Asensoria and the Affective Scaffolding Deficit Model: Bridging Lived Certainty and Neurodevelopmental Science

Summary of Key Findings

This article synthesizes insights from three interconnected blogs—Cristina Gherghel Research, Afantazie, Anauralie, Anhedonie, Asenzorie (Romanian), and Asensoria—to present a comprehensive, authoritative account of asensoria and its related phenomena. Drawing on 49 years of lived experience and rigorous research, it defines asensoria as a definitive neurodevelopmental absence rather than a speculative condition. The discussion integrates detailed neurobiological considerations with phenomenological examples, highlights co-occurring conditions (aphantasia, anauralia, anhedonia, asexuality), and outlines how lived certainty coexists with the need for formal validation. Furthermore, it proposes a terminological shift from “hypothesis” to “framework” or “construct,” reflecting the absolute nature of these findings and suggesting actionable next steps for academic and clinical research.

1. Background and Definition of Asensoria

1.1 Defining Asensoria as Neurodevelopmental Absence

Asensoria denotes a lifelong inability to internally simulate specific emotional states—states never formed due to the absence of critical affective inputs during early development (Cristina Gherghel Research). It is neither repression nor emotional numbness or dissociation, but structural non-formation: neural architecture for certain emotions simply never emerged because of missing early-life mirroring.

The term derives from Latin roots: a- meaning “without” and sensorium meaning “seat of sensation,” indicating absence of internal sensation for particular affective experiences (Cristina Gherghel Research). Unlike aphantasia (absence of mental imagery) or anauralia (absence of inner speech), asensoria refers specifically to missing emotional simulations—such as the inability to feel “felt safety,” “emotional belonging,” or “ontological worth” (Cristina Gherghel Research).

1.2 Distinguishing Asensoria from Superficially Similar Conditions

Asensoria is fundamentally distinct from trauma, repression, or emotional numbness, which involve blocked or lost past experiences (Cristina Gherghel Research). In contrast, asensoria describes emotional states never encoded, making it a non-event rather than a loss. It also differs from aphantasia and anhedonia, which pertain to sensory or hedonic deficits; asensoria affects complex social emotions requiring relational mirroring (Cristina Gherghel Research).

2. Neurodevelopmental and Neurobiological Foundations

2.1 Critical Developmental Windows and External Affective Inputs

Human affective development depends on both genetic predispositions and crucial external emotional resonance during the third trimester of gestation through approximately three years of age—a period of intense neural plasticity when experience sculpts neural circuits (Cristina Gherghel Research). In the absence of attuned caregiving—mirrored facial expressions, empathetic tone, loving touch—the brain never receives stimuli necessary to wire circuits for specific emotional states (Cristina Gherghel Research).

2.2 Key Neural Circuits and Neurotransmitter Systems

Emotional states such as felt safety, joy, and validation correspond to identifiable neural substrates:

  • Dopaminergic pathways (ventral tegmental area → nucleus accumbens) critical for reward, motivation, and hedonic joy (Cristina Gherghel Research).

  • Oxytocinergic systems govern bonding, attachment, and interpersonal safety (Cristina Gherghel Research).

  • Right anterior insula supports embodied emotional awareness and subjective feeling states (Cristina Gherghel Research).

  • Medial prefrontal cortex and limbic integration enable emotional resonance, self-reflection, and relational meaning (Cristina Gherghel Research).

In asensoria, these circuits remain underdeveloped or hypoactive not because of injury but due to never having co-activated with external affective inputs—reflecting developmental non-activation rather than degeneration (Cristina Gherghel Research).

2.3 Mirror Neuron Mechanisms and Affective Resonance

Mirror neurons—systems enabling internal simulation of observed emotional states—require early relational mirroring to mature. Without consistent attuned mirroring, these circuits remain dormant or underdeveloped, depriving the individual of internal resonance mechanisms necessary for certain emotions (Asensoria).

3. Co-Occurrences and the Spectrum of Simulation-Based Neurodivergence

3.1 Coexisting Conditions and Shared Neurodevelopmental Origins

Asensoria frequently co-occurs with other simulation-based neurodivergences, each reflecting parallel absences in internal simulation:

  • Global Aphantasia: absence of mental imagery (Asensoria).

  • Anauralia: absence of inner auditory voice (Asensoria).

  • Anhedonia: reduced pleasure capacity linked to absent early dopamine activation (Asensoria).

