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Drug Effects on the EEG

Updated: Mar 2




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


Antidepressants


depression


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).


MAOIs

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).



SSRIs

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).



Antipsychotics


antipsychotics


Clinical Presentation

The major antipsychotic classes include first-generation, second-generation (atypical), and third-generation agents.


First-generation agents (FGAs) like Haloperidol (Haldol) can produce akathisia (restless movement disorder), extrapyramidal symptoms (pseudo-Parkinsonism, tardive dyskinesia, and tardive dystonia), blurred vision, death and stroke in elderly with dementia-related psychosis, dizziness, hypertension, hypotension, neuroleptic malignant syndrome (rare), neuroleptic-induced deficit syndrome (analogous to the negative symptoms of schizophrenia), seizures (rare), and tachycardia.


Second-generation (atypical) agents (SGAs) like Clozaril (Clozapine) can produce death and stroke in the elderly with dementia-related psychosis, neuroleptic malignant syndrome (when used with another agent), sedation, seizures, tachycardia, and tardive dyskinesia (rare).


Third-generation agents (TGAs) like Aripiprazole (Abilify) can produce activation, akathisia, death and stroke in the elderly with dementia-related psychosis, dizziness, headache, impaired impulse control (rare), insomnia, loss of energy, neuroleptic malignant syndrome, sedation, seizures (rare), and tardive dyskinesia (theoretical risk).



EEG Measures

All FGAs do not produce identical EEG changes. Chlorpromazine (Thorazine), a sedating FGA, increases EEG coherence, reduces total power, increases delta and theta power, and reduces alpha and beta power. FGAs may slow the peak alpha frequency and produce synchronous slow-wave activity.


Chlorpromazine can increase sharp theta transients at frontal and temporal sites. Chlorpromazine can significantly slow the posterior dominant rhythm (PDR) (Demos, 2019). The attenuation of alpha-blocking in response to sensory stimuli may be associated with memory deficits produced by this drug (Saletu, 2010; Thompson & Thompson, 2016). High phenothiazine doses may produce bisynchronous spikes or polyspikes (Blume, 2006).


Haloperidol (Haldol), a nonsedating FGA, does not affect total power, increases delta and theta power, modestly decreases alpha power, and increases beta power (Saletu, 2010).


Excessive doses of the SGA Clozapine can increase delta and theta power, where theta appears diffusely (Blume, 2006).


Where dopamine receptor hypersensitivity produces extrapyramidal side effects like tardive dyskinesia, FGAs may cause extended trains of mixed fast/sharp transients, EEG slowing, and potentiation of latent epileptiform activity (J. Gunkelman cited by Thompson & Thompson, 2016).



Benzodiazepines


benzodiazepines


Clinical Presentation

The major benzodiazepine classes include long-acting agents, intermediate-acting agents, short-acting agents, and benzodiazepine receptor agonist (BZRA) hypnotics.


Long-acting agents like Diazepam (Valium) can produce ataxia, confusion, depression, dizziness, fatigue, forgetfulness, hallucinations (rare), hyperexcitability, hypotension (rare), mania (rare), nervousness, respiratory depression (overdose with respiratory depressants), sedation, slurred speech, and weakness (Stahl, 2017).


Intermediate-acting agents like Lorazepam (Ativan) can produce the same side effects as their long-acting counterparts (Stahl, 2017).


Short-acting agents like Alprazolam (Xanax) can also produce the same side effects as their long and intermediate-acting counterparts (Stahl, 2017).


Benzodiazepine receptor agonist (BZRA) hypnotics like Zolpidem (Ambien) can produce amnesia (dose-dependent), ataxia, dizziness, hallucinations (rare), headache, hyperexcitability, nervousness, respiratory depression (overdose with respiratory depressants), and sedation.



EEG Measures

Benzodiazepines do not increase delta or theta power. They reduce alpha and increase beta power, especially over 20 Hz. They can reduce the PDR (Demos, 2019). Benzodiazepines may increase spindling beta and inhibit epileptiform activity (Advokat et al., 2023; Bauer & Bauer, 2005; Blume, 2006; Knott, 2000; Thompson & Thompson, 2015; Van Cott & Brenner, 2003).



CNS Stimulants


CNS stimulants

The two main classes of CNS stimulants include amphetamines and nonamphetamine behavioral stimulants.


