Brainstem Auditory Evoked Potentials Components Research Articles

Brainstem auditory pathway maturation in term neonates with congenital cytomegalovirus infection: a cohort study.

Congenital cytomegalovirus infection (cCMVi) is a leading cause of sensorineural hearing loss (SNHL) and developmental delay. Brainstem auditory evoked potentials (BAEPs) recording allows assessment of central auditory pathway maturation in neonates. We aimed to characterize the effect of cCMVi on the maturation of the brainstem auditory pathway in term neonates. We retrospectively reviewed medical records of neonates born with cCMVi in 2010-2018 and characterized their auditory pathway maturation using brainstem auditory-evoked potentials (BAEPs). We compared inter-peak latency differences (IPLDs) of the main BAEP components (I-V, I-III, and III-V) in terms of cCMVi patients and healthy controls and described their changes in cCMVi patients throughout the first year of life. Of 101 cCMVi patients, 57 (56.4%) were considered symptomatic, 6 (5.9%) were small for gestational age, 6 (5.9%) had microcephaly, 4 (4%) had thrombocytopenia, 5 (6.6%) had hepatitis, 2 (2.1%) had retinitis, 47 (49.5%) had typical abnormalities on head ultrasound, 9 (8.9%)developed SNHL, and 34 (59.6%) received antiviral therapy. No significant difference was found between IPLDs of full-term cCMVi patients compared to controls throughout the entire auditory pathway (I-III, III-V, and I-V IPLDs), for both ears (p > 0.05). On serial BAEP examinations, cCMVi patients presented decreased IPLDs throughout the first year of life (p < 0.05 ofcompared 1st, 2nd, and 3rd BAEPs in both ears). Conclusions: Intrauterine cytomegalovirus infection does not affect the auditory brainstem maturation process in term neonates. Our findings support previous studies noting the normal neurodevelopmental outcome of asymptomatic cCMVi patients, suggesting antiviral treatment is not warranted in these cases. What is Known: •cCMVi is a leading cause of developmental delay and hearing loss. Treatment is recommended for patients with symptomatic diseases who are at significant risk of long-term sequelae. • It is unknown whether cCMVi affects the central nervous system maturation process. What is New: •We performed a neurophysiological evaluation of brainstem conduction by recording the BAEPs. We found that cCMVi has no significant impact on central conduction times along the auditory pathways in the brainstem at birth nor changes the neuronal maturation process during the first year of life. •Our findings suggest that cCMVi does not universally affect central nervous system maturation, supporting a highly selective approach when considering the benefits of antiviral therapy.

Continuous positive airway pressure treatment may negatively affect auditory maturation in preterm infants.

Nasal continuous positive airway pressure (CPAP) devices generate loud noise, which might harm auditory function and maturation. The function of auditory pathways can be examined by using brainstem auditory evoked potential (BAEP) and brainstem audiometry (BA) recordings. Our objective was to study whether CPAP treatment during the neonatal period is associated with abnormalities in BAEP and BA recordings. Included in this retrospective study were preterm infants (birth weight ≤1500g and/or gestational age ≤32weeks) born between 2002 and 2006 with a comprehensive clinical background and follow-up data, including the duration of CPAP treatment (n=162). BAEP and BA were recorded near the mean corrected age of one month. The following variables from BAEP and BA examinations were analysed: latencies of BAEP components I, III, V, interpeak intervals (IPI) I-V, I-III, III-V (ms), amplitude I and V (µV), amplitude ratio I/V and BA thresholds. In the adjusted analysis, a longer CPAP treatment leads to longer latencies of BAEP component III (p=0.01) and V (p=0.02) in the right ear. CPAP treatment may impair the auditory maturation and processing mediated via the dominant right ear. The hearing and neurodevelopment of the children who are treated with CPAP should be followed.

