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Research: FERGUSON and CASSADAY
Listed in Issue 89
Abstract
FERGUSON and CASSADAY, School of Psychology, University of Nottingham, Nottingham NG7 2RD, UK, eamonn.ferguson@nottingham.ac.uk, give theoretical accounts of Gulf War Syndrome from environmental toxins to psychoneuroimmunology and neurodegeneration.
Background
This review (123 references) deals with evidence that suggests it is often more parsimonious to explain non-specific illness as single symptom clusters than as a set of separate illnesses, even though a wide variety of symptoms can be included ranging from behavioural to cognitive to physiological. The superordinate syndrome, for instance Gulf War Syndrome GWS, could have its biological basis in the activity of pro-inflammatory cytokines, in particular interleukin-1 (IL-1), that give rise to what is known as the 'sickness response'. It is further argued that the persistence of non-specific illnesses may be in part due to a bio-associative mechanism. 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. Later on, these same smells could act as associative triggers to maintain the conditioned sickness response. Such associative mechanisms could be mediated through the hypothalamus and limbic system via vagal innervation and would provide an explanation for the persistence of a set of symptoms that should normally be self-limiting and short-lived. Evidence is also presented that the symptom pattern produced by the pro-inflammatory cytokines reflects a shift in immune system functioning towards a T-helper-1 profile. This position contrasts with other immunological accounts of GWS that suggest that the immune system demonstrates a shift towards a T-helper-2 (allergy) profile. Evidence pertaining to those two contrasting positions is reviewed.
Methodology
Results
Conclusion
References
Ferguson E, Cassaday HJ. Theoretical accounts of Gulf War Syndrome: from environmental toxins to psychoneuroimmunology and neurodegeneration. Behavioural neurology 13 (3-4): 133-147, 2001-2002.