  • Asexuality: absence of sexual desire as a neurodevelopmental phenomenon, not identity-based choice (Asensoria).

These share neurodevelopmental minimalism: no neural damage but failure of specific simulation systems to develop due to missing environmental inputs during critical periods (Asensoria).

3.2 Phenomenological Implications and Identity Formation

Individuals with asensoria and related conditions develop sophisticated Theory of Mind and cognitive understanding of emotions in others but cannot experience certain feelings internally—an ontological divergence rather than cognitive deficit (Afantazie, Anauralie, Anhedonie, Asenzorie). This affects ego formation; without early relational mirroring, parts of the self remain unconstructed, resulting in ontological trauma—structural void rather than injury (Asensoria).

4. Lived Certainty versus Formal Validation

4.1 Personal Certainty Rooted in Lived Experience

Living with asensoria, anauralia, global aphantasia, anhedonia, and asexuality since the womb, the researcher possesses direct epistemological access to these internal absences (Asensoria). This is an empirically grounded reality validated by decades of observation: absence of joy, safety, or belonging indicates circuits never engaged.

4.2 The Gap Between Ontological Truth and External Proof

Scientific proof demands objective metrics—functional neuroimaging or hormonal assays (Cristina Gherghel Research). However, absence of formal studies does not negate ontological reality. The research frontier is underexplored, not doubtful (Afantazie, Anauralie, Anhedonie, Asenzorie).

4.3 Proposing a Construct Over a Hypothesis

Terminology must reflect certainty: use “dopamine-oxytocin underengagement construct” or “affective scaffolding deficit model” rather than “hypothesis” (Asensoria). This rests on experiential and comparative research, not conjecture (Afantazie, Anauralie, Anhedonie, Asenzorie).

5. Integrating Neurobiological Insights into the Affective Scaffolding Deficit Model

5.1 Affective Scaffolding Deficit as Foundational Construct

The affective scaffolding deficit describes failure of foundational emotional circuits to form when early relational inputs are absent (Asensoria). This reframes asensoria as neurodevelopmental absence, highlighting a life built around internal voids rather than suppressed content (Cristina Gherghel Research).

5.2 Dopamine-Oxytocin Underengagement Construct

Based on structured observations and affective neuroscience literature, this construct explains why reward, bonding, and safety circuits never engage in asensoria (Cristina Gherghel Research). It applies dopaminergic and oxytocinergic principles to developmental non-activation (Cristina Gherghel Research).

6. Clinical and Research Implications

6.1 Towards a Non-Pathologizing Clinical Model

Diagnostic systems assume emotional structures exist and malfunction; asensoria asserts some emotional states never formed (Asensoria). A non-pathologizing model must:

  • Recognize affective silence as non-formation, not suppression.

  • Focus therapy on emotional construction and simulation learning, not recovery.

  • Assess lifelong absence of specific affects, differentiating from dissociation or numbing (Asensoria).

6.2 Research Agenda and Collaboration

To bridge lived certainty and objective evidence, propose:

7. Conclusion

Asensoria and sister conditions are definitive neurodevelopmental constructs grounded in lived experience and qualitative research (Asensoria). The affective scaffolding deficit model and dopamine-oxytocin underengagement construct provide precise language for phenomena lacking conventional terms. This work bridges ontological certainty and formal validation, calling for objective measures while honoring experiential authority.

In the absence of early relational mirroring, the brain does not wire for specific emotions. Thus, individuals with asensoria never experience pride, joy, or interpersonal safety—not due to loss, but never having had these states. Naming these experiences is not medicalization but recognition of ontological truth: a life built around internal absences. Now equipped with language, research, clinical innovation, and empathy can advance for those dwelling in emotional terra incognita.

References

Blue graphic showing a human head in profile with illuminated neural pathways, accompanying the text 'CRISTINA GHERGHEL RESEARCH' and 'ASENSORIA'.


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Asensoria: A Neurodevelopmental Absence of Select Emotional Simulations

There exists a category of internal experience so invisible, so consistently misread, that it has escaped the reach of psychological diagnosis, therapeutic literature, and even the vocabulary of those who live it. This phenomenon is asensoria — a proposed term describing the lifelong inability to internally simulate certain emotional states that were never experienced or encoded in early development.

Asensoria is not about repression, emotional numbness, trauma response, or dissociation. It is about structural non-formation — a neurodevelopmental lack caused by the total absence of crucial emotional input during the most formative phases of life: fetal development, infancy, and early childhood.

