Interpreting the Raw EEG: Occipital Intermittent Rhythmic Delta Activity (OIRDA)

Occipital Intermittent Rhythmic Delta Activity (OIRDA): A Developmental EEG Phenomenon with Clinical Nuance

Occipital intermittent rhythmic delta activity (OIRDA) is a well-characterized EEG pattern that typically appears in the pediatric population.

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OIRDA reflects a transient electrophysiologic signature of cerebral development, but one that can carry diagnostic weight in the context of certain epilepsy syndromes. OIRDA’s core features—rhythmicity, reactivity, and posterior localization—set it apart from pathological slow-wave activity. Yet, its interpretation hinges on the clinical backdrop in which it is found. In a healthy, neurologically intact child, OIRDA is a benign maturational variant that often requires no action.

But in a child presenting with staring spells, behavioral arrest, or suspected generalized seizures, OIRDA may point to underlying idiopathic generalized epilepsy. The tension between benignity and clinical significance makes OIRDA a pattern that demands contextual analysis, developmental awareness, and precision in interpretation.

The pediatric EEG offers a landscape that changes with age, brain maturation, and neurodevelopmental transitions. OIRDA, as a transient and age-dependent phenomenon, highlights this dynamism.

It typically emerges during early to mid-childhood, between the ages of 5 and 14, and typically disappears in adolescence. Unlike epileptiform discharges, which may persist into adulthood or herald chronic epilepsy, OIRDA often resolves as the occipital cortex and its thalamocortical connections mature. Thus, its presence offers not only a snapshot of current cerebral activity but also a developmental timeline that, when interpreted correctly, can aid in distinguishing between benign and pathologic processes.

Morphological and Physiological Basis of OIRDA

OIRDA is characterized by a distinct and reproducible set of electrographic features that enable its reliable recognition in pediatric EEG recordings.

Morphologically, OIRDA consists of rhythmic delta-frequency waveforms, typically in the range of 2 to 4 Hz, that appear intermittently in brief bursts.

These waveforms are maximal over the occipital scalp regions—particularly at electrodes O1 and O2—and frequently extend to adjacent posterior temporal and parietal channels.

The activity is bilaterally synchronous and symmetric, with each burst exhibiting a smooth, sinusoidal contour devoid of sharp deflections or complex morphology. The amplitude is moderate, typically ranging between 50 and 150 microvolts, and each run of activity exhibits a waxing and waning envelope that lasts several seconds. Raw EEG with OIRDA courtesy of Vogovitsyn and Sharkov (2020).

One of the defining features of OIRDA is its rhythmicity. Unlike polymorphic delta activity, which is irregular in both shape and timing, OIRDA maintains a consistent frequency and morphology within each episode. It also displays reactivity to eye opening—attenuating or disappearing when the eyes are opened and reappearing with eye closure or in relaxed wakefulness. This reactivity is a hallmark of physiologic occipital rhythms and distinguishes OIRDA from pathological occipital delta seen in structural or postictal conditions. The pattern typically emerges during drowsiness or calm wakefulness, in the absence of external visual stimuli.

From a physiological standpoint, OIRDA is believed to arise from cortical generators in the visual association areas, modulated by subcortical inputs, most notably the thalamus. The occipital cortex, highly interconnected with the thalamic relay nuclei, is particularly susceptible to transient rhythmic synchronization during developmental stages when thalamocortical circuits are still maturing. OIRDA is most commonly seen in children between the ages of five and fourteen and tends to disappear by late adolescence, reinforcing its role as a developmental electrophysiological marker. It is thought to represent a benign variant of posterior rhythm generation, reflecting temporarily heightened synchrony in the occipital cortex under thalamic modulation.

