T complex hemispheric asymmetries: effects of stimulus intensity

The T complex component of the human auditory evoked potential (AEP) is thought to be produced in auditory cortex, on the posterior lateral surface of the temporal lobe. Recorded over temporal scalp, it consists of an 80-90 ms positive peak, Ta, and a 120-140 negative peak, Tb. As part of an effort to develop the clinical usefulness of the T complex in assessing auditory cortical function, we studied the effects of change in monaural stimulus intensity (20-80 dB SL) on T complex latency, amplitude, and hemispheric differences in normal adults. Ta and Tb peak latencies decreased as stimulus intensity increased. These latency changes were not dependent on ear or hemisphere. Right hemisphere Ta latency was shorter with contralateral than with ipsilateral stimulation; while left hemisphere Ta latency was not dependent on the ear stimulated. Tb latency was shorter over the left hemisphere, and over the contralateral hemisphere. Ta-b amplitude increased as stimulus intensity increased. This amplitude change was not dependent on ear or hemisphere. Ta-b amplitudes were larger over the right hemisphere and over the contralateral hemisphere. Hemispheric asymmetries were not significantly affected by stimulus intensity.     

Auditory evoked potentials in patients with dementia of the Alzheimer type

Dementia of the Alzheimer type (DAT) disrupts the function of the central auditory nervous system as a result of temporal lobe pathology. Auditory brain stem response (ABR) and middle latency responses (MLR) were studied in a group of patients with DAT to determine whether a correlate of dementia existed in these electrophysiological potentials. Comparison of absolute and interwave latencies on ABR, and absolute latency and amplitude of the MLR in patients with DAT and normal aged controls showed no significant differences between groups for any measure. Further, no relationship with degree of dementia or temporal lobe involvement, as assessed through dichotic speech recognition studies, and auditory evoked potentials could be demonstrated. It was concluded that the temporal lobe atrophy and hypometabolism seen in DAT is not generally sufficient to disrupt the generating of ABR and MLR potentials; however, slow cortical and cognitive evoked potentials may be more sensitive to central auditory nervous system impairment in DAT.     

Neuro-audiological correlates in cerebral hemisphere lesions: Temporal and Parietal Lobe Tumors

Auditory test results and localizing neurological, radiological, surgical, and pathological findings are described in three cases representative of 14 patients with glioma in the temporal and parietal lobes of the brain. Low-pass filtered, alternate-binaural, simultaneous-binaural, and competing sentence discrimination tests yield abnormal scores in the ear contralateral to the affected hemisphere in patients with temporal lobe tumors. Patients with parietal lobe lesions may manifest abnormal auditory behavior from secondary involvement of the temporal lobe due to pressure, edema, or infiltration of tumor cells. In such instances, auditory functions seem to be less severely affected than in cases with primary temporal lobe tumor. Binaural resynthesis of low-band and high-band pass speech is abnormal with involvement of the brain stem.     

Contributions of medial geniculate body subdivisions to the middle latency response.

Ongoing studies in our laboratory, concerned with identifying the neural pathways responsible for the auditory middle latency response (MLR), have involved analysis of surface and intracranial potentials following pharmacologic inactivation (with lidocaine) of small regions in the guinea pig brain. Previous studies indicate that MLR surface waves recorded over the temporal lobe originate from pathways anatomically distinct from those that generate MLR waves recorded over the midline. The medial geniculate body (MG) contributes to both MLR responses. At issue here are the relative contributions of ventral and caudomedial subdivisions, which have been linked to primary and non-primary auditory pathways, respectively. Ventral and caudomedial subdivisions contributed to the surface-recorded MLR in a distinctive manner. Lidocaine injections to both areas reduced the amplitude of the surface temporal response. Caudomedial injections had a much greater effect on the surface midline responses than did injections in the ventral portion. Thus, the ventral division, a part of the primary auditory pathway, contributes chiefly to the temporal response. The caudomedial portion, which may be linked to non-primary auditory pathways, contributes to both responses.     

