CLINICAL NEUROSCIENCE OF
ADDICTION: NEUROBIOLOGICAL

DISRUPTIONS AND TRANSLATIONAL

MODELS OF SOCIAL DYSFUNCTION

NEUROCIENCIA CLÍNICA DE LA ADICCIÓN: DISRUPCIONES
NEUROBIOLÓGICAS Y MODELOS TRASLACIONALES DE
DISFUNCIÓN SOCIAL

Fabiano de Abreu Agrela Rodrigues

Department of Neurosciences and Genomics

Ricardo Santos Ferreira

Department of
Neurobusiness, Brazil & Portugal
Lincol Nunes Cruz

Department of Philosophy, Brazil & Portugal

Cássio Jandir Pagnoncelli

Department of Tecnology, Brazil & Portugal
pág. 8215
DOI:
https://doi.org/10.37811/cl_rcm.v9i3.18443
Clinical Neuroscience of Addiction: Neurobiological Disruptions and

Translational Models of Social
Dysfunction
Fabiano de Abreu Agrela Rodrigues
1
contato@cpah.com.br

https://orcid.org/0000
-0002-5487-5852
Department of Neurosciences and Genomics

Ricardo Santos Ferreira

contato@cpah.com.br

https://orcid.org/0009
-0001-6575-8520
Bachelor in Law, Master in Administration

Heraclitus Research and Analysis Center

(CPAH), Department of Neurobusiness

Brazil & Portugal

Lincol Nunes Cruz

contato@cpah.com.br

https://orcid.org/0009
-0008-7916-4062
Bachelor in Philosophy and Psychoanalyst

Heraclitus Research and Analysis Center

(CPAH), Department of Philosophy

Brazil & Portugal

Cássio Jandir Pagnoncelli

cassiopagnoncelli@gmail.com

https://orcid.org/0009
-0000-7114-7008
Heraclitus Research and Analysis Center

(CPAH), Department of Tecnology, Brazil &

Portugal

ABSTRACT

Background:
A comprehensive understanding of the neurobiological substrates that modulate social
behavior is essential for identifying etiologies and proposing effective approaches to social dysfunction

and addiction. Rather than relying on speculative or metaphysica
l premises, this framework is based on
measurable neurological alterations resulting from chronic environmental stress and early relational

deficits. These conditions may lead to maladaptive engrammatic patterns and dysregulated

neurocircuitry, with direct
implications for the emergence of compulsive behaviors. Aims: This study
aims to propose a conceptual refinement in the field of clinical neuroscience, with emphasis on the

integration of addiction medicine within a neuroevolutionary and precision
-based model. Methods: The
methodological approach combines descriptive observational analysis with a neuroethological

perspective, incorporating data from peer
-reviewed literature in behavioral neuroscience and
neuroimaging studies (fMRI), focused on the identifi
cation of patterns consistent with dysregulation in
dopaminergic and prefrontal
-limbic pathways. Conclusion: Based on consistent neuroscientific
parameters, we delineate a structured framework to interpret addiction
-related phenomena, introducing
a neurobiologically grounded model that contributes to clinical and theoretical advancement in the

understanding of a
ddictive behaviors.
Keywords: addiction, neurocircuitry, social behavior, dopaminergic pathways, neuroevolutionary
model

1
Autor Principal
Correspondencia:
contato@cpah.com.br
pág. 8216
Neurociencia Clínica de la Adicción: Disrupciones Neurobiológicas y
Modelos Traslacionales de Disfunción Social

RESUMEN

Antecedentes: Una comprensión integral de los sustratos neurobiológicos que modulan el
comportamiento social es esencial para identificar las etiologías y proponer enfoques efectivos frente a
la disfunción social y la adicción. En lugar de basarse en premisas especulativas o metafísicas, este
marco se fundamenta en alteraciones neurológicas medibles, producto del estrés ambiental crónico y de
déficits relacionales tempranos. Estas condiciones pueden conducir a patrones engramáticos
desadaptativos y a una neurocircuitería disfuncional, con implicaciones directas en la aparición de
conductas compulsivas. Objetivos: Este estudio busca proponer un refinamiento conceptual en el campo
de la neurociencia clínica, con énfasis en la integración de la medicina de la adicción dentro de un
modelo neuroevolutivo y basado en la precisión. Métodos: El enfoque metodológico combina un análisis
observacional descriptivo con una perspectiva neuroetológica, incorporando datos de literatura científica
revisada por pares en neurociencia del comportamiento y estudios de neuroimagen (fMRI), centrados
en la identificación de patrones consistentes con la desregulación de las vías dopaminérgicas y prefronto-
límbicas.Conclusión: Basándonos en parámetros neurocientíficos consistentes, delineamos un marco
estructurado para interpretar fenómenos relacionados con la adicción, introduciendo un modelo con base
neurobiológica que contribuye al avance clínico y teórico en la comprensión de las conductas adictivas.