Amphetamines like Amphetamine D, L (Adderall) can produce adverse cardiovascular effects, cardiac arrhythmia, dizziness, headache, hypertension, hypomania, insomnia, irritability, mania, nervousness, overstimulation, psychotic episodes, sexual dysfunction (long-term), suicidality, and worsened tics (Stahl, 2017).


Nonamphetamine behavioral stimulants like Methylphenidate (Ritalin) can produce adverse cardiovascular effects, cardiac arrhythmia, dizziness, headache, hypertension, hypomania, insomnia, irritability, mania, nervousness, overstimulation, priapism (rare), psychotic episodes, suicidality, and worsened tics (Stahl, 2017).



EEG Measures

Amphetamine (Adderall) reduces total power and reduces absolute delta, theta, alpha, and beta power (Saletu, 2010). Methylphenidate (Ritalin) reduces delta and theta power, increasing posterior alpha and low beta power for up to 6 hours following drug administration (Blume, 2006; Thompson & Thompson, 2015).


A client's level of arousal modulates the EEG response to a CNS stimulant. Stimulants increase alpha power in under-aroused, decrease alpha power in typically aroused, and do not alter alpha in anxious (fast-EEG) clients (J. Gunkelman, cited by Thompson & Thompson, 2015).



Mood Stabilizers


mood stabilizers


Clinical Presentation

The major mood stabilizer classes include lithium, first-generation anticonvulsants, second-generation anticonvulsants, atypical antipsychotics, and omega-3 fatty acids.


Lithium can produce arrhythmia, ataxia, bradycardia, cardiovascular changes, delirium, forgetfulness, hypotension, and lithium toxicity (Stahl, 2017).


First-generation anticonvulsants like Phenobarbital (Phenobarbital) can produce aggression, confusion, depression, dizziness, drowsiness, excitement, forgetfulness, hallucinations (rare), headache, insomnia, nightmares, and respiratory depression (in overdose or with other CNS depressants) (Stahl, 2017).


Second-generation anticonvulsants like Valproate (Depakene) can produce ataxia, bradycardia, dizziness, headache, sedation, suicidality, tachycardia, and weakness (Stahl, 2017).


Atypical antipsychotics like Olanzapine (Zyprexa) can produce death and stroke in the elderly with dementia-related psychosis, diabetes, dizziness, neuroleptic malignant syndrome (rare), orthostatic hypotension, pain (back, chest, extremity, joint), sedation, seizures (rare), and tardive dyskinesia (rare) (Stahl, 2017).


Omega-3 fatty acids do not produce significant side effects that would affect clinical presentation.



EEG Measures

Phenobarbital can induce rhythmic 18-26 Hz activity that starts in the frontal lobe and can progressively extend to the whole cortex. Progressively higher doses promote EEG slowing and reduced beta activity until slow-wave activity eclipses beta activity. Voltage can decrease until the brain enters an iso-electric state, like a medically induced coma (Blume, 2006; Thompson & Thompson, 2016). Barbiturate withdrawal may increase beta activity. Pentobarbital intoxication can result in triphasic waves.

Antiepileptic drug reduction may increase the frequency of focal spikes or spike waves (Blume, 2006).


Lithium can cause generalized asynchronous slowing that reduces the peak alpha frequency. Lithium may increase theta and beta power and greatly potentiate latent epileptiform activity. High lithium doses may produce bisynchronous spikes or polyspikes and increase delta and theta power, where theta appears diffusely (Blume, 2006). Lithium toxicity dramatically slows the EEG and causes triphasic discharges (Thompson & Thompson, 2016).


Neurotoxicity caused by high levels of antiepileptic drugs may cause diffuse delta and increased theta power. Valproic acid intoxication can produce triphasic waves (Blume, 2006).



Opioid Analgesics


opioid analgesics


Clinical Presentation

The major opioid analgesic classes include pure agonists, partial agonists, and mixed agonist-antagonists.


Pure agonists like Morphine (MS-IR) can produce agitation, confusion, dizziness, drowsiness, hallucinations, respiratory depression, and weakness (Advokat et al., 2023).


Partial agonists like Buprenorphine (Subutex) can produce headaches, insomnia, mood swings, orthostatic hypotension, respiratory depression, and sedation (Advokat et al., 2023; Stahl, 2017).


Mixed agonist-antagonists like Pentazocine (Talwin) can produce confusion (rare), depression, double vision (rare), drowsiness, excitement, insomnia, irregular heartbeat, irritability, sleepiness, very slow or very rapid breathing, and weakness (Advokat et al., 2023).



