They know their trauma by heart: An assessment of psychophysiological failure to recover in PTSD

Abstract

Background

Posttraumatic stress disorder (PTSD) develops following exposure to atraumatic event and is characterized by persistent intense reactivity to trauma related cues. Equally important, but less studied, is the failure to restore physiological homeostasis after these excessive reactions. This study investigates psychophysiological markers of sustained cardiac activity after exposure to reminders of traumatic event in PTSD patients.

Methods

Participants passively listened to neutral and personal traumatic event while electrocardiogram was continuously recorded. Heart rate (HR) and heart rate variability (HRV) were analyzed in 19 PTSD patients and 16 trauma-exposed controls.

Results

Both PTSD patients and trauma exposed controls exhibited a significant increase in HR to the exposure of their personal trauma. PTSD patients sustained the increase of HR while controls recovered to basal levels. In PTSD patients, sustained HR was positively associated with re-experiencing symptoms. The PTSD group also showed a reduced HRV (a measure of parasympathetic influence on the heart) during personal trauma exposure and lack of recovery.

Limitations

The sample size was small and PTSD patients were under medication.

Conclusions

Our findings provide an experimental account of the failure of PTSD patients to exhibit physiological recovery after exposure to trauma-related stimuli. PTSD patients exhibited a sustained tachycardia with attenuation of HRV that persisted even after cessation of the stressor. Re-experiencing symptoms facilitated engagement in the trauma cues, suggesting that, in their daily-life, patients most likely present repeated episodes of sustained over-reactivity, which may underpin the emotional dysregulation characteristic of PTSD.

Introduction

The diagnostic criteria for posttraumatic stress disorder (PTSD) require experiencing, witnessing, or being confronted with “an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others” (American Psychiatric Association, 1994). Diagnostic criteria also require that the individual experience intense fear, helplessness, or horror during the traumatic event. According to the DSM-IV, the definition of PTSD also includes three symptoms clusters: re-experiencing, avoidance and numbing, and hyperarousal. These symptoms must continue for more than 1 month and must cause significant distress and impairment. PTSD is a chronic illness, and it leads to significant public health consequences; including increased rates of unemployment, marital instability and suicide (Kessler, 2000); impaired role functioning and health problems (Zayfert et al., 2002); cognitive impairments (Mueller-Pfeiffer et al., 2010); and secondary mental disorders, such as substance dependence (Breslau, 2002, Breslau et al., 2003).

PTSD pathology includes an excessive reaction to internal or external cues that resemble the traumatic event. Researchers have provided many relevant pathophysiological insights into PTSD symptomatology using laboratory assessments, which typically employ non-invasive biological recordings related to trauma memories. Autonomic hyperarousal during trauma-related cues has been demonstrated in many different experimental paradigms, including hearing aversive unexpected sounds (Holstein et al., 2010), viewing pictures (Rabe et al., 2006), videos (Hauschildt et al., 2011) or words (Bremner et al., 2003) related to the trauma, or when the subject recounts and/or listens the traumatic event (Cohen et al., 1998, McTeague et al., 2010).

A meta-analysis of the psychophysiology of PTSD (Pole, 2007) showed that patients exhibit an elevated reactivity to external and internal trauma reminders. This striking excess in arousal and reactivity has led most investigators to emphasize biological systems involved in reacting to trauma-related cues. However, PTSD can also be conceptualized as a disorder related to failure of recovery mechanisms impeding the restitution of physiological homeostasis (Yehuda and LeDoux, 2007). Indeed, the meta-analysis by Pole (2007) highlighted that, rather than the reactivity to trauma-related cues, the most robust effect to note in PTSD was the failure to show recovery.

The personal trauma script-driven imagery protocol is widely used to elicit PTSD symptoms. In this paradigm, the participant listens to an autobiographical script and is instructed to mentally relive the event as vividly as possible during and after audio playback (Lang et al., 1980, Pitman et al., 1987). Physiological reactivity during personal threat imagery is significant in PTSD patients as well as in controls (McTeague et al., 2010). A previous study (Volchan et al., 2011) employed passive listening to personal trauma script (without imagery instructions), an experimental condition with more resemblance to real contexts. Volchan et al. (2011) showed that even without imagery instructions the trauma cue triggered a last-ditch defense response (tonic immobility) following the end of audio play in a larger proportion of PTSD patients than in trauma-exposed controls. The authors raised the possibility that re-experiencing symptoms was responsible for the different and sustained engagement of patients, relative to controls, following exposure to trauma cues without imagery instructions.

The aim of the present study is to investigate the psychophysiological markers of sustained cardiac activity after exposure to reminders of the traumatic event in PTSD patients. For this purpose, we contrasted the cardiac activity of trauma-exposed victims with and without PTSD, both during and after presentation of their personalized trauma script without imagery instructions. We hypothesized that PTSD patients would show more cardiac reactivity than controls during exposure to their trauma script and, most importantly, we hypothesized that patients would sustain this high reactivity after exposure, while controls would recover. Furthermore, we speculated that re-experiencing symptoms would be critical for the sustained reactivity in PTSD patients.