This developmental origin explains the benign nature of OIRDA in most neurologically normal children. However, in a subset of patients—particularly those with idiopathic generalized epilepsy—OIRDA may reflect an underlying susceptibility to abnormal thalamocortical synchronization. In these cases, OIRDA can appear alongside generalized spike-and-wave discharges or other interictal epileptiform activity. Although OIRDA itself is not epileptiform, its increased prevalence in patients with generalized epilepsies, especially childhood absence epilepsy, suggests that it may serve as an indirect indicator of cortical network instability or epileptogenic potential.

In conclusion, OIRDA is a well-formed, rhythmic, occipital delta pattern that reflects a transient developmental rhythm in the maturing brain. Its morphology—sinusoidal, bilateral, and reactive—places it among benign EEG variants when found in isolation. However, its physiological roots in thalamocortical circuitry, and its association with generalized epileptic syndromes in some contexts, lend it additional diagnostic importance. The key to interpreting OIRDA lies in integrating its electrographic features with the clinical history, neurological status, and broader EEG background.

Raw EEG Analysis

The above EEG segment presents a clear, classical example of OIRDA, a non-epileptiform yet clinically meaningful pattern most often seen in pediatric EEGs. The tracing reveals rhythmic, sinusoidal delta activity—approximately 2 to 3 Hz—that emerges abruptly and organizes into a well-formed, bilateral, and synchronous waveform. The activity is confined to the occipital regions, particularly evident in channels involving O1 and O2, including P3–O1, P4–O2, T5–O1, and T6–O2. The waveforms exhibit a smooth, sinusoidal contour, waxing and waning in amplitude over several seconds, while maintaining symmetry between the hemispheres. There is no evidence of phase reversal or sharp components, which confirms its non-epileptiform nature.

This rhythmic delta pattern is distinctly posterior and does not involve the frontal or central regions. The rest of the montage, particularly the anterior leads such as Fp1–F3 and Fp2–F4, remains electrically quiet during the burst, which further emphasizes the strictly occipital localization. The background EEG before and after the OIRDA episode appears well-organized and age-appropriate, with preserved posterior dominant rhythm (alpha activity), suggesting an otherwise normal record.

The presence of photic stimulation, as noted in the lower channel labels, is temporally near the emergence of the OIRDA, but the pattern does not appear to be photically driven. There is no photoparoxysmal response, and the morphology of the occipital delta is not time-locked to the photic stimuli, which reinforces the notion that this is a spontaneous rhythmic posterior pattern rather than a stimulus-induced phenomenon.

OIRDA is most commonly observed in children and is considered a benign age-related variant in neurologically normal individuals. It is frequently encountered during relaxed wakefulness or drowsiness and often disappears with eye opening or mental activation, though reactivity is not testable in this static image.

When seen in isolation, without clinical seizures or epileptiform discharges, OIRDA requires no intervention. However, in the context of seizure symptoms—such as brief behavioral arrests, staring spells, or confirmed absence seizures—OIRDA can serve as a supportive finding, particularly in idiopathic generalized epilepsies like childhood absence epilepsy.

Although not epileptiform in itself, OIRDA is more common in children with generalized epileptiform tendencies than in those without, and its presence should always prompt careful clinical correlation.

In summary, this EEG demonstrates a textbook pattern of OIRDA: bilateral, symmetric, rhythmic delta confined to the occipital regions, with sinusoidal morphology and no epileptiform features. Its appearance here is most likely benign, but its diagnostic weight depends entirely on the clinical context in which it occurs. In the hands of the informed clinician, it is a valuable clue—not a diagnosis, but a signal to interpret with care.

OIRDA as a Benign Variant in Healthy Children

In neurologically normal children, OIRDA is almost always a benign phenomenon. It tends to occur in the context of well-developed posterior dominant alpha rhythm and normal sleep-wake transitions. These children are typically brought for EEG evaluation due to nonspecific concerns such as headaches, family history of epilepsy, or incidental findings. When OIRDA is found in such individuals, without any coexisting epileptiform discharges or clinical seizures, it is considered a developmental pattern with no prognostic or diagnostic implication. Its frequency, amplitude, and morphology fall within predictable limits: 2 to 4 Hz, moderate amplitude (50–150 µV), and sinusoidal in shape.