EEG Measures

Immediately after morphine administration, during the euphoric high, alpha power increases, and the peak alpha frequency slows. Delta and theta power may increase, as well as time spent in REM sleep. Increasing the dose causes EEG slowing and may progress to an iso-electric brain like a barbiturate-induced coma (Thompson & Thompson, 2015).



Recreational Drugs


Caffeine


caffeine


Clinical Presentation

Caffeine increases alertness and reduces fatigue. In vulnerable individuals, caffeine can promote anxiety and nervousness, cardiac arrhythmia, hypertension, and insomnia (Advokat et al., 2023).



EEG Measures

Caffeine acutely reduces theta and alpha power with rebound increases in these bands (Thompson & Thompson, 2016).



Cannabis


cannabis


Clinical Presentation

Cannabis can produce increased blood pressure and heart rate; cerebral artery constriction; impaired attention, coordination, memory, perception, and reaction time; mild euphoria; reduced anxiety; relaxation; acute depressive reactions, panic attacks, and mild paranoia at very high doses; and altered sensory perception, confusion, delusions, depersonalization, disorientation, hallucinations, and paranoia at massive doses. Early use has been associated with increased schizophrenia risk (Advokat et al., 2023).


EEG Measures

Cannabis acutely increases frontal alpha and chronically promotes frontal interhemispheric connectivity (hypercoherence and phase synchrony) (Thompson & Thompson, 2015).



Cocaine


cocaine


Clinical Presentation

Cocaine can produce increased blood pressure, heart rate, and temperature; increased alertness and energy; reduced fatigue; mood elevation; insomnia; and mild depression during withdrawal. Higher plasma levels can be associated with agitation, anxiety, impulsivity, suspiciousness, paranoia, and paranoid psychosis; repetitive behavior; and cardiac arrhythmias, cardiorespiratory arrest, and strokes (Advokat et al., 2023).


EEG Measures

Cocaine decreases delta and theta and increases alpha and beta power (Bauer & Bauer, 2005; Herning et al., 1985). The cortical distribution of beta power is frontal and central, resembling the effects of barbiturates and benzodiazepines (Herning et al., 1994).




Ethanol


ethanol

Clinical Presentation

Ethanol can produce short-term psychological effects of aggressiveness and violence; behavioral disinhibition; impaired attention, memory, motor coordination, and problem-solving; reduced anxiety and fear; respiratory depression; seizure following abrupt withdrawal; shortsightedness and tunnel vision; and slowed perceptual speed (Advokat et al., 2023).


EEG Measures

Ethanol acutely increases theta and low-alpha power and decreases beta power above 20 Hz. Individuals diagnosed with alcohol use disorder or who are vulnerable to developing this disorder frequently present with elevated beta (> 20 Hz and between 24-26 Hz) and decreased 6-10 Hz and alpha power (Thompson & Thompson, 2015). Alcohol withdrawal may increase beta activity, spikes, and polyspikes (Blume, 2006).



Nicotine


nicotine


Clinical Presentation

Nicotine increases alertness and may improve cognitive performance in smokers (and possibly nonsmokers). Nicotine can produce side effects of dizziness and headache. Nicotine withdrawal may result in anxiety, depression, and insomnia. Tobacco tars primarily contribute to cancer and cardiovascular disorders linked to long-term tobacco consumption (Advokat et al., 2023).

EEG Measures

Like caffeine, nicotine acutely reduces theta and alpha power with rebound increases in these bands (Thompson & Thompson, 2016).


Detailed Summary Table


Drug Summary Table


Clinical Issues


Clinical issues

Clinicians must understand their scope-of-practice restrictions when discussing medication issues. Clients often seek alternative treatments when medication management is ineffective or has undesirable side effects.


A careful and comprehensive assessment may reveal a more appropriate medication approach. Best case, neurofeedback may correct underlying causal factors, resulting in general improvement and reduced need for further medication.

Recommended Medication Management Approaches


Discuss the scope and limitations of your professional license and your ability to address medication issues. Review your client's plans regarding medication.


Continue current prescriptions? If not, have they consulted with their prescribing physician?


Decrease or eliminate current medications? Your client's best choice is to discuss medication adjustment with the prescribing physician. If they wish to proceed without physician consultation, explain your limitations and ethical concerns about proceeding with neurofeedback training under these circumstances.


Medications often need to be adjusted due to the effects of training. The clinician or client must interact with the prescribing physician regarding these changes. As neurofeedback changes brain function and structure, medications may need to be titrated or withdrawn. Standardized psychological (e.g., Beck Depression Inventory) and performance (e.g., Computerized Continuous Performance Test) instruments may help inform the physician's decision.


