Repetition and Trauma

Toward A Teleonomic Theory of Psychoanalysis

Max M. Stern, Liselotte Bendix Stern

• Publisher: Routledge
• Year: 2013
• eBook ISBN: 9781134878857
• Topic: Psychology
• Subtopic: Applied Psychology
• Index: Psychology

The culmination of over three decades of investigation into traumatic processes, Repetition and Trauma is the late Max Stern's pioneering reconceptualization of trauma in the light of recent insights into the physiology and psychology of stress and the "teleonomic" character of human evolution in developing defenses against shock. As such, it is a highly original attempt to reformulate certain basic tenets of psychoanalysis with the findings of modern biology in general and neurobiology in particular.

At the core of Stern's effort is the integration of laboratory research into sleep and dreaming so as to clarify the meaning of pavor nocturnus. In concluding that these night terrors represent "a defense against stress caused by threatening nightmares," he exploits, though he interpretively departs from, the laboratory research on dreams conducted by Charles Fisher and others in the 1960s.

From his understanding of pavor nocturnus as a compulsion to repeat in the service of overcoming a developmental failure to attribute meaning to states of tension, Stern enlarges his inquiry to the phenomena of repetitive dreams in general. In a brilliant reconstruction of Freud's Beyond the Pleasure Principle, he suggests that Freud was correct in attributing the repetitive phenomena of traumatic dreams to forces operating beyond the pleasure principle, but holds that these phenomena can be best illumined in terms of Freud's conception of mastery and Stern's own notion of "reparative mastery."

1
Pavor Nocturnus

The pavor nocturnus of children and the night terror of adults, each of which can be defined broadly as an awakening in fright from a severe nightmare, represent expressions of anxiety of an intensity rarely witnessed directly in daytime intercourse, still less often in the analytic consulting room. Until the development of laboratory dream research in the mid-1950s, when for the first time the student of dreams had direct access to the sleeper and accordingly an opportunity to investigate his physiological experience at first hand and his psychological experience as reported immediately upon awakening, psychoanalytic commentators on night terror and pavor nocturnus had to rely largely on anecdotal reports from diverse sources and the impressionistic accounts of their own patients. The latter accounts, apparently in keeping with the traumatic nature of the nocturnal episode and the amount of time intervening between the occurrence and its report, generally provided but meager descriptions of the content of the nightmare preceding the attack. Even when the elicited content was more substantial, it was of a type rather different from that of the wish-fulfilling dreams that are the staple of the psychoanalytic interpretive method. Content was straightforward, if invariably sensational, and showed little of the elaborate and bizarre visual imagery and fantastic wordplay of the wish-fulfilling dream, in apparent support of Freud’s (1920) claim that traumatic nightmares were an exception to the wish-fulfilling nature of dreams. These accounts further suggested relatively little remembrance on the part of the patient of the attack itself—a retrograde amnesia, as it were, for events witnessed at first hand by parents, siblings, and spouses, and including, in the severest cases, bloodcurdling screams and somnambulism. Psychoanalysis, then, so largely concerned with the problem of neurosis, was practically impotent to examine one of the most striking expressions of the affect par excellence of neurosis, anxiety.

Although laboratory dream research has done much to remedy this situation, it is not without its own limitations of method—to which I shall refer later—having to do principally with the artificiality of the laboratory setting itself. Perhaps because of this, reports of such research tend generally to give short shrift to the subjective experience of the sleeper; anxiety is rated and quantified rather than described. Inasmuch as it is the anxiety that has attracted our interest in the first place, we are put as readers in the awkward position of having to judge a phenomenon whose terror has been abstracted and relativized. It might be best, then, to begin by presenting a composite portrait of the subjective experience of night terror—pre-1960, as it were—which we shall very often have to qualify, drawn as it is from the impressionistic accounts I mentioned earlier. Nevertheless, I think it will prove a useful device for orienting the reader to this most perplexing of human behaviors.

It seemed certain, before 1960, that night terror attacks were always preceded by a dream. In general, the stronger and more threatening the predominant sensations of the subsequent attack, the weaker was the recollection of the dream. The dream usually contained elements having reference to motility—running, climbing, gliding, falling, and the like. We often encountered scoptophilic and exhibitionistic fantasies and oral elements that were subsequently specifically represented in the anxiety accompanying the ensuing attack: fears of being eaten, of being unable to scream, of being choked. Auditory elements —speaking or being spoken to, hearing noises—were also noted.

As the dream unfolded it suddenly revealed its nightmarish character, in the form of a threat against the sleeper: attacks by humans, animals, ghosts, vampires; walls closing in on him, waves engulfing him, his crashing down from heights or being crushed by unknown powerful forces. Invariably the sleeper was helpless against the threat, which was nearly always connected with the most severe anxiety.

