The Neurophysiology of Dissociation

Dissociation as a clinical psychiatric condition has been defined primarily in terms of the fragmentation and splitting of the mind, and perception of the self and the body. Its clinical manifestations include altered perceptions and behavior, including derealization, depersonalization, distortions of perception of time, space and body and conversion hysteria. Using examples of animal models, and the clinical features of the whiplash syndrome, we have developed a model of dissociation linked to the phenomenon of freeze/immobility. Also employing current concepts of the psychobiology of posttraumatic stress disorder (PTSD), we propose a model of PTSD linked to cyclical autonomic dysfunction, triggered and maintained by the laboratory model of kindling, and perpetuated by increasingly profound dorsal vagal tone and endorphinergic reward systems. These physiologic events in turn contribute to the clinical state of dissociation. The resulting autonomic dysregulation is presented as the substrate for a diverse group of chronic diseases of unknown origin. During the last two decades of the 19 century, psychiatrists in Europe began to explore and define the peculiar behavior manifested by patients of theirs who fell under the diagnostic category of hysteria. Pierre Janet at the Salpetriere` described dissociation as phobias of memories, in the form of expressions of excessive or inappropriate physical responses to thoughts or memories of old traumas (Janet, 1920). After visiting Janet, Freud adopted many of these concepts of dissociation as a splitting of consciousness, often associated with bizarre physical symptoms and manifestations, and ultimately attributed such symptoms in his hysterical patients to a history of childhood sexual abuse (Freud, 1896). Evolution of the concept of dissociation led to the description of a constellation of varied clinical manifestations attributed to it, including altered perceptions of physical sensation, time, memory, and the perceptions of self and reality. Complex expressions of these states came to include conversion disorder, fugue states and multiple personalities (dissociative identity disorder) (Freud & Breur, 1953, MayerGross, W., 1935, Spiegal & Cardena, 1991, Bremner, et al, 1992). Thus the concept of dissociation evolved to include not only mental and emotional aberrations, but also stereotyped and unusual somatic perceptual and motor experiences and expressions. All of these symptoms and behaviors were felt to be the sequellae of prior life trauma. The basic mechanism of dissociation was felt to involve the splitting off of parts of memory or perception in order to escape intolerable anxiety triggered by those areas of the mind that retained elements of the traumatic conflict. Relief from that conflict through hysterical dissociation resulted in relief from anxiety, resulting at times in the seemingly blasé acceptance of disabling physical conditions (la belle indifference`). Freud, however, soon began revising his concepts of hysteria, and by 1925 had recanted his theories of the relationship of hysteria and dissociation to prior childhood trauma (Freud, 1959). He ultimately attributed the stories of childhood sexual abuse in his hysterical patients to fabrication, based on unacceptable sexual wishes and fantasies that they could not acknowledge. As a result, the role of childhood trauma in the etiology of dissociation was basically ignored for decades. The introduction of the diagnosis of Post Traumatic Stress Disorder (PTSD) into the Diagnostic and Statistical Manual of Mental Disorders, 3 edition (DSM III) in 1980 also resulted in the reclassification of many of the conditions formerly attributed to trauma and dissociation, and in some cases, ignored their association with prior life trauma (American Psychiatric Association, 1980). Van der Kolk et al (1998) note that in the DSM IV, dissociative symptoms are included under the diagnostic categories of not only Post Traumatic Stress Disorder, but also of Acute Stress Disorder, Somatization Disorder and Dissociative Disorders themselves (van der Kolk, et al, 1998). In fact, in the DSM IV, Dissociative Disorders do not include Conversion Disorder, which has now been placed under the Somatiform Disorders. Since the DSM III, the diagnosis of hysteria is nowhere to be found. Van der Kolk et al (1998) make a strong case for the consideration of dissociation, somatization and affect dysregulation as late expressions of trauma even in the absence of continuing criteria for the diagnosis of PTSD. In doing so, they echo the concerns of Nemiah (1995), who notes that the diagnoses of PTSD, conversion disorder and dissociation are connected by the common process of dissociation itself, whereas their disparate placement in different categories of the DSM IV inhibits investigation of the psychodynamics of trauma. This attempt to return to the concepts of a relatively broadly-based response of the organism to traumatic stress is critical to our consideration of the neurophysiology of trauma and its effects not only on systems of the brain and endocrine systems, but also on the body itself. When one accepts the tenet that the clinical expressions of a multitude of psychiatric syndromes derive not only de novo or through gene expression, but perhaps also through life experience and its lasting effects on brain physiology, one must return to the concept of a physiological continuum between many psychiatric diagnoses. CLINICAL TYPES OF DISSOCIATION One of the dilemmas of classification of symptoms of dissociation is that these symptoms assume many and varied forms and expressions. They may be emotional, perceptual, cognitive or functional. They may involve altered perception of time, space, sense of self and reality. Emotional expressions may vary from panic to numbing and catatonia. Altered sensory perceptions may vary from anesthesia to analgesia to intolerable pain. Motor expressions frequently involve weakness, paralysis and ataxia, but may also present as tremors, dysarthria, shaking and convulsions (Please see discussion of conversion reaction later). Cognitive symptoms