The Clinician Detective: Spindling Excessive Beta

Spindling excessive beta (SEB) is a specific electroencephalographic (EEG) phenomenon characterized by rhythmic, spindle-shaped bursts of beta frequency activity. SEB is a transdiagnostic biomarker. In abrupt onset and refractory cases, SEB should challenge neurofeedback providers and their medical colleagues to become detectives to identify its causes.

Beta denotes brain waves within the 13–30 Hz range, and "spindling" refers to a waxing-and-waning morphological pattern resembling sleep spindles, but occurring at higher frequencies. Unlike normal sleep spindles (typically 12–16 Hz during non-REM stage 2 sleep), SEB is pathologic when present diffusely during wakefulness (Krepel et al., 2021; Nuwer, 1997).

How to Identify SEB in the EEG

SEB is identified through a standard EEG interpreted by trained neurophysiologists. Visual analysis remains the gold standard, assessing for spindle-shaped beta activity in the 13–30 Hz range, typically distributed frontocentrally (Krepel et al., 2021). Primary clinical interpretation relies on pattern recognition and morphology (John et al., 1988; Swatzyna et al., 2015).

What Causes SEB?

The presence of SEB typically signals cortical dysregulation or hyperarousal. It is observed across a wide spectrum of psychiatric and neurological disorders, including attention-deficit/hyperactivity disorder (ADHD), anxiety disorders, post-traumatic stress disorder (PTSD), bipolar disorder, and in some cases of epilepsy (Hughes & John, 1999; Krepel et al., 2021). Functional studies have demonstrated that SEB is associated transdiagnostically with problems of impulse control, independently of specific DSM-5 diagnoses (Krepel et al., 2021).

Further strengthening this association, Swatzyna and colleagues (2015) found that in a large sample of refractory psychiatric cases, four EEG biomarkers—including SEB—were commonly present regardless of traditional diagnostic labels. Specifically, SEB was identified across disorders such as ADHD, autism spectrum disorder (ASD), mood disorders, and anxiety disorders. Importantly, the presence of SEB did not correlate strictly with any specific DSM-5 category but rather indicated underlying cortical dysregulation contributing to medication failure (Swatzyna et al., 2015).

Swatzyna et al. (2024) further validated these findings in a larger replication study of 1,233 patients, confirming that SEB, along with focal slowing, encephalopathy, and isolated epileptiform discharges, constituted the major biomarkers underlying treatment resistance. This work supports the emerging view that SEB reflects neurobiological dysfunction beyond traditional psychiatric nosology and is critical for guiding precision medicine approaches.

Furthermore, toxic encephalopathies, especially due to heavy metal exposure (e.g., lead, mercury), have been implicated in the genesis of SEB (Swatzyna et al., 2024). Structural injuries such as traumatic brain injury (TBI) and hypoxic or metabolic insults may also produce spindling beta by disrupting inhibitory-excitatory balance (Swatzyna et al., 2015).

Recent research suggests that genetic factors contribute to beta frequency abnormalities, with polymorphisms in GABA-A receptor genes affecting cortical beta power (Krepel et al., 2021; Porjesz et al., 2002).

Which DSM-5 Diagnoses Are Associated With SEB?

SEB has been linked with several DSM-5 diagnoses, including: Attention-Deficit/Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD), Bipolar Disorder, Generalized Anxiety Disorder, and Post-Traumatic Stress Disorder (PTSD; American Psychiatric Association, 2013; Hughes & John, 1999; Swatzyna et al., 2015; Swatzyna et al., 2024).

In autism specifically, routine EEG studies have demonstrated high rates of subclinical epileptiform activity and beta abnormalities, including SEB patterns, emphasizing the shared biological mechanisms between epilepsy, autism, and cortical dysregulation (Swatzyna et al., 2018).

It is important to recognize that EEG abnormalities are not diagnostic of psychiatric conditions but serve as neurophysiological markers that must be interpreted within the broader clinical context (Swatzyna et al., 2024).

Drugs That Worsen SEB

Certain pharmacological agents are known to exacerbate SEB. Benzodiazepines increase beta activity by enhancing GABAergic inhibition, paradoxically leading to excessive beta synchrony, particularly with chronic use (Fisher et al., 2014; Swatzyna et al., 2024).