Progressive myoclonus epilepsy without renal failure in a Chinese family with a novel mutation in SCARB2 gene and literature review

PurposeTo describe the clinical and genetic features of a Chinese progressive myoclonus epilepsy (PME) patient related with SCARB2 mutation without renal impairment and review 27 SCARB2-related PME patients from 11 countries. MethodsThe patient was a 27-year-old man with progressive action myoclonus, ataxia, epilepsy, dysarthria and absence of cognitive deterioration. Renal functional test was normal. Electroencephalography (EEG) showed progressively slowed background activity and sporadic generalized spike-and-wave discharges. Electromyography (EMG) showed slowed motor and sensory nerve conduction velocities and distal motor latency delay accompanied by normal compound motor action potential (CMAP) and amplitudes of sensory nerve action potential (SNAP). The amplitude of cortical components of brainstem auditory-evoked potential (BAEP) was normal with slightly prolonged latencies. Generalized atrophy, ventricle enlargement and white matter degeneration was observed in brain magnetic resonance imaging (MRI). Open muscle biopsy and genetic analysis were performed. Two hundred healthy individuals were set for control. Quantitative real time PCR (qPCR), western blotting and immunofluorescence were carried out to evaluate the fate of the SCARB2 mRNA and lysosomal-membrane type 2 (LIMP2) protein level. ResultsOne homozygous mutation in SCARB2 gene (c.1187 + 5G > T) was identified in the patient. Each of his parents carried a heterozygous variant. This mutation was not detected among the healthy controls and predicted to be damaging or disease causing by prediction tools. qPCR revealed a significantly lower level of SCARB2 mRNA in peripheral blood cell of the proband compared with his parents and healthy control individuals. Muscle biopsy showed mild variation in fiber size. Western blotting and immunofluorescence detected an extremely weak signal of LIMP2 protein from skeletal muscle of the proband. ConclusionIn this study, we identified a SCARB2-related PME patient with normal renal function and a novel homozygous splicing mutation. SCARB2 gene should be analyzed in patients with progressive action myoclonus, epilepsy, peripheral neuropathy, without cognitive deterioration or renal failure.

P286 Visual and brainstem auditory evoked potentials abnormalities in the patients with systemic lupus erythematosus

Objectives Lupus erythematosus (SLE) is a systemic disease with possible nervous system involvement, regarded as unfavorable prognostic factor. Evoked potentials (EP) are electrophysiological markers of disturbed central nervous system (CNS) function, even in subclinical stage of CNS disorders. The purpose of the study was to evaluate parameters of EP in the patients with SLE with or without neuropsychiatric manifestation (NPSLE). Methods The study comprised 53 patients with SLE (49 women, 4 men, aged 21–62, mean 38.3) and 40 healthy, age- and gender- matched controls. 33 patients were classified as having NPSLE. Visual evoked potentials (VEP) and brainstem auditory evoked potentials (BAEP) were performed in all the subjects. Latencies and amplitudes of VEP and BAEP components were compared between SLE patients and controls and between NPSLE and non-NPSLE patients. Results Mean latency of P100 component of VEP for the right eye was significantly longer (104.3 ms vs 102.06 ms; p = 0.05) and mean amplitude of the I component of BAEP for the right ear was significantly lowered (0.25 μ V vs 0.30 μ V; p = 0.04) in the SLE patients in comparison with the controls. No differences were found between NPSLE and non-NPSLE patients. Discussion Asymmetric abnormalities of EP correspond with multifocal brain damage in the course of SLE, although they are not specific for the background of the disease. Conclusions and significance Parameters of VEP and BAEP show asymmetric abnormalities in SLE patients, regardless of the clinical symptoms of CNS involvement. EP may be considered as electrophysiological markers of early CNS dysfunction in the course of SLE.

Prognostic value of SSEP and BAEP in a cohort of deeply sedated mechanically ventilated critically ill patients

