Neuroendocrinology<unk>  symptoms may result when a<unk>  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. During<unk>  experiences, the high levels of stress hormones secreted suppress hypothalamic activity that may be a major factor toward the development of<unk> .<unk>  causes biochemical changes in the brain and body, that differ from other psychiatric disorders such as major depression. Individuals diagnosed with<unk>  respond more strongly to a dexamethasone suppression test than individuals diagnosed with clinical depression. Most people with<unk>  show a low secretion of cortisol and high secretion of catecholamines in urine, with a norepinephrine/cortisol ratio consequently higher than comparable non-diagnosed individuals. This is in contrast to the normative fight-or-flight response, in which both catecholamine and cortisol levels are elevated after exposure to a stressor. Brain catecholamine levels are high, and corticotropin-releasing factor (CRF) concentrations are high. Together, these findings suggest abnormality in the hypothalamic-pituitary-adrenal (HPA) axis. The maintenance of fear has been shown to include the HPA axis, the locus coeruleus-noradrenergic systems, and the connections between the limbic system and frontal cortex. 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<unk> . The amygdala is responsible for threat detection and the conditioned and unconditioned fear responses that are carried out as a response to a threat. The HPA axis is responsible for coordinating the hormonal response to stress. Given the strong cortisol suppression to dexamethasone in<unk> , HPA axis abnormalities are likely predicated on strong negative feedback inhibition of cortisol, itself likely due to an increased sensitivity of glucocorticoid receptors.<unk>  has been hypothesized to be a maladaptive learning pathway to fear response through a hypersensitive, hyperreactive, and hyperresponsive HPA axis. Low cortisol levels may predispose individuals to<unk> : Following war trauma, Swedish soldiers serving in Bosnia and Herzegovina with low pre-service salivary cortisol levels had a higher risk of reacting with<unk>  symptoms, following war trauma, than soldiers with normal pre-service levels. Because cortisol is normally important in restoring homeostasis after the stress response, it is thought that trauma survivors with low cortisol experience a poorly contained—that is, longer and more distressing—response, setting the stage for<unk> . It is thought that the locus coeruleus-noradrenergic system mediates the over-consolidation of fear memory. High levels of cortisol reduce noradrenergic activity, and because people with<unk>  tend to have reduced levels of cortisol, it has been proposed that individuals with<unk>  cannot regulate the increased noradrenergic response to<unk>  stress. Intrusive memories and conditioned fear responses are thought to be a result of the response to associated triggers. Neuropeptide Y (NPY) has been reported to reduce the release of norepinephrine and has been demonstrated to have anxiolytic properties in animal models. Studies have shown people with<unk>  demonstrate reduced levels of NPY, possibly indicating their increased anxiety levels. Other studies indicate that people that suffer from<unk>  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. Dopamine levels in a person with<unk>  can contribute to symptoms: low levels can contribute to anhedonia, apathy, impaired attention, and motor deficits; high levels can contribute to psychosis, agitation, and restlessness. Several studies described elevated concentrations of the thyroid hormone triiodothyronine in<unk> . This kind of type 2 allostatic adaptation may contribute to increased sensitivity to catecholamines and other stress mediators. Hyperresponsiveness in the norepinephrine system can also be caused by continued exposure to high stress. Overactivation of norepinephrine receptors in the prefrontal cortex can be connected to the flashbacks and nightmares frequently experienced by those with<unk> . A decrease in other norepinephrine functions (awareness of the current environment) prevents the memory mechanisms in the brain from processing the experience, and emotions the person is experiencing during a flashback are not associated with the current environment. There is considerable controversy within the medical community regarding the neurobiology of<unk> . A 2012 review showed no clear relationship between cortisol levels and<unk> . The majority of reports indicate people with<unk>  have elevated levels of corticotropin-releasing hormone, lower basal cortisol levels, and enhanced negative feedback suppression of the HPA axis by dexamethasone. Neuroanatomy Regions of the brain associated with stress and<unk>  A meta-analysis of structural MRI studies found an association with reduced total brain volume, intracranial volume, and volumes of the hippocampus, insula cortex, and anterior cingulate. Much of this research stems from<unk>  in those exposed to the Vietnam War. People with<unk>  have decreased brain activity in the dorsal and rostral anterior cingulate cortices and the ventromedial prefrontal cortex, areas linked to the experience and regulation of emotion. 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<unk> . When someone with<unk>  undergoes stimuli similar to the<unk>  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<unk>  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<unk>  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<unk> . The BLA activates the central nucleus (CeA) of the amygdala, which elaborates the fear response, (including behavioral response to threat and elevated startle response). Descending inhibitory inputs from the medial prefrontal cortex (mPFC) regulate the transmission from the BLA to the CeA, which is hypothesized to play a role in the extinction of conditioned fear responses. While as a whole, amygdala hyperactivity is reported by meta analysis of functional neuroimaging in<unk> , there is a large degree of heterogeniety, more so than in social anxiety disorder or phobic disorder. Comparing dorsal (roughly the CeA) and ventral(roughly the BLA) clusters, hyperactivity is more robust in the ventral cluster, while hypoactivity is evident in the dorsal cluster. The distinction may explain the blunted emotions in<unk>  (via desensitization in the CeA) as well as the fear related component. In a 2007 study Vietnam War combat veterans with<unk>  showed a 20% reduction in the volume of their hippocampus compared with veterans having suffered no such symptoms. This finding was not replicated in chronic<unk>  patients<unk> ed at an air show plane crash in 1988 (Ramstein, Germany). Evidence suggests that endogenous cannabinoid levels are reduced in<unk> , 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. A 2020 study found no evidence for conclusions from prior research that suggested low IQ is a risk factor for developing<unk> .
Post-traumatic stress disorder
Borderline personality disorder
Acute stress disorder
Dissociative disorder not otherwise specified
Adjustment disorder
Exploding head syndrome
Stress-related disorders
Hodophobia