Psychosomatic Medicine 66:760-761 (2004)
© 2004 American Psychosomatic Society
Elevated Resting Heart Rate as a Predictor of Posttraumatic Stress Disorder After Severe Traumatic Brain Injury
Richard A. Bryant, PhD,
Jeno E. Marosszeky, MB BS,
Jenelle Crooks, RN and
Joseph A. Gurka, MB BS
From the School of Psychology, University of New South Wales, New South Wales, Australia; and the Department of Rehabilitation Medicine, Westmead Hospital, Sydney, Australia.
Address correspondence and reprint requests to Richard A. Bryant, PhD, School of Psychology, University of New South Wales, NSW, 2052, Australia. E-mail: r.bryant{at}unsw.edu.au
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ABSTRACT
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OBJECTIVE: This study indexed the relationship between resting heart rates (HRs) after injury and subsequent posttraumatic stress disorder (PTSD) in patients who sustained severe traumatic brain injury (TBI).
METHODS: Patients who sustained a severe TBI (N = 68) had their resting HR assessed 1 week and 1 month after injury, and they were assessed for PTSD 6 months after injury with the PTSD Interview, a structured clinical interview based on the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised.
RESULTS: PTSD was diagnosed in 23% of patients. PTSD participants had higher HRs at 1 week but not at 1 month after trauma than non-PTSD participants. This difference remained significant when the effect of posttraumatic amnesia was controlled, but it was not significant when the effect of Glasgow Coma Scale was controlled.
CONCLUSION: These findings accord with the proposal that fear conditioning can occur outside the level of awareness and contribute to PTSD development.
Key Words: posttraumatic stress disorder, • traumatic brain injury, • heart rate, • fear conditioning.
Abbreviations: PTSD = posttraumatic stress disorder;; HR = heart rate;; TBI = traumatic brain injury;; PTA = posttraumatic amnesia;; GCS = Glasgow Coma Scale;; PTSD-I = Posttraumatic Stress Disorder Interview;; SD = standard deviation.
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INTRODUCTION
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Fear conditioning models of posttraumatic stress disorder (PTSD) posit that arousal at the time of the trauma releases stress hormones (including norepinephrine and epinephrine) that subsequently lead to an overconsolidation of trauma memories (1,2). Consistent with the fear conditioning model, there is evidence that resting heart rates (HR) in the initial week after trauma exposure is higher in people who subsequently develop PTSD than in those who do not develop PTSD (3,4). One recent study reported that patients who sustain a severe traumatic brain injury (TBI) and are fully amnesic of their trauma could develop PTSD (5). This study found that PTSD patients experienced distress in response to reminders of the trauma, even though they could not recall the trauma itself. One possible explanation for this development is that fear conditioning occurred in the absence of awareness of the trauma. Animal and human research indicate that fear conditioning is located within the amygdala (6,7) and raises the possibility that PTSD may occur in these individuals at subcortical levels. To test this possibility, this study indexed the resting HR in the acute phase of the patients reported in the initial study of patients with PTSD after severe TBI (5). Fear conditioning models would predict that patients who developed PTSD should have higher resting HRs in the immediate period after trauma, despite amnesia of the event.
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METHODS
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Subjects
Over a 36-month period, 161 patients were admitted to a brain injury rehabilitation unit. Attempts were made to assess each patient 6 months after hospital discharge. Patients were not included because of inability to speak English (n = 4), insufficient cognitive ability to understand the interview (n = 22), refusal to participate (n = 27), inability to contact patient (n = 12), and absence of HR data from medical records (n = 28). Thus, 68 (54 males, 14 females) adults who had sustained severe TBI as a result of motor vehicle accidents (n = 48), industrial accidents (n = 8), or assaults (n = 12) were included in the study. Table 1 presents the patient characteristics for PTSD and non-PTSD patients. The duration of posttraumatic amnesia (PTA) was established with the Westmead PTA Scale (8). Severity of loss of consciousness was assessed using the Glasgow Coma Scale (GCS) score. The mean PTA and GCS scores indicate that the average level of TBI was very severe and that on average these patients had little recall for events that occurred in the initial month posttrauma. After a complete description of the study to the patients, written informed consent was obtained.