Somatosensory evoked potentials (SSEP) and brainstem auditory evoked potentials (BAEP) might be useful for predicting outcome in critically ill patients who require deep sedation and mechanical ventilation [1] . However, the impact on outcome of the assessment of brain dysfunction using SSEP and BAEP in this population remains unproven. In this pilot study, we investigated the prognostic value and clinical correlates of the lengthening of inter-peak latencies of SSEP and BAEP components, in a cohort of deeply sedated mechanically ventilated critically ill patients. Median nerve SSEP, BAEP and neurological examination were assessed at bedside, under deep sedation, before day 5 after admission, in intensive care unit (ICU). Interpeak latencies (IPL) of SSEP and BAEP were considered delayed when they were over the mean + 2.5 SD of the ones obtained from our cohort of healthy adults. Primary outcome was mortality in the ICU. Secondary outcome was post-sedation altered mental status defined as the occurrence of delirium or delayed awakening after discontinuation of sedation. Eighty six consecutive patients were enrolled, mean age 61 ± 19 years, and 65% with severe sepsis. Richmond Assessment Sedation Scale (RASS) score at inclusion was -5 (-5 to -4). Thirty seven patients (43%) died in the ICU. A prolonged subcortical-cortical conduction time (P14-N20 IPL SSEP component) i. e. > 5.3 ms, was found an independent predictor of in-ICU mortality after adjustment on total Sequential Organ Failure Assessment score (SOFA) [OR (95% CI) = 2.69 (1.05 to 6.85); P = 0.039]; and after adjustment on non-neurological SOFA [OR (95% CI) = 2.67 (1.05 to 6.81) ; P = 0.040]. Furthermore, delayed P14-N20 IPL SSEP component was associated with absent cough reflex. Finally, there was a trend for association between delayed III-V IPL BAEP component (ponto-mesencephalic conduction time) and post-sedation altered mental status (P = 0.053). These results support the hypothesis of brainstem dysfunction during critically illness [2] , [3] . Studies with larger sample are needed.

Padronização do potencial evocado auditivo de tronco encefálico utilizando um novo equipamento

Standardization of Brainstem Auditory Evoked Potential (BAEP) using a new device. To standardize BAEP responses using a new device developed (NDD) in Brazil. Analysis of absolute latencies, interpeaks and wave amplitudes of BAEP, using a new device developed to study normal-hearing groups (91 adults) and individuals (15 adults) with bilateral neurosensory hearing loss. Responses obtained in the EP15 hearing device/Interacoustics and the NDD were compared. For this, the following paramenters were used: non-filtered click of 100 microsecond (µs), totaling 2000 stimuli in rarefied polarity, stimulation frequency of 13.1 clicks/s, intensity of 80 decibels normalized hearing level (dB nHL), with a window of 10 milliseconds and bandpass filter between 100 and 3000 Hertz (Hz). Significance level was set at 0.05. Absolute latency and interpeak means for 76 normal-hearing individuals with the NDD were: wave I=1.50, III=3.57, V=5.53, I-III=2.06, III-V=1.96 and I-V=4.02. When analyzing results according to gender, there was a statistically significant difference for the absolute latencies of waves III and V and in interpeaks I-III and I-V. Mean amplitude value of wave I=0.384 microvolt (µV) and of wave V=0.825 µV. There was no statistically significant difference between the absolute latencies and interpeaks of the two devices in the same individual. The components of BAEP with the NDD in normal-hearing subjects were similar regarding the tested ears, with statistically lower latencies in women. The BAEP latencies in the same individual with NDD were similar to those obtained with the EP15 / Interacoustics. Normal values of BAEP were obtained in normal-hearing adults.

Localizing brain stem lesions with brain stem auditory evoked potentials.

Based on a survey of brain stem auditory evoked potentials (BAEPs) in animals and humans with localized brain stem lesions compared to the recognizability of BAEP components in normal materials, it was concluded that BAEP examination might localize lesions to a high or low level and diffusely within the brain stem. In 155 patients with multiple sclerosis, vascular disorders or other lesions from a neurological department, the involvement of the brain stem was clinically estimated to be negative, situated at a high or low level or diffuse. Correlation between location of the lesions assessed by clinical versus BAEP examination showed correspondence between negative and diffusely abnormal findings, but not with regard to levels within the brain stem. CT-scanning similarly failed to localize lesions to various levels. This was probably due to poorly circumscribed or widespread lesions. The main value of BAEP in neurological patients was to establish clinically silent lesions, especially in patients with multiple sclerosis and only spinal signs.

