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Abnormal auditory adaptation is a standard clinical tool for diagnosing auditory nerve disorders due to acoustic neuromas. In the present study we investigated auditory adaptation in auditory neuropathy owing to disordered function of inner hair cell ribbon synapses (temperature-sensitive auditory neuropathy) or auditory nerve fibres. Subjects were tested when afebrile for (i) psychophysical loudness adaptation to comfortably-loud sustained tones; and (ii) physiological adaptation of auditory brainstem responses to clicks as a function of their position in brief 20-click stimulus trains (#1, 2, 3 ... 20). Results were compared with normal hearing listeners and other forms of hearing impairment. Subjects with ribbon synapse disorder had abnormally increased magnitude of loudness adaptation to both low (250 Hz) and high (8000 Hz) frequency tones. Subjects with auditory nerve disorders had normal loudness adaptation to low frequency tones; all but one had abnormal adaptation to high frequency tones. Adaptation was both more rapid and of greater magnitude in ribbon synapse than in auditory nerve disorders. Auditory brainstem response measures of adaptation in ribbon synapse disorder showed Wave V to the first click in the train to be abnormal both in latency and amplitude, and these abnormalities increased in magnitude or Wave V was absent to subsequent clicks. In contrast, auditory brainstem responses in four of the five subjects with neural disorders were absent to every click in the train. The fifth subject had normal latency and abnormally reduced amplitude of Wave V to the first click and abnormal or absent responses to subsequent clicks. Thus, dysfunction of both synaptic transmission and auditory neural function can be associated with abnormal loudness adaptation and the magnitude of the adaptation is significantly greater with ribbon synapse than neural disorders. © 2013 The Author).

Objective: To define brain activity corresponding to an auditory illusion of 3 and 6 Hz binaural beats in 250 Hz or 1000 Hz base frequencies, and compare it to the sound onset response. Methods: Event-Related Potentials (ERPs) were recorded in response to unmodulated tones of 250 or 1000 Hz to one ear and 3 or 6 Hz higher to the other, creating an illusion of amplitude modulations (beats) of 3 Hz and 6 Hz, in base frequencies of 250 Hz and 1000 Hz. Tones were 2000 ms in duration and presented with approximately 1 s intervals. Latency, amplitude and source current density estimates of ERP components to tone onset and subsequent beats-evoked oscillations were determined and compared across beat frequencies with both base frequencies. Results: All stimuli evoked tone-onset P50, N100 and P200 components followed by oscillations corresponding to the beat frequency, and a subsequent tone-offset complex. Beats-evoked oscillations were higher in amplitude with the low base frequency and to the low beat frequency. Sources of the beats-evoked oscillations across all stimulus conditions located mostly to left lateral and inferior temporal lobe areas in all stimulus conditions. Onset-evoked components were not different across stimulus conditions; P50 had significantly different sources than the beats-evoked oscillations; and N100 and P200 sources located to the same temporal lobe regions as beats-evoked oscillations, but were bilateral and also included frontal and parietal contributions. Conclusions: Neural activity with slightly different volley frequencies from left and right ear converges and interacts in the central auditory brainstem pathways to generate beats of neural activity to modulate activities in the left temporal lobe, giving rise to the illusion of binaural beats. Cortical potentials recorded to binaural beats are distinct from onset responses. Significance: Brain activity corresponding to an auditory illusion of low frequency beats can be recorded from the scalp. © 2009 International Federation of Clinical Neurophysiology.

Objective To study objectively auditory temporal processing in a group of normal hearing subjects and in a group of hearing-impaired individuals with auditory neuropathy (AN) using electrophysiological and psychoacoustic methods. Methods Scalp recorded evoked potentials were measured to brief silent intervals (gaps) varying between 2 and 50 ms embedded in continuous noise. Latencies and amplitudes of N100 and P200 were measured and analyzed in two conditions: (1) active, when using a button in response to gaps; (2) passive, listening, but not responding. Results In normal subjects evoked potentials (N100/P200 components) were recorded in response to gaps as short as 5 ms in both active and passive conditions. Gap evoked potentials in AN subjects appeared only with prolonged gap durations (10–50 ms). There was a close association between gap detection thresholds measured psychoacoustically and electrophysiologically in both normals and in AN subjects. Conclusions Auditory cortical potentials can provide objective measures of auditory temporal processes. Significance The combination of electrophysiological and psychoacoustic methods converged to provide useful objective measures for studying auditory cortical temporal processing in normals and hearing-impaired individuals. The procedure used may also provide objective measures of temporal processing for evaluating special populations such as children who may not be able to provide subjective responses.

