Middle Latency Auditory Evoked Potentials Research Articles

Changes in Middle Latency Auditory-Evoked Potentials of the Rat Exposed to Styrene.

Effects of styrene exposure on middle latency auditory-evoked potentials (MAEPs), which reflect the central auditory function, were investigated. As significant delay in latencies of No, Po, Na, and Pa components and increases in the peak to peak intervals of MAEPs, but not amplitudes, were observed in a dose‐dependent manner. The present and our previous studies demonstrate that electrophysiological alterations occur before neuronal cell damage induced by styrene exposure. The present results suggested that styrene has a marked effect on the processing of auditory information related to MAEPs.

Topographic Analysis of Epidural Pure-Tone–Evoked Potentials in Gerbil Auditory Cortex

This study investigated the tonotopic organization of pure-tone-evoked middle latency auditory evoked potentials (MAEPs) recorded at the auditory cortical surface in unanesthetized gerbils. Multielectrode array recording and multiple linear regression analysis of the MAEP demonstrated different degrees of tonotopic organization of early and late MAEP components. The early MAEP components P1 and N1 showed focal topography and clear dependence in location and size of cortical area covered on pure-tone frequency. The later components P2 and N2 showed a widespread topography which was largely unaffected in location and size of cortical area covered by pure-tone frequency. These results allow delimitation of the neural generators of the early and late MAEP components in terms of the spectral properties of functionally defined neural populations.

Middle latency auditory evoked potentials in patients with parkinsonism.

The aim of this study was to assess the middle latency auditory evoked potential (MLAEP) findings in idiopathic Parkinson's disease (IPD) and in patients who are regarded as having atypical parkinsonian disorders (AP) and to determine whether MLAEPs could contribute to the differential diagnosis of IPD and AP.MLAEPs were evaluated in 19 control subjects and in a total of 35 patients with parkinsonism, of which 27 had IPD and 8 had AP. Among IPD patients, P1 was absent in 1 nondemented patient with young-onset Parkinson's disease (YOPD) (5%) and in 2 of 7 demented (28.5%) IPD patients. In the AP group, 3 of the 7 (42.8%) nondemented patients and the one patient with dementia showed the absence of P1. The absence of P1 was found to be significantly higher in AP patients than IPD patients (p=0.0335).In conclusion, MLAEPs were found to be normal in nondemented IPD patients with only a few exceptions. The absence of P1 in nondemented patients with parkinsonian symptoms may bring the diagnosis of IPD into question. The absence of P1 could be detected in AP patients at least as often as in demented IPD patients. Thus, the measurement of MLAEPs may be a clinically useful adjunct to the clinical examination of patients with parkinsonism.

Use of midlatency auditory-evoked potentials as indicator of unconsciousness in the dog: characterisation of the effects of acepromazine–thiopentone, medetomidine–thiopentone and medetomidine–butorphanol–midazolam combinations

Middle latency auditory-evoked potentials were measured in sedated and anaestetised dogs to determine their possible usefulness in monitoring of unconsciousness during anaesthesia and to compare the effects of anaesthetic protocols. There were three groups of five dogs: group I received acepromazine; groups 2 and 3 received medetomidine; 30 minutes later, groups 1 and 2 received thiopentone and group 3 received midazolam and butorphanol. Groups 2 and 3 received atipamezole 60 minutes after medetomidine was administered. Auditory-evoked potentials were recorded at time 15, 40 and 75 minutes. Thiopentone administration resulted in a profound modification of the pattern of response, and several peaks were no longer identified. In group 3, the administration of midazolam-butorphanol tended to increase the latency of the different peaks, but lesser than thiopentone did. Middle latency-evoked potentials appeared to be potentially useful in the monitoring of unconsciousness in the dog.

Equivalent dipoles for middle latency auditory evoked potentials using the dipole tracing method

During the last decade, new dipole localization techniques have prompted the search for the neuronal generators of evoked potentials. In this study we have reported the equivalent dipoles for the middle latency auditory evoked potentials (MAEPs) by the mean of these localization using the dipole tracing method. MAEPs that were recorded from 19 normal human subjects attending to random binaural clicks were analyzed using the dipole tracing method. Equivalent dipoles (EDs) were found, using both the single-dipole model and the two-dipole model, for components occurring from 0 to 60 ms after stimulus onset. The dipole analysis accounted for the real head geometry based on three-dimensional digitization of measured head shape, and the results were experimentally correlated to those of magnetic resonance imaging to increase the accuracy of ED localization. For components in the first 15 ms latency (P0 and Na), neither model provided EDs with reproducible high dipolality. Na was particularly difficult to analyze, as this component was often contaminated by myogenic potentials. The results provided by the two-dipole model for the Pa component (20–30 ms) showed three variations: in three subjects, one ED was located in each supratemporal cortex; in another three, one ED was located in the right temporal cortex and the other in the midbrain; and in the remaining thirteen subjects, both EDs were in the midbrain. The single-dipole model and the two-dipole model both found EDs in the midbrain for Nb. Further study is necessary to determine the cause or causes of the variety in our results. And it is also necessary to try the study using unilateral ear stimulation with/without contralateral masking noise for understanding the mechanism of the binaural interaction.

