How Benzodiazepines Affect the EEG

If you record enough EEGs, you eventually meet the benzodiazepine (BZD) signature. The patient looks calm, the tracing looks faster than usual, and the familiar posterior alpha rhythm feels washed out. That impression is not a mirage.

The story of “drug effects on the EEG” is nearly as old as modern electroencephalography itself. By the mid‑1970s, pharmaco‑EEG studies had already mapped characteristic spectral shifts produced by common anxiolytics: single oral doses of diazepam and bromazepam reliably increased fast activity above 13 Hz while attenuating posterior alpha—changes that closely tracked blood levels (Fink, Weinfeld, Schwartz, & Conney, 1976).

Later reviews and demonstrations consolidated the pattern, situating benzodiazepines among the most consistent “beta activators” on waking scalp EEG (Blume, 2006). At the neuronal level, GABA-𝐴 receptor modulation by BZDs dampens excitability and alters thalamo‑cortical dynamics, with predictable consequences in the beta and low‑gamma ranges (Lozano‑Soldevilla, 2018). These antecedents frame what you should expect today when you sit down to read a waking EEG in someone on a benzodiazepine: more fast activity—often frontocentral, often symmetric—and a background in which classical posterior alpha may be subdued.

Increased beta activity and decreased alpha/theta power are hallmark EEG changes after benzodiazepine administration, observed in both acute and chronic use (Bang et al., 2022; Friedman et al., 1992; Hotz et al., 2000; Nutt et al., 2015). QEEG studies confirm that BZDs induce a regular, smoothly formed beta rhythm, especially over frontal regions, regardless of sedation or tolerance (Bang et al., 2022; Nutt et al., 2015). Across the class, benzodiazepines tend to elevate fast beta activity while softening alpha, most clearly during relaxed wakefulness with eyes closed or quietly open (Buchsbaum et al., 1985; Fink, Weinfeld, Schwartz, & Conney, 1976; Yamadera, Kato, Ueno, Tsukahara, & Okuma, 1993). Technologists see it as a diffuse shimmer of low-to-moderate amplitude fast waves. Interpreters see it as a medication effect that can dominate the record unless you explicitly look for it.

Two Pharmacokinetic Families

Two pharmacokinetic families help you predict how long the EEG will wear that signature. The long-acting agents, such as diazepam (Valium), clorazepate (Tranxene), and clonazepam (Klonopin), have long half-lives or active metabolites that linger. Intermediate-acting drugs such as Lorazepam (Ativan), oxazepam (Serax), temazepam (Restoril), and alprazolam (Xanax), usually leave briefer EEG footprints that track more closely with the dosing window. Their EEG imprint can persist across recording sessions and even into the next day, especially with diazepam or clorazepate where nordazepam extends exposure (StatPearls overview).

Long-Acting Benzodiazepines

Consider diazepam (Valium) first, because it anchors the classic pattern. Controlled pharmaco-EEG mapping shows that within a few hours of a standard oral dose, relative beta power rises broadly while alpha power falls, and absolute theta often does not increase when vigilance is held steady.

Long-acting BZDs (e.g., flurazepam, diazepam) produce sustained increases in beta power and more persistent reductions in slow-wave activity, with effects sometimes lasting into withdrawal nights (Borbély et al., 1983; Friedman et al., 1992; Hartman et al., 2020).

Topographic displays emphasize reduced occipital alpha with more beta over central and parietal regions, which matches the clinical look of a faster, flatter background during wakefulness (Buchsbaum et al., 1985; Fink et al., 1976; Yamadera et al., 1993). Connectivity can shift as well.

One study found that diazepam increased interhemispheric beta correlations and reorganized frontal coupling, with some sex differences in the balance of alpha and theta changes (Romano-Torres, Borja-Lascurain, Chao-Rebolledo, del-Río-Portilla, & Corsi-Cabrera, 2002).

The take-home for practice is that diazepam reliably pushes the spectrum toward beta and away from alpha without necessarily adding generalized slowing when the patient remains alert.

