Prof. Joseph Levine

Talk 77: Therapeutic work with preverbal experiences of an adult including RGFT treatment adaptations for this work

By Prof. Levine & Dr. Salganik

Hello to our readers,

Identifying preverbal experiences in psychotherapy poses unique challenges because these early experiences occur before language development and are therefore encoded primarily through sensory, affective, and somatic pathways rather than through verbal memories.

Below, we offer a speculative but clinically informed exploration of psychotherapeutic strategies for accessing and interpreting such preverbal content.

Nonverbal Expression and Bodily Memory

Preverbal memories are often encoded somatically – through sensations, emotions, and physiological responses rather than through language.

Somatic Experiencing: Trauma-based therapies such as Peter Levine’s Somatic Experiencing help clients tune into subtle bodily sensations (Levin, 2010). Feelings of pressure, heat, nausea, or trembling, especially in response to triggers, may indicate distress or preverbal comfort.

Movement Therapies: Movement therapy or sensorimotor psychotherapy encourages expressive bodily movement.

Observing patterns, postures, muscle tension, and spontaneous gestures can help identify emotional states rooted in preverbal experiences (Ogden, Minton, & Pain, 2006).

Attachment-Based Observations

Attachment theory posits that early interactions with caregivers profoundly shape affective regulation and interpersonal behaviors.

Adult Attachment Interviews (AAI): Although subtle verbal, emotional, or behavioral cues during these structured interviews can indicate disruptions in preverbal attachment.

Individuals who exhibit unresolved emotional states or incoherent narratives may implicitly express preverbal relationship disorders (Main & Hesse, 1990).

Observing the dynamics of therapeutic relationships:

The therapeutic relationship often reflects early attachment styles. Patterns such as intense fear of abandonment, persistent distrust, or difficulty regulating emotional closeness may reflect preverbal relationship traumas or deficits (Schore, 2003).

Symbolic, Imaginative, and Artistic Exploration

Artistic and symbolic modes bypass language and directly engage preverbal experiences.

Art therapy and sand tray therapy: Creative expressions in art or sand tray therapy can symbolically represent preverbal emotional states. Colors, shapes, textures, and arrangements may correspond to early preverbal experiences, allowing clients to externalize unconscious memories (Kalff, 2003).

Guided imagery and dream work, guided imagery and metaphorical exercises often connect to early nonverbal content. Recurrent symbolic images or emotionally charged scenarios may indicate unresolved preverbal experiences (Hartman, 2010).

Emotional states and emotional flashbacks

Preverbal experiences usually manifest as diffuse emotional states rather than clear memories.

Affect regulation difficulties: Chronic emotional states such as unexplained sadness, anger, anxiety, or helplessness may reflect early preverbal trauma or neglect, as such emotions can precede explicit verbal memories (Van der Kolk, 2014).

Emotional flashbacks (Pete Walker's concept): Verbal trauma is often expressed through sudden emotional flashbacks – intense emotional states without narrative context.

Identifying and processing these flashbacks within therapy can help identify the sources of such preverbal experiences (Walker, 2013).

Implicit Relational Patterns

Implicit relational knowledge is formed during infancy and is encoded as procedural rather than episodic memory.

Relational Psychoanalysis: Through careful analysis of relational dynamics in therapy, clinicians can uncover implicit relational patterns that were formed during preverbal periods.

Interaction patterns such as withdrawal, dependency, dissociation, or anxious attachment can indicate the origins of preverbal relationships (Lyons-Ruth, 1998).

Hypnosis and Altered States of Consciousness

Hypnosis and trance states may facilitate access to implicit memory systems, bypassing conscious language barriers.

Hypnosis: Clinical hypnosis can gently guide the patient into deeper states of consciousness where preverbal experiences are expressed symbolically, emotionally, or somatically, and help integrate them into current narratives (Spiegel, 2013).

Support and speculation in neuroscience

Neuroscience highlights the importance of right-brain dominance in preverbal experiences, suggesting that nonverbal psychotherapy methods may more effectively focus on implicit emotional memories encoded in the limbic system and right hemisphere (Schore, 2019).

Future psychotherapeutic tools could include brain imaging and neurofeedback techniques to further elucidate these implicit memories.

Clinical Aspect (Speculative Example):

Consider a hypothetical patient who experiences intense anxiety, feelings of abandonment, and unexplained gastrointestinal discomfort. Somatic experience and art therapy reveal a recurring theme of emptiness and vulnerability symbolized by dark, empty containers in her drawings. Through guided imagery and gentle exploration, it emerges that she is experiencing feelings of profound isolation and abandonment that echo a preverbal period.

Observation of relationship patterns in therapy—attachment followed by abrupt withdrawal—further suggests a disrupted attachment in early infancy. Hypnosis and implicit referential methods gradually facilitate his emotional integration, suggesting that these experiences reflect preverbal neglect rather than explicit verbal memories.

Conclusion:

Although inherently speculative due to methodological and epistemological constraints, psychotherapeutic identification of preverbal experiences remains possible through careful integration of somatic approaches, attachment-based observations, creative methods, relational dynamics, and guided exploration of implicit emotional states.

Preverbal memories—formed in infancy before language acquisition—are encoded primarily as implicit, nonverbal, sensory, emotional, and somatic experiences. These memories are stored differently from explicit verbal memories and involve distinct neural mechanisms.

Why we usually don’t remember anything before the age of three:

The tendency for people to have few or no memories from before the age of three is known as childhood amnesia. It happens due to several factors related to brain development, memory formation, and the way we encode experiences. Here’s why:

• Immature Brain Structures: The hippocampus, a key brain region for storing long-term memories, is still developing in infancy and early childhood. Since it's not fully matured, it doesn't efficiently consolidate memories in a way that can be recalled later.
• Underdeveloped Language Skills: Memories are closely tied to language. Infants and toddlers experience events, but without the ability to put them into words or structured narratives, these memories remain inaccessible later in life.
• Lack of Self-Concept: Very young children haven’t fully developed a clear sense of self, which is necessary for autobiographical memory—memories connected to personal identity. Without this, their experiences don’t get stored in a way that makes them recognizable as personal memories.
• Differences in Encoding & Retrieval: Even when toddlers form memories, they may encode them in a way that's different from how older children and adults process information. Over time, the ability to retrieve early memories fades because the retrieval mechanisms change.
• Neural Pruning: During early childhood, the brain undergoes significant restructuring, strengthening important neural connections and eliminating unused ones. Some early memory pathways may be lost in this process.

Interestingly, while explicit memories from early childhood are rare, emotions, habits, and learned responses from that period still influence behavior subconsciously. So even if you don’t remember specific events from your infancy, they have shaped parts of who you are!

How Preverbal Internalizations Manifest Later in Life

Since these internalizations occur before a person can articulate or consciously recall them, beneath verbal awareness, preverbal internalizations manifest as deeply felt experiences, often with no recognizable source, they often emerge in indirect ways:

1. Emotional Triggers & Automatic Responses

• People may react to situations with strong emotions—such as anxiety, anger, or distrust—without knowing why.
• For example, someone who experienced inconsistent caregiving in infancy may later struggle with feelings of abandonment, even in secure relationships.
• These responses stem from deeply wired emotional associations rather than conscious thought.

