Theoretical accounts of Gulf War Syndrome: from environmental toxins to psychoneuroimmunology and neurodegeneration.
Non-specific illness includes a wide variety of symptoms: behavioural (e.g., reduced food and water intake), cognitive (e.g., memory and concentration problems) and physiological (e.g., fever). This paper reviews evidence suggesting that such symptoms can be explained more parsimoniously as a single symptom cluster than as a set of separate illnesses such as Gulf War Syndrome (GWS) and chronic fatigue syndrome (CFS). This superordinate syndrome could have its biological basis in the activity of pro-inflammatory cytokines (in particular interleukin-1: IL-1), that give rise to what has become known as the 'sickness response'. It is further argued that the persistence of non-specific illness in chronic conditions like GWS may be (in part) attributable to a bio-associative mechanism (Ferguson and Cassaday, 1999). In the case of GWS, physiological challenges could have produced a non-specific sickness response that became associated with smells (e.g., petrol), coincidentally experienced in the Persian Gulf. On returning to the home environment, these same smells would act as associative triggers for the maintenance of (conditioned) sickness responses. Such associative mechanisms could be mediated through the hypothalamus and limbic system via vagal nerve innervation and would provide an explanation for the persistence of a set of symptoms (e.g., fever) that should normally be short lived and self-limiting. We also present evidence that the pattern of symptoms produced by the pro-inflammatory cytokines reflects a shift in immune system functioning towards a (T-helper-1) Th1 profile. This position contrasts with other immunological accounts of GWS that suggest that the immune system demonstrates a shift to a Th2 (allergy) profile. Evidence pertaining to these two contrasting positions is reviewed.
Ferguson
E
E
School of Psychology, University of Nottingham, Nottingham, NG7 2RD, UK. eamonn.ferguson@nottingham.ac.uk
Cassaday
H J
HJ
D001244:Association; D016207:Cytokines / Q000276:immunology; D004781:Environmental Exposure / Q000009:adverse effects*; D015673:Fatigue Syndrome, Chronic / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology; D007375:Interleukin-1 / Q000276:immunology; D008032:Limbic System / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000209:etiology / Q000503:physiopathology; D018923:Persian Gulf Syndrome / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology* / Q000523:psychology; D011598:Psychoneuroimmunology; D012903:Smell / Q000276:immunology; D013313:Stress Disorders, Post-Traumatic / Q000276:immunology / Q000503:physiopathology; D013312:Stress, Physiological / Q000276:immunology / Q000503:physiopathology; D018417:Th1 Cells / Q000276:immunology
D016207:Cytokines; D007375:Interleukin-1