The maturational process of the auditory system in the first year of life characterized by brainstem auditory evoked potentials

ABSTRACTThe study of brainstem auditory evoked potentials (BAEP) allows obtaining the electrophysiological activity generated in the cochlear nerve to the inferior colliculus. In the first months of life, a period of greater neuronal plasticity, important changes are observed in the absolute latency and inter-peak intervals of BAEP, which occur up to the completion of the maturational process, around 18 months of life in full-term newborns, when the response is similar to that of adults. Objective: The goal of this study was to establish normal values of absolute latencies for waves I, III and V and inter-peak intervals I-III, III-V and I-V of the BAEP performed in full-term infants attending the Infant Hearing Health Program of the Speech-Language Pathology and Audiology Course at Bauru School of Dentistry, Brazil, with no risk history for hearing impairment. Material and Methods: The stimulation parameters were: rarefaction click stimulus presented by the 3A insertion phone, intensity of 80 dBnHL and a rate of 21.1 c/s, band-pass filter of 30 and 3,000 Hz and average of 2,000 stimuli. A sample of 86 infants was first divided according to their gestational age in preterm (n = 12) and full-term (n=74), and then according to their chronological age in three periods: P1: 0 to 29 days (n=46), P2: 30 days to 5 months 29 days (n=28) and P3: above 6 months (n= 12). Results: The absolute latency of wave I was similar to that of adults, generally in the 1st month of life, demonstrating a complete process maturity of the auditory nerve. For waves III and V, there was a gradual decrease of absolute latencies with age, characterizing the maturation of axons and synaptic mechanisms in the brainstem level. Conclusion: Age proved to be a determining factor in the absolute latency of the BAEP components, especially those generated in the brainstem, in the first year of life.

Mechanisms of intraoperative brainstem auditory evoked potential changes.

Brainstem auditory evoked potential (BAEP) changes during intraoperative monitoring may reflect damage to or potentially reversible dysfunction of the ear, the eighth nerve, or the brainstem auditory pathways up to the level of the mesencephalon. They may also be caused by other physiologic mechanisms such as anesthesia, hypothermia, and acoustic masking from drilling noise, or they may result from technical factors that prevent proper stimulus delivery or recording of an evoked potential that is actually present. Cochlear ischemia or infarction resulting from compromise of the internal auditory artery and inner ear damage during temporal bone drilling will affect all BAEP components, including wave I. Direct mechanical or thermal trauma to the eighth nerve will delay, attenuate, and possibly eliminate waves III and V, but wave I, which is generated at the cochlear end of the eighth nerve, may be preserved. During scraping of tumor off the eighth nerve, force applied in an ear-toward-brainstem direction can avulse the fragile fibers of the distal eighth nerve at the area cribrosa. Prolonging the I-to-III interpeak interval during retraction of the cerebellum and brainstem reflects stretching of the eighth nerve, and is often reversible. Vasospasm within the eighth nerve can cause similar, potentially reversible BAEP changes. Damage to the brainstem auditory pathways at or below the level of the mesencephalon will delay and attenuate or eliminate wave V. Wave III is affected similarly if the damage is at or caudal to the region of the superior olivary complex. These BAEP changes may reflect direct mechanical or thermal damage to the brainstem, brainstem compression, or ischemia or infarction resulting from vascular compromise. During BAEP monitoring, examination of the pattern of BAEP changes, analysis of their correlation with surgical maneuvers, and investigation for possible contributory technical factors can help to determine the cause of the BAEP changes and provide the appropriate information to the rest of the surgical team.

Brainstem triggers absence seizures in human generalized epilepsy

Simultaneous analysis of brainstem auditory evoked potentials (BAEPs) with reference to electroencephalography (EEG) was designed to examine the brainstem function corresponding to the EEG event. With this method, we investigated the brainstem function pre- and during the paroxysmal discharge in human absence seizures classified as primary generalized epilepsy (PGE). Two types of functional change in the lower brainstem were revealed as parameters of wave-III components (amplitude and area) of BAEPs without significant change in the upper brainstem. One was long-range biphasic fluctuation (acceleration followed by abrupt deceleration with the maximum −6.4±3.2 s before the seizure onset), and the other was rhythmic oscillation with 3 Hz. The latter, synchronized with the cortical spike-and-wave complex, imposed on the descending slope of the former. One important point is that both preceded the onset of cortical paroxysmal discharge. The results reappraise the classical hypothesis of “centrencephalic system” on seizure generating mechanism in human PGE. The results prove the primary triggering role of the lower brainstem that is independent of sleep-related synchronizations. The method is applicable to other types of EEG event for the investigation of brainstem involvement.

