Dutton, D.G. (2001)  The neurobiology of abandonment homicide. Aggression and Violent Behavior, 7, 1- 15.

 

 

                              The Neurobiology of Abandonment Homicide

 

 

 

 

 

                                                   Donald G. Dutton

 

                                           University of British Columbia

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Requests for reprints to:     dutton@interchange.ubc.ca  or Department of Psychology, University of British Columbia, Vancouver, B.C., Canmada, V6T 1Y7.

                                                                                    

 

 

 

 

Key words: homicide, trauma, attachment, neuropsychology, neurobiology

 

 

 

 

 

Neurobiology of Abandonment Homicide

 

 

 

 

 

 

 

                                                            Abstract

 

 

  A review is made of the typical modus operandi and psychological profile of uxoricide (wife murder) perpetrators. Typically most had traumatic childhoods and have current personality disorders (typically Dependent, Passive-Aggressive or Borderline P.D.). The uxoricide occurred during attempted abandonment of the relationship by the female was characterized by extreme violence and elements of disorganized behavior by the perpetrator. A review is also made of the neuroanatomy and neurobiology of aggression. It is found that the orbitofrontal cortex is implicated in control of aggressive impulses. This cortical area matures during the critical “rapprochment subphase” of early development (1.5- 2 years). Attachment dysfunction during this period may interfere with critical development. It is found that low levels of serotonin and high levels of norepinephrine (NE) are implicated in aggression. It is also found that low levels of serotonin and high levels of NE are long term neurobiological sequelae of trauma. Attachment trauma can occur during the rapprochment subphase. It is suggested that a biological basis may serve to connect early trauma experience with a specific rage response to abandonment and spousal homicide. Neural networks containing malignant memories may be the neural mechanism by which perceived abandonment generates such symbolic terror and rage.

 

 

 

 

 

Neurobiology of Abandonment Homicide

 

 

 

         This paper examines psychobiological moderators of a special category of homicides; those precipitated by abandonment by an intimate other or its’ anticipation. I am not referring to intimate homicides that are instrumental; planned for financial gain. I am describing reactive spousal homicides resulting either from a perception that a spouse is leaving or has left or those longer term “abandonments” predicated on emotional distancing and an ensuing “catathymic crisis” (Wertham 1937). Meloy (1992), Wilson & Daly 1993, Dutton & Kerry (1999) and others have written about this category from a number of perspectives. Although Wilson & Daly (1993) erroneously refer to these as “estrangement killings”, they are predicated on abandonment not estrangement which merely connotes separation. It is the perception that one is being left that triggers disproportionate rage and violence which often appears inexplicable to jurors. Wilson & Daly (1993) noted that such homicides are more likely for male-perpetrator, female victim combinations. Dutton & Kerry (1999), in a study of 90 incarcerated spousal killers, found that the majority were reactive unplanned events. Typically the man and woman had separated or were about to separate. The man was making one last desperate (and unsuccessful) attempt to convince the woman to stay in the relationship. The man then killed the woman, typically with a weapon found at the scene (frequently a knife or club) or strangulation. The number of blows/ stab wounds with a knife was extreme, qualifying the act as overkill (more violence than necessary for death to occur). Typically there was an incompetent attempt to move or hide the body but in such a way that it would inevitably be found. Post homicide suicidal ideation and/or unsuccessful suicide attempts were frequent. Many of the perpetrators left the scene with obvious blood traces and were quickly apprehended. Most had sketchy amnesia for the event (Swihart & Dutton 2001). In most cases there had been a history of domestic violence and prior separations. Most of the men had Dependent, Passive-Aggressive or Borderline personality disorders and non-aggressive

 

Neurobiology of Abandonment Homicide

 

criminal histories. Dutton & Kerry (1999) found that Psychopaths were more likely to kill for

instrumental reasons. The men who kill in response to abandonment have insecure attachments that serve ego integrating functions for them.