This feeling of helplessness was then experienced as having the character of reality, although still remaining in some way hallucinatorily connected with the ongoing nightmare. The sleeper attempted to scream, to cry for help, but was unable to utter a sound. He sought to fight back, but in vain. He was paralyzed, unable to breathe, with a sensation of dreadful pressure on the chest, similar to the precordial fear of annihilation; he had a sensation as though a band of iron were encircling his head, and a conviction of being overwhelmed by unconsciousness. Now he was certain that he was no longer dreaming, that he really was in the utmost peril. He knew that he would be able to save himself from this peril by waking up, but he could not wake up and with each passing moment felt the real end coming closer. He gathered himself for a last attempt at escape but could not move his body or limbs—until suddenly, with some violent effort, he woke to reality. Covered with perspiration, his heart racing madly, his breast heaving, he felt he had escaped a mortal danger.

The reader familiar with the literature may have noticed the more than passing resemblance between this composite description of night terror and Ernest Jones’s (1931) definition of nightmare as a distressing dream necessarily showing, among other features, three cardinal ones: agonizing dread, a sense of oppression and weight upon the chest that alarmingly interferes with respiration, and a conviction of helpless paralysis. Freud (1895) also noted difficulty in breathing and sweating as features of the adult night terror and elsewhere (1900) described a case of pavor nocturnus in a 13-year-old boy whose sleep was interrupted by severe attacks of anxiety accompanied by hallucinations: “He would wake up from an anxiety dream in terror, unable to cry out at first, until his voice came back to him and he was distinctly heard to say ‘No, no, not me!’” (p. 586). More recent psychoanalytic investigators have noted that the most severe night terror attacks are often accompanied by sleepwalking (Stern, 1951; Sperling, 1958; Mack, 1965; Schur, 1969).

The foregoing composite portrait invites the obvious question: Are the sensations of helpless paralysis, difficult breathing, and pressure on the chest based on actual physiological events? In imprecise but convenient shorthand, are they real? Real or not, do they instigate the observed responses of ample breathing, pounding heart, and violent movement? And, finally, given these questions, how can we delimit the attack itself? When does it begin and the nightmare end? We shall see that the results of laboratory dream research suggest answers to these questions. For the time being, however, I should like to propose that the pavor nocturnus attack, even while remaining hallucinatorily connected to the content of the nightmare, includes the features noted by Jones—agonizing dread, a sensation of difficult breathing, real or not, and a conviction of helpless paralysis, real or not—to which must be added the accelerated heart rate, ample respiration, and scream or violent movement that appear to end the attack, with somnambulism reserved for the severest cases. The definition recommends itself if only for being comprehensive.

I should now like to consider the questions I have raised in the light of a condition in which psychic events lead to a temporary breakdown in vital somatic functions. I refer to what has been variously called “primary shock” or “neurogenic shock of central origin.” In this condition, overintense mental activity leads to a series of physiological events that resemble the sensations or physiological events described in the pavor nocturnus attack. The discussion is based on the seminal research on stress conducted by Selye and his co-workers (1946, 1947, 1950) in the aftermath of World War II.

Shock and Countershock

Selye (1950) defines “systemic stress” as a condition in which “due to function or damage—extensive regions of the body deviate from normal resting state” (p. 9). He postulates that any stress mobilizes two responses: a specific one that seeks to alter the threat by producing an alloplastic change—a change in the environment—and a nonspecific systemic autoplastic response, called the “alarm reaction” and defined as the sum of all nonspecific phenomena elicited by sudden exposure to stimuli to which the organism is quantitatively or qualitatively not adapted. The alarm reaction is thus independent of the nature of the damaging agent and represents a response to damage as such. When stress is sufficient to overwhelm the defensive capabilities of the alarmed organism, it eventuates in full-blown shock: There is profound weakness, flaccidity of muscles, pallor, perspiration, a weak rapid pulse, and a low arterial blood pressure. As the reaction progresses, this deficiency affects the nervous system as well as other parts of the organism, paralyzing its functions: reflexes are abolished, there is no response to painful stimuli, the subject is lethargic or semi-comatose, the respiration becomes shallow and weak, and the blood pressure declines to zero. As the condition progresses further, there is stupor or coma, and finally death (Moon, 1942, p. 24). Most authors conceive of full-blown shock in terms of anoxia and circulatory failure and “a condition of depression of the vital activities of the body, associated with a marked and progressive fall in blood pressure” (Rose and Carless, quoted by Moon, 1942, p. 43). Although primary shock arising from psychic activity is much less severe than secondary shock—blood volume does not so precipitously decline and the primary circulatory disturbance of lowered blood pressure is usually only of short duration—it can lead to secondary shock with fatal consequences; Moon reports that death from circulatory failure occurs in various forms of psychopathology in which demonstrable lesions are lacking (p. 214). It should be noted that the “clinical features, functional disturbances, and visceral changes are almost identical whether death has occurred rapidly by shock or more gradually after grave illness: … Shock is merely the approach of death by its usual mechanism” (p. 214).