Palabras clave: adicción, neurocircuitería, comportamiento social, vías dopaminérgicas, modelo
neuroevolutivo

Artículo recibido 14 abril 2025

Aceptado para publicación: 20 mayo 2025
pág. 8217
INTRODUCTION

According to the American Society of Addiction Medicine (ASAM), addiction is defined as “a chronic,

treatable medical disease that involves complex interactions among brain circuits, genetics,

environment, and an individual’s life experiences. People with
substance use addiction engage in
compulsive behaviors and often continue despite harmful consequences”
1. This classification aligns
with the neurobiological frameworks that currently inform evidence
-based approaches to addiction
treatment.

Recent neurobiological advances, supported by molecular tracing techniques such as Arc
-driven
mGRASP, in conjunction with behavioral neuroscience and functional neuroimaging methods, have

contributed to a broader understanding of synaptic connectivity and
memory-related processes in
addiction. These findings allow for the refinement of clinical constructs in addiction medicine, with a

focus on measurable maladaptive neural configurations rather than speculative multidimensional

models
2.
Empirical data continue to demonstrate that exposure to early life stressors and emotionally adverse

conditions increases the risk for multiple psychopathologies, including substance use disorders (SUDs).

Computational models of memory engrams reveal that
overlapping neural circuits may sustain
pathological associations in response to such experiences. These patterns can persist into adulthood and

influence the development of comorbid conditions such as post
-traumatic stress disorder and affective
dysregula
tion3.
In the context of clinical research and decision
-making, the investigation of addiction-related
phenomena requires precision in interpretation and methodological restraint. The presence of

interpretative errors due to attentional network dysfunctions has b
een documented in studies examining
the relationship between structural damage and functional outcomes, suggesting the need for a cautious

and evidence
-based analysis of neurocognitive data4.
The accurate identification of etiologies and therapeutic targets for social behavior dysfunctions depends

on the recognition of specific neurological correlates. These include dysfunctional network patterns and

altered connectivity signatures that typical
ly emerge under sustained environmental stress or lack of
affective stimulation. These neurological anomalies have been observed in clinical presentations
pág. 8218
involving visual
-spatial processing impairments and attention deficits, reinforcing the argument that
social deficits in addiction may be rooted in identifiable cerebral alterations
5.
Clinical neuroscience provides a valid pathway for integrating these observations into a structured model

of precision medicine. Evidence from white matter disconnection studies supports the premise that

disruptions in connectivity, rather than isolated gr
ay matter lesions, play a central role in syndromes
affecting awareness and executive function. This conceptual shift informs the understanding of addiction

not as a singular behavioral manifestation but as a complex, network
-level dysfunction6.
Primary Neuro Determinism

The interaction between familial psychosocial dynamics and genetic
-epigenetic influences contributes
to the development of identifiable personality traits rooted in specific neurobiological dysfunctions. This

configuration, involving eight commonly observe
d clinical neurodysfunctions (CNDs), appears to
precede socioeconomic and educational variables in its impact on the early formation of emotional and

behavioral regulation patterns
6.
These dysfunctions, when acting in interpersonal contexts, particularly within early relational

environments, may give rise to maladaptive behavioral responses characterized as neurodysfunctional

interpersonal relationships (RINs). The observed microstruct
ural personality elements are primarily
oriented toward affective survival in both internal and social domains, particularly under emotionally

inconsistent conditions
7.
Such dysfunctional interpersonal patterns within family systems have been associated with increased

resistance to treatment and a higher risk of relapse in individuals with substance use disorders and other

behavioral addictions. These phenomena are unders
tood to arise from neurobiological triggers,
involuntary emotional unavailability, and impairments in volitional control and agency across members

of the relational group (8).