 

     Meloy (1992) describes a catathymic homicide  as delineated by “intense autonomic arousal, (and) overwhelming anger during the violence (p. 47)”.  Wertham (1937) had described  acatathymic crisis”: a seemingly unsolvable state of chronic, aversive emotional tension, viewed as inescapable. The tension builds in what Revitch & Schlesinger (1978) called an incubation period, and of which the perpetrator may be only partially conscious. Isolation and rumination on the faults of the eventual victim precede the violent act, which is carried out after building tension and the belief that the target is the cause of the intolerable tension.  With both reactive and incubation homicides there is a release from tension with the violent act and a return to baseline and “superficial normalcy”. Revitch & Schlesinger (1978) rightly saw the tension and violence as expressions of a “fight on the part of the patient for safeguarding his personality”. That is, the perpetrator either perceives (in abandonment cases) an impending loss of their ego-integrity or (in the case of incubation homicides) an invasion of their autonomy. It is this threat-to-the-self aspect that generates so much rage; the rage is a primitive reaction to a sense of incipient annihilation.

  Dutton (1998) developed and tested a theory, combining many of these elements in a non-lethal group of spouse assaulters. In a sample of 200 men, he related psychological assessments of the perpetrators to spouses’ reports of physical, sexual and emotional abuse. He also examined the developmental history of the perpetrators. These men also experienced abandonment rage and acted in a controlling way to avoid it, frequently questioning their spouses on their whereabouts, etc. The non-lethal abandonment rage stemmed from a triad of early developmental factors:

 

Neurobiology of Abandonment Homicide

abuse, being shamed and being insecurely attached. Development of attachment insecurity is

especially  acute during the “rapprochment subphase” of early development (1.5- 2). These, he argues constituted a form of trauma in an immature male with resulting difficulties in ego development and tendencies to use control and violence as guards against abandonment by intimates (Dutton 1995, 1999). The strength of the anxiety on which this rage was based could be inferred from paranoid reactions to the intimates use of space and time and from affective reactions to videotapes depicting intimate abandonment (Dutton & Browning 1988). Abusive men self reported significantly more arousal, anger and anxiety to a video depicting a woman’s independence (perceived as abandonment) than did other groups of men. They did not differ on responses to “neutral” conflict videos. Dutton (1994) demonstrated PTSD profiles in these men similar to those obtained from independently assessed war veterans. Both groups demonstrated “82C” elevations on the MCMI-11 found by other researchers (Roberts et al. 1982; Hyer et al, 1989)

 

Modus Operandi

  The key ingredients of abandonment homicides then are as follows: first, a male perpetrator with ego deficits related to early family-generated trauma and insecure attachment. Second, a perception of being abandoned by an intimate other, and a disproportionate arousal-rage reaction generated toward the woman (but which may deflect to children or others present and to the perpetrator himself), sometimes described as “overkill”. Finally, a “disorganized” or poorly implemented attempt to hide the body and conceal evidence (bloodstains) on the self. Men who flee the scene frequently did so with visible bloodstains and may be apprehended when noticed in public ( see State of Cal v. Henriquez, State of Washington v. Waldradt). To date there has been no attempt to examine the neurological or neurobiological features of such killings although a considerable body of literature has grown on many features of such homicides and of the

Neurobiology of Abandonment Homicide

 

neurobiology of aggression. Since I have argued that such homicidal rage has a trauma basis, and have developed that argument with regard to non-lethal intimate violence (Dutton 1998, 1999), I attempt here to review the growing literature on the neuropsychology of aggression; both its’ neuroanatomical and functional aspects. I also review the literature on neural development, especially as it is affected by trauma and trauma caused by separation. Needless to say, any attempt to explain a macrobehavioral pattern will, of necessity, be speculative. Nevertheless, there are components of that pattern upon which recent neurobiological studies can shed some light.

Neurobiology of aggression

  Kardiner (1941) first recognized that “explosive reactions” were part of the “traumatic neuroses” and stressed that explosive aggressive reactions were foreign to his patient’s pre-trauma personalities. He stated “The aggressiveness of the traumatic neurotic is not deliberate nor premeditated. His aggression is always impulsive; nor is it capable of being long sustained. Entirely episodic, it often alternates with moods of extreme tenderness.” (Kardiner, 1941, p. 97 cited in van der Kolk 1996).