Stimulants such as methylphenidate and amphetamines, by increasing cortical excitability, can enhance beta activity and potentially worsen spindling (Swatzyna et al., 2024). Selective serotonin reuptake inhibitors (SSRIs) have been reported to increase cortical beta power in susceptible individuals (Olbrich & Arns, 2013). Thus, clinicians are advised to exercise caution in patients with prominent SEB when prescribing CNS-activating agents.

Differential Diagnosis and Recommended Testing

When SEB is detected, the differential diagnosis could include metabolic encephalopathy (hepatic, renal, hypoxic causes), primary psychiatric disorders (e.g., ADHD, bipolar disorder),

sleep disorders (especially insomnia with hyperarousal), toxic encephalopathy (particularly heavy metal toxicity), and traumatic brain injury (TBI; Krepel et al., 2021; Swatzyna et al., 2024).

Recommended investigations include a comprehensive metabolic panel, extended EEG monitoring (if epileptiform activity is suspected), heavy metal screening (blood, urine), MRI of the brain (to assess for structural abnormalities), neuropsychological assessment (to define cognitive domains affected), and thyroid function testing.

Structured Diagnostic Checklist: Spindling Excessive Beta (SEB) Evaluation and Management

I. Initial Clinical Assessment

☐ Comprehensive Clinical History

• ☐ Symptom onset, duration, and progression

• ☐ Psychiatric history (ADHD, ASD, anxiety, bipolar disorder, PTSD)

• ☐ History of treatment resistance (≥2 failed medication trials)

• ☐ Medication history (especially benzodiazepines, stimulants, SSRIs)

• ☐ Environmental toxin exposures (lead, mercury, etc.)
  

☐ Behavioral and Cognitive Screening

• ☐ ADHD-RS (impulse control focus)

• ☐ Sleep questionnaires (PSQI, HSDQ)

• ☐ Anxiety and mood disorder scales

• ☐ ASD screening tools (if applicable)
  

☐ Neurological and Functional Examination

• ☐ Full neurological exam (reflexes, coordination)

• ☐ Basic cognitive screening (executive function, memory)
  

II. Neurophysiological Evaluation

☐ Routine EEG and Quantitative EEG (qEEG)

• ☐ Confirm presence of spindling beta (13–30 Hz, spindle morphology)

• ☐ Identify additional abnormalities (e.g., focal slowing, encephalopathy, isolated epileptiform discharges)

• ☐ Compare findings to Swatzyna’s neurobiomarker model (SEB as a marker of cortical dysregulation in refractory cases)

• 
  

III. Laboratory and Imaging Workup

☐ Toxicology and Metabolic Testing

• ☐ Blood and urine heavy metal testing (especially lead, mercury)

• ☐ Comprehensive metabolic panel (electrolytes, liver, kidney)

• ☐ Thyroid panel

• ☐ Nutrient levels (zinc, magnesium, vitamin D)

☐ Neuroimaging

• ☐ MRI Brain with DTI and FLAIR sequences (if structural lesion suspected)

☐ Extended EEG Monitoring

• ☐ If seizure activity, subtle epileptiform discharges, or a sleep disorder suspected

☐ Neuropsychological Testing

• ☐ Full battery evaluating executive function, attention, memory

  
  

IV. Differential Diagnosis Considerations

Based on Swatzyna’s findings, strongly consider:

• ☐ Refractory ADHD (potentially toxin-induced)

• ☐ Autism Spectrum Disorder with hidden epileptiform activity

• ☐ Generalized anxiety or PTSD with cortical hyperarousal

• ☐ Bipolar disorder (manic/mixed states with SEB overlay)

• ☐ Metabolic or toxic encephalopathies

• ☐ Traumatic brain injury sequelae

  
  

V. Treatment Strategy

☐ Address Identified Underlying Causes

• ☐ Chelation therapy for heavy metal toxicity (if indicated)

• ☐ Nutritional repletion (e.g., zinc, magnesium)

• ☐ Anti-inflammatory and detoxification protocols

• ☐ Sleep optimization strategies

• ☐ Neurofeedback or neuromodulation (where available)

☐ Medication Management

• ☐ Minimize agents exacerbating SEB (stimulants, benzodiazepines, SSRIs)

• ☐ Adjust psychotropics cautiously with EEG monitoring

☐ Follow-up

• ☐ Repeat EEG every 3–6 months to assess response

• ☐ Behavioral and functional reassessment

Illustrative Case Narrative: Jacob

Jacob, a 14-year-old boy, was initially diagnosed with ADHD after exhibiting chronic inattention, impulsivity, and emotional dysregulation. Stimulant medications worsened his symptoms. A baseline EEG demonstrated SEB over the frontal and central regions.

