Journal of Chronic Fatigue Syndrome: Volume 1, Issue 1, 1995

Titles and abstracts for the Journal of Chronic Fatigue Syndrome, Volume 1, Issue 1, 1995.

Volume 1, Issue 1, 1995

• The Birth of a Journal by Nancy Klimas & Roberto Patarca
• Guest Editorial - Psychoneuroimmunology and Chronic Fatigue Syndrome: Toward New Models of Disease
• Review - Chronic Fatigue Syndrome in Children

  "Abstract - Chronic fatigue syndrome (CFS), formerly called chronic Epstein-Barr virus syndrome, chronic mononucleosis, and numerous other names, is a symptom complex characterized by marked functional limitation which affects children as well as adults. The symptom complex, physical examination, laboratory evaluation, clinical course, and differential diagnosis are reviewed with particular emphasis upon CFS in children. Management consists of a comprehensive treatment plan including medical, educational, and psychosocial support wiih the aim of reducing both symptom and activity limitation. While etiology is unknown, the use of the term "chronic fatigue syndrome" is appropriate for children with marked functional limitation due to unexplained fatigue who have the associated symptom complex and physical examination findings characteristic of this condition."

• Long Term Improvements in Patients with Chronic Fatigue Syndrome Treated with Ampligen

  "Abstract- Fifteen patients who fit the CDC definition of chronic fatigue syndrome (CFS) and had evidence of severe reduction in performance levels by low Karnofsky performance scores (KPS) of 20-60 were treated with Ampligen. At baseline most patients showed evidence of cerebral dysfunction by neuropsychological testing, were antigen positive by cell culture assay for human herpesvirus-6 (HHV-6), and displayed reduced performance during exercise tolerance testing, as measured by oxygen consumption. These patients represented a subset of CFS patients with especially severe and sustained symptomatology. Following 1248 weeks of Ampligen therapy, sustained improvements were noted in KPS (p < 0.01). Cognitive function improved including IQ and memory. Oxygen uptake and treadmill duration during exercise tolerance testing was also improved after 24 weeks of treatment (p < 0.01). Reduction in Human herpesvirus 6 expression as measured by the giant cell assay was significant (p < 0.001). Patients continued to show significant improvement late in therapy, taking 8 to 12 weeks as baseline. It was concluded that while receiving Ampligen, the severely afflicted patients studied here derived long-lasting clinical benefit from the Ampligen therapy."

• The Assessment of Vascular Abnormalities in Late Life Chronic Fatigue Syndrome by Brain SPECT: Comparison with Late Life Major Depressive Disorder

  "Abstract- We report on brain SPECT analysis of regional cerebral blood flow (rCBF) in late life chronic fatigue syndrome (CFS) patients and compare their results with patients with late life depression and elderly normal controls 45 years and older. We attempted to distinguish CFS from normals and patients with depression and applied the findings to understand the pathophysiology of the illness. We studied 33 patients with CFS (55 ± 10 years), 26 patients with late life depression (62 ± 8 years), and 19 normal controls (66 ± 8 years); 43 other normal controls had only ¹³³Xe rCBF measurements (66 ± 8 years). We evaluated rCBF quantitatively with ¹³³Xe images and qualitatively with high resolution imaging using 99mTc-HMPAO. We found that rCBF in CFS measured by ¹³³Xe varied between 35 and 41 ml/min/l00g in both hemispheres, p < 0.0001 and 0.05; similar findings were observed in depression. In CFS 99mTc-HMPAO imagain demonstrated right orbitofrontal and marked right dorsofrontal hypoperfusion at 58% to 66% of the maximal activity in the brain, p , 0.001. In late life depression, hypoperfusion was primarily limited to the right orbitofrontal lobe, 42% and 57%, p , 0.001. In depression, the abnormalities were most striking in the left temporal lobe and particularly in the left anterior frontal lobes. CFS patients with major depressive disorder by DMS-III-R criteria did not differ in regional cerebral hypoperfusion from those without major depression. The pathophysiology of the illness may involve the dysregulation of a neural network which includes circuits between the hippocampus (located in the anterior temporal lobe) and the dorsolateral prefrontal cortex."