Middle-latency auditory-evoked magnetic fields in patients with auditory cortex lesions

OBJECTIVE: To demonstrate the influence of auditory cortex lesions on auditory middle-latency responses (AMLRs) and middle-latency auditory-evoked magnetic fields (MLAEFs) in humans. MATERIAL AND METHODS: A total of 15 normal subjects, 9 patients with left auditory cortex lesions and 1 patient with a right auditory cortex lesion were studied. MLAEFs were recorded from each hemisphere of the brain in a magnetically shielded room using a 37-channel SQUID gradiometer. Simultaneously, AMLRs were recorded from the scalp at the vertex, C3 and C4. Tone bursts were used as auditory stimuli. RESULTS: Pam responses of the MLAEF, which are typically evoked in the latency range of the Pa of the AMLR, and are localized at the auditory cortex as dipoles, were impaired or abolished over the left auditory cortex lesion in the patients with left-hemisphere lesions, but the Pa of the AMLR persisted. CONCLUSION: The main generator of the Pam in MLAEF was demonstrated to be the auditory cortex. The results also show that the Pa of the AMLR is evoked only partly from the auditory cortex.     

High pass digital and analog filtering of the middle latency response

Digital filtration with zero and standard-phase shift characteristics was performed on unfiltered auditory evoked potentials recorded from 10 adult subjects. Standard-phase shift filters were seen to distort the response. Mild phase shift distortion often augmented the IV/V-Na1 amplitude (auditory brain stem response). When recording the IV/V-Na1 amplitude on a narrow timebase (20 msec), we recommend using a phase shift filter that has a high-pass cutoff frequency approximating 15 Hz and a slope of 12 to 24 dB/octave, in order to take advantage of the observed phase shift augmentation. The augmentation of the IV/V-Na1 amplitude is at the expense of the IV/V-Na2 amplitude. Thus, this phase shift distortion is not desirable if a long timebase (50 msec) is used. If a high-pass standard-phase shift filter of 100 Hz is used to eliminate muscle artifact, a reduction in the IV/V-Na1 amplitude from phase shift distortion is seen compared to the zero-phase shift control. In site-of-lesion testing, a nondistorted waveform produced by digital zero-phase shift filtration is also desirable over a distorted analog response. It is recommended that the slow wave activity of the response be recorded with a timebase of at least 40 to 50 msec and with a filter that produces minimal or no phase shifting. The major recorded response will be the Na trough and Pa peak. Evoked response units with steep filters will phase shift the response and produce a reduction in the IV/V-Na amplitude and a concomitant augmentation of the latter middle latency response waveforms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sound localization: value in localizing lesions of the auditory pathway

Reports in the literature suggest that patients with otosclerosis, neural lesions such as acoustic neuroma, pontine lesions, and temporal lobe lesions may show abnormal sound localization ability. In the present experiment, 15 normal subjects and 22 patients with various auditory pathway lesions had sound localization testing using special apparatus. The results confirmed that patients with otosclerosis were unable to localize low frequency sounds. Those with temporal lobe lesions made judgments not significantly different from normal subjects. Patients with unilateral sensorineural deafness made errors localizing high frequency sounds. Those with acoustic neuromas made greater errors than those without, but the difference between these two groups just failed to reach statistical significance. The number of cases was however small, and further studies are in progress to attempt to define numerical criteria to assist clinical decisions with regard to the selection of patients for invasive investigations such as oil cisternogram.     

Psychophysical measures of central auditory dysfunction in multiple sclerosis: neurophysiological and neuroanatomical correlates

