Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

In this paper I briefly review the relationship between hypnotizability, dissociative experiences and traits, and electrocortical activity (i. e., visual event-related potentials, or ERPs), and present work-in progress on these issues with a sample of posttraumatic stress disorder (PTSD) and non-PTSD Gulf War veterans.

There are multiple converging research lines supporting a relationship between hypnotizability, dissociation and PTSD. Two studies have found that, as a group, individuals with PTSD exhibit higher hypnotizability than most other clinical and comparison groups (Spiegel, Hunt & Dondershine, 1988; Stutman & Bliss, 1985). It should be mentioned that hypnotizability includes an important dissociative component (Cardeņa & Spiegel, 1991). With respect to the relationship between trauma and dissociation, there is evidence that: a) dissociative disorder patients almost universally report a history of serious abuse (e.g., Putnam, 1989; Cardeņa et al., 1996); b) a trauma history predicts dissociative symptomatology in diverse clinical groups (e.g., Ogata et al., 1990; Chu & Dill, 1990); c) there is a significant positive correlation between PTSD and dissociative symptomatology (e.g., Carlson & Putnam, 1993; Hyer et al., 1993); d) "normal" populations exposed to natural disasters exhibit short-lived dissociative phenomena in (e.g., Cardeņa & Spiegel, 1993; Koopman, Classen & Spiegel, 1994); and e) dissociation around the time of trauma is a significant predictor of later PTSD (e.g., Classen et al., 1998; Marmar et al., 1994). Nonetheless, although the common association of trauma and dissociation is well established, the nature of such relationship is not clear, nor have the electrocortical underpinnings of dissociative experience been elucidated.

The literature on waking EEG and ERPs in PTSD is small, despite the hypothesis by Kolb (1987) and others that PTSD may be associated with cortical damage, and recent findings of decreased hippocampal volume among PTSD victims (see Bower, 1995). In a brief report on 18 Vietnam-era PTSD patients, Wolf and collaborators (1988) found no evidence for EEG abnormalities during sleep or awake recordings. A more detailed investigation (Gurvits et al., 1993) with 27 Vietnam-era PTSD patients revealed that they had significantly more neurological soft signs than a control group. The incidence of EEG abnormalities in the PTSD group (19%) was, however, not greater than that of the control group (21%), or very different from that estimated for the normal population (1-15%). These two articles implied that the waking EEG of PTSD patients does not contain obvious abnormalities. This conclusion is tempered, however, by limitations in these studies including the lack of use of advanced EEG analytical techniques. McCaffrey and collaborators (1993) evaluated two EEG epochs recorded at the beginning and after 5 seconds of exposure to various trauma-related and neutral odors in two groups, five Vietnam patients diagnosed with PTSD and five Vietnam patients with adjustment disorder. Of the six odors used, the greatest, and significant, effect for the PTSD group was found for "burnt hair," which the participants associated to war odors.

A different and more sensitive approach than spontaneous EEG is the measure of electrocortical activity after exposure to various stimuli, or ERPs. ERPs sample perceptual processes that occur in a well-defined, brief time period, locked to stimulus presentation (Coles, Gratton & Fabiani, 1991). There have been two published studies of event-related potential in PTSD patients. Paige and collaborators (1990) measured the ERPs and heart-rate responses to four different volume tones, presented randomly to a group of 12 PTSD and 6 combat controls. Results showed a noticeable difference between the two groups: nine of the 12 PTSD patients had a significant "reducer" pattern in which, in contrast to the comparison group, P2 (positive amplitudes about 200 msecs after exposure to stimuli) amplitudes at vertex (CZ) and temporal (particularly T3) locations remained stable or actually decreased as the intensity of the tones increased. This pattern was reversed for HR change, which increased significantly more for the PTSD group than for the controls as the tone volume increased. Self reported anxiety was significantly correlated with the decreases in peak voltage, suggesting that more anxious individuals show reduced cortical response to these stimuli.

Using a different paradigm with 18 PTSD patients and 20 controls, McFarlane, Weber and Clark (1993) presented a target discrimination task using infrequent tones as targets, with frequent and infrequent tones of different frequencies serving as distracters (i.e., an "oddball" paradigm). The reported data on vertex sites (i.e., Fz, Cz, and Pz) showed that the PTSD group had a significantly delayed N2 (negative potential around 200 msec after stimulus presentation) and a reduced P3 (positive deflection around 300 msec after stimulus presentation), although the reduced P3 was not significant at Fz. Contrary to results with normal populations, the PTSD group did not show a significant difference in the P3 for target and distracter tones, result that suggests impairment in the discrimination of relevant stimuli.

Thus, most studies suggest that PTSD patients exhibit elevated levels of dissociation, and electrocortical abnormalities, although these different variables have not been directly related. In this study, I seek to evaluate both types of variables.

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