the November 2014 issue.
Michael M. Zeineh, MD, PhD, James Kang, MD, Scott W. Atlas, MD, Mira M. Raman, MS, Allan L. Reiss, MD, Jane L. Norris, PA, Ian Valencia, BS, Jose G. Montoya, MD
Department of Radiology, Lucas Center for Imaging, Stanford University School of Medicine, 1201 Welch Rd, Room P271, Stanford, CA 94305-5488.
Abstract
PURPOSE
To identify whether patients with chronic fatigue syndrome (CFS) have differences in gross brain structure, microscopic structure, or brain perfusion that may explain their symptoms.
MATERIALS AND METHODS
Fifteen patients with CFS were identified by means of retrospective review with an institutional review board–approved waiver of consent and waiver of authorization. Fourteen age- and sex-matched control subjects provided informed consent in accordance with the institutional review board and HIPAA. All subjects
underwent 3.0-T volumetric T1-weighted magnetic resonance (MR) imaging, with two diffusion-tensor imaging (DTI) acquisitions and arterial spin labeling (ASL). Open source software was used to segment supratentorial gray and white matter and cerebrospinal fluid to compare gray and white matter volumes and cortical thickness. DTI data were processed with automated fiber quantification, which was used to compare piecewise fractional anisotropy (FA) along 20 tracks. For the volumetric analysis, a regression was performed to account for differences in age, handedness, and total intracranial volume, and for the DTI, FA was compared piecewise along tracks by using an unpaired t test. The open source software segmentation was used to compare cerebral blood flow as measured with ASL.
RESULTS
In the CFS population, FA was increased in the right arcuate fasciculus (P = .0015), and in right-handers, FA was also increased in the right inferior longitudinal fasciculus (ILF) (P = .0008). In patients with CFS, right anterior arcuate FA increased with disease severity (r = 0.649, P = .026). Bilateral white matter volumes were reduced in CFS (mean ± standard deviation, 467 581 mm3 ± 47 610 for patients vs 504 864 mm3 ± 68 126 for control subjects, P = .0026), and cortical thickness increased in both right arcuate end points, the middle temporal (T = 4.25) and precentral (T = 6.47) gyri, and one right ILF end point, the occipital lobe (T = 5.36). ASL showed no significant differences.
CONCLUSIONS
Bilateral white matter atrophy is present in CFS. No differences in perfusion were noted. Right hemispheric increased FA may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.
From Clinical Rheumatology, 14 October 2014.
What is in a name? Comparing diagnostic criteria for chronic fatigue syndrome with or without fibromyalgia
Mira Meeus(1,2,3), Kelly Ickmans (2,3,4,5), Filip Struyf (2,3), Daphne Kos(3,6,7), Luc Lambrecht(8), Barbara Willekens(9), Patrick Cras(9), Jo Nijs(2,3,4,5)
1. Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium
10. Rehabilitation Sciences and Physiotherapy, Ghent University, Campus Heymans (UZ) 3 B3, De Pintelaan 185, Ghent, Belgium
2. Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium
3. Pain in Motion International Research Group http://www.paininmotion.be
4. Departments of Human Physiology and & Rehabilitation Sciences, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel, Brussel, Belgium
5. Department of Physiotherapy and Rehabilitation, University Hospital Brussels, Brussel, Belgium
6. Division of Occupational Therapy, Artesis Plantijn University College Antwerp, Antwerp, Belgium
7. Rehabilitation Sciences, KU Leuven, Leuven, Belgium
8. Private practice for internal medicine, Ghent, Belgium
9. Department of Neurology, Faculty of Medicine, University and University Hospital Antwerp, Antwerp, Belgium
Abstract
The current study had two objectives. (1) to compare objective and self-report measures in patients with chronic fatigue syndrome (CFS) according to the 1994 Center for Disease Control (CDC) criteria, patients with multiple sclerosis (MS), and healthy controls, and (2) to contrast CFS patients who only fulfill CDC criteria to those who also fulfill the criteria for myalgic encephalomyelitis (ME), the 2003 Canadian criteria for ME/CFS, or the comorbid diagnosis of fibromyalgia (FM).
