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ABSTRACT: Previous studies of adults with posttraumatic stress disorder (PTSD) have found various abnormalities in the regulation of the hypothalamic-pituitary-adrenal axis, including enhanced suppression of cortisol following low-dose dexamethasone. The purpose of the present study was to investigate salivary cortisol responses to low-dose dexamethasone in adolescents with PTSD.
Forty-eight adolescents (20 with current PTSD, 9 trauma controls without PTSD, and 19 healthy nontraumatized controls) were enrolled in the study. On day 1, baseline saliva samples were obtained at 8 a.m. and 0.5 mg of dexamethasone was administered at 11 p.m. Cortisol and dexamethasone levels were assessed at 8 a.m. the following day.
Adolescents with current PTSD showed no difference in the suppression of salivary cortisol in response to low-dose (0.5 mg) dexamethasone compared to trauma controls without PTSD and nontraumatized controls. More severely affected PTSD subjects with co-occurring major depression showed higher pre- and post-dexamethasone salivary cortisol levels compared to controls.
The present study did not find evidence for enhanced suppression of salivary cortisol at 8 a.m. following low-dose dexamethasone in multiply traumatized adolescents with PTSD. This result differs from findings in adults with PTSD. Further investigations of hypothalamic-pituitary-adrenal axis abnormalities in traumatized children and adolescents are needed.
Journal of the American Academy of Child & Adolescent Psychiatry 12/2003; 42(11):1310-7. · 6.44 Impact Factor
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Journal of Nervous & Mental Disease 05/2003; 191(4):261-2. · 1.68 Impact Factor
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ABSTRACT: Alexithymia was measured in non-treatment seeking, community-dwelling Holocaust survivors using the Toronto Alexithymia Scale—Twenty Item Version (TAS-20). Scores of survivors with (n = 30) and without (n = 26) posttraumatic stress disorder (PTSD) were compared, and associations among alexithymia, severity of trauma, and severity of PTSD symptoms were determined. Survivors with PTSD had significantly higher scores on the TAS-20 compared to survivors without PTSD. TAS-20 scores were significantly associated with severity of PTSD symptoms, but not with severity of trauma. This study adds to our knowledge of the relationship between alexithymia and trauma by demonstrating that this characteristic is related to the presence of posttraumatic symptoms and not simply exposure to trauma.
Journal of Traumatic Stress 12/1996; 10(1):93-100. · 2.72 Impact Factor
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ABSTRACT: The present study was designed to explore several aspects of depressive phenomenology, including current symptoms, dependency (anaclitic) and self-criticism (introjective) themes, and issues of self-efficacy, in Holocaust survivors with and without posttraumatic stress disorder (PTSD). The Depressive Subscale of the Symptom Checklist-90 (SCL-90) and the Depressive Experiences Questionnaire (DEQ) were administered to 23 Holocaust survivors and 18 demographically-matched controls. Holocaust survivors with PTSD scored significantly higher on the SCL-90 depression scale, and portrayed more self-criticism on the DEQ, than Holocaust survivors without PTSD and demographically-matched non-exposed subjects. The data suggest that depressive symptoms in individuals who have been severely traumatized are more severe when associated with a concurrent PTSD. Furthermore, groups suffering different types of trauma may show similarities in psychological dimensions of depression.
Journal of Traumatic Stress 01/1994; 7(4):699-704. · 2.72 Impact Factor
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ABSTRACT: Neuroendocrine studies examining the hypothalamic-pituitary-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore, in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiology of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to different mechanisms of action for cortisol and its regulatory factors.
Biological Psychiatry 12/1991; · 8.28 Impact Factor
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ABSTRACT: Eight male alcoholic inpatients in their 2nd week of treatment were presented with, and instructed to consume, a beverage described at one session as containing alcohol and at another as not containing alcohol. The beverage on each occasion did not, in fact, contain alcohol. The results indicated that when subjects believed they had consumed alcohol, the change in insulin from baseline was significantly greater at 10, 20, and 30 min following consumption. The findings suggest that the insulin response of alcoholics following ingestion of a carbohydrate-containing beverage is enhanced by the anticipation of ethanol.
Alcoholism Clinical and Experimental Research 10/1991; 15(6):1001 - 1006. · 3.34 Impact Factor
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ABSTRACT: Platelet monoamine oxidase (MAO) activity was significantly lower in nonpsychotic, nonorganic, unmedicated male inpatients with DSM-III-R borderline personality disorder (BPD) than in nonpsychiatric controls. Patients with BPD who also met DSM-III-R criteria for antisocial personality disorder had significantly lower MAO activity than those with BPD alone. Low MAO activity in this sample did not appear to be related to the comoroid presence of major depressive disorder or a history of substance abuse.
Psychiatry Research 01/1990; · 2.52 Impact Factor
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ABSTRACT: Platelet α2-adrenergic receptor binding sites were measured in a group of patients with major depressive disorder (MDD) (n = 23) and in normal controls (n = 25). When all depressed subjects were compared to controls, there were no differences in either Kd (affinity of the ligand) or total binding site (number/platelet), although a significant change in the ratio of high to low affinity states was observed in the depressed group. When the depressed patients were subdivided into those with and without a co-occuring borderline personality disorder (BPD), the BPD group had significantly fewer α2 high affinity binding sites, while the group with depression alone had significantly more binding sites (both low and high affinity) than the control group. The results support the concept that assessment of comorbid diagnoses may be essential to biological studies of depression.
Psychiatry Research.
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ABSTRACT: The objective of this study was to obtain longitudinal data on lability of cortisol levels in posttraumatic stress disorder (PTSD) because previous studies have largely been based on sampling at a single time point and have yielded varying results.
This study measured urinary cortisol levels at admission, midcourse, and discharge during a 90-day hospitalization period in male Vietnam combat veterans with PTSD (N = 51).
Although there were no significant differences in the mean +/- SEM urinary cortisol levels between the admission (59.4 +/- 3.0 microg/d), midcourse (55.6 +/- 3.9 microg/d), and discharge (53.4 +/- 3.4 microg/d) values, marked lability of cortisol levels in individual patients was observed over time, with changes ranging from +93 to -58 microg/d from admission to midcourse. In addition, this hormonal lability defined discrete subgroups of patients on the basis of the longitudinal pattern of cortisol change during exposure treatment, and there were significant psychometric differences in the level of social functioning between these subgroups.
The findings do not support the concept of either a static "hypocortisolism" or "hypercortisolism" in PTSD, but rather suggest a psychogenic basis for cortisol alterations in PTSD in relation to psychosocial stress and indicate a central regulatory dysfunction of the hypothalamic-pituitary-adrenal axis characterized by a dynamic tendency to overreact in both upward and downward directions. The longitudinal findings fit with recent observations that cortisol elevations occur when acutely superimposed stressful conditions emotionally engage patients and overwhelm the usually dominating disengaging coping mechanisms associated with suppression of cortisol levels in PTSD. The findings emphasize the importance of longitudinal data in studies of the hypothalamic-pituitary-adrenal axis in PTSD.
Psychosomatic Medicine 64(2):238-46. · 3.97 Impact Factor
