Screen Trauma – Specifics of the Disorder and Therapy in Adults and Children

Violeta R. Manolova and Stoyan R. Vezenkov

Center for applied neuroscience Vezenkov, BG-1582, Sofia, e-mail: info@vezenkov.com

For citation: Manolova V.R. and Vezenkov S.R. (2025) Screen Trauma – Specifics of the Disorder and Therapy in Adults and Children. Nootism 1(1), 37-51, ISSN 3033-1765

*This paper was presented by Dr. Violeta Manolova at the Second Science Conference "Screen Children" on November 23, 2024, in Sofia, Bulgaria.

Abstract

Screen addiction has been widely recognized as a condition that disrupts cognitive, emotional, and physiological functioning, with severe implications for the brain and autonomic nervous system (ANS). However, the long-term effects of screen addiction extend beyond addiction itself, leading to persistent neurophysiological impairments collectively referred to as screen trauma. This study explores screen trauma as a distinct phenomenon, characterized by cortical fragmentation, autonomic dysregulation, and maladaptive brain functioning that does not resolve through screen detox alone.

Using quantitative EEG (qEEG) and ANS assessments, the study categorizes individuals into four groups: those without markers of screen addiction or trauma, those with screen addiction alone, those with screen trauma alone, and those with both conditions. Findings indicate that screen trauma results in rigid, non-adaptive brain functioning, making affected individuals highly vulnerable to life stressors and prone to psychological and physiological breakdowns.

A key contribution of this study is the introduction of euthymic screen time (EST) and hedonic screen time (HST) as distinct digital engagement patterns. EST, associated with work and learning, does not contribute to addiction, while HST, driven by dopamine-seeking behaviors, fosters screen addiction and its neurophysiological consequences. Prolonged HST exposure leads to screen aadiction and screen trauma, where seeking behaviors migrate from screen environments to other compulsive activities.

The study also highlights that children develop screen trauma much more rapidly than adults, leading to severe cortical dissociation, sensory-motor disintegration, and major developmental disorders, including autism-like symptoms. The earlier screen exposure begins, the more profound and irreversible the effects.

Lastly, the study examines therapy strategies, showing that screen detox alone is insufficient for recovery. Instead, a multimodal biofeedback approach is necessary to restore cognitive flexibility, emotional regulation, and autonomic stability in adults.

These findings emphasize the urgent need for early intervention and preventive strategies to mitigate the long-term impact of screen addiction and screen trauma.

Keywords: screen trauma, screen addiction, qEEG biomarkers, seeking, hedonic screen time

Introduction

Screen addiction is known to be associated with various functional impairments of the brain and nervous system, presenting a spectrum of symptoms (Firth et al., 2024; Li et al., 2024; Huang et al., 2024; Wu et al., 2023). Research on this phenomenon aims to clarify the underlying causes of addiction, related disorders, and the severe symptoms resulting from prolonged screen use. The causes and effects of screen addiction vary based on factors such as the age at which it develops, gender, and the duration of addiction before recovery. Many of these aspects are explained through the concept of "screen trauma," which we introduce and explore in detail in this report. Moreover, the presence of screen trauma provides clear evidence that the observed impairments and symptoms stem specifically from screen addiction rather than other contributing factors.

This study presents the concept of screen trauma, exploring its definition, origins, and the circumstances under which it arises, as well as the research approaches used to examine it. It clarifies the relationship between screen time, screen addiction, and screen trauma, offering a detailed description of cortical changes supported by specific biomarkers. Additionally, it examines the adverse effects on the autonomic nervous system (ANS) and provides an in-depth analysis of the symptomatology, its progression, and manifestations.

The study also includes cases of individuals affected by screen trauma, highlighting the distinctions between screen addiction and screen trauma both in terms of functional impairments and symptomatic presentation. Special attention is given to the differences in cortical and autonomic functioning and symptomatology in children and adolescents, as well as gender-based variations. Furthermore, the study outlines a general framework for therapy, emphasizing key aspects that require special consideration, and discusses the role of screen detox as a crucial component of the recovery process.

Initial Observations of Screen Trauma

We first identified screen trauma during therapy with individuals who showed no direct cortical indicators of screen addiction. Over several months, we conducted comprehensive functional assessments of the brain and nervous system, alongside structured interviews, with nine young men aged 20 to 30. Despite having no signs of screen addiction, they exhibited strikingly similar symptoms, including depressive-anxious states, compulsions, and psychosocial challenges that they struggled to manage. Interestingly, their self-reported screen time was minimal, close to zero, except for activities related to work and study.

At the cortical level, their brain function showed three distinct patterns, one of which fell within the normal range. However, another pattern suggested a form of neural dissociation, characterized by a faster-perceiving cortex (dominant frequency: 11–13 Hz) and a slower-executive cortex (dominant frequency: 4–8 Hz), both operating simultaneously. This pattern is commonly associated with unresolved trauma, indicating that despite the absence of traditional markers of screen addiction, these individuals exhibited trauma-related neurophysiological alterations. Findings from the alpha studies had suggested heightened distress and changes in cortical activity (Lobo et al., 2015).

Lower deep sleep and higher brain arousal, reflected in NREM delta and gamma power changes, had been identified as possible sleep markers of PTSD (Wang et al., 2020).

Theories of frontal asymmetry have linked frontal asymmetry to the relative activity of two hypothesized brain systems in the left and right hemispheres, respectively, sub-serving positive affect or approach motivation, and negative affect or withdrawal motivation. (Meyer et al., 2015)

This trauma pattern was entirely sufficient to explain the dysregulation of the autonomic nervous system (ANS) observed during assessments, as well as the symptoms these individuals experienced. The third identified brain activity pattern displayed some indicators of screen addiction, but they were too subtle to confirm a full-fledged addiction. These included inverted hemispheric activity, alpha peaks across all leads with open eyes, or strong occipital discharges, primarily in O1.

During therapy sessions using multimodal biofeedback, we observed oscilatory SCL (skin conductance level) responses that are typically linked to addictive functioning. These patterns had not been prominent during the initial assessment but manifested multiple times per session throughout the therapeutic process. This led us to suspect that each of these young individuals had a history of addiction that they were concealing. In therapeutic practice, it is not uncommon to encounter distorted or incomplete information from clients for various reasons. By the second month of therapy, after seeing significant improvements in HRV markers, we began gently encouraging clients to share any past trauma they had experienced. We approached the subject indirectly, carefully probing to avoid forcing them into a discussion they were not yet ready for—one that could potentially worsen their condition. Instead, we aimed to keep the door open for future discussions and processing.

However, the firm and consistent denials we received made us question our initial certainty about past trauma. While it is true that some individuals repress or deny their experiences, this kind of suppression is usually detectable through sensor readings. Yet, in this case, none of the nine young men showed physiological signs of avoidance or deception in their functioning. Realizing that such a coincidence seemed illogical, we shifted our focus to the hypothesis of addiction.

On one hand, the SCL readings displayed patterns typically linked to addictive behavior. On the other hand, the subtle cortical activity markers hinting at screen addiction suggested that we were overlooking something crucial. However, the observed functioning did not indicate an active addiction but rather a deep - seated residual effect—a lingering echo of past addiction.

