Current Perspectives on Posttraumatic Stress Disorder: From the Clinic and the Laboratory

Stephen R. Paige

Department of Psychology

University of Nebraska at Omaha

Omaha, Nebraska 68182

Running Head: Current Perspectives on PTSD

Current Perspectives on Posttraumatic Stress Disorder: From the Clinic and the Laboratory Integrative Physiological and Behavioral Science, 32, 5-8

The recognition by medical authorities of psychological malfunctioning resulting from trauma can be traced back well over 200 years (Kolb, 1984). The symptoms of traumatic syndromes were included as traumatic neuroses in the first edition of The Diagnostic and Statistical Manual of the American Psychiatric Association (DSM; American Psychiatric Association, 1952). However, the specific diagnosis was eliminated from DSM-II (American Psychiatric Association, 1968), and the symptoms were categorized in this edition as transient situational disturbances or gross stress reactions (Keane, 1993). It was not until DSMIII (American Psychiatric Association, 1980) was published, that Posttraumatic Stress Disorder (PTSD) was clearly delineated as a clinical syndrome, within the category of anxiety disorders.

Considerable controversies remain concerning the reliability and validity of the diagnostic criteria for PTSD ( Davidson, 1993; Davidson et al., 1993). PTSD's current nosological status is considered to represent "... an amalgam of symptomatic, pathogenic, and etiological classification" (Pitman, 1993, p. 182). Moreover, the diagnosis of PTSD is considered to be particularly vulnerable to high false positive rates (Fairbank et al., 1985; Hamilton, 1985; Sparr and Pankrantz,1983). PTSD is the only anxiety disorder for which the occurrence of an external event is specified as a diagnostic criterion (Rothbaum and Foa, 1993), however this status also remains controversial (Brett, 1993; Davidson, 1993; Herman, 1993; McNally and Saigh, 1993). Moreover, significant co-morbidity exists between PTSD and a number of other psychiatric disorders, suggesting alternative diagnostic strategies "DSM-IV and Beyond" ( Davidson, 1993; Davidson et al., 1993).

A substantial body of evidence, integrating literature examining animal models of stress (Antelman, 1988; Krystal et al., 1989; Pitman, 1988; Pitman, 1989; van der Kolk et al., 1985), has demonstrated that neurobiological changes are reliably correlated with the diagnosis of PTSD. Alterations in functioning of central and autonomic nervous system (Blanchard et al., 1982; Blanchard et al., 1986; Malloy et al., 1983; Pallmeyer et al., 1986; Pitman et al., 1987; Pitman and Orr, 1990; Orr, 1990; Paige et al., 1990), hypothalamic-pituitary-adrenal axis (Mason et al., 1986; Watson et al., 1986;Yehuda et al., 1991), as well as monoamine (Kosten et al., 1987), and endorphin (van der Kolk et al., 1985) neurotransmitter systems have been reported in persons who suffer from the symptoms of PTSD compared to similarly traumatized individuals without PTSD, nontraumatized normals, and other psychiatric patient groups.

Some of the current neurobiological perspectives on PTSD have also been influenced by Kardiner's (1941) classic characterization of the symptoms of PTSD as symptoms of a "physioneurosis." The concept of behavioral kindling of PTSD symptoms, based on experimental studies of limbic kindling (Goddard et al., 1969) and its relationship to temporal lobe seizures (Epstein, 1964; Epstein and Hill, 1966) are also intertwined into these neurobiological perspectives on PTSD (Everly, 1993; Kolb, 1987). Thus, there has been considerable interest in the psychophysiological and neuropsychological status of patients diagnosed with PTSD.

