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Fos-like immunoreactivity in the auditory brainstem evoked by bipolar intracochlear electrical stimulation: effects of current level and pulse duration.

Fos-like immunoreactivity was used to compare the auditory brain stem excitation elicited by bipolar electrical stimulation of the cochlea at various current levels relative to the electrically evoked auditory brain stem response threshold for a 50-micros/phase monophasic pulse. Fos-like immunoreactive cells were labeled in primary auditory brain stem regions. The distribution of labeled cells was restricted to regions known to be cochleotopically related to the stimulated region of the scala tympani. Some labeled cells were observed at 2x electrically evoked auditory brain stem response threshold. The number, density and spatial distribution of labeled cells were quantified in the dorsal cochlear nucleus and inferior colliculus, and found to increase with increasing level of stimulation. For 50-micros pulses, the location of labeled neurons remained reasonably restricted to narrow bands within each region until the 1Ox level of stimulation (20 dB above electrically evoked auditory brain stem response threshold) was reached. While a monotonic increase in Fos-like immunoreactivity with increasing stimulus level was observed in most nuclei, for cells of the superficial layer of the dorsal cochlear nucleus, a non-monotonic change with increasing stimulus level was seen. This dorsal cochlear nucleus non-monotonicity may indicate that, at higher levels of stimulation, a secondary indirect inhibitory input, probably associated with activation of deep layer dorsal cochlear nucleus cells, reduces excitatory responses at the superficial layer of the dorsal cochlear nucleus. Electrically evoked auditory brain stem response and Fos expression showed parallel changes as a function of stimulus level and pulse duration. The data indicate that discrete activation of cell populations within the central auditory pathways can occur with bipolar electrical stimulation to the highest levels of stimulation typically useful in humans. The data also indicate a close, but not identical, quantitative relationship between Fos-like immunoreactivity and electrophysiological response amplitude. These findings support the view that a study of Fos-like immunoreactivity can provide a powerful and quantitative tool for study of the dynamic response characteristics of cells of the central auditory system to electrical stimulation at suprathreshold levels. The data suggest that there is a monotonic increase in the number of neurons responsive to intracochlear electrical stimulation as a function of stimulus level, at least through the upper half of the dynamic range, but that this increase does not result in a complete loss of spatial selectivity. Coupled with previous psychophysical studies, these results suggest that the increase in the number of activated neurons is functionally beneficial, resulting in improved discrimination of changes in the electrical signals.

Animals↗

Auditory plasticity and hyperactivity following cochlear damage.

This paper will review some of the functional changes that occur in the central auditory pathway after the cochlea is damaged by acoustic overstimulation or by carboplatin, an ototoxic drug that selectively destroys inner hair cells (IHCs) in the chinchilla. Acoustic trauma typically impairs the sensitivity and tuning of auditory nerve fibers and reduces the neural output of the cochlea. Surprisingly, our results show that restricted cochlear damage enhances neural activity in the central auditory pathway. Despite a reduction in the auditory-nerve compound action potential (CAP), the local field potential from the inferior colliculus (IC) increases at a faster than normal rate and its maximum amplitude is enhanced at frequencies below the region of hearing loss. To determine if this enhancement was due to loss of sideband inhibition, we recorded from single neurons in the IC and dorsal cochlear nucleus before and after presenting a traumatizing above the unit's characteristic frequency (CF). Following the exposure, some neurons showed substantial broadening of tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition. The central auditory system of the chinchilla can be deprived of some of its cochlear inputs by selectively destroying IHCs with carboplatin. Selective IHC loss reduces the amplitude of the CAP without affecting the threshold and tuning of the remaining auditory nerve fibers. Although the output of the cochlea is reduced in proportion to the amount of IHC loss, the IC response shows only a modest amplitude reduction, and remarkably, the response of the auditory cortex is enhanced. These results suggest that the gain of the central auditory pathway can be up- or down regulated to compensate for the amount of neural activity from the cochlea.

