Use of Auditory Evoked Responses as a Measure of Recovery from Benzodiazepine Sedation

Milligan, K. R.; Lumsden, J. H.; Howard, Rick; Howe, Judy; Dundee, John W.

doi:10.1177/014107688908201009

Cited by 18 publications

(13 citation statements)

References 8 publications

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“…Summing up the current and earlier reported effects of benzodiazepines on event-related potentials (ERPs), midlatency ERPs (including P50) seem to be unaffected by benzodiazepines (Schwender et al, 1993), while the amplitudes of most if not all long-latency ERPs are decreased (Milligan et al, 1989;Nichols and Martin, 1993;Rockstroh et al, 1991;Semlitsch et al, 1995). Besides an enforced inhibition of neural circuits involved in the MMN generation by GABAergic interneurons, the observed reduction of the MMN could also stem from an attenuated efficacy in sensory information processing, as reflected by the decreased N100m (as a bottom-up process).…”

Section: Neuromagnetic Recordingsmentioning

confidence: 60%

“…Similarly, no difference in MMN was revealed between schizophrenic patients treated with high vs those with low doses of anxiolytic and hypnotic drugs, including benzodiazepines . A reduction of the MMN by benzodiazepines seems to be, nevertheless, likely to some extent, since a diminution of event-related components caused by benzodiazepines was found in several studies, as for the N100 (Rockstroh et al, 1991;Semlitsch et al, 1995), P200 (Semlitsch et al, 1995), and P300 (Milligan et al, 1989;Nichols and Martin 1993;Rockstroh et al, 1991;Semlitsch et al, 1995).…”

Section: Introductionmentioning

confidence: 98%

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Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m

Rosburg

Marinou

Haueisen

et al. 2004

Neuropsychopharmacol

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The mismatch negativity (MMN) as an auditory evoked potential is thought to reflect an early, preconscious attention process. While this component has gained great importance in studies on clinical populations and in basic research on auditory information processing, the involvement of different neurotransmitters in the generation of this component is less well understood. We investigated the impact of the benzodiazepine lorazepam as a GABA agonist on the neuromagnetic MMN (MMNm) and auditory evoked field component N100m. A group of 12 healthy subjects was studied in single blind trials under the following three conditions: after the intake of 1.25 mg lorazepam, 100 mg caffeine or placebo. Neuromagnetic recordings were obtained before drug intake and three times after it. Controlled visual attention was tested additionally using a version of the Continuous Performance Test (CPT). The neuromagnetic activity was reconstructed by a single moving dipole, and the dipole moment and its latency were compared between conditions and time points of measurement. Lorazepam diminished the signal detection performance in the CPT 25 min after drug intake. The source of the field component N100m was attenuated, most significantly in the recording 105 min after lorazepam intake. The attenuation of the MMNm under lorazepam became significant at 105 min, but was visually less apparent, because in all conditions a decrease of the MMNm dipole moment within the course of a session was observed. Besides the already known effects of benzodiazepines on controlled attention functions, preconscious attention functions as reflected in the MMN are impaired by acute benzodiazepine intake. MMN studies on clinical populations have to be controlled for the recording time because of the strong habituation of this component.

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Section: Neuromagnetic Recordingsmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 98%

Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m

Rosburg

Marinou

Haueisen

et al. 2004

Neuropsychopharmacol

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“…Therapeutic doses of BDZs are reported to prolong the latency and decrease the amplitude of P300 in normal subjects (Berchou et al 1986;Milliggam et al 1989;Shinotoh et al 1989;Fujiwara et al 1991;Rockstroh et al 1991). The time courses of the effects of BDZ on P300 seem to correlate with its elimination half-life.…”

Section: Discussionmentioning

confidence: 99%

“…1991;Rockstroh et al 1991). However, these reports did not determine whether or not there is a relationship between cognitive impairments and other effects of BDZs such as sleepiness, even though it has been suggested that sedation affects the ERP (Berchou et al 1986;Milliggam et al 1989).…”

