Kardiner (1959) observed that combat related PTSD comprises exaggerated physiological responses to stimuli that resemble or are associated with combat. In the past twenty years, psychophysiological research has confirmed his early clinical observations and extended our understanding of physiological responses to non-traumatic or neutral stimulus information. The following is a summary and discussion of the findings of this psychophysiolgical research.
The diagnostic criteria for PTSD include heightened physiological arousal in reponse to stimuli associated with the trauma (APA, 1994). Psychophysiological research has demonstrated that the response to traumatic stimuli or imagery in PTSD patients involves heightened startle responses and peripheral physiological hyperactivity, including increases in heart rate and blood pressure, muscle tension, and skin conductivity (Blanchard, Kolb, Gerardi, Ryan, and Pallmeyer, 1986; Blanchard, Kolb, Pallmeyer, and Gerardi, 1982; Blanchard, Kolb, and Prins, 1991; Boudewyns and Hyer, 1990; Gerardi, Blanchard, and Kolb, 1989; Pallmeyer, Blanchard, and Kolb, 1986; Pitman, Orr, Forgue, de Jong, and Claiborn, 1987). Several research groups have pursued the use of objective measures of physiological arousal in response to traumatic stimuli to discriminate war veterans with and without PTSD.
In a series of studies, Blanchard and co-workers have successfully discriminated veterans with or without PTSD on the basis of heart rate responses to combat sounds (Blanchard et al, 1986, 62% correct; Blanchard, Kolb, Pallmeyer, and Gerardi, 1982, 95% correct for veterans with PTSD and non-veteran controls; Blanchard, Kolb, and Prins, 1991, 75%-83% correct; Gerardi, Blanchard, and Kolb, 1989, 81% correct; Pallmeyer, Blanchard, and Kolb, 1986, 86.4% correct). They have measured various physiological processes in response to three conditions: (a) resting, (b) mental arithmetic, and (c) a combination of music, silence, and combat sounds that increase in loudness from 40 to 80 dB is steps of 20 dB over several presentations. Recently, Blanchard, Kolb, and Prins (1991) found that a discriminant function based on measures of heart rate alone correctly identified an initial sample of 84% of combat veterans with PTSD and 75% of all veterans. Furthermore, the same discriminant function correctly identified 83% of another sample of combat veterans with or without PTSD. Gerardi, Blanchard, and Kolb (1989) report good short term test-retest reliability. Also, Gerardi, Blanchard, and Kolb (1989) report that veterans with PTSD cannot consciously lower their physiological responses so that they appear to be without PTSD and, although veterans without PTSD can elevate their physiological responses to combat stimuli, it is still possible to discriminate them from veterans with PTSD with 85% accuracy using a discriminant function based on heart rate measures alone.
Pitman et al (1987) assessed heart rate, forehead electromyogram (EMG), and skin conductance in response to unique combat incidents recollected by combat veterans. That is, they recorded physiological arousal while veterans listened to a tape recording of a narrative of a unique combat event that was described in detail by a veteran. Although independent raters agreed that the traumatic content or severity of the events recalled were similar for veterans with or without PTSD, the physiological response to the unique combat imagery was greater in veterans with PTSD than veterans without PTSD (Pitman et al, 1987). Pitman et al (1987) found that skin conductivity (73%), rather than forehead electromyogram (67%) or heart rate (64%), provided the best predictive discrimination of veterans with or without PTSD. Pitman et al (1987) found that a step-wise discrimiant function, based on all three measures, correctly classified all PTSD veterans, with 79% accuracy for all veterans with or without PTSD. Thus, this evaluation has very good sensitivity to PTSD. Also, Pitman et al (1987) found that physiological arousal in response to the unique traumatic imagery was significantly associated with the frequency of intrusions related to those traumatic events. Pitman et al (1987) proposed that veterans with PTSD were "reliving" their traumatic experiences, whereas veterans without PTSD were merely "recollecting" their experience.
