Key words: PTSD, DESNOS, Complex PTSD, revictimization, allostatic model
During the 19th century, a picture was painted of trauma in which the focus was on pathologies of the victims, including notions of inherited "moral degeneracy," with little cognizance of the greater contextual factors, such as the traumatic events themselves, that contributed to the symptom picture. The role of trauma in the etiology of posttraumatic symptoms was incorporated into the DSM-III in 1980 and the PTSD category was initially viewed as an improvement over earlier categorizations of trauma, as it acknowledged that some experiences are so overwhelming that few people would escape unscathed. However, recent findings that not all persons who have suffered traumatic events develop PTSD have led some writers to discussion of a genetic component to PTSD. This article looks at this conclusion and the role of individual and contextual factors in relation to PTSD, Complex PTSD, and revictimization.
*Note: Some of the material in this article may be disturbing to some readers.
Within the helping professions, there has been a longstanding interest in the causes and effects of PTSD (hysteria). Historically, the effects of trauma were subsumed under the heading of hysteria, however, the traumatic origins of hysteria were not acknowledged until the 19th century. Before discussing some current research on PTSD and revictimization of persons who were abused as children, I would like to take a bit of a historical journey up through 19th Century Europe, and discuss the history of PTSD and child sexual abuse.
The History of Hysteria
The term "hysteria" originated in Egyptian and Greek medicine, and was derived from "hystera," meaning "uterus" (Veith, 1965). Although the symptoms of hysteria were recorded in as early as the ancient Egyptian papyri, the traumatic origins were not readily apparent until the physician Robert Carter noted in 1853 that the etiology of hysteria included external events (e.g., Veith, 1965). Ancient writers attributed etiology to the drying up of the uterus such that it would wander throughout the body seeking moisture and lead to various symptoms, depending upon where in the body the uterus ultimately settled. With movement into the Middle Ages, devils and demons were held responsible for psychological maladies, and persons with hysteria were persecuted as witches.
Around the end of the 16th century, Edward Jordan (1569-1632) postulated that the etiology of hysteria lay in natural, rather than supernatural, causes, and hysteria was linked to the brain. The founder of modern neurology, Thomas Willis (1621-1673) and his colleague, Sydenham, noted evidence provided by postmortem examinations that in females diagnosed with hysteria, the uterus was completely normal, thereby refuting the ancient notion of a 'wandering womb.' The physician Andrew Coombe (1797-1847) was the first to use the word "functional" in relation to nervous diseases, and with the phrenologists, the notion of function, rather than structure, became more widespread (Trimble, 1981).
During the 19th century, Charcot's student Janet noted the relationship between trauma and hysteria in their work with traumatized persons at the Saltpetriere in France. Janet went on to formulate a theory that emphasized the role of dissociation between cognition and affect in the etiology of hysteria (van der Kolk, Weisaeth, & van der Hart, 1996). Janet's views that posttraumatic sequelae were based in dissociation and that treatment consisted of synthesis and integration of traumatic material was accepted until psychoanalysis gained prominence around the turn of the century (van der Kolk, Weisaeth, & van der Hart, 1996).
Sexual Exploitation of Children
Ancient Greek civilization esteemed pedophilia, in particular, homosexual pedophilic activities between boys and men (Kahr, 1991; Rush, 1980). Some boys were raped and forced into sexual slavery, and many were castrated (Rush, 1980). According to Rush (1980, p. 17), the Bible and the Talmud encouraged sexual activity between men and very young girls. Ancient Roman literature provides numerous examples of sexual abuses of young girls and boys, including incest (Kahr, 1991). In 13th Century England, Church law was separated from civil law, wherein evolved the crime of statutory rape (Rush, 1980). Having intercourse with a female under the age of 12 was deemed a misdemeanor. During the 16th century, a girl could legally consent to sexual intercourse at age 10, and to marriage at age 12 (Rush, 1980).