We explored potential histories of substance use, including drugs, marijuana, alcohol, gambling, or prescription medications, but none appeared to be a contributing factor. Recognizing that clients often withhold or distort initial self - reports, we then asked a different question: what was their daily screen time?

Although we had no definitive indicators and the clients had initially denied excessive screen use, we still needed to explore this possibility. Once again, they insisted that their screen time was strictly limited and under full control. However, at the moment this topic was discussed, all of them exhibited strong SCL oscillations—a pattern typically associated with addictive functioning during state transitions, such as shifting from rest to exertion or vice versa.

Something about the way the first man firmly stated his position unsettled me. I could sense his irritation at my persistence on the subject. In the next session, I reframed the question: had his screen time ever been different from what it was now? Perhaps there had been a period of excessive pornography use or online gambling that he had avoided mentioning.

His response was strikingly simple and right in front of us all along. He admitted to a period of heavy gaming that lasted nearly two years, during which his symptoms had first emerged. He explained that he had realized he had developed an addiction, which severely impacted both his health and achievements. Determined to regain control, he had imposed a strict screen detox on himself—a process that was extremely difficult but one he had gradually managed to overcome. Now, he had been "clean" for over three years, meticulously monitoring his screen time, fully aware of the dangers of addiction, and committed to never letting it take hold of his life again. As he told his story, I had to interrupt him multiple times to help him restore his autonomic balance before he could continue.

The entire session revolved around this topic. When I asked why this information had not been shared during the initial assessment, the response was that it wasn’t important because the addiction had already been overcome. I then asked whether he connected his symptoms to the onset of his addiction. His answer was yes, but he believed there were other reasons for his current condition, as his symptoms had not only failed to improve after the detox but had worsened drastically. To him, this meant that something else was wrong, that he was somehow ill.

He had no idea what these reasons could be. He had not experienced any tragic or even significant events during that period—on the contrary, it had been marked by monotony and a lack of challenges. Conversations with the other eight participants, who exhibited similar functioning and symptomatology, followed a nearly identical pattern, revealing strikingly similar narratives: a period of severe screen addiction, the onset of symptoms, detox, and a subsequent worsening of symptoms and quality of life over the following years. The specific data from these cases are presented in the results.

This sparked our interest in gathering more data. We reviewed additional cases of adults between the ages of 20 and 50 whom we had studied over the past two years. What emerged was a remarkable pattern: most of them displayed the same markers as the young men described earlier but with an ongoing screen addiction. Some, however, exhibited similar brain activity patterns despite no current screen addiction. The symptoms remained consistent with those observed, all of which had originated during an intensive period of screen exposure.

I had worked personally with some of these cases and was familiar with the challenges involved in their recovery therapy. A common characteristic in most cases was one of three scenarios: either a detox phase followed by worsening symptoms and a subsequent return to screen use, intensive screen exposure up until the start of therapy, or continued screen use during therapy. As a result, the pace of recovery and the extent of improvement—both in terms of brain function and symptom reduction—varied significantly. This led us to consider the possibility that prolonged screen addiction could cause brain fragmentation and autonomic imbalance, similar to those observed in trauma - related conditions. To test this hypothesis, we conducted a detailed analysis of the original nine cases along with an additional 163, bringing the total to 172. This allowed us to identify overarching trends as well as specific variations influenced by different factors. From this, the concept of screen trauma emerged, guiding us into the research field of the multidimensional manifestations of a chronic condition.

Over time, the term screen trauma gained further significance as we observed similar patterns of "splitting" and fragmentation of brain activity in children. However, their brain functioning appeared even more dissociated and burdened with symptoms. Despite these differences, the hallmark of trauma remained the same—leaving an imprint that powerfully hinders and distorts the development of specific systems within particular dimensions.

To better understand the transition from screen time to addiction and trauma, we introduce two key terms related to how screen devices are used: euthymic screen time (EST) and hedonic screen time (HST).

Similar to our previous observations, screen addiction does not develop when screen devices are used for work and learning, as these activities keep the mind

alert and engage the cortex in task execution. In contrast, screen addiction emerges when screens are used to alter one’s state, inducing excitement, pleasure, or relaxation. Additionally, for addiction to form, prolonged daily screen stimulation over months is necessary.

Our earlier findings indicate that the time required to develop screen addiction, when screens are used for state modulation, varies significantly depending on age, gender, autonomic and cortical maturity, and lifestyle. The more developed and high-functioning the cortex, the slower the addiction develops, and the less severe its impact on the body. Nervous system maturity plays a similar role, with rigid and highly adaptive (younger) neural organizations being more vulnerable.

Euthymic Screen Time (EST).Definition:

Euthymic screen time refers to a type of digital engagement where the use of screen devices does not lead to addiction, is not driven by compulsive need, and does not cause negative psychophysiological effects. It is characterized by a stable autonomic nervous state and cortical alertness, contributing to cognitive activity and psycho-emotional balance.

Characteristics:

·Does not disrupt autonomic balance or destabilize the autonomic nervous system (ANS).

·Associated with cognitively engaging processes such as learning, work, analytical thinking, and complex information processing.

·Supports neurophysiological alertness by stimulating the frontal cortex and maintaining optimal cognitive function.

·Does not lead to symptoms of screen addiction.

·Is not linked to significant changes in dopaminergic regulation that could trigger compulsive use or addiction.

Examples of euthymic screen time:

·Using screen devices for work and education that require analysis, synthesis, and critical thinking.

·Communication that fosters social interaction and intellectual exchange rather than passive content consumption.

·Digital activities that promote personal development and productivity without causing cognitive overload or emotional destabilization.

Hedonic Screen Time (HST). Definition:

Hedonic screen time refers to a type of digital engagement where screen use is aimed at inducing pleasure, relaxation, emotional shifts, or psychophysiological state transitions (e.g., using screens to fall asleep). This type of screen time can lead to addiction, disrupted autonomic balance, and "cortical sleep" (a prolonged decrease in cognitive activity). It is often used as a mood regulation strategy.

Characteristics:

·Influences the autonomic nervous system, leading to dominance of either sympathetic or parasympathetic activity, depending on individual nervous system type and content type.

·Produces neurophysiological effects, such as increased dopamine activity (with stimulating content) or a sedative effect (with passive consumption).

·Frequently serves as a mechanism for stress avoidance, a compensatory strategy, or a tool for emotional regulation.

·Excessive use can reduce cortical activation, impairing cognitive function.

·Associated with risks of addiction and related symptoms such as irritability, anxiety, sleep disturbances, cognitive fatigue, attention deficits, and more.

Examples of hedonic screen time:

·Extended consumption of entertainment content that requires no cognitive engagement (e.g., passive social media scrolling, binge-watching TV series).

·Intensive use of digital platforms for virtual pleasures, such as high-adrenaline video games, online gambling, or pornographic content.

·Screen use as a transition between psychophysiological states, such as shifting from tension to relaxation (e.g., guided meditations) or from boredom to excitement (e.g., engaging in social media conflicts).