Given these findings, functional testing was pursued. A provoked urine heavy metal analysis revealed significant lead toxicity. Jacob underwent a medically supervised chelation therapy protocol, alongside zinc supplementation. Over 6 months, his cognitive and behavioral symptoms resolved, and a repeat EEG showed normalization of beta activity. He no longer met the criteria for ADHD.

This case highlights that what was initially diagnosed as a psychiatric disorder was in fact a reversible environmental encephalopathy—underscoring the importance of physiological investigation when SEB is present.

Conclusion

Spindling excessive beta (SEB) represents a critical neurophysiological marker of cortical dysregulation identifiable on the EEG. While traditionally overlooked or misattributed solely to psychiatric disorders such as ADHD or anxiety, SEB’s presence often signals deeper neurobiological dysfunctions, including toxic encephalopathies, metabolic derangements, and subtle structural or genetic anomalies. As emerging research from Swatzyna et al. (2015, 2024) and others demonstrates, SEB is highly prevalent in refractory psychiatric cases and transcends traditional DSM-5 categories, being detected across ADHD, autism spectrum disorder (ASD), mood disorders, and PTSD. This finding underscores the need to move beyond symptom-based models and toward precision diagnostics grounded in neurophysiology.

Clinicians encountering SEB must resist premature diagnostic closure. Instead, comprehensive evaluation—including toxicology screening, metabolic profiling, sleep assessment, and advanced neuroimaging—should be prioritized to uncover correctable underlying causes. Treating SEB’s root contributors rather than its neurobehavioral consequences can dramatically alter clinical outcomes, often eliminating the need for long-term psychiatric medications. The identification of SEB thus exemplifies the principle that "testing the organ we are treating"—the brain—must become central to modern psychiatric and neurodevelopmental practice.

Key Takeaways

1. Spindling excessive beta (SEB) is a non-specific EEG biomarker indicating cortical dysregulation, not a psychiatric diagnosis.

2. SEB is highly prevalent in refractory cases of ADHD, ASD, anxiety, mood disorders, and PTSD, reflecting underlying neurobiological dysfunction rather than pure behavioral pathology.

3. Heavy metal toxicity, metabolic encephalopathy, chronic sleep disorders, and subtle genetic vulnerabilities must be considered in the differential diagnosis of SEB.

4. Certain medications—especially benzodiazepines, stimulants, and SSRIs—can worsen SEB and should be used cautiously in affected individuals.

5. Proper identification and treatment of SEB’s underlying causes can lead to full symptom resolution, reversing misdiagnoses and preventing unnecessary chronic psychiatric treatment.

Glossary

ADHD-RS: ADHD rating scale, a standardized assessment tool to quantify symptoms of attention-deficit/hyperactivity disorder, particularly impulsivity and inattention.

attention-deficit/hyperactivity disorder (ADHD): a neurodevelopmental disorder characterized by chronic inattention, hyperactivity, and impulsivity.

autism spectrum disorder (ASD): a neurodevelopmental condition characterized by impaired social interaction, repetitive behaviors, restricted interests, and often associated with neurophysiological abnormalities such as spindling excessive beta.

benzodiazepines: a class of psychoactive medications that enhance GABAergic inhibition, commonly used for anxiety but known to exacerbate beta activity on EEG, especially with prolonged use.

beta: EEG frequency band ranging from 13–30 Hz, associated with cortical activation and cognitive processing; excessive activity may indicate cortical hyperarousal.

bipolar disorder: a psychiatric condition characterized by alternating episodes of mania/hypomania and depression, frequently associated with cortical dysregulation detectable on EEG.

chelation therapy: medical treatment involving agents to bind and remove heavy metals (e.g., lead, mercury) from the body.

comprehensive metabolic panel: blood test assessing kidney function, liver function, electrolyte balance, and other metabolic parameters.