During the witch hunt from the 15th to 18th centuries, children from at least the age of six (legal age for sexual consent in France) were held to be old enough to copulate with the devil, and thus old enough to stand trial and be persecuted as witches. Sexual offenders were passed off as evil spirits. In 1624, the chancellor to the Prince Bishop of Wurtzburg wrote "there have been 300 children of three and four who are said to have intercourse with the devil. I have seen children of seven put to death" (cited in Rush, 1980, p. 39). Rush reports that one child who was reportedly raped by an incubus was infected with virulent gonorrhea. Another attempted to divert attention from her pregnancy by claiming to be possessed by three devils (Rush, 1980, p. 40). Rush also notes that in France during the 17th century, alarming numbers of nuns and school girls reported being sexually tormented by demons, and they evidenced symptoms of dramatic convulsions, writhings, and vomiting.
Projection of adult pedophilic fantasies onto the children was evident. Kahr (1991, p. 202) notes:
...during the sixteenth
and seventeenth centuries, numerous little girls were
imprisoned,
tortured, and burnt at the stake because their tormentors insisted that
they had fornicated
with the Devil and had attempted to seduce innocent and
unsuspecting
men. If a man of this era wished to rape a young girl, he could blame
the assault
on the Devil.
During the 19th century, sexual exploitation of children was widespread (deMause, 1997; Masson, 1984). There was massive production and distribution of child pornography, including poetry (Kahr, 1991; Rush, 1980). Prostitution was legalized in 1873 in France, and girls had to be at least 14 years old to give consent. Ambroise Tardieu, eminent professor of legal medicine at the University of Paris, published an article in 1860 wherein he documented physical and sexual abuses of children, often by their own caretakers (cited in Masson, 1984). Krafft-Ebing noted that in France between 1829 and 1870, there were 36,176 cases of child rape/assault reported (cited in Masson, 1984, p. 25). During this era, masturbation was viewed as inherently pathological -- as being a symptom of mental illness (Krafft-Ebing, 1906/1924), to the extent that prepubescent children were institutionalized for excessive masturbation (Zambaco, 1882, cited in Masson, 1986). Recent empirical literature provides evidence that children who have been sexually abused may engage in excessive masturbation.
Children were also victimized at the hands of medical professionals. One physician in the 19th century described an institutional treatment protocol for curing masturbation in two young sisters (Zambaco, 1882, cited in Masson, 1986). Treatment involved corporal punishment, including whipping, being placed in a straightjacket, being tied down on the bed, and, finally, cauterization of the buttocks with a large heated rod iron; and torture by way of cauterization of the clitoris, labia majora, and the entrance to the vagina. These girls were 6 and 10 years of age.
Zambaco describes a scene of his treatment of the six-year old child. He wrote (pp 81-82):
Then I picked
up the enormous red hot ax, but I only cauterized her clitoris with a
tiny stylet,
three millimeters in diameter, that had been heated red-hot by an
alcohol lamp.
"If you do it again," I told her, "I will burn you with the large iron
ax, and I will
show no mercy.
A few days later:
A new cauterization.
I burned her three times on both labia majora, and once on
the clitoris,
and to punish her for her disobedience I cauterized her buttocks and
loins with the
dreaded large iron (p. 82).
Three days later: "Third cauterization of little Y, who sobs and screams" (p. 83). About one month later: "I cauterized the clitoris and the entrance to the vagina of both sisters" (p. 85).
Zambaco concludes (p. 88)
It is reasonable
to presume that cauterization with a red-hot iron deadens the
sensitivity
of the clitoris, and that if repeated a certain number of times, it can
entirely destroy
the clitoris. The second sensitive genital spot, the vulvar orifice, is
also deadened
by cauterization, and therefore one can easily imagine that children,
once their genitals
have become less sensitive, would be less likely to touch
themselves there.
He further wrote "...fear at the sight of the instruments of torture, and the images that a red-hot iron produces in the imagination of children, should also be counted among the beneficial effects of electrical cauterization" (p. 88).
