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THE NEUROPSYCHOBIOLOCY OF ADDICTION, TRAUMA AND DISSOCIATION

Daniel R. Schiele, MD, Ph.D.
Paper; 5th Annual Western Clinical Conference on Multiple Personality and Dissociation
Costa Mesa, CA April 10-12 1992

Inescapable shock is the only known biologic animal model equivalent to learned helplessness in humans. Addiction to dissociation and various co-dependent behaviors are the unavoidable sequelae of repetitive or overwhelming single-event trauma. Most focused symptomatic behavior (e.g., drug abuse, sexual promiscuity, perversions, self-mutations, binge eating and purging, etc.) reflect an emergency attempt to maintain and/or restore internal cohesion and harmony to a vulnerable self (1). For the "self"-in-formation, addiction to dissociation, a consequence of overwhelming trauma, represents a disorder in self-integration (2). This paper reviews the neuroanatomical, neurophysiological and neuropsychological parameters to dissociation as an addiction. Specifically the interrelatedness of the parameters to the BASK components (Behavior, Affect, Sensation and Knowledge) and to primary dissociation (neurophysiological-affective) arid secondary dissociation (cognitive-behavioral) (3) will be reviewed to formulate the common denominators to addiction, trauma and dissociation

In their discussion of Pierre Janet's relevance to the contemporary study of psychological trauma and dissociation, Bessel van der Kolk and Onno van der Hart (4) review Janet's thoughts on how mental processes transform traumatic experiences into psychopathology: what memory processes best is not specific events, but the quality of experience and the feelings associated with it; that an inverse relationship exists between the intensity of the emotional reaction ("vehement emotion") and the capacity to process traumatic memories conceptually (verbally); and that, information can best be retrieved, and memories reactivated, when a person is exposed to a situation, or is in a somatic state, reminiscent to the one in which the memory was first encoded. Prior to the turn of the century, psychiatrists accepted the notion that mental illness would be reflected in discrete neuroanatomical or physiological processes. Thus human experience would be encoded in memory in some persistent engram, a hypothesized discrete neurobiological or neurophysiological record that would be modified over time by experiential learning. Janet believed that when people are terrified, the usual cognitive schemata are inadequate to create a mental construct which places the experience in the perspective of prior knowledge schemes, causing it to be left unintegrated and to persist as a psychological automatism, and that a range of visceral, perceptual, emotional, or motoric (reenactment) symptoms could represent an involuntary reliving of elements of the trauma (4). Such unintegrated psychological automatism have come to be understood within the context of the BASK model of dissociation (5): Dissociation is today taken to mean the separation of an idea or thought process from the main stream of Consciousness and that dissociation can occur on any one or more levels of Behavior, Affect, Sensation and Knowledge. The inability to place memory in a cognitive-behavioral context leaves it to be arranged on a neurophysiological - affect level.

It is precisely those neurophysiological - affective and cognitive-behavioral symptoms that have come to be equated with the dissociative disorders and specifically the unique features of Posttraumatic Stress Disorder (6). The biphasic alteration of reliving and denial, with alternating intrusive symptoms (hyperactivity, explosive aggressive outbursts, startle responses, intrusive recollections in the form of nightmares and flashbacks, and reenactment of situations reminiscent of the trauma) and avoidant symptoms (emotional constriction, social isolation, retreat from family obligations, anhedonia, and a sense of estrangement) reflect the Psychological and physiological components of the trauma response (7). Posttraumatic Stress Disorder symptomatology, earlier thought synonymous with combat veterans, today is seen as more generic psychopathology, occurring within such conditions as MPD, Borderline Personality Disorder (BPD), the anxiety disorders, the eating disorders and the addictive disorders (2).

LEARNING PARADIGMS AND MPD, REACTIVE AND STRUCTURED SUBTYPES

Associative pairing of traumatic environmental cues set up classical and operant conditioning stimulus-response patterns. The characteristic biphasic response to trauma (intrusiveness - hyperarousal versus numbing - avoidance symptoms) set up the array of symptoms which define PTSD. Patterns of reactivity, either random or fixed, predispose to specific integrated or non-integrated altered states of consciousness. If dissociation is possible or even encouraged, the solution may be MPD, Reactive Type or MPD, Structured Type (8). If the human organism is allowed to retain an internal locus of control to freely anticipate and perceive in response to trauma and/or abuse, and internally dissociate any or all of the compnents of the BASK model, (the Behavior, the Affect, the Sensation. Or the Knowledge concerning the abuse and trauma), them MPD, Reactive Type may result; when the anticipation and perception of the abuse and/or trauma is pre-determined by an allowing escape from continuing hyperarousal only by dissociation limited predetermined direction, then MPD, Structured Type ensues (3).