The discrepancy in the predictive value of skin conductance and heart rate between the research studies cited above might be partially explained by an increase in skin conductivity to specific traumatic imagery. Pitman et al (1987) found that skin conductance, but not heart rate, was greater in response to specific combat imagery than general combat imagery and that skin conductance has better discriminative power than heart rate. Since skin conductivity is an indication of sympathetic arousal, the results of Pitman et al (1987) indicate that there is an increase in sympathetic arousal associated with specific traumatic imagery and that this increased sympathetic arousal is positively associated with the frequency of intrusions.
Furthermore, Brende (1982) reports that skin conductivity in response to traumatic imagery reflects the functioning of the contralateral hemisphere and that the left and right hemisphere play different roles in the symptoms of PTSD. Skin conductivity from the right hand is associated with hypervigilance and emotional numbing in PTSD and it reflects the function of the left hemisphere, which is related to logical, linguistic operations on information from the senses and the maintenance of high levels of vigilance for changes in stimulation (Brende, 1982). The relationship between hypervigilance and emotional numbing is not very clear. It could be expected that hypervigilance will produce irritability and volatile emotions rather than numbness. However, Brende (1982) asserts that hypervigilance in the left hemisphere could involve lateral inhibition of the emotional processing of the right hemisphere. Conversely, skin conductivity from the left hand reflects the activity of the right hemisphere, which processes or regulates traumatic imagery and its emotional impact in PTSD (Brende, 1982). Thus, skin conductivity may not only indicate the degree of physiological responsiveness to traumatic imagery but also the effective functioning of the left and right hemispheres in the processing of that imagery.
These findings of Pitman et al (1987) and Brende (1982) have interesting implications for the treatment of PTSD. They indicate that skin conductance biofeedback could be useful in the treatment of PTSD. Skin conductivity is easy to monitor and provides an objective indication of the physiological responses to traumatic imagery in any PTSD patient. This biofeedback could help PTSD patients to learn more about their physiological responses and promote the development of better control over those responses and the anxiogenic feedback properties of those physiological responses. The ability to control and reduce anxious physiological responses to traumatic stimuli or imagery could be an important aspect of the process of recovery. For instance, Boudewyns and Hyer (1990) used the physiological assessment technique of Pitman et al (1987) and found that therapeutic reductions in symptoms are associated with decreases in heart rate and especially skin conductance responses to traumatic imagery immediately after therapy. Boudewyns and Hyer (1990) also report that an exposure/flooding therapy reduces heart rate and skin conductance responses to traumatic imagery (see also Fairbank and Keane, 1982; Keane and Kaloupek, 1982; cited in Boudewyns and Hyer, 1990, p. 65). The research of Boudewyns and Hyer (1990) also illustrates that measures of physiological responses to traumatic imagery can be a valuable objective evaluation of therapeutic interventions.
However, the diagnostic utility of physiological discrimination is equivocal, at this stage. Firstly, there is considerable individual overlap between veterans with or without PTSD in their heart rate responses to combat stimuli (Blanchard et al, 1986). The technique of Blanchard et al (1986) can identify 90% of veterans without PTSD, but it can only identify 64% of veterans with PTSD. Gerardi, Blanchard, and Kolb (1989) report that even when veterans without PTSD attempt to elevate their physiological responses, measures of heart rate alone can be used to correctly identify 67% of veterans without PTSD and 89% of veterans with PTSD. Thus, their technique holds some promise of a simple physiological diagnostic indicator for Vietnam veterans, but further refinement is required to achieve higher rates of accuracy in detection of the presence or absence of PTSD and the technique is specific to combat related PTSD, it does not apply to PTSD that results from a variety of other traumatic incidents. Secondly, the flexibility of the technique of Pitman et al (1987) is attractive because it can be applied to PTSD of various origins and it has better sensitivity to combat PTSD than the technique of Blanchard et al (1986) and Gerardi, Blanchard, and Kolb (1989), but the overall discrimination rates achieved for combat veterans with or without PTSD are slightly lower than those found for the latter technique. Further evaluation of both techniques is required, but especially the technique of Pitman et al (1987) since it has not been the subject of much further research. Lastly, but most importantly, the procedures involve the presentation of traumatic stimuli or imagery to trauma surviors and may cause unneccesary psychological distress (Blanchard, Kolb, Pallmeyer, and Gerardi, 1982).