Wherever possible, involve your client in this process since physicians may not welcome your involvement in medication decisions. When given accurate information, clients may find interacting with the prescribing physician easier.

Drug Implications for Assessment and Neurofeedback


Consider drug effects when interpreting your initial assessment battery and subsequent reassessment testing. Develop training goals based on initial testing with medication. Retest with the same medication unless withdrawn to ensure a valid comparison.


Develop a personalized neurofeedback training strategy that does not attempt to train against a drug's principal effects on the EEG.


Quiz


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Glossary

alpha-blocking: arousal and specific forms of cognitive activity may reduce alpha amplitude or eliminate it entirely while increasing EEG power in the beta range.

alpha rhythm: 8-12-Hz and 8-13-Hz activity that depends on the interaction between rhythmic burst firing by a subset of thalamocortical (TC) neurons linked by gap junctions and rhythmic inhibition by widely-distributed reticular nucleus neurons. Researchers have correlated the alpha rhythm with "relaxed wakefulness." Alpha is the dominant rhythm in adults and is located posteriorly.


alpha spindles: regular bursts of alpha activity.


amplitude: the energy or power contained within the EEG signal measured in microvolts or picowatts.


anterior: near or toward the front of the head, for example, the anterior cingulate.

anterior cingulate: the division of the prefrontal cortex that plays a vital role in attention and is activated during working memory. It mediates emotional and physical pain and has cognitive (dorsal anterior cingulate) and affective (ventral anterior cingulate) conflict-monitoring components.


arousal: a process that combines alertness and wakefulness, produced by at least five neurotransmitters, including acetylcholine, histamine, hypocretin, norepinephrine, and serotonin.


asynchronous waves: neurons depolarize and hyperpolarize independently.


benzodiazepine receptor agonist (BZRA) hypnotics: nonbenzodiazepine BZRAs like zolpidem (Ambien) that are prescribed to treat insomnia.


beta rhythm: 12-36 Hz rhythm associated with arousal and attention generated by brainstem mesencephalic reticular stimulation that depolarizes neurons in the thalamus and cortex. The beta rhythm can be divided into multiple ranges.


bilateral synchronous slow waves: a pathological sign observed in drowsy children. When detected in alert adults, intermittent bursts of high-amplitude slow waves may signify gray matter lesions in deep midline structures. bisynchronous spikes: A spike is a sharply contoured waveform that lasts for a brief duration, typically under 70 milliseconds. Bisynchronous spikes occur in both hemispheres of the brain simultaneously or near-simultaneously, indicating a synchrony in brain activity across the hemispheres.


cerebral cortex: the layer of gray matter that covers the cerebral hemispheres. The cerebral cortex consists of gray matter and white matter.


complex: a sequence of waves.


continuous irregular delta: slow waves produced by white matter lesions seen in disorders like multiple sclerosis.


delta rhythm: 0-4 Hz, 0.5-3.5 Hz, and 1-4 Hz oscillations generated by thalamocortical neurons during stage-3 sleep.


diphasic wave: a wave that contains both a negative and positive deflection from the baseline.


dominant frequency: the EEG frequency with the greatest amplitude.


dual-action antidepressants: medications like duloxetine (Cymbalta) that activate 5-HT1 receptors to produce antidepressant and anxiolytic effects while they blockade 5-HT2 (agitation, restlessness, and sexual dysfunction) and 5-HT3 (nausea, headache, and vomiting) receptors to minimize their side effects.


EEG activity: a single wave or successive waves.


EEG coherence: shared oscillatory activity (identical waveform morphology) between two sites expressed as the square of the correlation coefficient between their frequencies.


EEG power: signal energy in the EEG spectrum. Most EEG power falls within the 0-20 Hz frequency range. EEG power is measured in microvolts or picowatts.


electroencephalogram (EEG): the voltage difference between at least two electrodes, where at least one electrode is located on the scalp or inside the brain. The EEG is a recording of EPSPs and IPSPs that occur primarily in dendrites in pyramidal cells located in macrocolumns, several millimeters in diameter, in the upper cortical layers.


fast cortical potentials: EEG rhythms that range from 0.5 to Hz-100 Hz. The main frequency ranges include delta, theta, alpha, sensorimotor rhythm, and beta.


first-generation antipsychotics (FGAs): FGAs like chlorpromazine (Thorazine) are prescribed to treat the positive symptoms of schizophrenia and exert their effects through D2 receptor blockade.