DEVELOPMENTAL LEARNING SCHEMA

Observations from infants are redefining traditional developmental learning concepts. Auditory pattern recognition is probably available to the late-term fetus: "conscious" recognition of variations of the maternal heart beat may be subjectively perceived. Stern (9) describes that the newborn is born with pattern recognition, temporal auditory recognition and associative capacity; that within weeks after birth, the infant has supermotor recognition, a common tactile/auditory/visual space in which the infant can associate how things should look from how they feel or sound from how they look without requiring involved learning schema usually thought later in cognitive development; that infants can abstract invariants of experience into categories and categories into prototypes between 3 and 10 months; that a basic unit of subjective experience (the "lived moment") can form interactions internally represented and generalized (RIGS-"representations of interactions, generalized; short things"); that RIGS are combined into scenarios by 9 months; and that affective attunement can occur by this same time indicating that intersubjective communication can be perceived and accurately reflected in corresponding maternal-infant interactions. The central developmental task of infancy and childhood is learning how to modulate behavioral states (10) and soothing transitions between various behavioral states with appropriate interaction and affective attunement with the primary caretaker. The mismatch of the infant-maternal affective attunement results in a failure of the autoregulation of infant physiological-affective behavioral states. The transitions between infant behavioral states exhibit psychophysiological properties that are highly similar to those observed across switches of alter personalities in multiple personality disorder (11)

THE NEUROANATOMY OF DISSOCIATION TRAUMA AND ADDICTION

The fortuitous discovery of chlorpromazine as effective in calming agitated psychotic patients heralded investigations into the mechanisms of actions of various psychotropic drugs and the belief that such drugs exert their effects by altering specific chemical processes involved in neuronal communication (12). Basic research efforts have pursued mapping of neuronal systems and the specific neuromodulators as etiologic factors in psychiatric illness. Contributions from the theoretical constructs in neural network theory (13), connectionism theory (14) or parallel distributed processing theory (15), in which drive, affect, meaning, knowledge, reality and present-state, all come together in the disturbed, constrained, holistic, probabilistic, self-organizing, layered network of the mind (16), afford a theoretical description of the engram as a discrete walled-off or dissociated neuronal network which persists over time, responsible for the neurophysiological--affective and cognitive-behavioral symptoms of the dissociative disorders.

Neural network theory implies certain basic principles: (a) large numbers of simple processing units with weighted connections between units form neural network pathways; (b) information in each pathway is represented as a pattern of spreading activation (c) knowledge is the set of connection weights and learning consists of adjusting the synaptic strengths between neurons (17); (d) axonal-dendritic pruning selectively removes less useful synaptic connections over time. (This concept of "neural darwinism" implies the "survival of the fittest" connections over time (18) and after a certain pruning threshold, a massive disruption of associative memory occurs (19); (e) neuromodulators not neurotransmitters of the state of processing information, act as filters or amplifiers rather than as initiators and carriers of information about the world (20); and consist of small numbers of neurons that induce widespread and diffuse effects (21); (e) the neural network does not store the memory of the trauma input itself, but rather it stores within its interconnections the predisposition to behave as though exposed to the traumatic input (22).

