The Clinician Detective: Pediatric Brain Dysregulation
- BioSource Faculty
- 1 hour ago
- 17 min read
Dr. Ronald Swatzyna, Director and Chief Scientist of the Houston Neuroscience Brain Center, inspired our Clinician Detective series. In his Association for Applied Psychophysiology and Biofeedback (AAPB) Distinguished Scientist address, he reminded his audience that the DSM-5 advises that general medical conditions be systematically ruled out before assigning a psychiatric diagnosis to ensure diagnostic validity and appropriate treatment planning. He argued that in abrupt onset and refractory cases, EEG biomarkers should challenge neurofeedback providers and their medical colleagues to become detectives to identify its causes. This collaborative approach allows each professional to contribute to assessment while "staying in their lane."
Dr. Swatzyna generously mentors professionals in his investigative method, including raw EEG interpretation, to train the next generation of neurofeedback clinicians.
This post is based on Dr. Swatzyna's thought-provoking BCIA webinar, "Neurofeedback Mystery Theater #1. Two Cases with Atypical Findings and Neurofeedback Response." We encourage you to purchase this neurofeedback mentoring webinar from BCIA.
Initial Clinical Presentation and Diagnostic Complexity
This case follows the neurophysiological and clinical progression of a male patient who entered treatment at the age of 5 with multiple neurodevelopmental and psychiatric diagnoses. The patient was diagnosed with Autism Spectrum Disorder (ASD), Attention-Deficit/Hyperactivity Disorder (ADHD), Generalized Anxiety Disorder (GAD), learning disabilities, and chronic sleep disturbance. These conditions had been documented by multiple prior providers, including pediatricians, psychologists, and educational specialists. Importantly, his clinical history was marked by multiple failed interventions—behavioral therapies, stimulant medications, and educational accommodations—that had yielded only partial or temporary benefit.
His developmental trajectory had been atypical from infancy. According to caregiver report, he had shown early speech delays, reduced social reciprocity, and repetitive motor behaviors. Despite early intervention services, his cognitive and social milestones continued to lag. Academic performance was below grade level, and his frustration tolerance was poor. Emotional dysregulation, particularly in overstimulating environments, resulted in aggressive outbursts and withdrawal behaviors. The child’s sleep was fragmented and nonrestorative, further exacerbating his daytime functioning.
A notable feature of his medical history was the frequency of upper respiratory infections, especially group A streptococcal pharyngitis. Although he had not received a formal diagnosis of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS), the repeated infections raised suspicion of immune-mediated neuroinflammation. His parents had expressed concern about abrupt behavioral shifts following illness, which further reinforced the need for a more integrative evaluation strategy.
This initial presentation highlighted the clinical reality that many children referred for neurofeedback are not arriving at the beginning of their treatment journey but at the midpoint—or even after multiple unsuccessful interventions.
Their conditions are often multifactorial, overlapping psychiatric, neurological, immunological, and developmental domains. Consequently, this case became an ideal candidate for longitudinal neurophysiological tracking and multidisciplinary collaboration.
Pharmacological and Neurofeedback Interventions
The treatment plan began with a dual approach combining pharmacotherapy and EEG-guided neurofeedback. Pharmacologically, the child was prescribed guanfacine, a selective alpha-2A adrenergic agonist known commercially as Intuniv. This agent reduces sympathetic nervous system activation by modulating norepinephrine release and is commonly used in pediatric ADHD for its calming, non-stimulant properties. Its sedating effects also made it suitable for addressing sleep disturbances and hyperarousal.
Over time, two additional medications were introduced: citalopram and clonidine. Citalopram, a selective serotonin reuptake inhibitor (SSRI), was added to address persistent anxiety symptoms and mood instability. By increasing extracellular serotonin concentrations in the central nervous system, SSRIs can reduce worry, improve emotional modulation, and assist with sensory overreactivity.