We studied a family with hereditary sensory motor neuropathy and deafness accompanying a missense mutation in the MPZ gene. Pathological examination of the cochlea in one of the family members revealed marked loss of auditory ganglion cells and central and peripheral auditory nerve fibres within the cochlea. The inner hair cells were of normal number with preserved morphology. The outer hair cells were normal in number except for a 30% reduction in just the apical turn. Examination of the sural nerve and the auditory nerve adjacent to the brainstem showed marked loss of fibres with evidence of incomplete remyelination of some of the remaining fibres. Studies of auditory function in surviving family members using electrophysiological and psychoacoustic methods provided evidence that the hearing deficits in this form of auditory neuropathy were probably related to a decrease of auditory nerve input accompanying axonal disease. Altered synchrony of discharge of the remaining fibres was a possible additional contributing factor.

Objectives : To define motor cortical excitability changes occurring at various times after non-fatiguing bimanual exercise of the index fingers. Methods : Twenty healthy right-handed subjects were studied with transcranial magnetic stimulation (TMS) of the right non-dominant hemisphere. They performed regular (3–4/s) repetitive opening–closing bilateral movements of the index finger onto the thumb. Motor evoked potentials (MEPs) of the left first dorsal interosseus (FDI) and rate of the repetitive finger movements were determined (1) before exercise, (2) immediately following 3 exercise periods of 30, 60 and 90 s, and (3) over a subsequent 30 min rest period. Results : Rate of movement did not show significant change during any of the exercise periods but did increase significantly when tested after 15 min of rest. MEPs immediately after 30 and 60 s of exercise were facilitated whereas MEPs after 90 s of exercise did not differ from baseline measures. MEP amplitudes were significantly increased after rest of approximately 15 min compared to the baseline MEPs. In contrast, motor potentials evoked by peripheral nerve stimulation were unchanged throughout the experimental test periods. Conclusions : Motor cortical excitability relating to an intrinsic finger muscle (FDI) was facilitated beginning 15 min after a brief period of non-forceful, repetitive activity of that muscle. This delayed facilitation of motor cortex after exercise may represent a form of short-term potentiation of motor cortical excitability.

Brain potentials evoked to non-targets in an auditory target detection task changed in amplitude, duration, polarity, and scalp topography as a function of position in the stimulus sequence relative to the target. (1) A negative prestimulus readiness like-potential, or RP, the poststimulus N100, and a late slow wave to non-targets immediately after the target were reduced in amplitude compared to non-targets immediately before the target. The amplitudes of these potentials after the target then increased in size as a linear function of the number of non-targets in the sequence. (2) The amplitudes of the positive components, P50 and P200, were larger to non-targets immediately after the target than to non-targets immediately before the targets. P50 amplitude then decreased to subsequent non-targets in the sequence in a linear manner; P200 amplitude was reduced equivalently to all subsequent non-targets. (3) The duration of the P200 component could extend into the time domain when the P300 to targets would occur. The P200 component to non-targets was therefore designated 'P200/300'. The duration of the P200/300 component was shorter to non-targets immediately after the target than to non-targets immediately before the targets. P200/300 duration then extended in a linear manner to subsequent non-targets in the sequence and approached the peak latency of the P300 evoked by targets. (4) The anterior/posterior scalp distribution of P50 and the polarity of the late slow wave to non-targets changed as a function of non-target position in the sequence. The subject's response to the targets (button press or mental count) influenced these sequential effects. Linear trends for sequence were present in the press but not the count conditions for the amplitude of the RP, N100, and P300; linear trends for P50, P200/300 duration, and the late slow wave were found in both the press and count conditions. Reaction time was speeded as a function of the number of preceding targets. These dynamic changes in the processing of auditory signals were attributed to an interaction of attention and the subjective expectancies for both the appearance of a target stimulus and the requirement to make a motor response.