Study Design

The study examines 172 individuals between the ages of 20 and 50 for qEEG markers of screen addiction, screen trauma, autonomic status, and symptomatology.

For each participant, data is collected and systematized, including:

·Gender and age at the time of the study.

·Period of intensive screen activity, including when it started, how long it lasted, whether it ended, and if so, how long ago.

·Whether a screen detox was attempted and what the results were.

·The level of awareness of screen addiction, assessed through behavioral patterns and complaints related to excessive screen time, compulsive behavior, seeking screen-based stimulation, displacement of real-life activities by virtual engagement, and signs of social withdrawal.

·The symptomatology that developed during addiction, its characteristics, and its progression over time.

· The symptoms studied are described both as individual cases and as summarized data. The primary focus is on:

·Sleep disturbances, including delayed sleep onset, reduced sleep duration, nocturnal awakenings with difficulty falling back asleep, and the presence of sleep apnea.

·Depressive and anxiety-related symptoms.

·Cognitive deficits, such as attention difficulties, memory impairments, distractibility, and lack of concentration.

·Social isolation and relationship difficulties, including lack of meaningful communication, absence of intimacy, and reluctance or inability to form interpersonal connections.

·Autonomic nervous system dysregulation and associated symptoms, such as palpitations, high blood pressure, panic attacks, headaches, dizziness, vertigo, and irritable bowel syndrome.

·Compulsive behavior and emotional dysregulation, including poor impulse control, impulsivity, and related manifestations.

EEG (qEEG) and Autonomic Balance Assessment

Electroencephalographic (EEG) recordings were conducted using a 19-channel monopolar montage, utilizing the Neuron-Spectrum-4P hardware system and Neuron-Spectrum.NET software, developed by Neurosoft LLC, Russia. The quantitative spectral analysis involved calculating amplitude values across different brain rhythm frequency ranges, along with other quantitative parameters processed through Neuron-Spectrum.NET. For comparison with a neurodynamic database, recorded metrics—including absolute and relative amplitude, coherence, phase delay, and Z-score—were analyzed using NeuroGuide Deluxe 3.3.0 from Applied Neuroscience, Inc., USA.

Alongside EEG recordings, autonomic peripheral indicators were measured, including heart rate (HR), heart rate variability (HRV), peripheral temperature, respiratory rate, skin conductance level (SCL), and electromyographic activity (EMG). These physiological parameters were recorded using the 8-channel Gp8 Amp system and analyzed with Alive Pioneer Plus, both developed by Somatic Vision Inc., USA. Various heart rate variability (HRV) indices, such as SDNN, total power, LF/HF ratio, smoothness index, stress index, SNS index, and PNS index, were further processed using Kubios HRV Scientific Lite.

Biofeedback Neurotherapy

Some of the adult participants underwent a five-month multimodal biofeedback therapy program, attending weekly 50-minute sessions.

Expected Outcomes

Based on previous research and our observations, we classified the participants into four groups, each representing distinct patterns of addiction progression, dysfunctions, and symptoms. For each group, we analyzed the trajectory of screen addiction, associated impairments, and symptomatology.

The primary method of differentiation was the qEEG test results, which served as the key criterion for categorizing the participants.

Group 1: Individuals with no markers of screen addiction or screen trauma.

Group 2: Individuals with markers of screen addiction.

Group 3: Individuals with markers of screen trauma.

Group 4: Individuals with markers of both screen addiction and screen trauma.

Results

Group 1. In 36 individuals, no markers of screen addiction or screen-related trauma were observed. The reported complaints in this group include: easy fatigability and irritability (36; 100%), sleep disturbances (33; 91.7%), increased anxiety (29; 80.6%), panic attacks (18; 50%), and lack of intimate life (9; 25%). Data from the autonomic nervous system (ANS) assessment indicated mild autonomic imbalance (18; 50%) accompanied by co-relaxation disturbances (18; 50%) and fatigue (36; 100%). These alterations appear to be the result of increased stress related to personal and professional responsibilities (27; 75%), as well as childcare and household duties managed with little external support (9; 25%).

Participants in this group reported euthymic screen time. They used digital devices primarily for work (27; 75%), studying (18; 50%), targeted information searches (36; 100%), and occasional movie watching, though not on a daily basis (36; 100%).

Within Group 1, several individual profiles showed some screen-based pleasurable activities; however, these were marginal in the context of the person’s overall activity, and thus no indicators of screen addiction were present. Recovery in this group generally proceeded relatively quickly. Through multimodal biofeedback interventions, maladaptive stress responses were addressed, triggering experiences were processed, mechanisms for rapid recovery were developed, and unhealthy habits and attitudes toward the body were modified. This process typically unfolded over approximately three months, followed by an additional two months of therapy to consolidate the achieved changes and prepare the individual for independently managing future challenges.

Therapy often included a phase of significant regression, typically occurring around the fifth to sixth week, after which a stable trend of recovery was observed.

Group 2: Individuals with qEEG Markers of Screen Addiction Without Screen Trauma

Group 2 includes 38 individuals who exhibited qEEG markers indicative of screen addiction (SA), yet without the presence of screen trauma (ST). The group consists of 27 men (71%) with a mean age of 29 years and 11 women (29%) with a mean age of 33 years. These individuals displayed neurophysiological alterations associated with prolonged digital exposure, as well as significant autonomic imbalance, resulting in cognitive, emotional, and somatic disturbances.

Based on self-reports, 18 participants (14 men and 4 women) identified the onset of their screen addiction between the ages of 12 and 18, 14 individuals (10 men and 4 women) between the ages of 18 and 24, and 6 individuals (3 men and 3 women) between the ages of 24 and 30.

Before starting therapy, some participants (7) had attempted unsuccessful screen detoxification, usually conducted independently and without external support. These detox periods lasted on average between two weeks and six months, after which individuals returned to their previous habits. The failed attempts to reduce screen time emphasize deficits in self-regulation and the inability to achieve lasting recovery without structured intervention.

qEEG analysis revealed typical neurophysiological markers of screen addiction, including increased theta activity (4–8 Hz) in the executive cortex, decreased beta activity in the frontal lobe, pronounced alpha peaks during eyes-open conditions, and reversed hemispheric activation. In men, these changes were more pronounced in the frontal areas, while in women, functional fragmentation was observed in the temporal and parietal regions, suggesting greater cognitive and emotional imbalance.

Autonomic nervous system (ANS) data indicated strong sympathetic dominance and co-activations, as well as low heart rate variability (HRV), all contributing to chronic physiological tension, anxiety, and dysregulation of internal systems. These autonomic disturbances manifested as elevated blood pressure and muscular tension, resulting in fatigue, poor emotional balance, and unstable regulatory function.