focal waves: EEG waves detected within a limited scalp, cerebral cortex, or brain area.


frequency: the number of cycles completed each second expressed in hertz (Hz).


frequency synchrony: when identical EEG frequencies are detected at two or more electrode sites. For example, 12 Hz may be simultaneously detected at O1-A1 and O2-A2.


frontal lobes: the most anterior cortical lobes of the brain that are divided into the motor cortex, premotor cortex, and prefrontal cortex.


gamma rhythm: 25-75 Hz, 35-45 Hz, 38-42 Hz, and 40 Hz oscillations that may speed information distribution and processing. Gamma bursts occur during problem-solving, and the absence of gamma is associated with cognitive deficits and learning disorders. Gamma is theorized as a "binding rhythm" that integrates sensory inputs into perception and consciousness.


generalized asynchronous slow waves: waves seen in sleepy children and those with elevated temperatures. This may indicate degenerative disease, dementia, encephalopathy, head injury, high fever, migraine, and Parkinson's disease in adults.

hertz (Hz): the unit of frequency, an abbreviation for cycles per second.


hypercoherence: abnormally-high functional connectivity between two sites.

intermediate-acting benzodiazepines: benzodiazepines with mean half-lives from 15-80 hours prescribed to manage anxiety.

irregular waves: successive waves that constantly alter their shape and duration.


irreversible MAO inhibitors (MAOIs): MAOIs like selegeline (Emsam) form permanent bonds with the MAO enzyme and are prescribed for major depressive disorder (MDD).


kappa rhythm: bursts of alpha or theta and is detected over the temporal lobes of subjects during cognitive activity.


lambda waves: saw-toothed transient waves from 20-50 μV in amplitude and 100-250 ms in duration detected over the occipital cortex during wakefulness. These positive deflections are time-locked to saccadic movements and observed during visual scanning, as during reading.


lateralized waves: waves that are primarily detected on one side of the scalp and may indicate pathology.


local synchrony: synchrony that occurs when the coordinated firing of cortical neurons produces high-amplitude EEG signals.


localized slow waves: waves that may indicate a transient ischemic attack (TIA) or stroke, migraine, mild head injury, or tumors above the tentorium. Deep lesions result in bilateral or unilateral delta.


long-acting benzodiazepines: benzodiazepines like diazepam (Valium) with mean half-lives ranging from 10-80 hours prescribed to manage anxiety.


mixed opioid agonist-antagonists: drugs like pentazocine (Talwin) that are kappa agonists and weak mu antagonists that are prescribed for pain management.


monoamine oxidase (MAO): an enzyme that degrades and inactivates the monoamine neurotransmitters dopamine, norepinephrine, and serotonin.


monoamine oxidase inhibitors (MAOIs): antidepressant drugs that interfere with MAO's breakdown of monoamines and increase monoamine availability and are prescribed to manage major depressive disorder (MDD).


monophasic wave: either a single negative (upward) or positive (downward) deflection from baseline.


mu rhythm: arch-shaped waves that range from 7-11 Hz with amplitudes typically below 50 μV detected over Cz and Pz in waking subjects. These waves are seen in the healthy EEG records of 7% of the population. While these waves resemble alpha, they contain sharp positive transients and curved negative segments. Mu waves are blocked or reduced by exposure to a tactile stimulus, planning to move, readiness to move, or moving a contralateral limb (making a fist).


multiple spike-and-slow-wave complex: multiple spikes associated with at least one slow wave.


partial opioid agonists: drugs like buprenorphine (Subutex) that produce less-than-maximal analgesia and are prescribed to manage pain.


peak alpha frequency: the highest-amplitude alpha frequency (8-12, 8-13 Hz) within an epoch.


phase: the degree to which the peaks and valleys of EEG waveforms coincide.


phase synchrony: synchrony when identical EEG frequencies are detected at two or more electrode sites, and the peaks and valleys of the EEG waveforms coincide. This is also called global synchrony. For example, EEG training may produce phase-synchronous 12-Hz alpha waves at O1-A1 and O2-A2.


polyphasic (multiphasic) wave: a wave that contains two or more deflections of opposite polarity from baseline.


polyspikes: a series of three or more consecutive spikes (≥ 10 Hz) lasting at least 300 milliseconds.


posterior: near or toward the back of the head.


pure opioid agonists: drugs like morphine that produce maximal analgesia and are prescribed for to manage pain.


