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In this section, basic findings are reviewed from endocrinology, neurochemistry, and brain circuitry research conducted on patients with a diagnosis of PTSD Table I. Core endocrine features of PTSD include abnormal regulation of Cortisol and thyroid hormones, though there is some disagreement about these findings in the literature. Of note, endocrine dysregulation is also found in patients diagnosed with TBI as a result of damage to the pituitary stalk. The hypothalamic-pituitary-adrenal HPA axis is the central coordinator of the mammalian neuroendocrine stress response systems, and as such, it has been a major focus of scrutiny in patients with PTSD Figure 1.

In short, the HPA axis is made up of endocrine hypothalamic components, including the anterior pituitary, as well as an effector organ, the adrenal glands. Upon exposure to stress, neurons in the hypothalamic paraventricular nucleus PVN secrete corticotropin-releasing hormone CRH from nerve terminals in the median eminence into the hypothalamo-hypophyscal portal circulation, which stimulates the production and release of adrenocorticotropin ACTH from the anterior pituitary. ACTH in turn stimulates the release of glucocorticoids from the adrenal cortex. Glucocorticoids modulate metabolism as well as immune and brain function, thereby orchestrating physiological and organismal behavior to manage stressors.

At the same time, several brain pathways modulate HPA axis activity. In addition, glucocorticoids exert negative feedback control of the HPA axis by regulating hippocampal and PVN neurons.

Sustained glucocorticoid exposure has adverse effects on hippocampal neurons, including reduction in dendritic branching, loss of dendritic spines, and impairment of neurogenesis. Although stressors as a general rule activate the HPA axis, studies in combat veterans with PTSD demonstrate decreases in Cortisol concentrations, as detected in urine or blood, compared with healthy controls and other com parator groups.

This surprising finding, though replicated in PTSD patients from other populations including Holocaust survivors, refugees, and abused persons, is not consistent across all studies. Sensitized negative feedback inhibition is supported by findings of increased glucocorticoid receptor binding and function in patients with PTSD.

In the context of the above discussion, prospective studies suggest that low Cortisol levels at the time of exposure to psychological trauma may predict the development of PTSD. This hypothesis is supported in principle by the finding that exogenously administered hydrocortisone shortly after exposure to psychological trauma can prevent PTSD. That said, it should be noted that glucocorticoids interfere with the retrieval of traumatic memories, an effect that may independently prevent or reduce symptoms of PTSD.

The hypothalamic-pituitary-thyroid HPT axis is involved in regulating metabolic versus anabolic states and other homeostatic functions, which it does by controlling the blood level of thyroid hormones. A possible role for the HPT axis in stress-related syndromes has been suspected for some time because it is known that trauma can trigger thyroid abnormalities.

Studies have been conducted, however, on Vietnam Veterans with PTSD who were found to have elevated baseline levels of both tri-iodothyronine T3 and thyroxine T4. Of note, the level of '13 in these subjects was disproportionately elevated relative to T4, implicating an increase in the peripheral deiodinization process. In these individuals, isolated T3 levels were elevated whereas T4 levels were normal. The authors suggest that elevated T3 may relate to subjective anxiety in these individuals with PTSD. Of note, catecholamine and serotonin as well as acetylcholine dysregulation is also found in patients diagnosed with TBI, presumably as a result of diffuse axonal injury.

Post-traumatic stress disorder: the neurobiological impact of psychological trauma

Further, mesolimbic DA has been implicated in fear conditioning. There is evidence in humans that exposure to stressors induces mesolimbic DA release, which in turn could modulate HPA axis responses. NE, on the other hand, is one of the principal mediators of autonomic stress responses through both central and peripheral mechanisms. The majority of CNS NE is derived from neurons of the locus ceruleus LC that project to various brain regions involved in the stress response, including the prefrontal cortex, amygdala, hippocampus, hypothalamus, periaqueductal grey, and thalamus. In addition, there is evidence for a feed-forward circuit connecting the amygdala and hypothalamus with the LC, in which CRH and NE interact to increase fear conditioning and encoding of emotional memories, enhance arousal and vigilance, and integrate endocrine and autonomic responses to stress.

In the periphery, stress-induced sympathetic nervous system activation results in the release of NE and epinephrine from the adrenal medulla, increased release of NE from sympathetic nerve endings, and changes in blood flow to a variety of organs as needed for fight-or-flight behavior. Because of its multiple roles in regulating arousal and autonomic stress responses, as well as promoting the encoding of emotional memories, NE has been a central focus of many studies investigating the pathophysiology of PTSD.