PTSD patients have high cardiovascular activity, including increased heart rates and diastolic and systolic blood pressure, during resting periods of laboratory research (Blanchard et al, 1986; Gerardi, Blanchard, and Kolb, 1989) and before a routine outpatients physical examination (Gerardi, Keane, Cahoon, and Klauminzer, 1994). Furthermore, PTSD patients have often demonstrated a heightened startle response to sudden loud tones, manifest in increased eye blink amplitude, heart rate, and skin conductivity, and diminished habituation of skin conductivity over several tone presentations (Butler, Braff, Rausch, Jenkins, Sprock, Geyer, 1990; Orr, Lasko, Shalev, and Pitman, 1995; Paige, Reid, Allen, and Newton, 1990; Shalev, Orr, Peri, Schreiber, and Pitman, 1992). An exception to these findings is that PTSD patients show no significant startle response to 2 sec of white noise presented at 80 dB (Pallmeyer, Blanchard, and Kolb, 1986). PTSD patients may be less responsive to the white noise, which had a longer duration and a different sound texture, than the sudden tones presented in other studies.
The physiological hyperactivity found in PTSD in these studies cannot be explained as a conditioned response. Shalev et al (1992) and Orr et al (1995) proposed that this physiological hyperactivity in PTSD might reflect a genetic disposition or an acquired sensitivity to autonomic reactivity and a diminished habituation of autonomic responses that could promote conditioned responses to trauma. Furthermore, Gerardi et al (1994) propose that PTSD patients activate a cognitive fear network during any laboratory or hospital visit and that this promotes physiological arousal.
The peripheral physiological response to traumatic or neutral stimulus information is a secondary manifestation of the response to this information. Unless these reactions are a highly learned or automatic reflex response, they must be initiated by cognitive appraisal of the information. In any case, the stimuli will activate cognitive evaluations that play an important role in the impact of these stimuli on psychological and physical health. An assessment of these cognitive responses is an important area of research that is gaining greater interest in recent years.
Combat veterans with PTSD demonstrate anomalies in evoked responses to traumatic images. Attias, Bleich, and Gilat (1996) found a larger N1 and P3 amplitude and a later N1 and P3 in response to rare non-target pictures of combat (20%) presented among rare target pictures of animals (20%) and common pictures of furniture and flowers (60%; see also Attias, Bleich, and Zinger, 1992). Veterans without PTSD had P3 amplitudes for targets that were much larger than those for non-target combat pictures, whereas veterans with PTSD had similar P3 amplitudes for both targets and non-target combat pictures (Attias, Bleich, and Gilat, 1996; Attias, Bleich, and Zinger, 1992). Also, the latency of the P3 in response to combat pictures was positively associated with the frequency of intrusions in veterans with PTSD (Attias, Bleich, and Gilat, 1996). Furthermore, a discriminant function, based on P3 amplitude in response to combat pictures alone, correctly identified 85-90% of veterans with PTSD and 95% of veterans without PTSD (Attias, Bleich, and Gilat, 1996).