Neuroanatomy

     Davidson, Putnam & Larson (2000) review the activity of brain circuitry regulating emotion:the orbital frontal cortex (OFC), amygdala, hypothalamus, anterior cingulated cortex and prefrontal cortex (PFC). The amygdala appears crucial for learning to associate stimuli with intrinsic punishment and reward.  In human neuroimaging studies, the amygdala is activated in response to cues connoting threat (such as facial signs of fear). In contrast, increasing intensity of angry facial expressions is associated with increased activation of the orbitofrontal cortex (OFC),

 

Neurobiology of Abandonment Homicide

 a cerebral structure that is located in the anterior undersurface and interior of the cortex and is especially developed in the right hemisphere. Using functional MRI scans, Davidson et al. found that impulsive-aggressive individuals do not show normal glucose metabolic functioning in the PFC area. Furthermore, lesions in the PFC or OFC areas produce syndromes characterized by impulsivity and aggression. Also, impulsive-aggressives (Temporal Lobe Epilepsy:TLE)  diagnosed with intermittent explosive disorder have left PFC areas that are 17% smaller than TLE’s without a history of aggression. The authors conclude that these neuroanatomical areas and the interconnections amongst them are central in the generation of impulsive aggression. Further they argue that the structure and function of this circuitry is affected by both genetic and early environmental factors.

 

      Studies on the development of these neuroanatomical areas has been extensively reviewed by Schore (1994) who concludes that “the infant’s affective interactions with the early human social environment directly and indelibly influence the postnatal maturation of brain structures that will regulate all future socioemotional functioning. The system that regulates this functioning is comprised of the orbitofrontal cortex (OFC). Because of its’ unique and extensive interconnections to other subcortical systems, the OFC represents an hierarchical apex of the limbic system which regulates emotional regulation. The critical period for maturation of the OFC occurs at the same temporal interval of interest to attachment researchers such as John Bowlby and psychodynamic theorists such as Melanie Klein (i.e. the “rapprochment subphase” or PreOedipal stage of development, occurring around age 1.5 to 2 years).

         Schore (1994) describes the development of impulse control or “automodulation of rage” as occurring because of “structural transformation (rewiring) of the  (OFC), a system governing internal inhibition ..this anatomical locus with its far reaching cortical and subcortical connections

 

Neurobiology of Abandonment Homicide

is equivalent to the frontal functional system which inhibits drive….its mature function is expressed in the braking mechanism of shame, which leads to inhibition and “drive restraint”  (p. 343).

 

 Perry (1995) argues that “the structural organization and the functional capabilities of the mature brain develop throughout life, with the vast majority of the critical structural organization taking place in childhood…due to the sequential development of the brain, disruptions of normal developmental processes early in life (e.g. during the perinatal period) which alter the brainstem or midbrain will necessarily alter the development of limbic and cortical areas because the critical signals these areas depend on for normal organization originate in these lower brain areas” (p 5). In a study of hyperaroused, reactive boys who had been exposed to prolonged domestic violence, Perry found that a subset of the boys developed predatory behavior. The boys described a soothing, calming effect when they began “stalking” a victim. Perry views aggressive acting out as a means of attempting to control inner aversive arousal and a persistent fear response developed through exposure to domestic violence. 

 

 Functional imaging studies of violent psychiatric patients have demonstrated decreased brain metabolism in prefrontal and medial temporal cortices (Volkow & Tancredi 1987), along with a higher incidence of structural abnormalities seen on CT scans (Wong et al., 1994). These findings lend support to a theory that prefrontal regions are involved in containing affective reactions and inhibit limbic regions normally involved in the expression of aggressive drives. Further evidence comes from a study by Raine et al. (1998) that tested the notion that impulsive, affectively aggressive individuals differed from predatory reactive aggressive persons. Citing past studies showing that the prefrontal and subcortical areas played a role in aggression, they did brain imaging studies (PET Scans) of 41 subjects in prison for murder or attempted murder and 41 non-

Neurobiology of Abandonment Homicide

violent controls. Affective murderers relative to controls had lower left and right prefrontal functioning, higher right hemisphere subcortical functioning and lower right hemisphere prefrontal/subcortical ratios. In contrast, predatory murderers had prefrontal functioning that was more equivalent to comparisons, while also having excessively high right subcortical activity. The analog, the authors argued, was that the prefrontal areas acted as a brake and the subcortical areas as an accelerator for violence.