The role of the hippocampus, thalamic nuclei and mammillary bodies in providing the substrate for acquiring and retaining new information (23) and parallels between learning-induced increases in hippocampal neuronal activity and long-term potentiation of memory (24) focus attention on the neuroanatomy of memory in non-traumatic and traumatic situations. Stone (25) summarizes research on memory: the long-term memory component (neocortex, including the frontal lobes) monitors and organizes thought and planning; the short term memory component translates tactile into visual impressions (amygdala) and subserves visual recognition (hippocampus); non-cognitive memory, a behavioral memory system involved in the development and reinforcement of habits even in the absence of recallable representations, is NOT dependent upon the limbic structures but rather upon the basal ganglia, the cudate and putamen (25). The basal ganglia earlier thought exclusively motor in function with limbic striatum connections serve an integrateve role for the limbic system which allows inherent goal oriented behavior, emotional output and suppression or inhibition of unwanted responses; connections of the basal ganglia and limbic structures with the orbitorfrontal cortex and thalamus appear to appropriate for effective cognitive and emotional recitative to the environment as well as playing a dominant role in the regulation of states of consciousness, alertness and attention (26). Programs in the noncognitive basal ganglia memory system permits speed reflex - like survival decisions: severe truama can overinscribe an engram program that can make new stimuli even faintly reminiscent of original noxious stimuli trigger the same catastrophic responcse (25). The thalamus, hypothalamus and corpus striatum, via dopamineggic transmission, facilitate intergration from cortical and limbic sites (27). The hypothalamus is involved in various emotional response patterns, rage, aggressivety, excitablity (25). Stimulation or of the lateral hypothalamus elicits anger while ablation produces placidity; lesions in the medial hypothalamus produces highly excitable animals in whom aggression can be easily provoked; electrical stimulation of the posterior hypothalamus, amygdala or midbrain enhances aggression, and ablation inhibits aggression (28).

THE NEUROMODULATORS OF TRAUMA AND ADDICTION

The locus ceruleus, hippocampus, amygdala, and anterior hypothalamus, the areas of the brain most concerned with emotions and stress, share a high density of both norepinephrine and opioid receptors (29, 30). Any cue associated with a noxious stimulus or interruption of behavior triggers the firing of the locus ceruleus, releasing norepinephrine (NE). Any situation that requires a rapid response or rapid selectivc- focus of attention to specific sources of information in the external environment releases NE. Dopamine appears to support and facilitate the situation and organization of sensory-motor associations critical during times of stress and flight or fight reactions (31). During waking states, NE and 5HT activity dominates, with inhibition of cholinergic output; thought content and cognition are consistent and continuous; affects are stable. During NREM sleep with balanced aminergic and cholinergic bursts of activity, thoughts are devoid of perceptive vividness or emotional tone. In REM sleep, thoughts are graphic, emotionally charged; images contain discontinuities, incongruities, uncertainties; cholinergic activity dominates (32). Modeling of this type may provide insight into possible functional roles of cognitive processes correlated with different neurobiological states, such as state dependent learning (32),

Opiate rece[tpr activity inhibits noradreneggic activity and vice versa (32, p. 44.). Inescapable shock depletes norepinephrine (NE) and dopamine and such NE depletion seems to be a conditioned response rendering certain NE receptors hypersensitive to subsequent NE stimulation (33, 34, 35). Van der Kolk, Greenberg and Boyd (34) proposed the physiological aspects of both opiate withdrawal and PTSD are related to central noradrenergic hyperactivity associated with a relative decrease in opiate receptor binding; such endogenous opioid release may result in a temporary sense of control, but withdrawal symptoms may occur. It is this transient relief on reexposure which may perpetuate an addictive cycle (35) which may lead to further loss of psychophysiological control (34). Redmond and Huang (36) proposed that acute anxiety reactions are related to increased activity in brain noradrenergic systems; electrical stimulation of the locus ceruleus induces a behavioral syndrome similar to that in natural fear-inducing situations. Drugs that reduce NE turnover (e.g., clonidine) are useful in treating panic attacks in humans, whereas drugs that increase NE turnover (e.g., yohimbine) produce anxiety states in humans. It has been proposed that it is the ability of TCAs and MAO inhibitors to decrease locus ceruleus firing, NE turnover, and beta-adrenergic receptor function that underlies the efficacy of the noradrenergic system in ameliorating panic attacks (37).

The human response to trauma is either unmodulated anxiety, often accompanied by motoric discharge that includes acts of aggression against the self or others, or else social and emotional withdrawal (38). Many traumatized people continue to respond to minor stimuli with an intensity appropriate only to emergency situations. The degree of the autonomic arousal determines the intensity of the emotional response. Van der Kolk, Greenberg and Boyd (34) hypothesized that the repetitive reliving of the trauma, particularly under stress, is caused by the stress-induced reactivation of the locus ceruleus - hippocampus - amygdala pathways. It is the long term potetitiation of certain pathways, neural network engrams, that predispose to certain characteristic neurophysiological affective and cognitive-behavioral response patterns.

