Emotion and trauma

Director of Teaching
University of Toulon

Emotion and trauma

by B. Cyrulnik, France

Without emotion, there can be no memory. An event needs to arouse neurological circuits that leave a memory potential “like a scar in brain tissue” (William James) or rather like a path carved out of the neuronal undergrowth. Everyday experience teaches us that what is a major event for one person may only be a minor incident for another. Thus trauma is defined not by the event in itself, but by its psychological impact. Memory is a heterogeneous system made up of neurology, affectivity, verbality, and cultural narratives. The biological component of emotion is physically determined by the functioning of a neuronal circuitry that mediates events and chemical compounds. Feeling is an emotion triggered by the representation of remembered images or individual and collective narratives. Healthy memory evolves, reworked over a lifetime, while traumatic memory stays fixed, but can be reworked employing targeted techniques.

Medicographia. 2013;35:265-270 (see French abstract on page 270)

A memory is said to be traumatic when a past event causing an emotional shock at the time is followed by a sustained aftershock of altered self-representation. Healthy memory is a heterogeneous system made up of neurobiology, interpersonal relationships, and collective narratives reworked over a lifetime. Traumatic memory, on the other hand, remains fixed on the recollection of misfortune and ceases to incorporate incoming self-representational data. Unable to rework the memory, the victim endures psychic agony as a prisoner of the past. Differing radically from an ordeal that a person confronts and overcomes before moving on, trauma fixes the mind on the memory of perpetually recurrent misfortune. Psychoanalysis likens traumatic memory to a break-in by a foreign body that plays havoc with the psychic apparatus. Neither internal conflict nor Oedipal neurosis,1 traumatic memory is the fear of death paralyzing the machinery of the mind.

Without emotion, there can be no memory. An event needs to arouse neurological circuits that leave a memory potential “like a scar in brain tissue”2 (William James) or rather like a path carved out of the neuronal undergrowth.3 Everyday experience teaches us that what is a major event for one person may only be a minor incident for another. Thus trauma is defined not by the event in itself, but by its psychological impact.4 This becomes easier to understand if we differentiate between emotion, caused by a cerebral stimulus or ingestion of a substance, and feeling, defined as emotion triggered by mental representation (a scenario made up of images and words).


Emotion is regulated primarily by a neuronal substrate. The orbitofrontal cortex plays an important role in emotivity: with its connections to the amygdala and anterior cingulate cortex, it modulates the affective connotation of events. When prefrontal inhibition is impaired by disease or accident, the “unleashed” amygdala over stimulates the anterior cingulate limbic circuit. In such cases, the slightest event triggers uncontrollable emotion that spreads to the hypothalamus, midbrain, and brainstem nuclei: the motor expression of emotion becomes uncontrollable.5

Figure 1
Figure 1. Attachment figure: the secure external base will be internalized
in the infant’s memory.

© Toronto Star/Andrew Francis Wallace/Getty Images.

A baby that experiences traumatic fright before it has learned to speak is unable to master or rework its representation of the trauma. It seeks support from an external secure base to relieve the emotion caused by the terrifying experience. When the attachment figure is present, the infant huddles close (Figure 1). But when that figure is absent or dysfunctional (dead, sick, or abused by partner, past, or community), the infant is insecure and loses the ability to learn emotional control. More crucially still, the event inscribes amygdala hyperactivity into its brain, triggering emotional panic at the slightest subsequent event. The infant’s pain threshold tumbles so that it becomes frightened and hurt by anything: it perceives the slightest facial expression of annoyance or impending remonstrance from an adult as an aggression equivalent (Figure 2).6,7 When a child’s developmental niche becomes so impoverished as to descend into sensory deprivation, the dendritic spines fail to establish connections. Neuroimaging shows atrophy8 while the overworked amygdala becomes hypertrophic.9


A child may be particularly given to emotion even when the affective component of its developmental niche is stable and well structured. Such emotivity is genetically determined, encoded in all mammals by a group of genes that under synthesize a synaptic serotonin transporter protein. Fifteen percent of all mammals come into the world deprived of the natural emotional tranquility conferred by serotonin. If misfortune happens to strike, these 15% of minor serotonin transporters are seriously wounded. Faced by the slightest event, such children seek to downplay its emotional potential by self-centered behavior such as gaze aversion, rocking, twirling, and nail-biting. When emotion overwhelms them (as readily happens), it triggers auto-aggressive behavior. Frightened by any relationship, they have never learned to direct toward others the interactive rituals that make for peaceful coexistence. The paradoxical result is that auto-aggressive behavior has a tranquilizing effect.