 

 Hence, the relative balance of activity between the two areas was important and consistent with Schore’s developmental emphasis on the OFC area as a braking mechanism. Schore

(1994:344) attributes the development of stress regulating strategies to practicing “distress-relief sequences” which “ facilitate a transition from distress to quiet alertness….. relief is neurophysiologically expressed in the diminution of sympathetic and activation of parasympathetic activity…distress-relief sequences, which are composed of sequential periods of sympathetic hyperaroused distress (separation protest, narcissistic rage) followed by parasympathetic relief thus reflects a shift of limbic system predominance”. Pine (1990) concludes that as a result of particular experiences with a reliable caregiver the infant develops an expectation of relief which allows for delay in the face of need and acts to regulate inner states….prefrontal cortical structures are known to mediate the highest control of “bridging temporal gaps”  (p. 344)

  

  Raine, Bushsbaum & Lacasse (1997) found brain abnormalities in murderers who had pleaded NGRI (Not Guilty by Reason of Insanity). Using PET scans and a continuous performance challenge task, they found 41 murderers (compared to matched controls) showed reduced glucose metabolism in the prefrontal cortex, superior parietal gyrus, left angular gyrus and the corpus callosum. Abnormal asymmetries were also found for the murderers (left hemispheric function

Neurobiology of Abandonment Homicide

lower than right) in the amygdala, thalamus, and medial temporal lobe. The authors speculated that a “network of abnormal cortical and subcortical brain processes may predipose to violence in murderers –pleading NGRI” (p. 495).

 

Neurobiological Functioning

 Coccaro (1996) and Coccarro & Kavoukian (1996) have examined the role of monoamine transmitters (serotonin, norepinephrine and dopamine) in human aggression and violence, using postmortem brain studies of individuals who had committed suicide or had been killed in accidents. Suicide victims tended to have lowered serotonin levels compared to accident victims. Furthermore, individuals who had used a violent means of committing suicide had even lower levels of serotonin (5-HT) in their cerebrospinal fluid (CSF). Coccarro & Kavoukian also reports studies linking low serotonin levels with histories of aggressive behavior in naval recruits. As the authors put it “this suggested that, in some populations at least, reduced CSF 5-HIAA (a metabolite of serotonin) concentration predisposes humans to aggression directed both at the self and the other” (p. 69). Studies of brain receptors generally support the hypothesis that self-directed aggression is associated with reduced serotonin activity. Typically suicide victims have reduced numbers of receptor sites compared to accident victims. Comparisons of groups low or normal in serotonin (5-HT) levels, revealed that 5-HT function is specifically associated with physically assaultive behaviors as measured by the Buss-Durkee assault scale. Stanley et al (in press) assessed whether serotonin dysfunction was related to aggression in the absence of a history of suicidal behavior. They did a median split for aggression on 64 patients with no suicidal history. The aggressive group had significantly lower levels of a serotonin metabolite drawn from cerebrospinal fluid (CSF 5-HIAA) concentrations than did the non-aggressive group. Aggressive individuals also scored higher on self-report measures of hostility, impulsiveness and sensation seeking. Stoff & Vitiello (1996) examined the role of serotonin in adolescent

Neurobiology of Abandonment Homicide

aggression. They noted that animal behavior studies indicated that increasing or decreasing serotonin (5-HT) activity produced concomitant decreases or increases in aggression and that these results were consistent with the human data collected by Coccaro & Kavoussi (1996). Stoff and Vitiello reviewed 25 studies and noted that aggressive tendencies and cerebrospinal serotonin  concentrations (obtained by lumbar puncture) are both highly stable over the life cycle. Decreased levels of CSF concentrations of 5- HIAA were obtained in children and adolescents with Conduct Disorder, and low 5-HT levels were generally related to aggressiveness in adolescent populations.

