Pharmaco‐EEG profiles of antidepressants. Pharmacodynamic studies with fluvoxamine.

Saletu, B.; Grünberger, J; Rajna, Péter

doi:10.1111/j.1365-2125.1983.tb02128.x

Cited by 57 publications

(33 citation statements)

References 13 publications

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“…This augmentation was more marked after repeated doses (8 to 9% after 10 mg and 9 to 11% after 25 mg) than after an acute dose (4% after 10 mg Time (h) Figure 1 Time course of the EEG changes in the relative beta activity (20- Mean elimination half-life ranged between 7 to 9 h both after a single dose and after repeated administration. AUCs from 0 to 12 h and from 0 to infinity were not (0) [11]. The EEG profile of desipramine 50 mg was similar to that seen after 6 mg methamphetamine 6 mg [11].…”

Section: Eegmentioning

confidence: 68%

“…The EEG profile of desipramine 50 mg was similar to that seen after 6 mg methamphetamine 6 mg [11]. A similar profile was seen with antidepressants whose action involves the dopamine (DA) or noradrenaline (NA) systems, such as tranylcypromine, a potent nonreversible MAO-inhibitor, or nomifensine, a DA and NA reuptake inhibitor [8,11].…”

Section: Eegmentioning

confidence: 76%

“…Amitriptyline, a sedative tricyclic antidepressant often used as a positive reference in clinical pharmacology trials, induced the same profile as imipramine 75 mg when given in doses ranging from 25 to 75 mg [11,12]. Brain mapping studies indicated that the increases in slow delta and theta waves occurred mainly in the fronto-temporal areas, the reduction in the alpha range in the occipital areas, and the increase in beta activity in the fronto-central regions [13][14][15].…”

Section: Eegmentioning

confidence: 99%

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EEG profile of litoxetine after single and repeated administration in healthy volunteers.

Patat¹,

Trocherie²,

Thebault³

et al. 1994

Brit J Clinical Pharma

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1 Litoxetine is a selective serotonin reuptake inhibitor with antidepressant activity in animal models and in depressed patients. 2 This double-blind, cross-over, placebo-controlled study was carried out in 12 healthy young male volunteers. The aim was to assess the EEG profile of litoxetine in parallel with its pharmacokinetics after a single dose or multiple administrations for 4 days (6 doses) of two dosages (10 mg and 25 mg). Spectral analysis of four EEG leads (F4-T4, F3-T3, T4-02 and T3-01) was done up to 12 h post-dose. 3 In single or multiple doses, litoxetine induced EEG changes characterised by a doserelated increase in fast beta energies, mainly beta 2, without any changes in slow waves (delta and theta). A slight reduction in alpha activity occurred only after repeated doses. 4 EEG changes occurred after a single oral administration and lasted at least 12 h with litoxetine blood concentrations ranging from 4 to 10 ng ml-'. With repeated administrations, the pharmacodynamic steady-state was achieved as the increase in beta 2 energies was the same before and 12 h post-dose. These effects occurred with litoxetine blood concentrations ranging from 3 to 7 ng ml-1 with the 10 mg dosage and from 8 to 18 ng ml-1 with the 25 mg dosage. The EEG profile did not change after 4 days of repeated administration, indicating that tolerance did not develop. 5 Cmax and AUC showed proportionality between the administered dosages of 10 and 25 mg. Mean tmax ranged from 3 to 4 h and mean elimination half-life from 7 to 9 h independently of the dosage. Pharmacokinetic steady-state was achieved on day 4. Litoxetine did not accumulate with a twice daily regimen. 6 In conclusion, the EEG profile of litoxetine resembles those previously described with non-sedative antidepressants. Such EEG changes generally occur at therapeutic dosages.

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Section: Eegmentioning

confidence: 68%

Section: Eegmentioning

confidence: 76%

Section: Eegmentioning

confidence: 99%

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EEG profile of litoxetine after single and repeated administration in healthy volunteers.

Patat¹,

Trocherie²,

Thebault³

et al. 1994

Brit J Clinical Pharma

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Section: Previous Studies Have Shown That Changes In Brain Functionmentioning

confidence: 99%

“…Prior work with "pharmaco-EEG" techniques has shown that the administration of antidepressant compounds yields reproducible changes in EEG activity in healthy control subjects within a few hours of dosing (Saletu et al 1982(Saletu et al , 1983(Saletu et al , 1986(Saletu et al , 1987(Saletu et al , 1987Grunberger 1985, 1988;Sannita et al 1983;Sannita 1990;Itil et al 1984;Herrmann et al 1991;Luthringer et al 1996). The relationship of these immediate EEG changes in control subjects to eventual clinical response in a depressed population is unclear.…”

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confidence: 99%

Early Changes in Prefrontal Activity Characterize Clinical Responders to Antidepressants