One hundred six participants (48 CFS patients diagnosed following the 1994 CDC criteria, 19 MS patients, and 39 healthy controls) completed questionnaires assessing symptom severity, quality of life, daily functioning, and psychological factors. Objective measures consisted of activity monitoring, evaluation of maximal voluntary contraction and muscle recovery, and cognitive performance.
CFS patients were screened whether they also fulfilled ME criteria, the Canadian criteria, and the diagnosis of FM. CFS patients scored higher on symptom severity, lower on quality of life, and higher on depression and kinesiophobia and worse on MVC, muscle recovery, and cognitive performance compared to the MS patients and the healthy subjects.
Daily activity levels were also lower compared to healthy subjects.
Only one difference was found between those fulfilling the ME criteria and those who did not regarding the degree of kinesiophobia (lower in ME), while comorbidity for FM significantly increased the symptom burden.
CFS patients report more severe symptoms and are more disabled compared to MS patients and healthy controls. Based on the present study, fulfillment of the ME or Canadian criteria did not seem to give a clinically different picture, whereas a diagnosis of comorbid FM selected symptomatically worse and more disabled patients.
From the Journal of Neuroimmunology, 15 October 2014.
Viral load and T-helper-1-cell cytokines in myalgic encephalomyelitis
Irina Malashenkova, Sergey Krynskiy, Daniil Ogurtsov, Nikita Hailov, Galina Kazanova, Olga Gurskaya, Maria Jarova, Igor Zuikov, Elvira Domonova, O.yu Silveystrova, Nikolay Didkovskiy
Abstract
OBJECTIVES
Myalgic encephalomyelitis (ME) is a polymorphic clinical entity. In some patients, chronic infection with Epstein–Barr virus (EBV), human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7) is regarded as an important pathogenetic factor that contributes to
chronic neuroinflammation. We determined a relationship between EBV, HHV-6 and HHV-7 viral load in the saliva and serum levels ofpro-inflammatory cytokines (IFNalpha, IFNgamma, IL-1, IL-2) in a group of ME patients.
(Seemingly incomplete abstract but the rest is behind a paywall).
From Advances in Clinical Chemistry. 2014;66:121-72.
Chapter Five – Metabolism in chronic fatigue syndrome.
Christopher W. Armstrong*, †, Neil R. McGregor‡, Henry L. Butt§, Paul R. Gooley*, †,
* Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria, Australia
† Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, Victoria, Australia
‡ Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Parkville, Victoria, Australia
§ Bioscreen, Bio21 Molecular Science and Biotechnology Institute, Parkville, Victoria, Australia
Abstract
Chronic fatigue syndrome (CFS) is a poorly understood condition that presents as long-term physical and mental fatigue with associated symptoms of pain and sensitivity across a broad range of systems in the body.
The poor understanding of the disorder comes from the varying clinical diagnostic definitions as well as the broad array of body systems from which its symptoms present.
Studies on metabolism and CFS suggest irregularities in energy metabolism, amino acid
metabolism, nucleotide metabolism, nitrogen metabolism, hormone metabolism, and oxidative stress metabolism. The overwhelming body of evidence suggests an oxidative environment with the minimal utilization of mitochondria for efficient energy production. This is
coupled with a reduced excretion of amino acids and nitrogen in
general.
Metabolomics is a developing field that studies metabolism within a living system under varying conditions of stimuli. Through its development, there has been the optimisation of techniques to do large-scale hypothesis-generating untargeted studies as well as hypothesis-testing targeted studies. These techniques are introduced and show an important future direction for research into complex illnesses such as CFS.
From the Australian article above – the research suggested –
METABOLIC irregularities in ALL of the following areas:
– energy metabolism, amino acid, nucleotide, nitrogen, hormone & oxidative stress metabolism.
Almost NO use of mitochondria for efficient energy production & reduced excretion of amino acids & nitrogen.
Wow – amazing that all this has gone unnoticed in very ill patients for so long.
Given that metabolism is a basic underlying principal for maintaining life itself, it might seem like a sensible area for basic study in medical training.