Within this framework, it becomes necessary to consider clinical approaches that target family
-level
dynamics. Specifically, strategies incorporating the understanding of Family Coping processes and

Family Schema configurations
both of which are grounded in neurobiological and psychological
structures
may enhance intervention outcomes by addressing the emotional survival systems that
sustain maladaptive cycles (8).
pág. 8219
The set of ONCs (Observed Neuroclinical Conditions) refers to a cluster of behavioral tendencies

formed through early affective interaction. These configurations are partially dependent on

neurobiological substrates and are linked to a spectrum of psycholo
gical phenomena, including
internalizing and externalizing temperaments, personality traits, affective dysregulation, and

mechanisms of stress response (9).

According to current literature, the ONCs involve the following clinical and neurobiological features

(10):

1.
Neurological Deficit of Family Synchrony (DNSF),
2.
Maladaptive amygdalar-limbic modulation related to family schemas,
3.
Hormonal and immune-inflammatory dysregulation,
4.
Dysfunctions in neuropsychodynamic feedback and mirror systems within family interactions,
5.
Dysregulation of the dopaminergic reward system and dopamine homeostasis,
6.
Neural network impairments involving emotional engrams and deficits in both primary and
higher
-order cognitive processing (associated with the conceptual framework of
Neuroschematic Survival Syndrome),

7.
Secondary simultanagnosia and executive cognitive limitations (1),
8.
Dissociative neuroadaptive disorders of consciousness.
Specific manifestations within this framework include:

Secondary Simultanagnosia: a visual-perceptual limitation preventing the simultaneous
recognition of multiple elements within the visual field (1);

Secondary Alexithymia: reduced access to internal affective states, impairing emotional self-
awareness;

Secondary Anosognosia: inability to accurately infer or recognize others’ affective states;
Anosodiaphoria: attenuated concern or awareness regarding one's health status, often
accompanied by affective indifference.

These dysfunctions, collectively representing a survival
-based emotional personality architecture,
reflect a form of maladaptive habituation embedded in disrupted neurocognitive circuits. The resulting
pág. 8220
engrammatic structures function as stable, but dysfunctional, neural patterns
also referred to as
emotional engrams, neural signatures, or maladaptive cognitive schemas (11).

Neurobiopsychosocial Conditioning

Biopsychosocial conditioning within family environments involves the simultaneous activation of

multiple cognitive
-affective schemas over extended periods. These schemas are frequently reactivated
by specific environmental or interpersonal cues originating
within the family context (12). This process
is associated with adaptive mechanisms for coping with chronic stressors, often involving abrupt

amygdala hyperactivation. This hyperactivation leads to a restricted attentional field and decreased

affective mo
dulation, which in turn may contributeimplicitly and without deliberate intentionto
patterns of emotional neglect (12).

Vygotsky's theoretical model distinguishes between elementary and higher psychological functions,

offering a developmental framework for understanding cognitive complexity (13). Higher psychological

functions encompass operations such as voluntary attentio
n, intentional memorization, conceptual
abstraction, symbolic thought, reasoning, imagination, goal
-directed behavior, and language-mediated
cognition. These functions are considered “higher” because they emerge through cultural mediation and

are not reduc
ible to reflexive or instinctual responses, which are more characteristic of elementary
biological mechanisms shared with non
-human species (13,14).
When biopsychosocial conditioning becomes neurofunctionally dysregulated, it reflects impairments in

neurocognitive systems responsible for attentional anchoring, intersubjective perception, and emotional
-
cognitive integration. This includes deficits in ne
ural connectivity associated with value-directed
attentional capture (VDAC), reduced attention during interpersonal exchanges across verbal, nonverbal,

and symbolic domains, and disruptions in the recognition of agency and intentionality (14
16).
Further dysfunctions encompass disturbances in motivation processes regulated by valence attribution,

involuntary emotional responses such as alexithymia, deficits in visuospatial awareness like

simultanagnosia, and limitations in recognizing internal or e
xternal states consistent with anosognosia.
Memory systems
both episodic and schematicare also implicated, contributing to the consolidation
of maladaptive emotional engrams within these disrupted circuits (17
20).
pág. 8221
These conditions are often subtle and difficult to detect in standard clinical assessments. However, their

impact is significant, manifesting as micro
-level distortions in awareness (micro-dissociations),
cognitive
-affective biases, and decision-making errors anchored in survival-oriented emotional
frameworks. These processes undermine neurosemantic integration and contribute to persistent patterns

of social dysfunction (21).

