Neurobiological sensitization models of post-traumatic stress disorder: their possible relevance to multiple chemical sensitivity syndrome.

Neurological sensitization has been proposed as a model for post-traumatic stress disorder (PTSD) (Lipper et al., 1986; van der Kolk, 1987; Friedman, 1988; Post et al., 1988, 1994; Charney et al., 1993). Laboratory paradigms in which repeated exposure to a discrete stimulus is associated with progressive intensification of a neurophysiologic, behavioral, or pharmacologic response has many parallels with the sequence of events that precipitates PTSD. Investigators with other clinical interests have also been attracted to sensitization models. Specifically, Bell and associates (1992) have proposed that olfactory-limbic kindling is a very good model for understanding the etiology of multiple chemical sensitivity (MCS) syndrome. A number of articles in this volume have addressed the goodness-of-fit between this model and MCS. My major assignment is to review laboratory data and clinical observations pertinent to sensitization models of PTSD. I will show that although there are intriguing parallels between the two phenomena, one must have great respect for the complexity and polymorphism of both sensitization and PTSD before grasping for simplistic theoretical conclusions. Secondly, I will address the following question; if both PTSD and MCS can be understood as sensitization phenomena, are PTSD patients at greater risk to develop MCS and vice versa? This article is divided into four sections: a) a description of three distinct sensitization phenomena; b) a description of the symptoms of PTSD; c) a review of the applicability of sensitization models to the clinical phenomenology of PTSD; and d) a review of the hypothesis that PTSD patients might be more vulnerable to MCS.