PubMed Health⌕ Search

Biomedical subjects

Thomas C Neylan

Publications and source records attributed to Thomas C Neylan.

At least 19 recordsLinked to original sources
PubMed2025

Brain dynamics reflecting an intra-network brain state is associated with increased posttraumatic stress symptoms in the early aftermath of trauma.

Post-traumatic stress (PTS) encompasses a range of psychological responses following trauma, which may lead to more severe outcomes such as post-traumatic stress disorder (PTSD). Identifying early neuroimaging biomarkers that link brain function to PTS outcomes is critical for understanding PTSD risk. This longitudinal study examines the association between brain dynamic functional network connectivity (dFNC) and current/future PTS symptom severity, and the impact of sex on this relationship. By analyzing 275 participants' dFNC data obtained ~2 weeks after trauma exposure, we noted that brain dynamics of an inter-network brain state link negatively with current (r=-0.197, p corrected = 0.0079) and future (r=-0.176, p corrected = 0.0176) PTS symptom severity. Also, dynamics of an intra-network brain state correlated with future symptom intensity (r = 0.205, p corrected = 0.0079). We additionally observed that the association between the network dynamics of the inter-network and intra-network brain state with symptom severity is more pronounced in female group. Our findings highlight a potential link between brain network dynamics in the aftermath of trauma with current and future PTSD outcomes, with a stronger effect in female group, underscoring the importance of sex differences.

Journal Article↗
PubMed2006

Increased cortisol in women with intimate partner violence-related posttraumatic stress disorder.

BACKGROUND: Alterations of hypothalamic-pituitary-adrenal (HPA) axis function and sympathetic-adrenal activity have been proposed as key factors in biological models of posttraumatic stress disorder (PTSD). METHODS: We examined neuroendocrine function in female survivors of intimate partner violence (IPV) with lifetime (current or remitted) PTSD (n=29) and in women who were exposed to IPV but never developed PTSD (n=20). Salivary cortisol was collected as a marker of HPA axis function at 1, 4, 9, and 11 h after awakening. Platelet epinephrine and norepinephrine were assayed as markers of sympathetic-adrenal activation. RESULTS: Women with lifetime PTSD had significantly higher cortisol levels across the day compared to abuse-exposed participants without PTSD, after controlling for age, depression, severity, and latency of abuse. There were no significant group differences in levels of platelet catecholamines. CONCLUSIONS: Elevated cortisol levels may be a biomarker of IPV-related lifetime PTSD, reflecting long-lasting changes associated with trauma-exposure or possibly a reflection of risk for PTSD in women.

Adult↗
PubMed2006

Neuropsychological functioning in posttraumatic stress disorder and alcohol abuse.

Studies have shown differences in neuropsychological functioning between groups with posttraumatic stress disorder (PTSD) and control participants. Because individuals with PTSD often have a history of comorbid alcohol abuse, the extent to which an alcohol confound is responsible for these differences remains a concern. The current study compares neuropsychological testing scores in 4 groups of veterans with and without PTSD (PTSD+ and PTSD-, respectively) and with and without a history of alcohol abuse (ETOH+ and ETOH-, respectively): n for PTSD+/ETOH- = 30, n for PTSD+/ETOH- = 37, n for PTSD-/ETOH+ = 30, and n for PTSD-/ETOH- = 31. Results showed that PTSD, when alcohol, educational level, vocabulary, and depression are controlled for, was associated with decreased verbal memory, attention, and processing speed performance. Alcohol abuse history was associated with decreased visual memory performance. By controlling for alcohol and depression, the authors can more conclusively demonstrate that verbal memory and attention differences are associated with PTSD.

Adult↗
PubMed2006

No improvement of posttraumatic stress disorder symptoms with guanfacine treatment.

OBJECTIVE: The authors report an 8-week, double-blind, randomized controlled trial of guanfacine versus placebo for posttraumatic stress disorder (PTSD). METHOD: Veterans with chronic PTSD who were medication-free or receiving stable pharmacotherapy were randomly assigned to guanfacine (N=29) versus placebo (N=34). RESULTS: Guanfacine had no effect on PTSD symptoms, subjective sleep quality, or general mood disturbances. Guanfacine was associated with a number of side effects. CONCLUSIONS: These results do not support the use of alpha 2 agonists in veterans with chronic PTSD.

Adrenergic alpha-Agonists↗
PubMed2006

Neuroendocrine regulation of sleep disturbances in PTSD.