• Dysregulated Expression of Soluble Immune Mediator Receptors in a Subset of Patients with Chronic Fatigue Syndrome: Cross-Sectional Categorization of Patients by Immune Status

  "Abstract-Individuals with chronic fatigue syndrome (CFS) have significantly increased proportions of activated CD8+T cells, decreased natural killer (NK) cell cytotoxic and lymphoproliferative activities, elevated serum levels of tumor necrosis factor (TNF)-α and detectable TNF-β, interleukin (IL)-lβ, and IL-6 mRNA in peripheral blood mononuclear cells (PBMC). We report here that CFS patients as a group also have significantly higher levels, as compared to controls, of soluble TNF receptor type I (sTNF-RI or sCDl20a), sIL-6R (sCD126) and β2-microglobulin (β2-m), but not of IL-1 receptor antagonist (IL-1Ra). Correlative and population distribution studies that included lymphoid phenotypic distributions and function as well as soluble immune mediator expression levels revealed the existence of at least two mainly nonoverlapping immunological categories among CFS patients with either: (1) dysregulaled TNF-α/β expression in association with changes in the serum levels of IL-lα, IL-4, sIL-2R and IL-lRa, PBMC-associated expression of IL-1β, IL-6 and TNF-β mRNA, and T cell activation; or, (2) interrelated and dysregulated expression of sTNF-RI, sIL-6R, and β2-m and significantly decreased lymphoproliferative and NK cell cytotoxic activities. This preliminary systematization is of usefulness in the diagnosis, follow-up, and characterization of possible etiological agents for CFS."

• National Institutes of Health Workshop Statement NIH Technology Assessment Workshop on the Persian Gulf Experience and Health April 27-29,1994
• Literature In Review

See also

• Journal of Chronic Fatigue Syndrome for other Issues

See chronic fatigue syndrome.

etiology The cause of origin, especially of a disease.

1. of or relating to the brain or the intellect 2. of, relating to, affecting, or being the cerebrum.}

cerebral 1. of or relating to the brain or the intellect 2. of, relating to, affecting, or being the cerebrum.

1. (verb) analysis (as of an ore or drug) to determine the presence, absence, or quantity of one or more components. 2. (noun) In biochemistry, any laboratory protocol used to test a sample for one or more qualities.

assay 1. (verb) analysis (as of an ore or drug) to determine the presence, absence, or quantity of one or more components. 2. (noun) In biochemistry, any laboratory protocol used to test a sample for one or more qualities.

cognition Thought processes, including attention, reasoning, and memory.

(rCBF) - The amount of blood flow to a specific area of the brain in a particular period of time.

regional cerebral blood flow (rCBF) - The amount of blood flow to a specific area of the brain in a particular period of time.

regional cerebral blood flow (rCBF) - The amount of blood flow to a specific area of the brain in a particular period of time.

T cell A type of white blood cell which is mostly produced or matured in the thymus gland (hence T-cell) and is involved in the adaptive immune response on a cellular level. Also known as a T lymphocyte. (Learn more: www.youtube.com)

The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)

serum The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)

α α / Α. Greek letter alpha or alfa (a symbol used in science), equivalent to "a".

β / Β. Greek letter beta (a symbol used in science), equivalent to "b".

β β / Β. Greek letter beta (a symbol used in science), equivalent to "b".

A chemical that reduces or helps block the activity of another chemical in the body. For example, most antihistamines are H1 antagonists because they block the H1 histamine receptor, which helps relieve allergy symptoms. The opposite of an agonist.

antagonist A chemical that reduces or helps block the activity of another chemical in the body. For example, most antihistamines are H1 antagonists because they block the H1 histamine receptor, which helps relieve allergy symptoms. The opposite of an agonist.

etiology The cause of origin, especially of a disease.

See National Institutes of Health.

National Institutes of Health (NIH) - A set of biomedical research institutes operated by the U.S. government, under the auspices of the Department of Health and Human Services.