 

Coccarro & Kavoussi (1996) also review animal studies for other neurotransmitter systems such as norepinephrine (NE), dopamine (DA) and endogenous opioids. These include findings that increased NE function in the brain correlates positively with the number of shock- induced aggressive episodes in rodents (Stolk, Connor, Levine & Barchas 1974). Agents that enhance NE function (i.e. tricyclic/MAOI antidepressants) increase shock-induced fighting in rodents (Eichelman & Barchas 1975). Stimulating post synaptic noradrenergic receptors in the hypothalamus facilitates aggression in cats (Barrett, Edinger, & Siegel 1990). In humans, clinical treatment with these agents is associated with agitation and irritability, especially in subsets of patients with borderline personality disorder (Cowdry & Gardner 1988; Soloff, George, Nathan, Schultz & Perel 1986). Similarly, agents that diminish noradrenergic function diminish aggression.

 

  In humans, CSF and plasma measures of NE are positively related to a scale measuring impulsivity (Roy, de Jong & Linnoila 1989). Coccaro & Kavoukian (1996) hypothesize that a neuropsychological model of impulsive aggression in humans is modulated by serotonin system function; the lower the functional status of the serotonin system, the more likely the individual is to respond to “threat, frustration or aversive circumstances with an aggressive outburst” (p. 80).

Neurobiology of Abandonment Homicide

The role of other neurotransmitter systems (NE, DA, opiates) lies in their role in perceiving threat or frustration and in activating the cognitive and motor systems necessary for aggression. This model suggests a person who is generally reactive to threat with aggression. However, most spousal killers have no record of conviction for aggression outside an intimate relationship (Dutton & Kerry 1999). Dutton (1998) has suggested that insecure attachment is a trauma source for both lethal and non-lethal spouse abusers. Insecure attachment would indicate an inability to self-soothe and a consequent reliance on the intimate other to provide soothing. In addition, in men who experienced traumatic childhoods, attachment or threat of lost attachment may produce a variety of psychobiological reactions similar to PTSD reactions (Dutton 1995, 1999). If the threat of attachment loss is a distinct stressor in these men, then the psychobiological reactions described by Cocarro & Kavoussi (1996) would occur with greatest intensity to perceived abandonment. Another line of research has shown that separation per se produces alterations in neurotransmitter function.

 

Psychobiology of  Attachment-Separation trauma

 

     Van der Kolk (1987a and b) showed how primate research had demonstrated that social attachment was related to core neurobiological functions in the primate brain. In mammalian species, dependency on adult caregivers has become so strong that separation from the mother alone, even without external danger, produces distress reactions including cardiac and respiratory depression, elevated plasma cortisol levels. Animals separated from their mothers generate endogenous opioids. When opioid receptor sites are blocked in male monkeys, need for social attachment increases. Furthermore, trauma seems capable of altering brain anatomy.  As revealed by MRI’s, subcortical areas in traumatized individuals become physically altered by the trauma. Stein et al. (1994) found a 7% reduction in hippocampal volume in women with PTSD who had suffered

Neurobiology of Abandonment Homicide

repeated childhood sexual abuse. Gurvitz, Shenton & Pitman (1995) found that Vietnam Vets

with the most intense combat experience and most severe PTSD had average hippocampal shrinkage of 24%.

 

     Van der Kolk (1987) reviews the neurobiological consequences of disruptions of attachment during critical periods of early development. Noting that separation from the mother produces a protest/despair response in all primates, van der Kolk argues that “social attachment is not only a psychological event; it is related to the development of core neurobiological functions in the primate brain” (p. 39-40). Separation distress is mediated by endogenous opioids, when these are mimicked by a dose of morphine, the separation distress call does not occur. Blocking opiate receptors greatly enhances the need for social attachment. Social isolation diminishes brain opiate receptor density in mice. The brain circuits that mediate separation distress are related to those that mediate pain: stimulation of the parts of the thalamus, amygdala, hypothalamus and neocortex all elicit distress vocalizations in animals (p. 41). As van der Kolk puts it “there is now some evidence that pain perception, separation distress, and affiliative behavior are all mediated, at least in part, by the brain opiate system, and that all three are related to discrete and interconnected neuroanatomical systems” (.p 41). While these studies used non-human subjects, van der Kolk does note that “opiates do have the capacity to relieve feelings of separation and alienation in human adults. It is conceivable that unalleviated separation distress during infancy makes a person more likely to seek the comfort of actions that stimulate the opioid system to

cope with adult separation distress.