Clorazepate (Tranxene) tells a similar story in anxious outpatients treated over one to two weeks. Topographic EEG demonstrated decreased occipital alpha and parietal delta with increased beta distributed over posterior-frontal and central areas. Clinically, that reads like anxiolysis without frank sedation, and it reminds you not to overcall symmetric, medication-related fast activity as muscle artifact (Buchsbaum et al., 1985).

Clonazepam (Klonopin) adds a twist in activation procedures. During hyperventilation, healthy controls typically show negative DC shifts and surges of alpha and theta. Clonazepam dampens those responses, reducing the DC shifts and preventing the expected alpha or theta increase while introducing beta activity at modest plasma levels (Rockstroh, 1990). If your patient is taking clonazepam, a flat hyperventilation trial may be a drug effect rather than an indicator that your activation was ineffective.

Intermediate-Acting Benzodiazepines

Intermediate-acting agents (e.g., temazepam, flunitrazepam) also increase beta and reduce slow-wave power, but these effects are generally shorter-lived and less pronounced after discontinuation (Arbon et al., 2015; Borbély et al., 1983; Tan et al., 1998; 2003).

Lorazepam (Ativan), oxazepam (Serax), temazepam (Restoril), and alprazolam (Xanax), usually leave briefer EEG footprints that track more closely with the dosing window (StatPearls overview). That time course matters when you are deciding whether a surprising power spectrum reflects the brain or the pharmacy.

Intermediate-acting agents can look different when you zoom in on microstructure. Lorazepam (Ativan), in a careful EEG and MEG classification study, reduced the proportion of alpha and fast-theta patterns while increasing delta, slow-theta, mixed delta–beta, and polyrhythmic segments. The authors did not find an independent rise of beta power in that analytic framework, which underscores that what you observe depends on both the drug and the method you use to quantify it (Fingelkurts et al., 2004).

Oxazepam (Serax), tested at 20 and 40 mg in a placebo-controlled crossover, reduced alpha-1 power and modulated beta-1 in ways that tracked behavioral vigilance and event-related potentials, reinforcing the state-sensitivity of these effects (van Leeuwen et al., 1995).

Alprazolam (Xanax), finally, highlights connectivity rather than power. At clinically relevant exposures it decreases linear coupling and increases nonlinear couplings across the scalp, with a dose–concentration relationship that suggests broad network reconfiguration during quiet wakefulness (Alonso, Mañanas, Romero, Hoyer, Riba, & Barbanoj, 2010).

These nuances point to a simple operating rule for both raw EEG and qEEG: band-power changes under benzodiazepines are consistent in direction for alpha and beta, but theta and delta depend on dose, vigilance, and analytic approach. In well-controlled resting recordings with the patient clearly awake, long-acting agents often leave theta and delta relatively unchanged.

In paradigms that admit drowsiness drift, or in microstructural approaches that classify transient patterns, slow activity becomes more prominent, especially with lorazepam (Fingelkurts et al., 2004; Yamadera et al., 1993). This is why vigilance control is not optional. Following IPEG guidance on stable eyes-closed and eyes-open epochs, consistent referencing, careful artifact control, and transparent preprocessing lets your conclusions rest on the brain rather than the methodology (Jobert et al., 2012).

A Practical Guide

What to document up front (matters for interpretation).

Begin by recording the benzodiazepine agent, route, approximate timing and size of the most recent dose(s), and whether dosing was scheduled or as‑needed; this information frames what you expect to see on the EEG.

At light to moderate effect, BZDs characteristically augment symmetric frontocentral beta activity and attenuate the posterior dominant rhythm (PDR), whereas deeper sedation progresses to generalized theta–delta slowing and, at anesthetic levels or in the ICU, may reach discontinuity or burst‑suppression (Brown et al., 2010; Smith, 2005).

Document the behavioral state, including the level of arousal and any recent sleep deprivation, because drowsiness modulates both alpha and beta expression.