Clonidine, another alpha-2 adrenergic agonist, was used adjunctively to enhance sedation, stabilize mood, and target impulsive behaviors. Together, these medications reflected a thoughtful, layered response to a clinical picture that defied monotherapy.
In tandem, the patient underwent neurofeedback training informed by quantitative electroencephalography (qEEG). Neurofeedback involves training the brain to regulate its own activity by providing real-time feedback on electrical oscillations. The technique leverages principles of operant conditioning—reinforcing desired brainwave patterns and discouraging dysregulated activity. Protocols were tailored to the child’s initial EEG findings and adjusted based on subsequent assessments.
The goal of treatment was not merely symptom reduction but functional reorganization of the brain’s electrical activity—particularly in the alpha and beta frequency ranges.
The therapeutic strategy focused on enhancing alpha rhythms (8–12 Hz), which are generated by synchronized activity between the thalamus and cortex and are essential for calm, focused wakefulness. At the same time, efforts were made to reduce excessive beta activity (13–30 Hz), particularly in the high beta range, which can be associated with anxiety, cognitive overload, and behavioral agitation.
Serial EEG Findings and Developmental Trends
Over the span of 8 years, the patient underwent five formal EEG and qEEG assessments. These recordings served as both diagnostic tools and progress markers, revealing detailed information about cortical function, oscillatory maturity, and systemic perturbations.
The initial EEG, performed at age 5, revealed bifurcated alpha peaks in the occipital cortex—two dominant frequencies appearing simultaneously at 7.08 Hz and 8.54 Hz. In typically developing children, a single dominant alpha peak is expected, with frequency increasing progressively with age.
Bifurcation of the alpha rhythm implies competing thalamocortical oscillators, often reflecting developmental asynchrony or disrupted neural entrainment. This phenomenon is not benign; it can interfere with attentional coherence, sensory integration, and cognitive fluidity.
Additional findings included pronounced beta excess in the 16–20 Hz range, especially over the right posterior temporal cortex. This pattern is frequently seen in individuals with hyperarousal, cognitive strain, or emotional dysregulation. Critically, the morphology of this beta activity—its sharpness, duration, and symmetry—confirmed that it was cortical in origin rather than a byproduct of electromyographic (EMG) artifact, which can contaminate EEG readings through scalp muscle tension.
The second EEG, conducted after 20 neurofeedback sessions, showed partial improvement. The slower of the alpha peaks had migrated slightly to 7.81 Hz, but the dominant rhythm remained below age-appropriate norms. The posterior temporal dominance persisted. Importantly, spindling beta patterns—characterized by symmetrical, rhythmic beta bursts—had dissipated.
These patterns, often seen in neuroinflammatory states or benzodiazepine withdrawal, are considered markers of cortical instability. Their disappearance indicated some therapeutic benefit. The theta/beta ratio, while statistically within normative range, was misleading on face value. The raw EEG revealed that the elevated ratio stemmed not from excessive theta activity but from suppressed sensorimotor rhythm (SMR), which plays a vital role in attention and motor inhibition.
A third EEG at age 6 captured a transient improvement. The alpha peak had accelerated to 9.28 Hz, a promising development. However, this was followed by a regression: posterior alpha slowed again, and theta activity increased. Morphological markers—such as waveform shape, smoothness, and symmetry—deteriorated, and interhemispheric coherence declined. These changes mirrored a period of emotional and academic instability, reinforcing the link between cortical oscillations and behavioral function.
At age 10, the fourth EEG revealed further progress. The alpha peak reached 10.5 Hz, a frequency considered optimal for focused wakefulness in children. Coherence maps normalized, and excess beta diminished. However, subtle posterior slowing was noted, hinting at a possible future reversal. This EEG represented a high-water mark in the child’s cortical development, but the electrophysiological trends that followed were concerning.