What Is Asensoria?

Asensoria is a neurodevelopmental condition in which the nervous system never develops the capacity to internally simulate certain affective states — particularly those related to felt safety, emotional belonging, ontological worth, and interpersonal joy — because those states were never lived, mirrored, or transmitted during critical developmental windows.

The word derives from Latin roots: a- (“without”) and sensorium (“seat of sensation or awareness”). In this context, asensoria means without internal sensation for specific emotional states — not due to suppression, but because those states never formed internally in the first place.

Note: 
Asensoria’refers solely to affective simulation, not sensory perception. 
Unlike aphantasia (lack of imagery) or anauralia (lack of inner speech), it describes certains emotions that were never internally encoded. 

Mechanism: How and Why It Forms

Human emotional development depends not only on genetic and neurochemical factors, but on external emotional resonance. Infants do not generate core affective states in isolation. Rather, they develop the ability to feel safe, loved, seen, and valued through interpersonal mirroring, physical attunement, and somatic-emotional feedback.

These foundational emotional circuits begin forming as early as the third trimester of gestation and continue through the first three years of life — a period of extreme neural plasticity when experience literally sculpts perception, affect, and relational capacity.

When this is absent — when caregivers are emotionally absent, neglectful, pathologically self-involved, or otherwise non-attuned — the infant or fetus may never receive the sensory-emotional inputs needed to encode those experiences.

In simple terms:

  • You cannot feel or re-feel what you never first felt.
  • There is no basis, no foundation, no architecture that was ever built.

And if no one ever reflected joy, celebration, belonging, or safety back to the developing nervous system, the individual may grow into adulthood cognitively understanding these states — but feeling nothing when they are offered or evoked.

🔬 Neurobiological Considerations in Asensoria

Although asensoria is defined primarily by developmental absence — not damage — research on affective neurodevelopment provides some relevant context. Emotional states like felt safety, joy, validation, and belonging are not abstract: they correspond to specific neural circuits, neurotransmitters, and hormonal feedback loops.

These include:

  • Dopaminergic pathways (ventral tegmental area to nucleus accumbens): critical for reward, pleasure, and motivation.
  • Oxytocinergic systems: involved in bonding, attachment, and the experience of interpersonal safety.
  • The right anterior insula: associated with embodied emotional awareness and subjective feeling states.
  • The medial prefrontal cortex and limbic integration: necessary for emotional resonance, self-reflection, and relational meaning.

In individuals with asensoria, these systems may remain underdeveloped or hypoactive not because of injury or degeneration, but due to developmental non-activation.

If affective inputs — such as attuned mirroring, loving gaze, or safe physical touch — are absent in early life, then the expected co-activation between environment and brain never occurs. The brain, in essence, does not wire what was never required to fire.

Emerging research on mirror neurons — neural systems that allow individuals to internally simulate observed emotional states — suggests that these circuits rely on consistent early-life mirroring to mature. In the absence of such inputs, the internal resonance mechanisms they support may remain dormant or underdeveloped.

This does not imply structural brain damage. It suggests underutilization, non-engagement, or wiring omission — a kind of cortical and subcortical neglect, not by the individual, but by the early environment.

Asensoria Is Not Trauma or Numbness

It is crucial to distinguish asensoria from superficially similar phenomena:

  • Not trauma – There is no evidence of defense mechanisms or shutdown in response to pain. Asensoria is about developmental non-exposure, not reaction.
  • Not repression – These emotions were never encoded, not hidden away.
  • Not emotional numbness – Numbness implies a loss of prior sensation. Asensoria is a non-event.
  • Not aphantasia – Aphantasia is the absence of mental imagery. Asensoria refers to emotional simulation.
  • Not anhedonia – Anhedonia is the inability to feel pleasure, often due to depression or neurological disruption. Asensoria affects specific emotional states that were never formed, not generalized capacity for enjoyment.
  • Not alexithymia – The person may be highly articulate about emotions, just not able to feel specific ones internally.
  • Not dissociation – Dissociation involves detachment from an experience that was once present. Asensoria refers to emotional experiences that were never installed to begin with.
  • Not Reactive Attachment Disorder – RAD results from inconsistent or disrupted caregiving and leads to attachment dysfunction. Asensoria describes the total absence of certain internal emotional simulation due to never having been mirrored, not inconsistent attachment formation.

Asensoria is the structural absence of certain emotional channels, not their blockage, suppression, or loss.

What Emotional States Are Missing?

