Evoked responses in anaesthesia

Thornton, Claire; Sharpe, Roger

doi:10.1093/bja/81.5.771

Cited by 148 publications

(75 citation statements)

References 74 publications

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“…A possible explanation for why we did not find a significant effect for the LDAEP of the P2 component in our experiments is that the mean amplitude of the P2 component is lower in rats than in humans (Sambeth et al, 2003). Furthermore, anesthesia reduces the AEP amplitudes, probably through a concomitant inhibition of the excitatory postsynaptic potentials of cortical pyramidal cells (Maclver et al, 1996;Schwender et al, 1997;Thornton and Sharpe, 1998;Antunes et al, 2003). As the animals in our study were anesthetized, the amplitude of the P2 component might have been decreased to a level at which differences were not significantly measurable whereas the naturally higher N1 component still showed a pronounced LDAEP.…”

Section: Discussionmentioning

confidence: 64%

Loudness Dependence of Auditory Evoked Potentials as Indicator of Central Serotonergic Neurotransmission: Simultaneous Electrophysiological Recordings and In Vivo Microdialysis in the Rat Primary Auditory Cortex

Wutzler

Winter

Kitzrow

et al. 2008

Neuropsychopharmacol

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Serotonin released in synapsis is one of the key neurotransmitters in psychiatry and psychopharmacology. The loudness dependence of auditory evoked potentials (LDAEP) has been proposed as a marker for central serotonergic neurotransmission. Several findings in animals and humans support this hypothesis. However, the in vivo measurement of cortical extracellular serotonin levels has never been performed simultaneously with the recording of auditory evoked potentials. The interrelationship between low cortical serotonergic activity and strong LDAEP is yet to be proven. The auditory evoked potentials were recorded in the epidura above the primary auditory cortex of male Wistar rats whereas extracellular serotonin levels in the primary auditory cortex were measured by in vivo microdialysis before and after i.p. application of the selective serotonin reuptake inhibitor citalopram. At baseline, the correlation of coefficients between the LDAEP, especially of the N1 component, and extracellular serotonin levels in the primary auditory cortex was negative. The increase of serotonin levels after citalopram application was significantly related to a decrease of LDAEP of the N1 component (r ¼ À0.86, p ¼ 0.003). These data support the view that the LDAEP is closely modulated by cortical serotonergic activity. Thus, the LDAEP might serve as an inversely related marker of synaptically released serotonin in the CNS.

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Section: Discussionmentioning

confidence: 64%

Loudness Dependence of Auditory Evoked Potentials as Indicator of Central Serotonergic Neurotransmission: Simultaneous Electrophysiological Recordings and In Vivo Microdialysis in the Rat Primary Auditory Cortex

Wutzler

Winter

Kitzrow

et al. 2008

Neuropsychopharmacol

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“…12 Alterations of sensory evoked potentials by general anesthetics 13 likely reflect changes in the strength and temporal pattern of dipole activation because general anesthetics impair synaptic transmission. 14 Localization of the generators of the human 40-Hz ASSR with BESA has proposed that the response mainly arises from six concurrently active dipoles: D1, a cortical, tangentially oriented dipole in the contralateral supratemporal plane; D2, a cortical, radially oriented dipole in the contralateral supratemporal plane; D3 and D4, duplicating D1 and D2 in the ipsilateral supratemporal plane; D5, a vertically oriented dipole in the midline brainstem; and D6, a laterally oriented dipole in the midline brainstem.…”

mentioning

confidence: 99%

Attenuation of the 40-Hertz Auditory Steady State Response by Propofol Involves the Cortical and Subcortical Generators

et al. 2008

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Background:The 40-Hz auditory steady state response (40-Hz ASSR) provides a reliable marker of anesthetic-induced unconsciousness. Brain electric source analysis indicates that the 40-Hz ASSR arises from cortical and subcortical generators. The authors used source analysis to assess the effect of propofol anesthesia on the cerebral generators of the 40-Hz ASSR. They also examined the effect of propofol on two auditory evoked potentials of cortical origin: the N1 and the sustained potential.Methods: Eleven healthy human volunteers were anesthetized with propofol given in target-concentration mode at the minimal concentration causing unconsciousness. The 40-Hz ASSR was recorded before, during, and after anesthesia. The source model consisted of five concurrently active generator dipoles: two in the contralateral auditory cortex (one tangentially oriented, one radially oriented), two in the ipsilateral auditory cortex (same orientations), and one in the midline brainstem.Results: During anesthesia, the strength of the cortical and brainstem dipoles was reduced to the same extent (to 54% of baseline for the four cortical dipoles pooled vs. 53% for the brainstem dipole). Dipole strength during anesthesia was significantly less (P < 0.01) than during baseline and recovery for both cortical and brainstem dipoles. The N1 and sustained potential were no longer recordable during anesthesia.Conclusions: The attenuation of the 40-Hz ASSR during propofol anesthesia results from a reduction of similar magnitude of the activity of the cortical and brainstem generators. The N1 and sustained potential are so profoundly attenuated during propofol anesthesia that they are no longer recordable from the scalp.

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“…The AEP Monitor uses active acoustic stimulation, delivered through headphones, to generate middle latency auditory evoked potentials (MLAEP) (Kurita et al 2001). Anaesthetics or sedation alters EEG latency and amplitude (Drummond 2000;Thornton and Sharpe 1998) and these changes are used to generate the A-line ARX Index TM (AAI) (Mantzaridis and Kenny 1997). BIS and AAI have a range from zero, where patient's EEG is isoelectric, to 100, when patients are awake (Nishiyama and Hanaoka 2004;Rampil 1998).…”

Section: Norwood Usa) and Alaris Auditory Evoked Potentials (Aep) Momentioning

confidence: 99%

A review of the utility of EEG depth of anaesthesia monitors in the paediatric intensive care environment

McKeever

Johnston

Davidson

2012

Intensive and Critical Care Nursing

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Evoked responses in anaesthesia

Cited by 148 publications

References 74 publications

Loudness Dependence of Auditory Evoked Potentials as Indicator of Central Serotonergic Neurotransmission: Simultaneous Electrophysiological Recordings and In Vivo Microdialysis in the Rat Primary Auditory Cortex

Loudness Dependence of Auditory Evoked Potentials as Indicator of Central Serotonergic Neurotransmission: Simultaneous Electrophysiological Recordings and In Vivo Microdialysis in the Rat Primary Auditory Cortex

Attenuation of the 40-Hertz Auditory Steady State Response by Propofol Involves the Cortical and Subcortical Generators

A review of the utility of EEG depth of anaesthesia monitors in the paediatric intensive care environment

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