 

   van der Kolk (1996) has described numerous studies done on psychobiological reactions to separation trauma. van der Kolk recognizes attachment- disruptions as traumatizing (see also van der Kolk 1987, Dutton 1998, inter alia). Attachment disruption/ separation from the mother

Neurobiology of Abandonment Homicide

generates hyperarousal and difficulty in modulating arousal (Pitman 1995). In primates, neurotransmitter changes include decreased hypothalamic serotonin, (Coe et al. 1985), increased adrenal gland catechoamines (Coe et al 1983), and changes in plasma cortisol (Coe et al 1985), heart rate, body temperature, and sleep (Reite et al 1981). Studies of Vietnam veterans with PTSD showed elevated catecolamine levels (epinephrine and norepinephrine (NE)) Kosten et al. 1987. Increasing NE by injecting a drug (yohimbine) which blocks adrenergic receptors, produced panic attacks and flashbacks in veterans (Southwick et al. 1993).  Hence, war-induced PTSD appears to chronically increase sympathetic nervous system activity.

 

Interpersonal traumas experienced at early ages also produce profound physiological effects. This occurs because attachment is the most secure defense against trauma. When the attachment bond itself is disrupted, the ability to modulate arousal is lost. van der Kolk & Fisler (1994) found that traumatized adults who had childhood histories of neglect had extremely poor prognoses. van der Kolk (1987) describing the “separation cry and the trauma response’ lists a variety of neurotransmitter changes related to attachment and separation. In addition to those listed above for war veterans, separation from the attachment object produces release of adrenocotropic hormones (ACTH) and decreases in cortisol responsiveness (Mason 1967). Cortisol suppression has also been discovered in rape victims with histories of prior assault (Resnick et al. 1995). When cortisol is suppressed, ACTH produces increased serotonin metabolism and hence, lower serotonin levels. These, in turn have been linked to aggression as demonstrated above (van der Kolk 1996, Coccaro & Kavoukian 1996).  In adults with histories of prior trauma, the current trauma produces trauma-generated spiraling self- amplifying arousal reactions. In this group, aggression is a frequent response to the terror or uncontrollable arousal and anxiety.

 

Neurobiology of Abandonment Homicide

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          The capacity to reduce arousal is the major maternal quality that reinforces the early infants’ attachment to its’ mother (Mason 1968). Infants raised in abusive households experience extreme arousal from the abuse and simultaneously cannot be soothed by a mother who is unavailable by virtue of being an abuse victim (Dutton 1998). These children are traumatized and experience the psychobiologic reactions common to trauma victims. These include unmodifiable arousal, and a complex long term reactions comprised of polar opposites: hypermnesia vs. amnesia, hyperactivity to trauma stimuli vs. psychic numbing, traumatic reexperiencing vs. repression.

 

Klein (1980) noted that both panic attacks and depression are rooted in a neurological sensitivity to abandonment precipitated by early life experiences. As van der Kolk (1987) points out, “it is likely that certain childhood experiences make people vulnerable to disorders of the neurotransmitter systems, which may be activated under stress, particularly after the loss of affiliative bonds.”(p. 46)

 

When separation from the mother occurs, a variety of neurotransmitter changes are generated in the infant. Drugs that increase noradrenergic activity in the brain can reverse the effects of separation and social isolation. (Suomi  et. al., 1978). Hence, the secretion of noradrenalin is implicated in the separation response. Drugs that decrease the availability of the catecolamines (norepinephrine and dopamine) also aggravate the behavioral expression of separation stress in separated monkeys. Hence, NE is implicated in both separation stress and aggression (see Coccaro & Kavoussi 1996).  Serotonin appears to increase affiliative behaviors and decrease fear and anxiety. Dominant male monkeys have higher levels of serotonin than subordinate males. Inhibition of serotonin increases fear and impulsive aggression. Hence, low serotonin levels are also implicated in aggression (Coccaro & Kavoussi 1996), increased fear/anxiety and decreased

Neurobiology of Abandonment Homicide

tendencies to affiliate. Thwarted attempts to affiliate, conversely may lower serotonin levels in already chronically stressed (and cortisol-suppressed men), increasing the likelihood of violence. Coccaro et al. (1997) found that certain serotonin measures correlated well with tendencies to assaultive behavior in non-criminally aggressive personality disordered men. It is non-aggressive personality disordered men who fit the profile of potential spousal killers (Dutton & Kerry 1999).