cortical dysregulation: disruption in normal cortical function, often reflected in abnormal eeg patterns like spindling excessive beta, linked to psychiatric and neurological disorders.

cortical excitability: increased responsiveness or reduced threshold of cortical neurons, which may manifest as enhanced beta frequency activity.

diffusion tensor imaging (DTI): an advanced MRI technique that evaluates structural integrity of white matter tracts, useful in assessing neurological conditions such as traumatic brain injury.

electroencephalographic (EEG): relating to the EEG, a method of recording electrical activity of the brain through scalp electrodes.

electrolytes: ions in the blood (e.g., sodium, potassium, chloride) critical for physiological processes and neurological functioning.

encephalopathy: generalized dysfunction or disease of the brain, identifiable through EEG abnormalities, including diffuse slowing or spindling, excessive beta.

epileptiform discharges: abnormal EEG patterns characteristic of epilepsy or subclinical seizure activity, such as spikes or sharp waves.

focal slowing: localized reduction in EEG frequency indicative of cortical dysfunction or structural brain lesions.

fluid-attenuated inversion recovery (FLAIR): MRI sequence enhancing visualization of brain lesions and structural abnormalities, especially in white matter.

functional testing: assessments used to evaluate physiological and biochemical processes, such as nutrient levels or toxin burden, to identify underlying conditions contributing to clinical symptoms.

GABA-A receptor genes: genes encoding gamma-aminobutyric acid (GABA) type-A receptors, genetic polymorphisms of which can influence cortical beta power.

generalized anxiety disorder: a psychiatric disorder marked by excessive, chronic worry and anxiety associated with cortical hyperarousal evident on the EEG.

heavy metal toxicity: poisoning due to exposure to metals such as lead or mercury, known to cause neurological dysfunction, including EEG abnormalities.

hepatic encephalopathy: cognitive dysfunction resulting from liver dysfunction, characterized by metabolic disturbances detectable via the EEG.

HSDQ: Holland Sleep Disorders Questionnaire, a tool to screen for various sleep disorders.

hyperarousal: heightened physiological and cortical activation, frequently seen in anxiety disorders and PTSD, detectable as elevated beta activity on the EEG.

hypoxic encephalopathy: neurological dysfunction resulting from inadequate oxygen supply to the brain, which may produce characteristic EEG changes.

impulse control: the ability to inhibit impulsive behaviors; impaired control correlates with EEG biomarkers such as spindling excessive beta.

isolated epileptiform discharges: discrete abnormal EEG waveforms indicative of subclinical seizure potential or cortical irritability.

magnetic resonance imaging (MRI): neuroimaging technique used to visualize brain structure in high resolution, important in evaluating structural abnormalities associated with EEG changes.

metabolic encephalopathy: neurological dysfunction caused by metabolic imbalances (e.g., electrolyte disturbances, renal or liver failure), associated with characteristic EEG abnormalities.

methylphenidate: stimulant medication commonly prescribed for ADHD, known to increase cortical excitability and beta frequency activity.

neuromodulation: therapeutic techniques (e.g., neurofeedback, transcranial magnetic stimulation) used to alter neural activity and cortical dysregulation.

neurophysiological markers: biological indicators of neurological function, such as specific EEG patterns (e.g., spindling excessive beta), used to assess underlying pathology.

neuropsychological assessment: structured evaluation of cognitive functions such as memory, attention, and executive function.

non-REM stage 2 sleep: a normal sleep stage characterized by sleep spindles (12–16 Hz) and K-complexes.

polymorphisms: genetic variations in DNA sequences influencing gene function and biological outcomes, such as cortical beta activity.

post-traumatic stress disorder (PTSD): psychiatric disorder triggered by trauma exposure, characterized by intrusive symptoms, hyperarousal, and associated EEG abnormalities.

precision medicine: a medical approach tailoring treatment to individual patient characteristics, informed by biomarkers like EEG patterns such as spindling excessive beta.

provoked urine heavy metal analysis: diagnostic procedure involving administration of a chelating agent prior to urine testing to detect elevated heavy metal levels.