A cardinal feature of patients with PTSD is sustained hyperactivity of the autonomic sympathetic branch of the autonomic nervous system, as evidenced by elevations in heart rate, blood pressure, skin conductance, and other psychophysiological measures. Accordingly, increased urinary excretion of catecholamines, and their metabolites, has been documented in combat veterans, abused women, and children with PTSD.

In addition, patients with PTSD exhibit increased heart rate, blood pressure, and NE responses to traumatic reminders. Interestingly, prospective studies have shown that increased heart rate and peripheral epinephrine excretion at the time of exposure to trauma predict subsequent development of PTSD. It is important to note, however, that this finding contradicts those from an earlier study.

Serotonin 5HT , is a monoamine neurotransmitter synthesized from the amino acid tryptophan. Neurons containing 5HT originate in the dorsal and median raphe nuclei in the brain stem and project to multiple forebrain regions, including the amygdala, bed nucleus of the stria terminalis, hippocampus, hypothalamus, and prefrontal cortex. Not surprisingly, given its connectivity and broad homeostatic role, 5HT has been implicated in the modulation of affective and stress responses, as well as a role in PTSD.

Although the mechanisms are not entirely clear, the effects of 5HT on affective and stress responses vary according to stressor intensity, brain region, and receptor type. It is believed that 5HT neurons of the dorsal raphe mediate anxiogenic effects via 5HT 2 receptors through projections to the amygdala and hippocampus. In contrast, 5HT neurons from the median raphe are thought to mediate anxiolytic effects, facilitate extinction and suppress encoding of learned associations via 5HT 1A receptors. Chronic exposure to stressors induces upregulation of 5HT 2 and downregulation of 5HT 1A receptors in animal models.

Further, 5HT 1A knockouts exhibit increased stress responses.

Tri-brain Trauma Therapy

A recent small and controversial study suggests that the street drug 3,4-Methylenedioxymetharnphetamine also known as. Glutamate is the primary excitatory neurotransmitter in the brain. Exposure to stressors and the release of, or administration of, glucocorticoids activates glutamate release in the brain. Among a number of receptor subtypes, glutamate binds to N -methyl D -aspartate NMDA receptors that are localized throughout the brain.

The NMDA receptor system has been implicated in synaptic plasticity, as well as learning and memory, thereby contributing in all likelihood to consolidation of trauma memories in PTSD. The NMDA receptor system is also believed to play a central role in the derealization phenomena and dissocation associated with illicit and medical uses of the anesthetic ketamine. CRH neurons are also found in widespread circuitry throughout the brain, including the prefrontal and cingulate cortices, central nucleus of the amygdala, the bed nucleus of the stria terminais, hippocampus, nucleus accumbens, periaqueductal gray, and locus coeruleus LC as well as both dorsal and median raphe.

Direct injection of CRH into the brain of laboratory animals produces physiological stress responses and anxiety-like behavior, including neophobia fear of new things or experiences , enhanced startle, and facilitated fear conditioning. Anxiety -like behaviors have been specifically linked with increased activity of amygdalar CRH-containing neurons that project to the LC.

Of note, glucocorticoids inhibit CRH-induced activation of LC noradrenergic neurons, providing a potential mechanism by which low Cortisol may facilitate sustained central stress and fear responses. In animal experiments, both exogenous administration of a CRH 1 , receptor antagonist, and experimental knockout of the CRH 1 receptor, produce attenuated stress responses and reduced anxiety. A recent experiment demonstrated that CRHj receptor blockade impacted not only gastrointestinal measures of chronic stress, but also prevented stress-induced hair loss in rodents.

By contrast, CRH 7 knockout mice demonstrate stress sensitization and increased anxiety, suggesting a role for CRH 2 receptor activation in reducing stress reactivity. Endogenous opioid peptides including the endorphins and enkephalins act upon the same CNS receptors activated by exogenous opioid molecules such as morphine or heroin. Endogenous opioids exert inhibitory influences on the HPA axis.

Naloxone, an opioid receptor antagonist, increases HPA axis activation as evidenced by exaggerated HPA axis response to naloxone. PTSD patients exhibit increased CSF p-endorphin levels, suggesting increased activation of the endogenous opioid system. Alterations in endogenous opioids may be involved in certain PTSD symptoms such as numbing, stress-induced analgesia, and dissociation.

Of additional interest, the nonselective opioid receptor antagonist, naltrexone, appears to be effective in treating symptoms of dissociation and flashbacks in traumatized persons. Characteristic changes in brain structure and function have been identified in patients with PTSD using brainimaging methods. These areas interconnect to form a neural circuit that mediates, among other functions, adaptation to stress and fear conditioning. Changes in these circuits have been proposed to have a direct link to the development of PTSD. A hallmark feature of PTSD is reduced hippocampal volume.