Asensoria does not involve a blanket absence of emotion. Individuals with asensoria may feel:

  • Sadness
  • Grief
  • Compassion
  • Love or others
  • Loyalty
  • Existential despair
  • Anger (in some cases)

What they cannot feel — because these states never formed — are specific affective responses typically built through early mirroring and bonding. These may include:

  • Feeling loved
  • Felt safety
  • Emotional belonging
  • Joy in being seen
  • Felt pride
  • Validation
  • Ontological affirmation 
  • Being protected
  • Celebratory recognition

These states are not simply "hard to feel." For the asensoric individual, they are non-existent. The concept is cognitively clear — but internally, it’s like staring at a blank screen.

Concrete Lived Examples of Asensoria
These illustrate the internal experience of asensoria — not as dysfunction or emotional detachment, but as a developmental non-installation of specific affective states. The individual is not emotionally shut down; rather, the emotional channel in question was never formed.

1. Love Without Resonance

“I know I’m loved. They tell me all the time. But I feel nothing.”

This is not avoidance, fear, or guardedness. The individual cognitively registers expressions of love — even believes them — yet feels no corresponding inner warmth, safety, or connection. The internal simulation of being loved was never installed because the original experience never occurred.

2. Praise Without Pride

“When someone compliments me, I believe them. But inside, it’s just... silence.”

The words are heard and understood. The intellect agrees. But the nervous system remains inert. There is no surge of being seen, no inner glow of validation. Not due to low self-worth, but because the neurological framework for feeling celebrated was never established.

3. Achievements Without Satisfaction

“I’ve done great things in life. I know it. What I’ve accomplished, alone and against all odds, is extraordinary. And yet, I have never, ever felt any satisfaction.”

This is not modesty, not depression, not imposter syndrome. It is the structural absence of the emotional template for felt fulfillment. The reality of the achievement is clear, but the mechanism for registering that reality as joy, pride, or internal recognition simply does not exist.

4. No Hatred, No Boundaries

“I don’t think I’m a saint. I just don’t feel hate. Even when people hurt me very badly.”

This is not moral superiority, repression, or trauma response. It is the absence of an internal template for hatred. In some individuals with asensoria, certain emotional states — including hate, vengeance, or outrage — were never installed. This does not negate their capacity for compassion or justice.

If a child is never mirrored — never granted the right to anger, never permitted to protest — then the emotional infrastructure for justified rage may never develop. What remains is not forgiveness or transcendence, but a structural absence. The affective architecture required to generate hatred as a felt experience was never formed.

Why “Lack” Is Not Pathologizing

Asensoria is not a disorder. It is not damage. It is not mental illness.

It is a neurodevelopmental absence — a structural void that formed because certain external experiences never occurred. Just as a language not heard in infancy may never be wired into the brain, emotional states not mirrored during development may never form. This is not dysfunction. It is simply missing formation due to missing input.

The term “lack” in this context is clinical, not judgmental. It names the non-installation of an internal emotional architecture, not its removal or decay.

How Asensoria Differs from Other Conditions

Condition

Core Feature

Key Difference from Asensoria

Aphantasia

Inability to form mental imagery

Involves a specific affective inability

Alexithymia

Difficulty naming or identifying emotions

The person with asensoria recognizes emotions but does not experience them in certain registers

Emotional Numbness

Loss of emotion due to trauma

Does not imply loss, but rather a deficit in forming certain affective states

Anhedonia

Loss of pleasure

Asensoria affects specific emotional states, not generalized pleasure

Dissociation

Detachment from emotion or experience

Some emotional states have never existed

Prerequisite for Asensoria

The defining condition for the development of asensoria is Arelationality — a total absence of relational mirroring or emotional attunement during critical developmental windows.

Asensoria originates in arelationality from genesis — the total absence of mirroring in the developmental crucible. But its consequences are ontological: a lifelong absence of internal emotional architecture, a self that was never ushered into being through relation.

Coexistence with Other Conditions

Although distinct, asensoria can coexist with: 

  • Aphantasia – the absence of visual imagination
  • Anauralia – the absence of an inner voice
  • Asexuality – the absence of sexual attraction
  • Anhedonia – the inability to experience pleasure

These phenomena are not identical but collectively indicate a severe form of neuropsychological underdevelopment—a profound neurodevelopmental minimalism of cerebral and emotional functions. This suggests a life structured around internal absences, not as a result of resilience or trauma, but due to a complete lack of exposure.