The Sudden Collapse in Cortical Amplitude
By age 13, the fifth EEG marked a dramatic inflection point. Although the alpha rhythm persisted at a seemingly healthy 10.74 Hz, the amplitude of all EEG signals had collapsed. The tallest waveforms measured just 0.54 microvolts. In pediatric populations, expected resting EEG amplitudes range between 10–30 μV. A reduction of this magnitude—more than 90% from previous baselines—cannot be attributed to artifact, electrode placement, or normal developmental decline.
Amplitude, or waveform height, reflects the number of synchronously firing neurons and the integrity of synaptic function.
A global drop in amplitude suggests either a disruption in metabolic support—such as mitochondrial failure—or widespread cortical inhibition. The low-voltage EEG pattern, particularly when associated with normal or high alpha frequency, is characteristic of toxic-metabolic encephalopathy or neuroinflammatory syndromes. It is not a feature of uncomplicated ASD or ADHD.
Concurrently, automated spike detection software identified 51 spike-wave discharges. These brief, sharply contoured waveforms can represent subclinical epileptiform activity or cortical irritability. Visual inspection confirmed that these were true cortical events, not artifacts. Their emergence—absent from all prior studies—pointed to a new pathophysiological process affecting cortical excitability.
Functional Decompensation and the Search for Root Cause
Behaviorally, the patient began exhibiting profound dysregulation. Once considered manageable, he now demonstrated persistent aggression, defiance, and academic collapse. His sleep deteriorated, mood lability intensified, and executive functioning eroded. The clinical picture was no longer consistent with static developmental delay—it now suggested active physiological decline.
In response, the clinician referred the family to a functional medicine practitioner specializing in systemic contributors to brain dysfunction. The integrative evaluation uncovered two key findings: significant gut dysbiosis and high levels of urinary mycotoxins, indicating chronic mold exposure.
Gut dysbiosis—an imbalance in the intestinal microbiota—has been implicated in neurodevelopmental disorders, especially ASD.
The gut-brain axis, mediated through immune, hormonal, and neural pathways, influences neurotransmitter availability and systemic inflammation.
In this case, the child’s limited diet, history of gastrointestinal complaints, and behavioral symptoms aligned with microbial imbalance.
Mold toxicity is a well-documented disruptor of mitochondrial function. Mycotoxins interfere with ATP production and reduce the release of nitric oxide (NO), a signaling molecule that regulates cerebral blood flow and neutralizes oxidative waste. In the absence of adequate NO, reactive oxygen species (ROS) accumulate, leading to oxidative stress, synaptic dysfunction, and neuroinflammation. These processes contribute directly to the EEG findings of low amplitude and high-frequency spiking.
Treatment Response and Multidisciplinary Integration
The patient underwent a comprehensive treatment plan that included antimicrobial protocols, dietary reform, mitochondrial support, and environmental remediation. Within 2 months, behavioral symptoms began to subside. He became more engaged in school, his mood stabilized, and his sleep improved. Teachers and administrators noted the dramatic turnaround, and the family was invited to share their story on a regional health broadcast, “Hatching for Health.”
The clinical recovery affirmed the hypothesis that brain dysfunction had been driven by systemic physiological disruption—not a primary neurological disease. The neurofeedback protocols had been effective insofar as the brain had metabolic integrity.
Once that support was withdrawn through toxic injury, even optimal training could not compensate.
This case catalyzed a shift in clinical practice. The team began proactively screening for physiological contributors in all cases of unexplained EEG voltage suppression, emerging spikes, or neurofeedback failure. Functional medicine became a standing component of the diagnostic algorithm, not a last resort.
Timeline
Age 5
EEG Findings: Initial EEG revealed two competing alpha peaks at 7.08 Hz and 8.54 Hz, suggesting unstable thalamocortical entrainment. There was excess beta activity in the 16–20 Hz range, especially over the right posterior temporal region.