Regardless of whether they are genetically hypersensitive or have amygdala hypertrophy induced by early deprivation, such children experience the frustration inevitably encountered in any game or conflictual situation as a source of violent stress. Any encounter triggers outward- and/or inward-directed aggression. Every emotional alert takes long to die down. Forever on standby, the hypothalamic-pituitary-adrenal axis increases mean circulating cortisol levels. The limbic cells that are supersensitive to cortisone swell in response, the ion channels open and let in potassium. The Na+/K+ gradient is reversed, causing such hyperosmolarity that the cell bursts. This process accounts for the limbic atrophy seen in depressed patients11 who progress from hypersensitivity to the slightest event to memory disturbance and affective indifference (Figure 3).12


During normal development, the same deprivation has different effects depending on when it occurs. It leaves its imprint on every human being who needs other people in order to complete his or her development. A sensory figure featuring at a sensitivemoment in a child’s development becomes a key object that the child perceives over and above any other. From that point onwards a circuit is traced in its implicit memory, attaching the child to the familiar figure. Whether mother, father, peer, or place, this attachment figure makes the child feel secure and gives it the strength to explore its world with pleasure. Without such a figure, the child panics, runs in all directions, suffers emotional diarrhea, becomes accident-prone and is unable to process information correctly (Figure 4).13

Figure 2
Figure 2. Interaction with an environmental factor: facial expressions.

Abbreviations: cACC, caudal anterior cingulate cortex; rACC, rostral anterior cingulate cortex;
vmPFC, ventromedial prefrontal cortex.
After reference 7: Hamann. Nature Neurosci. 2005;8(6)701-703. © 2005, Nature Publishing Group.

Failed imprinting may be due as much to the child’s environment as to its development. A deprived niche (a dead or depressed mother, conjugal violence, or underprivilege14) leaves no reassuring imprint in a child’s biological memory. Similarly, genetic disease causing a deficiency of acetylcholine, endogenous opioids or oxytocin undermines the biological basis for imprinting.15 Drugs may have the same effect: β-blockers, certain antidepressants and interferon (in 50% of prescriptions) make the body indifferent to contextual information.

Memory no longer retains an imprint once blunted emotion prevents an object or event from standing out in a child’s experience. In a world without emotion, everything is the same, there are no value judgments, no event is worth inscribing in memory, and no figure stands out for potential attachment.

Genetic determinants create a predisposition rather than determine an ineluctable fate. Minor serotonin transporters who live in a reassuring environment soon develop enough self-confidence and affective stability to begin exploring with pleasure. Conversely, major serotonin transporters living in longstanding isolation acquire an emotional vulnerability that subjects them to their impulses and the stimuli of others. This may account for the emotional storms in borderline states. Having suffered a torrent of early childhood traumas, the prefrontal lobes in such individuals fail to acquire the ability to inhibit emotion. Stimuli are too intermittent to develop the frontolimbic connections that could control the expression of emotion.16 A distorted interactional spiral then becomes established in which such children, who are incapable of controlling their impulses, sabotage the emotional reactions of those around them, thus jeopardizing their affective relationships with their attachment figures.17

Figure 3
Figure 3. Limbic atrophy.

Dynamic evaluation of genetic vulnerability factors in depression, according to
presence or absence of “s” allele. Structural, correlated, and functional high-resolution
MRI (1 mm3) in more than 100 subjects. Cingular atrophy is evidenced in
“s” allele carriers. This determinant of emotivity is not a determinant of resilience.
After reference 12: Pezawas et al. Nature Neurosci. 2005;8(6):828-834. © 2005,
Nature Publishing Group.

Figure 4
Figure 4. Attachment figure and imprinting.

A and B: In the presence of the attachment/imprinting object the duckling feels
secure and is able to learn how its environment works. C: In the absence of
the attachment/imprinting object, the duckling panics and fails to learn anything.
This leads to a propensity for accidents, emotional diarrhea, and immunodepression,
as all new information is experienced as traumatic.

The insecurity of a child whose sensory niche has been deprived by parental misfortune (death, disease, marital breakdown, underprivilege) leads it to perceive its world as an unending series of alarms. The resulting prefrontal hypotrophy and limbic atrophy subject the child to its environmental stimuli since it is unable either to plan ahead or use its memory. Everything and anything frightens the child and triggers reactions of fight or flight.