Engrams

An engram refers to a persistent and detectable physical or molecular alteration within a neural network,

resulting from activity
-dependent processes in specific neuronal populations. These changes occur in
response to episodic stimuli and can be reactivat
ed by partial or complete re-exposure to the original
conditions, thereby enabling memory retrieval (22). Experimental evidence shows that repeated

exposure to the same contextual stimulus leads to consistent activation of the same cell ensembles,

commonly
tracked through the expression of immediate early genes (IEGs) such as c-Fos, Arc, and the
activity
-regulated cytoskeleton-associated protein (22).
In the hippocampus, engram cells have been identified as forming synaptic connections with other

neurons participating in the encoding of the same memory episode (22). These engram networks operate

as coordinated assemblies of memory
-encoding cells, and their reactivation is both necessary and
sufficient for the conscious retrieval of stored experiences (22
27).
Furthermore, experimental models have demonstrated that artificial activation of engram circuits can

produce memory distortions, including the generalization of fear to unrelated contexts or the induction

of context
-specific memories never actually experienced (2227). Evidence from optogenetic studies,
such as those conducted by Kitamura et al., indicates that engrams form simultaneously in the

hippocampus and the medial prefrontal cortex (mPFC) during the initial phase of memory encoding,

although mPFC en
gram cells remain inactive during recent memory retrieval and are classified as “silent
engrams” (22
27).
The relatively low degree of overlap between neuronal populations activated during memory acquisition

and later recall
typically between 10 and 40 percentsuggests a dynamic restructuring of engrams
throughout the memory consolidation process. This reorgan
ization reflects the capacity of neural
pág. 8222
networks to adapt their composition to optimize selectivity and behavioral relevance of stored

information (22
27).
Competition among neurons within a brain region for inclusion in an engram is modulated by neuronal

excitability. Cells with higher excitability levels have an increased probability of being recruited into

the memory trace, influencing the spatial and func
tional configuration of the engram ensemble (2830).
Structural plasticity in engram cells includes increased synaptic strength and dendritic spine density,

along with preferential downstream connectivity to other engram
-encoded neurons, even during resting
or offline states (28
30).
Advances in molecular neuroscience have enabled selective manipulation of these cell populations using

promoter
-specific gene expression strategies, allowing for precise targeting of engram-related processes
at the cellular and circuit levels. These method
ologies incorporate constitutively active proteins or
activity
-inducible genetic markers to isolate and characterize engram cell subtypes (2830).
Conceptual Memory

The encoding and retrieval of memory are mediated by specific subpopulations of neurons, referred to

as cellular engrams. In the human brain, memory formation frequently involves the association of

semantically or perceptually related concepts, a process s
upported by distributed yet selective neural
assemblies (31
33).
According to the Hebbian learning principle, synaptic connections between neurons exhibiting

temporally correlated activity are progressively strengthened, whereas those between neurons with

weakly correlated activity tend to undergo synaptic depression or
elimination. This process enhances
the probability that the neural activation pattern present during encoding will be reactivated during

subsequent retrieval, establishing a synaptic engram as a memory substrate within coactive neuronal

ensembles (31
33).
In the human medial temporal lobe (MTL), individual neurons referred to as “concept cells” exhibit

invariant responses to representations of specific persons, places, or abstract elements. These neurons

selectively increase their firing rates upon exposure
to stimuli associated with a particular conceptual
domain (34
37). The activity of a concept cell reflects the encoding of a discrete representational unit,
suggesting that each concept is represented by a distinct and distributed subset of neurons. When
a
pág. 8223
stimulus is presented, the coactivation of
γN neurons defines the engram of a single concept, while the
overlap between two unrelated concepts is estimated as
γ²N, where N denotes the total number of
neurons in the relevant cortical region (34
37).
Experimental data confirm that individual neurons can become responsive to newly learned associations,

particularly when two concepts are presented in paired configurations. In such cases, the proportion of

shared neurons increases from less than one perce
nt for unrelated concepts to approximately four to five
percent for concept pairs that have undergone associative learning, supporting the hypothesis that neuron

sharing facilitates cognitive integration and memory binding (38
39).
Theoretical models such as those proposed by Romani and Tsodyks demonstrate that memory engrams

maintain structural independence from network size constraints. Nonetheless, they allow for statistically

significant overlap between certain engram pairs, enab
ling sequential activation under conditions of
oscillatory or periodic background input. This mechanism may underlie the neurobiological basis for

concept sequencing and inferential reasoning (40
43).
Persistent structural connectivity has also been observed in animal models. Long
-term potentiation of
Arc
-expressing neurons between hippocampal subfields such as dCA3 and CA1 has been demonstrated
following continuous learning, confirming the stability an
d traceability of functional engrams in vivo.
These findings contribute to the clinical characterization and potential targeting of memory circuits (40

43).