Participants presented with a wide spectrum of cognitive, emotional, and somatic symptoms. Cognitive impairments were most prominent—90% reported difficulty concentrating, 83% experienced mental fatigue, and 68% had short-term memory deficits. Emotional disturbances were also significant—87% reported anxiety, 79% irritability, and 42% depressive episodes. Panic attacks affected 36% of participants, more frequently associated with deeper autonomic dysregulation in women and compulsive tendencies in men. Sleep disorders affected more than two-thirds of the group—71% reported difficulty falling asleep, 46% had frequent nocturnal awakenings, and 82% woke without feeling rested. Social difficulties were also widely reported—64% cited communication problems, 59% reported social isolation, and 43% had difficulty forming long-term interpersonal relationships. Compulsive behavior was a key characteristic, with 84% showing a persistent urge to check social media and 55% experiencing obsessive thoughts about screen-related stimuli even without access to devices.

Average screen time ranged between 6 and 10 hours daily. Men spent 85% of that time on hedonic screen time (HST), while the proportion was 70% for women. Women demonstrated a higher proportion of euthymic screen time (EST)—30% compared to 15% in men—indicating greater engagement with work and educational content. Although participants engaged in activities generally considered beneficial to cognitive and autonomic health—such as reading, cognitive games like chess, physical exercise, dance, some social interactions, and academic work—these were insufficient to neutralize the impact of HST and the development of screen addiction and its symptoms.

Many individuals reported experiencing stagnation in recent years, actively avoiding novelty and challenges, and expressing a fear of change.

Out of the 38 individuals assessed, 26 began therapy. Three discontinued during the first month, and two more dropped out during the initial therapeutic crisis. Thus, 21 participants completed the therapeutic program.

Within the first third of the therapeutic process, screen stimuli were significantly reduced. However, unlike other cases of autonomic dysregulation, where therapeutic crises typically emerge around the fifth week, this group displayed a delayed therapeutic crisis, appearing around the 9th to 10th week. This delay suggests impaired neuroplasticity and slower recovery processes compared to individuals without screen addiction. From that point forward, progress was uneven, with frequent regressions and symptom fluctuations. In some cases, therapy followed a weekly cycle of improvement followed by significant worsening, a pattern that could persist for four to six weeks.

Therapists were able to distinguish participants who adhered to detox recommendations during therapy program from those who continued to engage in excessive HST. Individuals who failed to reduce HST exhibited slower progress and unsatisfactory therapeutic outcomes.

After five months of therapy, 17 out of 21 participants (15 men and 2 women) achieved full recovery, marked by the disappearance of screen addiction markers, restored autonomic balance, and a 92% reduction in symptoms. Their EST became unrestricted, while HST was limited to just a few hours per week. During therapy, they learned to recognize early signs of autonomic dysregulation and to manage screen use responsibly. Recovery among women was approximately 30% slower than in men, based on the time taken for initial improvements and symptom resolution.

In the remaining four participants (all men), some improvements in autonomic balance and symptoms were observed. However, each time progress was made, HST levels returned to a point where symptoms re-emerged, effectively negating therapeutic gains. Their final functional assessments continued to indicate persistent screen addiction, and overall outcomes were deemed unsatisfactory.

Group 3: Individuals with qEEG Markers of Screen Trauma Without Active Screen Addiction

Group 3 consists of 15 individuals (13 men and 2 women) who exhibited qEEG markers of screen trauma (ST), but without active screen addiction (SA) at the time of assessment. All participants linked the onset of their symptoms to a prior period of intense screen addiction, which was followed by a complete screen detox. However, instead of improvement, the detox phase was accompanied by a worsening of symptoms. Over the course of several years, symptom severity remained stable or progressively worsened, with no signs of spontaneous recovery.

Regarding the subjective onset of screen addiction, 6 individuals (4 men and 2 women) reported the age range of 12–18, and 9 individuals (all men) indicated the age range of 18–24.

These individuals did not engage in compulsive digital device use, and hedonic screen time (HST) was minimized. Nonetheless, even during euthymic screen time (EST), addiction-like functioning was triggered, involving neurophysiological and behavioral mechanisms typical of addiction. Even while using screens for work or academic purposes, they reported elevated internal tension, impaired state regulation, and a heightened drive for additional stimulation.

qEEG analysis revealed fragmented cortical functioning, marked by simultaneous activation of alpha and theta peaks. This pattern is indicative of impaired impulse control and the emergence of animalistic behavioral templates, where instinctual reactions override rational cognition.

The main neurophysiological and autonomic changes included:

Hypersynchronization of alpha activity (10–12 Hz) with eyes open, followed by dysregulated theta activity (4–7 Hz) in the frontal cortex during cognitive tasks.
Decoupling of functional brain networks, characterized by concurrent fast perceptual cortex rhythms (alpha 11–13 Hz) and slow executive cortex rhythms (4–8 Hz)—a profile typical of unresolved trauma and poor regulatory flexibility.
Episodic beta activity surges (21–26 Hz) in the frontal lobe alternating with hypofunction, reflecting nervous system dysregulation.
An oscillatory SCL profile, where state transitions become heavily dependent on external triggers.

Autonomic nervous system (ANS) assessments showed pronounced vagotonic dominance, with intermittent sympathetic activations:

Predominant parasympathetic activity at rest, accompanied by low heart rate variability (HRV) and inability to transition into sympathetic response under stress or cognitive load (a "freeze" response), including tonic muscular tension and abrupt increases in skin conductance (SCL) after task completion.
Cortical shutdown patterns, where sudden stimuli caused sharp drops in both alpha and beta activity, suggesting incomplete adaptation of the nervous system to screen-induced stress responses.

Participants exhibited persistent patterns of addiction-like functioning, which had migrated from screen use to other behaviors. A core feature of this group was the “seeking” drive—an intense internal need for external stimulation, manifesting as constant pursuit of stimulating environmental factors. These included excessive social interaction, participation in high-adrenaline physical activities, and continuous engagement with intellectually demanding tasks.

Alongside this seeking behavior, participants experienced craving, a compulsive urge to fulfill the stimulation need, without attaining a lasting sense of satisfaction. As a result, they became trapped in repetitive activity loops, offering only temporary relief, followed by renewed tension. This cycle often escalated into seeking migration, where individuals shifted from one source of stimulation to another—e.g., from intense exercise to risky behavior, from heavy socialization to self-isolation, or from academic engagement to impulsive decisions.

Substitute compulsive behaviors sustaining these addiction mechanisms included:

Escalating physical activity with no accompanying sense of fulfillment.
Social instability, such as frequent changes in peer groups and short-lived relationships lacking emotional depth.
Pursuit of one-time, high-risk adrenaline experiences, temporarily creating a sense of control or gratification.
Overcommitment to academic or professional work, leading to frequent burnout episodes. Despite these efforts being aimed at social and professional integration, individuals struggled to maintain consistency over time.

Their high motivation was marked by cycles of intense effort followed by emotional or functional collapse, reinforcing a deep internal sense of deficiency and renewed seeking behavior. Many exerted substantial effort to "fit in" socially, yet their behavior often bordered on socially unacceptable. For example, they formed intense but short-lived interpersonal connections or deliberately instigated conflicts as a way to sustain internal tension. Their personality functioning frequently included manipulative tendencies, with social interactions used primarily as a means to regulate internal emotional states.