Erosion of the soul

Once stress has been so overwhelming as to have consumed the capacity to respond, the physiological reactions of the burned-out amygdala induce a state of psychic numbness. An amygdala rendered dysfunctional by physiological burnout or head injury leads to anhedonia. Nothing excites such individuals anymore. They lose all taste for life.

Amygdala response is what determines whether an item of information is stored in memory. An alert amygdala ensures that some facts will become memory events. A numbed or lesioned amygdala, on the other hand, lets nothing through to memory. Thus the soldiers who took propranolol during the Iraq War in 1991 avoided the hypermnesia of posttraumatic stress syndrome, but conversely experienced enormous gaps in memory.18

Anhedonia—the inability to enjoy life—was described in the 19th century in melancholics, neurasthenics, and those with early dementia. The following variants were identified:
_ Reactive anhedonia in subjects who once enjoyed life, but eventually experienced “erosion of the soul” after a trauma or cascade of painful events.
_ Anhedonia as a personality trait reflecting a hyporeactive amygdala, in a subject whose life since childhood had been deprived, bleak, and led at slow pace in social isolation.

Prospective studies speak of “chronic depression” and psychotic tendencies.19 These traits are common among risk takers who depend on strong stimuli to feel alive. Other instances include the astonishing anesthesia of psychotics capable of walking on a broken leg, remaining upright with peritonitis, or slicing into their forearms with no change in facial expression. Evidence suggests that such agenesis of the amygdala is due to the numbing of amygdala reactivity by opioid hypersecretion in response to early interactions in the first few months of life.20

Victims of the prefrontal leukotomies practiced between 1935 and 1960 or patients with crude lobotomies caused by head injuries were found to have lost the ability to inhibit their behavioral or mental responses. Having lost the neurologic substrate required for the representation of time (memory and anticipation), such patients become incapable of imagining the effect that their words or acts could have (later) in the mind of someone else. Incapable of empathy, they give free rein to their impulses, as is seen after lobotomy, in frontotemporal dementia, sexual deviation, and in children under 4 who have yet to develop a theory of mind. As prisoners of the here and now, incapable of combining representation of the past with that of the future, they are unable to give meaning to what they perceive. They become detached from an existence that no longer holds meaning for them, switching between overreaction and indifference, depending on the stimuli emanating from those around them. When people are busy around them, they can become agitated; but when things calm down again, they become immobile, bereft of either internal language or emotion. Empathy

Patients whose amygdala has been destroyed by lobotomy become totally indifferent. If you ask them to lay their hand on the table and you then pretend to strike it with a hammer, they do not even flinch, since they do not anticipate feeling pain. They remain stone-faced and devoid of empathy in front of any manifestation of pain or suffering in another person. Yet paradoxically they can be hurt by their own indifference of affect. Lobotomized patients often say: “I miss the time when I felt pain and suffering. I at least felt alive.” Does this mean that pain and suffering are part of the human condition and that they help us develop the empathy that enables everyone to live together? The minor frustrations that are inevitable in daily life (eg, a delayed feed or temporary absence of its mother for an infant, a physical malaise or a relationship issue) cause minor levels of discomfort or distress that train us in empathy. Child survivors of natural disasters, war, or serious illness show an astonishing acceleration of emotional maturity.21

Affective anesthesia thus has a variety of causes:
_ Dysfunctional frontolimbic circuitry due to early deprivation of environmental stimuli leading to amygdala burnout.
_ Erosion of the soul caused by a cascade of insidious trauma such as underprivilege or an unwelcoming environment (soul-destroying work, harassment, racism).
_ Ingestion of amygdala-numbing substances such as propranolol, β-blockers, or certain psychotropic agents.
_ Lobotomy due to head injury.22

Recent neuroimaging data confirm the time-honored neurologic concept of the complementarity of opposites between pleasure and pain.23 Dopaminergic and opioid systems preferentially stimulate the ventral segmental area of the brainstem.24 But excessive stimulation of the inferior longitudinal fasciculus (pleasure area) eventually stimulates the lateral spinothalamic fasciculus (pain area), and vice versa. We see this pair of opposites at work in attachment behavior: an infant moves away from its secure attachment figure and explores its environment until it experiences fright, at which point it scuttles back to huddle deliciously close to its mother. An infant that experiences neither fright nor frustration is numbed by the absence of stimuli and neither mentalizes nor develops an attachment figure.25 Perhaps, when poets write that magic consists of transforming pain by endowing it with inordinate nobility (“nothingmakes us greater than great pain… the most beautiful songs are the most despairing”24), they are simply giving voice to this combination of contrary emotions.

