Initial Posttraumatic Urinary Cortisol Levels Predict Subsequent PTSD Symptoms in Motor Vehicle Accident Victims Douglas L. Delahanty, A. Jay Raimonde, and Eileen Spoonster Background: This study was designed to examine the relationship between urinary hormone levels collected upon admission to the trauma unit following a motor vehicle accident and posttraumatic stress disorder symp- tomatology 1 month later. Methods: Fifteen-hour urine samples were collected from 63 male and 36 female motor vehicle accident victims and were used to assess levels of catecholamines and cortisol reflecting peritraumatic and acute-phase posttraumatic levels. Presence of posttraumatic stress disorder symptom- atology was assessed 1 month after the accident. Results: Motor vehicle accident victims subsequently diagnosed with acute posttraumatic stress disorder ex- creted significantly lower levels of cortisol in 15-hour urines collected upon admission to the hospital. In addi- tion, urinary levels of cortisol predicted a significant percentage of the variance in intrusive and avoidant thoughts 1 month after the accident. Conclusions: The results of our study suggest that initial cortisol levels in the immediate aftermath of a traumatic event contribute, in part, to subsequent symptoms of posttraumatic stress disorder. Biol Psychiatry 2000;48: 940 –947 © 2000 Society of Biological Psychiatry Key Words: Urinary cortisol, posttraumatic stress disor- der, neuroendocrine Introduction T he psychophysiology of posttraumatic stress disorder (PTSD) has been the focus of a number of recent studies, with research indicating that neuroendocrine lev- els may differentiate between those victims who meet PTSD criteria and those who do not. Despite mixed findings (for exceptions, see Lemieux and Coe 1995; Pitman and Orr 1990), the majority of studies have found lower 24-hour urinary cortisol excretion in victims with PTSD compared with victims without PTSD and normal control subjects (Mason et al 1986; Yehuda et al 1990, 1991, 1993, 1995a, 1995b; for a review, see Friedman 1991), suggesting a downregulation of the hypothalamic– pituitary–adrenal (HPA) axis in PTSD. Further support for altered HPA functioning stems from findings of greater numbers of lymphocyte glucocorticoid receptors (Yehuda et al 1991, 1993) and exaggerated dexamethasone (.5mg dose) suppression of cortisol excretion (Halbreich et al 1989; Yehuda et al 1993, 1995) in PTSD patients. Aug- mented adrenocorticotropic hormone response has also been noted after metyrapone treatment (Yehuda et al 1996), leading Yehuda and colleagues to suggest that PTSD is characterized by an enhanced sensitivity of the glucocorticoid negative feedback loop at the pituitary. Studies examining basal catecholamine levels in pa- tients with PTSD also have reported mixed results. Whereas PTSD patients and control subjects do not differ in levels of plasma norepinephrine and epinephrine (Blan- chard et al 1991; McFall et al 1990; Southwick et al 1994), findings concerning 24-hour urinary catecholamine excre- tion have suggested greater catecholamine excretion in PTSD patients versus control subjects (Lemieux and Coe 1995; Kosten et al 1987; Yehuda et al 1992; see Friedman 1991 for a review). The majority of these studies have examined neuroen- docrine levels in chronic PTSD patients who have pre- sented with PTSD for more than 20 years, making con- clusions concerning onset of altered neuroendocrine levels difficult. Determining whether neuroendocrine abnormal- ities reflect altered acute responses to the traumatic stres- sors that persist long after the event or long-term presence of PTSD is impossible. Recent research has attempted to address this issue by examining neuroendocrine levels of trauma victims during the acute phase of responding to traumatic events. Resnick et al (1995) examined plasma cortisol levels within 51 hours after a rape (mean = 12.0  15.6 hours) in 37 adult female victims. Women with prior assault or rape histories demonstrated lower plasma cortisol levels and were more likely to develop PTSD than were women without similar trauma histories; From the Department of Psychology, Kent State University, Kent (DLD), and Summa Health System, Akron (AJR, ES), Ohio. Address reprint requests to Douglas L. Delahanty, Kent State University, Depart- ment of Psychology, 118 Kent Hall, Kent OH 44242. Received November 17, 1999; revised April 12, 2000; accepted April 14, 2000. © 2000 Society of Biological Psychiatry 0006-3223/00/$20.00 PII S0006-3223(99)00896-9