Post-withdrawal changes in middle-latency auditory evoked potentials in abstinent human alcoholics

We investigated the effects of chronic alcoholism on middle-latency auditory evoked potentials (MAEP) in 14 male alcoholics with 1–6 weeks of abstinence (without other severe disorders) and 13 age-matched male social-drinker controls. The peak amplitude of a positive deflection (Pa) of the MAEP, peaking at about 30 ms post-stimulus, was significantly larger in the alcoholics than in the controls ( P<0.01), and notably, a significant negative correlation ( r=−0.65) was observed between the Pa amplitude and duration of abstinence in the alcoholics. The present results suggest that the post-withdrawal brain hyperexcitability in the alcoholic brain, gradually recovering with abstinence, could be objectively and non-invasively studied with the MAEP.

On-line analysis of middle latency auditory evoked potentials (MLAEP) for monitoring depth of anaesthesia in laboratory rats

In laboratory animals as well as in human beings a depth of anaesthesia, where the subject has no pain or recall of events from the surgery, should be provided. Haemodynamic parameters such as heart rate and blood pressure are not a guarantee for an optimal depth of anaesthesia, especially when using neuromuscular blocking agents (NMBA). A number of studies suggest that the Middle Latency Auditory Evoked Potentials (MLAEP) contain information about the state of consciousness in humans. The purpose of this study was to examine whether the AEP could serve as an indicator of depth of anaesthesia in rats. The AEP was elicited with a click stimulus and monitored in an 80 ms window synchronised to the stimulus. The AEP was extracted applying an Auto Regressive Model with Exogenous Input (ARX-model) from which a Depth of Anaesthesia Index (DAI) was calculated. DAI was normalised to 100 while awake and decreasing gradually to a level between 50 and 20 as the rat was anaesthetised. Nine rats were anaesthetised and included in the study. Four doses of Hypnorm vet.® and Dormicum® were given as a total, each with 5 minutes interval. Clinical signs of the level of anaesthesia were observed simultaneously with the AEP. The results showed that in four rats DAI decreased to a level below 30 while anaesthetised. In the remaining five rats the AEP was only decreased to a level below 45. The results indicated that a simple dosing regimen based on weight was unable to give the same depth of anaesthesia in individual rats. The decrease in the DAI correlated well with the loss of stimulus response. In conclusion, MLAEP could be used as an indicator of depth of anaesthesia in rats during Hypnorm vet.® and Dormicum® administration. However studies applying other anaesthetic drugs should be carried out, before a conclusion of the general utility of the method can be made.

Auditory steady-state responses to click trains from the rat temporal cortex

In order to investigate the mechanisms underlying the generation of steady-state responses (SSRs), auditory evoked potentials elicited by click trains presented at several stimulation rates (30, 40, 50, 60 Hz) were recorded in 7 awake rats by means of epidural electrodes placed over the temporal cortex. Mean amplitude-rate function calculated on the recorded responses appeared almost flat and showed the maximum value at 50 Hz, while mean phases showed a linear increase when increasing the stimulation rate. In each rat, predictions of the recorded responses at 30, 40, 50 and 60 Hz were synthesized by superimposing middle-latency auditory evoked potentials (MAEPs) at suitable time intervals at each rate. Mean amplitudes calculated on the predicted curves decreased linearly when increasing the stimulation rate and appeared higher in comparison to those obtained from the recorded SSRs. Predicted phases showed a linear increase when increasing the stimulation rate and were leading with respect to corresponding phase values calculated for recorded SSRs. Our findings indicate that the MAEP superimposition mechanism does not adequately predict the generation of temporal recorded SSRs in rats. This was explained by admitting that phenomena related to the recovery cycle and, to a lesser extent, to rate-dependent facilitating effects come into play.