Central and Peripheral Neural Responses in Acromegaly

To assess the function of the central and peripheral nervous systems in patients with untreated acromegaly. We recorded the somatosensory evoked potentials (SSEPs) and brain stem auditory evoked potentials (BAEPs) in 10 patients with untreated acromegaly of brief duration and in 20 age- and sex-matched healthy control subjects to evaluate the function of the central nervous system and at least the median and tibial components of the peripheral nerves. Electrophysiologic studies were done at the time of diagnosis and before the initiation of any treatment for acromegaly. We also studied the distal motor latency, nerve conduction velocity, compound muscle action potentials, and F response in the peroneal nerve; the sensory nerve conduction velocity and sensory potential amplitude were measured in the sural nerve. The mean duration of acromegaly (expressed as time elapsed since patients first recognized signs or symptoms) was 2.4 years. The N(9) and N(13) latencies in median SSEPs and the N(22) latency in tibial SSEPs were significantly prolonged in patients with acromegaly in comparison with the control group; however, central nervous system components of SSEPs and all components of BAEPs were normal. We also noted abnormalities in peroneal motor and sural sensory nerves. No correlation was found between the neurophysiologic data and the basal growth hormone level, the fasting blood glucose level, or the duration of disease. Our results suggest that peripheral, but not central, nervous system involvement exists in patients with untreated acromegaly of short duration.

Binaural interaction and the effects of stimulus intensity and repetition rate in human auditory brain-stem

Binaural interaction (BI) components in brain-stem auditory evoked potential (BAEP) and their changes with stimulus intensity and repetition rate were examined in human adult. Seven BI components were identified, which occurred between the latency range of 5 and 11 ms and coincided consistently with the latency range of BAEP waves IV–VII. Waves DV and DVII, occurring at the downslopes of BAEP-waves V and VII, respectively, were the two most prominent and reproducible BI components. Wave DVII existed consistently at high, moderate and, in most cases, low stimulus intensities, suggesting that this component is neurogenic although acoustic cross-talk may account for a part of its waveform at high stimulus intensities. The latencies of all BI components increased as a function of decreasing stimulus intensity, while the interpeak intervals, especially DV–DVII, were essentially constant at different intensity levels. The amplitudes of BI components decreased slightly with decreasing intensity. As click repetition rate increased, BI wave latencies and interpeak intervals increased slightly and amplitudes decreased slightly. When repetition rate increased to above 20/s, BI components became poorly differentiated. Lower repetition rates, e.g. 10/s, are therefore preferred for routine derivation of the BI. The changes in the latency and amplitude of BI components with stimulus intensity and repetition rate were associated or concomitant with those of the corresponding BAEP components in monaural and binaural potentials. In view of the concomitant relationship between BI and BAEP latency, we designate BI components in association with the corresponding BAEP components.

Binaural interaction and the effects of stimulus intensity and repetition rate in human auditory brain-stem

Binaural interaction (BI) components in brain-stem auditory evoked potential (BAEP) and their changes with stimulus intensity and repetition rate were examined in human adult. Seven BI components were identified, which occurred between the latency range of 5 and 11 ms and coincided consistently with the latency range of BAEP waves IV–VII. Waves DV and DVII, occurring at the downslopes of BAEP-waves V and VII, respectively, were the two most prominent and reproducible BI components. Wave DVII existed consistently at high, moderate and, in most cases, low stimulus intensities, suggesting that this component is neurogenic although acoustic cross-talk may account for a part of its waveform at high stimulus intensities. The latencies of all BI components increased as a function of decreasing stimulus intensity, while the interpeak intervals, especially DV–DVII, were essentially constant at different intensity levels. The amplitudes of BI components decreased slightly with decreasing intensity. As click repetition rate increased, BI wave latencies and interpeak intervals increased slightly and amplitudes decreased slightly. When repetition rate increased to above 20/s, BI components became poorly differentiated. Lower repetition rates, e.g. 10/s, are therefore preferred for routine derivation of the BI. The changes in the latency and amplitude of BI components with stimulus intensity and repetition rate were associated or concomitant with those of the corresponding BAEP components in monaural and binaural potentials. In view of the concomitant relationship between BI and BAEP latency, we designate BI components in association with the corresponding BAEP components.