ADDICTION TO TRAUMA AND DISSOCIATION

PTSD symptoms take on a biphasic repetition-compulsion pattern (intrusive recollections, revivification-autonomic hyperarousal) or magical fantasy undoing pattern (psychic numbing, denial, avoidance). The human response to trauma is summarized by Van der Kolk and Greenberg (35, p. 64-66): that the central nervous system seems to react to any overwhelming threatening and uncontrollable experience in a consistent pattern; that traumatized people tend to respond in an all-or-nothing way with either unmodulated anxiety, often with motoric discharges that includes acts of aggression against the self or others, or else social and emotional withdrawal; that PTSD symptoms seem to underlie the psychopathology of a number of psychiatric disorders (MPD, BPD, the addictive disorders, including the eating disorders, certain anxiety and a panic states); and that the intensity of the autonomic arousal, formerly adaptive preparation to cope with stress, eventually becomes itself a precipitant of fear and emergency responses.

The animal model of inescapable shock parallels the equivalent of learned helplessness in humans. Animals exposed to inescapable shock develop analgesia when exposed to another stressor shortly afterward; this response is mediated by endogenous opioids and is reversed by nalozone, and that chronic stress induces a physiological state that resembles dependency on high levels of exogenous opioids; and when severely stressed, subsequent fear and the accompanying opioid secretion attenuates the perceived intensity of subsequent shocks (35, p. 71-72). It is this "addiction to trauma", that characterizes the morbid human fascination to chronic reexposure to dangerous situations in PTSD victims

THE BIOPSYCHOSOCIAL MODEL OF ADDICTION

Concepts derived from basic research into the disease model of addiction suggest addiction is the result of a genetic predisposition, environmental cueing, and behavioral sensitization which sets up conditioned neurophysiological-affective and cognitive-behavioral patterns of responsivity. Wallace (39) summarized recent research on the biopsychosocial disease model of alcoholism: that in animals, when the serotonin level is reduced, ethanol consumption increased and vice versa; that in humans, that decreased noradrenergic activity was correlated to increased relapse rates; that relapses may occur in response to excessive stimulation, stress and high arousal-related discomfort, and others to boredom, restlessness and an inability to experience pleasure; and citing Cloninger (40), that Type I alcoholics are thought high in traits of harm avoidance and reward dependency and low in novelty seeking while Type II alcoholics are low in harm avoidance and reward dependency but high in novelty seeking.

MPDs often unconsciously recreate, reenact and repeat traumatic situations from the past again and again; one of the explanations of traumatic reenactment comes from the Karpman Drama Triangle (41) which envisions the alcoholic family system as a triangle of persecutor, victim and rescuer. Patients with MPD recreate this abuse triangle with personalities that fall into the three categories (42). Object relations theory would describe this triad as identification-interjection with the abuser, victim or the rescuer. Thus each alternative engram of state-dependent object relatedness constitutes the personality alters, fragments, traces and functions which comprise the MPD system or the various dissociated states or PTSD psychopathology.

ADDICTION TO LIVING ON THE EDGE: THE PSYCHODYNAMICS OF SELF-MUTILATION

MPD patients often polarize between chronic reexposure to life-threatening situations or excessive self-protective avoidance of risk-taking and human contact. MPD patients consistently describe being "addicted to the adrenaline rush of living on the edge between life and deity"', addicted to cheating death or cheating pain. This polarization is a seeming repetition-compulsion to activities that others would be afraid to try.

The psychodynamics of dissociation must include the understanding that addiction to dissociation, in and of itself, constitutes a transitional object relationship to a threatened "self"-concept. ["Self" as used in this discussion is self-as-agency, rather than limited to self-as representation: (1)]. Addiction to dissociation, like any other addiction, provides an opportunity for magical-thinking mastery and magical-undoing control, to overcome a sense of powerlessness, hopelessness, and learned helplessness. The dehumanization, the objectification, the depersonalization and the derealization forces activated in a setting of inescapable trauma, threaten the physical and psychic integrity of an "integrated" "self" concept

