Hypothalamic–Pituitary–Adrenal Axis Activity and Sleep in Posttraumatic Stress Disorder (original) (raw)
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Background: Nightmares and insomnia in PTSD are hallmark symptoms, yet poorly understood in comparison to the advances toward a biological framework for the disorder. According to polysomnography (PSG), only minor changes in sleep architecture were described. This warrants alternative methods for assessing sleep regulation in PTSD. Methods: After screening for obstructive sleep apnea and period limb movement disorder, veterans with PTSD (n = 13), trauma controls (TCs, n = 17) and healthy controls (HCs, n = 15) slept in our sleep laboratory on two consecutive nights with an IV catheter out of which blood was sampled every 20 min from 22:00 h to 08:00 h. Nocturnal levels of plasma adrenocorticotropic hormone (ACTH), cortisol, melatonin were assessed in conjunction with PSG registration, as well as subjective sleep parameters. Results: PTSD patients showed a significant increase in awakenings during sleep in comparison to both control groups. These awakenings were correlated with ACTH levels during the night, and with the subjective perception of sleep depth. Also, heart rate (HR) was significantly increased in PTSD patients as compared with both control groups. The diurnal regulation of ACTH, cortisol and melatonin appeared undisturbed. PTSD patients exhibited lower cortisol levels at borderline
Neuroendocrine Regulation of Sleep Disturbances in PTSD
2006
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.
Psychoneuroendocrinology, 2017
Disturbed sleep is a core feature of posttraumatic stress disorder (PTSD), characterized in part by decreased delta power sleep that may result from stress-related alterations in corticotropin releasing factor (CRF), hypothalamic pituitary adrenal axis (HPA) regulation and glucocorticoid signaling. Overnight HPA axis response mediating sleep disturbances in men and women with PTSD was examined using a metyrapone challenge. Metyrapone blocks cortisol synthesis, removing negative feedback, and increases the release of hypothalamic CRF and pituitary adrenocorticotropic hormone (ACTH). Laboratory-based polysomnography was used to monitor the sleep of 66 medically healthy, medication-free men and pre-menopausal follicular phase women including 33 with chronic PTSD (16 women and 17 men) and 33 age- and sex-matched controls (14 women and 19 men) over 3 consecutive nights. Participants completed an overnight metyrapone challenge after an adaptation and baseline night of sleep and ACTH was o...
Nocturnal/daytime urine noradrenergic measures and sleep in combat-related PTSD
Biological Psychiatry, 1995
In association with sleep recording, subjects saved their urine for 24 hours in three 8-hour collections in order to obtain "daytime" (8:00 AM to 4-00 PM, 4-00 P M tO MN) and "nocturnal" (MN to 8:00 AM) catecholamine measures. PTSD patients had decreased sleep efficiency relative to controls and increased REM density; 24-hour norepinephrine and MHPG (the more centrally derived metabolite ) did not differ between patients and controls. "Nocturnal" excretion of MHPG minus the average of the two "daytime" values was negative in the controls, slightly' positive in the patients, and differed significantly between the two groups. "Nocturnal minus daytime" MHPG also correlated negatively with total sleep time in the PTSD patients (R = -.45, p < .05). Our data support a relationship of nondiminished central noradrenergic activity at night, and sleep disturbance, in chronic', combat-related PTSD.
Implications of Hypothalamic-Pituitary-Adrenal Axis Functioning in Posttraumatic Stress Disorder
Journal of the American Psychiatric Nurses Association, 2011
BACkgrounD: Cortisol secretions serve as the barometer of the hypothalamic-pituitary-adrenal (HPA) axis, which regulates and controls responses to stress. Studies of cortisol secretions in patients with posttraumatic stress disorder (PTSD) reveal inconsistent results. PurPoSe: Current research on HPA axis functioning in PTSD is examined to elucidate the neuroendocrine contributions in the disorder, identify current treatment's impact on the HPA axis, and consider implications for nursing care and areas for future research. FInDIngS: There is evidence for HPA dysregulation in PTSD, which contributes to widespread impairment in functions such as memory and stress reactivity and to physical morbidity via processes such as allostatic load. There is limited, but building, evidence that dehydroepiandrosterone (DHEA), which is released simultaneously with cortisol, may provide anti-glucocorticoid and neuroprotective effects. ConCluSIon: Current treatments such as selective serotonin reuptake inhibitors and psychotherapy may have a beneficial impact on the HPA axis in PTSD populations. Somatic approaches to treating PTSD have not yet been studied in relation to their impact on HPA axis parameters in PTSD patients. Treatment studies of DHEA or glucocorticoids have not yet used HPA axis endpoints. PTSD treatment studies that include measures of HPA axis target mechanisms and consider HPA axis regulation as an additional treatment outcome are warranted.