regular or monomorphic waves: successive waves with identical shapes. Regular waves may resemble sine waves (sinusoidal) or maybe arched (resembling wickets) or saw-toothed (asymmetrical and triangular).


second-generation antipsychotics: SGAs like clozapine (Clozaril) are prescribed to treat the positive symptoms of schizophrenia and antagonize D2 receptors less effectively than D1 receptors and significantly less than 5-HT2 receptors.


selective norepinephrine reuptake inhibitors (SNRIs): drugs like atomoxetine (Strattera) that specifically interfere with norepinephrine reuptake for the management of major depressive disorder (MDD).


selective serotonin reuptake inhibitors (SSRIs): drugs like fluoxetine (Prozac) that specifically interfere with serotonin reuptake for the management of major depressive disorder (MDD).


sharp transients: sequences that contain several sharp waves.


sharp waves: waves that resemble spikes with a pointed peak with a longer 70-200-ms duration.


short-acting benzodiazepines: benzodiazepines like alprazolam (Xanax) with mean half-lives ranging from 2.5 to 12 hours are prescribed to manage anxiety.


spike: a negative transient with a pointed peak at conventional paper speeds, 20-70-ms duration, and 40-100 μV amplitude.


spike-and-slow-wave complex: a spike followed by a higher amplitude slow wave at 3 Hz. In an absence seizure, the amplitudes are very high (e.g., 160 μV).


spindle waves: waves that originate in the thalamus and occur during unconsciousness and stage II sleep.


synchronous: adverb meaning that groups of neurons depolarize and hyperpolarize simultaneously.


synchrony: the coordinated firing of pools of neurons. EEG signals can display local synchrony, frequency synchrony, and phase synchrony.


theta rhythm: 4-7 Hz rhythm generated a cholinergic septohippocampal system that receives input from the ascending reticular formation and a noncholinergic system that originates in the entorhinal cortex, which corresponds to Brodmann areas 28 and 34 at the caudal region of the temporal lobe.


third-generation antipsychotics (TGAs): drugs like aripiprazole (Abilify) that is a partial agonist at D2 and 5-HT1A receptors and an antagonist at 5-HT2 receptors prescribed for the management of the positive and negative symptoms of schizophrenia.


total power: the sum of the voltages in all EEG frequency bands.


transient: a single wave or sequence of regular waves, called a complex, distinguishable from background EEG activity.


triphasic waves (TWs): medium-to-high-amplitude sharp transients that often involve a negative-positive-negative sequence. TWs are distributed diffusely and symmetrically with frontal predominance.


waveform: the shape and form of an EEG signal.



References


Advokat, C. D., Comaty, J. E., & Julien, R. M. (2023). Julien's primer of drug action: A comprehensive guide to the actions, uses, and side effects of psychoactive drugs (15th ed.). Worth Publishers.

Dias Alves, M., Micoulaud-Franchi, J. A., Simon, N., & Vion-Dury, J. (2018). Electroencephalogram modifications associated with atypical strict antipsychotic monotherapies. Journal of Clinical Psychopharmacology, 38(6), 555–562. https://doi.org/10.1097/JCP.0000000000000953

Banoczi, W. R. (2005). How some drugs affect the electroencephalogram (EEG). Am J END Technol, 45, 118-129. PMID: 15989074

Barry, R. J., Clarke, A. R., Hajos, M., McCarthy, R., Selikowitz, M., & Bruggemann, J. M. (2009). Acute atomoxetine effects on the EEG of children with attention-deficit/hyperactivity disorder. Neuropharmacology, 57(7-8), 702–707. https://doi.org/10.1016/j.neuropharm.2009.08.003

Bauer, G., & Bauer, R. (2005). EEG drug effects and central nervous system poisoning. In E. Niedermeyer & F. Lopes da Silva (Eds.). Electroencephalography: Basic principles, clinical applications, and related fields (5th ed.). Lippincott Williams & Wilkins.