Record concurrent sedatives or analgesics—opioids, propofol, dexmedetomidine, ketamine—because pharmacodynamic interactions can reshape the background and reactivity (Brown et al., 2010). Pretest probability is the likelihood of a condition before a test is administered, that is, the chances of a condition based on knowing only its likelihood in the population from which the subject is taken (e.g., chances that a person has tonic-clonic seizures based on knowing only that they come from the general population). Depending on the pretest probability, and how sensitive and specific a test is, a test result must be interpreted differently.

Finally, specify the clinical question (e.g., spell classification, epilepsy localization, or encephalopathy assessment); pretest probability determines how you weigh borderline patterns and whether you prioritize seizure capture, structural slowing, or reactivity (Hirsch et al., 2013; Smith, 2005).

Acquisition parameters that help (and won’t hide BZD effects).

Acquire from the outset in both referential and bipolar montages. A quiet non‑cephalic reference (when available) makes anterior fast activity easier to appreciate, while longitudinal and transverse bipolar chains test physiologic fields and guard against misinterpreting artifact as “seizure” (Hirsch et al., 2013; Smith, 2005).

Use a high‑pass (low‑frequency) filter at approximately 0.5–1 Hz to preserve slow components and a low‑pass (high‑frequency) filter at 70–100 Hz so that BZD‑related beta (typically 18–30 Hz) is not attenuated; reserve the notch filter for true line‑noise problems, as notch can distort fast activity and mask diagnostically useful beta (Smith, 2005).

Sampling rates of at least 200–256 Hz are acceptable for routine studies, with ≥500 Hz preferred when spike detail matters. Starting sensitivities of 7–10 μV/mm at a 10–15 s/page time base are reasonable, with adjustments to reveal fields and morphology as needed.

Keep impedances below 5 kΩ and balanced within roughly 1–2 kΩ to optimize the low‑amplitude fast activity that BZDs accentuate (Smith, 2005).

The benzodiazepine “signature” on waking EEG—how it looks and how to verify it.

What, concretely, should you anticipate on the benzodiazepine tracing? In alert wakefulness, the most reproducible signature is increased low‑to‑mid beta activity that is broadly distributed yet typically most prominent frontocentrally, low‑to‑medium in amplitude, and strikingly symmetric. These characteristics are robust across laboratory and bedside contexts and have been replicated in pharmacologic and behavioral paradigms (Blume, 2006; Fink et al., 1976; van Lier, Drinkenburg, van Eeten, & Coenen, 2004).

At the same time, the posterior alpha background often appears attenuated in amplitude even if the peak frequency remains in the alpha range (Fink et al., 1976; Lozano‑Soldevilla, 2018). In some patients you may notice brief runs of “spindling” beta—spindle‑shaped, rhythmic bursts in the 18–26 Hz range, frequently anterior‑weighted and bilateral—which historically have been associated with sedative‑hypnotics including benzodiazepines (Blume, 2006).

With deeper sedation, fast activity may coexist with mild background slowing—an effect long recognized with many antiseizure and sedative drugs (Blume, 2006).Under light to moderate BZD effect, expect symmetric, frontocentral‑predominant, low‑amplitude beta often clustered in spindle‑like bursts around 18–26 Hz. The PDR remains present but may be partially attenuated; physiologic eye‑opening attenuation of posterior alpha should still be demonstrable unless sedation is deep (Brown et al., 2010; Smith, 2005).

As dose or susceptibility increases, the background slows into generalized theta and delta, and at ICU‑level sedation, discontinuity or burst‑suppression can appear; in parallel, interictal epileptiform activity may be reduced given the GABA‑A–mediated anticonvulsant action of BZDs (Brown et al., 2010; Smith, 2005).

To confirm that fast activity is cortical beta rather than artifact, evaluate topography, bandwidth, and behavior. Cortical beta is typically symmetric and maximal over frontocentral regions, with a relatively narrow‑band rhythmic quality; by contrast, EMG is broad‑band, irregular, often asymmetric, and accentuated over frontotemporal or jaw leads.

Simple bedside maneuvers—asking the patient to relax the forehead and jaw or to open the mouth briefly—reduce EMG but spare cortical beta. Finally, ensure that the pattern maintains a plausible physiologic field across montage changes; electrode pops and line noise usually do not (Smith, 2005).