Central auditory function was assessed in 15 patients with multiple sclerosis (MS) to determine whether the demyelinating lesions resulted in disruption of temporal processing. Auditory evoked potential (AEP) recordings included all three latency regions: Auditory brain stem responses (ABRs), midlatency responses (MLRs), and long-latency responses (LLRs). Two psychophysical tasks thought to involve temporal processing were used: a monaural-processing task (gap-detection) and a binaural-processing task (masking level difference; MLD). Further, AEP abnormalities and psychophysical performance deficits were related to lesion location, based on magnetic resonance imaging (MRI) scans. Reduced MLDs were seen in six MS subjects. Abnormal MLDs were always accompanied by abnormal ABRs and MLRs, and compared to subjects with normal MLDs, the subjects with abnormal MLDs were more likely to have bilateral abnormalities in the AEPs. Further, MLR indices of abnormal binaural interaction appeared to be specifically related to the psychophysical measure of binaural processing. The MRI data of these patients indicated widespread involvement of the auditory pathway. MS subjects with abnormal MRI signals restricted to levels caudal to the lateral lemniscus did not have abnormal MLDs. Gap-detection thresholds were more resistant to the effects of the demyelinating lesions; only two subjects had abnormal gap-detection thresholds. These subjects had extensive AEP abnormalities (bilaterally, in all three latency regions). The gap-detection thresholds were most specifically related to abnormalities of the LLRs. In addition, the subjects with elevated gap-detection thresholds were the only ones with a prolonged interval between the ABRs and MLRs. Thus, efficient neural conduction between the upper brain stem and auditory cortex appears to be crucial for normal monaural temporal processing. The results indicate that demyelinating lesions can cause deficits in temporal processing in the central auditory pathway. However, auditory temporal processing is not a unitary phenomenon since abnormalities at different levels of the auditory system disrupt different types of temporal processing. Finally, abnormal psychophysical performance was not seen in all subjects with AEP and MRI evidence of involvement of the auditory pathway; rather, these psychophysical measures appeared to be sensitive to disruption only in specific portions of the auditory system.     

Infarction of the superior temporal gyrus: a description of auditory evoked potential latency and amplitude topology

P1 and N1 of the cortical auditory evoked potential (AEP) were studied with multiple electrodes in 10 normal subjects and 6 patients with left middle cerebral artery infarction. Patients were selected based on neurological examination and on CT scans showing both (1) infarction limited to the vascular territory and (2) involvement of posterior portion of superior temporal gyrus. Waveforms recorded from C3, Cz, and C4 were examined for peak latency and amplitude of P1 and N1 on all subjects. Topographic displays of amplitude over P1 and N1 latency ranges were also examined. In normals, P1 was identified in 9 of the 10 subjects at all three electrode sites. In patients, P1 was identified at C3 in only 1 of the 6. N1 was present at all three electrodes in the 10 normal subjects and in 5 of the 6 patients. The remaining patient had N1 at C4 and Cz only. Examination of amplitude topology showed as asymmetric evolution of P1 and N1 in the patients. This asymmetry was not present in normals. The results of this study are consistent with theory that P1 arises from primary auditory cortex. Results further suggest multiple generators for N1. Additional study correlating topographic display from multichannel recordings with CT or MRI in brain-injured patients may bring more insight into N1 generators.     

Phase audiometry in neuroaudiological practice.

Six groups of subjects, altogether 107 in number, were studied with phase audiometry. Three control groups were studied (normal-hearing healthy controls, persons with cochlear hearing losses, and patients with neurological disease not affecting the auditory system), and three patient groups were studied (patients with cerebellopontine angle tumours, with brainstem lesions, and with temporal lobe lesions). Two phase audiometers were used. The sensitivity was 85% for patients with cerebellopontine angle tumours, 71% for patients with brainstem lesions, and 69% for patients with temporal lobe lesions. There was good agreement between the phase audiometers, though one of them (BIAB Phase Audiometer) had better results for two of the patient groups. Phase audiometry can be recommended in neuroaudiological practice.     

Differential age effects for components of the adult auditory middle latency response.

The middle latency components of the auditory evoked response were obtained from a young (20-24 years of age) and an older (51 to 71 years of age) group of normal-hearing, healthy female subjects. Recording procedures and stimulus repetition rates were chosen to promote the resolution of both Pa and Pb. The absolute and peak-to-peak amplitudes of Pa and Pb were significantly larger for the older subjects at all stimulus rates. An amplitude reduction of Pb with increasing stimulus rate was much more pronounced for the young than for the older subjects. This, combined with a shorter latency for Pb in the older subjects, may have contributed to partial and/or complete fusion of Pa and Pb observed in 10 of the 17 older subjects. An apparent positive shift in the response baseline for older subjects also may have contributed to the age-related amplitude effects.     