2. Body & Nervous System Responses

• Preverbal experiences are stored in the limbic system and autonomic nervous system, leading to physiological reactions like increased heart rate, muscle tension, or even unexplained physical discomfort.
• Somatic Memory: Unexplained bodily reactions—tension, digestive issues, or chronic stress—tied to unprocessed early experiences.
• A person who experienced neglect or distress as an infant may have a heightened fight-or-flight response even in non-threatening situations.

3. Attachment & Relationship Patterns

• Preverbal internalizations dictate whether someone feels secure or insecure in relationships.
• If an infant internalized safety through responsive caregiving, they tend to develop secure attachment, fostering trust and confidence.
• If an infant experienced unpredictability or neglect, they may later exhibit avoidance, anxiety, or emotional detachment without understanding why.
• Recurring Emotional Patterns: Feeling unseen, fearing abandonment, or difficulty trusting, despite no conscious reason.
• Behavioral Repetition: Gravitation toward unstable relationships, self-sabotaging moments of success, or emotional avoidance.

4. Implicit Beliefs About Self & Others

• Without verbal reinforcement, early experiences create unspoken beliefs like:
  • "I am loved" or "I must earn love."
  • "The world is safe" or "I must be hyper-vigilant."
  • "People will understand me" or "I must not express emotions."
• These foundational beliefs dictate how someone interacts with others and approaches challenges.

Because these patterns don’t originate in explicit thought, traditional cognitive-based approaches aren’t enough to modify them.

These early internalizations—beliefs, emotional patterns, and learned behaviors formed in infancy—continue shaping a person's thoughts, relationships, and reactions throughout life. Here's how they typically manifest across different ages:

Infancy (0-2 years)

• Internalizations are primarily emotional and sensory, based on the caregiver’s responsiveness.
• A securely attached infant develops a foundation of trust and safety, while inconsistent care may lead to anxiety or avoidance.
• These experiences shape implicit memory, influencing how the brain later responds to stress and relationships.

Early Childhood (2-6 years)

• Internalized messages about love, worth, and emotional expression start to solidify.
• Children who experience warmth and validation tend to develop confidence; those exposed to criticism or neglect may internalize self-doubt.
• Emotional regulation patterns begin to emerge, shaped by caregivers’ responses to distress.

Middle Childhood (6-12 years)

• Early internalizations influence social interactions and self-image.
• A child who has internalized encouragement may approach challenges with resilience, while one exposed to excessive criticism might fear failure.
• Cognitive development allows them to start reflecting on these patterns, though they are largely subconscious.

Adolescence (12-18 years)

• Early internalizations shape identity formation, self-worth, and peer relationships.
• Unresolved attachment patterns may manifest in friendships and romantic relationships.
• Internalized fears or insecurities from childhood may become more evident, influencing choices in risk-taking and self-expression.

Adulthood (18+)

• By this stage, internalizations deeply affect decision-making, emotional responses, and interpersonal relationships.
• Early self-worth beliefs impact career choices, relationships, and overall emotional well-being.
• With self-awareness, individuals can recognize unhelpful patterns and work to reshape them through reflection and experience.

These foundational beliefs remain influential, but they are adaptable. With awareness and effort, people can reframe early internalizations and develop healthier perspectives.

The beautiful thing is that internalizations aren’t set in stone. While they form the foundation, people can reflect on them, challenge unhelpful patterns, and reshape their perspectives over time.

The following is an overview of the brain mechanisms associated with preverbal memories.

Brain mechanisms involved in preverbal memories

Implicit memory system and subcortical structures

Preverbal memories are primarily implicit, meaning they are recalled unconsciously and indirectly, often through emotions, behaviors, or physical sensations.

Amygdala:

Central to encoding emotional content of early experiences.

Responsible for implicit fear conditioning and emotional memory (LeDoux, 2012).

Hippocampus (Early Developmental Role):

Although the hippocampus is best known for explicit memory, early nonverbal emotional and spatial associations can be implicitly encoded with it in infancy (Riggins et al., 2020).

Basal nuclei and cerebellum:

Related to procedural memories, body habits, and motor responses learned in infancy.

Early interactions (such as rocking or soothing) can be encoded as procedural preverbal memories (Squire & Dede, 2015).

Right-hemisphere dominance

Preverbal experiences, which are primarily emotional, sensory, and relational, involve greater activity of the right hemisphere of the brain.

Right orbitofrontal cortex (OFC):

Vital for emotional regulation and social bonding.

Processes implicit emotional and relational memories formed through interactions with caregivers (Schore, 2019).

Right temporoparietal regions:

Facilitate body awareness and somatic experience – important for encoding sensory aspects of preverbal memories (Damasio, 2010).

Default Mode Network (DMN)

The default mode network mediates introspective thought, autobiographical memory, and emotional self-representation.

Although preverbal memories are implicit, emotional self-awareness and implicit autobiographical impressions may be processed through early DMN activity, laying the foundation for later narrative memory formation (Buckner & DiNicola, 2019).

Brainstem and Midbrain (Arousal and Regulatory Systems)

Preverbal memory involves basic homeostatic and autonomic regulation.

Brainstem nuclei, such as the locus coeruleus and periaqueductal gray (PAG), encode implicit arousal patterns—such as stress and safety—that are established early in infancy (Porges, 2011).

Scientific evidence supporting the brain mechanisms of preverbal memory

The following lines of evidence highlight the neurobiological basis for preverbal memories:

Infant Studies and Preconditioning

Classic research (e.g., Rovee-Collier's mobile kicking experiments) demonstrates that preverbal infants form strong implicit memories through operant conditioning, even without explicit awareness (Rovee-Collier & Cuevas, 2009).

Attachment and Brain Imaging Studies

Imaging studies show that adults with attachment insecurity—likely stemming from disrupted early preverbal experiences—show altered activity in limbic regions (amygdala, OFC) during social-emotional tasks (Buchheim et al., 2008).

The dominance of the right hemisphere in processing emotional facial expressions and relational cues further confirms the neuroanatomical basis for preverbal and implicit relational memories (Schore, 2019).

Trauma Research and Neuroscience

Preverbal trauma (e.g., neglect, infant abuse) leads to structural and functional changes in regions associated with implicit memory, such as the amygdala, hippocampus, and prefrontal cortex (Teicher & Samson, 2016). Adults with early preverbal trauma often exhibit heightened amygdala responsiveness, dysregulated OFC function, and impaired hippocampal processing (Van der Kolk, 2014).

Clinical Evidence: Somatic and Emotional Flashbacks

Clinical evidence suggests that patients who experience early preverbal trauma exhibit somatic flashbacks—implicit memories triggered by sensory or emotional stimuli without conscious recall of narrative details, consistent with neural pathways involving the amygdala, insula, and subcortical regions (Ogden, Minton, & Pain, 2006).

Neurodevelopmental Evidence from Animal Models

• Research in animals (primates, rodents) highlights that early maternal separation or disruptions in care affect amygdala maturation, HPA axis dysregulation, and emotional dysregulation—suggesting similar mechanisms in human preverbal memory formation (Tottenham, 2012).

Summary of key brain mechanisms and structures:

Conclusion:

Scientific evidence from neuroscience, clinical research, developmental psychology, and animal studies strongly supports the involvement of the amygdala, right hemisphere, basal ganglia, and related subcortical structures in the encoding and storage of preverbal memories.

These neural systems operate primarily through implicit, emotionally and sensory-coded mechanisms that are accessible through nonverbal therapeutic interventions.