Behavioral Findings: The child presented with speech delay, sensory sensitivities, aggression, and fragmented sleep. Emotional regulation was poor, especially in overstimulating settings.
Treatment: Neurofeedback was initiated with protocols targeting alpha enhancement and beta reduction. Guanfacine was prescribed to address hyperactivity and sleep disruption.
Age 5.5
EEG Findings: Alpha peak slowed to 7.81 Hz, beta excess improved, and previously noted spindling beta activity resolved. Low sensorimotor rhythm (SMR) contributed to an elevated theta/beta ratio.
Behavioral Findings: Mild improvements were seen in focus and emotional stability. However, regulation remained inconsistent.
Treatment: Citalopram and clonidine were added to manage mood and impulsivity. Neurofeedback continued with revised protocols.
Age 6
EEG Findings: Alpha frequency accelerated to 9.28 Hz, indicating temporary progress. However, posterior alpha later slowed again and theta increased. Morphological coherence decreased.
Behavioral Findings: Transient behavioral gains were followed by regression in attention and emotional control.
Treatment: Neurofeedback protocols were adjusted to account for new slowing. No changes were made in pharmacological therapy.
Age 10
EEG Findings: Alpha rhythm reached 10.5 Hz, appropriate for age. Coherence maps normalized and beta excess resolved. Mild posterior slowing persisted.
Behavioral Findings: This marked the patient’s best functional period. He was performing well in school and mood was stable.
Treatment: Maintenance neurofeedback sessions continued. No medication changes were needed.
Age 13
EEG Findings: Alpha remained stable at 10.74 Hz, but amplitude collapsed to 0.54 μV—more than a 90% reduction. Automated detection flagged 51 spike-wave discharges in frontal and central regions.
Behavioral Findings: Aggression, academic failure, sleep disturbance, and emotional volatility re-emerged. The child’s functioning deteriorated rapidly.
Treatment: The patient was referred to functional medicine. Workup revealed gut dysbiosis and mold toxicity. A comprehensive detoxification and microbiome restoration plan was initiated.
Recovery (Age 13.5)
Summary: After two months of systemic treatment, the patient’s sleep, focus, and emotional regulation improved dramatically. He returned to full academic participation and was featured on Hatching for Health as a recovery case.
Conclusion: The Brain as a Systemic Mirror
This case underscores the value of longitudinal EEG tracking, multidisciplinary care, and systemic thinking.
A child’s brain is not a sealed unit but a living interface with the body’s immune, metabolic, and microbial systems. When that interface is damaged, it reflects disturbances not only in waveform patterns but in behavior, cognition, and development.
For clinicians, the lesson is both humbling and empowering. When amplitude declines, alpha frequencies regress, or new discharges appear, the EEG is telling a story. That story is not limited to synaptic transmission or cognitive state—it may reflect gut imbalance, mitochondrial failure, or hidden environmental exposure. The job of the neurophysiologist is not merely to interpret the map, but to ask: what landscape is it mapping?
In that question lies the future of integrative neurodiagnostic care.
Lessons Learned
This case offered an uncommon opportunity to observe, over nearly a decade, how the brain’s electrical rhythms mirror and sometimes precede clinical change. Serial EEG recordings documented a trajectory that moved from unstable alpha rhythms and excess beta to a period of apparent neurophysiological normalization—followed by a dramatic and unexpected collapse in amplitude and emergence of spike-wave activity. These shifts were not merely diagnostic curiosities; they directly paralleled the child’s behavioral functioning and guided clinical decisions.
The most powerful insight was the essential value of longitudinal EEG. Without tracking brain activity over time, the late-stage decline in cortical voltage would have been missed, and the severity of the underlying pathology may have gone unrecognized until symptoms worsened further.