Animals↗

Different effects of intracochlear sensory and neuronal injury stimulation on expression of synaptic N-methyl-D-aspartate receptors in the auditory cortex of rats in vivo.

CONCLUSIONS: The expression of synaptic N-methyl-D-aspartate (NMDA) receptors in the auditory cortex is dynamic and is bidirectionally regulated by auditory activity. Furthermore, the time course of changes in the level of NR2A protein differs after sensory and neuronal injury stimulation, which modulate different changes in synaptic plasticity. OBJECTIVE: To examine the effects of different types of auditory activity on the expression of synaptic NMDA receptors (NMDARs) in the auditory cortex of rats. MATERIAL AND METHODS: We prepared synaptosomes from the auditory cortices of postnatal Day 28 ototoxic-deafened Sprague-Dawley rats and postnatal Day 28 Sprague-Dawley rats subjected to noise trauma that were given various treatments and compared them to the synaptosomes of 1-6-week-old normal Sprague-Dawley rats. The expression of different NMDAR subunits in the synaptosomes was investigated by means of Western blotting. RESULTS: Changes in NR1 and NR2B proteins were not significant during different types of auditory activity. The level of NR2A protein increased remarkably during postnatal development and as a result of electrical intracochlear stimulation, auditory deprivation and noise trauma. Seventy-two h after a 2-h period of sensory electrical intracochlear stimulation, the expression of NR2A protein returned to the level caused by auditory deprivation. Seventy-two h after a 3-h period of noise trauma, elevation of the level of NR2A protein was unchanged. We also confirmed that elevation of the level of synaptic NR2A protein was sensitive to protein synthesis inhibitor and NMDAR antagonist. However, transcription inhibitor had no effect on NR2A protein expression.

Animals↗

Pathophysiological changes of the central auditory pathway after blunt trauma of the head.

It is the aim of the present paper to correlate clinical symptoms of auditory dysfunction (tinnitus, hyperacusis, hearing loss) one year on average after a blunt trauma of the head with objective audiological test results (otoacoustic emission and auditory brainstem response testing, impedance audiometry) and to compare these findings to controls without history of head trauma. Thirty-one patients (24-56 years) were included. They were largely female (n = 26). The clinical and otolaryngological examination (including otoscopy) of all patients revealed no pathological abnormalities. Pure-tone audiograms were normal with one exception (pre-existing noise-induced hearing loss) as well as tympanograms. The main auditory symptoms were tinnitus (n = 9), hyperacusis (n = 2) and a reported transient hearing loss immediately after the trauma (n = 16) (which had improved at the time of examination). The results of testing the central auditory pathway showed that the transiently evoked otoacoustic emissions (otoemissions) revealed statistically significant differences between amplitude differences of all patients as well as patients with tinnitus and controls in the linear, but not in the non-linear stimulation mode. A complete loss of stapedial reflex responses was found in 12 of the patients and a partial (irregular) loss (in at least more than two frequencies) in four additional patients. Auditory brainstem responses (ABR) were normal in all patients, but 76% had lowered loudness discomfort levels (LDL). Blunt trauma of the head can lead to auditory dyfunction, probably as a result of diffuse axonal injury of the central auditory pathway. An initial sensorineural hearing loss after the trauma (as a result of the inner ear fluid concussion) was transiently reported only. Auditory symptoms play a minor role in the so-called "postconcussive syndrome," but should be considered and evaluated fully.

Adult↗

A sensitive period for the development of the central auditory system in children with cochlear implants: implications for age of implantation.

