What is the most common drug effect on EEG?

October 10, 2025 •

4 min read

While many variations exist, an increase in beta wave activity and a mild increase in theta waves are the most common electroencephalogram (EEG) alterations associated with medication [1.2.2, 1.10.4]. Answering 'What is the most common drug effect on EEG?' involves understanding how different drug classes interact with the brain's electrical signals.

Quick Summary

The most frequent medication-induced change on an EEG is an increase in beta activity and sometimes a mild theta increase. Different drug classes, such as sedatives, antidepressants, and antipsychotics, produce predictable, dose-dependent alterations in brainwave patterns.

Key Points

Most Common Effect: An increase in beta wave activity and a mild increase in theta waves are the most common EEG alterations from medication [1.2.2, 1.10.4].
Benzodiazepines & Barbiturates: These sedatives are the classic cause of increased beta frequency activity on an EEG [1.9.1].
Antidepressant Variety: SSRIs typically increase beta activity, while tricyclic antidepressants (TCAs) often cause an increase in slow waves (theta and delta) [1.2.1, 1.10.3].
Antipsychotic Slowing: Many antipsychotics, especially clozapine and low-potency agents, induce a general slowing of the EEG, with more delta and theta waves [1.7.1, 1.7.2].
AEDs and Alpha Rhythm: Conventional antiepileptic drugs like phenytoin and carbamazepine can slow the brain's dominant posterior alpha rhythm [1.8.2].
Dose-Dependence: Most drug effects on the EEG are dose-dependent, with higher doses or toxicity often leading to more pronounced slowing or abnormal patterns [1.2.3].
Reversibility: Many drug-induced EEG changes, even severe ones, can fully resolve to normal after the offending medication is discontinued [1.2.2, 1.11.3].

Understanding Drug Effects on EEG Brainwaves

An electroencephalogram (EEG) is a non-invasive test that records the brain's electrical patterns through small electrodes attached to the scalp. These patterns, known as brainwaves, are categorized by their frequency into bands: Delta, Theta, Alpha, and Beta. Medications can significantly and often predictably alter these brainwaves [1.2.3]. The most common drug-induced EEG changes involve an increase in beta activity (>13 Hz), often seen with sedative medications like benzodiazepines and barbiturates, and a mild increase in theta activity (4–8 Hz) [1.2.2, 1.9.1, 1.10.4].

Drug effects are typically dose-dependent and can range from no discernible effect to significant background slowing, the introduction of intermixed theta and delta waves, or even epileptiform activity [1.2.3, 1.10.1]. In severe overdose situations, patterns like burst suppression or an electrically silent ("flat") EEG can occur [1.2.3]. It is crucial for clinicians to recognize these patterns, as a drug-induced abnormality may be fully reversible once the medication is discontinued [1.2.2, 1.11.3].

The Role of Different Brainwaves

Delta (0.5–4 Hz): Associated with deep, dreamless sleep and encephalopathy [1.6.2].
Theta (4–8 Hz): Linked to drowsiness, early sleep stages, and is sometimes a marker for cortical dysfunction or seen with sedatives [1.4.3, 1.6.2].
Alpha (8–13 Hz): The dominant rhythm in a relaxed, awake state with eyes closed. Suppression of alpha activity is a common drug effect [1.4.3].
Beta (>13 Hz): Prominent during states of concentration and problem-solving. A medication-induced increase in beta activity is a very common finding, particularly with anxiolytics and sedatives [1.9.1, 1.10.3].

Specific Drug Classes and Their EEG Signatures

Different categories of drugs have distinct and recognizable effects on the EEG, which can be valuable for both diagnostics and monitoring therapeutic effects or toxicity.

Sedatives and Anxiolytics (Benzodiazepines & Barbiturates)

This class of drugs is well-known for causing a significant increase in beta activity [1.9.1]. Benzodiazepines like Diazepam (Valium) and Alprazolam (Xanax) reliably increase beta power, which is considered a biomarker for their modulation of GABA-A receptors [1.4.1]. This effect is often widespread but can be most prominent in the frontocentral regions of the brain [1.4.3]. At lower, anxiolytic doses, the primary effect is this beta increase. At higher, sedative doses, an increase in delta power (especially in the occipital region) and a decrease in alpha power may also be observed [1.4.1]. Similarly, barbiturates also tend to increase fast beta wave activity [1.5.1].

Antidepressants

Antidepressants have varied effects depending on their class:

SSRIs (Selective Serotonin Reuptake Inhibitors): Drugs like fluoxetine (Prozac) and sertraline (Zoloft) often cause a mild increase in beta activity and may decrease frontal alpha waves [1.10.3]. Some studies suggest that specific EEG changes, like changes in alpha power, can even predict a patient's response to SSRI treatment [1.6.5].
TCAs (Tricyclic Antidepressants): TCAs are known to increase both delta and theta (slow wave) activity while also potentially increasing fast beta activity [1.2.1, 1.10.3]. They can also lower the seizure threshold and elicit spike-wave discharges [1.2.1, 1.11.1].
MAOIs (Monoamine Oxidase Inhibitors): These typically produce an activating EEG profile with increased fast beta activity and a decrease in slower frequencies [1.6.2, 1.10.3].