Early Memory in Animal Models: A Comprehensive Review

Introduction:

Infants of all species undergo rapid brain development, forming memories even before they can passably communicate or explicitly recall events.

Researchers use animal models—from rodents to primates—to study how very early experiences are encoded and stored.

It is noteworthy that animals exhibit preverbal memory for early life events, which can shape their behavior and brain function later in life. This review synthesizes evidence from scientific studies on early life memory, covering species and developmental stages, types of early experiences, forms of memory, behavioral indicators of retention, basic neurobiology, and long-term effects.

The findings highlight that preverbal memory systems do exist and are functionally significant, with implications for understanding human infant memory and development.

Species and developmental stages in early memory studies

Animal models provide insight into infant memory because their developmental timelines can be aligned with human infancy. Key species include rodents (rats and mice) and nonhuman primates (monkeys), which offer complementary advantages:

Rodents: Newborn rats and mice are neurologically immature at birth, and undergo accelerated brain development after birth. Milestones that take years in humans occur within days or weeks in rodents.

For example, peak synapse formation (synaptogenesis) occurs in the fourth postnatal week in rats, whereas it occurs around 2–4 years of age in humans (whereas in great apes it occurs at ~1–2 years of age).

Thus, a rodent pup on day 7-10 after birth roughly corresponds to a human infant in many neurodevelopmental respects.

This rapid maturation allows researchers to model "infancy" and track its effects over a feasible time frame.

Nonhuman primates: Infant monkeys (e.g., rhesus macaques) are more neurologically advanced at birth and develop more slowly, closer to humans.

Their brain organization (cortex, hippocampus, amygdala) is highly homologous to humans, making them excellent models for complex cognitive and socioemotional development. For example, a one-year-old monkey is roughly equivalent to a human toddler in some memory abilities.

Studies in infant monkeys reveal how early damage to the hippocampus or amygdala and early social experiences affect memory development in ways that parallel human outcomes.

Relevance to Human Linkages:

By choosing species whose developmental stages map to human infancy, scientists ensure that early memory findings are developmentalally meaningful. Rodent pups can model the brain of a preverbal human infant (during which hippocampal and cortical circuits are still maturing), while primate infants bridge the gap to the human condition with a relatively longer childhood than rodents.

Collectively, these models emphasize that even very young brains encode information that can influence behavior long after infancy, similar to human infants.

Types of Early Life Experiences Studied

Researchers have identified various early life experiences that can leave lasting memory traces. The most commonly studied experiences include adverse and deprivation experiences that occur during the neonatal or infant period:

Maternal separation (early care deprivation): This paradigm involves separating infants from their mothers for extended periods (e.g., several hours a day during the first 2 weeks of life). In rodents, repeated maternal separation is a form of early life stress that alters the pup's environment and maternal care.

Such separations can have profound effects—for example, rat pups that are separated from their mothers daily later exhibit enhanced retention of fear memories formed in infancy compared to unseparated controls.

The mechanism is related to exposure to stress hormones (corticosterone in rodents), as mimicking separation by administering corticosterone exogenously to rat pups also prolongs the retention of these memories.

In primates, analogs include peer rearing or inconsistent maternal care; infant monkeys raised without their mothers (or under unpredictable care) experience psychosocial stress that affects their emotional memory systems (e.g., altered attachment and fear responses).

These models mimic neglect or inconsistent care in humans.

Early trauma and aversive conditioning: Even during early infancy, animals can undergo traumatic experiences (mild electric shocks, pain, or fear conditioning) and later show evidence of memory for these events. It should be noted that while young rodents (under 2 weeks old) typically undergo infantile amnesia (rapid forgetting), traumatic learning can leave latent traces.

Contextual fear conditioning (combining a context with a mild shock) in rat pups illustrates this: Rat pups may not show fear after a delay, but a reminder cue can restore a strong fear memory long after the original event.

Alberini and colleagues found that an experience learned during the period of infantile amnesia is not truly erased—it is stored as a latent memory that can be reactivated later in life.

This suggests that early trauma is encoded in the brain even if the infant does not later overtly recall it. Similarly, in infant monkeys or other species, stressful events (e.g., a mild shock or the smell of a predator) can lead to later changes in avoidance or anxiety, indicating early encoded emotional memory. These paradigms mimic early human traumas (such as painful medical procedures or infant abuse) in a controlled manner.

Sensory or social deprivation: Limiting the infant's sensory experiences (touch, sight, smell) or social interactions can examine the role of early stimulation in memory development. For example, some rodent studies use early sensory deprivation by raising pups in environments with reduced tactile stimulation or limited nesting materials (leading to fragmented maternal care).

These infants often show cognitive and emotional deficits later in life, such as impaired spatial learning or altered social behaviors. In classic primate studies, infants deprived of normal maternal contact and social interaction (e.g., Harlow’s rhesus monkeys raised with surrogate mothers) developed abnormal social and emotional behaviors.

While these older studies emphasized attachment, more recent studies link early social deprivation to changes in memory processing and stress reactivity (e.g., difficulty with appropriate fear learning, or memory problems resulting from atypical brain development).

Sensory deprivation by specific methods—such as blocking vision during critical periods (in cats or rodents)—profoundly alters the formation of neural circuits; although this is more about the wiring of the sensory system than "episodic" memory, they emphasize that prior experience (or lack of such experience) disqualifies the brain's ability to learn later.

Other early stressors: Researchers are also looking at mild exposure to stress or improvements in early experience. Early handling (briefly taking puppies outside for a few minutes a day) is a mild stressor that paradoxically can have a positive effect on later stress regulation and memory (promoting resilience). This contrasts with severe stressors such as prolonged maternal separation, which highlights that the intensity and timing of early experiences matter.

Additionally, studies on prenatal stress (stress on the mother during pregnancy) show that stress hormones can affect the fetal brain, leading to postnatal memory and emotional differences. While prenatal exposure precedes “learning” per se, it sets the stage for infant behavior.

Enriched early childhood experiences (extra toys, social play) have also been studied, showing that providing more stimulation at an early age can facilitate certain memory abilities later, an interesting side effect of deprivation studies.

Each of these early life experiences provides a window into how a baby’s brain encodes events. Remarkably, even experiences in the first days or weeks of life (before animals are weaned) can influence long-term behavior.

This suggests that the developing brain remembers early adversity or enrichment, although often in indirect ways.

Types of Memory at an Early Age: Emotional, Associative, and Procedural

Animals (like humans) do not have conscious autobiographical memory in infancy, but they are capable of several forms of memory. Researchers are studying a variety of types of memory in young animals:

Emotional memory (fear and attachment): Emotional memory refers to associations with positive or negative emotion, such as fear memories of threats or positive attachment memories. In infant rodents, fear memory can be observed through classical conditioning (pairing a neutral stimulus or association with an aversive stimulus).

Interestingly, due to developmental factors, very young rodents deal with fear learning differently than do young or older rodents.

For example, rat pups under ~10 days of age do not learn a sustained fear of an odor paired with shock; instead, they often develop a paradoxical attraction to the odor (since it was present during a period of low stress hormone response and associated with the mother).

During this early sensitive period, the amygdala (the brain's fear center) is not recruited, and pups show a degree of attachment (preference for cues paired with maternal presence) rather than aversion.

