MCS: Journal Abstracts
Neurogenic inflammation as a pathway distinct from antigen-driven, immune-mediated inflammation may play a pivotal role in understanding a broad class of environmental health problems resulting from chemical exposures. Recent progress in understanding the mediators, triggers, and regulation of neurogenic inflammation is reviewed. Evidence for and speculations about a role for neurogenic inflammation in established disorders such as asthma, rhinitis, contact dermatitis, migraine headache, and rheumatoid arthritis are presented. The sick building syndrome and multiple chemical sensitivity syndrome have been defined as clinical entities in which exposure to chemical inhalants gives rise to disease. Current data on the existence of chemical irritant receptors in the airway and skin are discussed; neurogenic inflammation arising from stimulation of chemical irritant receptors is a possible model to explain many of the aspects of chemical sensitivities.
Address correspondence to W. J. Meggs, Room 4W54, Brody Building, Department of Emergency Medicine, East Carolina University School of Medicine, Greenville, NC 27858 USA.
Illness from low
levels of environmental chemicals: relevance to chronic fatigue syndrome
This article summarizes (1) epidemiologic and clinical data on the symptoms of maladies in association with low-level chemicals in the environment, i.e., environmental chemical intolerance (CI), as it may relate to chronic fatigue syndrome (CFS) and fibromyalgia; and (2) the olfactory-limbic neural sensitization model for CI, a neurobehavioral synthesis of basic and clinical research. Severe CI is a characteristic of 20-47% of individuals with apparent CFS and/or fibromyalgia, all patients with multiple chemical sensitivity (MCS), and approximately 4-6% of the general population. In the general population, 15-30% report at least minor problems with CI. The levels of chemicals reported to trigger CI would normally be considered nontoxic or subtoxic. However, host factors--e.g., individual differences in susceptibility to neurohormonal sensitization (amplification) of endogenous responses--may contribute to generating a disabling intensity to the resultant multisystem dysfunctions in CI. One site for this amplification may be the limbic system of the brain, which receives input from the olfactory pathways and sends efferents to the hypothalamus and the mesolimbic dopaminergic [reward] pathway. Chemical, biologic, and psychological stimuli can initiate and elicit sensitization. In turn, subsequent activation of the sensitized limbic and mesolimbic pathways can then facilitate dysregulation of behavioral, autonomic, endocrine, and immune system functions. Research to date has demonstrated the initiation of neurobehavioral sensitization by volatile organic compounds and pesticides in animals, as well as sensitizability of cardiovascular parameters, beta-endorphin levels, resting EEG alpha-wave activity, and divided-attention task performance in persons with CI. The ability of multiple types of widely divergent stimuli to initiate and elicit sensitization offers a new perspective on the search for mechanisms of illness in CFS and fibromyalgia with CI.
PMID: 9790486, UI: 99005147
Bell IR, Baldwin CM, Schwartz GE, Department of Psychiatry, University of Arizona, Tucson Veterans Affairs Medical Center, 85723, USA.
Prevalence and Overlap
of Chronic Fatigue Syndrome and Fibromyalgia Syndrome Among 100 New Patients
with Multiple Chemical Sensitivity Syndrome
Background: Several studies have reported on extensive two-way overlaps found among chronic fatigue syndrome (CFS), fibromyalgia syndrome (FMS) and multiple chemical sensitivity syndrome (MCS) but none have yet reported on the overlap of all three. This study assesses the prevalence of pure MCS, MCS-CFS, MCS-FMS and the overlap of all three among 100 consecutive new patients evaluated for MCS in a private practice specializing in occupational and environmental medicine.
Methods: Sixty-eight females and 32 males diagnosed with MCS-based on a medical history of multiple chronic symptoms in multiple organs triggered by multiple chemical exposures at or below previously tolerated levels - were also evaluated for CFS and FMS using the diagnostic criteria of the US Centers for Disease Control and the American College of Rheumatology, respectively.
Results: Eighty-eight percent of the 100 MCS patients met criteria for CFS, 49% met criteria for FMS, and 47% met both. Slightly more male than female MCS patients had CFS: 91% vs. 87%; while FMS was more than twice as common among female MCS patients: 59% vs. 28%. The majority of women, 56%, met criteria for all three disorders, and an additional 31% had both MCS and CFS. This pattern was reversed in men, only 28% of whom had all three, compared to 63% with MCS and CFS but no FMS. MCS alone was diagnosed in only 10% of the women and 9% of the men. Even rarer was the overlap of MCS and FMS without any CFS, found in just 2 women.
Conclusions: At least in this clinic population, MCS seldom occurs alone. The enormous range of diagnostic overlaps reported here and in previous studies of various overlaps among CFS, FMS and MCS highlights the need to screen for all three disorders in studies of any one and to report results in these terms. We recommend this be made standard practice in both clinical settings and research protocols.
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