Selye (1949,1950) subdivides the alarm reaction into two more or less distinct phases: shock, an initial manifestation of systemic damage, and countershock, a defensive homeostatic response to the damage. The phase of shock is characterized by lowered body temperature and lowered blood pressure, depression of the nervous system, decrease in muscle tone, deranged capillary and cell membrane permeability, decreased blood volume due to a loss of fluids to the tissues, and gastrointestinal disturbances. The vasomotor center in the medulla sends out efferent vasoconstrictor and vasodilator impulses to the blood vessels by way of the spinal cord and sympathetic nerves, causing a fall in blood pressure followed by a disturbance of fluid balance through increased capillary and cell membrane permeability. When blood pressure and blood volume thus decline, physiological reactions take place that tend to compensate for the deficiency. These make up the phase of countershock.

Selye found that adrenocorticotropic hormone (ACTH) plays a major role in the defense of the body against systemic injury. Stimulation of the hypothalamus, which regulates vital autonomic activities, produces (1) intensified activity in the sympathoadrenal system and (2) strong reactions in the skeletal effectors of the body. (1) Increased secretion of adrenaline results in the release of corticotropic hormone from the anterior lobe of the pituitary gland. In response to corticotropin, the adrenal cortex enlarges, and secretion of cortical hormone is augmented. Organic corticoids produce changes in organic and inorganic metabolism; inorganic corticoids cause retention of sodium with resultant increase in blood volume, a plethora that contributes to elevation of blood pressure. (2) Stimulation of the caudal portion of the hypothalamus causes increased muscular activity. When experimentally induced in animals, hypothalamic stimulation resulted in a reaction termed “sham rage” consisting of struggling, biting, spitting, snarling, clawing movements, lashing of the tail, dilation of the pupils, increased blood sugar, rapid heart rate, rise in blood pressure, and increased secretion of adrenaline. Wortis and Mowrer (1942) reported cases of human sham rage as a result of uninhibited hypothalamic discharge. Inasmuch as the defensive role of adrenaline consists in increasing circulatory activity and oxygen supply, it may be said to facilitate muscular activity; increased muscular activity in turn intensifies the secretion of adrenaline and its effect on the adrenal cortex.

The successful defense of the organism against stress thus shows an exquisite balancing of homeostatic forces. Even the initial phase of shock seems to serve a signal function. In reviewing it, one is inevitably reminded of Freud’s (1926) description of signal anxiety, wherein the ego submits “to a slight attack of the illness in order to escape its full strength” (p. 162). In general, Selye seems to have been deeply influenced by Freud’s ideas on trauma as I characterize them in Chapter 3.

Selye (1950) also noted, however, that there is an antagonistic effect of various corticoids. Desoxycorticosterone (DCA), for example, at first increases the excitability of the nervous system; in a second phase, it produces a reversible depression. “If very large doses of DCA suddenly enter the blood stream … there is a preliminary stage of excitation followed by [an] anesthesia [so deep] that major operations can be performed … [under it]. In certain experimental conditions, DCA produced a state of experimental catalepsy” in rats. DCA-treated rats, for example, showed extraordinary hypersensitivity and irritability with profuse salivation. They jumped or bit when the experimenter attempted to hold them. “After this they fell to the floor apparently in an unconscious state” (pp. 666-668).

All of this, I submit, is remarkably like the sequence of events we observe in infants subjected to severe deprivation. In the early infantile period, frustrations such as loss of mothering or delayed sucking are responded to by three different forms of primitive stress reaction, which follow one another according to the degree of frustration experienced: (1) agitation, consisting of mass activity, restlessness, startle pattern, crying, vigorous body movements, and muscular tension; (2) catatonoid reaction, consisting of refusal to suck, breathing difficulties, constipation, hypertension, and rigidity of all body muscles with an extensor reaction of the muscles of the back, interspersed with periods of violence and screaming, culminating in; (3) full shock, with stupor, general loss of muscle tone and of reflex excitability throughout the body, pallor, gastrointestinal disturbances (diarrhea), and death (Ribble, 1939, 1941). We see, that is, the identical sequence of excitation and depression observed in DCA-treated rats and in humans in full-blown shock; and we see it not only in the general movement from agitation to full shock, but also in the intervening catatonoid stage, wherein violent activity is interspersed with inhibition. The catatonoid reaction thus seems to recapitulate in microcosm the general trend in the development of full-blown shock. One might even describe the entire sequence as “catatonoid.”

