The sympathetic branch of the autonomic nervous system gives rise to a specific set of physiological responses to physical or psychological stress. The body's response to stress is also termed a 'fight or flight' response, and it is characterised by an increase in blood flow to the skeletal muscles, heart, and brain, a rise in heart rate and blood pressure, dilation of pupils, and an increase in the amount of glucose released by the liver.
The onset of an acute stress response is associated with specific physiological actions in the sympathetic nervous system, both directly and indirectly through the release of adrenaline and, to a lesser extent, noradrenaline from the medulla of the adrenal glands.
These catecholamine hormones facilitate immediate physical reactions by triggering increases in heart rate and breathing, constricting blood vessels. An abundance of catecholamines at neuroreceptor sites facilitates reliance on spontaneous or intuitive behaviours often related to combat or escape.
Normally, when a person is in a serene, non-stimulated state, the 'firing' of neurons in the locus ceruleus is minimal. A novel stimulus, once perceived, is relayed from the sensory cortex of the brain through the thalamus to the brain stem. That route of signalling increases the rate of noradrenergic activity in the locus ceruleus, and the person becomes more alert and attentive to their environment.
If a stimulus is perceived as a threat, a more intense and prolonged discharge of the locus ceruleus activates the sympathetic division of the autonomic nervous system.
The other major player in the acute stress response is the hypothalamic-pituitary-adrenal axis. Stress activates this axis and produces neuro-biological changes. These chemical changes increase the chances of survival by bringing the physiological system back to homeostasis.
The autonomic nervous system controls all automatic functions in the body and contains two subsections within it that aid the response to an acute stress reaction. These two subunits are the sympathetic nervous system and the parasympathetic nervous system.
The sympathetic response is colloquially known as the 'fight or flight' response, indicated by accelerated pulse and respiration rates, pupil dilation, and a general feeling of anxiety and hyper-awareness. This is caused by the release of epinephrine and norepinephrine from the adrenal glands.
Studies have shown that patients with Acute Stress Disorder have overactive right amygdalae and prefrontal cortices; both structures are involved in the fear-processing pathway.
If symptoms persist past one month, the diagnosis of PTSD is explored. There must be a clear temporal connection between the impact of an exceptional stressor and the onset of symptoms; onset is usually within a few minutes or days but may occur up to one month after the stressor.
Also, the symptoms show a mixed and rapidly changing picture; although 'daze' depression, anxiety, anger, despair, hyper-activity, and withdrawal may all be seen, no one symptom dominates for long. The symptoms usually resolve rapidly where removal from the stressful environment is possible. In cases where the stress continues, the symptoms usually begin to diminish after 24–48 hours and are usually minimal after about three days.
Symptoms of PTSD generally begin within the first 3 months after the inciting traumatic event, but may not begin until years later.
In the typical case, the individual with PTSD persistently avoids trauma-related thoughts and emotions, and discussion of the traumatic event, and may even have amnesia of the event.
However, the event is commonly relived by the individual through intrusive, recurrent recollections, dissociative episodes of reliving the trauma ("flashbacks"), and nightmares.
While it is common to have symptoms after any traumatic event, these must persist to a sufficient degree (i.e., causing dysfunction in life or clinical levels of distress) for longer than one month after the trauma to be classified as PTSD. Some following a traumatic event experience posttraumatic growth.
Trauma survivors often develop depression, anxiety disorders, and mood disorders in addition to PTSD.
Resolving these problems can bring about improvement in an individual's mental health status and anxiety levels.
PTSD has been associated with a wide range of traumatic events. The risk of developing PTSD after a traumatic event varies by trauma type and is highest following exposure to sexual violence.
Men are more likely to experience a traumatic event, but women are more likely to experience the kind of high-impact traumatic event that can lead to PTSD, such as interpersonal violence and sexual assault.
An individual that has been exposed to domestic violence is predisposed to the development of PTSD. There is a strong association between the development of PTSD in mothers that experienced domestic violence during the perinatal period of their pregnancy.
Those who have experienced sexual assault or rape may develop symptoms of PTSD.[52][53] PTSD symptoms include re-experiencing the assault, avoiding things associated with the assault, numbness, and increased anxiety and an increased startle response.
The likelihood of sustained symptoms of PTSD is higher if the rapist confined or restrained the person, if the person being raped believed the rapist would kill them, the person who was raped was very young or very old, and if the rapist was someone they knew. The likelihood of sustained severe symptoms is also higher if people around the survivor ignore (or are ignorant of) the rape or blame the rape survivor.
PTSD symptoms may result when a traumatic event causes an over-reactive adrenaline response, which creates deep neurological patterns in the brain. These patterns can persist long after the event that triggered the fear, making an individual hyper-responsive to future fearful situations.[20][80] During traumatic experiences the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of PTSD.
The HPA axis that coordinates the hormonal response to stress, which activates the LC-noradrenergic system, is implicated in the over-consolidation of memories that occurs in the aftermath of trauma.