Blume, W. T. (2006). Drug effects on EEG. Journal of Clinical Neurophysiology, 23(4), 306-311. https://doi.org/10.1097/01.wnp.0000229137.94384.fa

Bos, D. J., Oranje, B., Veerhoek, E. S., Van Diepen, R. M., Weusten, J. M., Demmelmair, H., Koletzko, B., de Sain-van der Velden, M. G., Eilander, A., Hoeksma, M., & Durston, S. (2015). Reduced symptoms of inattention after dietary omega-3 fatty acid supplementation in boys with and without Attention Deficit/Hyperactivity Disorder. Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology, 40(10), 2298–2306. https://doi.org/10.1038/npp.2015.73 Bromm, B., Ganzel, R., Herrmann, W. M., Meier, W., & Scharein, E. (1986). Pentazocine and flupirtine effects on spontaneous and evoked EEG activity. Neuropsychobiology, 16(2-3), 152–156. https://doi.org/10.1159/000118317 Brunner, D. P., Dijk, D. J., Münch, M., & Borbély, A. A. (1991). Effect of zolpidem on sleep and sleep EEG spectra in healthy young men. Psychopharmacology, 104(1), 1–5. https://doi.org/10.1007/BF02244546 Cajochen, C., Kräuchi, K., von Arx, M. A., Möri, D., Graw, P., & Wirz-Justice, A. (1996). Daytime melatonin administration enhances sleepiness and theta/alpha activity in the waking EEG. Neuroscience Letters, 207(3), 209–213. https://doi.org/10.1016/0304-3940(96)12517-9 Carley, D. W., & Farabi, S. S. (2016). Physiology of sleep. Diabetes Spectrum: A publication of the American Diabetes Association, 29(1), 5–9. https://doi.org/10.2337/diaspect.29.1.5

Demos, J. N. (2019). Getting started with neurofeedback (2nd ed.). W. W. Norton & Company.

Dijk, D. J., & Cajochen, C. (1997). Melatonin and the circadian regulation of sleep initiation, consolidation, structure, and the sleep EEG. Journal of Biological Rhythms, 12(6), 627–635. https://doi.org/10.1177/074873049701200618 Eschmann, G., Irrgang, V., & Rüther, E. (1983). Effects of beta-receptor blockers in pharmacology EEG. Neuropsychobiology, 10(2-3), 190–192. https://doi.org/10.1159/000118008 Flachenecker P. (2013). A new multiple sclerosis spasticity treatment option: Effect in everyday clinical practice and cost-effectiveness in Germany. Expert Review of Neurotherapeutics, 13(3 Suppl 1), 15–19. https://doi.org/10.1586/ern.13.1 Fontani, G., Corradeschi, F., Felici, A., Alfatti, F., Migliorini, S., & Lodi, L. (2005). Cognitive and physiological effects of Omega-3 polyunsaturated fatty acid supplementation in healthy subjects. European Journal of Clinical Investigation, 35(11), 691–699. https://doi.org/10.1111/j.1365-2362.2005.01570.x Goldstein, L., Murphree, H. B., & Pfeiffer, C. C. (1968). Comparative study of EEG effects of antihistamines in normal volunteers. The Journal of Clinical Pharmacology and the Journal of New Drugs, 8(1), 42–53. https://doi.org/10.1002/j.1552-4604.1968.tb00091.x Han, G., Matsumoto, S., Diaz, J., Greene, R. W., & Vogt, K. E. (2022). Dihydropyridine calcium blockers do not interfere with non-rapid eye movement sleep. Frontiers in Neuroscience, 16, 969712. https://doi.org/10.3389/fnins.2022.969712 Hasan, M., Pulman, J., & Marson, A. G. (2013). Calcium antagonists as an add-on therapy for drug-resistant epilepsy. The Cochrane Database of Systematic Reviews, 2013(3), CD002750. https://doi.org/10.1002/14651858.CD002750.pub2

Herning, R. I., Glover, B. J., Koeppl, B., Phillips, R. L., & London, E. D. (1994). Cocaine-induced increases in EEG alpha and beta activity: Evidence for reduced cortical processing. Neuropsychopharmacology, 11(1), 1-9. https://doi.org/10.1038/npp.1994.30


Herning, R. I., Jones, R. T., Hooker, W. D., Mendelson, J., & Blackwell, L. (1985). Cocaine increases EEG beta: A replication and extension of Hans Berger's historic experiments. Clinical Neurophysiology, 60(6), 470-477. https://psycnet.apa.org/doi/10.1016/0013-4694(85)91106-X

Khajehpour, H., Mohagheghian, F., Ekhtiari, H., Makkiabadi, B., Jafari, A. H., Eqlimi, E., & Harirchian, M. H. (2019). Computer-aided classifying and characterizing of methamphetamine use disorder using resting-state EEG. Cognitive Neurodynamics, 13(6), 519–530. https://doi.org/10.1007/s11571-019-09550-z

Knott, V. J. (200). Quantitative EEG methods and measures in human psychopharmacological research. Human Psychopharmacology, 15, 479-498. https://doi.org/10.1002/1099-1077(200010)15:7<479::AID-HUP206>3.0.CO;2-5