Comparison of the effects of halothane, isoflurane and methoxyflurane on the electroencephalogram of the horse

We have investigated in eight ponies the effects of three different end-tidal concentrations of halothane, isoflurane and methoxyflurane on median (F50) and 95% spectral edge (F95) frequencies of the EEG and the second differential (DD) of the middle latency auditory evoked potential (MLAEP). The three concentrations of each agent were chosen to represent approximately the minimum alveolar concentration (MAC), 1.25 MAC and 1.5 MAC for each agent. During halothane anaesthesia, F95 decreased progressively as halothane concentration increased, from mean 13.9 (SD 2.6) at 0.8% to 11.9 (1.1) at 1.2%. DD was lower during anaesthesia with the highest concentration (21 (6.5)) compared with the lowest (27.6 (11.4)). There were no significant changes in F50. During isoflurane anaesthesia, there was a small, but significant increase in F95 between the intermediate and highest concentrations (10.2 (1.5) to 10.8 (1.6)). There were no changes in F50 and DD. Values of F95, F50 and DD at all isoflurane concentrations were similar to those of halothane at the highest concentration. During methoxyflurane anaesthesia, F95 and F50 decreased progressively as methoxyflurane concentration was increased, from 21.3 (0.7) and 6.5 (1), respectively, at 0.26%, to 20.1 (0.6) and 5.6 (0.8), respectively, at 0.39%. DD was lower during anaesthesia with the highest concentration of methoxyflurane (25.7 (7.8)) compared with the lowest (39.7 (20.6)). Values of F95, F50 and DD at all methoxyflurane concentrations were higher than those seen with halothane at the lowest concentration. The different relative positions of the dose-response curves for EEG and MLAEP changes compared with antinociception (MAC) changes suggest differences in the mechanisms of action of these three agents. These differences may explain the incomplete adherence to the Meyer-Overton rule.

Delayed recovery of auditory cortical evoked potentials is correlated with cortical neuronal death after transient cerebral ischemia in awake gerbils

Early detection of irreversible neuronal change after transient cerebral ischemia is important so that adequate treatment can be initiated within the therapeutic window. We have examined the correlation between changes in middle-latency auditory evoked potentials (MAEPs) and histological changes in the auditory cortex of awake Mongolian gerbils subjected to 4 min or 12 min of transient cerebral ischemia. Post-ischemic MAEPs were characterized by the appearance of a markedly large negative and positive component at approximately 17–22 ms latency in both groups. Delay in the appearance of the high amplitude (maximal amplitude at 45 min after recirculation in the 12-min ischemia group) precedes the slowly developing death of neurons in the auditory cortex that results from transient cerebral ischemia.

Effects of aging on middle-latency auditory evoked potentials: A cross-sectional study

The results of previous studies comparing the middle-latency auditory evoked potentials (MAEPs) of young and elderly subjects have suggested that thalamic inhibitory deficits underlie age-related increases in MAEP amplitudes. MAEPs were recorded from 73 healthy subjects aged between 20 and 86 years. The latencies of MAEPs recorded at Fz were subjected to two-way analyses of variance for the effects of age group and sex. Amplitude data were subjected to analyses of covariance with age group and sex as between-subjects factors, electrode position as within-subject factor, and individual perceptual thresholds as covariates. Variables exhibiting significant effects of age group were further investigated by regression analysis. Age correlated positively with Na, Na-Pa, and Nb-Pb amplitudes. The distribution of Na-Pa amplitude over the scalp varied with age. The observed age-related increases in amplitude are believed to reflect diminished capacity of subcortical and related cortical systems to inhibit the response to repetitive auditory stimuli that require no attentional effort. Possible age-related changes in the cortical distribution of MAEPs are also discussed.

Intérêt diagnostique des potentiels évoqués auditifs de latence moyenne (PEALM) dans la sclérose en plaques

This study was aimed at assessing the interest of middle latency auditory evoked potentials (MLAEP) recordings in multiple sclerosis (MS). Brainstem auditory evoked potentials (BAEP) and MLAEP were recorded in 40 control subjects and 65 patients who had MS according to Poser's criteria. Na and Pa latencies were significantly delayed in the MS group. These abnormalities were detected in 60% of the patients. In 26% of the cases with normal BAEP, abnormalities of MLAEP were present. In 71% of the patients abnormalities of both BAEP and MLAEP were observed. These results suggest the ability of MLAEP recordings to detect lesions of the auditory pathways rostral to the pons and show the value of their combined recordings in MS patients.

The P1 component of the middle latency auditory potential may differentiate a brainstem subgroup of Alzheimer disease.