Neurodysfunctional Family Interpersonal Relationships

The quality of early family interactions plays a central role in child development, attachment formation,

and mental health outcomes. Several studies have established the correlation between caregiver

responsiveness and neuropsychological maturation in the
child (4547). Exposure to childhood
adversity, including chronic stress and parental depression, has been shown to affect the dynamics of

the mother
-father-child triad, disrupting interactional quality and emotional attunement within the
family system (4
547).
Triadic synchrony
defined as temporally coordinated behaviors involving physical proximity,
affectionate contact, and mutual gaze between both parents and their infant
has been associated with
pág. 8224
parental oxytocin levels. These synchronous interactions contribute to the formation of secure relational

patterns during early development (45
47).
Oxytocin has emerged as a key modulator of social behavior, implicated in mechanisms underlying

trust, empathy, affiliation, and the regulation of interpersonal interactions, particularly in parent
child
bonding. Behavioral studies suggest that parental se
nsitivity correlates positively with endogenous
oxytocin production, reinforcing its role in shaping attachment
-specific behaviors (48,49).
Evidence also supports the intergenerational transmission of stress
-related vulnerabilities. Parents with
histories of adverse childhood experiences (ACEs) often display increased levels of depressive

symptoms, which in turn compromise their responsiveness
to their children. This reduced sensitivity
affects both dyadic and triadic interactions within the family, contributing to less effective emotional

regulation and behavioral involvement in children (48,49).

Maternal and paternal sensitivity appear to be mutually reinforcing. Higher sensitivity in parent
child
dyads is associated with more adaptive triadic coordination, enhancing the child's capacity for emotional

regulation and relational engagement. Converse
ly, reduced synchrony correlates with the emergence of
internalizing symptoms in children, particularly in contexts where parental mental health is

compromised (48,49).

Notably, improvement in children's psychological outcomes has been observed when maternal

depressive symptoms are alleviated. However, this effect is not uniform across cases. In families where

mothers report histories of early trauma
such as emotional abuse, sexual abuse, or physical neglect
traditional interventions may have limited efficacy. In these contexts, maladaptive parenting strategies,

including lower acceptance and increased psychological control, tend to persist independently of

perinatal facto
rs (48,49).
These findings underscore the necessity of early, targeted interventions that address both the

psychological health of the parent and the relational mechanisms that mediate parent
child interaction.
Enhancing positive parenting behaviors through structured
, neurobehavioral frameworks may contribute
to improved developmental trajectories in at
-risk offspring (48,49).
pág. 8225
Intrusive Neurodysfunctional Interpersonal Relationships

The concept of alienation encompasses multiple dimensions in interpersonal dynamics and is frequently

observed in family systems. Functionally, it is characterized by bidirectional influence. One individual

may encroach upon the rights or autonomy of anoth
er through overt or covert behaviors, often driven
by affective control mechanisms, behavioral regulation, volitional imposition, and financial self
-interest.
These behavioral patterns, commonly associated with parental affective neglect and authoritariani
sm,
manifest within a relational context where the alienator exhibits dominance and the alienated assumes a

submissive role (50).