Figure 5
Figure 5. Memory of a psychologically traumatic syndrome.

Images of a terrifying event tend to become pervasive within the subject’s mental
life, whereas the precise memory of the traumatic event tends to fade.
Man aiming gun. © Micha Klootwijk/123RF.

Reworking emotion

It is thus possible to rework the pain in a feeling by ennobling it or transforming it into poetry. In doing so we become author- actors in the representation of our life stories.26

The memory of a psychologically traumatic syndrome is constraining and painful: an image of terror takes over our thoughts, seeps into our mental lives, and constantly recurs, haunting us in particular in nightmares (Figure 5). The memory of a terrifying event is said to ease over time, but it is more accurate to say that time gives the “victim” an opportunity to develop the relationships that will help rework the memory so that he or she is no longer its victim. Emotion is transformed by meeting someone with whom one can share a narrative. Words have to be found in which to address the person we trust.

Healthy memory adjusts its representation of the past to current circumstances: 73 14-year-old boys answered a 28-point questionnaire describing how they perceived their current situation: “Is religion helpful to you?”, “What do you enjoy most?”, “Is the discipline you receive upsetting to you?” Thirty-four years later, the investigators recontacted 67 of the ex-adolescents, now aged 48, and re-asked the same questions: the answers were astonishingly different. Twenty-eight percent of the 14-year-olds had replied that they “enjoyed school and homework least”; this figure jumped to 58% at age 48. One adolescent in four considered that he enjoyed peer relationships most, a proportion that expanded to one in two of the 48-year-olds. Eight adolescents in ten (82%) were upset by the corporal punishment they received, whereas at age 48 the upset was remembered by only about a third (28%).27 The emotion we experience at the time is different from the emotion we remember. It is in the present that we become drunk on the Baudelaire’s “wine of memory” and the reconstituted past. Reworking of the emotion associated with memory is thus the general rule. Predictably, the memory associated with the least reworked emotion is the memory of horror.

Three factors combine to keep a memory intact and accurate or allow it to fade into haziness:
Time of occurrence of the traumatizing experience. Preverbal terror leaves a trace in biological memory, but no memory. The persons concerned do not know why they have been made sensitive to this type of event: they have source amnesia. Later in life, they may become able to find images and/or words to represent the source event or situation that has given the particular taste to their world, but it will not necessarily be factually accurate (false allegations of rape, impressions of persecution, mistaken identity). If terror strikes when a person is depressed or has been made vulnerable by previous trauma, there is a high probability of the image of the terrifying event becoming part of a psychologically traumatic syndrome, comprising a fascination with the aggressor who is recalled in hyper-real focus, while the setting in which the aggression occurred remains hazy.28
_ The emotion of horror. We do not need to experience horror in order to strengthen our memory of horrific images. People only have to be shown one series of horrific images and another of attractive images. A month later, they clearly remember the horrific images, but retain only vague recollections of the attractive photographs.29 Horror has a fascination that fixes memory, whereas pleasure has a relaxing effect that traces in memory a readiness for well-being that is devoid of individual images.30
_ The power of words. The words that accompany photographs have a strongly reworking effect on memory. When horrific photographs are shown with an accompanying commentary that gives meaning to the horror involved (the making of a hero, a noble sacrifice, or dramatic fiction), the horror of the memory will be largely blurred. But if attractive photographs are shown with an uplifting commentary, the attractive memory becomes clearer.

Even written words are involved in the reworking of memory. When the written words trawl a painful past for the details of an atrocity in order to commit them to paper, the mental work required can concentrate the mind to a degree approximating to psychological trauma syndrome. Primo Levi dwelled on Auschwitz to the point of suicide, while Jorge Semprún described his drafts on his experience of Buchenwald as having bled for 20 years. Conversely, when “victims” write on trauma to give others the pleasure of understanding or to create a work of art (novel, film, art, or poetry), they rework the representation of what they have suffered.31 In restoring the past by “the wine of remembrance,” collective narratives play a major role in attenuating or exacerbating a traumatic memory.32 When traumatized parents are sustained by the cultural narratives that surround them, they give their children the impression of emerging victorious. But when the cultural context isolates, aggresses, or despises them, the unresolved trauma suffered by the parents destabilizes the children.


Whether triggered by an affectively and/or socially deprived environment, organic lesion, or enveloping narrative, emotion is what gives taste to the world we perceive. It is by shaping the environment that shapes us that we enjoy a measure of freedom. _

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Keywords: affective relationships; cultural narratives; neurological circuits; sensory deprivation