The P1 component of the middle latency auditory evoked potential (MLAEP) was found to be absent in 47.5% of 101 patients with Alzheimer disease (AD). Lack of a P1 component recently has been associated with a more rapid decline in cognitive performance. The blink reflex (BR) was tested in 36 patients with probable AD and 17 elderly control subjects. All subjects also underwent P1 recording. Patients lacking a P1 potential showed a significant increase in latency of the contralateral R2 response of the BR. The P1 component and the R2 response may differentiate a subgroup of AD patients with involvement of the brainstem, especially the reticular formation.

Effects of ketamine on CNS-function

The present review summarises the main actions of racemic ketamine and ketamine enantiomers on central nervous system receptors. The primary CNS action of ketamine appears to be a non-competitive block of N-methyl-D-aspartate receptors. Although numerous other receptors (e.g., GABA, nicotinic acetylcholine, opiate, voltage-operated channels) have been reported to interact with ketamine, their role in inducing dissociative anaesthesia is still under discussion. In humans, characteristic electroencephalographic (EEG) changes after administration of ketamine are dose-dependent increases in delta, theta, and beta power. In equipotent doses S-(+)-ketamine induces similar EEG changes. However, in comparison to racemic ketamine and S-(+)-ketamine, R-(-)-ketamine does not suppress the EEG to the same extent. Former studies suggested that ketamine is a proconvulsive agent; however, recent studies have demonstrated anticonvulsive and even neuroprotective properties. In humans, low-dose ketamine has no influence on early cortical peaks of somatosensory evoked potentials (SEP). Larger doses induce increases in SEP amplitude while latencies are unchanged. Recent data indicate that analgesia induced by low-dose ketamine may be quantitated by specific pain-related SEP. Significant reductions of pain-induced cortical potentials may be correlated with subjective pain ratings. Brain-stem auditory evoked potentials (AEP) are not influenced by ketamine. Interestingly, in contrast to many other anaesthetics, middle-latency AEP were not altered by racemic and S-(+)-ketamine. This observation may indicate insufficient suppression of auditory stimulus processing during ketamine anaesthesia. Motor evoked responses to transcranial electrical or magnetic stimulation in humans are not markedly suppressed by ketamine.

P261 Middle latency auditory evoked potential (MLAEP) monitoring in midazolam induced anesthesia

Brainstem cavernous malformations (BCM) have a high incidence of bleeding and rebleeding and carry a high rate of neurologic morbility. Locations in the tectal plate that represent a small percentage of BCMs have rarely been reported in the literature. The authors present a case of a patient with such localization who was successfully operated.A 24-year-old male known for having a tectal plate cavernoma with obstructive hydrocephalus, previously treated by shunting in another hospital, was admitted in our institute because of increasing headaches, gradual drowsiness, and the inability to stand up. Investigations revealed a compressive cavernoma lateralized on the left side of the tectal plate and a residual hydrocephalus in spite of the previous shunting. A new shunting procedure did not improve clinical conditions. Thus, an aggressive surgical resection was decided upon and was performed through an occipital-transtentorial approach with the aid of intraoperative brainstem and middle latency auditory evoked potentials (BAEPs/MLAEPs) monitoring. Total resection was achieved without significant deterioration except a hypovoltage of wave V after stimulation of the right ear, demonstrating a left collicular dysfunction. The patient was discharged on the 36th day after surgery. Seven months later, audiometry was normal, in spite of the persistence of the hypovoltage of the V wave after stimulation of the right ear, and functional status appraised using the Karnofsky score was at 100%. Professional activity could be resumed.Tectal plate cavernomas (TPC) represent a special entity of BCM. They are surgically accessible lesions on the dorsal aspect of the brainstem. Our preferred approach is the occipital-transtentorial approach. The use of intraoperative auditory evoked potentials monitoring make the surgical resection safer.

Middle latency auditory evoked potentials in epilepsy.

Middle latency auditory evoked potentials (MLAEPs) have been recorded after cortical lesions and seizure surgery. We recorded interictal MLAEPs in 14 patients with well documented complex partial and secondary generalized seizures. Na and Pa potentials did not differ in latency between patients and controls, although both were longer among seizure patients. Pa and Na were significantly reduced in amplitude in complex partial seizure patients compared to controls. These findings accord with previous suggestions that MLAEPs may be generated subcortically but modulated by temporal lobe structures. MLAEPs may be of value in differentiating temporal and extratemporal epilepsy. They may also help clarify interictal cognitive or behavioral symptoms related to epilepsy or the effects of antiepileptic medication.