A stepwise reading workflow tailored to BZD exposure.

On first pass, establish the state (awake versus drowsy) and test reactivity with standardized eye-opening and closure tests.

Describe the PDR—its frequency, symmetry, and reactivity—and note the presence, symmetry, and persistence of anterior beta superimposed upon the waking background. Comment on continuity and on whether slowing, if present, is generalized or focal (Brown et al., 2010; Hirsch et al., 2013; Smith, 2005).

During the second pass, adjudicate artifacts versus physiology. Fast frontal “hash” warrants deliberate separation of BZD‑related beta from EMG using the maneuvers above; also screen for EOG, ECG, line noise, and breach rhythm over skull defects, which can mimic focal fast activity but usually has clear localization and higher amplitude (Smith, 2005).

One of your most important jobs during review is to separate medication‑related fast activity from myogenic artifact. EMG contamination is common, broadband, and can extend down into alpha and even delta ranges; weak facial muscle activation can masquerade as cerebral beta across much of the scalp (Goncharova, McFarland, Vaughan, & Wolpaw, 2003; Muthukumaraswamy, 2013; Shackman, McMenamin, Slagter, Maxwell, Greischar, & Davidson, 2009).

Several pragmatic tests help. First, look for distribution and morphology: benzodiazepine‑related beta is typically rhythmic or quasi‑rhythmic, often frontocentral, and shows a coherent field across montages, whereas EMG tends to be fragmented, irregular, and maximal at edge electrodes, especially over frontalis and temporalis (Goncharova et al., 2003; Muthukumaraswamy, 2013). Second, check reactivity: have the patient relax the jaw, swallow, or briefly change facial tone; EMG often drops out abruptly, while medication‑related beta persists (Shackman et al., 2009). Third, avoid “fixing” the display with aggressive high‑frequency filtering; over‑attenuation not only degrades legitimate fast activity but also risks morphing muscle into spike‑like transients (Sinha et al., 2016). If artifact remains a major confound, annotate it clearly; you can also examine higher‑density montages for spatial clues or, where appropriate, apply artifact‑focused offline methods—but interpret denoised segments cautiously and document any processing (Shackman et al., 2009; Muthukumaraswamy, 2013).

On the third pass, search for epileptiform activity and other abnormalities. Recognize that BZDs can suppress spike yield—particularly generalized spike–wave—so consider extending recording, capturing drowsiness or stage N2 sleep, and employing multiple montages to improve sensitivity when the clinical question requires it (Smith, 2005).

In encephalopathic patients, apply standardized ACNS terminology for rhythmic and periodic patterns (e.g., GPDs, LPDs, GRDA/LRDA with appropriate modifiers), and privilege spatiotemporal evolution when diagnosing seizures along the ictal–interictal continuum; heavy BZD exposure can slow, fragment, or suppress such patterns and should be weighed in interpretation (Hirsch et al., 2013).

Technician‑level, practical operations—what to do and what to avoid.

Technologists should annotate the exact timing of eyes‑open/closed periods, photic stimulation (if used), and any tactile or auditory stimuli, together with observed behavioral responses, because reactivity helps distinguish drug effect from encephalopathy (Hirsch et al., 2013).

Coaching relaxation of forehead, jaw, and neck muscles reduces EMG contamination and unmasks genuine cortical beta (Smith, 2005). When clinically safe, capturing early drowsiness can increase the diagnostic yield for interictal discharges even in the presence of BZDs (Smith, 2005).

Impedances should be verified and optimized at setup and as needed during the study to preserve low‑amplitude fast rhythms. Conversely, avoid default application of notch filtering; address line noise first by improving reference and ground connections.

Do not overfilter—e.g., avoid high‑pass settings above ~1 Hz that erase slow components and artificially sharpen transients.

Finally, refrain from labeling persistent fast frontal activity as ictal without demonstration of evolution and a physiologic field, and remember that triphasic‑appearing generalized periodic discharges are not pathognomonic of metabolic disease and must be interpreted within the sedation context and with attention to reactivity (Hirsch et al., 2013; Smith, 2005).