This over-consolidation increases the likelihood of one's developing PTSD. The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat.
Other studies indicate that people that suffer from PTSD have chronically low levels of serotonin, which contributes to the commonly associated behavioral symptoms such as anxiety, ruminations, irritability, aggression, suicidality, and impulsivity.Serotonin also contributes to the stabilization of glucocorticoid production.
The amygdala is strongly involved in forming emotional memories, especially fear-related memories. During high stress, the hippocampus, which is associated with placing memories in the correct context of space and time and memory recall, is suppressed.
According to one theory this suppression may be the cause of the flashbacks that can affect people with PTSD. When someone with PTSD undergoes stimuli similar to the traumatic event, the body perceives the event as occurring again because the memory was never properly recorded in the person's memory.
The amygdalocentric model of PTSD proposes that the amygdala is very much aroused and insufficiently controlled by the medial prefrontal cortex and the hippocampus, in particular during extinction. This is consistent with an interpretation of PTSD as a syndrome of deficient extinction ability.
The basolateral nucleus (BLA) of the amygdala is responsible for the comparison and development of associations between unconditioned and conditioned responses to stimuli, which results in the fear conditioning present in PTSD.
While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in PTSD, there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder.
Evidence suggests that endogenous cannabinoid levels are reduced in PTSD, particularly anandamide, and that cannabinoid receptors (CB1) are increased in order to compensate. There appears to be a link between increased CB1 receptor availability in the amygdala and abnormal threat processing and hyperarousal, but not dysphoria, in trauma survivors.
PTSD was classified as an anxiety disorder in the DSM-IV, but has since been reclassified as a "trauma- and stressor-related disorder" in the DSM-5. The DSM-5 diagnostic criteria for PTSD include four symptom clusters: re-experiencing, avoidance, negative alterations in cognition/mood, and alterations in arousal and reactivity.
The International Classification of Diseases and Related Health Problems 10 (ICD-10) classifies PTSD under "Reaction to severe stress, and adjustment disorders." The ICD-10 criteria for PTSD include re-experiencing, avoidance, and either increased reactivity or inability to recall certain details related to the event.
A diagnosis of PTSD requires that the person has been exposed to an extreme, life-threatening stressor. Any stressor can result in a diagnosis of adjustment disorder and it is an appropriate diagnosis for a stressor and a symptom pattern that does not meet the criteria for PTSD.
The symptom pattern for acute stress disorder must occur and be resolved within four weeks of the trauma. If it lasts longer, and the symptom pattern fits that characteristic of PTSD, the diagnosis may be changed.
In extreme cases of prolonged, repeated traumatization where there is no viable chance of escape, survivors may develop complex post-traumatic stress disorder. This occurs as a result of layers of trauma rather than a single traumatic event, and includes additional symptomatology, such as the loss of a coherent sense of self.
Complex post-traumatic stress disorder (C-PTSD; also known as complex trauma disorder) is a psychological disorder that can develop in response to prolonged, repeated experience of interpersonal trauma in a context in which the individual has little or no chance of escape.
C-PTSD relates to the trauma model of mental disorders and is associated with chronic sexual, psychological and physical abuse and neglect, chronic intimate partner violence, victims of kidnapping and hostage situations, indentured servants, victims of slavery and human trafficking, sweatshop workers, prisoners of war, concentration camp survivors, residential school survivors, defectors of cults or cult-like organizations, and narcissistic child abuse.
Situations involving captivity/entrapment (a situation lacking a viable escape route for the victim or a perception of such) can lead to C-PTSD-like symptoms, which can include prolonged feelings of terror, worthlessness, helplessness, and deformation of one's identity and sense of self.
Children can suffer chronic trauma such as maltreatment, family violence, and a disruption in attachment to their primary caregiver. In many cases, it is the child's caregiver who caused the trauma. The diagnosis of PTSD does not take into account how the developmental stages of children may affect their symptoms and how trauma can affect a child’s development.
The term developmental trauma disorder (DTD) has been proposed as the childhood equivalent of C-PTSD.[11] This developmental form of trauma places children at risk for developing psychiatric and medical disorders.
Repeated traumatization during childhood leads to symptoms that differ from those described for PTSD. Cook and others describe symptoms and behavioural characteristics in seven domains:
- Attachment – "problems with relationship boundaries, lack of trust, social isolation, difficulty perceiving and responding to others' emotional states"
- Biology – "sensory-motor developmental dysfunction, sensory-integration difficulties, somatization, and increased medical problems"
- Affect or emotional regulation – "poor affect regulation, difficulty identifying and expressing emotions and internal states, and difficulties communicating needs, wants, and wishes"
- Cognition – "difficulty regulating attention; problems with a variety of 'executive functions' such as planning, judgement, initiation, use of materials, and self-monitoring; difficulty processing new information; difficulty focusing and completing tasks; poor object constancy; problems with 'cause-effect' thinking; and language developmental problems such as a gap between receptive and expressive communication abilities."