 

 In abuse-traumatized men, hyper activity to separation is central (Dutton et al, 1994), they experience “Fearful” attachment styles, but use anger and control to avoid abandonment (e.g. threats to the attachment-object, monitoring of her use of time and space, undermining of her self confidence).  As van der Kolk (1996) points out, chronic physiological arousal and the inability to regulate autonomic reactions to internal and external stimuli affects people’s capacity to utilize emotions as signals. Some attempt to compensate for this chronic arousal by “shutting down” – avoiding stimuli that remind them of the trauma and by emotional numbing to both trauma related and everyday experience (Litz & Keane 1989).

 

PTSD, Anger and Violence

   Beckham & Moore & Reynolds (2000) reviewed several studies indicating elevated anger in Vietnam Veterans with PTSD. Hiley-Young et al (1995) found PTSD to be related to violence; 58% of a male sample of 177 reported previous violence towards their wife. Vietnam Vets with PTSD reported 13-22 acts of interpersonal violence in the preceding year compared to 0-3 acts in non-PTSD vets. (Beckham et al. 1992).  Beckham et al (1995) found that childhood physical abuse, combat exposure, current alcohol use and PTSD severity all contributed to interpersonal violence. According to Dutton’s (1998) model, the alcohol use would itself be a

 

Neurobiology of Abandonment Homicide

 consequence of early abuse/insecure attachment and the other predictors (with the obvious exception of combat exposure) would apply as well to non-vet groups. 

Dutton (1995) found that men in treatment for wife assault had similar profiles on the MCMI-11 to two independent samples of Vietnam veterans (Hyer et al, 1989: Roberts et al. 1982). This consisted of elevations on the 8 (Passive-Aggressive), 2 (Avoidant) and C (Borderline) Scales of the MCMI. Dutton found significant correlations between trauma symptoms and wives’ reports of abuse by her husband. Men with “82C” profiles were most abusive. Furthermore, men with the highest levels of trauma symptoms had experienced the least parental warmth and the most parental abuse. Later, Dutton (1998, 1999) found that parental shaming, in combination with abuse and lack of secure attachment produced adult trauma symptoms related to intimate abuse.

 

Targeting of the Violence

      The choice of an intimate partner as the target of the abandonment rage underscores the origin of that rage; abandonment by a parent. The abandonment terror is transferred to the adult partner because the ego deficits generated by the original trauma necessitate a current partner to maintain ego integrity (Dutton 1998).  The prospect of loss generates a subjective distress describes as extreme anxiety (Dutton & Kerry 1999). Below we consider whether neural networks contain the malignant memories that serve to target aggression toward the abandoning object.

 

Memory Retrieval and Abandonment Rage

 

    There are two issues concerning memory in intimate homicides; memory for the act and memories of the original trauma that are triggered by abandonment. Swihart, Yuille & Porter (1999) have discussed the “red-outs” that occur in spousal homicides. They suggest that extreme

 

Neurobiology of Abandonment Homicide

rage states (red-outs) create an inability to access state dependent memories. There is some evidence that re-creating the homicidal setting under hypnosis produces both the rage and the memory. This apparently occurred with Sirhan Sirhan’s recall of his assassination of Robert Kennedy. They suggest that both state dependence and the discrepancy between the act and the perpetrator s’ self image generate an inaccessible/repressed memory. Another possibility is that the rage and the memory loss have a shared, traumatically-generated neurobiological basis.