Beyond tracking frequency and coherence, this case emphasized EEG amplitude—or microvoltage—as a critically underappreciated marker of brain health. The amplitude of the peak alpha frequency increases from approximately 20–30 µV at age 5 to 40–60 µV or higher by age 14, reflecting neurodevelopmental maturation and enhanced cortical synchrony. These changes are robust, reproducible, and have important implications for the understanding of normal cognitive and neural development (Gasser et al., 1988; Matousek & Petersén, 1973). While frequency metrics often dominate clinical interpretation, amplitude reflects the vitality of large-scale cortical networks. The near-total suppression of amplitude seen at age 13 could not be explained by artifact or developmental variation. It signaled diffuse cortical underactivation, likely due to mitochondrial dysfunction and systemic inflammation triggered by mold exposure and gut dysbiosis. This electrophysiological signal prompted a shift in the diagnostic framework and led directly to a functional medicine referral. The child’s recovery after gut and environmental interventions affirms the central premise that cortical dysfunction is often rooted in systemic pathology—and that neurofeedback cannot succeed if the brain lacks the metabolic capacity to respond to training.
The case also illustrates the limits of quantitative EEG when used in isolation. The distinction between suppressed sensorimotor rhythm and elevated theta power, for example, was obscured in summary ratios and only clarified by inspecting waveform morphology. Similarly, automated spike detection algorithms flagged epileptiform discharges that required human confirmation to rule out artifact. Most critically, this case redefines the role of the neurofeedback clinician—not just as a technician guiding brainwave training, but as a systems-oriented diagnostician. Integrative collaboration with functional medicine, openness to caregiver insight, and willingness to revisit assumptions were pivotal to the outcome. In the end, this case challenges practitioners to listen to the EEG not as a static output but as the voice of the brain in systemic distress—and to respond with a broader, more biologically informed model of care.
Key Takeaways
EEG amplitude is a critical biomarker of cortical function; a significant reduction in voltage over time may signal mitochondrial dysfunction, neuroinflammation, or toxic exposure.
Alpha rhythm maturation follows a predictable developmental trajectory, and deviations—such as bifurcated or persistently slow alpha—warrant further investigation for neurodevelopmental delay or thalamocortical dysregulation.
Longitudinal EEG assessment enhances diagnostic accuracy, revealing dynamic changes that may be missed in isolated recordings or quantitative summaries alone.
Behavioral regression should prompt systemic inquiry, especially when accompanied by new electrophysiological abnormalities; metabolic, toxic, or immunologic causes must be considered.
Interdisciplinary collaboration, particularly with functional medicine, can uncover treatable physiological contributors to neurocognitive dysfunction that lie outside traditional psychiatric paradigms.
Glossary
academic performance: a measure of a child’s cognitive and functional success in educational settings, often influenced by neurodevelopmental, emotional, and environmental factors. Persistent difficulties may suggest underlying cognitive or regulatory dysfunction.
aggressive outbursts: sudden episodes of physical or verbal aggression. In neurodevelopmental disorders, these may reflect poor emotional regulation, sensory overload, or cortical dysregulation.
alpha rhythms: brainwave activity in the 8–12 Hz range, typically recorded over posterior scalp regions during relaxed wakefulness. Generated through synchronized thalamocortical oscillations, alpha rhythms reflect the brain’s resting baseline. Their maturation follows a predictable developmental trajectory.
amplitude (EEG): the vertical height of EEG waveforms, measured in microvolts (μV). Amplitude reflects the degree of synchronized neural firing; low amplitude may signal cortical underactivation or metabolic suppression.
anxiety: a state of heightened arousal and worry, often accompanied by increased beta activity in EEG. It may be idiopathic or secondary to neurodevelopmental, environmental, or physiological factors.
Attention-Deficit/Hyperactivity Disorder (ADHD): a neurodevelopmental condition characterized by symptoms of inattention, hyperactivity, and impulsivity. EEG studies often reveal altered beta and theta activity.
automated spike detection software: computerized algorithms used to identify potential epileptiform discharges in EEG recordings. These tools flag waveforms that resemble spikes or sharp waves, but require human confirmation due to artifact sensitivity.