Another prominent physician, Alfred Fournier, after observing tissue damage of the genitalia of young female children, concluded that the lesions and other physical damage were due, not to actual sexual assault, but to "simulated sexual abuse" (cited in Masson, 1986, p125). He wrote:
In brief, these
cases consist of artificially produced vulvar lesions on a young child
which are meant
to resemble the lesions of sexual abuse, and the imputation of this
abuse to a carefully
selected perpetrator, to serve the simulator's self interest" (pp
125-126).
He also notes the comments of a colleague, Brouardel, who stated "girls accuse their fathers of fantasized sexual abuse, either of them or of other children, in order to achieve their liberty, so that they can give themselves over to debauchery, etc." (1880, cited in Masson,1986, p. 120 footnote).
Another physician, C.S. Fere, wrote:
It would not
have been without interest to see if the majority of little girls who
become the victims
of these degenerates [pedophiles] are not themselves
predisposed
to it by belonging to a special category; a large number of these girls
are hereditarily
tainted and present organic anomalies. Often they are prematurely
developed and
have a peculiar genital physiognomy which is mirrored by a
particular expression
in their eyes. This contrasts with the childlike lower part of
the face and
the rest of the body. It is this look which somehow brings them to the
attention of
depraved men" (cited in
Masson, 1986, pp. 15-16.)
The Aetiology of Hysteria
In The Aetiology of Hysteria, Freud (1896/1962) postulated that early sexual trauma was the cause of hysteria, however, he later changed his position. According to Masson (1984), Freud's renunciation of the seduction theory in favor of the Oedipal theory occurred after Freud received, in his words, "an icy reception from the asses" (cited in Masson, 1984) at a Psychoanalytic Conference. He wrote: "I was at last obliged to recognize that these scenes of seduction had never taken place, and that they were only fantasies which my patients had made up" (cited in Masson, 1984, p. 11). The psychohistorian Lloyd deMause argues that Freud's renunciation of the seduction theory was less politically motivated than Masson argues. According to deMause (1997), Freud was well aware of the sexual abuses that were inflicted upon children, and even held that they can be beneficial in that men who had been abused as young boys by women tended to escape neurasthenia.
Freud, although he acknowledged the existence of child sexual abuse, held that sexual abuse per se was not harmful to the child unless it resulted in unconsummated excitation. It was only later that the abuse could cause problems, if later events triggered the memory of the earlier abuse (deMause, 1997). Thus, according to deMause, Freud largely held actual child sexual abuse, per se, to be harmless. Much of traditional psychoanalysis operated on the Oedipal assumption, treating actual memories of sexual abuse as fantasies (DeMause, 1991; Masson, 1984; van der Kolk, Waisaeth, & van der Hart, 1996). Denial on the part of others, including mental health professionals, itself constitutes one form of revictimization.
Although Freud (1920/1961) gave some acknowledgement to the role of trauma in hysteria in Beyond the Pleasure Principle following the first World War, he never came to integrate his ideas of the role of war trauma in hysterical symptoms and his earlier ideas on the role of childhood sexual abuse in symptoms of hysteria (van der Kolk, Weisaeth, & van der Hart, 1996).
The role of trauma in the etiology of certain psychological symptoms was acknowledged by the American Psychiatric Association in 1980. Before that time, post traumatic symptoms (or symptoms of hysteria) were not recognized as such by the medical establishment, but were viewed as being due to individual pathology, rather than trauma. van der Kolk (2000) notes that as late as the 1970s, incest was held to be incredibly rare in a major textbook of Psychiatry. In 1980, the construct of Post Traumatic Stress Disorder (PTSD) was incorporated into the Diagnostic and Statistical Manual of Mental Disorders, based on a symptom picture that was common to rape trauma survivors, battered women, Vietnam veterans and abused children (van der Kolk, Weisaeth, & van der Hart, 1996). At the same time, the construct of "hysteria" disappeared from the DSM system, and was divided into several different mental disorders (van der Kolk, Pelcovitz, Roth, Mandel, McFarlane, & Herman, 1996, p. 85).