These results reflect an early and later attentional sensitivity to threatening information in PTSD. An increase in N1 amplitude reflects an automatic allocation of attentional resources to identification and discrimination of the physical attributes of stimulus information and suggests that PTSD patients are very sensitive to the stimulus attributes of traumatic images (Attias, Bleich, and Gilat, 1996; Attias, Bleich, and Zinger, 1992). An increase in P3 amplitude and P3 latency in response to combat pictures indicates greater attention to the subjective significance or meaning of the traumatic images and a longer duration of attention to those images, which depends on prior exposure and sensitivity to their traumatic content (Attias, Bleich, and Gilat, 1996; Attias, Bleich, and Zinger, 1992). Furthermore, attention to the traumatic images interfered with the capacity to respond to neutral target images (Attias, Bleich, and Zinger, 1992). These results provide tentative support for the hierarchical cognitive action theory of PTSD proposed by Chemtob et al (1988), which postulates that attention to traumatic information diminishes processing of neutral information.
Rauch et al (1996) investigated regional cerebral blood flow (rCBF) in PTSD patients presented with a narrative containing traumatic imagery that was generated and presented according to the technique of Pitman et al (1987). In comparison with a relaxed state, PTSD patients had increased rCBF during traumatic imagery in limbic and paralimbic structures of the right hemisphere, including anterior cingulate, posterior medial orbitofrontal, insular, and anterior and medial temporal cortex, as well as the amygdala (Rauch et al, 1996). A further increase in rCBF was identified in secondary visual cortex and decreases in rCBF were located in left inferior frontal cortex (Broca’s area) and left middle temporal cortex during traumatic imagery (Rauch et al, 1996). These patterns of rCBF during traumatic imagery indicate that the secondary visual cortex is involved in mental imagery and areas of the limbic system in the right hemisphere are activated during the emotional recollection of a traumatic experience (Rauch et al, 1996). Furthermore, traumatic imagery diminishes linguistic activity in Broca’s area, which supports the contention that traumatic memories may be encoded as sensory and emotional elements without linguistic or semantic analysis or encoding (Rauch et al, 1996).
Fig, Liberzon, Steventon, Minoshima, and Koeppe (1995) also investigated rCBF in response to combat sounds in veterans with PTSD. They found increases in rCBF in left and right parahippocampal gyrus, the left striatum, and the upper brain stem. They attibute these findings to (a) an arousal response initiated in the upper brain stem, and (b) activation of traumatic memory networks initiated in the parahippocampal - amygdala region.
Shalev, Attias, Bleich, Shulman, Kotler, and Shahar (1988) found that war veterans with or without PTSD, matched for pure tone audiometry, have similar speech perception thresholds, speech discrimination capacities, and they could equally tolerate an increasing intensity of a continuous series of spoken words without any traumatic content. However, many PTSD veterans showed deficits in both the discrimination of speech from noise presented to the left ear and the ability to selectively attend to a passage presented to the left ear while another louder passage is presented in the right ear (Shalev et al, 1988). Since the information from the left ear projects to the right hemisphere, these deficits could reflect a persistent dominance of the rational, logistic focus of the left hemisphere over the wholistic, imaginative activity of the right hemisphere (Shalev et al, 1988). The dominant left hemisphere information processing bias could reflect the inhibition of persistent traumatic intrusions and emotions that are generated in the right hemisphere or a disconnection of the imaginative or figurative intelligence of the right hemisphere from the linguistic, verbal intelligence of the left hemisphere (Shalev et al, 1988). Moreover, this suppresion of the linguistic transformation of imaginative intelligence could promote a maladaptive displacement or expression of that intelligence in violent impulses or outbursts and psychosomatic disorder (Shalev et al, 1988). For instance, Brende (1982) reports that skin conductivity from the left hand, which reflects the activity of the right hemisphere, is associated with traumatic imagery and its emotional impact in PTSD (Brende, 1982).