may involve confusion, dysphasia, dyscalculia and severe deficits in attention. Perceptual symptoms include ignoral and neglect. Memory alteration may appear as hypermnesia in the form of flashbacks, or as amnesia in the form of fugue states or more selective traumatic amnesia. The varied symptoms of dissociation therefore mimic the intrinsic bipolar nature of the defining symptoms of PTSD (arousal, reexperiencing, avoidance). Time perception is often greatly altered, most commonly characterized by a sense of slowing of time (Terr, 1983). Altered perception of self (depersonalization) may manifest as an out-of body experience, or a sense of intense familiarity (de ja` vu) (Pynoos, et al, 1987). In its most extreme expression, depersonalization may encompass perception of several separate states of self in the form of distinct and separate personalities (dissociative identity disorder), each with distinct personality characteristics and even physical attributes (Mayer-Gross, 1935). Strange persons or events may appear familiar, whereas familiar faces and scenes may appear alien and strange. Abnormal memories also constitute a significant dissociative phenomenon. Simple amnesia for the traumatic event is common, and may present as complete amnesia, or as distorted or inaccurate memory content (Torrie, 1944, Terr, 1983). Fugue states present an extreme state of amnesia, characterized by periods of time for which the dissociative patient has no memory, often triggered by exposure to cues reminiscent of prior trauma. During that time, the person may appear distracted and may not remember personal facts. More often, they may appear confused, histrionic, socially inappropriate or bizarre (Fisher, 1945). Perhaps the most unique symptom of dissociation is that of flashbacks. These episodes are distinctive in that they involve intense arousal and reexperiencing, symptoms more related to acute PTSD than to dissociation (Mellman, & Davis, 1985). During these episodes, which may last briefly or for several hours or even days, the person will also usually experience more typical dissociative experiences such as depersonalization. Sensory processing and perception may be greatly distorted. During flashbacks, the person may appear confused and detached, but later may report vivid sensory and memory experiences, often associated with intense emotions and states of arousal. The accuracy of the associated memories may be variably valid or distorted. Conversion reaction and hysteria no longer are described in the DSM IV under dissociation (American Psychiatric Association, 1994). In fact the DSM IV goes so far as to assert that if dissociative and conversion-based symptoms occur in the same patient, both diagnoses must be made. The neurophysiological and pathophysiological basis for dissociation proposed in this paper, however, demands that conversion be reintroduced as a specific form of dissociation, one that is closely linked to somatic perceptual alterations that are an acceptable and in fact intrinsic feature of the dissociative process. The model presented proposes that the atypical neurologic symptoms and signs that characterize conversion constitute perceptual alterations based on prior trauma, and represent the same splitting of consciousness that produces disorders of perception of time, space, reality and self presented above. As such, conversion may be associated with the same spectrum of positive and negative phenomena as PTSD as well as other symptoms of dissociation (analgesia/pain, paralysis/seizures). MEMORY, TRAUMA AND DISSOCIATION Disorders of memory constitute one of the diagnostic categories for PTSD in the form of reexperiencing. As noted above, this may be in the form of hypermnesia, amnesia or distortion of memory. Trauma-based memory phenomena often involve declarative (explicit, semantic) memory in the form of variably accurate verbal and imaginal recall of the traumatic event. Declarative memory, the form of memory that relates to facts and events, initially involves hippocampal and prefrontal cortical pathways and plays an important role in conscious recall of trauma-related events. It also is notoriously inaccurate, and subject to decay. Procedural memory relates to acquisition of motor skills and habits, to the development of emotional memories and associations, and to the storage of conditioned sensorimotor responses. Procedural memory is unconscious, implicit and extremely resistant to decay, especially if it is linked to information of high emotional or threat-based content (van der Kolk, 1994). Although declarative memory may account for much of the arousal-based cognitive symptoms of PTSD, procedural memory provides the seemingly unbreakable conditioned link that perpetuates the neural cycle of trauma and dissociation. Endogenous opiate reward systems very likely contribute to the establishment of conditioned procedural memory in trauma. Researchers have known for decades that exposure to overwhelming trauma in combat often results in a sustained period of analgesia. Soldiers wounded in battle frequently require much lower doses of morphine than in other types of incidental injury (Beecher, 1946). Stress-induced analgesia is a well-documented phenomenon in many forms of traumatic stress (van der Kolk, Greenberg, Orr & Pittman, 1989). Release of endorphins at the time of acute stress has a distinct survival benefit. An animal ministering to his wounds due to pain at the time of aggressive, life-threatening injury would suffer significant compromise of his defensive capabilities. Endorphins also persist during freeze/immobility, rendering the animal analgesic in the face of the injury from the attack. This also has potential survival value, since the persistence of immobility in the face of painful injury might serve to end the predatoris attack behavior. In the event of lack of completion of the freeze/immobility response, however, persistent recurrent dissociation with associated endophinergic reward might well potentiate the kindled trauma reflex. Endorphinergic influences might also contribute to the phenomenon of compulsive trauma reenactment (van der Kolk, 1989).