Nature, Nurture, and Allostasis
Shalev (1996), in a summary of research on the role of the magnitude of the stressor in PTSD, notes that dangerousness of a rape incident and intensity of a torture experience or extent of physical injury are significant contributors to the onset of PTSD. The DSM-IV states that the severity, duration, and proximity of exposure to the traumatic event are the most important factors in the onset of PTSD, and that the "disorder can develop in individuals without any predisposing conditions, particularly if the stressor is especially extreme" (American Psychiatric Association, 1994, p. 427). With the inclusion of the PTSD construct, there was some movement away from looking at constitution as a contributing factor (Yehuda & McFarlane, 1995). However, the pendulum now appears to be swinging back, based on more recent evidence that not everyone who undergoes a traumatic event develops PTSD. Twin studies on combat veterans have also suggested a genetic component to the onset of PTSD (True et al, 1993).
Other writers have documented symptoms that correlate to various degrees with PTSD, but that go beyond the symptoms included in the PTSD construct. These symptoms have been variously referred to as Complex PTSD (Herman, 1992) and as Disorders of Extreme Stress, Not Otherwise Specified (DESNOS) (Pelcovitz, et al, 1996). The focus here is on the effects of trauma on human development and functioning over time, with the acknowledgment that severe stress over time may have a profound effect on normative developmental processes. Thus, with the notion of Complex PTSD or DESNOS, there is the suggestion that extreme stress, including familial factors, strongly impinges on normative development.
McEwen (2000) states that genetic factors play a large role in terms of risk for stress-related disorders. He postulates that any given disorder is a function, not of a single gene, but of polygenetic variants (e.g., mutations on more than one gene), in interaction with behavioral and environmental factors, as well as the disease processes per se. He presents evidence to the effect that ongoing life stressors affect brain chemistry and functioning, which increase the individual's risk for disorder. He discusses evidence (p. 114) that genetic expression is a partial function of the external environment:
It is now well known that
genes are regulated by hormones, neurotransmitters and other chemical signals
that
are produced in response
to signals from the external and internal environment. For example, stress
is reported
to activate immediate early
gene expression, and these immediate early genes, like e-fos, are believed
to activate
other genes and thus regulate
aspects of cell structure and function...
He further notes that there is evidence that the encoding of information and controlling of behaviors by the brain itself acts to change brain structure and chemical processes -- that is, the activity of the brain itself alters its own structure. Most promising for survivors of trauma is the evidence he provides that the stress-induced structural changes in the brain are potentially reversible when the contextual factors, including lifestyle behaviors, are such that they are conducive to neuronal repair.
Criteria for DESNOS
It is unclear as to whether the symptoms of DESNOS constitute a more severe variant of simple PTSD, or whether they constitute a distinct disorder. DESNOS includes three symptom clusters and three characterological features. These latter features include relationship disruptions, changes to identity, and repetition of harm including revictimization and self-destructive behavior. These three features were included in a characterological cluster based on theory that these are disruptions in personality based in severe, ongoing stress, rather than being symptomatic of simple PTSD. McEwen's (2000) work can be interpreted to suggest that ongoing child abuse affects cortical and subcortical functioning, which may evidence itself as alterations in personality. The proposed criteria for DESNOS include alterations in regulation of affect and impulses; alterations in attention or consciousness; alterations in self-perception; alterations in relations with others; somatization; and alterations in systems of meaning (Pelcovitz, et al, 1996).