OBJECTIVE: The aim of the present experiment was to assess the consequences of cochlear implantation at different ages on the development of the human central auditory system. DESIGN: Our measure of the maturity of central auditory pathways was the latency of the P1 cortical auditory evoked potential. Because P1 latencies vary as a function of chronological age, they can be used to infer the maturational status of auditory pathways in congenitally deafened children who regain hearing after being fit with a cochlear implant. We examined the development of P1 response latencies in 104 congenitally deaf children who had been fit with cochlear implants at ages ranging from 1.3 yr to 17.5 yr and three congenitally deaf adults. The independent variable was the duration of deafness before cochlear implantation. The dependent variable was the latency of the P1 cortical auditory evoked potential. RESULTS: A comparison of P1 latencies in implanted children with those of age-matched normal-hearing peers revealed that implanted children with the longest period of auditory deprivation before implantation-7 or more yr-had abnormal cortical response latencies to speech. Implanted children with the shortest period of auditory deprivation-approximately 3.5 yr or less-evidenced age-appropriate latency responses within 6 mo after the onset of electrical stimulation. CONCLUSIONS: Our data suggest that in the absence of normal stimulation there is a sensitive period of about 3.5 yr during which the human central auditory system remains maximally plastic. Plasticity remains in some, but not all children until approximately age 7. After age 7, plasticity is greatly reduced. These data may be relevant to the issue of when best to place a cochlear implant in a congenitally deaf child.

Adolescent↗

Auditory processing in patients with Charcot-Marie-Tooth disease type 1A.

HYPOTHESIS: It is unclear whether Charcot-Marie-Tooth (CMT) disease, type 1A, causes auditory processing disorders. Therefore, auditory processing abilities were investigated in five CMT1A patients with normal hearing. BACKGROUND: Previous studies have failed to separate peripheral from central auditory processing disorders. MATERIALS AND METHODS: Five genetically confirmed CMT1A cases in patients with normal hearing underwent behavioral and objective testing. Pure tone audiometry, speech audiometry, and OAE assessment were followed-up by an auditory processing test battery comprising sentences-in-noise test, pattern recognition tests, words-in-noise test, dichotic digit test, filtered speech test, binaural fusion test, and categorical speech perception test. Subsequently, ABR and ERP measurements were conducted. RESULTS: Either the behavioral or objective test scores of 4 out of the 5 CMT1A patients did not differ significantly from those of subjects with normal hearing. Significantly lower scores of one patient on auditory processing tests and ABR measurements could be ascribed to subnormal hearing. CONCLUSION: The authors conclude that CMT1A patients with normal peripheral hearing have auditory processing abilities that were not indicative for an auditory processing disorder. Furthermore, the presence of a peripheral hearing loss complicates the interpretation of auditory processing abilities.

Acoustic Stimulation↗

Early otitis media with effusion, hearing loss, and auditory processes at school age.

OBJECTIVES: To examine the effect of conductive hearing loss (HL) secondary to otitis media with effusion (OME) in the first 3 years of life on physiologic, peripheral, and higher-order behavioral auditory measures examined at school age. METHODS: Peripheral hearing sensitivity for conventional and extended high-frequency audiometric ranges, physiologic (distortion product otoacoustic emissions, contralateral and ipsilateral acoustic middle ear muscle reflexes), auditory brain stem response (ABR), and higher-order auditory processing measures (masking level difference; Virtual Auditory Localization, Speech Intelligibility Gain; adaptive Pediatric Speech Intelligibility task) were examined at the end of the second grade of elementary school in two cohorts (North Carolina, N = 73, and New York, N = 59). All participants (mean age, 8 years) were followed prospectively in infancy and early childhood (7 to 39 months) for middle ear status and hearing loss (using pneumatic otoscopy/tympanometry and repeated conditioned behavioral audiometric response procedures). Multivariate analyses were conducted to address whether early OME and early conductive HL were related to physiologic, peripheral, and higher-order auditory processes. RESULTS: Early hearing loss and OME were significantly associated with peripheral hearing at school age; extended high-frequency thresholds accounted for the result. Similarly, hearing loss in early life and OME were significantly associated with the acoustic middle ear muscle reflex: The contralateral stimulation condition accounted for the association. Significant associations with both early OME and early HL were also found for the auditory brain stem response measure and were explained by the correlations between early hearing loss and the ABR Wave V latency but not other ABR indices. There were no reliable associations between either early OME or early HL on any other auditory processes evaluated at the end of second grade. CONCLUSIONS: Extended high-frequency hearing and brain stem auditory pathway measures in childhood were significantly associated with children's experiences with OME and hearing loss from 7 to 39 months of age. However, no significant associations were found for psychoacoustic measures of binaural processing or a behavioral adaptive speech-in-noise test at school age.