感音神经性聋患者听觉皮层BOLD-fMRI研究

目的利用血氧水平依赖的功能磁共振成像（blood oxygenation level dependent functional magnetic resonance imaging,BOLD—fMRI）技术观察感音神经性聋患者纯音刺激时大脑听觉皮层激活情况,探讨感音神经性聋的中枢客观检查方法。方法对22例单侧中重度感音神经性聋患者（耳聋组）和15例健康志愿者（对照组）行听觉刺激BOLD-fMRI检查,比较两组纯音刺激时听觉皮层激活的体积和信号强度。结果对照组纯音刺激单耳时,对侧听觉皮层激活体积和信号强度明显大于同侧（P〈0．01）,表现为对侧半球传导优势;耳聋组刺激健侧时健侧听觉皮层激活体积和信号强度大于患侧,但差异无统计学意义（P〉0．05）。结论感音神经性聋患者纯音刺激健耳时对侧听觉半球传导优势消失,其听觉皮层可能发生了结构重塑。     

Temporal envelope processing in the human auditory cortex: response and interconnections of auditory cortical areas

Temporal envelope processing in the human auditory cortex has an important role in language analysis. In this paper, depth recordings of local field potentials in response to amplitude modulated white noises were used to design maps of activation in primary, secondary and associative auditory areas and to study the propagation of the cortical activity between them. The comparison of activations between auditory areas was based on a signal-to-noise ratio associated with the response to amplitude modulation (AM). The functional connectivity between cortical areas was quantified by the directed coherence (DCOH) applied to auditory evoked potentials. This study shows the following reproducible results on twenty subjects: (1) the primary auditory cortex (PAC), the secondary cortices (secondary auditory cortex (SAC) and planum temporale (PT)), the insular gyrus, the Brodmann area (BA) 22 and the posterior part of T1 gyrus (T1Post) respond to AM in both hemispheres. (2) A stronger response to AM was observed in SAC and T1Post of the left hemisphere independent of the modulation frequency (MF), and in the left BA22 for MFs 8 and 16Hz, compared to those in the right. (3) The activation and propagation features emphasized at least four different types of temporal processing. (4) A sequential activation of PAC, SAC and BA22 areas was clearly visible at all MFs, while other auditory areas may be more involved in parallel processing upon a stream originating from primary auditory area, which thus acts as a distribution hub. These results suggest that different psychological information is carried by the temporal envelope of sounds relative to the rate of amplitude modulation.     

Cortical centres underlying auditory temporal processing in humans: a PET study

We have used positron emission tomography (PET) to test a specific hypothesis of a neural system subserving auditory temporal processing (acoustical stimulus duration discrimination). Maps of the cerebral blood flow distribution during specific stimulations were obtained from five normally-hearing and otherwise healthy subjects. The auditory stimuli consisted of sounds of varying duration and of auditorily presented words in which the duration of the initial phoneme was manipulated. All stimuli alternated with conditions of silence in a subtraction paradigm. The blood flow distribution was mapped with O-15-labelled water. The results demonstrated that stimuli requiring recognizing, memorizing, or attending to specific target sounds during temporal processing generally resulted in significant activation of both frontal lobes and the parietal lobe in the right hemisphere. Based on these results, we hypothesise that a network consisting of anterior and posterior auditory attention and short-term memory sites subserves acoustical stimulus duration perception and analysis (auditory temporal processing).     

Differential Ear Effects of Profound Unilateral Deafness on the Adult Human Central Auditory System

This study investigates the effects of profound acquired unilateral deafness on the adult human central auditory system by analyzing long-latency auditory evoked potentials (AEPs) with dipole source modeling methods. AEPs, elicited by clicks presented to the intact ear in 19 adult subjects with profound unilateral deafness and monaurally to each ear in eight adult normal-hearing controls, were recorded with a 31-channel system. The responses in the 70–210 ms time window, encompassing the N_1b/P₂ and Ta/Tb components of the AEPs, were modeled by a vertically and a laterally oriented dipole source in each hemisphere. Peak latencies and amplitudes of the major components of the dipole waveforms were measured in the hemispheres ipsilateral and contralateral to the stimulated ear. The normal-hearing subjects showed significant ipsilateral–contralateral latency and amplitude differences, with contralateral source activities that were typically larger and peaked earlier than the ipsilateral activities. In addition, the ipsilateral–contralateral amplitude differences from monaural presentation were similar for left and for right ear stimulation. For unilaterally deaf subjects, the previously reported reduction in ipsilateral–contralateral amplitude differences based on scalp waveforms was also observed in the dipole source waveforms. However, analysis of the source dipole activity demonstrated that the reduced inter-hemispheric amplitude differences were ear dependent. Specifically, these changes were found only in those subjects affected by profound left ear unilateral deafness.     