Revictimization
Childhood abuse, whether sexual, physical, or emotional, can have profound effects on the developing child’s sense of safety, feelings about self and others, relationships with others, cognitions (beliefs), and general sense of well-being. Empirical research shows that adults with a history of child sexual abuse trauma frequently report retraumatization in adulthood (Briere & Runtz, 1987; Cloitre, Scarvalone, & Difede, 1997; Dutton, Burghardt, Perrin, Chrestman, & Halle, 1994; Fergusson et al, 1997; Follette, Polusny, Bechtle, & Naugle, 1996; Fryer & Miyoshi, 1994; Gorcey, Santiago, & McCall-Perez, 1986; Kemp et al., 1991; Koverola, Proulx, Battle, & Hanna, 1996; Mayall & Gold, 1995; Neumann et al., 1996; Russell, 1984; Schaaf & McCanne, 1998; Stevenson and Gajarsky, 1992; Wyatt, Guthrie & Notgrass, 1992; Zeitlin, McNally, & Cassiday, 1993).
Prevalence rates of revictimization of adults who were abused as children vary depending on many factors, including variations in study methodology. Rates of revictimization during adulthood for those sexually abused as children range from 24% (Mayall & Gold, 1995) to 33.3% (Schaaf & McCanne, 1998) to 44% (Wyatt, Guthrie, & Notgrass, 1992) to 65% (for males) and 72% (for females) (Stevenson & Gajarsky,1992). Adult revictimization rates of persons physically abused as children are reported as at 50.9% in one study that looked at physical abuse specifically (Schaaf & McCanne, 1998). For combined physical and sexual abuse during childhood, Schaaf and McCanne (1998) report an adult revictimization rate of 77.4%. Adult victimization of persons not reporting any form of childhood abuse range from 16.9% (Mayall & Gold, 1995) to 31.3% (Schaaf & McCanne, 1998).
A review of literature on revictimization suggests that adults who were abused as children and who are revictimized as adults may be at higher risk of revictimization because: (a) they have learned maladaptive ways of thinking, coping, and relating to others (Messman and Long, 1996); (b) they may be attempting to attain mastery of the trauma (Chu, 1992; Levy,1998); (c) their posttraumatic symptoms may predispose them to be more vulnerable to revictimization (Chu, 1992), including a biologically-mediated "inescapable shock" response upon exposure to danger (van der Kolk, et. al, cited in Chu, 1992); (d) the abuse may result in problems with self/identity development, such that the individuals interact with abusive persons in a manner that is in accord with their negative view of themselves (Chu, 1992); (e) they may have developmental disturbances in affect regulation, which may relate to problems with self/identity, numbing responses, inescapable shock, alexithymia, and/or dissociation, and may predispose them to either not feel or not pay attention to "danger signals" (Cloitre, 1998; van der Kolk, 1996); and (f) they may experience Finkelhor and Browne’s (1985) traumagenic dynamics of child sexual abuse, which may increase the risk of subsequent revictimization (Mayall & Gold, 1995).
Empirical studies have offered support for a relationship between revictimization and PTSD symptoms (Cloitre, Scarvalone, & Difede, 1997; Koverola, et al, 1996; Schaaf & McCanne, 1998) and also between revictimization and interpersonal and self problems (Cloitre, Scarvalone, & Difede, 1997).
A recent preliminary analysis of predictors of revictimization in persons who experienced sexual and/or physical abuse before the age of 18 was conducted (Dietrich, Haverkamp, Figley & van der Kolk, 1999), which utilized the DSM-IV Field Trials data on DESNOS (Pelcovitz, et. al, 1996). Revictimization was measured by way of the Structured Interview for Disorders of Extreme Stress (SIDES) lifetime revictimization item, which reads "I find that other traumatic experiences keep happening to me" (yes or no). The item does not request elaboration on the type of traumatic events experienced. Of the persons who experienced physical and/or sexual abuse/assault before the age of 18, 45.9% reported that they had been revictimized since their original trauma. PTSD diagnosis predicted revictimization in this group, as well as some DESNOS variables. The role of PTSD varied with child sexual abuse subgroups.