Auditory Cortex↗

Central auditory development in children with cochlear implants: clinical implications.

A common finding in developmental neurobiology is that stimulation must be delivered to a sensory system within a narrow window of time (a sensitive period) during development in order for that sensory system to develop normally. Experiments with congenitally deaf children have allowed us to establish the existence and time limits of a sensitive period for the development of central auditory pathways in humans. Using the latency of cortical auditory evoked potentials (CAEPs) as a measure we have found that central auditory pathways are maximally plastic for a period of about 3.5 years. If the stimulation is delivered within that period CAEP latencies reach age-normal values within 3-6 months after stimulation. However, if stimulation is withheld for more than 7 years, CAEP latencies decrease significantly over a period of approximately 1 month following the onset of stimulation. They then remain constant or change very slowly over months or years. The lack of development of the central auditory system in congenitally deaf children implanted after 7 years is correlated with relatively poor development of speech and language skills [Geers, this vol, pp 50-65]. Animal models suggest that the primary auditory cortex may be functionally decoupled from higher order auditory cortex due to restricted development of inter- and intracortical connections in late-implanted children [Kral and Tillein, this vol, pp 89-108]. Another aspect of plasticity that works against late-implanted children is the reorganization of higher order cortex by other sensory modalities (e.g. vision). The hypothesis of decoupling of primary auditory cortex from higher order auditory cortex in children deprived of sound for a long time may explain the speech perception and oral language learning difficulties of children who receive an implant after the end of the sensitive period.

Auditory Cortex↗

Central auditory system plasticity and aural rehabilitation of adults.

Until recently, researchers used behavioral measures of identification and discrimination of speech and nonspeech stimuli to assess the effects of auditory deprivation, enhancement, and training. Recent advances in our ability to measure electrical activity in the auditory system in response to sound have made it possible for us to study how changes in auditory input (because of hearing loss, auditory input modification, or training) affect the function of the central auditory system. This article reviews the evidence of changes in the auditory cortex in mature animals and in humans with acquired sensorineural hearing loss as well as changes associated with auditory training in persons with normal hearing. The results of studies that measure psychoacoustic and speech-recognition performance of persons with hearing loss, with and without hearing aids, are interpreted within the framework of our new knowledge about plasticity of the auditory system. Applications of electrophysiologic techniques to hearing aid research and clinical practice are highlighted.

Aging↗

Intrinsic and extrinsic contributions to auditory selectivity in a song nucleus critical for vocal plasticity.

The development, maintenance, and perception of learned vocalizations in songbirds are likely to require auditory neurons that respond selectively to song. Neurons with song-selective responses have been described in several brain nuclei critical to singing, but the mechanisms by which such response properties arise, are modified, and propagate are poorly understood. The lateral magnocellular nucleus of the anterior neostriatum (LMAN) is the output of an anterior forebrain pathway (AFP) essential for learning and maintenance of song, processes dependent on auditory feedback. Although neurons throughout this pathway respond selectively to auditory presentation of the bird's own song, LMAN is the last stage at which responses to this auditory information could be transformed before being transmitted to vocal motor areas, where such responses may influence vocal production. Indeed, previous extracellular studies have indicated that LMAN's auditory selectivity is greater than that at earlier stages of the AFP. To determine whether LMAN local circuitry transforms or simply relays song-related auditory information to vocal control neurons, it is essential to distinguish local from extrinsic contributions to LMAN's auditory selectivity. In vivo intracellular recordings from LMAN projection neurons, coupled with local circuit inactivation, reveal that much of LMAN's song selectivity is supplied by its extrinsic inputs, but selective blockade of GABA receptors indicates that local inhibition is required for the expression of song selectivity. Therefore, LMAN neurons receive highly song-selective information, but LMAN's local circuitry can mask these selective inputs, providing a mechanism for context-dependent auditory feedback.