颞叶癫痫患者的中枢听功能初探

目的采用汉语最低听觉功能测试（minimal auditory capabilities inchina，MACC）中背景噪声下言语测听法（speech-perception-in-noise test，SPIN），评价颞叶癫痫患者的中枢听觉功能。方法对9例经脑电图和MRI、CT检查后神经内科确诊的颞叶癫痫患者，进行SPIN、听性脑干反应（auditory brainstem response，ABR）测试。选择19例年龄、性别相匹配的健康人做对照组，进行SPIN测试。所有受试者均经询问病史、耳科检查及纯音测听、声导抗测定除外传导、感音神经性及混合性聋，且纯音听阈均在25dB以内。SPIN测试材料中测试言语和噪声材料，采用独立声道录制，通过预实验选择测试信噪比（S／N）为-25dB。测试时，每受试句均朗读2次，并对2次的结果分别进行记录和比较。结果在ABR测试中，癫痫患者仅V波潜伏期左耳较右耳延长，且差异有统计学意义（P〈0．05），余各波潜伏期及波间期差异均无统计学意义（P〉0．05）；在SPIN测试中，健康对照组第1次聆听左右耳间得分比较，差异无统计学意义（P〉0．05），第2次聆听时，差异有统计学意义（P〈0．05）；颞叶癫痫患者左右耳间得分比较，第1次和第2次聆听的差异均无统计学意义（P〉0．05），而颞叶癫痫患者无论在单耳、双耳聆听以及第1次和第2次聆听的SPIN得分，与健康对照组相比，差异均有统计学意义（P〈0．01）。由于9例癫痫患者中有3例为右侧颞叶病变，余为双侧颞叶病变，故未对左、右侧颞叶病变与左、右利手的关系可能对实验造成的影响进行统计分析。结论本组颞叶癫痫患者在纯音测听、ABR检查无明显异常，而SPIN测试言语识别率明显低于对照组，差异有统计学意义，证明颞叶癫痫患者具有中枢听功能障碍，同时提示SPIN是一项敏感、无创的中枢听觉功能检查方法，建议临床上将其作为听处理套查方法之一。     

Robin sequence: review of treatment modalities for airway obstruction in 110 cases

INTRODUCTION: Children diagnosed with attention deficit disorder (ADD) can present with different abnormalities in electrophysiological studies. OBJECTIVE: The purpose of this paper is to compare brainstem auditory (short latency) evoked responses (BSAER) and long latency auditory evoked responses (LLAER) in school children with and without ADD. MATERIALS AND METHODS: A normative study was carried out, 20 normal subjects were studied. All these patients underwent a study protocol including BSAER and LLAER. Eighteen school children diagnosed as ADD were included in the active group. Eighteen school children were selected as controls. All children from both groups underwent BSAER and LLAER. BSAER and LLAER results from both groups of patients were compared. RESULTS: Brainstem transmission was significantly longer in children with ADD. The latency of P300 was significantly longer in children with ADD. Also, mean amplitude of P300 was significantly decreased in children with ADD. CONCLUSION: The results of this study indicates that school children with ADD show significant abnormalities in BSAER and LLAER. These electrophysiological procedures involving the auditory system can be useful for the diagnosis of children with ADD.     

Changes in the Electrically Evoked Compound Action Potential over time After Implantation and Subsequent Deafening in Guinea Pigs