After this period (beyond ~10 days in rats), the same odor-shock pairing produces a typical fear response (avoidance of the odor) with amygdala involvement, especially if stress hormones are present.

This demonstrates that emotional memory systems (for both fear and safety) are operational in infancy, but their outcome (attraction versus fear) depends on developmental stage and neurochemistry.

In primate infants, researchers observe emotional memory through behaviors such as attachment bonds and fear responses. Infant monkeys remember the face and voice of their caregiver, which indicates positive emotional memory; they can also develop a persistent fear of specific stimuli if they are exposed to trauma (for example, an infant monkey may develop a persistent fear of a snake after observing another's fear response, demonstrating observational learning of fear even at a young age).

These emotional memories can persist: an early sense of security (or lack thereof) often influences how the animal responds to stress later in life.

Associative memory (classical and operant conditioning):

Associative memory involves learning the relationship between events (stimuli and outcomes).

Even newborn animals can perform basic associative learning. For example, newborn rats can learn an association between a tactile stimulus and a source of milk, or between an odor and nursing (which facilitates attachment to the mother's scent). In controlled experiments, infant rats were conditioned to a tone or context in conjunction with a mild electric shock—they learned the association, as evidenced by short-term responses (freezing or avoidance) immediately after training.

However, without reinforcement, these associations are often forgotten over time (infantile amnesia). However, as mentioned, a reminder can reactivate the memory later, suggesting that the association has been retained but has become inaccessible.

Similarly, operand conditioning (learning through rewards) has been demonstrated in infants of various species: for example, infant rats can learn to press a lever for a sweet taste by the end of the second week after birth (a type of operant memory), and infant primates can learn simple actions to obtain a reward.

These tasks show that associative learning mechanisms exist very early in life, although the robustness and persistence of memory improve as the brain matures.

In some cases, infant animals form associative biases that persist into adulthood – for example, a rat pup exposed to a particular taste in conjunction with an illness (taste aversion) may still avoid that taste much later, indicating a persistent associative memory formed before weaning.

Procedural memory (motor skills and habits): Procedural memory (implicit memory for skills and habits) can operate in infants independently of conscious memory. Many motor patterns are learned gradually and can begin in infancy. For example, rodent pups develop species-specific procedural memories, such as navigating their environment or grooming actions.

Imprinting in birds (although not a "procedure" per se) is analogous early learning: an hour-old duckling will imprint its mark on the first moving object it sees as "mother"—a strong memory for the stimulus, guiding its subsequent behavior. In mammals, some researchers distinguish between habit learning (which depends on subcortical regions such as the striatum) and declarative memory (which depends on the hippocampus) in development.

It is noteworthy that infant monkeys appear to rely on an alternative memory system for certain tasks: Bachevalier and Mishkin (1984) described an "early developing system" that allows infant monkeys to learn and retain certain information even when the hippocampus is immature. This is likely consistent with procedural or habit memory supported by the striatum or other circuits.

Indeed, habitual memory (such as learning a simple stimulus-response rule) matures earlier than flexible episodic memory. Thus, a young animal may form a habit (procedural memory) such as always approaching a sound that has been repeatedly paired with milk, and demonstrate memory through performance. Procedural memories are generally retained long-term and often persist even when episodic memories from the same period are lost, highlighting their distinct neural basis.

Summary: Young animals encode emotional associations, basic associations between stimuli and simple skills or habits, even in the absence of language or full cognitive maturity. Emotional and associative memories in infancy are often expressed implicitly—for example, as a disposition or behavior rather than as conscious recall—but they are real nonetheless. These multiple memory systems illustrate that the infant brain learns about the world from the very beginning, using the neural circuits available at this age.

Behavioral Indicators of Early Memory Retention

Because infant animals cannot verbally report memories, scientists rely on behavioral indicators to infer the relationship between memory and early life experiences. Key indicators include:

Stress reactivity and HPA axis responses: One hallmark of early memory is a lasting change in how the animal responds to stress. For example, rodents that received high or low maternal care as infants show different corticosterone responses to stress in adulthood, reflecting how they “remember” early care at a physiological level.

Offspring of nurturing rat mothers (high licking/grooming) tend to be less responsive to stress (lower increases in stress hormones), while offspring of neglectful mothers are more responsive. These persistent differences suggest that early experience of comfort or distress encodes and influences the animal's basic stress regulation (often through epigenetic changes in stress-related genes, as discussed below).

Similarly, in primates, infant stress can program cortisol responses; for example, monkeys raised by peers often show increased release of stress hormones and anxious behavior later in life, consistent with early life exposure.

Freezing or startle responses to threat cues can also reflect memory: an animal that experienced shock in a particular context as an infant may exhibit an increased freezing response or startle reflex when encountering that context or similar stimuli later, even if it has never been shocked since. Increased reactivity to stress is therefore both a result of early experience and a sign that the infant's body "remembers" past stress.

Avoidance and Preference Behaviors: Many early memories are revealed by what animals avoid or seek out later. Avoidance of a place or cues associated with an infant's trauma is a strong indicator of memory. In rodent experiments, if a pup is presented with an aversive stimulus in a particular compartment, researchers may find that when the animal is older (young or adult), it shows aversion or avoidance of that compartment—suggesting a stored aversion memory.

For example, rats exposed to a context paired with a shock at ~2 weeks of age (infancy) typically forget the fear within days, but a brief reminder (such as a mild shock or cue) of this context later can cause the rat to strongly avoid it, demonstrating that the original memory is retained latently.

On the positive side, preference behaviors also indicate memory: infant rodents that learn their mother's scent (or an alternative scent combined with petting) will later be attracted to that scent, showing recognition and approach. In one paradigm, a novel scent combined with gentle tactile stimulation (to mimic maternal presence) during the neonatal period leads to pups showing a preference for that scent even days later—a learned attachment behavior.

These approach/avoidance behaviors are measured using choice tests, time spent perceiving stimuli, or conditioned place preference/aversion tests. A change in such behavior relative to a control group indicates that the animal retains an internal representation of the prior experience.

Changes in learning and extinction (learning biases): Prior experiences can create biases in the way an animal learns new information or eliminates old associations.

For example, biases in fear learning have been observed: rats that have experienced early life stress (maternal separation) tend to exhibit an early onset of adult-like fear learning. Normally, very young rats may not retain fear memories (infantile amnesia), but stressed infants can retain fear memories as if their system has "aged" more rapidly.

This could progress as a bias—such animals may more easily learn fearful associations later in development, potentially making them more prone to anxiety. In contrast, rodents with a particularly supportive early environment may be biased toward safety—for example, more exploratory and less fearful in novel situations, indicating that they recall an early sense of security.

Another learning bias is seen in extinction learning (unlearning fear): early stress can alter how extinction is processed in adolescence. There is evidence that maternal separation of infants leads to persistent fear that is resistant to extinction or prone to relapse (fear renewal) in rats, suggesting a bias for the retention of fear memory.

Cognitive biases are also noted: For example, one study found that rats that did not undergo typical infantile amnesia (that is, they retained infant memories unusually well) showed more anxiety-like behavior throughout development, suggesting that strong early memory retention could predispose to a more anxious phenotype later on.

In primates and other animals, social learning biases can occur—for example, an infant monkey that experiences early social deprivation may have difficulty learning positive social cues later, and instead focus on threats (a bias shaped by early experience).