Acoustic Stimulation↗

The latency of auditory nerve-brainstem responses in sensorineural hearing loss.

The use of auditory nerve-brainstem responses in differential diagnosis of hearing loss is based on several properties of these responses including response latency. The auditory nerve response latency has been shown to be prolonged in conductive hearing loss. The latency of the brainstem responses is also often prolonged in retrocochlear hearing loss. However, the effect of sensorineural hearing losses on auditory nerve response latency is not clear. Several authors report that response latency is prolonged in sensorineural loss, whereas others claim that it is unchanged. To study this, auditory nerve-brainstem responses to 75 dB HL clicks were recorded in normal-hearing subjects and in those with various degrees of high-frequency sensorineural hearing loss. In the more extreme hearing losses, the auditory nerve response could not be seen in the response trace, so the latency of the earlobe positive wave from the region of the inferior colliculus was considered as mirroring auditory nerve response latency, since the time interval between these two waves has been shown to be constant. The average latency of the more severe hearing loss group (more than 40 dB hearing loss at 4kHz) was found to be only 0.35 ms longer than that of the normal-hearing group. This value is smaller than that seen in most conductive and retrocochlear hearing losses. This result warrants continued use of prolonged auditory nerve response latency (greater than 0.35 ms) as an indicator of conductive hearing loss. Possible explanations for smaller latency prolongation than expected of the auditory nerve response in sensorineural hearing loss are discussed based on the properties of single auditory nerve fibers.

Audiometry↗

Enhancement of REM sleep with auditory stimulation in young and old rats.

Auditory stimulation applied during rapid eye movement (REM) sleep enhances the duration of REM sleep in cats and humans. The present experiment investigated whether auditory stimulation would enhance REM sleep in young (3-6 months) rats, and also in old (22-24 months) rats which have impaired REM sleep. Baseline sleep records were obtained on two days. Sleep patterns were then assessed during auditory stimulation test sessions. In young rats, auditory stimulation was administered during each REM sleep bout. In old rats, auditory stimulation was administered on a fixed schedule (10 min of stimulation alternating with 15 min quiet). The day after the stimulation session, an additional sleep record (Day 2) was obtained for each rat. In young rats, auditory stimulation enhanced both REM sleep duration and total REM sleep time. In the old rats, which showed impaired sleep measures as compared to young animals, auditory stimulation enhanced both total REM sleep time and the number of REM sleep periods. Residual proactive effects of auditory stimulation (Day 2) were observed in both young and old rats. Thus, auditory stimulation is an effective manipulation with which to augment REM sleep in both young and old rats, and partially attenuates REM sleep impairments in old rats.

Acoustic Stimulation↗

Effects of auditory stimulation during rapid eye movement sleep in healthy volunteers and depressed patients.

Auditory and somesthesic forms of stimulation have substantially increased rapid eye movement (REM) sleep in cats. We investigated whether auditory stimulation, applied during REM sleep or outside REM sleep, would have similar effects in normal volunteers. We also administered auditory stimulation to depressed patients during REM sleep. Subjects were studied during 1 acclimatization night, 2 baseline nights, 4 consecutive nights with auditory stimulation, and 1 followup night without auditory stimulation. Normal volunteers were randomly divided into Group R, which received auditory stimulation during each REM sleep episode, and Group NR, which received auditory stimulation at the end of each REM sleep episode. Depressed patients (Group D) received auditory stimulation during each REM sleep period. Only Group R showed increased REM sleep time during the nights of auditory stimulation and throughout the followup night. This group also increased their sleep efficiency. Group NR showed reduced sleep efficiency due to an increase in both the duration and frequency of awakenings. Group D did not show increased REM sleep time, but did show shortened REM sleep episodes, increased REM sleep frequency, and increased duration of awakenings. Group D did not show clinical changes.