Studies that have conducted quantitative analysis of the sleep electroencephalogram (EEG) have demonstrated decreased delta sleep in PTSD. Elevations in both hypothalamic (neurohormonal) and extrahypothalamic (neurotransmitter) corticotropin releasing factor (CRF) release is associated with decreased delta sleep activity. We present data from several studies examining the effect of metyrapone administration on the sleep EEG in PTSD and control subjects. Plasma ACTH, cortisol, and 11-deoxycorticol were obtained the morning following polysomnographic sleep recordings before and after metyrapone administration. Delta sleep was measured by period amplitude analysis. The results demonstrate: a) decreased delta sleep in male subjects with PTSD; b) metyrapone administration resulted in an activation of the sleep EEG and a robust decrease in quantitative delta sleep; c) the sleep and endocrine (increase in ACTH) responses to metyrapone were significantly decreased in PTSD in two different study samples; and d) the metyrapone-related disruption to sleep in both samples was predicted by the increase in ACTH measured the following morning. These findings strongly suggest that the delta sleep response to metyrapone is a measure of the brain response to a hypothalamic CRF challenge. The attenuated delta sleep and endocrine response to metyrapone challenge in PTSD is consistent with a model of enhanced negative feedback regulation or downregulation of CRF receptors in an environment of chronically increased CRF activity.

Corticotropin-Releasing Hormone↗
PubMed2006

Association between alexithymia and neuroendocrine response to psychological stress in police academy recruits.

Alexithymia has been associated with both posttraumatic stress disorder and neuroendocrine responses to stress. This study examined the relationship of alexithymia to salivary cortisol and 3-methoxy-4-hydroxy-phenylglycol (MHPG) in a sample of police academy recruits exposed to a video stress challenge. Alexithymia scores were negatively associated with catecholamine response to the video challenge but no association was found between alexithymia scores and cortisol reactivity.

Affective Symptoms↗
PubMed2006

Increased cortisol in women with intimate partner violence-related posttraumatic stress disorder.

Intimate partner violence (IPV) is a chronic and recurrent traumatic stressor associated with PTSD; however, its biological correlates are not well understood. This study examined diurnal salivary cortisol and platelet catecholamines in women with lifetime IPV-related PTSD and in women exposed to IPV who did not develop PTSD. Cortisol was elevated in women with lifetime PTSD compared to controls. No differences were found for platelet catecholamines.

Biomarkers↗
PubMed2005

PTSD symptoms predict waking salivary cortisol levels in police officers.

This study examines whether pre- or post-dexamethasone salivary cortisol is related to cumulative critical incident exposure, peritraumatic responses, or post-traumatic stress disorder (PTSD) symptom severity. Thirty active duty police officers completed the study protocol, which included measures of peritraumatic emotional distress, peritraumatic dissociation, duty-related trauma exposure, and PTSD symptoms. Salivary cortisol was consolidated into three outcome variables: (1) pre-dexamethasone free cortisol levels at 1, 30, 45, and 60 min after awakening, (2) post-dexamethasone cortisol levels at the identical wake times, and (3) percentage of cortisol suppression. Control variables included age, gender, average daily alcohol use, night shift work, routine work environment stressors, and salivary dexamethasone levels. Zero order correlations showed that greater levels of PTSD symptoms, peritraumatic distress, and peritraumatic dissociation were associated with lower levels of pre-dexamethasone cortisol levels on awakening, but were not associated with the other two cortisol variables. A trend was also noted for older subjects to have lower pre-dexamethasone cortisol on awakening. When these four predictors were entered simultaneously in a regression analysis, only age and PTSD symptom severity significantly predicted pre-dexamethasone awakening cortisol levels. These results replicate previous research indicating a relationship between greater PTSD symptoms and lower levels of basal cortisol on awakening, and extend this finding to a previously unstudied non-treatment seeking population, urban police.

Adult↗
PubMed2005

Association between childhood trauma and catecholamine response to psychological stress in police academy recruits.

BACKGROUND: Childhood trauma is a risk factor for anxiety disorders in adulthood. One possible mechanism for this association is an increased neuroendocrine response to stress in adults with a history of childhood trauma. METHODS: In a cross-sectional study, 76 police academy recruits (mean [+/-SD] age 28 +/- 5 years, 10 female) were exposed to a video depicting real-life officers exposed to highly stressful incidents. Salivary cortisol and 3-methoxy-4-hydroxy-phenylglycol (MHPG, the major metabolite of norepinephrine) were collected at baseline, immediately after the video, and 20 min after the video. Childhood trauma before age 14 was assessed with an interview (Life Stressor Checklist-Revised). RESULTS: Exposure to the video elicited significant MHPG and cortisol responses in both groups. Recruits with childhood trauma histories (n = 16) had a significantly greater MHPG response, as evidenced by a group effect (F = 8.0, p < .01), and a group x time interaction (F = 4.1, p < .05). The cortisol response did not differ between groups. CONCLUSIONS: Police academy recruits with childhood trauma histories have an increased catecholamine response to psychological stress. This might serve as a risk factor for anxiety disorders in recruits, and these findings might generalize to other groups with a history of childhood trauma.

