Chronic Fatigue Syndrome and the Body's Immune Defense System.

Patarca-Montero R. Binghamton, NY 13904-1580, The Haworth Medical Press, 2002, hardcover/paperback, 122 pp, ISBN: 0-7890-1529-3 (hardcover), 0-7890-1530-7 (paperback), $34.95 (hardcover), $19.95 (paperback).

Although the author did not give a purpose statement for the book or an indication of its intended audience, I believe the best audience for this book would be readers who have a good working knowledge of the immune system and who are interested in learning about the research on the relationship between chronic fatigue syndrome (CFS) and the immune system. The author begins with a short overview of the immune system; the role of T cells, B cells, and interleukins; and major differences between cellular immunity (which is mediated by T-helper type 1 cells [Th 1 cells]) and humoral immunity (which is mediated by T-helper type 2 cells [Th 2 cells]).

The author gives a brief overview of the role of Th 2-cell predominance in autoimmune disorders. Patarca-Montero states that, although CFS has an unknown etiology, some evidence suggests that CFS is caused by a chronic infection or an infection that leaves autoimmune sequelae. This results in a shift of T-helper-cell responses in patients with CFS where Th 2-cell responses are predominant over Th 1-cell responses. This shift has led researchers to look at interventions that may cause a shift from the Th 2 response in patients with CFS to a Th 1-predominant pattern.

The rest of the book reviews the relationship among the immune, nervous, and endocrine systems. The author states that these relationships may be mediated, in part, by the sympathetic nervous system, which may suppress the Th 1 response. The hypothalamic-pituitary-adrenal axis and the sympathetic nervous system are both linked with the immune system. The author also points out that persistent noxious stimulation of the neuroimmunological circuitry can lead to multi-organ pathology. Some research cited by the author suggests that CFS is related to deficient neuroendocrine-immune communication and that patients with CFS show a high comorbidity with other stress-associated syndromes and autoimmune conditions associated with endocrine dysfunction. Although controversial, the author points out that some researchers have found that patients with CFS can be categorized using immunological findings. According to the author, the literature is mixed on whether patients with CFS have a higher incidence of allergic responses; however, some research seems to point to an autoimmune response as a causative factor of CFS.

The author also reviews the literature looking for a relationship between CFS and other infectious diseases. The review reveals that viruses have been implicated in playing a role in causing CFS but they have not been considered to be a primary cause. The Epstein-Barr virus and other herpesviruses have been associated with CFS. Although the research is inconclusive, several bacteria, including Chlamydia, Rickettseiae, and Yersinia, have also been linked to CFS. CFS has also been associated with inhalation of fungal spores. One hypothesis is that acute microbial infections may trigger an autoimmune response.

The cited research indicates a relationship between stress and the severity of CFS symptoms. There appears to be some commonality between CFS symptoms and the symptoms experienced by soldiers returning with Gulf War syndrome (another syndrome where Th 2 response predominates). As the author suggests, CFS may be related to a shift from Th 1 responses to Th 2 responses. Therefore, various interventions, including vaccines and lymph node cell reinfusion, have been tried in order shift the balance of responses from Th 2 to Th 1 cells. Panax ginseng may have some effect on shifting the balance between the helper cells.

Overall, the author does an excellent job of reviewing the literature regarding CFS and the immune system. The author includes 30 pages of references (most of which are peer reviewed). The author does not include any tables or figures to support the text. Although the book would be very valuable to immunologists and others interested in the cellular events that might be related to CFS, I don't think the book would be useful to physical therapist clinicians. The book may serve as a limited reference for physical therapist faculty involved in teaching pathology to physical therapist students. The book does not discuss examination or intervention techniques for CFS that would be of interest to a clinical physical therapist.

Thomas M Mohr, PT, PhD

University of North Dakota

Grand Forks, ND

Dr Mohr is Professor and Chairman in the Department of Physical Therapy. His teaching responsibilities are in neuroscience, physiology, biomechanics, and electrophysiology. His research interests are in electromyography, biomechanics, and electrotherapy.