Autism Spectrum Disorder (ASD): a neurodevelopmental condition characterized by deficits in social communication, restricted interests, and repetitive behaviors. EEG findings in ASD may include abnormal alpha maturation, focal slowing, or posterior asymmetry.
behavioral therapies: interventions targeting behavior regulation, often including applied behavior analysis (ABA), parent training, or cognitive-behavioral strategies.
beta activity: EEG frequency range between 13–30 Hz, associated with alertness and cognitive effort. Excess beta during rest is often linked to hyperarousal, anxiety, or compensatory overactivation.
beta excess: elevated beta power in resting EEG, particularly in frontal or posterior regions. It may be endogenous or reflect muscle tension, stimulant use, or environmental stress.
bifurcated alpha peaks: the appearance of two distinct alpha frequencies in the EEG spectrum. Often reflects developmental immaturity or oscillatory instability in thalamocortical networks.
citalopram: a selective serotonin reuptake inhibitor (SSRI) used in treating anxiety and mood disorders. By increasing serotonin availability, it can modulate affective and sensory processing.
clonidine: an alpha-2 adrenergic receptor agonist that decreases norepinephrine release. Commonly prescribed for hyperarousal, sleep disturbance, and impulse control in pediatric populations.
coherence: a qEEG measure of synchrony or functional connectivity between regions. High coherence may indicate hypercoupling; low coherence may reflect disconnection or maturational delay.
cognitive overload: a state of diminished processing efficiency due to excessive demands on attention and executive systems. May correlate with high-frequency EEG activity and behavioral regression.
cortical excitability: a measure of the brain's responsiveness to stimulation. It is inferred in EEG through features like amplitude, spike occurrence, and rhythmic variability.
developmental asynchrony: a discrepancy in the maturation of different neurocognitive domains, often seen in ASD or learning disabilities. EEG may reflect this via mixed frequency profiles.
educational accommodations: school-based adjustments designed to support students with learning or behavioral challenges, including modified instruction, extra time, or individualized supports.
emotional dysregulation: a diminished capacity to manage emotional responses, often leading to outbursts, anxiety, or withdrawal. EEG may show beta excess, reduced SMR, or alpha instability.
executive functioning: a set of cognitive processes including working memory, impulse control, planning, and cognitive flexibility. Disruptions are common in ADHD, ASD, and frontal lobe dysfunction.
fragmented sleep: disruption in normal sleep architecture, resulting in frequent awakenings and poor restorative rest. Common in neurodevelopmental disorders, and often associated with EEG slowing and elevated theta during wakefulness.
frustration tolerance: the ability to manage distress when goals are blocked. Low frustration tolerance is often linked to emotional dysregulation, poor inhibitory control, and cortical immaturity.
functional medicine: an integrative medical model focused on identifying and treating root physiological causes of illness. Practitioners often assess gut health, toxins, nutrition, immune markers, and mitochondrial function.
guanfacine: an alpha-2A adrenergic receptor agonist used in ADHD and anxiety treatment. It lowers sympathetic activity and improves impulse control and emotional regulation.
Group A streptococcal pharyngitis: a bacterial throat infection that, in susceptible individuals, may trigger autoimmune neuropsychiatric symptoms (as in PANDAS). Associated with post-infectious behavioral shifts.
high-beta range: EEG activity above 20 Hz within the beta band. Excessive high beta is often associated with stress, overactivation, or stimulant effects.
hyperarousal: a state of increased central nervous system activation, reflected in EEG by elevated beta and suppressed alpha or SMR. Frequently seen in anxiety and trauma-related disorders.
impulse control: the ability to inhibit inappropriate or maladaptive behaviors. Poor impulse control is central to ADHD and can be associated with low SMR and elevated frontal beta.
interhemispheric coherence: a measure of connectivity between homologous brain regions across hemispheres. Reductions can indicate disrupted integration; increases may suggest compensatory hypercoupling.