Interpretation and reporting pearls.

In routine reports, it is appropriate to explicitly attribute typical features to BZD exposure when the pattern and clinical information align. For example, one might write: “Continuous waking background with symmetric frontocentral beta activity consistent with benzodiazepine effect; posterior dominant rhythm 10 Hz with normal reactivity,” thereby acknowledging the sedation‑related signature while preserving standard descriptors (Brown et al., 2010; Smith, 2005).

Benzodiazepines can also change what you do not see.

Because they enhance GABAergic inhibition, they may suppress interictal epileptiform discharges (IEDs) or raise the threshold for activation during brief routine studies. Thus, absence of spikes on a BZD‑exposed tracing does not exclude an epileptic tendency, and ACNS‑style wording in the Impression and Clinical Correlation should make that clear (Tatum et al., 2016).

Where the diagnostic question hinges on interictal expression—pre‑surgical evaluation, epilepsy classification, or suspected photosensitivity—consider whether a repeat EEG after safe, clinician‑supervised medication adjustments would be informative; if so, recommend that option in neutral, non‑directive language (Blume, 2006; Tatum et al., 2016).

Conversely, in certain sleep‑potentiated epileptic encephalopathies, high‑dose benzodiazepines can intentionally reduce spike burden and increase spindles—illustrating how medication effects can cut both ways depending on clinical goals (long‑term effects reviewed in Fernández et al., 2013; see also diazepam‑related spindle increases in Stoyell et al., 2021). Your report should integrate these possibilities without implying treatment recommendations. When no epileptiform discharges are captured in a patient taking BZDs, add a caveat that short‑term benzodiazepine exposure can suppress spike frequency and may reduce the sensitivity of the study for interictal abnormalities, particularly generalized spike–wave (Smith, 2005).

In encephalopathic or ICU contexts, use ACNS terminology to describe rhythmic or periodic patterns and comment on reactivity; for example: “Generalized rhythmic delta activity without evolution (GRDA) on a sedated background; the pattern and limited reactivity may reflect drug effect; no electrographic seizures recorded” (Hirsch et al., 2013). Such phrasing is both descriptive and transparent about the confounding influence of medication.

Common pitfalls specific to benzodiazepine exposure.

Several recurring errors are worth anticipating. The first is misreading BZD‑related beta as EMG artifact; this is prevented by attending to symmetry and bandwidth and by using relaxation maneuvers to suppress muscle activity while cortical beta persists (Smith, 2005).

The second is overlooking subtle focal abnormalities: abundant fast activity can mask low‑amplitude focal slowing, so temporarily lowering sensitivity and reviewing in bipolar montages can reveal interhemispheric or regional asymmetries (Smith, 2005).

A third error is under‑calling encephalopathy on the assumption that drug exposure explains all abnormalities; although heavy BZD dosing can produce diffuse slowing, nonreactive backgrounds and loss of continuity remain concerning and carry prognostic weight irrespective of medication (Brown et al., 2010; Hirsch et al., 2013).

Finally, avoid inferring that a normal or near‑normal EEG excludes epilepsy in the acute BZD window; medication may have transiently reduced interictal discharge frequency, and repeating or sleep‑depriving the EEG when clinically indicated can improve diagnostic yield (Smith, 2005).

Best Practices

Two final practical habits round out high‑quality readings. First, keep the patient’s state in view: the beta‑dominant picture is clearer during alertness than during drowsiness, when theta intrudes and alpha wanes for non‑pharmacologic reasons (St. Louis & Frey, 2016). Record enough artifact‑free eyes‑closed and eyes‑open epochs to characterize the PDR and its reactivity (Sinha et al., 2016).

Second, describe what you see with plain language that a non‑EEG clinician can use.

A model sentence might be: “During wakefulness, there is diffuse, symmetric, frontocentrally predominant low‑to‑medium amplitude fast beta activity with attenuation of the posterior alpha rhythm; given the documented lorazepam use before recording, these features are most consistent with benzodiazepine effect; no epileptiform discharges were captured.”