All 15 individuals began therapy. Two dropped out within the first two months, while the remaining 13 completed the therapeutic process. A major therapeutic challenge was the seeking behavior, indicative of persistent addiction-related functioning. Repetitive engagement in substitute activities created an illusion of safety and satisfaction, which in reality was a compulsive mechanism participants were reluctant to relinquish.

Multimodal biofeedback was employed not only to restore ANS balance but also to enhance cognitive stability and sensorimotor integration. By the end of the therapy, there was an average symptom reduction of 76%, with the most significant improvements seen in cognitive clarity and autonomic regulation. Recovery among women was approximately 45% slower than among men, based on the timeline from initial improvement to symptom remission.

Despite measurable progress, long-term stability remains a challenge, as addiction-based patterns tend to reactivate under social, emotional, or physiological stressors.

Group 4: Individuals with qEEG Markers of Both Screen Addiction and Screen Trauma

Group 4 includes 83 individuals (66 men and 17 women) who presented qEEG markers indicative of both screen addiction (SA) and screen trauma (ST). These individuals had a history of prolonged and intensive hedonic screen time (HST) exposure that led to addiction-related functioning. Regarding the subjective onset of their screen addiction, 21 individuals (17 men and 4 women) reported the age range of 12–18, 47 individuals (39 men and 8 women) indicated 18–24, and 15 individuals (10 men and 5 women) reported 24–30 years.

The consequences of this screen addiction evolved into chronic neurophysiological and autonomic dysfunctions that were never compensated. For an extended period, these individuals believed they were in control of their daily lives, unaware of the depth of the underlying disturbances. They described their lives as stable, secure, and predictable, without overt psychophysiological breakdowns. However, upon deeper analysis, this stability was revealed to be rigid and pseudo-adaptive, resulting from fixation on routine behaviors and avoidance of novelty and challenge.

Rather than developing genuine psychological resilience, they had formed rigid cognitive and behavioral patterns, which ultimately collapsed under pressure. A sudden life event—such as divorce, job loss, financial collapse, or health crisis—triggered intense and unmanageable symptomatology that they were unable to regulate. Their nervous systems had been conditioned by long-term exposure to controlled environments and repetitive patterns of addicted functioning, making them ill-equipped to handle stress and novelty. The screen addiction had contributed to the formation of a non-plastic, non-adaptive nervous system, incapable of adjusting to sudden changes due to a lack of flexibility, coping mechanisms, and adaptive capacity. When routine was disrupted, regulatory mechanisms collapsed, leading to trauma-mode functioning.

qEEG analysis revealed combined profiles, showing both addiction-related and trauma-related neural activity. On the one hand, there were markers of addiction, such as frontal beta hyperactivity (22–28 Hz), associated with anxiety, tension, and overcontrol. Concurrently, chaotic alpha activity was observed, correlating with impulsivity and cognitive instability. On the other hand, trauma-related biomarkers were evident, including elevated alpha activity in the occipital lobe (10–12 Hz) and slowed frontal theta peaks (4–7 Hz). This fragmented brain functioning led to disintegration of cognitive coordination and disrupted state regulation.

Assessment of the autonomic nervous system (ANS) revealed severe regulatory impairments. The sympathetic system was chronically overburdened and ineffective in responding to actual stressors, creating a dual profile of vagotonic dominance and co-relaxation dysfunctions. These dysfunctions resulted in an inability to transition smoothly between states, with individuals depending on external triggers to regulate their nervous system activity. This mechanism made them highly dependent on environmental stability and vulnerable to abrupt changes.

Within months of a critical life event, these individuals entered a deep symptomatic phase. Physiological symptoms included chronic fatigue, sleep disturbances, autonomic disorders, dizziness, somatic complaints, panic attacks, sexual dysfunction, depression, and obsessive-compulsive features. Psychosocially, they withdrew from active life, experiencing a loss of agency. This withdrawal often coincided with increased belief in conspiracies, astrology, fate, and other external systems of control. A key element was the absence of perceived personal responsibility: although they felt powerless to change their lives, they simultaneously sought quick fixes to reduce physical symptoms.

Average screen time for this group ranged between 8 and 12 hours per day. Men spent approximately 70% of this time in HST, while women spent about 55%. Few participants had attempted screen detox (7 individuals), but all attempts were unsuccessful. Abrupt reduction in screen use often exacerbated symptoms, leading to substitution with other forms of addiction.

Out of the 83 individuals, 54 began therapy. Eleven dropped out during the first two months, leaving 43 who completed the therapeutic program, of whom only 36 demonstrated stable recovery. The primary challenge in therapy was the deeply ingrained addictive and compensatory behaviors, combined with the clients' firm belief that they were not in control of their lives or functioning. These individuals relied heavily on external stabilizers, and when such structures were removed, autonomic instability and emotional chaos surfaced.

Multimodal biofeedback was the principal tool used to stabilize the nervous system. It was applied both to reduce chaotic cortical patterns and to enhance self-regulation capacity.

Group 4 represents the most complex clinical profile, where screen addiction and screen trauma interact to create a rigid, non-learning nervous system and fragmented brain functioning. When stressors emerged, these individuals were unable to adapt, resulting in severe neurophysiological breakdowns and reversion to trauma-based functioning. Instead of perceiving crises as opportunities for growth, they retreated into psychological defense mechanisms, including conspiratorial thinking, feelings of helplessness, and abdication of responsibility.

Recovery in women was approximately 40% slower than in men, based on the time from first signs of improvement to symptom remission. Recovery in this group was the longest and least stable, and even post-therapy, individuals remained prone to relapse. These findings underscore the necessity of long-term therapeutic engagement to prevent re-entry into the addiction-trauma cycle.

Summary of Results and Discussion

This study examines screen addiction (SA) and screen trauma (ST) as interconnected yet distinct phenomena, both of which lead to profound neurophysiological, autonomic, and psychosocial changes. Through qEEG analysis and autonomic balance assessments, participants were classified into four distinct groups, enabling a detailed analysis of different addiction and trauma profiles.

Group 1: Individuals Without Markers of Screen Addiction or Screen Trauma (36 Participants)

This group did not exhibit significant neurophysiological impairments; however, some participants reported elevated anxiety, sleep disturbances, and fatigue, which were primarily linked to high levels of life stress rather than screen use. Their screen engagement was predominantly euthymic (EST), with no signs of addiction-driven behavior.

Distinctive Biomarkers:

·Normal qEEG profile with no significant deviations in cortical activity.

·Mild autonomic imbalance (indicative of nervous system fatigue).

Group 2: Individuals with qEEG Markers of Screen Addiction but Without Screen Trauma (38 Participants)

This group exhibited distinct neurophysiological markers of addiction, including increased theta activity, frontal hypoactivation, and sympathetic dominance, which contributed to anxiety and autonomic dysfunctions. Participants engaged in high levels of hedonic screen time (HST) and struggled to discontinue screen use without therapeutic intervention.

Recovery was possible but occurred at a slower pace, with frequent regressions throughout the process.

Distinctive Biomarkers:

·Increased theta activity (4–8 Hz) in the frontal lobe, associated with cognitive suppression and compulsivity.