A Contextual Developmental Model of Revictimization
Victoria Follette and colleagues (1998) favour a contextual perspective of trauma, rather than a disease model of trauma. In this viewpoint, looking at the social and learning factors that are involved in the formation of post-traumatic symptoms is preferable to looking at so-called pathologies of the individual. They make reference to the finding that many people do not in fact develop PTSD following trauma exposure, and the corresponding conclusion that PTSD is not normal. They ask:
Will increased public and professional awareness
of this finding create a different societal situation for the trauma
survivor, in which the likelihood of viewing posttrauma
problems as psychopathologies of the individual ("blaming
the victim") increase? Rather, we hope that a dialectic
emerges that encompasses both healthy, adaptive
responses and more symptomatic responses to trauma
as normal.
Susan Wooley (1996) similarly favors a contextual perspective of revictimization. She expresses some concern that focusing on personality characteristics will result in a "blaming the victim" stance, rather than holding perpetrators accountable for their actions. She wrote, in response to the argument that not looking at characterstics of the individual is akin to stifling scientific inquiry:
It would be unfortunate indeed if women’s commitment
to helping victims and to bringing the issues surrounding
abuse to light should operate to stifle inquiry
and debate, demanding an alignment with victims so blind that their
full dilemma cannot be seen and denying, for example,
that abuse does in fact change people, distorting their
relational development in ways that truly effective
therapies must address (p. 200).
I empathize with the concerns expressed by these writers. With the accumulating evidence that premorbid factors increase the risk of posttraumatic pathologies, there is a concomitant risk of regressing to earlier notions where individual factors are emphasized, such as the view expressed by Fere at the beginning of this article. The risk is that there may result a black-and-white view, particularly among some followers of certain groups who tend to minimize sexual abuse and where children may be seen not only to cause themselves to be abused (e.g., through a certain "expression in their eyes"), but as inadvertently causing themselves (via predispositions) to fall ill as a result of abuse. It is, therefore, important for researchers and clinicians to stay mindful and avoid a mindset that emphasizes univariate, linear, causation. McEwen's (2000) work is exemplary in this regard -- his allostatic model emphasizes the interaction between a myriad of variables, including reciprocal effects of environment (e.g., abuse), brain structure and function, individual interpretations, lifestyle, disease processes, and genetic expression. His model not only provides many possible avenues of intervention, but offers hope for those who, perhaps, can benefit from hope the most.
Summary and Conclusions
In summary, the 19th century history of trauma painted a picture that focused on pathologies of the victims, with little cognizance of the greater contextual factors that contributed to the symptom picture. Freud was among the first to notice a connection between symptoms of hysteria and child sexual abuse, however, Freud later withdrew his position and changed his Seduction Theory to his Oedipal Theory. Janet's views on dissociation and its' relation to hysteria were largely ignored for decades.
The role of trauma in the etiology of posttraumatic symptoms was incorporated into the DSM-III in 1980 (American Psychiatric Association), and there was a move away from looking at premorbid vulnerability as the contributing factor. However, recent findings that not all traumatized persons develop PTSD, along with findings from Veteran twin studies, has led some writers to emphasize a genetic component to PTSD. Others have noticed a symptom pattern that goes beyond simple PTSD in persons who have experienced chronic trauma, particularly during childhood, including repeated revictimization.
The question as to whether the disruptions in development seen in chronically traumatized children are a function of inherent pathologies/vulnerabilities; a function of the severity, length, and other characteristics of the trauma; a function of greater environmental factors; or a function of some combination of the above, has not been answered conclusively. At this point in time, it may be too early to state with any certainty which of these factors are more or less pathogenic of PTSD, of developmental disruptions (as in DESNOS), and/or of revictimization. However, it seems pretty clear that there is no one, single, factor that results in poor outcome, and that there is no one particular type of outcome.