The mechanism behind benign OIRDA is not entirely understood, but it is believed to reflect transient instability in the thalamocortical regulatory loops that govern occipital rhythms. During early childhood, these loops are still undergoing synaptic pruning and myelination. Rhythmic delta oscillations in the occipital regions may thus emerge as a transient byproduct of this developmental tuning. Supporting this view is the observation that OIRDA disappears in adolescence as alpha rhythm stabilizes and cortical excitability matures.

Benign OIRDA is reactive—it attenuates or disappears with eye opening and reappears during eye closure or light drowsiness. This reactivity mirrors the behavior of the normal alpha rhythm, providing additional reassurance that the activity is physiologic. Importantly, benign OIRDA never occurs in isolation from a normal background; the rest of the EEG should show age-appropriate features, including symmetric alpha rhythm, normal sleep architecture if present, and absence of focal or generalized epileptiform discharges.

In such cases, the identification of OIRDA should be followed by reassurance to the family, and no further testing or treatment is required. This is an important point for general pediatricians and non-neurologist clinicians:

OIRDA, when encountered in the EEG report of a neurologically normal child, does not in itself warrant anti-seizure medications, imaging, or repeat EEG unless other clinical concerns exist.

OIRDA in the Context of Epilepsy Syndromes

The benign nature of OIRDA shifts significantly when seen in the setting of idiopathic generalized epilepsies, particularly childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), and other forms of primary generalized epilepsy. In these children, OIRDA often coexists with generalized spike-and-wave discharges or may precede them in the course of the disease. Its presence should raise a flag for the clinician to probe more deeply into subtle seizure symptoms, such as behavioral arrest, inattentiveness, staring spells, automatisms, or brief interruptions in activity. Parents may report “blank spells” or episodes of unresponsiveness lasting a few seconds. In this context, OIRDA is no longer incidental—it becomes a soft electrographic clue that further investigation is warranted.

Several features distinguish OIRDA with epileptogenic significance from the benign variant. First, it may show asymmetry, either in amplitude or duration, with one occipital lead demonstrating a more prominent discharge. Second, the rhythmic delta may show higher amplitude than expected (>150 µV), raising concern for cortical irritability. Third, it may persist into adolescence or adulthood in patients with active epilepsy, which is atypical for the benign form. Lastly, it is often recorded in close proximity to generalized discharges, or is provoked during periods of hyperventilation or drowsiness—states that are known to precipitate absence seizures.

When these features are present, the EEG should be interpreted in conjunction with the clinical presentation. If generalized spike-and-wave activity is present, the diagnosis of idiopathic generalized epilepsy is straightforward. In more ambiguous cases, an extended EEG, including sleep, hyperventilation, and photic stimulation, may help unmask subtle epileptiform activity. Ambulatory or video EEG monitoring may also be indicated if clinical events are frequent but electrographically elusive.

It is also important to emphasize that OIRDA does not meet the criteria for an epileptiform pattern on its own. It is a rhythmic, non-sharp, sinusoidal delta activity.

However, its presence in a seizure-prone child, particularly when associated with abnormal clinical behaviors, raises the index of suspicion and should guide the decision to initiate further diagnostic and therapeutic steps.

Differentiating OIRDA from Other Posterior Delta Patterns

The posterior EEG territory can exhibit a variety of slow-wave phenomena, and careful differentiation is crucial to prevent diagnostic errors.

Among the most common confounders is posterior slow waves of youth (PSWY). This pattern, also seen in children, consists of polymorphic, non-rhythmic delta activity superimposed on the alpha rhythm.

Unlike OIRDA, PSWY is irregular in frequency and shape, lacks a waxing and waning envelope, and is not composed of sinusoidal waves. It is also reactive, but its irregular morphology makes it easier to distinguish with experience. PSWY is benign and, like OIRDA, does not require further intervention.