It is in this context that a symposium on PTSD was held at the 1995 Annual Meeting of the Pavlovian Society of North America in Baltimore, Maryland which provided the impetus for the present Special Issue. It is particularly appropriate for the intellectual descendants of Pavlov and Gantt to be interested in PTSD, not only because of its integrative physiological and behavioral psychopathology, but also because some theoretical accounts of its etiology postulate that acuteand chronic anxiety states become associated with the aversive nature of traumatic events through both classical and instrumental conditioning (Keane & Kaloupek, 1982; Lewis & Hare, 1978; Pitman, 1988). For example, Kolb (1984; 1987) has postulated that a conditioned emotional response links fear inducing traumatic stimuli with a startle response which generalizes to include other fear arousing conditions which therefore may induce the conditioned response. Conditioning theories of the etiology of PTSD are specifically addressed in the theoretical paper by Dykman, Ackerman and Newton (this volume). As they point out, these accounts are largely based on a two-factor theory of learning (Mowrer, 1947; 1960), which they argue is a less parsimonious explanation of the etiology of PTSD than the process of emotional sensitization in genetically susceptible individuals which they offer as an alternative hypothesis. What may be almost as exciting for Pavlovians is that these authors review data collected in the Pavlovian Laboratory at Johns Hopkins University under the direction of Dr. W. Horsley Gantt, as well as their own later work in Arkansas, and work by others, as support for their intriguing hypothesis.

The presumed curative mechanism of behavioral re-exposure therapies for PTSD such as implosion and flooding is the extinction of trauma-related fear/anxiety states through controlled imaginal re-exposure to the trauma, with concomitant physiological arousal hypothesized as a precondition for extinction to occur. Woodward et al., (this volume) examine the arousal levels of six Vietnam veteran inpatients in group trauma re-exposure therapy for combat-related PTSD via continuously measured heart rate (HR) and videotape during eleven, approximately two and one half hour therapy sessions. They found that the precondition for extinction, an increases in arousal as indexed by an increase in HR, is evident in patients actively engaged in imaginal re-exposure to their personal traumas (flooding). However, no such increase was evident in patients in grouptherapy not directly engaged in personal imaginal re-exposure. Therefore, group trauma re-exposure therapy may not provide the precondition for extinction of trauma-related fear/anxiety states and thus may not produce “vicarious” flooding in non-engaged participants.

Dykman and his colleagues (Dykman, McPherson, Ackerman, Newton, Mooney, Wherry, and Chaffin, this volume) offer some empirical evidence bearing on questions of the etiology of PTSD, specifically childhood PTSD, by contrasting behavioral rating scale and structured psychiatric interview data in three groups (sexual abuse, physical abuse, or both) of abused children (N=109) and a group of 16 non-abused controls. PTSD was diagnosed in 50% of the abused children, with the highest rate of PTSD in children experiencing both sexual and physical abuse. Sexually abused children exhibited a higher incidence of PTSD than physically abused children and the most frequent co-morbid condition with PTSD was Separation Anxiety.

The third contribution from Dykman’s lab at Arkansas Children’s Hospital (McPherson et al., this volume) is an event-related brain potential (ERP) study of the abused children from their clinical sample. ERPs, a series of voltage fluctuations (components) recorded from the scalp (as EEG), are time-locked to a stimulus and averaged over repeated stimulus presentations in order to provide neurophysiological measures with precise temporal resolution. These potentials have shown their sensitivity to CNS processing of sensory and cognitive information in hundreds of studies of normative and psychopathological groups (Verleger, 1988).

One hundred seventy four sexually and/or physically abused children and twelve non-abused controls were tested in a modified auditory ERP augmentation/reduction paradigm in an attempt to investigate differences in CNS manifestations of sensory processing among various subject groupings based on PTSD diagnosis and PTSD symptom clusters. Augmentation is thetendency of vertex ERP component amplitudes to increase as a function of stimulus intensity, while vertex component amplitudes level off or actually decrease as a function of stimulus intensity in reduction (e.g., Buchsbaum and Silverman, 1968). Abused children diagnosed with PTSD had a significantly larger mean slope of the linear function relating P2-N2 ERP component amplitude to the intensity of the evoking auditory stimulus (augmenting) than abused subjects without PTSD. A similar P2-N2 augmentation effect was found when abused subjects with the highest number of number of re-experiencing symptoms (top 25%) were compared to the 25% of abused subjects with the least number of re-experiencing symptoms. However, the 25% of abused subjects with the greatest number of arousal symptoms had a significantly smaller mean slope (reduction) of the linear function relating N1-P2 ERP component amplitude to the intensity of the evoking auditory stimulus than the 25% of abused subjects with the least number of arousal symptoms.