Such intrusive interactions are often subtle and normalized within dysfunctional environments. They are

maintained by maladaptive conditioning mechanisms that serve momentary relief functions, frequently

co
-occurring with other interpersonal strategies that obscure their pathological nature (50). These
behaviors typically originate during early developmental stages and reflect alterations in familial role

expectations. These may involve role inversion, hyper
-authoritarianism, or deficits in caregiving due to
emotional absence or neglect (51
52).
Violations of relational boundaries and personal autonomy are consistent with maladaptive expressions

of selfishness. These are hypothesized to emerge from involuntary neuroadaptive patterns linked to

neurodevelopmental emotional dysfunctions (NDE) or ONCs
. In this context, the punitive or aversive
nature of the behavior is tied to a diminished perception of relational responsibility (51
52).
Individuals exhibiting these traits may present selective deficits in affective processing, despite retaining

functional cognitive capacity in survival
-oriented domains. This dissociation is reflected in reduced
flexibility of thought, impaired conceptual
reasoning, and compromised social-affective functioning.
Symptomatically, such profiles may resemble traits observed in pervasive developmental conditions,

including restricted empathy, underdeveloped communication, diminished resilience, and a narrow

rang
e of social interests (5152).
Neurobiological evidence suggests that affiliative bonds
mediated by systems such as oxytocincan
rapidly shift from attraction to aversion. Feldman and colleagues have demonstrated that the same neural

substrates implicated in attachment and empathy also
contribute to antagonistic emotional responses.
pág. 8226
These systems, initially structured within the maternal
-infant bond, are later adapted for broader social
functioning and group cohesion among mammals (51
52).
The concept of the affiliative brain, as defined in these studies, has been associated with vulnerabilities

to specific psychopathologies, including dissocial personality disorder, borderline personality disorder,

and subtypes with sociopathic or psychopat
hic features (5354). Trajectories leading to antisocial
behavior include disorganized attachment, early life maltreatment, parental rejection, negative

attribution of others’ mental states (low mentalization), verbal deficits, impulsivity, and increased p
eer
affiliation with antisocial individuals (53
54).
A key factor in the emergence of these dysfunctions is the absence of sensitive parental responsiveness,

also known as mentalism. This refers to the caregiver’s inability to detect and appropriately respond to

the child’s affective and developmental cues.
Intrusive parenting behaviors, which involve disregarding
the child's autonomy and imposing adult
-centric priorities, reflect a disruption in the neural substrates
responsible for family synchrony (53
54).
Intrusive parental conduct is characterized by a pattern of adult
-centered interactions, in which parents
assert control over tasks that the child is developmentally capable of handling independently. This

behavior suppresses autonomy, disregards the child
’s emotional feedback, and often reflects an
immaturity in caregiving capacity (55). Consequences of such patterns include restricted emotional

exploration, inhibition of independent coping skills, and heightened physiological arousal in the child.

These r
esponses interfere with emotional regulation, particularly the ability to manage fear and
perceptions of safety (55).

As a result, parental intrusiveness is considered a significant risk factor for altered neurodevelopment in

socioemotional domains. It may result in persistent neurobiological alterations and sequelae that

compromise healthy psychological maturation (56).

Secondary Neuro Determinism

Secondary Neuro Determinism (SND) refers to unconscious and involuntary stress
-response
mechanisms primarily oriented toward emotional survival, often manifesting as adaptive strategies

within physical, economic, or relational contexts. These responses are
frequently observed in both
pág. 8227
family systems and occupational environments, where behavioral patterns emerge as coping

mechanisms under chronic stress exposure (57).

In this state of neuroactivation, individuals often remain unaware of the presence of secondary emotional

gains, particularly those mediated by dysfunctional relational dynamics within neurodysfunctional

interpersonal relationships (RINs). Behaviors such a
s compulsive routines or dopaminergic
reinforcement cycles may arise as attempts to manage psychosocial stress. However, these behaviors

also paradoxically induce instability and reinforce maladaptive affect regulation strategies (57).

Both primary and secondary survival
-based neurodeterminisms may operate concurrently, giving rise
to observable behavioral deviations such as exaggerated self
-importance or maladaptive conduct in
professional contexts (58).

Coping and Addiction

Behaviors initiated as stress
-coping strategies may, under certain conditions, evolve into habitual
patterns. When these behaviors serve dual functions
both alleviating aversive emotional states and
activating reward circuitry
the risk of transition into addiction increases, particularly in the presence
of genetic predispositions or highly pleasurable reinforcement cycles (59).