Brain-stem auditory evoked potential monitoring. Variations of stimulus artifact in brain death

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 subjects with brain death (mean age, 33.2 ± 15.1 years) and 20 healthy volunteers (mean age, 29.8 ± 6.8 years). Brain death was due to head injury (n = 14), encephalitis (n = 3), brain-stem hemorrhage (n = 1), cerebellar hemorrhage (n = 1) or cerebral infarction (n = 1). The presence, latency and amplitude of the individual BAEP components and variations of the stimulus artifact were evaluated. The mean ( ± S.D.) amplitude of the stimulus artifact was 0.26 ± 0.12 μV in the brain-dead subjects and 0.09 ± 0.05 μv in the control group ( P < 0.001, t test). The causes of the phenomenon of increasing stimulus artifacts in the evolution of brain death remain unclear.

Peaks of brainstem auditory evoked potentials in dogs.

The effects of electrode configuration and click polarity on brainstem auditory evoked potentials (BAEP) in dogs were investigated to clarify the inconsistent nomenclature for each peak. Four positive peaks (waves 1, 2, 3 and 4) before a deep negative trough and a fifth positive peak (wave 5) following the trough were the basic components of BAEP in dogs, which were easily identified regardless of recording conditions such as electrode configuration and click polarity. Additional peaks tended to be present when a noncephalic reference electrode and/or single-polarity (rarefaction or condensation) click stimuli were used. The Roman nomenclature for the individual positive peaks of BAEP in dogs is confused owing to variations in the observed waveforms among researchers, but click polarity and/or reference electrode position can explain all the previously reported variations in BAEP waveforms in dogs. When the criteria concerning 'wave V' in the guidelines of BAEP in human beings are applied to avoid further confusion of Roman nomenclature in dogs, it is recommended that the basic five positive peaks (waves 1, 2, 3, 4 and 5 as identified easily with Ai-Vertex configuration and alternating clicks) are designated as waves I, II, III, V and VI, respectively. Wave IV (wave 3b) occurs occasionally before wave V in dogs.

Brainstem Auditory Evoked Potentials

Brainstem auditory evoked potentials (BAEPs) have obtained widespread clinical application in assessing neurologic and audiologic problems. Seven waves (I-VII) are usually recorded in the first 10 ms following broad-band and high-intensity clicks. Latencies of waves I, III, and V, interpeak latencies of I-III, III-V, and I-V, and the amplitude ratio of wave V to wave I are common parameters evaluated for assessing clinically relevant abnormalities of BAEPs. Usually two-channel recordings are obtained: vertex (Cz) to ipsilateral ear and Cz to contralateral earlobe derivation. Evaluating different components in the two derivations helps their identification, particularly when the BAEPs are abnormal. Several technical and subject-related factors affect the amplitude and latencies of BAEP components besides lesions and dysfunctions involving the peripheral auditory structures and brainstem auditory pathways. BAEPs have maximal clinical utility in evaluating comatose patients, in patients with suspected demyelinating disorders, posterior fossa tumors, or in audiologic evaluation, especially in infants. They are also used for intraoperative monitoring of eighth-nerve and brainstem function during different types of posterior fossa surgery.