Is it reversible or treatable?

At present, the answer lies more in hypothesis than scientific certainty. Further neurological and behavioral research is required to determine whether, and under what conditions, the cultivation of these emotions is possible. Theoretically, change can occur, though it is likely as challenging as reshaping a deeply entrenched personality pattern.

In my view, consistent self-observation combined with genuinely connective human relationships might stimulate the formation of these affective states, although the probability remains low. Even structured interventions such as Dialectical Behavior Therapy (DBT) could be attempted, but the process would be lengthy and yield uncertain results.

Why Naming Asensoria Matters

Without a term like asensoria, people who live with these internal absences are misdiagnosed, blamed, shamed, or pathologized in ways that erase the truth of their experience. They are told:

  • “Just let yourself feel.”
  • “You’re blocking it.”
  • “You need to learn to receive love.”

But you cannot receive what your system doesn’t recognize. You cannot resonate with a frequency your nervous system was never tuned to detect.

Individuals who experience an affective scaffolding deficit are frequently told to “open up” or “learn to receive,” without recognizing that these states were never internally wired. Understanding the neurodevelopmental origins — including dopamine-oxytocin under engagement — validates their lived reality, moving beyond blame or pathologization.

Naming asensoria is not about medicalizing a person. It’s about giving language to an invisible developmental reality that affects millions — especially those born into emotional neglect, psychopathic parenting, institutional care, or total mirroring failure. 

Final Summary: Asensoria at a Glance

Asensoria is the developmental absence of specific affective emotional states — such as being loved, safe, validated or celebrated — due to non-exposure and non-mirroring in early life. It is not loss. It is not damage. It is internal nonexistence.
It describes what happens when the human self is built in an arelational void, without emotional reflection or affirmation.
Those with asensoria are not broken.
They are unmirrored.
The condition is lifelong unless deeply and consistently mirrored later in life — a rarity, but not an impossibility.
In the absence of such mirroring, the person may go through life seeing everything, knowing everything, but feeling only within the narrow band of what was formed early on. Pride, joy, celebration— these are not repressed. They are blank fields. Unknown territory. 
Emotional terra incognita.
And now, finally, we have a name. Asensoria. 

Methodological Note

The data and observations presented in this section originate from a qualitative study conducted on adult subjects who were born and raised in a familial environment marked by an extreme overlap of destructive dynamics: a sociopathic maternal figure, entirely indifferent to the child's existence, and a sadistic-psychopathic paternal figure who systematically persecuted any form of emotional expression. In this context, the child was never emotionally mirrored. Isolated and alone, the child was ignored by both the mother and siblings, while attempts at emotional expression were reversed by the father — a process of constant anti-mirroring.

This study is part of the ongoing research project “Panthropic Abuse and Existential Trauma,” which is scheduled for publication in the near future. 

Further Reading
For in-depth explorations of abuse, trauma, personality disorders, C-PTSD, mental health, women’s health, neurodivergence, and emotional development, read my books on Amazon:
https://amzn.to/3GXZcKg, 

Or visit my Romanian-language blog, where I translate and expand these concepts for a local audience:
https://neurodivergentasitrauma.blogspot.com/.

Abstract illustration of a brain with branches symbolizing the interconnection between neuroscience and human behavior research.

I am Cristina Gherghel, author of numerous blogs and books dedicated to human behavior, trauma, abuse, psychology, and mental health. I share my perspective not only from the standpoint of rigorous research but also through personal experience, living with multiple forms of neurodivergence (and related conditions):

  • Global aphantasia
  • Asensoria
  • Anauralia
  • Anhedonia
  • Asexuality
  • C-PTSD (Complex Post-Traumatic Stress Disorder)
  • And others

I have detailed this personal experience on the "About the Author" page, where I explore the long-term impact of systemic and relational abuse on psychic architecture. 

The conditions described here — aphantasia, asensoria, anauralia, anhedonia, and asexuality — are insufficiently understood in the specialized literature. Current explanations for their causes are often inconsistent with how they manifest in lived reality.

This is why I am developing my own model, based on observation and comparative research, which analyzes the differences and overlaps among these neurodivergent conditions and their connection to early trauma, ontological abuse, and subtle forms of self-instrumentalization.

This article is part of a broader ongoing effort to clearly differentiate between these conditions — not only as clinical definitions but as lived experiences with a profound impact on thought processes, relationships, perception, and identity construction.

Thank you for your interest in and support for my work. 

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