Another important differential is occipital polymorphic delta activity, which may reflect underlying structural pathology in the occipital cortex, such as a tumor, an infarct, cortical dysplasia, or postictal slowing. This activity is typically irregular, non-rhythmic, and non-reactive to eye opening. It may be asymmetric and may persist during alert wakefulness, unlike OIRDA. Structural correlates are often evident on MRI, and the EEG must be interpreted in light of these findings.

Finally, eye movement artifacts—particularly those related to vertical eye motion or blinks—can contaminate the occipital leads with slow waves. However, these are usually frontally predominant, brief, and time-locked to EOG channels. They do not show the rhythmic sinusoidal morphology or occipital confinement of true OIRDA. Proper electrode placement and use of polygraphic channels (EOG) help eliminate this confusion.

A precise understanding of these differences allows clinicians to interpret OIRDA accurately, avoid over-treatment, and recognize when it carries real diagnostic weight.

Clinical Integration and Longitudinal Perspective

OIRDA should never be interpreted in a vacuum. Its true significance emerges only when viewed in the context of the child’s clinical history, developmental profile, and the rest of the EEG. The clinician must ask: is this a normal child with no history of seizures or cognitive concerns? Or is this a child with subtle episodes, behavioral pauses, or school decline that may suggest an idiopathic epilepsy syndrome? EEG is a powerful diagnostic tool, but its value lies in its integration with the patient’s lived experience.

Over time, OIRDA tends to fade as the child matures. In those without epilepsy, it may disappear completely by adolescence, reflecting the stabilization of thalamocortical circuitry. In children with generalized epilepsy, it may persist longer, especially if seizures remain active. For this reason, serial EEGs may help track disease progression or remission, particularly when correlated with clinical response to antiseizure therapy.

The educational role of the clinician is also crucial in this context. Parents who are told their child’s EEG shows “rhythmic delta activity” may be alarmed unless this finding is explained carefully.

A clear distinction must be made between epileptiform activity and benign variants. Overdiagnosis can lead to unnecessary medications, imaging, and emotional burden. Under-recognition, on the other hand, can delay the diagnosis of an epilepsy syndrome that responds well to early treatment.

Critical Information for Clinicians

OIRDA's significance is not intrinsic to the waveform itself, but is determined entirely by the clinical context. OIRDA can be either benign or pathologic, and misinterpreting it in either direction has consequences—ranging from unnecessary treatment and parental anxiety to missed diagnoses of epilepsy in children who would benefit from early intervention. OIRDA requires careful interpretation, not reflexive action.

First and foremost, we wish clinicians knew that OIRDA is not an epileptiform discharge. It does not reflect hyperexcitability or paroxysmal depolarization, and in isolation, it is not a seizure pattern.

It should not trigger antiepileptic prescription unless accompanied by definitive epileptiform features—such as generalized spike-and-wave discharges—or clear clinical seizures. We have seen children started on levetiracetam or valproic acid based solely on the presence of OIRDA on EEG, with no supporting clinical or electrographic evidence of epilepsy. This practice is not only unnecessary but potentially harmful, exposing children to cognitive, behavioral, and metabolic side effects without cause.

Second, we wish clinicians treating children would take time to clarify the neurologic history before acting on an EEG report that includes OIRDA. The presence of OIRDA in a healthy, alert, seizure-free child with a normal neurological examination almost always represents a benign maturational pattern, particularly if the rest of the EEG background is normal and there are no coexisting epileptiform discharges. In such cases, reassurance—not medication—is the appropriate response. Communicating this clearly to families helps avoid reinforcing fear or stigma surrounding normal childhood EEG findings.