     The trauma origin of this abandonment rage also accounts for the memory difficulties.  As van der Kolk (1996) puts is “ the loss of recollections for traumatic experiences is also well documented” (283). Siegfried et al (1990) found that memory is impaired in animals when they can no longer actively influence the outcome of a threatening situation. Panic interferes with effective memory processing; both excessive endogenous opioids and norepinephrine interfere with the storage of explicit memory. The extreme emotion generated by abandonment may by retained separately from details of the actions involved (see Christianson 1992). Christianson suggests that specific details of an event and emotional details of an event may be retained separately, and that emotional experiences may use different mechanisms (not necessarily conscious) to process and store information. Thus, it may be possible to remember only the specific details or the emotional details of an event. The individual may remember that a strong emotion was felt (anger, anxiety), but cannot remember precise details or sequencing of events. In addition, abusive husbands with histories of abuse-victimization report higher trait dissociation (Swihart & Dutton 2001), suggesting that they would be most prone to abandonment-rage dissociation and subsequent memory problems. For obvious reasons, no psychobiological data exists on human subject samples in such circumstances.

 

 

Neurobiology of Abandonment Homicide

 

 Van der Kolk (1996) points out that severe stress generates endogenous opioids which inhibit pain and reduce panic. However, oversecretion of endonenous opioids and NE both interfere with the storage of experience in explicit memory. Siegfried et al. (1990) observed memory impairment in animals who can no longer influence the outcome of a threatening sitation. The animals freeze, panic and secrete endogenous opioids, as if preparing for pain or death.  Van der Kolk suggests that freezing/numbing responses may serve to remember situations of overwhelming stress. He also suggests that dissociative reactions in response to trauma may be analogous to the freezing complex in animals. Coccaro & Kavoussi (1996) found increased NE activity to be associated with aggression. Increased NE might also inhibit storage of memory for aggression, especially aggression occurring as an impulsive acting out to an abandonment panic state.

 

 Schwartz & Perry (1994) provide a potential explanation for a second memory issue, why abandonment represents such a traumatic stimulus for spousal homicide perpetrators. Abandonment in early childhood produces a stress response that includes “ a cascade of cellular and molecular processes that alter brain structure and function to create an adaptive record of survival-related information ‘ (p. 312) Neurotransmitter receptor/effector activation then alters intracellular chemical constituents. One important effect is the sensitization of receptors to similar future neurotransmitter stimulation in all synaptically connected neurons. These “neural networks” are comprised of “threat-sensitized interconnected neurons” that organize the brain of a survivor into functional neural networks that might include parts of the limbic system and amygdala. These networks become the “preferred new means for integrating sensation, perception, evaluation, processing, and memory storage and retrieval associated with threat-related information” (p. 313).

 

Neurobiology of Abandonment Homicide

What Schwartz & Perry call malignant memories  are “patterned dysfunctional contents of neural network activities integrating survival- related perception, memory, arousal, cognition, affect, somatic and psychological state, and behavior. Triggered by external sensory or internal cognitive, affective or somatic cues, a malignant memory invades experience with high levels of noxious arousal and can include cognitive distortions, memory changes, dissociative and somatic states, and behavioral and affective overactivity….activation of a malignant memory results in maladaptive states and behaviors.” (p. 313) According to Schwartz & Perry, malignant memories, rooted in early development trauma, are likely to manifest later as disorders of self, personality, or ego functions, including cognitive development and regulation of object relations, attention, affect and arousal. These malignant memories, stored in neural networks functionally cut off from higher cortical function can generate high arousal rage states and actions which later are poorly recalled in part, because they never were stored in higher consciousness. Some form of personality disorder would be expected in the perpetrator, typically Dependent or Borderline P.D. (see Dutton & Kerry 1999).   

   The purpose of this review was to establish that evidence has accumulated for a neurobiological link between abandonment and homicidal rage. The evidence is mainly of the sort where similar neural structures (e.g. the orbitofrontal cortex) or processes (low serotonin, high NE) are both a consequence of trauma during a crucial maturational period and implicated in spousal homicide. The “steering function” to the wife-target may be a neural network containing malignant memories of early abandonment. Of course, such a review also points out what is not yet known. Why, for example, would alterations in development of a neural structure or function produce rage? Bandura (1979) pointed out that Delgado’s famous work on hypothalamic stimulation produced different responses in animals of different social stature. This review should not be read as an attempt to remove the contextual features from intimate rage, merely to suggest that those very features may trigger intense neurobiological reactions in men with certain brain features.

Neurobiology of Abandonment Homicide

 

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Neurobiology of Abandonment Homicide