Procedures
Patients were interviewed by a rehabilitation consultant who was trained in the assessment procedures by the first author. Diagnosis of PTSD was made by using the Posttraumatic Stress Disorder Interview (PTSD-I) (9). The PTSD-I is based on the criteria of the Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition, Revised, and has good construct validity (sensitivity = 0.92) and test-retest diagnostic agreement (
value, r = 0.61). Dissociative amnesia was excluded as a possible symptom of PTSD because of the confound between dissociative amnesia and TBI-related amnesia. Additional information was obtained from medical records, including age, duration of PTA, duration of hospital stay, and GCS score. Treating physicians or nursing staff that were unaware of patients’ PTSD status manually recorded resting HR on a 6-hourly basis during hospital admission. HR was sampled continuously for 1 minute as the patient lay in a hospital bed and was subsequently recorded in the patient’s medical record as beats per minute. To achieve comparability with previous HR studies (3,4), this study indexed HR approximately 1 week after trauma and 1 month after trauma. To increase the reliability of indexing resting HR, three 1-minute periods were sampled at 6-hourly periods, and the average of these three measures was calculated to obtain mean resting HR values.
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RESULTS
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The 68 patients who participated in the 6-month assessment did not differ from the 93 who did not participate in terms of age, years of education, or PTA. Nonparticipants (mean = 5.48, standard deviation [SD] = 3.62) had lower GCS scores than those who participated (mean = 8.00, SD = 3.78, t [124] = 2.96, p < .01).
PTSD was diagnosed in 23% (n = 16) of patients. Table 1 presents the mean HR data of PTSD and non-PTSD patients. A planned comparison of HR between PTSD and non-PTSD patients indicated that patients with PTSD had higher resting HR approximately 9 days after trauma than patients who did not develop PTSD (t [66] = 2.03, p < .05). To determine the influence of loss of consciousness and length of amnesia on HR levels, these analyses were repeated by entering each variable as a covariate. Although covarying for PTA did not alter the group difference (t [66] = 4.19, p < .05), the difference was not significant when controlling for GCS score (t [66] = 1.39, p = .24). There was no difference in resting HR between groups at 1 month after injury (t [66] = 0.52, p = .65).
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DISCUSSION
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The finding that PTSD patients had higher HR levels than non-PTSD patients is consistent with previous reports (3,4), although it contrasts with another report that found that PTSD patients had lower initial HR levels than non-PTSD patients (10). The intriguing aspect of the current finding is that PTSD patients were amnesic of their trauma, and they only met criteria for PTSD because, despite no intrusive memories or nightmares of the trauma, they reported psychological distress or physiological reactivity in response to trauma-related cues. One interpretation of this finding is that these patients experienced fear conditioning at a level that did not require awareness of the trauma experienced. The conditioned fear response involves the central nucleus of the amygdala stimulating sympathetic activation, which can be reflected in increased HR and need not involve cortical regions associated with conscious awareness (11). The finding that group differences disappeared when GCS score was controlled for suggests that dense loss of consciousness may limit the role of HR in PTSD development. Alternately, it is possible that more intense coma may limit the likelihood of subsequent PTSD, and that HR may predict PTSD because it is negatively related to coma intensity. This possibility is underscored by the negative correlation between GCS and HR (r = –0.36, p < .01). Overall, these data may suggest that fear-conditioned responses during trauma can occur in the absence of awareness. The absence of a difference 1 month after trauma accords with one previous prospective study of HR and PTSD (3) and is consistent with evidence of a lack of elevated baseline HR in chronic PTSD (12). It is possible that adrenergic activation in the acute rather than the chronic phase is important in the overconsolidation of trauma memories and the contribution to subsequent PTSD.
Inferences from this study are limited in a number of ways. First, HR was collected via medical records rather than through tightly controlled experimental conditions. Second, the sample was not consecutive and may not be representative of brain injury patients. Third, the possibility that participants had learned about their traumas through indirect means (e.g., conversations with others, photographs) may have provided them with some awareness of what had occurred. Fourth, the small sample size and limited data that was collected precluded studying the possibility that other baseline factors that correlated with HR may have contributed to PTSD development. Finally, the absence of any neuroimaging data precludes firm inferences concerning the neural pathways associated with fear conditioning in these patients. These pilot data do suggest, however, that patients who sustain severe TBI may represent an interesting population in which to study the mechanisms of fear conditioning in neural networks that do not involve awareness.
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ACKNOWLEDGMENTS
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This research was supported by a National Health and Medical Research Council Program Grant.
Received for publication April 4, 2004.
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ABSTRACT
INTRODUCTION