Third, in children who do have seizure-like symptoms—particularly brief staring spells, unresponsiveness, or behavioral arrests—the presence of OIRDA should not be dismissed as benign, especially if it shows asymmetry, high amplitude, or persistence beyond early adolescence. In these scenarios, OIRDA should be seen as a potential marker of idiopathic generalized epilepsy, most often childhood absence epilepsy or juvenile absence epilepsy. Clinicians should investigate further with a thorough seizure history, sleep-deprived EEG, and potentially video EEG monitoring to capture events and confirm the diagnosis. If generalized spike-and-wave activity is identified, appropriate antiepileptic therapy should be initiated, often with ethosuximide, valproic acid, or lamotrigine, depending on the seizure type and clinical profile.

Fourth, we wish more clinicians understood the age-dependent nature of OIRDA. In healthy children, it is a transient developmental finding that typically resolves by adolescence. Its persistence into late adolescence or adulthood is unusual and, if present, should prompt a search for ongoing epilepsy, cortical abnormalities, or atypical maturational trajectories. Conversely, its appearance in younger children (<3 years) or adults is rare and should not be assumed to be OIRDA without careful scrutiny—it may represent polymorphic delta activity, artifact, or other pathology.

Finally, we wish that referring physicians would view EEG findings, such as OIRDA, as one piece of a larger clinical picture. EEG is not a test that gives yes-or-no answers about seizure disorders. It is a tool of physiologic inference, and its patterns only acquire meaning in the presence of good clinical history, developmental understanding, and a nuanced diagnostic framework. The knee-jerk prescription of anticonvulsants based on ambiguous or benign EEG patterns is one of the most avoidable errors in pediatric neurology.

When OIRDA is interpreted with precision and integrated into the full clinical picture, it becomes a useful developmental marker, and in certain cases, a helpful pointer to generalized epilepsy. But when misunderstood or misapplied, it can lead to overdiagnosis, overtreatment, or diagnostic complacency. We want clinicians to ask not just what the EEG shows, but what it means in the child sitting in front of them. That’s how OIRDA fulfills its diagnostic potential—not as an isolated rhythm, but as part of a child’s neurological story.

The Clinician Detective's Challenge

OIRDA is not just a waveform—it is a clue. It appears quietly in the background of pediatric EEGs, rhythmic and symmetrical, unassuming in its morphology, and often overlooked. But for the attentive clinician, OIRDA invites inquiry. It poses a question rather than offers an answer. Is this the sign of healthy cerebral maturation, or is it the soft footprint of an evolving generalized epilepsy? The task of the clinician is to interpret OIRDA not in isolation, but as part of a broader neurophysiologic landscape—one shaped by age, symptoms, developmental history, and the rest of the EEG.

Like all good clinical clues, OIRDA is a subtle indicator. It does not shout with spikes or sharp waves. It doesn’t demand immediate treatment or signal an emergency. Instead, it waits—rhythmic, reactive, and revealing—only to those who know what they’re looking for. In a child with no seizures, no neurologic symptoms, and a normal background, OIRDA may be a benign maturational rhythm, a brief developmental echo of thalamocortical synchrony. But in another, it may be the earliest hint of childhood absence epilepsy, especially if accompanied by clinical events or coexisting generalized discharges. Its diagnostic value lies not in its appearance, but in its context—the hallmark of any meaningful clinical sign.

The clinician detective does not respond to OIRDA reflexively. They resist the urge to prescribe antiseizure medication simply because the EEG carries a label. They also avoid the mistake of dismissing it as irrelevant. Instead, they ask: Who is this child? What brought us to this EEG? What are the parents seeing? What else does the recording show?

In this framework, OIRDA becomes what it truly is—a physiologic message requiring interpretation, not categorization. The EEG becomes a witness, not a verdict.

This is the essence of the clinician’s task—not to react to every pattern, but to recognize what deserves pursuit, what warrants reassurance, and what must be watched.

