It was Kardiner,A., a disciple of Freud, who presented a diagnostic concept of “traumatic neurosis” practically equivalent to the current diagnosis of PTSD. He described five principal features of PTSD; (1) persistence of startle response and irritability, (2) proclivity to explosive outbursts of aggression, (3) fixation on the trauma, (4) constriction of the general level of personality functioning, and (5) atypical dream life (van der Kolk, 1991). In his “Traumatic Neurosis of War” (Kardiner, 1941) Kardiner called the condition “physioneurosis”, stressing that war neurosis has many psychological as well as physiological features. His idea was practically carried over to PTSD in DSM-III (1980).
Kardiner, A (1941) Traumatic Neurosis of War . Paul B. Hoeber, New York, 1941.
van der Kolk, BA. (1991) The Biological Response to Psychit Trauma: Mechanisms and Treatment of Intrusion and Numbing. Anxiety Research 4:199-212.
The way traumatic memories are ingrained in our body
Trauma primarily affects our limbic system. Limbic system is in charge of modulating emotion necessary for our self-preservation, and behaviors such as eating, fight/flight, and reproduction. Therefore, trauma’s impact on this area affect reaches very wide range of our life. The areas in the limbic system which are most involved in trauma are hippocampus and amygdala. Amygdala deals with memories so long as they are emotionally meaningful. At the moment of trauma, amygdala is typically over activated and memory is strongly encoded, which will be reactivated later in the form of flashbacks. Hippocampus’s involvement in the formation of traumatic memories is also quite significant in the formation of trauma memories. Usually, hippocampus forms episodic memories of the daily events. However, if the experience is emotionally overwhelming, activities of hippocampus are suppressed partially due to the inhibitory signals from overexcited amygdala. Consequently, memories of traumatic event become blurred in time and space, and often become a subject to amnesia.
To recapitulate some of the discussions in the Chapter 6, recent researches revealed that decreased volume of hippocampus might be implicated in PTSD and other psychiatric disorders. It began with the study of Bremner (1995) who reported that Viet Nam veterans have on average 8% of volume reduction of their right hippocampus. Since then the relationship between memory problems in PTSD and this volume decrease has been investigated by many researchers. However, some studies indicated that originally low volume of hippocampus can predispose people to develop PTSD and it is still unclear whether low hippocampal volume is the result of, or cause for PTSD.
Bremner, J.D.: Acute and chronic responses to psychological trauma. Where do we go from here? Am J Psychiatry, 156;349-351, 1999.
Neuroendocrinological implication has also been noted in trauma reactions. When traumatic incident occurs, so-called HPA (hypothalamic - pituitary - adrenal) axis is activated and glucocorticoid hormones are secreted. Glucocorticoid hormones help us go through trauma by inhibiting initial acute physiological response to stress. In PTSD, there is a chronic increase of the blood level of catecholamine due to the fact that the alarm switch is continually turned on upon frequent flashbacks. On the other hand, level of glucocorticoid hormones is rather decreased in PTSD, and it no longer gets increased when new stress occurs. If we take into consideration that concomitant secretion of catecholamine gives emotional value to the experience (with palpitation and sweating, for example) and therefore intensifies the memory, in PTSD flashback experiences themselves potentially further strengthen traumatic memories. Therefore, this hormonal abnormality in PTSD can perpetuate the impact of traumatic memories.
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