Addiction is clinically characterized by a neuropsychological dependency on the coping behavior,

evidenced by the inability to cease the behavior despite genuine attempts and preserved motivation to

change (59). Across different forms of addiction, individ
uals commonly experience deficits in judgment,
reduced predictive awareness, and impaired self
-referential processing (59).
Functional neuroimaging studies have shown evidence of abrupt, automatic activations within the

amygdala, which operate as neurobiological triggers for mesolimbic reward pathways. These findings

support the hypothesis that maladaptive coping behaviors are
reinforced through dysregulated
connectivity between affective and dopaminergic systems (59). Despite this evidence, no comprehensive

synthesis of mediating or moderating factors has been established to inform structured prevention or

treatment programs fo
r substance use disorders (SUDs) (59).
Most existing studies focus on isolated moderators or mediators within individual levels of the

socioecological framework, which limits the understanding of multifactorial contributors to behavioral

pathology. A broader, integrative model could guide more
conscious and effective clinical interventions
pág. 8228
(59). Furthermore, variations in exposure, individual response patterns, and access to services

significantly influence clinical outcomes and should be included in evaluative frameworks (59).

Although some meta
-analyses have attempted to address contextual factors in relational environments,
results have not demonstrated sufficient robustness. This suggests the need for evaluators to adopt a

critical and motivated stance, regardless of clinical
specialization, to facilitate meaningful behavioral
change (60).

In several cases, behaviors such as problem gambling may not conform strictly to addiction models but

instead reflect maladaptive coping strategies developed to manage unmet emotional needs. Dysregulated

coping and internet addiction are not mutually exclu
sive; rather, dysfunctional coping can act as a
predictor of addictive behaviors. This positions certain maladaptive behaviors as forms of psychological

self
-medication (60).
The dopaminergic midbrain, particularly the substantia nigra and ventral tegmental area (SN/VTA),

plays a central role in processing reward stimuli (60). This region is also sensitive to novelty, indicating

shared mechanisms between novelty detection and r
eward processing. The hippocampus, which is
implicated in encoding novel experiences, exhibits anticipatory responses distinct from those of the

SN/VTA when processing expected versus unexpected novelty (61).

Memory recall is significantly enhanced for anticipated novel stimuli when compared to those that are

unexpected, suggesting differential encoding and consolidation pathways (62). These differences are

reflected in functional connectivity profiles of SN/VT
A regions during reward prediction tasks (63).
Specifically, stimuli predictive of reward that are novel enhance the functional connectivity between

medial SN/VTA and mesolimbic targets, including the nucleus accumbens, hippocampus, and primary

visual cort
ex (64).
This connectivity likely enables the integration of novelty and reward signals, contributing to the

modulation of memory processes associated with emotionally salient or motivationally relevant events.

The medial SN/VTA may act either as a convergence poin
t for novelty-reward interactions or as a
modulatory hub for memory encoding related to reward
-predictive novelty (65).
pág. 8229
METHODS

The methodological design adopted in this study was descriptive and observational, with field
-based
ethnographic components. This was integrated with an extensive literature review focused on behavioral

neurobiology in both human and animal models. The sel
ected studies were primarily based on analyses
using functional magnetic resonance imaging (fMRI) and were retrieved from indexed databases such

as PubMed and Web of Science. Article inclusion followed a contextual analysis protocol to ensure

relevance and
alignment with the neurobiological framework under investigation.
DISCUSSION

The application of a pragmatic research paradigm reflects a methodological alignment with the need to

address complex, real
-world phenomena through empirical inquiry. This approach prioritizes functional
solutions to social and clinical problems, emphasizi
ng translational potential. In the context of addiction
medicine, the integration of experiential data with structured observational protocols aligns with

pragmatic epistemology, which posits that meaning is derived from lived experience and is essential f
or
constructing applicable knowledge.

This study presents a comprehensive model within the domain of precision medicine that offers a

structured, evidence
-informed framework for clinical decision-making in addiction. The methodology
enabled the identification of functional patterns and clinica
l categories relevant to complex, uncontrolled
behavioral disorders.

Mixed methods research continues to be adopted in healthcare sciences, where pragmatism serves not

only as a philosophical foundation but also as a practical strategy for integrating patient
-oriented
perspectives and empirical rigor. The synergy between me
thodological pluralism and stakeholder
engagement enhances both the depth and applicability of health
-related research outcomes (6667).
CONCLUSION

Based on descriptive observational field research, a novel conceptual and clinical model was identified.

This model contributes to the understanding of addiction as a multifactorial condition and opens new

investigative pathways by offering a resolution
-oriented framework for intervention.
Declaration of Conflicts of Interest

The authors declare no conflicts of interest relevant to the content or execution of this study.
pág. 8230
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