Addiction to dissociation constitutes a narcissistic (preservation of the "self") attempt at mastery and control by the initiation of either interpersonal or intrapsychic action, physical movement away or towards a noxious stimulus, or mental distancing' as in dissociation when no escape is possible, and represents a powerful energizing, reinforcing and soothing internal "self-object", which in itself is a transitional object. In the absence of available consistent caretakers external to the self, the potential for escape, fantasy-based or reality-based, in a physical no-escape situation is limited to death, catatonia, psychosis, or dissociation and to the primitive ego defense mechanisms available: splitting, projective identification, introjection and denial. The catatonic, psychotic or dissociative solution represents some primitive narcissistic defense to initiate action, to move away, to feel something other than the pain of the original Primary Dissociative Experience (43, 44), with the reenactment-revivification of all its attendant neurophysiological-affective symptoms, (as compared with The Secondary Dissociative Experience, the cognitive-behavioral symptoms).

PSYCHODYNAMICS OF SELF-MUTILATION

Favazza (45) described self-mutilation as the deliberate destruction or alteration of body tissue without conscious suicidal intent. Self-mutilation includes the cutting, biting, bruising, abrading, burning and scratching of the skin, trichotillomania, self-amputation of body parts, etc. (46). Psychodynamic explanations for self-mutilation are thought to be pre-oedipal or preverbal and physical in nature since the incidence of self mutilation is high among eating disorders, antisocial personality disorder and borderline personality disorder (BPD) (46). Although Bliss (47) first reported the occurrence of self-mutilation with a MPD, the association between depersonalization and/or dissociation and self-mutilation was highest among MPDs (48%), present in psychogenic amnesia (27%) and in dissociative disorder not otherwise specified.(23%), but not in psychogenic fugue; in the MPDs 58% experienced amesia for the self-mutilation, and the self-mutilation was performed by an alter personality. Coons and Milstein (46) summarize other studies on self-mutilation: that self-mutilation is a venting of aggression, particularly against the self; that self-mutilation may relieve feelings of tension, anxiety, guilt and depersonalization; may provide gratification such as gaining attention from others; and may attain a feeling of euphoria or provide a sense of security.

Self-mutilation has long been considered synonymous with borderline personality disorder. BPD as defined in DSM-III-R is characterized by at least five of the following features: impulsivity, intense yet unstable interpersonal relationships, inappropriate anger, identity disturbance, affective instability, intolerance of being alone, self-injurious acts, a sense of emptiness or boredom (6). When a BPD feels the absence of an object relationship, brief psychotic episodes, panic states or impulsive acts to ward off the subjective experience of aloneness and badness occur; or a prolonged dissociative episode of either the depersonalization or derealization type may occur (48). These reactions detach the BPD from either the reality of bodily distress or the environmental situation that evokes the intolerable distress. During dissociative episodes, nihilistic fears occur that may give rise to self-mutilation to confirm being alive by feeling pain; frequently such self-mutilation is accompanied by restitutive fantasies in which the absent object is either believed to be performing the act or is being punished by the act, but in either case is still involved (48)

Only recently is it accepted that MPD and BPD commonly coexist. When MPD and BPD coexist, one is dealing with trauma in the context of probable severe developmental deficits and an early structural disturbance manifested by pervasive splitting as well as a posttraumatic organization indicated by dissociation, and alternative states of consciousness (49) with desperate attempts to ward off unwanted overwhelming somatosensory hyperarousal when psychic numbing or analgesia has failed (35). Self-mutilation often employs reliance on primitive defense mechanisms (denial, projection, splitting and dissociation), isolation and constriction of affect; repetition-compulsion attempts to recreate, master and control painful affects initiated during abuse experiences; the suspension of reality testing in favor of regressive modes of thinking (analogic, concrete, trance-logic thinking); and the loss, of ego boundaries that summate to determine the self-mutilation as an attempt to dispel badness or aloneness

ADDICTION TO SELF-MUTILATION

Addiction to self-mutilation constitutes a transitional object that behaviorally numbs physiological pain. It represents an internal "body talk" attempt at self-soothing in the MPD, the BPD, the eating disorder patient and those experiencing a panic attack, as well as others temporarily, feeling disruptions in human relatedness or overwhelming trauma. It is relief through preverbal concretized thinking and physiological messages which are designed to stave off emerging feelings of depersonalization or derealization. Entering into a state of existential nothingness, a depersonalized objectless void so feared yet equated with death of the "self", is resisted; instead a dissociated state is chosen by the "self", rather than giving in to a death instinct. This dissociated vertical split allows the fantasy of the magical-rescuer to (self-soothe) and restore a ("good-mother") object relatedness when no escape from pain is possible.