Sensitization of the Hypothalamic-Pituitary-Adrenal Axis in Posttraumatic Stress Disorder
Annals of the New York Academy of Sciences, 1997
Posttraumatic stress disorder (PTSD) is a psychiatric condition that can occur in individuals who have experienced traumatic events. The symptoms of PTSD were initially conceptualized as reflecting a natural process of adaptation to extraordinarily adverse life event~.l-~ However, in recent years prevalence studies have clarified that PTSD only occurs in a percentage of those exposed to trauma."' Furthermore, among trauma survivors who develop this disorder, a substantial proportion appear to show full remission of their symptoms over time.6 This observation demonstrates that chronic PTSD represents a specific type of adaptation to trauma, which may not necessarily reflect typical or even normative stress responsiveness.1°
A Multidimensional Approach to Post-Traumatic Stress Disorder - from Theory to Practice, 2016
Stress-induced alterations in sleep have been linked to the development of posttraumatic stress disorder (PTSD) and sleep complaints and disturbances in arousal are continuing symptoms in patients. PTSD-related changes in sleep have not been fully characterized but involve persistent disturbances in both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS). PTSD is considered a disorder of the fear circuitry, which includes the amygdala, dorsal anterior cingulate, hippocampus, and ventromedial prefrontal cortex. Currently, several animal models are used to examine the underlying neurobiology of PTSD; however, sleep has been characterized in only a limited number of models. Intense conditioned fear training, which may best model PTSD in rodents, can produce reductions in REMS as well as alterations in NREMS that may vary with mouse and rat strains. The amygdala, a central region in current concepts of PTSD, plays significant roles in regulating the stress response and changes in stress-induced alterations in arousal and sleep. This chapter reviews sleeprelated findings in patients with PTSD and in animal experimental paradigms currently utilized to model the disorder, as well as the neurobiology that has been linked to disturbed sleep in PTSD. It will also discuss the impact of PTSD treatments on sleep disturbances.
Sleep and posttraumatic stress disorder: a review
Clinical Psychology Review, 2003
Research seeking to establish the relationship between sleep and posttraumatic stress disorder (PTSD) is in its infancy. An empirically supported theory of the relationship is yet to emerge. The aims of the present paper are threefold: to summarise the literature on the prevalence and treatment of sleep disturbance characteristic of acute stress disorder (ASD) and PTSD, to critically review this literature, and to draw together the disparate theoretical perspectives that have been proposed to account for the empirical findings. After a brief overview of normal human sleep, the literature specifying the relation between sleep disturbance and PTSD is summarized. This includes studies of the prevalence of sleep disturbance and nightmares, content of nightmares, abnormalities in rapid eye movement (REM) sleep, arousal threshold during sleep, body movement during sleep, and breathing-related sleep disorders. In addition, studies of the treatment of sleep disturbance in individuals with PTSD are reviewed. We conclude that the role of sleep in PTSD is complex, but that it is an important area for further elucidating the nature and treatment of PTSD. Areas for future research are specified. In particular, a priority is to improve the methodology of the research conducted.
Sleep parameters improvement in PTSD soldiers after symptoms remission
Scientific Reports, 2021
Eye movement desensitization and reprocessing (EMDR) is a psychotherapy for the treatment of posttraumatic stress disorder (PTSD). It is still unclear whether symptoms remission through EMDR therapy is associated with a beneficial effect on one of the PTSD symptoms, sleep disturbance. Our objective was therefore to study sleep parameters before and after symptom remission in soldiers with PTSD. The control group consisted of 20 healthy active duty military men who slept in a sleep lab with standard polysomnography (PSG) on two sessions separated by one month. The patient group consisted of 17 active duty military with PTSD who underwent EMDR therapy. PSG-recorded sleep was assessed 1 week before the EMDR therapy began and 1 week after PTSD remission. We found that the increased REMs density after remission was positively correlated with a greater decrease of symptoms. Also, the number of EMDR sessions required to reach remission was correlated with intrasleep awakenings before treatment. These results confirm the improvement of some sleep parameters in PTSD after symptoms remission in a soldier's population and provide a possible predictor of treatment success. Further experiments will be required to establish whether this effect is specific to the EMDR therapy. Abbreviations EMDR Eye movement desensitization and reprocessing PSG Polysomnography PTSD Posttraumatic stress disorder TST Total sleep time SPT Sleep period time SOL Sleep onset latency REM Rapid eye movement SE Sleep efficiency SME Sleep maintenance efficiency WASO Wake after sleep onset Sleep disturbances represent a key factor in the genesis and maintenance of psychiatric disorders 1. An estimated 90% of people with posttraumatic stress disorder (PTSD) report difficulty initiating and maintaining sleep 2,3. Even in the absence of nightmares, sleep problems remain the most frequently reported complaint in PTSD 4. Self-reported poor sleep quality is only minimally explained by psychiatric comorbidity, age, and sex in these patients, which suggests an important role of the syndrome in the sleep impairment 5. The severity of PTSD symptoms are positively correlated with sleep disturbances 6. Sleep problems may in turn worsen daytime PTSD symptoms 7 , and contribute to comorbid psychiatric disorders such as major depression 8-11 , suicidal behaviour 12 , and substance abuse 13. Sleep disturbances in PTSD are also correlated with a decreased