Empirical literature on risk and/or resiliency factors in CSA has examined the role of several different variables. Characteristics of the abuse circumstances, internal mediating processes, and factors external to the individual have been found to have an effect on the outcome of CSA (Morrow & Smith, 1995; Pynoos, Steinberg, & Goenjian, 1996; Shalev, 1996). Coping skills and strategies, including cognitive strategies, appear to play a strong mediating role between the traumatic stressor event (CSA) and the outcome (Cicchetti et al., 1993; Spaccarelli, 1994; Trickett & Putnam, 1993; Wyatt & Newcomb, 1990). For example, effectively dealing with a stressor may act to enhance one’s sense of competence and resourcefulness, leading to successful adaptation to subsequent stressors (Briere, 1997; Haggerty & Sherrod, 1996; O’Leary & Ickovics, 1995).
The empirical research seems fairly consistent in the finding that when abuse is prolonged, severe, involves a family member, and is associated with neglect and lack of social support, that the effects are more damaging (Binder, McNiel, & Goldstone, 1996; Coffey et al., 1996; Tsai, Feldman-Summers, & Edgar, 1979; van der Kolk, 1996; Wyatt & Newcomb, 1990). It has been suggested that the role of the severity of the stressor (e.g., depth of penetration in rape or child sexual abuse) may not play an especially significant role in outcome (e.g., Lam & Grossman, 1997; cf American Psychiatric Association, 1994; Shalev, 1996; Wyatt & Newcomb, 1990). However, a particularly severe traumatic event (such as a particularly brutal rape, or rape of a small child with full penetration) will lead to significant tissue damage. It stands to reason that the physiological response to such trauma would increase the likelihood of biological numbing/peritraumatic dissociation, which has been shown to be predictive of PTSD (e.g., see van der Kolk, van der Hart, & Marmar, 1996). The concomitant release of stress hormones (which may be more likely with particularly brutal stressors), results in structural impairments over time (McEwen. 2000). Thus, it seems very plausible that looking only at subjective appraisal (e.g., Lazarus, 1990; 1993) or only at the biological stress response (i.e., Selye, 1936; 1956) in isolation is insufficient to account in full for outcome. It is likely that subjective factors and the nature of the traumatic stressor event(s) interact with each other and with contextual factors to result in the variations in outcome observed in those who have suffered enduring trauma.
Research suggests that not all people who have experienced trauma go on to develop PTSD. What can we conclude from this? Did this research include chronically and severely traumatized persons who were still in the formative stages of development? Did this research utilize traumatized populations who experienced less severe forms of trauma, or trauma after the personality was fully developed, or trauma of shorter duration or lesser intensity?
Is PTSD the only possible outcome of trauma? What about the documented relationship between trauma and ADHD (Putnam, 1997; 2000), anxiety disorders (Marshall, et.al, 2000), somatization (Pelcovitz, et. al, 1996), personality disorders (Pelcovitz, et al, 1996) and other psychiatric conditions (McEwen, 2000)? Should all of these disorders be re-classified based on postulated etiologies? Should the DSM pay more attention to the contextual factors within diagnostic formulations (i.e., incorporate them into Axes I and II), rather than keeping contextual factors on a separate axis?
What about the role of family environment? Is a family environment that is invalidating more pathogenic than abuse itself? Might it depend on the severity of the invalidation (e.g., Herman, 1992)? The severity of the abuse? What about social support external to the family, such as the role of teachers and other influential individuals in the child's socialization?
The effect of chronic child abuse on self-development and post-traumatic symptoms is particularly complex, with a myriad of possible variables contributing. There is wide variation in outcome, including variations in presentation of symptoms of DESNOS. To the extent that our mainstream research paradigm and statistical methodology is premised on univariate physical causation, and to the extent that the effects of chronic abuse on child development is multivariate, we may gain more depth in understanding by utilizing case methodology, and building from there (Richters, 1998). Alternatively, prospective longitudinal studies (e.g., Putnam, 2000) can provide fuller understanding.
The field of traumatic stress studies is still in its infancy, and much more remains unknown than known. As such, we need to use care in our theoretical formulations, and proceed with some caution in terms of postulating non-abuse/neglect factors alone since people can be, and are, seriously hurt by trauma. Much more study is needed to shed light on these complex issues.
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