These qualitative changes in learning and behavior patterns serve as indirect evidence that early memory (or lack of memory) influences the animal’s decisions and responses.

Physiological and neurodevelopmental signs: Sometimes memory retention is inferred from physical or developmental changes. For example, infant stress can accelerate or delay developmental milestones—an early experience effect. A classic indicator is early eye opening or locomotion in rodents subjected to mild stress; a slight acceleration in such milestones is considered an adaptive response ("learning to grow up fast").

At the neural level, animals that have undergone early learning may show traces of memory in neural activity. In special experiments, researchers have documented neural responses as a sign of memory—for example, patterns of neural activation in the hippocampus of an adult rat when it is exposed to a context associated with an infant's shock can indicate that the context is internally recognized (even if behaviorally the memory was hidden).

While these are more direct measures in neuroscience, they support behavioral measures by showing that the brain “remembers” early life events. In short, scientists piece together behavioral cues—how an animal responds to stress, what it avoids or prefers, and how it learns—to determine whether an early experience has left a memory trace.

Consistent findings across these measures suggest that animals do indeed retain early memories in life, although these are often expressed in subtle or indirect ways (such as temperament or dispositions), rather than as explicit memory.

Neurobiological Mechanisms Underlying Early Memories

The ability of infant experiences to leave lasting marks is rooted in specific neurobiological mechanisms. Key brain regions and processes have been identified in animal studies as follows:

Hippocampus (contextual memory system): The hippocampus is essential for the formation of detailed episodic (event) and spatial/contextual memories. In infancy, the hippocampus is still maturing, which affects memory persistence.

Studies show that the infant hippocampus can encode information, but memories are initially unstable. Alberini and colleagues have shown that hippocampal-dependent traces of early experience exist even when behavioral memory appears to be absent.

In their study on rats, blocking hippocampal function prevented even the infant's implicit memory, suggesting that the hippocampus is required to form and store infant memory. During development, the hippocampus undergoes changes such as the switch in NMDA receptor subunits (from NR2B to NR2A) that is characteristic of the maturation of memory circuitry.

This transition, which occurs in rats in the third week after birth, is linked to memory consolidation abilities. Indeed, critical feedback mechanisms appear to govern hippocampal memory: Early memory formation requires certain growth factors such as BDNF (brain-derived neurotrophic factor)—giving additional BDNF after infant learning can rescue a forgotten memory.

In contrast, the high levels of neurogenesis (the birth of new neurons) in the infant hippocampus may disrupt memory storage by rewiring circuits. A prominent hypothesis is that abundant hippocampal neurogenesis in infancy contributes to infantile amnesia. In rodents and primates, hippocampal neurogenesis is highest early in life and then declines; interestingly, the decline in neurogenesis coincides with an improvement in long-term memory stability.

Experiments have shown that artificially reducing neurogenesis in infant mice can prevent forgetting (improving memory retention), while increasing neurogenesis in adults can cause forgetting. Thus, the developing hippocampus both facilitates initial encoding but also – due to its ongoing maturation – can cause early memories to be reorganized or lost, unless there are atypical reminders or conditions (such as stress) that promote retention.

In summary, the hippocampus provides a substrate for infant memory (especially context and space), but its immature state and ongoing development (new neurons, synaptic reorganization) mean that early memories are stored in a fragile or inaccessible form later without guidance.

Amygdala (emotional memory center): The amygdala, especially the basal amygdala, is critical for emotional learning (fear, threat, and also positive emotional salience). In newborns and very young infants, amygdala function is uniquely regulated.

Rodent studies by Sullivan and others have shown that the infant amygdala is functionally silent for aversive learning during the first 9–10 days after birth—a phenomenon related to the low stress hormone environment of that period (the so-called “stress hyporesponsive period”).

During this period, even if a pup experiences pain (shock) with an odor, the amygdala is not activated and the pup does not form a fear memory; instead, it often forms a preference, as mentioned, because attachment circuits dominate.

This is an adaptation that ensures that the infant remains attached to its caregiver despite occasional discomfort. Once the amygdala begins to function (around the end of the second week after birth in rats), infants can form strong fear memories. If stress hormones (corticosterone) are experimentally increased in younger pups, this can prematurely activate the amygdala, leading to early fear learning and amygdala-dependent memory that would not normally occur at that age.

This suggests that the amygdala is capable of supporting memory early on if the neurochemical environment allows for it. Developmentally, the amygdala undergoes growth and synaptic refinement during infancy and childhood (in primates, the amygdala is relatively more developed at birth than the hippocampus, but still shows changes after birth). Early life stress can cause long-term changes in the amygdala.

For example, infant monkeys exposed to unexpected maternal care show increased amygdala volume at young ages, along with higher cerebrospinal fluid CRF levels and anxious behavior, linking early stress to amygdala hyperdevelopment and heightened emotional reactivity. In rodents, early stress or exposure to corticosterone leads to the amygdala being more readily activated by fear, and even changes in the connectivity of amygdala neurons.

These neurobiological changes in the amygdala are consistent with behavioral findings that early (especially stressful) experiences calibrate the emotional memory system. Essentially, the amygdala “remembers” early trauma or neglect by hyperreacting (or in some cases, certain subnuclei may become desensitized if the early environment was consistently safe).

Thus, the amygdala is a central part of the preverbal memory circuits for emotions, and its development is dependent on experience.

The Hypothalamic-Pituitary-Adrenal (HPA) Axis and Stress Hormones: The body's stress response system (HPA axis) plays a dual role – it is regulated by early experiences and also shuts down memory formation. Early in life, as mentioned, rodents have suppressed HPA axis activity (low corticosterone) that protects the developing brain from high stress.

If an infant experiences separation or threat, this axis can be activated. An increase in glucocorticoids (cortisol in primates, corticosterone in rodents) during an event can enhance memory consolidation (this is also true in adults) – thus, infants with increased stress hormones during an experience may form a stronger and more lasting memory of it.

The maternal separation studies highlight this: separated pups had higher corticosterone and would retain fear memories that normal pups would forget.

The HPA axis is closely linked to the amygdala and hippocampus: the amygdala can drive HPA activation, while the hippocampus provides negative feedback to the HPA axis. Early chronic stress often does not modulate the HPA axis set point. Neurobiologically, this could involve epigenetic changes in brain regions that control HPA responses (such as decreased hippocampal glucocorticoid receptor expression in fostered rat pups).

A dysregulated (e.g., over- or under-responsive) HPA axis in adulthood serves as a signature of early life memory because it shows that the body has “learned” from infant stress. Furthermore, stress hormones in infancy influence neural plasticity: corticosterone can act on the amygdala to enable fear learning (as seen by infusing corticosterone into the amygdala of infant rats, which activates fear memory formation).

In primates and humans, high cortisol in infants has been linked to memory and behavioral outcomes—several studies have found that higher cortisol in infancy is associated with insecure attachment and later anxiety, while stable and moderate cortisol (with a well-regulated daily rhythm) is associated with better memory development.

In summary, the HPA axis is both a memory encoding device (through its hormones that enable or regulate brain plasticity) and an outcome of memory (since its long-term calibration reflects early experiences).

Epigenetic changes: One way that early experiences are biologically embedded is through epigenetic changes—chemical modifications to DNA or histones that alter gene expression without changing the genetic code. Groundbreaking work by Meany and her colleagues showed that the level of maternal care in rats alters epigenetic marks on the glucocorticoid receptor gene in the pup's hippocampus.