·Reduced beta activity (12–20 Hz) in the frontal cortex, leading to poor cognitive regulation, low concentration, and impulsivity.

·Alpha dysregulation with open eyes, characterized by delayed and fragmented alpha peaks.

·Reversed hemispheric activity—heightened right-hemisphere activity and frontal hypoactivation in the left hemisphere, linked to emotional instability and anxiety.

·Sympathetic dominance in the autonomic nervous system (ANS), evident through:

oLow heart rate variability (HRV)

oIncreased skin conductance level (SCL)

oImpaired recovery mechanisms

Group 3: Individuals with qEEG Markers of Screen Trauma but Without Active Screen Addiction (15 Participants)

These individuals had a history of screen addiction, but after screen detox, their symptoms worsened instead of improving. qEEG analysis revealed fragmented cortical functioning, characteristic of unresolved trauma.

Participants exhibited persistent seeking and craving mechanisms, which had shifted away from screen use and onto non-digital compulsive behaviors, such as:

·Excessive physical activity (compulsive exercise)

·Risky social interactions

·Intense intellectual overexertion

Although therapy resulted in a 76% reduction in symptoms, addiction mechanisms remained active, suggesting a deeply ingrained pattern of dysregulation.

Distinctive Biomarkers:

·Fragmented cortical functioning—simultaneously increased occipital alpha activity (10–12 Hz) and slowed frontal theta peaks (4–7 Hz), indicative of unprocessed trauma.

·Functional dissociation between sensory and executive cortex, leading to:

oCognitive disintegration

oAsynchronous neural activity

oAttention instability

·Oscillatory SCL activity profile, indicating difficulty transitioning between states without external triggers.

·Episodic beta hyperactivity (21–26 Hz) in the frontal lobe, linked to anxiety and hyperarousal.

·Predominant parasympathetic (vagotonic) activity at rest, but with sudden sympathetic surges under stress.

Group 4: Individuals with qEEG Markers of Both Screen Addiction and Screen Trauma (83 Participants)

This group represents the most complex clinical profile, consisting of individuals who had functioned for a long time in a rigid and pseudo-adaptive environment, actively avoiding change and challenges.

While they initially experienced a period of relative stability, their symptoms worsened dramatically when exposed to a major life stressor (e.g., divorce, job loss, financial difficulties), leading to severe neurophysiological decompensation.

These individuals exhibited conspiratorial thinking, a sense of helplessness, and a loss of personal agency, making recovery the most difficult among all groups.

Only 36 out of 83 participants achieved lasting stability after therapy, highlighting the long-term risks associated with this dual condition.

Distinctive Biomarkers:

Combined addiction and trauma profiles, including:

·Frontal beta hyperactivity (22–28 Hz)

·Chaotic alpha activity

·Theta dysregulation

Cortical fragmentation, leading to a disconnect between cognitive processing and emotional regulation.

Chronic sympathetic hyperactivation, followed by a

sudden breakdown in autonomic regulation, resulting in physiological collapses under stress.

Severe autonomic dysfunction, characterized by:

·Unstable heart rate variability (HRV)

·Dizziness and autonomic crises

·Somatic dysfunction

Tendency toward abrupt cognitive shutdowns, where cortical activity "switches off" under excessive stress.

Key Findings

1.Screen addiction and screen trauma are distinct but interconnected phenomena.

·Screen addiction (SA) is characterized by addiction-driven behavior.

·Screen trauma (ST) is a consequence of untreated SA, leading to profound neurophysiological dysregulation.

2.Screen detox does not always lead to recovery.

·In some individuals, symptoms worsen after detox, suggesting that the issue extends beyond addiction.

·Long-term neurophysiological consequences persist even when screen time is reduced.

3.Neurophysiological changes in screen trauma resemble those in traumatic disorders.

·qEEG analyses show fragmented cortical functioning, leading to difficulties in cognitive coordination and state regulation.

4.Seeking and craving mechanisms can persist even after stopping screen use.

Individuals replace screen addiction with other compulsive behaviors, such as:

· Risk-taking activities

· Extreme sports

Excessive academic or professional efforts

5.Recovery is possible but depends on the depth of dysregulation.

·Groups 1 and 2 show faster and more stable therapeutic progress.

·Groups 3 and 4 experience unstable recovery and high relapse risk, requiring long-term therapeutic support.

6.The rigidity of the nervous system caused by screen addiction reduces adaptability.

·Long-term screen addiction lowers neuroplasticity, making individuals highly vulnerable to life changes.

·Group 4 demonstrates extreme difficulty in adapting to stress and unpredictable circumstances.

7.The earlier screen addiction begins, the earlier screen trauma develops, leading to more severe consequences.

·Men are 2–3 times more vulnerable than women.

·Women recover 40% more slowly than men.

8.Multimodal biofeedback is an effective therapeutic tool, but its success depends on therapist expertise.

·Therapists must analyze the client’s entire functional profile, including:

o Direct and indirect stimulation mechanisms that sustain unhealthy states.

o Methods to restructure these mechanisms in therapy, especially when faced with strong client resistance.

o Clients who continue engaging in HST show slower progress and higher relapse rates.

o Many clients attempt to shift responsibility onto the therapist, assuming a childlike or manipulative role.

o A therapist’s ability to recognize and neutralize these behaviors is critical for successful treatment.

Screen Trauma in Children

42 children aged 2-12 years were examined for markers of screen addiction and/or screen trauma and here are the results collected from the testing and subsequent therapy.

Early screen addiction disrupts brain development by activating infantile behavioral patterns, which remain deeply reinforced in the brain from the time addiction first takes hold. These patterns persist for years, failing to integrate into later developmental stages. We refer to this condition as fragmentation—a state where different brain functions develop unevenly and fail to synchronize, leading to sensory, motor and cognitive disintegration. The longer screen addiction persists, the more severe the fragmentation becomes. This progressive disruption in brain function has contributed to the legitimization of ASD as a diagnosis.

At the neurological level, screen addiction slows cortical activity within key intrinsic networks, causing:

•Fragmented and disorganized cortical activity

•Asynchronous development and maturation across intrinsic connectivity networks

•Local hyperconnectivity combined with trans-cortical hypoconnectivity

•Significant frequency mismatches between cortical regions

In many cases, dominant frequencies across different brain areas differ by more than 2 Hz, indicating a lack of synchronized neural development. Each network functions at a different developmental stage, with varying levels of maturity and no proper coordination.

Another characteristic of fragmentation is the so-called splitting—where two or even three dominant frequencies appear simultaneously in a single EEG recording. For example, 2–5 Hz, 7–9 Hz, and/or 11–13 Hz may be present with open eyes and persist even with closed eyes.

In some cases, dominant frequencies are higher with closed eyes than with open eyes, clearly indicating the burden that the visual system imposes on cortical activity. Normally, when the eyes are closed, a single alpha peak with a specific frequency should emerge across all recordings, known as the dominant frequency. However, in the digital era, such clear alpha responses have become increasingly rare. Today, alpha and/or theta peaks appearing even with open eyes have become a common finding, reflecting altered cortical functioning.