learning disabilities: neurologically based processing disorders that interfere with reading, writing, math, or executive function. EEG may reveal focal slowing, coherence abnormalities, or delayed alpha maturation.
longitudinal neurophysiological tracking: repeated EEG evaluations over time to observe changes in brain function. Useful for monitoring intervention effects and detecting emerging pathology.
microbiota: the collective microorganisms in the gut. Imbalances (dysbiosis) can affect brain function via the gut-brain axis and are increasingly implicated in neurodevelopmental conditions.
morphology (EEG): the shape, sharpness, and symmetry of EEG waveforms. Helps differentiate normal rhythms from pathological discharges or artifact.
mitochondrial failure: inadequate energy production due to mitochondrial dysfunction. In EEG, this may manifest as globally suppressed amplitude or slow background rhythms.
mood lability: rapid and unpredictable mood changes, often seen in neurodevelopmental and mood disorders. May correlate with EEG irregularities such as alpha instability or increased beta variability.
mycotoxins: toxic secondary metabolites produced by fungi. Known to impair mitochondrial function, induce oxidative stress, and alter brain metabolism.
neuroinflammation: Inflammatory processes in the central nervous system that impair synaptic function and neuroplasticity. EEG signs may include spindling beta, slowing, and low voltage.
neurophysiological maturity: the degree to which a child’s EEG patterns align with age-expected rhythms, coherence, and amplitude. Delays may signal developmental disruption or pathology.
operant conditioning: a behavioral principle where reinforcement increases the likelihood of desired behavior. Used in neurofeedback to shape cortical oscillations.
Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS): a proposed condition in which streptococcal infections trigger immune responses that affect basal ganglia function, leading to acute-onset tics, OCD, and behavioral change.
posterior temporal cortex: a region involved in language comprehension and social cognition. EEG abnormalities here are common in ASD and language-based learning disorders.
quantitative EEG (qEEG): computer-processed EEG used to quantify spectral power, coherence, asymmetry, and other metrics, often compared to normative databases.
sensorimotor rhythm (SMR): an EEG frequency in the 12–15 Hz range located over the sensorimotor cortex. Enhancing SMR is associated with improved attention, motor inhibition, and emotional regulation.
sleep disturbance: disruption of normal sleep quantity or quality, common in children with neurological and psychiatric disorders. Often contributes to daytime dysfunction and altered EEG profiles.
speech delay: delayed acquisition of spoken language relative to developmental norms. May signal broader neurodevelopmental issues and correlate with EEG language area abnormalities.
spike-wave discharges: EEG patterns consisting of a sharp spike followed by a slow wave. Indicative of cortical irritability or epileptiform potential.
spindling beta: rhythmic bursts of beta-frequency activity that may appear symmetrical. Often associated with neuroinflammation or sedative withdrawal.
stimulant medications: pharmacologic agents (e.g., methylphenidate) that increase dopamine/norepinephrine levels to enhance attention. Can affect EEG by increasing beta activity and reducing theta.
sympathetic nervous system activation: a component of the autonomic nervous system responsible for arousal, vigilance, and stress responses. Excess activity may be reflected in high beta EEG and somatic hyperreactivity.
theta activity: EEG activity in the 4–8 Hz range. Prominent theta at rest in older children may reflect underarousal or cortical immaturity.
theta/beta ratio: a qEEG-derived metric often used in ADHD research, comparing slow-wave theta to fast-wave beta activity. Elevated ratios may reflect inattention but are highly context-sensitive.
upper respiratory infections: nasal passage, sinus, pharynx, or larynx infections. Recurrent episodes in children have been implicated in autoimmune neuropsychiatric syndromes.
withdrawal behaviors: social or emotional retreat often observed in overstimulating or stressful environments. These behaviors may reflect sensory processing issues or affective dysregulation.
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