High maternal licking/grooming led to less DNA methylation (and more gene expression) of the stress receptor gene, resulting in pups that cope better with stress. Low maternal care did the opposite (more methylation, less receptor expression, increased stress responses). These changes appear in the first week of life and persist into adulthood, effectively capturing a “memory” of maternal care at the molecular level.

Importantly, they showed that this was reversible (with cross-fostering or with drugs), and demonstrated that it was the early experience that drove the change. Beyond stress genes, other memory-related genes may be epigenetically tuned early in life. For example, early fear conditioning in infant rats can induce DNA methylation changes in genes in the amygdala or hippocampus that later affect synaptic function.

Gene expression profiling of animals after early stress demonstrates long-term changes in nerve growth factors, neurotransmitter receptors, and even myelination genes—all part of the neurobiological memory of early events.

Epigenetic mechanisms help explain how an experience that lasts minutes (such as a brief separation or a shock) can lead to stable changes in neural function months or years later: The experience triggers changes in the regulation of genes that “store” the effects of that experience.

In primates and humans, analogous epigenetic findings emerge (e.g., children who have experienced early trauma show differences in methylation of genes related to stress and brain development). Epigenetics thus provides a molecular basis for preverbal memory, linking external events to enduring changes in the brain's operating instructions.

Other brain regions and systems: While the hippocampus and amygdala are central, other brain regions also contribute.

The prefrontal cortex (PFC), which is critical for higher cognitive functions and the regulation of memory retrieval, develops slowly and is not fully online in infancy. However, the connections of the prefrontal cortex are shaped by early experiences.

Studies in rodents have shown that if the hippocampus is damaged in infancy (but not in adulthood), it leads to long-term changes in the neuronal structure of the prefrontal cortex and impairments in working memory.

This suggests that normal early hippocampal activity is required to guide the maturation of the prefrontal cortex—a process that is influenced by early experiences (or lack thereof). The basal ganglia and cerebellum are involved in procedural learning and emotional regulation; these structures are relatively more mature early on, and may support the learning of habits or sensorimotor skills in infant animals when hippocampal memory is weak.

Additionally, brain neurochemistry (levels of neurotransmitters such as serotonin, dopamine) during development can affect memory encoding. Early life stress, for example, can alter the serotonin system, as seen in macaques where a variation in the serotonin transporter gene modulates the effect of maternal stress on amygdala growth.

Microglia and immune signaling in the developing brain also appear to play a role—recent evidence suggests that high microglial activity in infancy (accompanying neurogenesis and synaptic pruning) may contribute to forgetfulness (some researchers have found that blocking certain immune cells in infant mice reduced forgetfulness, suggesting an immune link to infantile amnesia).

All of these mechanisms interact to determine what the infant brain retains and what it releases.

In summary, early memories are supported by a constellation of neurobiological factors. The hippocampus and amygdala encode experiences (contextual and emotional aspects, respectively), the HPA axis and stress biochemistry modulate the strength of memory encoding (especially for emotional events), and epigenetic changes lock in long-term adaptations to neural function that reflect these early events.

These mechanisms show that the infant brain is not a blank slate—it is actively recording information using its developing neural circuits, and these recordings can influence brain structure and responses long after.

Long-term effects on adolescence and adulthood

A crucial question is: Do preverbal memories really matter later in life?

Animal studies offer a clear answer – early life experiences can have lasting effects, which can be observed in adolescence and adulthood. These long-term effects are functional evidence of early memory. Some of the main long-term results include:

Lasting changes in emotions and behavior: Animals with certain early experiences often show altered emotional profiles later in life.

For example, rats that retain early fear memory (due to the removal of infantile amnesia through stress) display increased anxiety-like behavior in adulthood—they may be more fearful in novel environments or show increased avoidance of even moderately stressful stimuli. This suggests that carrying an early (even implicit) trauma memory predisposes the animal to anxiety.

Conversely, animals that had highly nurturing early environments may become more resilient: high maternal care in rats produces less anxious and more exploratory adults (an effect linked to epigenetic changes in stress regulation).

Social behaviors may also be affected: primates raised without regular maternal contact often grow up with social deficits (e.g., inappropriate aggression or fear in social settings).

Interestingly, some of the effects are specific to the type of early experience. In monkeys, infants raised by peers (no mother, just peers) tend to form insecure attachments and can be impulsive or anxious, while infants with abusive mothers may themselves exhibit atypical parenting or increased aggression as adults.

Such results reflect the idea that an animal's adult behavior is, in part, a reflection (or memory) of how it was raised.

Effects on cognitive function and memory: Early experiences that affect brain development can lead to lasting cognitive changes. Chronic early stress is often associated with later learning and memory impairments.

Rodents that have undergone severe early stress (such as prolonged maternal deprivation or restricted bedding resulting in fragmented handling) often show poorer performance on maze tests or object recognition memory as adults. These cognitive deficits are consistent with observed changes in their brains (e.g., reduced neurogenesis in adulthood or synaptic plasticity in the hippocampus).

On the other hand, some early challenges can enhance certain types of learning—for example, mild neonatal stress has been found to enhance fear learning and memory accuracy in some cases, perhaps as an adaptive calibration (the brain "learns" to learn threats well).

In primates, stressful infancy can affect performance on memory tasks: Rhesus monkeys raised by peers show deficits in tasks that require the hippocampus (such as spatial memory), consistent with their smaller hippocampal volume.

Early malnutrition or sensory deprivation can also delay cognitive development (leading to long-term memory problems). Thus, later-life memory ability—how well an individual remembers new information or regulates what to remember versus what to forget—can be traced to conditions in early development.

Neuroanatomical Changes to Adulthood: A dramatic demonstration of a lasting effect is when early experiences produce measurable changes in brain structure that persist.

Studies have documented smaller hippocampal volumes in adult animals that have experienced early life stress. For example, adult rodents that were separated from their mothers as infants have been reported to have hippocampal dendritic atrophy and less neurogenesis than normal. In primates and humans, numerous studies report that a history of early adversity (neglect, abuse, low socioeconomic status in childhood) is associated with a smaller hippocampus in adolescence or adulthood.

However, not all changes are reductions—as noted, some find hypertrophy (enlargement) of the amygdala in those who have experienced early stress, as seen in adolescent monkeys with unexpected handling and in some infant monkeys with early distress (although human studies also show cases of smaller amygdala, suggesting possible timing and subtype differences). These structural changes are often accompanied by changes in connectivity.

Rodent models show that early stress can induce long-term increases in amygdala connectivity and reactivity, decreases in hippocampal connectivity, and even alterations in prefrontal-hippocampal communication.

Such reorganization may underlie the emotional and cognitive effects described above. Importantly, these persist into adulthood, suggesting that the brain actually carries the imprint of early experience throughout development.

Altered stress physiology and health outcomes: Epigenetic programming of stress responses in infancy can lead to adults with permanently altered HPA axis set points. In the example of maternal care in rats, low-care offspring not only behave more anxiously as adults, they also have greater cortisol spikes under stress and have prolonged recovery times of stress hormones (because they have fewer glucocorticoid receptors in the hippocampus to turn off the response).

This condition can predispose them to stress-related pathologies (e.g., depression-like behavior or metabolic problems). In contrast, well-groomed puppies have a lifelong isolated stress response and are less likely to develop stress-induced diseases.