OIRDA teaches restraint and discernment. It reminds us that not every wave is pathology, and not every benign variant is harmless. Like any good clue, it sharpens our clinical reasoning, not by answering the question, but by asking the right one.

Key Takeaways

1. OIRDA is a rhythmic 2–4 Hz occipital delta pattern typically seen in children and often represents a benign maturational EEG variant.

2. In isolation and with a normal neurological exam, OIRDA does not indicate epilepsy and does not warrant antiepileptic treatment.

3. When associated with clinical seizures or generalized spike-and-wave discharges, OIRDA may support a diagnosis of idiopathic generalized epilepsy, such as childhood absence epilepsy.

4. Key distinguishing features of OIRDA include its occipital localization, rhythmic sinusoidal morphology, bilateral symmetry, and reactivity to eye opening.

5. Clinical context is essential—OIRDA must be interpreted alongside history, developmental status, and background EEG features to determine its significance.

Glossary

alpha rhythm: a normal EEG rhythm of 8–13 Hz observed in the posterior head regions during relaxed wakefulness with eyes closed; considered a marker of intact thalamocortical function in older children and adults.

amplitude: the voltage of an EEG waveform, measured in microvolts (µV); reflects the degree of synchrony in underlying neuronal activity.

anterior-to-posterior lag: a temporal delay in the appearance of an EEG waveform as it moves from anterior to posterior regions; commonly seen in triphasic waves and indicative of subcortical rhythm propagation.

artifact: any non-cerebral signal captured by EEG, such as eye movement, muscle activity, or electrical interference; must be distinguished from true cortical signals to avoid misinterpretation.

background activity: the baseline rhythmic activity seen in an EEG, usually referring to the posterior dominant rhythm; assessment of this helps determine overall cerebral function.

benign variant: A non-pathologic EEG pattern that may deviate from adult norms but is normal for a specific age or state; examples include OIRDA and posterior slow waves of youth.

bilateral symmetry: a characteristic of EEG patterns that appear equally on both hemispheres; suggests generalized rather than focal cortical involvement.

cortical generators: brain regions in the cerebral cortex that produce rhythmic electrical activity observable on the scalp EEG.

delta activity: EEG waveforms with frequencies between 0.5 and 4 Hz; normal during deep sleep but often abnormal when seen in awake adults or diffusely during encephalopathy.

diencephalon: a midline brain structure comprising the thalamus and hypothalamus; often implicated in the generation of rhythmic EEG activity and in disorders associated with FIRDA and triphasic waves.

electrooculography (EOG): a technique for recording eye movements using electrodes placed near the eyes; helps distinguish ocular artifacts from cerebral EEG activity.

encephalopathy: a general term for diffuse brain dysfunction, typically due to metabolic, toxic, or systemic causes; associated EEG findings may include generalized slowing or triphasic waves.

epileptiform: refers to EEG features such as spikes or sharp waves that are associated with an increased risk of seizures.

eye movement artifact: slow-frequency signals caused by eye motion, especially blinks or vertical movements; can mimic delta activity if not properly identified using EOG leads.

frontal intermittent rhythmic delta activity (FIRDA): an abnormal EEG pattern consisting of rhythmic 1–3 Hz delta waves over the frontal regions; seen in subcortical dysfunction and various encephalopathies.

generalized spike-and-wave: a common epileptiform pattern in idiopathic generalized epilepsy, consisting of synchronous spike-and-slow wave complexes occurring across the entire scalp.

hyperventilation: a common EEG activation procedure that can provoke generalized discharges, particularly in absence epilepsy.

idiopathic generalized epilepsy: a group of genetically mediated epilepsy syndromes without structural brain abnormalities, characterized by generalized discharges and typically normal development.

ictal: refers to the period during a seizure, characterized by evolving rhythmic or spike activity on EEG.

intermittent: describes activity that occurs in sporadic bursts rather than continuously; a feature of patterns such as OIRDA and FIRDA.