That phrasing places the fast activity in context, names the likely contributor (with documentation), and avoids over‑interpretation (Tatum et al., 2016).

Key Takeaways

1. Class hallmark: benzodiazepines commonly ↑beta and ↓alpha during relaxed wakefulness.
   

2. Kinetics shape the record: long-acting agents yield more persistent EEG changes; intermediate-acting effects are briefer.
   

3. Slow bands are conditional: theta/delta shifts depend on dose, vigilance, and analysis rather than the drug class alone.
   

4. Connectivity can flip: some agents reduce linear but increase nonlinear coupling, so results depend on the metric.
   

5. Methods decide clarity: strict IPEG-style vigilance control and transparent pipelines turn medication effects from confounds into context.

Glossary

absolute power: total spectral energy within a frequency band (e.g., μV²/Hz), independent of other bands; often contrasted with relative power.

activation procedures: standardized maneuvers (e.g., hyperventilation, photic stimulation) used to elicit physiological reactivity during EEG.

alpha (α; ~8–12 Hz): posterior dominant rhythm in relaxed wakefulness that typically decreases after benzodiazepines.

alpha attenuation: reduction of alpha amplitude or power, commonly posteriorly, seen after benzodiazepine administration.

alpha1 / alpha2: sub-bands (e.g., ~8–10 Hz; ~10–12 Hz) sometimes reported separately; alpha1 tends to fall under oxazepam.

anxiolysis: reduction in anxiety symptoms with preserved alertness; clorazepate patterns with β↑ and α↓ can accompany clinically observed anxiolysis.

band definitions (IPEG): standardized ranges for δ, θ, α, β to harmonize pharmaco-EEG reporting across labs. band‑pass (filters): display or acquisition limits (e.g., ~1–70 Hz) used to visualize EEG; excessive high‑frequency attenuation can obscure true fast activity and distort spikes.

beta (β; ~13–30 Hz): fast activity that increases diffusely with benzodiazepines, often central/parietal predominant.

beta1 / beta2: lower and higher β sub-bands (lab-specific boundaries) used in qEEG; β1 may track performance changes with oxazepam.

CAP (cyclic alternating pattern): a marker of NREM sleep instability; reduced by benzodiazepines.

cephalic reference: montage referencing to another scalp electrode (e.g., A1/A2); reference choice can alter absolute vs relative findings.

clinical state control: procedures ensuring stable wakefulness (eyes-closed/open epochs, prevention of drowsiness) to avoid slow-wave confounds.

coherence (linear): frequency-domain correlation between two signals; can increase or decrease with benzodiazepines depending on band and region.

connectivity (nonlinear): coupling metrics capturing non-linear dependencies; often increases under alprazolam despite reduced linear coupling.

DC shift: slow baseline potential change; hyperventilation typically produces negative shifts that clonazepam attenuates.

delta (δ; ~0.5–4 Hz): slowest waking band; may remain low at anxiolytic doses but can rise with sedation or microstructural reorganization.

diffuse fast activity: widespread low-to-moderate amplitude β that smooths the background; a medication hallmark rather than EMG when symmetric and integrated.

drowsiness drift: gradual state change toward Stage N1 features (increased θ/δ, vertex waves) that can confound pharmaco-EEG if not controlled.

electromyographic (EMG) artifact: a non‑cerebral signal from muscle activity that contaminates scalp EEG—broadband, often frontal/temporal, and easily mistaken for fast cerebral rhythms if not tested for reactivity and distribution encephalopathic: pertaining to, or exhibiting signs of, encephalopathy—a diffuse brain dysfunction (toxic, metabolic, infectious, hypoxic-ischemic, degenerative, etc.) that typically presents with altered mental status (inattention, confusion, reduced arousal) and, on EEG, generalized slowing (↑ theta/delta) often with state-inappropriate background and, in some metabolic etiologies, triphasic-appearing waves (reversible if the cause is corrected).

epileptiform discharge (interictal): sharp transients (spikes/sharp waves) reflecting cortical hyperexcitability; may be suppressed by benzodiazepines during routine exams.