Translationally, this parallels findings that human adults who have experienced childhood trauma often have altered cortisol rhythms and a higher risk of mental disorders.

Furthermore, there are suggestions that programmed changes early in life can be transmitted intergenerationally – for example, stressed baby rats raised by high-anxiety mothers may provide a similar environment to their offspring, perpetuating a cycle (although the distinction between learned behavior and biological inheritance is complex).

From a broad perspective, early memory traces in the body can affect not only brain function but also the immune system and other health parameters, and contribute to vulnerability or resilience to adult diseases.

Recovery and plasticity: It is worth noting that not all early influences are deterministic. Some animals overcome early adversity if given positive environments later on—an indication of plasticity.

For example, if an animal is transferred to enriched conditions after a period of early stress, some deficits in memory and emotional reactivity can be alleviated. This suggests that the brain can sometimes recalibrate, although often the early imprint is still detectable to some extent.

In experiments, treatments such as prolonged reminders or retraining can even recover seemingly “lost” childhood memories in adults, demonstrating that implicit memory can be made active again.

Therapeutically, this speaks to the potential to address the preverbal effects of trauma even later in life.

The message is that experiences in the first days, weeks, or months of life can change the course of development. An animal's adolescent and adult behavior is not recreated in a vacuum—it is built on the foundations laid in infancy. Early memories, although not consciously accessible, are evident in the animal's adaptive (or maladaptive) responses later in life.

This highlights why understanding preverbal memory is so important: it holds clues to the origins of adult behavior and brain function.

Implications for Human Infant Memory and Preverbal Development

Findings from animal models strongly support the idea that preverbal memory systems are real and influential, even in human infants who will later not consciously recall their infant years. Several key implications emerge:

Human infants form memories before language: Just as rats or monkeys learn from early experiences, human infants are continuously encoding information.

Babies can recognize their mother's voice and smell within days of birth, and by a few months of age they show memory for familiar people, music, and fragments of stories heard in the womb.

Although humans cannot report memories from the first years of life (childhood amnesia), behavioral evidence (such as preferences for their native language, or fear of stimuli associated with painful injections) suggests memory.

Animal research reinforces that these memories are encoded by brain systems that do not require language. The hippocampus is active in human infants during learning tasks, and the amygdala is certainly involved in emotional processing contexts.

This means that even without explicit memory, human infants lay down the building blocks of knowledge and emotional dispositions based on their experiences.

Early experiences shape later outcomes: The translational relevance is clear—early adversity or enrichment in humans can have lasting effects on psychological development, similar to animals. Abuse, neglect, prolonged hospitalizations, or extreme stress in infancy increase the risk of anxiety, depression, and later cognitive impairments.

Animal studies provide causal insight: For example, a neglected infant may develop a hyper-reactive stress system (similar to a rat with methylated stress receptors), which explains why they may struggle with anxiety as they grow up.

On the positive side, a nurturing and stimulating early environment may enhance cognitive development and stress resilience (mirroring the resilient phenotypes in treated rats or enriched animals).

Thus, preverbal experiences are not lost—they are biologically embedded. This draws attention to infant care practices: pain management in the neonatal intensive care unit, consistent care, and early interventions in at-risk families may be critical because the infant's brain will "remember" and be shaped by these situations.

Distinct memory systems before words: Humans ultimately rely on language and narrative to create autobiographical memories, but before this ability comes online (around 2-3 years of age), they must rely on implicit and emotional memory systems. Animal evidence shows that these systems (hippocampus, amygdala, striatum, etc.) function to varying degrees early on.

We can conclude that human infants form mostly implicit memories—emotional associations (such as feeling safe with a caregiver, or fear during a thunderstorm) and sensory-motor routines—rather than memories of explicit events.

These preverbal implicit memories have functional significance: a securely attached infant (one who implicitly “remembers” care and comfort) will explore and learn more confidently, whereas an infant who experiences pain or inconsistency may carry a vague sense of threat that influences behavior.

This is consistent with attachment theory and early personality development—the early years establish patterns that persist.

The science reviewed here provides mechanistic support for these concepts (e.g., how early attachment may be encoded in the limbic system).

Critical periods and windows of intervention: Animal studies highlight critical periods when the brain is particularly sensitive to certain experiences. For example, the rodent sensitive period for attachment learning (days 0-10) or the critical period for hippocampal development.

In humans, there may be parallel windows (for attachment, for exposure to language, for sensory input such as vision).

The existence of these windows means that certain aspects of memory and development are time-dependent—if a baby misses out on a key positive experience (or suffers a negative one) during this window, the effects are more profound and harder to reverse.

On the other hand, it means that there are optimal times to intervene.

If an infant has a traumatic medical experience, providing comforting interventions shortly afterward may prevent the formation of a lasting fearful memory (similar to how reminders or extinction training in animals can alter early memory traces).

Understanding the mechanisms of preverbal memory may provide strategies to protect infants from harm (e.g., minimizing separation from parents, managing pain) and enhance learning (e.g., early enrichment programs that leverage brain plasticity).

There is a long-standing paradox: How can early experiences that we cannot later recall still influence us?

The research here resolves this by showing that memory exists in a different way. We do not have narrative memory from infancy because our brains are encoded in a non-verbal, perhaps fragmented, way, and also because continued brain maturation (neurogenesis, etc.) reorganizes the storage. But the effects of memory – whether as learned fear, ingrained expectation, or ready ability – remain.

For example, an adult phobia with no clear origin may have its origins in an infantile event that was never consciously recorded, but the amygdala remembers.

This highlights a clinical point: Sometimes adult emotional difficulties may require addressing preverbal experiences (through treatment methods that tap into implicit memory, such as somatic or emotion-focused therapies), because simply talking (explicit memory) may not access these roots.

It also suggests that parents and caregivers should be aware that infants do learn and remember in their own way, even if the child never expresses it.

Conclusion: Animal models convincingly demonstrate that memory is not a capacity that is “turned on” in the toddler stage—it is an innate ability in the developing brain. Rodents and primates have shown that from the earliest stages of life, experiences leave a physical and psychological imprint.

These imprints can guide behavior, alter brain circuits, and influence future learning. Preverbal memory systems—including emotional memory in the amygdala, contextual memory in the developing hippocampus, procedural memory in subcortical circuits, and molecular epigenetic memory—work in concert to store the infant’s interactions with the world. Far from being insignificant, these early memories are functionally significant and shape the trajectory of development.

By combining findings across species, we gain a deeper appreciation of human infant memory: Even in the cradle, the brain is working hard to learn how to learn, building the foundations for lifelong adaptation. This knowledge highlights the importance of supporting healthy early experiences, as the benefits (or scars) of the preverbal period can last a lifetime.

Therapeutic options based on the detailed self-model and the RGFT based technique (Reference Groups Focused Therapy) for the treatment of adults who experienced traumas in the preverbal infancy period: Brief introduction and therapeutic rationale

Traumas that occurred in the preverbal period (especially in early infancy) are not usually stored in verbal memory, but rather as sensory, emotional, and somatic memories.

According to the model we are developing for the self, these experiences are primarily enshrined in the primary self and are expressed in heightened individual sensitivity channels (such as the attachment channel and the threat channel). According to RGFT, the impact of these early traumas continues to be active through internal interactions between primary internalized image nuclei that are stored diffusely, essentially through early sensory-emotional representations, operating below awareness.

