Specific Mechanisms Potentially Contributing To The Pathophysiology Of Ptsd

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While the precise mechanisms whereby even well-established biological risk factors may influence a person's acute response to trauma have not yet been fully elaborated, it is important to consider the possibilities. With respect to the neuroendocrine alterations, for example, since cortisol inhibits its own release through negative feedback at the level of the pituitary and the hypothalamus, lower circulating cortisol levels may disrupt (or delay) the process of physiological stress recovery by failing to inhibit the activation of the hypothalamus/pituitary. This failure of inhibition will result in increased corticotropin releasing factor (CRF)

stimulation, in synergy with other neuropeptides, such as arginine vasopressin, resulting in a higher magnitude adrenocorticotropin hormone (ACTH) response, which in turn might further stimulate the sympathetic nervous system through a direct effect [42]. Moreover, since glucocorticoids inhibit norepinephrine release from sympathetic nerve terminals, relatively lower cortisol levels may be expected to prolong norepinephrine availability at synapses, both in the periphery and in the brain [43]. Importantly, enhanced negative feedback inhibition may be present at the time of the trauma (i.e., may be a pre-trauma risk factor), and may contribute to the premature suppression of ACTH and cortisol among individuals at increased risk for the development of PTSD in response to trauma [44].

There may be consequences of increased catecholamine levels in the acute aftermath of a trauma in promoting the consolidation of the traumatic memory. Indeed, adrenergic activation in the presence of low cortisol has been shown to facilitate ''learning'' in animals [45]. If this was the neurohumoral state of an individual during and in the immediate aftermath of a traumatic exposure, the event would not only be strongly encoded in memory, but associated with extreme subjective distress. This level of distress, in turn, would set the stage for the occurrence of perceptual and cognitive distortions in the acute aftermath of the event, particularly regarding the estimation of danger and subjective assessment of ability to respond effectively to the threat. Such altered beliefs would serve to further inhibit recovery by leading to a failure to quell fearful recollections. The repeated experience of the trauma memory with its associated fear response, as may occur at the time of an intrusive recollection or in response to a traumatic reminder, serves to enhance, rather than reduce, the association of trauma-related and distorted cognitions with the fear response, further increasing the likelihood of spontaneous re-emergence of the memory. In this way, re-experiencing symptoms becomes a form of re-traumatization, that not only perpetuates, but can intensify the intrusive and arousal symptoms of PTSD, and provide further provocation for avoidance behaviors. This cascade can produce a series of secondary biological changes. Indeed, the exaggerated startle response in PTSD is not observed until one month following trauma, and not earlier, reflecting the developmental progression of at least some aspects of the pathophysiology of PTSD [44].

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