Thus addiction to dissociation and addiction to self-mutilation as transitional objects become understandable and potentially analyzable within the holding environment of the therapeutic hour. The therapist serves as a transitional object to each dissociated ego state within various psychiatric disorders containing the posttraumatic response pattern. Like other addictions, these conditioned patterns, of state-dependent relatedness are hard to relinquish. Understanding the psychobiosocial disease model of addiction and the psychodynamic parameters inherent within dissociation allows working through, integration, healing and resolution of trauma and the replacement of an addiction with more mature coping mechanisms.

REFERENCES
Below

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1 Gabbard GO: Psychodynamic Psychiatry in Clinical Practice. Washington, D.C., Am. Psych. Press, 1990.
2. Schiele DR: Working with the Trauma Survivor: Capistrano by the Sea Hospital Seminars. Dana Point, CA., July 26-27, 1991
3. Ray S: Beyond Psychotherapy and Abreaction: Dissociative Memory Work. Paper presented at the 4th Regional Conference of Multiple Personality and Dissociation. Newport Beach, Ca., April 12-14, 1991.
4. van der Kolk BA, van der Hart 0: Pierre Janet and the breakdown of adaptation in psychological trauma. Am J Psych 1989; 146: 1530-1540
5. Braun BG: The BASK model of dissociation. Dissoc 1988; 1:4-23.
6. American Psychiatric Association. (1987) Diagnostic and statistical manual of mental disorders (3rd Ed., Rev), AM Psych Press: Washington, D.C.
7. van der Kolk BA: Psychological trauma. Washington, D.D., Psych Press, 1987.
8. Ray S, Reagor PA: Beyond psychotherapy and abreaction:
dissociative memory work. Paper presented at 4th Western Regional Conference on Multiple Personality and Dissociation. April 12-14, 1991 Newport Beach, CA.
9 Stern DN: Infancy: a theoretical playground for the study of mind. Paper presented as 144th Annual Meeting, American Psychiatric Association New Orleans, LA., May 11-16, 1991.
10. Wolff PH: The development of behavioral states and the expression of emotions in early infancy. Chicago, University of Chicago Press, 1987.
11. Putnm FW: Multiple personality disorder. New York, Guilford Press, 1989.
12. Martin MB, Owen CM, Morihissa JM: An overview of neurotransmitters and neuroreceptors, in Textbook of Neuropsychiatry. Edited by Hales RE, Yudofsky SC. Washington, D.C., Am Psych Press, 1987.
13. Hoffman RE: Computer simulations of neural information processing and the schizophrenia-mania dichotomy. Archive Gen Psychiat 1987; 44: 178-188.
14. Fodor JA, Psynshyn ZW: Connectionism and cognitive architecture: a critical analysis. Cognition 1988; 28: 7-71.
15. Rumelhart DE, McClelland JL, PDP Research Group: Parallel distributed processing: Explorations in the microstructure of cognition. Vols. I-II Cambridge, The MIT Press, 1986.
16. Globus, OG: The Self-organizing mind: a neural network approach to mental functioning. Personal Communication. May, 1989.
17. Cohen JD, Servan-Schreiber D: Introduction to neural network models in psychiatry. Psych Annals 22: 113-118, 1992.
18. Edelman GM: Neural Darwinism: The theory of neuronal group selection, New York, NY: Basic Books, 1987.
19. Hoffman RE: Attractor neural networks and psychotic disorders. Psych Annals 22: 119-124, 1992.
20. Sutton JP, Mamelak AN, Hovson JA: Modeling states of waking and sleeping. Psych Annals 22: 137-143, 1992.
21. Servan-Schreiber D: Cohen JD: A neural network model of catecholamine modulation of behavior. Psych. Annals 22: 125-130, 1992.
22. Li D, Spiegel D: A neural network model of dissociative disorders. Psych Annals 22: 144-147, 1992.