ERP (event-related potential): stimulus-locked averaged potentials; can covary with oxazepam-induced vigilance changes.

eyes-closed (EC): recording condition maximizing posterior α; critical for detecting α attenuation after benzodiazepines.

eyes-open (EO): condition reducing posterior α; still useful for observing diffuse β increases. eyes‑open/eyes‑closed reactivity: standard elicitation to assess PDR appearance and attenuation; important for separating alpha from other rhythms and for characterizing benzodiazepine effects on background.

filter (high-pass/low-pass): band-limiting operation; settings should meet pharmaco-EEG standards to avoid distorting power estimates.

high-pass filter: a signal-processing filter that attenuates frequencies below a chosen cutoff so very slow voltage shifts (baseline drift, sweat, movement-related DC shifts, and slow cortical potentials) are reduced while preserving faster EEG rhythms; in routine adult EEG, the high-pass cutoff is commonly set near 0.5–1.0 Hz.

hyperventilation (HV): activation that increases α/θ and induces negative DC shifts in healthy adults; clonazepam blunts these responses.

interictal epileptiform discharges (IEDs): brief, paroxysmal EEG transients — classically spikes (≈20–70 ms) or sharp waves (≈70–200 ms) — that have a pointed peak, a rapid return to baseline and are typically followed by an after-going slow wave; they occur between clinical seizures and, when genuine, show a plausible cortical field and reproducibility across montages.

IPEG: International Pharmaco-EEG Society, which publishes core recording and analysis guidelines.

line noise (50/60 Hz): mains interference that can masquerade as β-range elevation; must be managed to interpret benzodiazepine β correctly.

low-pass filter: a signal-processing filter that attenuates frequencies above a chosen cutoff so high-frequency noise and muscle (EMG) contamination are reduced while preserving physiologic beta and lower-gamma rhythms; routine low-pass/display cutoffs are often 70–100 Hz, with higher limits required for studies of high-frequency oscillations.

microstructure (EEG/MEG): segmentation of short-lived oscillatory patterns; lorazepam increases slow-pattern segments and reduces α/fast-θ.

montage: arrangement of references and derivations; source, average, and noncephalic references can shift absolute power maps (Yamadera et al., 1993).

noncephalic reference: extracephalic reference (e.g., linked ears, mastoids with careful setup); used to reduce shared scalp activity at the cost of other biases.

PDR (posterior dominant rhythm): the occipital alpha rhythm in relaxed wakefulness; typically attenuated by benzodiazepines.

pharmaco-EEG: EEG/qEEG approach examining drug effects on brain activity using standardized recording/analysis pipelines.

power spectral density (PSD): distribution of power across frequencies; basis for absolute and relative band power metrics.

pretest probability: the likelihood of a condition before a test is administered, that is, the chances of a condition based on knowing only its likelihood in the population from which the subject is taken.

qEEG (quantitative EEG): numerical/spectral/topographic/connectivity analyses of EEG data, used as an adjunct to clinical interpretation.

relative power: proportion of total power in a specific band; diazepam often shows relative β↑ even when absolute power is reference-dependent.

sedation (EEG): state-related slowing with increased θ/δ and reduced reactivity; distinct from the non-slowing β/α pattern at anxiolytic benzodiazepine doses.

spectral leakage: spread of energy between frequency bins due to windowing; mitigated by appropriate epoching and windows.

theta (θ; ~4–7 Hz): band with variable behavior under benzodiazepines; may decrease (diazepam, women) or increase in microstructure (lorazepam).

topographic mapping: spatial display of band power/coherence across the scalp; a sensitive way to visualize benzodiazepine β↑ and α↓ patterns.

vigilance control: explicit procedures to maintain alert wakefulness and prevent drowsiness; essential for pharmaco-EEG validity.

volume conduction: passive spread of electrical fields across scalp leading to apparent correlations; affects interpretation of coherence/connectivity.

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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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