PSQI: Pittsburgh Sleep Quality Index, a questionnaire assessing sleep quality and disturbances.

quantitative EEG (qEEG): an advanced EEG analysis technique providing statistical and spectral analysis of brain wave frequencies and spatial distributions.

renal encephalopathy: cognitive and neurological dysfunction resulting from kidney failure, characterized by specific EEG abnormalities.

selective serotonin reuptake inhibitors (SSRIs): antidepressant medications that increase cortical serotonin levels, occasionally exacerbating cortical beta power on the EEG.

spatial distribution: geographic pattern or scalp locations where EEG abnormalities are found, important in clinical interpretation of EEG patterns.

spectral power: quantitative measure of EEG wave amplitude within specific frequency bands, critical in qEEG analyses.

spindling excessive beta (SEB): an abnormal EEG phenomenon characterized by rhythmic, spindle-shaped bursts of beta frequency activity (13–30 Hz), indicative of cortical dysregulation.

stimulants: psychoactive drugs that increase cortical activity and alertness, potentially exacerbating EEG beta activity in susceptible individuals.

thyroid function testing: assessment of thyroid hormones (e.g., TSH, T3, T4), relevant in evaluating metabolic contributions to neurological dysfunction.

toxic encephalopathy: brain dysfunction due to toxin exposure (e.g., heavy metals), frequently characterized by specific EEG abnormalities like spindling excessive beta.

traumatic brain injury (TBI): physical brain injury resulting from external trauma, potentially disrupting cortical inhibitory-excitatory balance, leading to EEG abnormalities.

vitamin D: a fat-soluble nutrient important for neurological function, deficiency of which is associated with various cognitive and mood disorders.

waxing-and-waning: descriptive term indicating cyclical or rhythmic changes in amplitude characteristic of spindle-shaped EEG waveforms.

zinc: essential mineral involved in neuronal function and neurotransmission; deficiency can exacerbate cortical dysregulation detectable on the EEG.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596

Fisher, R. S., Scharfman, H. E., & deCurtis, M. (2014). How can we identify ictal and interictal abnormal activity? Epilepsia, 55(6), 87–93. https://doi.org/10.1111/epi.12528

Hughes, J. R., & John, E. R. (1999). Conventional and quantitative electroencephalography in psychiatry. Journal of Neuropsychiatry and Clinical Neurosciences, 11(2), 190–208. https://doi.org/10.1176/jnp.11.2.190

John, E. R., Ahn, H., Prichep, L., Trepetin, M., Brown, D., & Kaye, H. (1988). Developmental equations for the electroencephalogram. Science, 210(4475), 1255–1258. https://doi.org/10.1126/science.7433992

Krepel, N., van Dijk, H., Sack, A. T., Swatzyna, R. J., & Arns, M. (2021). To spindle or not to spindle: A replication study into spindling excessive beta as a transdiagnostic EEG feature associated with impulse control. Biological Psychology, 165, 108188. https://doi.org/10.1016/j.biopsycho.2021.108188

Nuwer, M. R. (1997). Assessment of digital EEG, quantitative EEG, and EEG brain mapping. Neurology, 49(1), 277–292. https://doi.org/10.1212/WNL.49.1.277

Olbrich, S., & Arns, M. (2013). EEG biomarkers in major depressive disorder: Discriminative power and prediction of treatment response. International Review of Psychiatry, 25(5), 604–618. https://doi.org/10.3109/09540261.2013.816269

Porjesz, B., Begleiter, H., Bihari, B., & Kissin, B. (2002). Event-related brain potentials in individuals at risk for alcoholism. Alcohol, 8(5), 335-339. https://doi.org/10.1016/0741-8329(91)90056-C

Swatzyna, R. J., Morrow, L. M., Collins, D. M., Barr, E. A., Roark, A. J., & Turner, R. P. (2024). Evidentiary significance of routine EEG in refractory cases: A paradigm shift in psychiatry. Clinical EEG and Neuroscience. https://doi.org/10.1177/15500594231221313

Swatzyna, R. J., Tarnow, J. D., Tannous, J. D., Pillai, V., Schieszler, C., & Kozlowski, G. P. (2014). EEG/QEEG technology identifies neurobiomarkers critical to medication selection and treatment in refractory cases. Journal of Psychology and Clinical Psychiatry, 1(7), 00046. https://doi.org/10.15406/jpcpy.2014.01.00046