Section: Introductionmentioning

confidence: 99%

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Effects of a small dose of triazolam on P300 and resting EEG

Urata

Uchiyama

et al. 1996

Psychopharmacology

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The aim of the present study was to clarify whether cognitive impairments caused by benzodiazepines (BDZs) are a consequence of their specific direct effects on cognitive function or whether they are explained as secondary effects of increased sleepiness. Ten healthy men (mean age, 33.9 years) participated in two experimental sessions in a randomized cross-over, double-blind study: in one session subjects were given a placebo and in the other they were given 0.125 mg triazolam (TRZ). Each experimental session was conducted on 1 day. After a pre-drug EEG recording and an event-related potential (ERP) recording, under an oddball paradigm, subjects took the TRZ or placebo orally at 1000 hours. Thereafter, EEG and ERP recording sessions, following the same procedure as the pre-drug sessions, were conducted at 1, 2, 4, 6 and 8 h after drug administration. The EEG and ERP recordings from Cz and Pz referred to the bilaterally linked ear electrodes were used. We found that P300 latency was significantly prolonged in TRZ condition at 2 h (Pz) and 4 h (Cz and Pz) after TRZ, and that the P300 amplitude was significantly reduced at 2 h (Cz and Pz) and 4 h (Pz) after TRZ, compared to the same times after placebo. The absolute power values for the theta (4-7 Hz), alpha 1 (8-9 Hz), and alpha 2 (10-12 Hz) bands did not differ at any measurement time between the treatments. Only the beta band (13-19 Hz) power value was significantly elevated after the TRZ administration (versus placebo). No significant sedative effects were detected in subjective measurements. These results indicate that a single oral dose of 0.125 mg TRZ caused cortical changes without distinct general sedation or subjective sleepiness.

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Acute effects of the anxiolytics suriclone and alprazolam on cognitive information processing utilizing topographic mapping of event-related brain potentials (P300) in healthy subjects

Semlitsch

Anderer

Saletu

1995

Eur J Clin Pharmacol

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In a double-blind, placebo-controlled, cross-over study, acute effects of suriclone--a cyclopyrrolone derivative--were investigated by means of topographic mapping of event-related potentials (ERPs). Fifteen normal volunteers, aged 22-35 years, received randomized, oral single doses of placebo, 0.1 mg, 0.2 mg and 0.4 mg suriclone and 1 mg alprazolam as a reference compound. ERPs were investigated in an auditory oddball paradigm before and 3 h after intake of each drug. In addition to 17 EEG leads, vertical and horizontal electro-oculograms (EOGs) were recorded. After EOG minimization and artifact identification, the peak latencies of the spatial average were determined by an automatic procedure. Compared to placebo, no significant effects of the low and middle doses of suriclone on N1 amplitude were observed; the highest dosage reduced N1 amplitude, as did 1 mg alprazolam to an even greater extent. While no consistent effects on P2 amplitude were observed after suriclone, alprazolam reduced P2 amplitude. P300 amplitude was reduced only after the highest dosage of suriclone, but much more so after alprazolam. P300 latency was not affected significantly by suriclone, but a marked prolongation of P300 latency was observed after 1 mg alprazolam. Concerning N1 and P2 effects, alprazolam, but not suriclone, may have an inhibitory influence on stimulus-induced cortical arousal. Concerning P300 effects, the used doses of suriclone were superior to 1 mg alprazolam, which seemed to have reduced cognitive information processing capacity and prolonged stimulus evaluation time. Self-rated well-being (adjective checklist) showed subtle beneficial effects after 0.1 mg and 0.2 mg, but marked sedative effects after both 0.4 mg suriclone and 1 mg alprazolam.

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Use of Auditory Evoked Responses as a Measure of Recovery from Benzodiazepine Sedation

Cited by 18 publications

References 8 publications

Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m

Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m

Effects of a small dose of triazolam on P300 and resting EEG

Acute effects of the anxiolytics suriclone and alprazolam on cognitive information processing utilizing topographic mapping of event-related brain potentials (P300) in healthy subjects

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