Paige et al (1990) found that Vietanam veterans with or without PTSD have different evoked potentials (EPs) to increasing intensity of an auditory tone (i.e., 780 Hz for 500 msec at 74, 84, 94, and 104 dB SPL). Veterans with PTSD decrease P2 amplitude with increasing sound volume, whereas veterans without PTSD increase P2 amplitude with increasing sound volume. This diminution in the P2 amplitude is positively associated with levels of anxiety, but not depression or measures of PTSD symptoms (Paige et al, 1990). The vertex P2 amplitude in response to increasing auditory intensity provided a PTSD:no PTSD discrimination sensitivity of 75% (9 of 12 PTSD veterans), a specificity of 83.3% (5 or 6 non-PTSD veterans), and a positive predictive accuracy of 90% (Paige et al, 1990). Paige et al (1990) argue that the diminution of P2 amplitude in response to intense auditory stimuli reflects a sensitivity to intense stimuli that activates a process of protective inhibition — the nervous system inhibits stimulation that would otherwise overload its capacity for accurate discrimination and pose difficulty dealing with further information. Furthermore, their results indicate that the diminution in P2 amplitude or protective inhibition was prominent in the left temporal area rather than the right temporal area in veterans with PTSD. This could reflect two possibilities: (a) the threshold of overwhelming stimulation is lower in the left hemisphere than in the right hemisphere, or (b) the capacity for inhibition of intense stimulation in the left hemisphere is better than the right hemispere in PTSD veterans.
McFarlane, Weber, and Clark (1993) found that PTSD patients have a slower response time and both later N200 and smaller P300 ERPs for infrequent stimuli in a three tone auditory discrimination task, where the tones were below a starte response threshold (70 dB SPL). A diminution of P300 ERPs in PTSD reflects a difficulty in the evaluation of the significance or relevance of stimulus information (McFarlane, Weber, and Clark, 1993; Charles et al, 1995). This difficulty could be related to an abnormality of catecholamine neurotransmission in PTSD, since catecholamines improve the capacity for attention and discrimination (McFarlane, Weber, and Clark, 1993).
Metzger, Orr, Lasko, and Pitman (1996) recently employed the auditory three tone discrimination task and found diminished P300 amplitude for target stimuli in unmedicated Vietnam veterans with PTSD. However, half of these veterans had comorbid diagnoses of major depression or dysthymia and depression accounted for the observed P300 amplitude abnormality. Furthermore, several unmedicated veterans with PTSD and comorbid panic disorder demonstrated normal P3 amplitudes to targets that were larger than those found in unmedicated veterans with PTSD. It is noteworthy, in this regard, that PTSD patients have diminished noradrenergic function whereas PD patients and PTSD patients with comorbid PD have normal or hyperactive noradrenergic function. Also, there were no ERP abnormalities in another group of medicated Vietnam veterans with PTSD. The medicated veterans with PTSD were taking one or several of a variety of psychoactive substances that affect catecholamines (sertonin, noradrenaline, and dopamine), acetylcholine, or gamma-aminobutyric acid (GABA). Thus, their study highlights (a) the influences of co-morbid diagnoses of depression and panic disorder on information processing in PTSD and (b) that a variety of psychoactive medications are related to normal stimulus evaluation or short-term memory updating in PTSD.
Semple et al (1993, 1995) investigated rCBF in veterans with PTSD and substance-abuse (SA) and age matched controls during an auditory continuous performance task (ACPT). The task required attention to a series of low pitched tones (500 Hz), presented for one second approximately every two seconds, and the discrimination of fifteen 67 dB tones from thirty 75 or 86 dB tones (Semple et al, 1993, 1995). PTSD-SA patients correctly indentified targets, although their d’ measure of attention and detection was lower than that of controls (Semple et al, 1993, 1995). Also, they made more false positive responses (Semple et al, 1993, 1995). PTSD-SA patients had normal rCBF in the right prefrontal cortex, but a lack of a normal increase in rCBF in the angular gyrus of the right parietal cortex in response to the ACPT (Semple et al, 1993, 1995). Furthermore, rCBF in the parietal cortex was positively associated with the accuracy of ACPT performance (Semple et al, 1993, 1995). Also, PTSD-SA patients abstained from substance use for several weeks before the study and the rCBF of PTSD-SA patients was not consistent with findings of rCBF in SA alone, suggesting that the results are due to PTSD more so than SA (Semple et al, 1993, 1995).
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