Slower-than-normal peaks observed both with open and closed eyes are, in our view, highly reinforced cortical activity patterns that correspond to the age at which they were most relevant. For example, 2–5 Hz peaks are characteristic of ages 1–3 years. These imprints may result from traumatic events at that developmental stage or serve as a developmentalanchor left by screen addiction or other addiction. This phenomenon is particularly severe when screen addiction begins about the age of one, profoundly disrupting early brain organization and functional integration. The result is a self-reinforcing cycle of neurological fragmentation, where attention, sensory processing, and executive functions become fixated on screen-based stimuli at the expense of real-world interaction and cognitive growth.

For children under six years old, all screen time is hedonic because their cortical alertness, analytical thinking, and interpretation skills are not yet fully developed. As a result, they cannot properly process overstimulation from animations, movies, or digital games. This makes them highly susceptible to screen addiction, which develops rapidly, and even more vulnerable to screen trauma, which emerges even faster than in adults.

As cognitive and language skills develop in older children, these tendencies slow down but never fully disappear. The degree of risk depends on the child's overall psychophysiological development and social environment. Despite these variations, the risk of screen addiction remains lifelong. The more developed the brain and nervous system, the longer the individual can resist the addictive pull, but the potential for addiction always exists.

A common parental response is to deny giving screens to their child. Many parents insist their child has never used screens, but during initial assessments and therapy, evidence of screen exposure often becomes clear based on specific neurophysiological changes and the persistence and severity of symptoms. While stopping screen exposure leads to significant improvement in many children, in about 50% of cases, symptoms remain, indicating long-term functional changes that impact the child’s overall development.

During the testing and therapy process, therapists can often determine at what age screen exposure began and how intense it was. This is revealed through observed functional changes and symptom persistence. Parental dishonesty about screen use is frequently uncovered in therapy when parents contradict themselves or when one parent, usually the father, unknowingly reveals that the other parent was not truthful.

At the beginning of therapy, parents often go to great lengths to convince therapists that something specific happened to their child, triggering a sudden and severe regression. They describe how, almost overnight, their child stopped speaking, lost eye contact, or withdrew from social interactions. The most common explanations they offer include vaccine reactions, severe infections such as complicated flu episodes often accompanied by seizures, or a distressing incident at daycare that left the child traumatized and displaying new symptoms.

However, both neuroscientific research and clinical experience indicate that the types of neurological disruptions seen in children with screen addiction and screen trauma do not occur overnight or as a result of a single event, no matter how distressing it may be. What is more likely is that the child's nervous system, already rigid, maladaptive, and resistant to learning, collapses when faced with a significant challenge—whether it be a high fever, an emotionally charged situation, or a conflict they cannot process and integrate due to underlying but unrecognized developmental delays.

The younger the child was when introduced to screens and the more intense their screen exposure – regardless of their age – the more minor an environmental stimulus needs to be to trigger a severe maladaptive reaction, pushing them into a mode of "trauma and automation." Even natural developmental leaps, which require an increased adaptive capacity, can become triggers for regression in these children. Instead of making a developmental leap, they experience a setback, one that has been building over weeks and months of excessive screen stimulation overloading their nervous system and brain.

Regression in these children is not just a temporary setback but a return to earlier homeostatic phases – developmental states that predate their first exposure to screens. From that point onward, their growth is marked by maladaptive reactions to nearly any stimulus and repeated regressions at every developmental leap their growing body demands. Instead of progressing naturally, they become stuck in automatized behaviors and compulsive attempts at integration – trapped in a body that continues to grow but lacks the internal developmental resources to regulate itself. These children exist in a state of disconnection, caught between an inner world they cannot structure and an outer world to which they are entirely addisted to its screen stimuli. Their entire orientation is toward screen-based stimulation, as they fail to recognize the significance of any other aspects of the external world. Instead, everything outside of screens becomes merely secondary and instrumental, existing only to serve the screen-driven compulsions formed through addiction. Without clear reference points to differentiate between inner and outer reality, they fail to develop a coherent sense of self or presence in either world. In this state, where people hold no intrinsic value, the ability to form relationships, self-awareness, or independent thought never emerges. There is no need for language or communication, as the child has never experienced the necessity of engaging with others or with themselves in a meaningful way. This is the foundation of psychotic development. When the screens of a child with early screen trauma are stopped, it becomes clear that they are not needed to maintain its states. The development has stalled in helplessness and egolessness, which does not respond to either internal

or external changes.

The compulsions and self-stimulatory behaviors observed in children with screen trauma are the only mechanisms they know to completely shut themselves off from external or internal stimulithat they cannot process but that nonetheless trigger rigid nervous system reactions. Every new environment, person, or circumstance either fails to register at all in the child’s perception or induces sheer terror.

In cases where screen trauma develops later, at ages 4, 6, or 8, the physical symptoms may vary, but the core patterns remain consistent—automatized behaviors, compulsions, loss of language skills, and confusion in social interactions. These issues persistently destabilize development, making delays and stagnation visibly apparent.

Since screen addiction and screen trauma have become near-universal phenomena over the past decade, children without any symptoms of regression or dysfunction are now the exception rather than the rule. As a result, both society and even professionals have become increasingly tolerant of milder forms of developmental delays and dysfunctions, normalizing behaviors that, in earlier generations, would have been seen as clear warning signs. Today, mild cognitive, emotional, or behavioral impairments are dismissed, simply because they appear minor in comparison to the 20% autism rate and 40% ADHD prevalence.

This shift in perception has given rise to the myth of neurodiversity, which reframes uneven developmental profiles as something inherently natural—ranging from severe impairments to minor psychophysical symptoms, developmental delays in some areas, and so-called “compensatory hyper-qualities” in others. These exaggerated strengths—whether in memory, pattern recognition, or intense focus—are often overstated by both parents and teachers as a way to justify or mask the child’s broader neurological dysfunction. Instead of addressing the root issue, many parents wait for their child to "grow out" of the symptoms or place their hopes on a psychologist or speech therapist to "work on" what is, in reality, an underlying neurophysiological disorder caused by screen trauma—something these specialists often fail to even recognize.

For children with early-onset screen trauma, where excessive screen exposure occurred before language development, screens themselves cease to be the primary issue once the trauma is fully established. By this stage, screen addiction is no longer necessary to sustain their maladaptive state. As a result, these children do not actively seek out screens and do not react with tantrums when screens are taken away—not because they have “overcome” the addiction, but because their neurological structure has already been permanently shaped by it. The "split" cortical functioning observed in children with early screen trauma keeps them in a state of complete neutrality toward the world. They no longer need to be "soothed" by external stimuli because their neurological systems have already shut down into a state of permanent detachment. Unlike children with post-linguistic screen trauma, who still oscillate between different levels of awareness, these children may not seek any screen stimulation—not out of self-regulation, but because their cognitive engagement with the world has already collapsed.