The catatonoid reaction is so named because of its resemblance to the more well-known catatonic syndrome, first described by Kahlbaum. In this, stupor, immobility and rigidity, and vegetative disorders—of the circulatory, respiratory, and digestive systems—are interspersed with occasional brusque impulsions (raptus). There is decreased metabolism and temperature, lowered blood pressure, bradycardia, difficulty breathing, loss of appetite, refusal of food, constipation, increased muscle tone but lowered muscular and cerebral activity, and the characteristic states of extreme motor excitement alternating with depersonalized stupor.

It is highly significant, I think, that all the substances that were used experimentally to produce catatonia (adrenaline, acetylcholine colibacilli, and so on) have likewise been found effective for the experimental induction of shock (de Jong, 1945; Baruk, 1949). Could it be that catatonia represents the last phase in a long line of defenses against shock? The catatonoid reaction itself seems to result from a blocking of higher cortical centers, probably as a consequence of anoxia, and represents a biological regression to a more vegetative existence, a dedifferentiation of the organism. Some of its manifestations are reminiscent of the rigidity observed in decerebrate animals (Sherrington, 1906), and it corresponds to the reaction of “dead faint” in animals, a kind of catatonic stupor known as “fright rigidity.” Its defensive function can be understood in terms such as these: Anoxic decortization diminishes in some degree the action of the cortex and thus the registration of inflowing stressful stimuli. Since the organism as a whole functions as a sensorimotor unit, this blocking causes a paralysis of controlled—of volitional—motor activity. At the same time, however, the increased tone of the muscular system, resulting from stimulation of lower brain centers, causes an increase in the supply of adrenaline. Catatonic rigidity thus facilitates respiration and steps up the supply of oxygen, which in turn facilitates the uncontrolled impulsions characteristic of the disorder. There is, in other words, a minimum of energy output, as reflected in lowered metabolism, with a very high order of muscular capacity and the same exquisite balance of homeostatic forces we saw in Selye’s countershock, but at a much lower, more primitive level.

Let me summarize our findings so far: The alarm reaction consists of sequential phases of inhibition and excitation—there is the depression of function of the initial phase of shock, followed by the agitation of the countershock phase. The first is a physiological alert mechanism, the second a restitutive response to alarm. If we hypothesize a similar alert mechanism in the frustrated infant, then the reaction of agitation can be seen to serve the countershock function. The succeeding catatonoid reaction would then represent yet another phase of inhibition—at least with regard to the characteristic stupor, vegetative disorders, and rigid immobility—and yet another phase of excitation—the paroxysmic motor impulsions. The sequence, then, would be inhibition (initial phase of shock), excitation (agitation response), inhibition (catatonoid depression of function), and excitation (catatonoid impulsion). Hereinafter I shall refer to the complex of agitation and catatonoid reaction as countershock.

I must now anticipate my argument to some extent by stating that laboratory dream research has unequivocally established that the pavor nocturnus attack proper takes place in a “modified waking state” in which the “subject is dissociated, is relatively unresponsive to the environment, shows decreased cortical responsiveness, and may be delusional and/or hallucinating” (Fisher, Kahn, Edwards, and Davis, 1974a, p. 388)—in a condition of stupor, in other words. The relevance of this to the foregoing should be apparent. If we define the catatonoid reaction, in its essence, as a condition of stupor and increased muscle tone with paroxysmic motor impulsions, have we not defined a condition very much like the complex of observed responses in pavor nocturnus? In particular, the violent movement and, as we have now seen, dissociated, stuporous state observed in the full-blown attack? Do we not find in both conditions the same curious coexistence of motility and stupor? There are, moreover, certain casual descriptive correspondences between the two conditions: the sensations of helpless paralysis—possibly rigid—difficult breathing, and pressure on the chest of pavor nocturnus, with the rigid immobility, difficult breathing, and vegetative disorders of the catatonoid reaction. The accelerated heart and respiratory rates observed in pavor nocturnus would be consistent with a preceding agitation phase. Might it not be the case, then, that the helpless para...

Table of contents

• Cover
• Title
• Copyright
• Table of Contents
• Acknowledgments
• Editor’s Preface
• Author’s Preface
• Bibliography of Max M. Stern, M.D.
• Introduction
• Chapter 1. Pavor Nocturnus
• 2. Regression Explanations
• 3. Trauma and the Repetition Compulsion
• 4. Reparative Mastery
• 5. The Teleonomic Principle
• References
• Author Index
• Subject Index