Acoustic Stimulation↗

Effects of selected pharmacological agents on avian auditory and vestibular compound action potentials.

Glutamate is currently the consensus candidate for the hair cell transmitter in the inner ear of vertebrates. However, other candidate transmitter systems have been proposed and there may be differences in this regard for auditory and vestibular neuroepithelia. In the present study, perilymphatic perfusion was used to deliver prescribed concentrations of ten drugs to the interstitial fluids of the inner ear of hatchling chickens (n = 124). Dose-response curves were obtained for four of these pharmacological agents. The work was carried out in part to distinguish further the neuroepithelial chemical receptors mediating auditory and vestibular compound action potentials (CAPs). Kainic acid (KA) eliminated both auditory and vestibular responses. D-alpha-Aminoadipic acid (DAA) and dizocilpine maleate (MK-801), both NMDA-specific antagonists, failed to alter vestibular CAPs at any concentration. MK-801 significantly and selectively reduced auditory CAPs at concentrations equal to or greater than 1 mM. Similarly, kynurenic acid (4-hydroxyquinoline-2-carboxylic acid, 1 mM), a glutamate antagonist, significantly reduced auditory but not vestibular CAPs. A non-NMDA glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), reduced vestibular CAPs significantly but only at the highest concentration tested (1 mM). In contrast, CNQX reduced auditory responses at concentration as low as 1 microM. The CNQX concentration effective in reducing auditory CAPs by 50% (EC(50)) was approximately 20 microM. Glutamate (1 mM) as well as alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), a glutamate agonist, significantly reduced auditory CAPs (AMPA EC(50)=100 microM). Bicuculline, a GABA(A) receptor antagonist, and L-NAME, a nitric oxide synthase inhibitor, failed to alter responses from either modality. These findings support the hypothesis that glutamate receptors mediate auditory CAPs in birds. However, the results underscore a remarkable difference in sensitivity of the vestibular neuroepithelium (here gravity receptors) to non-NMDA receptor antagonists. The basis of the vestibular insensitivity to glutamate blockers is unknown but it may reflect differences in receptors themselves, differences in the transmission modes available to vestibular synapses or differences in the access of compounds to vestibular neuroepithelial receptors from the interstitial-perilymphatic fluid spaces.

Action Potentials↗

Auditory-visual speech integration by adults with and without language-learning disabilities.

UNLABELLED: Auditory and auditory-visual (AV) speech perception skills were examined in adults with and without language-learning disabilities (LLD). The AV stimuli consisted of congruent consonant-vowel syllables (auditory and visual syllables matched in terms of syllable being produced) and incongruent McGurk syllables (auditory syllable differed from visual syllable). Although the identification of the auditory and congruent AV syllables was comparable for the two groups, the reaction times to identify all syllables were longer in the LLD compared to the control group. This finding is consistent with previous research demonstrating slower processing in learning disabled individuals. Adults with LLD also provided significantly fewer integration-type or McGurk responses compared with their normal peers when presented with speech tokens representing a mismatch between the auditory and visual signal. These results suggest the poor integration for auditory-visual speech previously documented in children with poor language skills also occurs in adults with LLD. LEARNING OUTCOMES: The reader will be able to (1) describe the McGurk effect; (2) describe group differences (language learning disabled and control adults) in auditory and auditory-visual speech perception of consonant-vowel syllables.

Acoustic Stimulation↗

Auditory receptive fields in primate superior colliculus shift with changes in eye position.