These ERP findings in abused children with PTSD seem to be at odds with the ERP findings in Vietnam veterans with combat-related PTSD tested with an augmentation/reduction paradigm (Paige et al., 1990). However, there are obvious differences in subject characteristics such age, type of trauma, and time since the trauma, as well as significant differences in the paradigms employed, such as the intensities of the tones, the number of different intensities of tones, a passive versus a forewarned reaction time task with reward, inter-trial interval, and differences in vertex ERP components. Each of these variables could act individually or in combination as possible mediators accounting for the differences in the direction of the amplitude/intensity functions between these two studies. Therefore, further research is necessary to establish the reliability of these findings and to determine whether or how variables such as differences in subject groups, type of trauma, symptoms, and variations in the experimentaleliciting and measurement conditions might mediate the direction of the modulation of stimulus intensity in PTSD.

Taken together, the results of these two ERP studies suggest that subjects with PTSD process the intensity of auditory stimuli differently than their peers, and that this difference in the processing of auditory intensity information by both samples of PTSD subjects occurs with maximum amplitude at the vertex, about 100-250 msec following stimulus onset. Consistent with a number of independent procedures, including dipole localization models (Scherg and Von Camon, 1985) and brain electrical activity mapping analyses (Faux et al. 1987), these vertex potentials are thought to result from the summation of activity in bilateral supra-temporal areas and therefore implicate temporal lobe cortical structures as the anatomical substrate underlying the differential processing of auditory intensity information by the PTSD subjects in both these studies.

In a paper from the Harvard Psychophysiology Lab, Metzger et al (this volume) report on their attempt to concomitantly measure P3 ERP component amplitudes and latencies to trauma-related colored words and to replicate delayed color naming reaction time (RT) in PTSD and control subjects (emotional Stroop effect) in order to investigate the cognitive processing stage in which the trauma-related words might interfere with the color naming task.. As these authors point out, interference during the input or encoding stage can be attributed to facilitated semantic priming of trauma-related memories due to the intrusive hyper accessibility (activation) of these traumatic memories in PTSD subjects, thereby interfering with the encoding of color information.

P3 is a relatively large positive ERP component elicited by task-relevant stimuli with a typical latency range of 300-600 msec from stimulus onset. P3 latency has been established as a mental chronometric measure of stimulus recognition (the input or encoding stage ), independent ofthe response stage of processing (McCarthy and Donchin, 1981). Therefore, Metzger et al hypothesize that P3 latency would be delayed to trauma-related colored words in individuals with PTSD, given that color encoding is disrupted by the priming of trauma-related words in the input or encoding stage. Thus, if the source of the emotional Stroop effect in PTSD lies in the priming by intrusive memory networks, the P3 latency measure should parallel the delayed color naming RT for trauma-related words. Alternatively, delayed color-naming RT in the Stroop task by PTSD subjects may also result from emotional and/or attentional biases that interfere with response execution.

In a study specifically designed to examine generalized attentional dysfunction in PTSD, Golier et al., (this volume) compare 24 male Vietnam comat veterans with PTSD to 15 normal male control subjects on a sensitive, performance-based measure of sustained visual attention, the Identical Pairs Version of a modified continuous performance test (CPT-IP). Although there is considerable evidence that PTSD is characterized by a cognitive processing bias for trauma-related information (see Metzger et al., this volume), the data on more generalized neurocognitive deficits in PTSD are equivocal (Yehuda et al., 1995). Moreover, it has been claimed that PTSD subjects fail to discriminate relevant from irrelevant non-trauma-related (neutral) stimuli (McFarlane et al., 1993). Therefore, Golier et al employ measures borrowed from signal detection theory (Swets et al., 1961) to provide independent measures of their subjects’ ability to discriminate signal from noise (D’) and to err by overresponding or underresponding (á) and thus aid in the delineation of the boundaries of possible attentional disturbance in PTSD.

As evidenced in this brief introduction, the papers included this Special Issue attempt to provide examples of PTSD research from both the clinic and the laboratory. However, this issueis not intended to be a comprehensive survey of the literature on PTSD, nor is it intended to be a tutorial on PTSD theory and research methodologies. Rather, this Special Issue on PTSD is an attempt to communicate the enthusiasm engendered by the symposium on PTSD held at the recent Pavlovian Society meeting and to express the appeal of PTSD research for students of the physiological and behavioral sciences.

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