Milena Mortara
Cecilia Riccardi
Posttraumatic stress disorder (PTSD) is a psychiatric condition that develops in some individuals after experiencing events involving threat of injury, physical integrity or death. PTSD consists of three clusters of symptoms:
1- re-experiencing (eg recurrent nigthmares about trauma, flashbacks...)
2- avoidance (eg avoindance of trauma reminders...)
3- hyperarousal (eg insomnia, hypervigilance...)
Individuals with PTSD are at greater risk for other mental and physical health problems, including suicidal behaviors, cardiovascular diseases and gastrointestinal diseases.
Experiencing negative feelings as “fear, helplessness or horror” is believed to be a cause of PTSD. Sources of such feelings are, for axample: physical, emotional or sexual abuse, drug addiction, medical complication. Nowadays PTSD symptoms are typical in individuals with occupations exposed to war or disaster.
NEUROENDOCRINOLOGY
PTSD symptoms result when a traumatic event causes an over-reactive adrenaline response. Adrenaline creates deep neurological patterns that can persist long after the event that triggered the fear. Prolonged exposure to stress (“long-term sensitization”) can make an individual hyper-responsive to future fearful situations.
PTSD is associated with low secretion of cortisol and high secretion catecholamines, with a norepinephrine/cortisol ratio higher than normal. This is in contrast to the normative fight-or-flight response, in which both catecholamines and cortisol are elevated. The strong cortisol suppression suggests abnormality in the hypotalamic-pituitary-adrenal axis.
Cortisol stimulates gluconeogenesis (formation, in the liver, of glucose from certain amino acids, glycerol, lactate and/or propionate) and it activates anti-stress and anti-inflammatory pathways. It downregulates the Interleukin-2 receptor (IL-2R) on "Helper" (CD4+) T-cells. This results in a decrease in B-cell antibody production and in the the release of substances in the body that cause inflammation.
Cortisol plays an important role in glycogenolysis, the breaking down of glycogen to glucose-1-phosphate and glucose, in liver and muscle tissue. Glycogenolysis is stimulated by epinephrine and/or norepinephrine, however cortisol facilitates the activation of glycogen phosphorylase, which is essential for the effects of epinephrine on glycogenolysis. The final result is an increasing production of ATP.
Low cortisol levels may predispose individuals to PTSD. Swedish soldiers serving in Bosnia-Herzegovina with low pre-service salivary cortisol level had a higher risk of reacting with PTSD symptoms following war trauma, than soldiers with normal pre-service levels. According to recent studies, early interventions such low-dose cortisol administration and propanolol treatment immediately after trauma exposure may have positive effects. We may suppose that an increased intracellular ATP, due to cortisol, could have protective effects. Therefore any condition that causes a decrease of ATP levels - such as hypoxia, iron or Q-coenzyme deficiency – may predispose to the development of the disease, combined with a severe stress or trauma.
Salivary cortisol, posttraumatic stress symptoms, and general health in the acute phase and during 9-month follow up, 2001
NEUROANATOMY
Two areas of the brain have been identified as altered in PTSD: amygdala and hyppocampus. Combat veterans of the Vietnam war with PTSD showed a 20% reduction in the volume of their hyppocampus compared with veterans who suffered no such symptoms. The hyppocampus is associated with the ability to plays memories in the correct contest of space and time, and with the ability to recall the memory; during high stress times its activity in suppressed. This suppression in hypothesized to be the cause of the flashbacks that often plaugue PTSD patientts.
Amygdala has been shown to be strongly involved in the formation of emotional fear-related memories; in PTSD it is associated with hyperarousal.
SLEEP IN PTSD
Impaired sleep is a common complaint among patients with PTSD. Sleep disturbance seems to be a core feature, and sleep disruption following a traumatic event may constitute a specific mechanism involved in the patophysiology of cronic PTSD.