For children with post-linguistic screen trauma, two dominant states are observed. The first is complete disengagement, a severe fragmentation where multiple functional modes are disrupted at once, leading to near-total cognitive shutdown. The second is partial disengagement, a less severe fragmentation where two functional modes remain disconnected, resulting in a semi-responsive but dissociative state.

In these children, removing screen exposure triggers extreme reactions, as their nervous system depends on external stimuli to regulate state transitions between disengagement and partial engagement. Without screens, they exhibit stimulus-seeking behavior, migrating toward alternative forms of triggering and mediation to maintain their dysregulated arousal patterns.

These triggers may be external, such as sweet foods, music, specific objects, or places, or they may manifest as self-generated compulsive activities, including spinning toy cars, arranging objects in repetitive sequences, or engaging in other stereotypical behaviors. These compulsions do not serve a functional or exploratory purpose; instead, they act as neurological crutches, helping the child navigate between states of hyperarousal and shutdown in the absence of screens.

The recovery of these children through the therapy we apply achieves several key breakthroughs simultaneously rather than in stages. It allows them to overcome addiction-driven functioning and behavior, stop the migration of seeking, awaken their nervous system and brain, and improve the functioning and parenting approach of their caregivers. This integrated process leads to the disappearance of symptoms and a return to the natural course of development, though with lasting marks from the lost time.

Children who have undergone therapy programs based on repetitive, conditioning methods that aim for "socially acceptable behavior" face greater challenges in recovery. These approaches reinforce the children's automatisms, further deepening their fragmentation instead of restoring them. When applied to an already fragmented brain, educational interventions turn children into mere carriers of information that they neither understand nor know how to use for development. Rather than supporting progress, these efforts create an additional blockage, preventing natural cognitive and emotional growth.

There is no way to call these methods—neither the procedures nor their outcomes—humane. For decades, children with early screen addiction and fragmented functioning were misclassified as autistic, described as being "alone in their own world." But they are not in a world of their own; they have no world at all. They lack representations of external realities and, most critically, of themselves. Investments in structured educational activities and conditioning-based programs only deepen their fragmentation and disintegration, both at the level of the brain and the level of consciousness.

Verbal children with screen trauma, though still fragmented, often have their deficits partially compensated by language development. This group forms the majority of those diagnosed with Asperger’s syndrome and savant abilities—children who are hyper-organized around highly specialized, almost mechanical domains such as mathematics, spatial reasoning, puzzle-solving, and repetitive pattern recognition, yet are entirely lost in human interactions. The social world, with its constant need for adaptation, emotional involvement, and empathy, remains incomprehensible to them.

Not all autistic, inclusive Asperger children have screen trauma – this is evident. However, all children with early screen trauma meet the full diagnostic criteria for autism, while older children with prolonged exposure exhibit autistic traits or fit the Asperger profile. The severe neurodevelopmental consequences of early addiction—especially in cognitive and social skills—are well documented in scientific literature and lead to identical outcomes.

Similar effects are observed in children born to mothers with substance addictions. Some inherit the addiction, while others do not, but research has shown that postnatal environment determines whether recovery is possible. This explains why some of these children are later diagnosed with autism while others are not. With screen trauma, the process is reversed. These children are born healthy, develop normally, and then begin to regress shortly after their first exposure to screens.

There is no need for surprise when recognizing that early addiction-driven functioning leads to bodily dissociation, blocking the formation of both a psychological and social identity. This phenomenon has been extensively studied in cases of alcohol, drug, and opioid dependencies, all of which have been shown to disrupt early personality development. Screen addiction, despite being digital rather than chemical, follows the same fundamental neurological patterns.

What is new in this phenomenon is that screen addiction is now widespread across all ages, even in infants. Screen time is easily accessible, legal, and socially accepted, and the most common “dealers” are parents, babysitters, grandparents, kindergarten teachers, and even therapists—many of whom are

themselves addicted to screens. Their own disconnection from real human experiences in favor of screen ones has dulled the natural instincts that, if not present in every parent, were at least once deeply ingrained in mothers and grandmothers. Or at least, they were—until two generations ago.

Key findings

Early screen Exposure causes lasting neurodevelopmental fragmentation. Screen trauma disrupts the brain’s natural developmental trajectory by reinforcing infantile brainwave patterns, leading to fragmented neural integration. This results in long-term deficits in attention, sensory processing, and executive function.
Screen trauma can mimic Autism Spectrum Disorders (ASD). Children with screen trauma—especially before language development—often exhibit autism-like symptoms, including language loss, social withdrawal, and compulsive behaviors. These children may meet full criteria for ASD despite being born neurotypical.
Neurological effects persist after screen removal. Even after screen exposure is stopped, around 50% of children continue to show symptoms due to structural and functional changes in the brain, indicating that the damage is not fully reversible without intensive intervention.
Screens replace real-world engagement and identity formation. Children with early screen trauma become disconnected from reality, fail to form a coherent sense of self, and lose interest in interpersonal communication. Their world becomes entirely screen-oriented, impairing language, empathy, and social cognition.
Traditional behavioral therapies can worsen fragmentation. Standard educational and behavioral programs that focus on compliance and repetition may reinforce neurological dysfunction instead of resolving it. Effective recovery requires therapeutic approaches that awaken neurocognitive and relational systems, not just enforce surface-level behavior.

Conclusion

This study presents screen trauma as a distinct phenomenon, arising as a consequence of prolonged screen addiction but manifesting as a persistent neurophysiological imprint that does not improve with detox and does not resolve spontaneously. The primary mechanisms underlying screen trauma are fragmentation and dissociation of cortical activity, leading to disintegration of cognitive, motor, and sensory functions. This is the body's response to an overwhelming, unnatural, and repetitive stimulation.

The findings indicate that screen addiction and screen trauma are not interchangeable conditions. While screen addiction is characterized addicted cortical and ANS functioning, screen trauma represents a deep neural fixation on specific developmental patterns, blocking the brain’s adaptability and plasticity. Once established, screen trauma results in rigid, maladaptive functioning, which can remain latent for years and later be triggered by stress, significant life changes, or attempts at developmental progression.

In children with early screen addiction, the effects are even more pronounced in the face of long-term cognitive, social, and emotional disintegration. In severe cases, this form of fragmentation creates a neurophysiological profile that overlaps with autism spectrum disorder (ASD), leaving the individual trapped in regressive behavioral patterns, with little capacity for independent development or integration into social environments.

Clinical practice shows that screen detox alone does not lead to recovery in individuals with established screen trauma. The lack of immediate improvement after discontinuing screen exposure confirms that the impairments are deeply embedded in cortical organization and cannot be overcome without targeted therapeutic intervention. Seeking behavior tends to migrate toward various non-screen-based stimulatory and compulsive activities, reinforcing maladaptive patterns.

The conclusions of this study emphasize the need for early prevention, as screen trauma is a self-sustaining process that becomes increasingly difficult to reverse over time. Future directions should focus on strategies to limit hedonic screen time for all individuals, but especially for children, the development of methodologies for early detection of fragmented functioning, and the implementation of therapeutic approaches aimed at addressing the deep neurophysiological consequences of screen addiction.

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19.03.2025

issue01-April2025