Trauma and Stressor Related Disorders and Disasters
John A. Leman, M.S.
PhD Student
Northeastern University
Roslindale, Massachusetts, United States
Emily Mintz, B.A.
Clinical Research Coordinator
Massachusetts General Hospital
Roslyn, New York, United States
Donald Robinaugh, Ph.D.
Assistant Professor
Northeastern University
Boston, Massachusetts, United States
Emma R. Toner, M.A.
Clinical Psychology PhD Student
University of Virginia
Charlottesville, Virginia, United States
Alexa Skolnik, B.A.
Graduate Student
University of Toledo
Ottawa Hills, Ohio, United States
Scott P. Orr, Ph.D.
Senior Investigator & Associate Professor of Psychology, Department of Psychiatry
Harvard Medical School
Charlestown, Massachusetts, United States
Naomi M. Simon, M.D., Other
Professor of Psychiatry
NYU School of Medicine
New York, New York, United States
Background
Prolonged Grief Disorder (PGD) is a bereavement-specific syndrome characterized by persistent, distressing and impairing grief. There are several lines of evidence implicating heightened autonomic reactivity in the phenomenology of PGD. Most notably, PGD is commonly conceptualized as a stress response syndrome like post-traumatic stress disorder (PTSD). PTSD is characterized by heightened autonomic reactivity to both trauma-related stimuli and to unconditioned startling stimuli (e.g., loud tones). Given the shared conceptual frameworks, frequent comorbidity, and syndromic overlap between PTSD and PGD, we investigated whether autonomic reactivity to loud tones was similarly elevated in those with PGD.
Methods Bereaved adults with (n=28) and without (n=26) elevated PGD symptoms—according to the Inventory of Complicated Grief ( >=30)—completed the Loud Tones procedure, a well-established assessment of startle response that has been used in clinical studies of PTSD. In this procedure, participants’ heart rate (HR), skin conductance response (SC), and left orbicularis oculi (EMG) were assessed in response to the delivery of fifteen loud tones (95-dB, 1000-Hz pure tones for 500-ms at random intervals through headphones). From this task, we derived three response outcomes (one each for HR, SC, and EMG) reflecting mean change from pre-to-post-tone. In addition, we derived two habituation indices for both SC and EMG: (1) the number of trials prior to reaching two successive nonresponse trials and (2) the slope of the regression line where square root of the response score is regressed on the log trial number (rate of habituation). Results We found no difference between groups for six of our seven outcomes (ts< =1.67, ps >=.09). The obicularis rate of habituation was faster in those without elevated PGD (M=-1.75) than in those with elevated PGD (M=-1.15), t(44) = -2.09, p=.04. However, this finding should be interpreted with caution due to the inflated Type 1 error from multiple comparisons as well as the absence of group differences for other indices of habituation. Discussion Our results fail to provide strong support for the notion that startle response is potentiated in those with PGD. Accordingly, despite the frequent comorbidity and syndromic similarities of PTSD and PGD, our results suggest that the mechanisms underlying these conditions may be distinct. Importantly, our study only examined whether PGD was characterized by heightened reactivity to startling stimuli. In future research, it will be important to investigate whether those with PGD exhibit elevated autonomic reactivity to grief-related cues, as this reactivity may be important to understanding the somatic sensation-laden experiences (e.g., “waves” of grief) described by those with PGD.