- Self-concept – "fragmented and disconnected autobiographical narrative, disturbed body image, low self-esteem, excessive shame, and negative internal working models of self".
Adults with C-PTSD have sometimes experienced prolonged interpersonal traumatization beginning in childhood, rather than, or as well as, in adulthood. These early injuries interrupt the development of a robust sense of self and of others.
Because physical and emotional pain or neglect was often inflicted by attachment figures such as caregivers or older siblings, these individuals may develop a sense that they are fundamentally flawed and that others cannot be relied upon.
This symptom is neither included in the diagnosis of dissociative disorder nor in that of PTSD in the current DSM-5 (2013). Individuals with Complex PTSD also demonstrate lasting personality disturbances with a significant risk of revictimization.
In the 1980s, various researchers and clinicians suggested that PTSD might also accurately describe the sequelae of such traumas as child sexual abuse and domestic abuse.
PTSD descriptions fail to capture some of the core characteristics of C-PTSD. These elements include captivity, psychological fragmentation, the loss of a sense of safety, trust, and self-worth, as well as the tendency to be revictimized. Most importantly, there is a loss of a coherent sense of self: this loss, and the ensuing symptom profile, most pointedly differentiates C-PTSD from PTSD.
C-PTSD better describes the pervasive negative impact of chronic repetitive trauma than does PTSD alone. PTSD can exist alongside C-PTSD, however a sole diagnosis of PTSD often does not sufficiently encapsulate the breadth of symptoms experienced by those who have experienced prolonged traumatic experience, and therefore C-PTSD extends beyond the PTSD parameters.
If a traumatic event was life-threatening, but did not result in a death, then it is more likely that the survivor will experience post-traumatic stress symptoms.
C-PTSD may share some symptoms with both PTSD and borderline personality disorder.[38] However, there is enough evidence to also differentiate C-PTSD from borderline personality disorder.
While standard evidence-based treatments may be effective for treating post traumatic stress disorder, treating complex PTSD often involves addressing interpersonal relational difficulties and a different set of symptoms which make it more challenging to treat.
Dr. Judith Lewis Herman, in her book, Trauma and Recovery, proposed that a complex trauma recovery model that occurs in three stages:
- establishing safety,
- remembrance and mourning for what was lost,
- reconnecting with community and more broadly, society.
Herman believes recovery can only occur within a healing relationship and only if the survivor is empowered by that relationship. This healing relationship need not be romantic or sexual in the colloquial sense of "relationship", however, and can also include relationships with friends, co-workers, one's relatives or children, and the therapeutic relationship.
It has been suggested that treatment for complex PTSD should differ from treatment for PTSD by focusing on problems that cause more functional impairment than the PTSD symptoms. These problems include emotional dysregulation, dissociation, and interpersonal problems.
In practice, the forms of treatment and intervention varies from individual to individual since there is a wide spectrum of childhood experiences of developmental trauma and symptomatology and not all survivors respond positively, uniformly, to the same treatment. Therefore, treatment is generally tailored to the individual.
Recent neuroscientific research has shed some light on the impact that severe childhood abuse and neglect (trauma) has on a child's developing brain, specifically as it relates to the development in brain structures, function and connectivity among children from infancy to adulthood.
Dr. Martin Teicher, a Harvard psychiatrist and researcher, has suggested that that the development of specific complex trauma related symptomatology (and in fact the development of many adult onset psychopathologies) may be connected to gender differences and at what stage of childhood development trauma, abuse or neglect occurred.
For example, it is well established that the development of dissociative identity disorder among among women is often associated with early childhood sexual abuse.
While standard evidence-based treatments may be effective for treating standard post traumatic stress disorder, treating Complex PTSD often involves addressing interpersonal relational difficulties and a different set of symptoms which make it more challenging to treat.
Complex post trauma stress disorder is a long term mental health condition which is often difficult and relatively expensive to treat and often requires several years of psychotherapy, modes of intervention and treatment by highly skilled, mental health professionals who specialize in trauma informed modalities designed to process and integrate childhood trauma memories for the purposes of mitigating symptoms and improving the survivor's quality of life. Delaying therapy for people with complex PTSD, whether intentionally or not, can exacerbate the condition.
Despite the fact that there is no one treatment which has been designed specifically for the adult complex PTSD population (with the exception of component based psychotherapy) several therapeutic interventions and modalities that may be used by mental health professionals, many of which are efficacious or used in the treatment of post traumatic stress disorder and have been adapted for use for the complex trauma client.
Some of the most common forms of treatment for complex trauma include:
Trauma-exposed individuals often receive treatment called psychological debriefing in an effort to prevent PTSD, which consists of interviews that are meant to allow individuals to directly confront the event and share their feelings with the counselor and to help structure their memories of the event.
One of the primary arguments for a new disorder has been the claim that individuals who experience complex post traumatic stress symptomatology are often misdiagnosed, and as a consequence may be given inappropriate or inadequate treatment interventions.