Adult↗
PubMed2005

A meta-analysis of cortisol response to challenge in human aging: importance of gender.

An increased cortisol response to challenge is associated with a variety of age-related disorders such as Alzheimer's disease, depression, diabetes, metabolic syndrome, and hypertension. Among the healthy elderly, an increased cortisol response to challenge may be a risk factor for developing these age-related disorders. We searched Pubmed, Embase, PsychInfo, Biosis, and Digital Dissertations (January 1966-June 2003) and included 45 parallel-group (young vs. old subjects) studies that used either a pharmacological or psychological challenge in healthy volunteers and measured cortisol response to challenge. We calculated effect sizes (Cohen's d) for the standardized mean differences between groups. Compared to younger controls (n=670, mean age 28 years +/-5), older subjects (n=625, 69+/-6) showed a larger cortisol response to challenge defined as stronger response to stimulation or less inhibition after a suppression test (d=0.42, 95% confidence interval (CI), 0.26-0.57). The effect of age on cortisol release was significantly stronger in women (d=0.65, 95% CI 0.34-0.97) than men (d=0.24, 95% CI 0.02-0.47). Our results demonstrate that aging increases the cortisol response to challenge. This effect of age on cortisol response is almost three-fold stronger in women than men. Prospective studies should explore whether the higher cortisol response in the elderly is a risk factor for developing neuropsychiatric and medical disorders.

Adult↗
PubMed2005

Hypothalamic-pituitary-adrenal axis activity and sleep in posttraumatic stress disorder.

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis and sleep disturbances have been described separately in post-traumatic stress disorder (PTSD). It is not known if HPA alterations and sleep disturbances are associated in PTSD. This study examined sleep and HPA activity in 20 male medication-free subjects with PTSD and 16 matched healthy controls. Two nights of polysomnography were obtained and 24-h urinary cortisol was collected during day 2. Subjects self-administered a low-dose (0.5 mg) salivary dexamethasone test at home. Compared with controls, PTSD subjects had higher 24-h urinary microg cortisol/g creatinine (mean+/-SD 40+/-17 vs 28+/-12, p=0.03) but not significantly higher 24-h urinary cortisol (mean+/-SD 52+/-15 microg/day vs 43+/-23, p=0.19). PTSD subjects showed a trend towards less cortisol suppression after dexamethasone (73%+/-18 vs 83%+/-10, p=0.06). In the combined sample, delta sleep was significantly and negatively correlated with 24-h urinary cortisol (r=-0.36, p=0.04), and with 24-h urinary cortisol/g creatinine on a trend level (r=-0.34, p=0.06). Our results suggest that increased cortisol is negatively associated with delta sleep. This may contribute to sleep abnormalities in conditions associated with elevated cortisol, possibly including PTSD. Future studies should explore the temporal relationship between HPA activity, sleep disturbances, and psychopathology after a traumatic event.

Adult↗
PubMed2005

Depressive symptoms and 24-hour urinary norepinephrine excretion levels in patients with coronary disease: findings from the Heart and Soul Study.

OBJECTIVE: Depressive symptoms are associated with an increased risk of cardiac events in patients with heart disease. Elevated catecholamine levels may contribute to this association, but whether depressive symptoms are associated with catecholamine levels in patients with heart disease is unknown. METHOD: The authors examined the association between depressive symptoms (defined by a Patient Health Questionnaire score > or =10) and 24-hour urinary norepinephrine, epinephrine, and dopamine excretion levels in 598 subjects with coronary disease. RESULTS: A total of 106 participants (18%) had depressive symptoms. Participants with depressive symptoms had greater mean norepinephrine excretion levels than those without depressive symptoms (65 microg/day versus 59 mug/day, with adjustment for age, sex, body mass index, smoking, urinary creatinine levels, comorbid illnesses, medication use, and cardiac function). In logistic regression analyses, participants with depressive symptoms were more likely than those without depressive symptoms to have norepinephrine excretion levels in the highest quartile and above the normal range. Depressive symptoms were not associated with dopamine or epinephrine excretion levels. CONCLUSIONS: In patients with coronary disease, depressive symptoms are associated with elevated norepinephrine excretion levels. Future longitudinal studies are needed to determine whether elevations in norepinephrine contribute to adverse cardiac outcomes in patients with depressive symptoms.