The electrically evoked compound action potential (eCAP) is a direct measure of the responsiveness of the auditory nerve to electrical stimulation from a cochlear implant (CI). CIs offer a unique opportunity to study the auditory nerve’s electrophysiological behavior in individual human subjects over time. In order to understand exactly how the eCAP relates to the condition of the auditory nerve, it is crucial to compare changes in the eCAP over time in a controlled model of deafness-induced auditory nerve degeneration. In the present study, 10 normal-hearing young adult guinea pigs were implanted and deafened 4 weeks later, so that the effect of deafening could be monitored within-subject over time. Following implantation, but before deafening, most examined eCAP characteristics significantly changed, suggesting increasing excitation efficacy (e.g., higher maximum amplitude, lower threshold, shorter latency). Conversely, inter-phase gap (IPG) effects on these measures – within-subject difference measures that have been shown to correlate well with auditory nerve survival – did not vary for most eCAP characteristics. After deafening, we observed an initial increase in excitability (steeper slope of the eCAP amplitude growth function (AGF), lower threshold, shorter latency and peak width) which typically returned to normal-hearing levels within a week, after which a slower process, probably reflecting spiral ganglion cell loss, took place over the remaining 6 weeks (e.g., decrease in maximum amplitude, AGF slope, peak area, and IPG effect for AGF slope; increase in IPG effect for latency). Our results suggest that gradual changes in peak width and latency reflect the rate of neural degeneration, while peak area, maximum amplitude, and AGF slope reflect neural population size, which may be valuable for clinical diagnostics.

     

An alternative diagnostic test for active Ménière's disease and cochlear hydrops using high-pass noise masked responses: the complex amplitude ratio

We [Don et al.: Otol Neurotol 2005;26:711-722] previously demonstrated that patients diagnosed with an active case of Ménière's disease could be distinguished from non-Ménière's normal-hearing subjects by a special auditory brainstem response method involving clicks and ipsilateral high-pass masking pink noise. Specifically, auditory brainstem responses to clicks presented alone and clicks with masking noise high-pass filtered at 8, 4, 2, 1 and 0.5 kHz were recorded. It was shown that the level of masking noise sufficient to progressively mask the response to clicks in non-Ménière's normal-hearing subjects was insufficient to appropriately mask the responses in Ménière's disease subjects, resulting in an obvious undermasked component. A relative latency measure of wave V or the undermasked component in the response to clicks with 0.5 kHz high-pass masking noise and wave V in the response to clicks presented alone clearly distinguished these two groups on an individual level, thus making it a valuable clinical tool. However, determining the peak latency of wave V or the undermasked component can be difficult in some cases. In anticipation of this difficulty, we investigated and present in this paper several amplitude measures that may help in the evaluation of these cases. One amplitude measure, the 'complex amplitude ratio', appears to be a good alternative when the latency measure of the undermasked component is difficult to determine.     

突发性聋患者听觉中枢在功能性核磁的表现

目的 利用血氧水平依赖性的功能性磁共振成像（blood oxygen level dependent functional MRI,BOLD～fMRD技术,观察突发性聋患者在接受纯音刺激时听觉中枢的变化。方法研究对象分为两组,突发性聋患者13例（均为左耳患病）为试验组,12例双耳听力正常的健康成年志愿者作为对照组。通过CoolEditPr02软件编辑1000Hz、127dB纯音,刺激模式采用ON／OFF组块设计,通过耳机分别给予右耳及双耳音频刺激,采用荷兰Philips Achieva3．0T磁共振成像系统,采集脑部的BOLD—fMRI数据,最后通过SPM2软件对数据进行统计学分析（组分析）,得到脑功能活动的图像。结果右耳接受纯音刺激时听力正常组主要中枢激活区在双侧颞上回、左枕叶、左额上回,此外还有左小脑、双侧海马及双侧旁中央小叶激活,听觉中枢表现为右侧优势偏向;突聋组见双侧颞上回,以及左侧海马、右枕叶和左侧距状裂区激活,听觉中枢表现为左侧优势偏向,突聋组听中枢激活容积小于正常组。双耳同时刺激时,听力正常组激活区主要在双侧颞中回,右侧扣带回和左胼胝体亦明显激活;突聋组双侧颞中回,以及右侧颞上回、右小脑、右侧额下回及右楔前叶激活,两组听觉中枢均表现为右侧优势偏向。听力正常组与突聋组比较,正常组左小脑、左胼胝体区明显激活,突聋组出现新的激活区右侧颞上回、右侧额下回及右小脑区：突聋组听中枢激活容积小于正常组。结论突聋患者在单耳刺激时听觉中枢出现优势偏向的改变,提示单侧耳聋的病人听觉皮质存在着结构重组;听觉中枢具有可塑性。突聋患者在双侧刺激时通过听觉重组使双耳对外界声音的感知尽量达到正常水平;突聋患者听觉中枢不仅本身存在重组现象,且同视觉皮质之间也发生了感觉交互作用。