38 to 73% of individuals with PTSD across studies reported experiencing recurrent nightmares about trauma, whereas only 6 to 12% of trauma-exposed individuals without PTSD reported having nightmares. Prospective studies showed that insomnia immediately prior to trauma exposure and soon after trauma predicted the subsequent development of PTSD.
Polysomnography (PSG) studies have found increased delta power (0.2-4 Hz) during the entire sleep period in violent crime victims with PTSD compared to healthy controls. Even alterations of beta spectral power (20-32 Hz) in PTSD as been reported; increased beta power was observed during the entire sleep period, but less beta power during REM sleep in veterans with chronic PTSD compared to veterans without PTSD. Therefore reduced beta power during REM was associated with more severe PTSD symptoms and nightmares.
These findings suggest that REM sleep disruption is not only a characteristic of established PTSD, but also a contributor to the development of it.
In PTSD patients the most consistent PSG findings are:
- difficulty in sleep initiation and maintenance, including poor sleep efficiency
- decreased total sleep time
- increased number of awakenings
- longer stage 1 sleep
- shorter slow-wave sleep
- increased REM density
Prospective studies examining associations between sleep characteristics in acute phase of trauma and subsequent development of PTSD sympotms indicated that nightmares about trauma within 2 weeks of a serious injury predicted PTSD at 6 weeks and 1 year post-injury. Some studies pointed out that posttraumatic nightmares respond to treatment with prazosin,which blocks a1-adrenoreceptor-mediated-noradrenergic activity; the event needs to be investigated further.
Polysomnography in patients with post-traumatic stress disorder, 2010
IMPACT OF IMPAIRED SLEEP ON THE DEVELOPMENT OF PTSD SYMPTOMS IN COMBAT VETERANS: A PROSPECTIVE LONGITUDINAL COHORT STUDY, 2013
SEX DIFFERENCES
Women have a higher lifetime prevalence of PTSD (10% in women vs. 5% in men) as well as a greater risk of developing PTSD after trauma exposure. Initially the explanation was women's higher risk for exposure to traumatic events such as rape and molestations. However several meta-analysis revealed women's higher susceptibility even after controlling for type of trauma, especially following exposure to trauma more frequentely experienced by men. Therefore trauma type is not the only factor contributing to the women's greater risk of developing PTSD.
Given the role of sleep in PTSD, it is possible that sex differences in sleep contribute to the increased prevalence in women. In general population, women are more likely than men to report having sleep initiation and maintenance problems, as well as nightmares.
Sex hormones and their fluctuations throughout the menstrual cycle contributed to the relationship between sex and sleep. Women report greater subjective sleep disturbances and lowered sleep quality during the late-luteal phase when both estrogen and progesterone are declining and during menstruation when both the hormones are low compared to the mid-follicular phase when estrogen is rising and progesterone is low.
In humans exogenously administered estrogen and progesterone promoted sleep.
One's sex, sleep, and posttraumatic stress disorder, 2012
Gender differences in sleep during the aftermath of trauma and the development of posttraumatic stress disorder, 2012
EVOLUTIONARY THEORY
Evolutionary psychology views fears and reactions caused by fears as adaptations that may have been useful in the ancestral environment in order to avoid or cope with various threats. Defensive behaviours depend on how close the threat is: avoidance, vigilant immobility, withdrawal, aggressive defence, complete frozen immobility. PTSD may correnspond to and be caused by overactivation of such fear circuits. Thus, PTSD avoidance behaviors may correnspond to withdrawal from threats. Heightened memory of past threats may increase avoidance of similar situations in the future as well as be a prerequisite for analyzing and develop a better defensive strategy if the threat should reoccur.
There may be evolutionary explanations for differences in resilience to traumatic events. It is bizarre to realize that PTSD is rare following traumatic fire; which may be explained by events such as forest fires long being part of the evolutionary hystory of mammals. On the other hand PTSD is much more common following modern warfare.