neuronal synchrony: a state in which groups of neurons fire together rhythmically, producing measurable EEG waveforms such as delta or alpha rhythms.

occipital intermittent rhythmic delta activity (OIRDA): a rhythmic delta activity seen over the occipital regions in children; often benign but may be associated with idiopathic generalized epilepsy.

parieto-occipital region: the area at the junction of the parietal and occipital lobes; a common site for pediatric rhythmic activity such as OIRDA.

paroxysmal: describes EEG activity that appears suddenly and often episodically, such as epileptiform discharges.

phase reversal: a point in bipolar EEG montage where the polarity of waveforms in adjacent electrodes changes direction, indicating a focal source of activity.

photoparoxysmal response: an abnormal EEG reaction to photic stimulation, typically characterized by spike-and-wave or polyspike activity; often seen in photosensitive epilepsy.

photic stimulation: A procedure during EEG in which flashing lights are used to activate occipital and generalized cortical responses; helps detect photosensitive epilepsy.

physiologic rhythm: a normal EEG rhythm generated by healthy brain networks, such as alpha rhythm or sleep spindles; contrasts with pathological slowing or epileptiform activity.

posterior dominant rhythm: the alpha rhythm seen over occipital leads during relaxed wakefulness with eyes closed; serves as an indicator of alertness and cortical integrity.

posterior slow waves of youth: a benign EEG pattern seen in children and adolescents, characterized by irregular delta waves superimposed on the posterior alpha rhythm.

reactivity: the ability of EEG rhythms to change in response to external stimuli such as eye opening, alerting, or tactile input; suggests preserved cerebral responsiveness.

rhythmicity: the regular, repeating nature of an EEG waveform, with consistent frequency and morphology; a key feature in patterns like OIRDA and triphasic waves.

sinusoidal waveform: a smooth, repetitive wave shape that defines many physiologic EEG rhythms, such as OIRDA; contrasts with sharp, jagged epileptiform patterns.

subcortical structures: brain regions located beneath the cerebral cortex, including the thalamus and basal ganglia; involved in the generation of rhythmic EEG activity in both normal and pathological states.

thalamocortical circuit: the network connecting the thalamus with the cerebral cortex; central to the generation of rhythmic EEG patterns and implicated in conditions such as absence epilepsy and metabolic encephalopathy.

triphasic waves: a distinctive EEG pattern consisting of a three-phase waveform, commonly seen in metabolic encephalopathies such as hepatic or uremic encephalopathy.

waveform morphology: the shape and structure of EEG waveforms, including features such as phase, polarity, frequency, and amplitude; essential for accurate EEG interpretation.

References

Ebersole, J. S., & Pedley, T. A. (2003). Current practice of clinical electroencephalography (3rd ed.). Lippincott Williams & Wilkins.

Niedermeyer, E., & da Silva, F. L. (2017). Electroencephalography: Basic principles, clinical applications, and related fields (7th ed.). Oxford University Press.

Nogovitsyn, V., & Sharkov, A. (2020). EEG in genetic generalized epilepsies. Epilepsy and Paroxysmal Conditions,12(1S), 23-40.

https://doi.org/10.17749/2077-8333.2020.12.1S.S23-S40

Panayiotopoulos, C. P. (2007). The epilepsies: Seizures, syndromes and management. Bladon Medical Publishing. https://doi.org/10.1007/978-1-84628-644-5

About the Author

Fred Shaffer earned his PhD in Psychology from Oklahoma State University. He earned BCIA certifications in Biofeedback and HRV Biofeedback. Fred is an Allen Fellow and Professor of Psychology at Truman State University, where has has taught for 50 years. He is a Biological Psychologist who consults and lectures in heart rate variability biofeedback, Physiological Psychology, and Psychopharmacology. Fred helped to edit Evidence-Based Practice in Biofeedback and Neurofeedback (3rd and 4th eds.) and helped to maintain BCIA's certification programs.

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