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Drug Effects on the EEG

Updated: May 22

Understanding psychopharmacology is important to neurofeedback because drugs can affect a client's clinical presentation, EEG, assessment, and training success. Reviewing a list of the medications and social drugs, your client is currently taking is essential. In some cases, different members of a drug class can produce different effects. Individual responses to medications can vary widely and may depend on factors like dosage, individual physiology, and the presence of other medical conditions.

A single dose of a prescription psychotropic drug can markedly change the EEG within 1-3 hours of administration. Families of psychotropic drugs that share therapeutic equivalence (e.g., chlorpromazine-like neuroleptics and haloperidol-like neuroleptics) produce similar systematic EEG changes (Knott, 2000). A drug's plasma level, which depends on the dose, distribution volume, and metabolism, influences the magnitude of EEG alterations, which should be symmetrical and often widespread.

Common EEG changes include slowing background activity, increased beta activity, epileptiform activity, triphasic waves, and widespread delta and increased theta activity (Blume, 2006).

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Prescription Drugs



Clinical Presentation

The major antidepressant classes include tricyclic antidepressants (TCAs), second-generation atypical antidepressants, selective serotonin reuptake inhibitors (SSRIs), dual-action antidepressants, irreversible MAO inhibitors, and selective norepinephrine reuptake inhibitors (SNRIs). The symbol indicates a dangerous side effect.

Tricyclic antidepressants (TCAs) like Imipramine (Tofranil) can produce anxiety, blurred vision, dizziness, fatigue and weakness, psychotic symptoms (rare), sedation, seizures (rare), sexual dysfunction, and suicidality (rare) (Stahl, 2017).

Selective serotonin reuptake inhibitors (SSRIs) like Fluoxetine (Prozac) can produce agitation, anxiety, headache, insomnia, mania (rare), sedation, seizures (rare), sexual dysfunction, suicidality (rare), and tremors (Stahl, 2017).

Dual-action antidepressants like Duloxetine (Cymbalta) can produce hypomania (rare), hypertension, insomnia, sedation, sexual dysfunction, and suicidality (rare) (Stahl, 2017).

Irreversible MAO inhibitors like Selegeline (Emsam, Eldepryl) can produce confusion, dizziness, dyskinesia, hallucinations, headache, hypertensive crisis, mania (rare), seizures (rare), and suicidality (rare) (Stahl, 2017).

Selective norepinephrine reuptake inhibitors (SNRIs) like Atomoxetine (Strattera) can produce abdominal pain, anxiety, agitation, aggression, dizziness, dysmenorrhea, dyspepsia, elevated heart rate, fatigue (especially in children), hypertension, hypomania and mania (rare), orthostatic hypotension, priapism, sedation, sexual dysfunction, and suicidality (rare) (Stahl, 2017).

EEG Measures

TCAs Sedating TCAs like Amitriptyline (Elavil) and imipramine (Tofranil) increase theta and fast-beta power and decrease alpha and total power (Knott, 2000; Saletu, 2010; Thompson & Thompson, 2016). However, nonsedating TCAs that resemble Desipramine (Norpramin) increase alpha and fast beta (Knott, 2000).

At higher doses, sedating TCAs can increase delta and widespread theta power (Bauer & Bauer, 2005; Van Cott & Brenner, 2003).

TCAs can cause asynchronous slow waves and increase sleep spindles (Thompson & Thompson, 2015). TCAs and SSRIs can provoke spikes or polyspikes. Excessive TCA doses can increase delta and theta power, where theta appears diffusely (Blume, 2006).


The nonselective, irreversible MAO inhibitor Iproniazid (Marsalid) increases theta to a smaller degree than Amitryptiline (Elavil) while it increases fast-beta power to a greater degree. MAO inhibitors like Isocarboxazid (Marplan) increase 20-30 Hz power while decreasing power in slower and high frequencies like CNS stimulants (Thompson & Thompson, 2015).


The SSRIs Fluoxetine (Prozac), paroxetine HCl (Paxil), and Sertraline HCl (Zoloft) modestly increase 18-25 Hz frontocentral beta and decrease anterior alpha power (Thompson & Thompson, 2016).

The nonsedating SSRI Citalopram (Celexa) decreases total, delta, theta, and alpha power, while it increases beta power (Bauer & Bauer, 2005; Saletu, 2010; Van Cott & Brenner, 2003).

High SSRI doses may produce bisynchronous spikes or polyspikes. Serotonin syndrome is associated with triphasic waves, which signal toxic encephalopathy (Blume, 2006).