Cook¹,

Leuchter

Morgan

et al. 2002

Neuropsychopharmacology

183

169

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Previous studies have shown that changes in brain functionClinicians long have observed a lag time of several weeks between the initiation of antidepressant treatment and clinical response for many patients (Hyman and Nestler 1996;Katz et al. 1996). Some individuals do have early symptomatic improvement, and this has been reported to predict further improvement over the next several weeks (Nierenberg et al. 1995). Reports have suggested that some physiologic changes are seen shortly after initiation of treatment (Sulser 1989;Beck 1995;Dahmen et al. 1997). No clinically practical physiologic predictor of treatment response has yet been identified with these techniques, however, and the relationship of early physiologic changes to eventual clinical outcome remains incompletely understood.Quantitative electroencephalography (QEEG) has been used as a physiologic measure in efforts to address these questions. Prior work with "pharmaco-EEG" techniques has shown that the administration of antidepressant compounds yields reproducible changes in EEG activity in healthy control subjects within a few hours of dosing (Saletu et al. 1982(Saletu et al. , 1983(Saletu et al. , 1986(Saletu et al. , 1987(Saletu et al. , 1987 Grunberger 1985, 1988;Sannita et al. 1983;Sannita 1990; Early Prefrontal Changes in Depression 121Itil et al. 1984;Herrmann et al. 1991;Luthringer et al. 1996). The relationship of these immediate EEG changes in control subjects to eventual clinical response in a depressed population is unclear. Other QEEG work with depressed subjects has found that changes from baseline in theta power early in the course of treatment may characterize groups of depressed patients who are more likely to respond to antidepressant treatment (Ulrich et al. 1994). Unfortunately, the overlap in the value of these changes between responder and nonresponder groups precluded the use of this measure in response prediction for individual subjects, and prior research did not indicate how to relate changes in theta power to other measures of regional brain activity (e.g., regional cerebral blood flow or metabolism). We previously have shown that absolute and relative power are complementary measures of brain activity (Leuchter et al. 1993). A relatively new QEEG measure, "cordance," combines information from both absolute and relative power measures (Leuchter et al. 1994a(Leuchter et al. , 1994b. The algorithm yields two indicators: a categorical value ("concordant" or "discordant" state) and a numerical value for each electrode. In an earlier report with the categorical measure , we observed that depressed subjects exhibiting the concordant state prior to treatment had better treatment outcomes when treated with fluoxetine than did subjects with the discordant state. In this report, we use the num*erical values of cordance, because they allow examination of changes in regional brain activity with treatment. In validation against data collected simultaneously with [H 2 15O]-positron emission tomography (PET), cordance values in the the...

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EEG, MAO-A inhibition, pharmacokinetics and safety of befloxatone in the elderly

Patat¹,

Dubruc²,

Deschamp³

et al. 1997

Hum. Psychopharmacol. Clin. Exp.

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Befloxatone is a new reversible and selective MAO‐A inhibitor. The present study aimed to assess the pharmacodynamics (EEG profile and MAO‐A inhibition using plasma levels of DHPG), pharmacokinetics and safety after a single dose of 10 mg of befloxatone compared to amitriptyline 50 mg in a randomized, double‐blind, three‐way crossover, placebo‐controlled trial involving 12 elderly subjects. Befloxatone did not show any sedative profile on EEG as no significant changes occurred in slow delta and theta waves or in alpha waves. In contrast, befloxatone produced a non‐significant decrease in delta relative power and a significant increase in the (12–40 Hz) beta waves compared to placebo and/or amitriptyline depending on the EEG lead. MAO‐A inhibition by befloxatone was evidenced by a significant reduction in DHPG plasma levels (peak activity of −85 per cent and AUC0–24 h of −46 per cent compared to placebo). The pharmacokinetics parameters obtained after a single 10‐mg oral dose of befloxatone were: tmax, 2 h; Cmax, 33·7 ng/ml; t1/2β, 14·5 h; AUC0–∞, 255 ng/ml for befloxatone and tmax, 2 h; Cmax, 29·4 ng/ml; t1/2β, 16 h; AUC0–∞, 596 ng/ml for its main metabolite, O‐demethyl befloxatone. These parameters are in the same range as those obtained in healthy young subjects. In conclusion, the present study demonstrated that a single oral dose of 10 mg of befloxatone is safe in the elderly, possesses potent MAO‐A inhibition activity and the EEG profile of a non‐sedative antidepressant and did not justify dose adjustment compared to young subjects. © 1997 John Wiley & Sons, Ltd.

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Pharmaco‐EEG profiles of antidepressants. Pharmacodynamic studies with fluvoxamine.

Cited by 57 publications

References 13 publications

EEG profile of litoxetine after single and repeated administration in healthy volunteers.

EEG profile of litoxetine after single and repeated administration in healthy volunteers.

Early Changes in Prefrontal Activity Characterize Clinical Responders to Antidepressants

EEG, MAO-A inhibition, pharmacokinetics and safety of befloxatone in the elderly

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