Aged↗
PubMed2005

Comparisons between high and low peritraumatic dissociators in cardiovascular and emotional activity while remembering trauma.

Peritraumatic dissociation (PD) is one of the best predictors of posttraumatic stress disorder (PTSD). In this pilot study, we examined cardiovascular psychophysiology and negative emotions in 19 adults who, retrospectively, reported experiencing high or low levels of PD during the worst trauma of their lives. In a contiguous series of ten-minute phases, they rested, thought about, talked about, and recovered from talking about their index trauma. We hypothesized that greater PD would be associated with more negative emotion, lower cardiovascular activity, and greater discordance between negative emotions and cardiovascular activity. Our main findings were that PD was associated with lower blood pressure prior to talking about the trauma, greater negative emotion while talking about the trauma, and greater emotional and cardiovascular discordance throughout the experiment. These findings add to the very limited empirical data on physiological concomitants of peritraumatic dissociation and may aid in developing preventive interventions for PTSD.

Adult↗
PubMed2004

Attention, learning, and memory in posttraumatic stress disorder.

This study compared attention and declarative memory in a sample of combat veterans with posttraumatic stress disorder (PTSD, n = 24) previously reported to have reduced concentrations of the hippocampal neuronal marker N-acetyl aspartate (NAA), but similar hippocampal volume compared to veteran normal comparison participants (n = 23). Healthy, well-educated males with combat-related PTSD without current depression or recent alcohol/drug abuse did not perform differently on tests of attention, learning, and memory compared to normal comparison participants. Further, hippocampal volume, NAA, or NAA/Creatine ratios did not significantly correlate with any of the cognitive measures when adjustments for multiple comparisons were made. In this study, reduced hippocampal NAA did not appear to be associated with impaired declarative memory.

Alcoholism↗
PubMed2004

Current concepts in pharmacotherapy for posttraumatic stress disorder.

OBJECTIVE: This article describes current approaches to the pharmacologic treatment of posttraumatic stress disorder (PTSD) and reviews the classes of pharmacologic agents used in the treatment of PTSD. Pharmacotherapy for PTSD that is comorbid with other psychiatric disorders is highlighted. METHODS: The primary-source literature was reviewed by using a MEDLINE search. Secondary-source review articles and chapters were also used. Results from studies of the psychophysiology of PTSD are outlined in the review to help inform treatment choices. The review gives more consideration to controlled studies than to open clinical trials. Recommendations for treatment are evidence based. RESULTS AND DISCUSSION: A growing body of evidence demonstrates the efficacy of pharmacologic treatment for PTSD. The effectiveness of the selective serotonin reuptake inhibitors sertraline and paroxetine in large-scale, well-designed, placebo-controlled trials resulted in their being the first medications to receive approval from the U.S. Food and Drug Administration for the treatment of PTSD. Observation of psychophysiologic alterations associated with PTSD has led to the study of adrenergic-inhibiting agents and mood stabilizers as therapeutic agents. Controlled clinical trials with these classes of medication are needed to determine their efficacy for treating PTSD. Finally, the choice of medication for treating PTSD is often determined by the prominence of specific PTSD symptoms and the pattern of comorbid psychiatric conditions.

Antidepressive Agents↗
PubMed2003

Cortisol levels are positively correlated with hippocampal N-acetylaspartate.

BACKGROUND: This study examined the relationship of hypothalamic-pituitary-adrenal measures and hippocampal N-acetylaspartate (NAA) in posttraumatic stress disorder (PTSD) patients and control subjects. METHODS: Eleven patients with combat-related PTSD and 11 control subjects were evaluated with magnetic resonance spectroscopy as well as by morning salivary cortisol samples before and after administration of low-dose dexamethasone (.5 mg). RESULTS: Left hippocampal NAA was strongly associated with both pre-dexamethasone cortisol levels (n = 22, r =.53, p =.013) and post-dexamethasone cortisol levels (n = 22, r =.63, p =.002). After accounting for clinical symptom severity and hippocampal volume, cortisol levels accounted for 21.9% of the variance (F = 5.6, p =.004) in left hippocampal NAA and 12.6% of the variance (F = 3.2, p =.035) in right hippocampal NAA. CONCLUSIONS: This study shows a positive relationship between cortisol levels and hippocampal NAA in subjects without hypercortisolemia. Within the range of values seen in our subjects, cortisol may have a trophic effect on the hippocampus.

Aspartic Acid↗