23. Erickson KR: Amnestic disorders. Pathophysiology and patterns of memory dysfunction. West J Med 1990; 152: 159-166.
24. Teyler TJ, Discenna P: Long-term potentiation as a candidate mnemonic device. Brain Res Rev 1984; 7: 15-28.
25. Stone NH: Toward a psychobiological theory of borderline personality. Dissoc 1988; 1: 15.
26. Modell JG, Mountz JM, Curtis GC, Greden JF: Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive-compulsive disorder J Neuropsychiat 1989; 1: 27-36.
27. Iverson DS: Brain lesions and memory in animals: A reappraisal, in Deutsche JA (Ed.), the Physiological Basis of Memory. New York: Academic Press, pp. 139-198.
28. Snyder SR: The New Biology of Mood. New York: Pfizer, 1988.
29.S, Langer SZ: Morphine and beta endorphin inhibit release of noradrenaline from cerebral cortex but not of dopamine from rat striatum. Nature 271: 559-560, 1978.
30. Korf J, Bunney BS, Aghajanian CK: Noradrenergic inhibition of spontaneous activity. Eur J Pharmacol 25: 165-169, 1974.
31. Cohen JD, Servar-Schreiber D: Aneural network model of disturbances in the processing of context in schizophrenia. Psych Annals 22: 131-136, 1992.
32. Anisman JL, Ritch M, Sklar LS:Catecholamine depletion in mice upon exposure to stress: mediation of the escape deficits reduced by inescapable shock. J Comp Physiol Psychol 93: 610-625, 1979.
33. Anisman HL, Ritch M, Sklar LS: Noradrenergic and dopaminergic interactions in escape behavior. Psychopharmacology 74: 263- 268, 1981.
34. van der Kolk BA, Greenberg MS, Boyd H, et al: Inescapable shock, neurotransmitters and addiction to trauma: towards a psychobiology of post traumatic stress. Biol Psychiatry 20: 314-325, 1985.
35. van der Kolk BA, Greenberg MS: psychobiology of the trauma response: hyperarousal, constriction and addiction to Trauma, traumatic reexposure, in Psychological Trauma Edited by van der Kolk, BA Washington, D.C., Am Psych Press, 1987, pp 63--87.
36. Redmond DE, Huang YH: New evidence for a locus coeruleus--norepinephrine connection with anxiety. Life Sci 25: 2149-2162.
37. Redmond DE: New and old evidence for the involvemenet of a brain norepinephrine system in anxiety, in Phenomenology and Treatment of Anxiety. Edited by Fann WE, Karacan I, Pokory, et al. New Yotk, Spectrum Books, 1979,pp 152-203.
38. Krystal H. Trauma and Affects. Psychoanal Stud Child 33::81-116, 1978.
39. Wallace J: The new disease model of alcoholism, West J Med 1990; 152: 502-505.
40. Cloninger CR: Genetic and environmental factors in the development of aicholism. S Psychiatric Treat Eval 1983; 10: 78-83.
41. Karpman S: Fairy tales and script drama analysis. Transactional Analysis Bulletin, 1968; 7: 39-43.
42. Turkus JA: Psychotherapy and case management for multiple personality disorder. Psych Clin of North Am 1991; 14: 649-660.
43. Ray S: Beyond Psychatherapy and Abreaction: Dissociative Memory Work. Paper presented at the 4th Regional Conference on Multiple Personality and Dissociation. Newport Beach, Ca, 12-14, April 1991.
44. Neswald DW: Working with in Adult MPD Survivors of the Primal Dissociative Experiences Satanic Ritualistic Abuse. Personal Communication. August 1991.
45. Fatrazza AR: Why patients mutilate themselves. Hospital and Community Psychiatry 1989; 24: 22-30.
46. Coons PM, Mustein V: Self-mutilation associated with dissociative disorders. Dissoc 1990; 3: 81-87.
47.Bliss EL: Multiple personalities: a report of 14 cases with implications for schizophrenia. Archives of General Psychiatry 1980; 37: 1388-1397.
48. Gunderson JO: Borderline Personality Disorder. Washington DC: Am Psychiatric Press, 1984.
49. Fink D: The co-morbidity of multiple personality disorder and DSM III R axis II disorders. Psych Clin of North Am 1991;14: 546-566.

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