Antipsychotics

Antipsychotic effects on the EEG can differ greatly between agents:

Typical (First-Generation) Antipsychotics: Low-potency neuroleptics like chlorpromazine often cause EEG slowing, characterized by increased delta and theta power and decreased alpha activity [1.7.1]. High-potency agents like haloperidol may cause an increase in alpha and beta power [1.7.1].
Atypical (Second-Generation) Antipsychotics: Clozapine stands out for its profound impact, frequently inducing significant EEG slowing (increased delta and theta) and carrying a higher risk of epileptiform discharges [1.7.2, 1.7.4]. Olanzapine can also cause notable EEG slowing [1.7.3]. In contrast, agents like aripiprazole and blonanserin may show no significant effect on spectral power [1.7.1].

Antiepileptic Drugs (AEDs)

While the primary goal of AEDs is to suppress seizure activity, they also alter the background EEG. Older AEDs like Carbamazepine, Phenytoin, and Phenobarbital are associated with a slowing of the posterior alpha rhythm [1.8.1, 1.8.2]. Carbamazepine and Phenobarbital can also produce generalized intermittent slow waves [1.8.2]. Phenytoin may increase the percentage of power in the theta and delta bands [1.8.4]. Newer generation AEDs generally have less impact on background rhythms [1.8.2].

Comparison of Drug Effects on EEG


Drug Class	Primary EEG Effect	Common Frequency Changes	Clinical Notes
Benzodiazepines	Beta Accentuation	↑ Beta, ↓ Alpha, ↑ Delta (high dose) [1.4.1, 1.4.3]	Effect is a biomarker for GABA-A receptor modulation [1.4.1].
Barbiturates	Beta Accentuation	↑ Beta, possible ↑ Slow Wave [1.5.1]	Can cause abnormal EEGs in a significant percentage of individuals [1.5.1].
Antidepressants (SSRIs)	Mild Beta Increase	↑ Beta, ↓ Alpha [1.10.2, 1.10.3]	EEG patterns may help predict treatment response [1.6.4, 1.6.5].
Antidepressants (TCAs)	Diffuse Slowing & Beta Increase	↑ Theta, ↑ Delta, ↑ fast Beta [1.2.1]	Can lower seizure threshold and produce epileptiform activity [1.2.1].
Antipsychotics (Clozapine)	Significant Diffuse Slowing	↑ Delta, ↑ Theta, ↓ Alpha [1.2.4, 1.7.1]	High risk of EEG abnormalities and epileptiform discharges [1.7.2].
Antiepileptic Drugs (Conventional)	Background Slowing	↓ Alpha Frequency, ↑ Slow Waves [1.8.2]	Effects can be mistaken for underlying pathology; cautious interpretation is needed [1.8.2].

Conclusion

The answer to What is the most common drug effect on EEG? points to an accentuation of beta activity, a change prominently caused by widely prescribed sedatives and anxiolytics [1.2.2]. However, the full picture is far more complex. Nearly every class of psychotropic and neurologic medication leaves a signature on the EEG, from generalized slowing with antipsychotics and some AEDs to specific frequency shifts with different types of antidepressants [1.2.3, 1.10.1]. Recognizing these patterns is essential for neurologists and psychiatrists to distinguish between a benign drug effect, a sign of drug toxicity, a predictor of therapeutic response, or an underlying neurological condition.

For further reading on this topic, a comprehensive review can be found in a paper by W. T. Blume, titled "Drug Effects on EEG," which offers detailed insights into how various medications influence EEG readings. Link

Frequently Asked Questions

Yes, many medications can cause EEG changes that are classified as abnormal. The most common is an increase in beta activity from sedatives, but drugs can also cause slowing (increased theta/delta waves) or even epileptiform discharges. These changes are often reversible upon stopping the drug [1.2.2, 1.2.3].

Increased beta activity can be a normal finding during states of concentration. However, when it is a prominent feature, it is often caused by medications, especially benzodiazepines (like Xanax, Valium) and barbiturates. It can also be associated with anxiety or cortical irritability [1.9.1, 1.9.3].

Several drug classes can cause EEG slowing, which means an increase in slower theta and delta waves. These include tricyclic antidepressants, many antipsychotics (notably clozapine), and some conventional antiepileptic drugs like phenytoin [1.2.1, 1.7.2, 1.8.4].

Yes, certain antidepressants, particularly tricyclic antidepressants (TCAs) and clozapine, are known to lower the seizure threshold and can sometimes induce epileptiform discharges (spikes and sharp waves) on an EEG [1.2.1, 1.11.2].

No, not all drugs have a discernible effect on the EEG. The effects are highly dependent on the drug's mechanism of action, dose, and individual patient susceptibility. For example, some newer antiepileptic and antipsychotic drugs show minimal impact on background EEG rhythms [1.2.3, 1.7.1, 1.8.2].

Benzodiazepines enhance the effect of the neurotransmitter GABA at the GABA-A receptor. This modulation of the brain's primary inhibitory system leads to characteristic changes in cortical network oscillations, including a prominent increase in beta frequency activity [1.4.1].

While an EEG can show patterns highly characteristic of certain drug classes (e.g., prominent beta activity suggesting benzodiazepine use), it cannot definitively identify a specific medication. The patterns are class-specific rather than drug-specific, and clinical correlation is always required.