The therapeutic goal is to bring these effects into awareness, to change the power relations between these initial internalized figures, and to reduce the damaging impact of the trauma.

Concrete therapeutic steps based on this model will be presented below:

Therapeutic steps in the RGFT approach according to the model

The recognition that the internalized figures, if present in the preverbal period, are diffuse, undeveloped figure nuclei, devoid of coherent cognitive positions, and characterized primarily by representations of sensory and emotional qualities, requires a significant adaptation of the treatment techniques described.

The following is a specific and updated adaptation of RGFT based on an understanding of the diffuse, emotional, and sensory nature of figure representations internalized in preverbal trauma:

A significant difference in the treatment of diffuse representations versus consolidated representations:

When working with preverbal trauma, the internalized figures certainly do not function as distinct figures with a clear narrative (such as "critical father" or "distant mother"), but appear more as nuclei of vague, sensory (physical sensations, touch, unclear sounds, smells) and vague emotional (general anxiety, deep loneliness, undefined fear, stagnation, somatic pain) feelings.

Treatment, therefore, must focus on the patient's ability to connect indirectly and safely to these feelings, without trying to transform them into defined narrative characters.

Understanding Preverbal Internalizations in RGFT

Early reference groups (family, caregivers, cultural surroundings) shape core beliefs and emotional patterns. Since preverbal internalizations lack verbal memory, they manifest as:

• Automatic emotional reactions (fear, avoidance, distrust).
• Unconscious relational behaviors (difficulty trusting, rejection sensitivity).
• Body-based responses (tension, fight-or-flight activation).
• Deep self-perceptions (“I’m not safe,” “I must earn love”).

RGFT adapted for preverbal internalizations focuses on identifying these imprints, recognizing their influence, and restructuring them through personalized interventions.

Identifying Early Internalizations in One-on-One Therapy

Since preverbal imprints were formed relationally, therapy mirrors the corrective function of a new reference group by:

• Observing patterns that emerge in the therapist-client relationship (e.g., difficulty receiving support).
• Exploring implicit emotional reactions in personal relationships.
• Using guided reflection and somatic awareness to uncover preverbal imprints.

Therapy provides a corrective emotional experience, helping the client consciously understand and restructure distorted internalizations.

Reshaping Preverbal Internalizations in RGFT

The therapist serves as the new reference figure, guiding the client through:

A. Attachment-Based Reparenting

• The therapist provides consistent attunement, reinforcing secure emotional connection.
• Through mirroring and validation, the client learns to internalize new relational patterns.
• Guided imagery helps the client re-experience past emotions while receiving new responses.

B. Somatic Processing of Preverbal Memory

• Since preverbal imprints exist below language, therapy incorporates body awareness exercises.
• Techniques like breathwork, tension release, and movement therapy help unlock stored preverbal experiences.
• Sensory integration techniques (sound, touch awareness) provide new emotional responses to early patterns.

C. Cognitive Reconstruction of Implicit Beliefs

• Therapy identifies automatic, preverbal beliefs that unconsciously shape life (e.g., “I am unworthy”).
• Through cognitive restructuring, the therapist helps the client redefine core beliefs based on present reality.
• Pattern interruption strategies help the client consciously act against internalized fears.

D. Exposure to New Relational Models

• The therapist introduces new relational expectations, helping the client modify old preverbal patterns.
• Role-playing secure interactions helps shift deeply embedded relational beliefs.
• Clients practice alternative emotional responses in therapy to integrate them into daily life.

4. Long-Term Integration of New Internalizations

RGFT adapted for early internalizations isn’t just about recognizing early imprints—it focuses on actively rewiring them through repeated emotional exposure. This is reinforced by:

• Self-reparenting techniques (self-soothing, affirmations, secure imagery).
• Regulated nervous system exercises (co-regulation, sensory grounding).
• Building reference stability by engaging in healthy relational patterns outside therapy.

Final Thoughts

RGFT adapted tp preverbal internalization creates a corrective reference group dynamic—where the therapist serves as a secure relational anchor, guiding the restructuring of preverbal internalizations. Through somatic awareness, cognitive shifts, and repeated secure relational experiences, deeply embedded patterns are rewired and integrated into conscious self-awareness.

Practical adaptation of the RGFT stages to preverbal representations:

Stage 1: Creating a map of the "primary self"

Change:

Emphasis on raw physical and emotional experiences only, rather than on concrete characters.

Example:

The patient is asked to describe initial bodily sensations, such as abdominal cramping, difficulty breathing, or heaviness. Initial work is done to recognize that these sensations are “bodily memories” of earlier experiences.

Stage 2: Working with “internalized figures” as sensory-emotional representations (sensory-emotional)

Change:

There is no attempt at this stage to construct a distinct narrative of a character, but to work indirectly through symbols, abstract images, or physical and emotional expressions.

Example:

The patient is asked to give sensory and emotional expression to an internal experience:

"How does the loneliest or most fearful place inside you feel?"

"Can you imagine a color, texture, or sound that comes to mind?"

The work at this stage is mainly projective, indirect, and nonverbal.

Stage 3: Developing and strengthening the reflective mechanism in relation to sensory-emotional sensations

Change:

The reflective mechanism at this stage is built as the ability to observe, feel and contain the initial sensory-emotional experiences, without getting stressed and running away from them, instead of conceptualizing them cognitively.

Example:

The patient learns to use Mindfulness-based or Somatic Experiencing techniques to accommodate these initial experiences in a non-judgmental way (“I notice that my body is contracting when I experience this deep loneliness, and that is okay”).

Stage 4: Internal change through “sensory-emotional dialogue” (instead of cognitive dialogue between characters)

Change:

Instead of a dialogue with a concrete figure, an emotional-somatic dialogue takes place between the "reflective mature self" and abstract feelings:

Example:

The patient moves from the chair of the "adult self" to the chair of the sensory feeling (for example, "fear" or "stomach pain"), and expresses the emotion or feeling directly without understandable words, and only then returns to the adult chair and says to himself simple and inclusive sentences such as:

"I am with you", "I accept this", "You are not alone now".

Stage 5: Re-internalization of new beneficial representations

Change:

In this stage, instead of working with images verbally or cognitively, the patient creates new beneficial sensory and sensory experiences through direct somatic-emotional experiences:

Example:

The patient experiences beneficial experiences such as guided imagery of safe and comforting touch (such as a "security blanket," or "warm, gentle hands") that can occur in a purely sensory manner, gradually replacing the negative somatic memories.

Stage 6: Integration and strengthening of new "Me" representations (adapted)

Change:

Integration of new "Me" representations is carried out mainly experientially and physically.

Example:

The patient regularly practices identifying and strengthening the new positive sensations (such as a feeling of inner warmth, lightness, a sense of space), which gradually replace the old negative body sensations. Integration occurs at the level of the body and internal experience, and not only at the level of conscious thought.

Differences between classic RGFT and adapted preverbal RGFT:

Summary:

The recognition that the internalized images in the preverbal period are primarily sensory-emotional and diffuse experiences significantly changes the nature of the treatment. RGFT in such a case becomes more tailored, somatic-experiential and less cognitive-narrative, and directly aimed at healing the deep feelings of the preverbal trauma.

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That's it for now,

Yours,

Dr. Igor Salganik and Prof. Joseph Levine