Task-dependent modulation of spinal reflexes

The binaural interaction component (BIC) of the brain-stem auditory evoked potential (BAEP) was studied in 13 normally hearing adults by subtracting the response to binaural clicks from the algebraic sum of monaural responses. Eight or 16 electrodes on the head and neck were referred to a non-cephalic site, the binaural stimuli were delivered either simultaneously or with an inter-aural time difference (Δt) of 0.2–1.6 msec, and masking noise was presented to the non-stimulated ear.With simultaneous binaural clicks a BIC was identifiable in every subject, the most consistent peaks being a scalp-positive potential (P1) peaking approximately 0.2 msec after wave V and a scalp negativity (N1) 0.7 msec later. Similar potentials were identifiable in 6/7 subjects with Δt fo 0.4 msec, 5/7 at 0.8 msec but only 1/7 at 1.2 msec. This suggests that the BIC may be associated with sound localization mechanisms which are sensitive to a similar range of Δt. On increasing Δt from 0.0 to 0.8 msec, the BIC was progressively delayed by approximately half the inter-aural time difference, with no suggestion of increasing temporal dispersion. This supports the notion of a ‘delay line coincidence detection’ mechanism in which the BIC represents the output of binaurally responsive neurones, probably in the superior olivary complex, which are ‘tuned’ to a particular Δt by the relative lengths of presynaptic axons relaying input from either ear.The distribution of the BIC in sagittal and coronal electrode chains was compared with that of binaural BAEP components I–VI and found to bear the closest resemblance to wave IV. It is suggested that both components may originate largely in the lateral lemnisci.

Diethylbenzene inhalation-induced electrophysiological deficits in peripheral nerves and changes in brainstem auditory evoked potentials in rats.

Motor and sensory conduction velocities (MCV and SCV), amplitude of the sensory action potential (ASAP) of the tail nerve and parameters of brainstem auditory evoked potentials (BAEP) were studied in male Sprague-Dawley rats after prolonged inhalation exposure to a commercial isomer mixture of diethylbenzene (DEB mixture) containing 6% 1,2-DEB. The MCV, SCV and ASAP were studied in one control group (10 rats) and three groups of 12 rats exposed to 500, 700 or 900 ppm DEB mixture for 6 h daily, 5 days per week, for 18 weeks. Rats used for recording BAEP (one control group and two other groups of 15 rats) were exposed to 600 and 800 ppm DEB mixture. The exposure time was the same. Rats exposed to DEB mixture exhibited a time- and concentration-dependent decrease in MCV, SCV and ASAP and a time- and concentration-dependent increase of both the peak latencies of all BAEP components and the interpeak (I-V) differences.

Alteration of brainstem auditory evoked potentials in diethylbenzene and diacetylbenzene-treated rats.

Male Sprague-Dawley rats were treated either with 1,2-diethylbenzene (1,2-DEB) or its putative active metabolite, 1,2-diacetylbenzene (1,2-DAB). Experimental rats and appropriate controls were examined electrophysiologically for brainstem auditory evoked potentials (BAEP). Oral administration of 1,2-DEB (75 or 100 mg kg-1 once a day, 4 days a week, for 8 weeks) and intraperitoneal injection of 1,2-DAB (10 or 15 mg kg-1 once a day, 4 days a week, for 8 weeks) produced time- and dose-dependent increases in the peak latencies of all BAEP components as well as in interpeak (I-V) differences, and a decrease in the amplitudes of all the components. The absolute and interpeak latencies recovered partially during an 8-week (1,2-DEB) or a 10-week (1,2-DAB) recovery period, whereas there were long-lasting decreases in peak amplitudes.

Temperature-dependent hysteresis in somatosensory and auditory evoked potentials

Fourteen adult patients undergoing open heart surgery under induced hypothermia had median nerve, short-latency somatosensory evoked potentials (SSEPs) recorded during cooling (from 36°C to 19°C) and subsequent rewarming. Similar data on another group of patients who had brain-stem auditory evoked potentials (BAEPs) were also analyzed. Hypothermia produced increased latencies of the major SSEP and BAEP components and the latencies returned to normal with subsequent warming. The temperature-latency relationship during the cooling phase was significantly different from that during the warming phase. For SSEP components the temperature-latency relationship was linear during cooling and curvilinear during warming, whereas for BAEP it was curvilinear both during cooling and warming. Furthermore, the regression curves were different during the two phases of temperature manipulation, particularly for temperatures below 30°C both for SSEP and BAEP components. At the onset of warming there was an initial exaggerated warming response on the evoked potential (EP) latencies and amplitude of the EP components. The temperature-latency regression curves were uniformly less steep during the warming phase compared to those during cooling. These findings suggest the existence of hysteresis in the relationship between temperature and EP latencies. The latencies at a given temperature below 30°C depend on whether that temperature is reached during cooling or during warming.