The process by which sensory signals are transformed into commands for the control of movement is poorly understood. A potential site for such a transformation is the superior colliculus (SC), which receives auditory, visual and somatosensory inputs and contains neurones that discharge before saccadic eye movements. Along the primary sensory pathways, signals coding the spatial location of auditory, visual and somatosensory targets are based on distinctly different coordinate systems, and it is not known whether each type of sensory input uses a separate motor pathway or if they are converted into a common coordinate system in order to share a single pre-motor circuit. Sensory neurones in the SC have spatially restricted receptive fields (RFs) and are organized into maps across the collicular surface. Acute experiments have shown a rough correspondence between the spatial positions of RFs of neurones encountered along a single dorsal-ventral penetration of the colliculus, regardless of the modality of the effective stimulus, suggesting that auditory, visual and somatosensory maps might be in register. However, in these conditions the head-centred auditory system and the retinotopic visual system are aligned because the eyes are in the primary orbital position. Moreover, other data have suggested that the primate SC is organized in motor, not sensory, coordinates, although in the cat, eye position was found to have no effect on auditory receptive fields. We therefore sought here to determine what happens to the registration of the auditory and visual maps in the alert, behaving animal. Monkeys, with heads fixed, were trained to make delayed saccadic eye movements to auditory or visual targets from one of three initial fixation points while the activity of single neurones was recorded extracellularly. We found that the auditory receptive fields shifted with changes in eye position, allowing the auditory and visual maps to remain in register.

Acoustic Stimulation↗

Changes in visual and auditory response time during conscious sedation with propofol.

BACKGROUND: Using a push-button device, we investigated whether visual or auditory response time would increase with increasing sedation, and assessed the responsiveness score of the Observer's Assessment of Alertness/Sedation (OAA/S) scale at the point of first loss of response to visual or auditory stimulation. METHODS: In experiment 1 we applied visual and auditory stimulation to 19 patients as the propofol target plasma concentration (CPT) was increased to determine whether the visual or auditory response would be lost first. Thirty patients were each then infused with propofol, starting at a CPT of 0.3 microg ml(-1) and increasing by increments of 0.2 microg ml(-1), during which visual (experiment 2) or auditory (experiment 3) stimulation was applied when the effect-site concentration (CE) of propofol reached CPT. Visual response time (VRT), auditory response time (ART), CE and total amounts of propofol, and OAA/S score at the first loss of visual/auditory response were measured. RESULTS: Visual response disappeared earlier than auditory response in 84.2% of the patients. Visual response time and ART were linearly prolonged as the CE of propofol increased. The CE and total amounts of propofol at the first loss of visual response were 1.2 +/- 0.4 microg ml(-1) and 57.9 +/- 16.7 mg, compared with 1.4 +/- 0.5 microg ml(-1) and 71.6 +/- 26.1 mg, respectively, at the first loss of auditory response. The median (range) OAA/S scores at the first loss of visual and auditory response were 4 (3-4) and 3 (2-4), respectively. CONCLUSION: VRT and ART were linearly prolonged with increasing sedation. Visual response may be useful in monitoring conscious sedation.

Acoustic Stimulation↗

Auditory influences on visual temporal rate perception.

Visual stimuli are known to influence the perception of auditory stimuli in spatial tasks, giving rise to the ventriloquism effect. These influences can persist in the absence of visual input following a period of exposure to spatially disparate auditory and visual stimuli, a phenomenon termed the ventriloquism aftereffect. It has been speculated that the visual dominance over audition in spatial tasks is due to the superior spatial acuity of vision compared with audition. If that is the case, then the auditory system should dominate visual perception in a manner analogous to the ventriloquism effect and aftereffect if one uses a task in which the auditory system has superior acuity. To test this prediction, the interactions of visual and auditory stimuli were measured in a temporally based task in normal human subjects. The results show that the auditory system has a pronounced influence on visual temporal rate perception. This influence was independent of the spatial location, spectral bandwidth, and intensity of the auditory stimulus. The influence was, however, strongly dependent on the disparity in temporal rate between the two stimulus modalities. Further, aftereffects were observed following approximately 20 min of exposure to temporally disparate auditory and visual stimuli. These results show that the auditory system can strongly influence visual perception and are consistent with the idea that bimodal sensory conflicts are dominated by the sensory system with the greater acuity for the stimulus parameter being discriminated.

Acoustic Stimulation↗