Matousek M. (1987). EEG assessment of the sedative and excitatory properties of CNS-active compounds in the patients with depression. Neuropsychobiology, 17(1-2), 118–120. https://doi.org/10.1159/000118348 Montgomery, P., Burton, J. R., Sewell, R. P., Spreckelsen, T. F., & Richardson, A. J. (2013). Low blood long chain omega-3 fatty acids in UK children are associated with poor cognitive performance and behavior: a cross-sectional analysis from the DOLAB study. PloS one, 8(6), e66697. https://doi.org/10.1371/journal.pone.0066697 Newton, T. F., Cook, I. A., Kalechstein, A. D., Duran, S., Monroy, F., Ling, W., & Leuchter, A. F. (2003). Quantitative EEG abnormalities in recently abstinent methamphetamine dependent individuals. Clinical Neurophysiology: Official Journal of the International Federation of Clinical Neurophysiology, 114(3), 410–415. https://doi.org/10.1016/s1388-2457(02)00409-1 Ott, G. E., Rao, U., Lin, K. M., Gertsik, L., & Poland, R. E. (2004). Effect of treatment with bupropion on EEG sleep: Relationship to antidepressant response. The International Journal of Neuropsychopharmacology, 7(3), 275–281. https://doi.org/10.1017/S1461145704004298 Patrick, R. P., & Ames, B. N. (2015). Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: Relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior. FASEB journal: Official Publication of the Federation of American Societies for Experimental Biology, 29(6), 2207–2222. https://doi.org/10.1096/fj.14-268342

Saletu, B., Anderer, P., Saletuzyhlarz, G. M. (2010). EEG mapping and tomography in drug evaluation. Medicographia, 32, 190-200. https://doi.org/10.1177/155005940603700205

Simeon, J. G., Ferguson, H. B., & Van Wyck Fleet, J. (1986). Bupropion effects in attention deficit and conduct disorders. Canadian Journal of Psychiatry. Revue Canadienne de Psychiatrie, 31(6), 581–585. https://doi.org/10.1177/070674378603100617

Stahl, S. M. (2017). Stahl's essential psychopharmacology prescriber's guide (6th ed.). Cambridge University Press.

Tashkin D. P. (2013). Effects of marijuana smoking on the lung. Annals of the American Thoracic Society, 10(3), 239–247. https://doi.org/10.1513/AnnalsATS.201212-127FR Thanacoody, H. K., & Thomas, S. H. (2005). Tricyclic antidepressant poisoning: Cardiovascular toxicity. Toxicological Reviews, 24(3), 205–214. https://doi.org/10.2165/00139709-200524030-00013 Thomaides, T., Tagaris, G., & Karageorgiou, C. (1996). EEG and topographic frequency analysis in migraine attack before and after sumatriptan infusion. Headache, 36(2), 111–114. https://doi.org/10.1046/j.1526-4610.1996.3602111.x

Thompson, M., & Thompson, L. (2015). The biofeedback book: An introduction to basic concepts in applied psychophysiology (2nd ed.). Association for Applied Psychophysiology and Biofeedback.


Van Cott, A., & Brenner, R. P. (2003). Drug effects and toxic encephalopathies. In J. S. Ebersole & T. A. Pedley (Eds.). Current practice of clinical electroencephalography (3rd ed.). Lippincott Williams & Wilkins.

van der Post, J., Schram, M. T., Schoemaker, R. C., Pieters, M. S., Fuseau, E., Pereira, A., Baggen, S., Cohen, A. F., & van Gerven, J. M. (2002). CNS effects of sumatriptan and rizatriptan in healthy female volunteers. Cephalalgia: An International Journal of Headache, 22(4), 271–281. https://doi.org/10.1046/j.1468-2982.2002.00344.x Zajicek, J., Fox, P., Sanders, H., Wright, D., Vickery, J., Nunn, A., Thompson, A., & UK MS Research Group (2003). Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): Multicentre randomised placebo-controlled trial. Lancet, 362(9395), 1517–1526. https://doi.org/10.1016/S0140-6736(03)14738-1 Zhu, J., Coppens, R. P., Rabinovich, N. E., & Gilbert, D. G. (2017). Effects of bupropion sustained release on task-related EEG alpha activity in smokers: Individual differences in drug response. Experimental and Clinical Psychopharmacology, 25(1), 41–49. https://doi.org/10.1037/pha0000109


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