Derecho al sufragio en Ecuador

Even nonpsychiatric physicians generally place nonphysiological findings in the diagnostic category of a “conversion reaction,” or conversion hysteria. This psychiatric condition was described in de-tail by Janet and Freud.^1,2As noted earlier, conversion is considered to be a protection against intolerable levels of anxiety or phobias. The anxiety is “converted” into symptoms in organs or other parts of the body, and usually presents as sensory or motor neurological symp-toms. These symptoms tend to represent the mental conflict creating the anxiety, and also meet some need of the patient—provide “sec-ondary gain”—on an unconscious basis. Conversion of an intolerable anxiety to a physical symptom indeed provides great emotional re-lief, hence the frequently documented indifference to the disabling physical condition (la belle indifference). Hysterical paralysis, for example, has been seen regularly in traumatized soldiers suffering from “shell shock” or “battle fatigue.” Hysterical paraplegia at the turn of the century was classically attributed in women to sexual am-bivalence—i.e., to a confused mixture of erotic feelings and disgust with regard to sexuality.²The very term “hysteria” derives from the Greek word for the uterus, hystera, essentially branding conversion reaction as a feminine condition. These young women were initially suspected, and are now thought to have been, victims of incest, and the secondary gain achieved is now believed to have been a form of protection from further exposure to their source of trauma.

In the DSM-IV, conversion has been assigned to the category of somatiform disorders, and is technically not felt to represent a true dissociative disorder. As part of the thesis of this chapter, however, I believe that all somatiform disorders constitute subsets of the dissociative response, and that they have a measurable physiological basis and origin. Conversion reaction, then, is an example of regional somatic dissociation as a reaction to trauma.

It is apparent that the patient with a conversion reaction will al-most always have been a victim of trauma in the past, usually in addi-tion to the new trauma that may have precipitated the conversion symptoms. Often this past trauma will have been severe childhood abuse. Children typically dissociate in the face of traumatic stress, as

Somatic Dissociation 107

we have noted. They sustain this tendency to freeze in the face of per-ceived threat as they grow older, with each episode of dissociation tending to reinforce the susceptibility to freeze in the face of subse-quent threat. As a result, adults with a history of child abuse typically experience a greater tendency to freeze at the moment of subsequent trauma and to develop dissociative symptoms. Dissociation is the pri-mary predictor for the later development of PTSD.²²Individuals who actively dissociate at the time of a traumatic event are much more likely to develop subsequent symptoms of PTSD than those who do not.^23-25People with a history of trauma or PTSD also are susceptible to arousal, freezing, and retraumatization after exposure to arousal stimuli unrelated to prior traumatic life experiences.²⁶They also have trouble differentiating relevant from irrelevant stimuli with regard to content and meaning of threat.²⁷The tendency to freeze in the face of trauma appears to be a self-fulfilling prophecy, rendering the victim increasingly sensitive to traumatization with ever-decreasing sever-ity and specificsever-ity of threat exposure. This phenomenon of sensitiza-tion to increasingly minor and apparently irrelevant threat in victims of childhood trauma, may well explain the remarkable incidence of dissociative symptoms and PTSD in my patients with a history of childhood trauma injured in relatively trivial MVAs.

Although poorly understood, a number of neurophysiological pro-cesses likely contribute to the clinical phenomenon of dissociation.

Recently, attention has been drawn to the role of the dorsal medial prefrontal cortex (MPFC), or anterior cingulate, in PTSD.²⁸Reference has been made to this region with regard to concepts of brain plastic-ity in PTSD in Chapter 5. Hamner noted that lesions of the anterior cingulate may facilitate the acquisition of fear conditioning, suggesting that this region may provide a gating function inhibiting fear condi-tioning.²⁹You will recall that the amygdala receives input from the locus ceruleus in states of potential threat, and evaluates that infor-mation for its emotional or arousal-based content. Continued activa-tion of the amygdala by further input from the locus ceruleus may then set up a state of fear conditioning. The gating or control function of the anterior cingulate is believed to occur through inhibition of ac-tivation of the amygdala at the time of fear arousal. Lack of this

inhi-bition of fear conditioning by the cingulate may lead to increased sensitivity to internal and external trauma-related cues.

In Hamner’s model, inhibition of the anterior cingulate by exces-sive adrenergic input from the locus ceruleus with traumatic arousal may limit this gating function of the cingulate on the amygdala. This in turn, would allow exposure of the amygdala to overwhelming in-ternal and exin-ternal arousal cues, thereby producing the exaggerated emotional and behavioral symptoms of PTSD. Once established, lo-cus ceruleus/amygdala kindling would continue to suppress anterior cingulate function, and perpetuate the conditioned fear response (see Figure 8.1). In addition, the anterior cingulate appears to play a role in emotionality, selective attention, and certain social functions, includ-ing emotional attachments and parentinclud-ing, as well as generation of the concept of the self in relation to society. Fragmentation of these func-tions through inhibition of the anterior cingulate in PTSD may ex-plain the inability of its victims to form social bonds, to manifest avoidance and isolation, and to experience fragmentation of the sense of self that typifies dissociation.

Dissociation almost certainly is also mediated at least in part by endorphinergic influences, which may in turn explain the dissociative phenomena of numbing, confusion, and cognitive impairment. Cer-tainly the analgesia associated with the freeze, or immobility, response—

the precursor and extreme expression of dissociation—is related to endorphinergic mediation. Current theory also strongly relates endog-enous opioids to the phenomenon of trauma reenactment.³⁰Increasing sensitization to dissociate in the face of threat may well be based on opioid reward systems.

Dissociation, or freezing, may represent the perpetuating mecha-nism that fuels the kindled arousal/memory feedback circuit of sus-tained PTSD. If so, it may be the reason why victims of prior traumatic stress, especially childhood abuse, are so susceptible to the development of PTSD symptoms in otherwise minor episodes of life stress, including low velocity MVAs, as noted in my patient popula-tion. The underlying neurochemistry and neurophysiology of dissoci-ation is likely to be of critical importance to the understanding of its role in trauma.

Somatic Dissociation 109

*SocialBehavior *SenseofSelf *GatingofAmygdala Activity *EmotionalMeaning *FacilitationofArousal *FearConditioning

*Arousal ImpairedGatingof FearConditioning

High-LevelInput FIGURE8.1.Theoreticalroleoftheanteriorcingulateinpost-traumaticstressdisorder.Theanteriorcingulatemayexertab ingactiononactivationoftheamygdala,andthereforeprovideagatingmechanismonthedevelopmentoffearconditioning traumaticstress.Excessiveorprolongedarousalinputfromthelocusceruleusinunresolvedtraumamayimpairthisgating actionthroughcingulateinhibition,therebypotentiatingfearconditioningandtraumatickindlinginPTSD.

110

THE AUTONOMIC NERVOUS SYSTEM