Autoregressive Modeling with Exogenous Input of Middle-Latency Auditory-Evoked Potentials to Measure Rapid Changes in Depth of Anesthesia

Obtaining an adequate depth of anesthesia is a continuous challenge to the anesthetist. With the introduction of muscle-relaxing agents the traditional signs of awareness are often obscured, or difficult to interpret. These signs include blood pressure, heart rate, pupil size, etc. However, these factors do not describe the depth of anesthesia (DA) in a cerebral activity sense. Hence, a better measure of the DA is required. It has been suggested that Auditory-Evoked Potentials (AEP) can provide additional information about the DA. The general method of extracting AEP is by use of a Moving Time Average (MTA). However, the MTA is time consuming because a large number of repetitions is needed to produce an estimate of the AEP. Hence, changes occurring over a small number of sweeps will not be detected by the MTA average. We describe a system-identification method, an autoregressive model with exogeneous input (ARX) model, to produce a sweep-by-sweep estimate of the AEP. The method was clinically evaluated in 10 patients anesthetized with alfentanil and propofol. The time interval between propofol induction and the time when the Na-Pa amplitude was decreased to 25% of the initial amplitude was measured. These measurements showed that ARX-estimated compared to MTA-estimated AEP was significantly faster in tracing transition from consciousness to unconsciousness during propofol induction (p < 0.05).

Insulin-associated modulation of neuroendocrine counterregulation, hypoglycemia perception, and cerebral function in insulin-dependent diabetes mellitus: evidence for an intrinsic effect of insulin on the central nervous system.

Evidence for an intrinsic effect of insulin on the central nervous system is accumulating. To test the hypothesis that insulin per se may modulate neuroendocrine counterregulation, hypoglycemia perception, and cerebral function in insulin-dependent diabetes mellitus, we examined 27 patients without any sign of classical autonomic neuropathy or evidence of so-called hypoglycemia unawareness. We used the hyperinsulinemic (0.67 vs. 2.00 mU/kg.min), stepped hypoglycemic (5.6/3.5/2.4/2.0 mmol/L) clamp technique to assess the patient's awareness of and response to equivalent hypoglycemic stimuli under different degrees of physiological hyperinsulinemia (approximately 270 vs. approximately 810 pmol/L) after an overnight euglycemic clamp (5.6 mmol/L). Simultaneously, the patient's cerebral function was assessed from his electrophysiological activity and neuropsychological skills. Higher degrees of physiological hyperinsulinemia caused enhanced neuroendocrine response (adrenaline, P < 0.05; noradrenaline, P < 0.03; GH, P < 0.02; beta-endorphin, P < 0.03; ACTH, P = 0.12; cortisol, P = 0.06; PRL, P = 0.08) and symptom awareness (total symptoms, P < 0.04; autonomic symptoms, P < 0.02; neuroglycopenia symptoms, P < 0.05; sweating, P < 0.05; heart pounding, P < 0.02; trembling, P < 0.01; lack of concentration, P < 0.02) to occur. Deteriorations of electrophysiological activity (middle latency auditory-evoked potentials, P < 0.04; Pa peak latencies, P < 0.05; Pa-V interpeak latencies, P = 0.08) and neuropsychological skills (Stroop test, P < 0.05; trail making, P = 0.12) were more pronounced the higher the insulin level, but at similar blood glucose concentrations. We conclude that insulin-associated modulation of neuroendocrine counterregulation, hypoglycemia perception, and cerebral function may occur in insulin-dependent diabetes mellitus, which indicates an intrinsic effect of insulin on the human brain.

PS-9-3 Investigation on middle latency auditory evoked potentials (MLAEPs): do P50 latencies correlate with the reaction times?

PS-9-3 Investigation on middle latency auditory evoked potentials (MLAEPs): do P50 latencies correlate with the reaction times?

The P1 component of the middle latency auditory evoked potential predicts a practice effect during clinical trials in Alzheimer's disease.

Thirty-five patients with probable Alzheimer's disease who were enrolled in an experimental drug trial of linopirdine underwent repeated testing that included recording the middle latency auditory evoked potential (MLAEP), the Mini-Mental State Examination (MMSE), and the Alzheimer's Disease Assessment Scale Cognitive Subscale (ADASCOG). Patients lacking the P1 component of the MLAEP exhibited a significantly greater decline in cognitive function as measured by the ADASCOG over 56 weeks. This decline appeared to be due to a less robust practice effect, which was maximal in all patients at 16 weeks. At the end of 56 weeks the entire group of patients was near baseline with respect to the ADASCOG. This lack of the annualized decline expected from other longitudinal studies may be explained by practice and placebo effects. The MMSE did not exhibit a practice effect and showed the expected decline in scores.