Trauma and the Triune Brain - Post-Traumatic Stress Disorder

The hippocampus is implicated in the control of stress responses, declarative memory, and contextual aspects of fear conditioning. Not surprisingly, the hippocampus is one of the most plastic regions in the brain. As mentioned above, prolonged exposure to stress and high levels of glucocorticoids in laboratory animals damages the hippocampus, leading to reduction in dendritic branching, loss of dendritic spines, and impairment of neurogenesis.

These findings were generally replicated in most but not all subsequent work. Studies using proton magnetic resonance spectroscopy further observed reduced levels of N-acctyl aspartate NAA , a marker of neuronal integrity, in the hippocampus of adult patients with PTSD.

Hippocampal volume reduction in PTSD may reflect the accumulated toxic effects of repeated exposure to increased glucocorticoid levels or increased glucocorticoid sensitivity, though recent evidence also suggests that decreased hippocampal volumes might be a pre-existing vulnerability factor for developing PTSD. Studies using functional neuroimaging have further shown that PTSD patients have deficits in hippocampal activation during a verbal declarative memory task.

The amygdala is a limbic structure involved in emotional processing and is critical for the acquisition of fear responses. The functional role of the amygdala in mediating both stress responses and emotional learning implicate its role in the pathophysiology of PTSD. The medial prefrontal cortex PFC comprises the anterior cingulate cortex ACC , subcallosal cortex, and the medial frontal gyrus. The medial PFC exerts inhibitory control over stress responses and emotional reactivity in part by its connections with the amygdala. It further mediates extinction of conditioned fear through active inhibition of acquired fear responses.

A recent twin study suggests that, unlike the hippocampus, volume loss in the ACC is secondary to the development of PTSD rather than a pre-existing risk factor. Not surprisingly, given the connectivity between the amygdala and medial PFC, interactions in activation patterns between these regions have been reported in PTSD, though the direction of the relationship is inconsistent across studies.

A number of studies have investigated the fundamental question as to whether the neurobiological changes identified in patients with PTSD represent markers of neural risk to develop PTSD upon exposure to extreme stress as opposed to abnormalities acquired through traumatic exposure or, most likely, a combination of both. Similarly, the reduced size of the hippocampus in PTSD has remained an unresolved question for many years.

There has been considerable debate as to whether this brain region shrinks as a result of trauma exposure, or whether the hippocampus of PTSD patients might be smaller prior to trauma exposure.

Studies in twins discordant for trauma exposure have provided a means to address this question, though without complete resolution. Gilbertson and colleagues 72 studied 40 pairs of identical twins, including Vietnam Veterans who were exposed to combat trauma and their twins who did not serve in Vietnam, and measured hippocampal volumes in all subjects.

As expected, among Vietnam Veterans, the hippocampus was smaller in those diagnosed with PTSD as compared with those without a diagnosis. However, this brain region was abnormally smaller in non-PTSD twins as well, despite the absence of trauma exposure and diagnosis. These findings suggest that a smaller hippocampus could be a pre-existing, potentially genetic, neurodevelopmental, and almost surely multifactorial vulnerability factor that predisposes to the development of PTSD and perhaps other stress-spectrum disorders. Recent results from the same study group indicate, as above, that gray matter loss in the ACC seems on the contrary to be an acquired feature.

In short, not all individuals who face potentially catastrophic trauma go on to develop PTSD. Why some individuals will develop PTSD following trauma, whereas others do not, is of paramount importance. Because the majority of trauma survivors do not go on to develop PTSD, it is crucial going forward to understand vulnerability and resiliency factors.

In this section, the role of genetic factors, gender differences, and early developmental stress experiences in moderating risk for developing PTSD in response to psychological trauma are discussed as is the increased risk for developing PTSD in the context of co-occurring physical traumas including TBI.

Studies on the genetics of PTSD have been hampered by a variety of factors, such as genetic heterogeneity similar phenotypes develop from different genotypes and incomplete phenotypic penetrance a person with genetic risk for PTSD, who is not exposed to trauma, will not develop PTSD.

Despite these confounds, there is accumulating evidence that risk for PTSD is heavily influenced by genetic factors. Evidence from family and twin studies has long suggested a heritable contribution to the development of PTSD. In addition, there is evidence for heritable contributions to some of the neurobiological endophenotypes of PTSD as discussed above, such as decreased hippocampal volume 72 or exaggerated amygdala reactivity. This finding suggests that genetically determined features of DA transmission may contribute to the development of PTSD among trauma survivors.


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