The purpose of this study was to compare cortical brain responses evoked by amplitude modulated acoustic beats of 3 and 6 Hz in tones of 250 and 1000 Hz with those evoked by their binaural beats counterparts in unmodulated tones to indicate whether the cortical processes involved differ. Event-related potentials (ERPs) were recorded to 3- and 6-Hz acoustic and binaural beats in 2000 ms duration 250 and 1000 Hz tones presented with approximately 1 s intervals. Latency, amplitude and source current density estimates of ERP components to beats-evoked oscillations were determined and compared across beat types, beat frequencies and base (carrier) frequencies. All stimuli evoked tone-onset components followed by oscillations corresponding to the beat frequency, and a subsequent tone-offset complex. Beats-evoked oscillations were higher in amplitude in response to acoustic than to binaural beats, to 250 than to 1000 Hz base frequency and to 3 Hz than to 6 Hz beat frequency. Sources of the beats-evoked oscillations across all stimulus conditions located mostly to left temporal lobe areas. Differences between estimated sources of potentials to acoustic and binaural beats were not significant. The perceptions of binaural beats involve cortical activity that is not different than acoustic beats in distribution and in the effects of beat- and base frequency, indicating similar cortical processing. © 2010 Elsevier B.V. All rights reserved.

Objective: Auditory temporal processes in quiet are impaired in auditory neuropathy (AN) similar to normal hearing subjects tested in noise. N100 latencies were measured from AN subjects at several tone intensities in quiet and noise for comparison with a group of normal hearing individuals. Methods: Subjects were tested with brief 100 ms tones (1.0 kHz, 100-40 dB SPL) in quiet and in continuous noise (90 dB SPL). N100 latency and amplitude were analyzed as a function of signal intensity and audibility. Results: N100 latency in AN in quiet was delayed and amplitude was reduced compared to the normal group; the extent of latency delay was related to psychoacoustic measures of gap detection threshold and speech recognition scores, but not to audibility. Noise in normal hearing subjects was accompanied by N100 latency delays and amplitude reductions paralleling those found in AN tested in quiet. Additional N100 latency delays and amplitude reductions occurred in AN with noise. Conclusions: N100 latency to tones and performance on auditory temporal tasks were related in AN subjects. Noise masking in normal hearing subjects affected N100 latency to resemble AN in quiet. Significance: N100 latency to tones may serve as an objective measure of the efficiency of auditory temporal processes. © 2009 International Federation of Clinical Neurophysiology.

Objective: To define cortical brain responses to large and small frequency changes (increase and decrease) of high- and low-frequency tones. Methods: Event-Related Potentials (ERPs) were recorded in response to a 10% or a 50% frequency increase from 250 or 4000 Hz tones that were approximately 3 s in duration and presented at 500-ms intervals. Frequency increase was followed after 1 s by a decrease back to base frequency. Frequency changes occurred at least 1 s before or after tone onset or offset, respectively. Subjects were not attending to the stimuli. Latency, amplitude and source current density estimates of ERPs were compared across frequency changes. Results: All frequency changes evoked components P50, N100, and P200. N100 and P200 had double peaks at bilateral and right temporal sites, respectively. These components were followed by a slow negativity (SN). The constituents of N100 were predominantly localized to temporo-parietal auditory areas. The potentials and their intracranial distributions were affected by both base frequency (larger potentials to low frequency) and direction of change (larger potentials to increase than decrease), as well as by change magnitude (larger potentials to larger change). The differences between frequency increase and decrease depended on base frequency (smaller difference to high frequency) and were localized to frontal areas. Conclusions: Brain activity varies according to frequency change direction and magnitude as well as base frequency. Significance: The effects of base frequency and direction of change may reflect brain networks involved in more complex processing such as speech that are differentially sensitive to frequency modulations of high (consonant discrimination) and low (vowels and prosody) frequencies. © 2008 International Federation of Clinical Neurophysiology.

Objectives: To examine auditory cortical potentials in normal-hearing subjects to intensity increments in a continuous pure tone at low, mid, and high frequency. Methods: Electrical scalp potentials were recorded in response to randomly occurring 100 ms intensity increments of continuous 250, 1000, and 4000 Hz tones every 1.4 s. The magnitude of intensity change varied between 0, 2, 4, 6, and 8 dB above the 80 dB SPL continuous tone. Results: Potentials included N100, P200, and a slow negative (SN) wave. N100 latencies were delayed whereas amplitudes were not affected for 250 Hz compared to 1000 and 4000 Hz. Functions relating the magnitude of the intensity change and N100 latency/amplitude did not differ in their slope among the three frequencies. No consistent relationship between intensity increment and SN was observed. Cortical dipole sources for N100 did not differ in location or orientation between the three frequencies. Conclusions: The relationship between intensity increments and N100 latency/amplitude did not differ between tonal frequencies. A cortical tonotopic arrangement was not observed for intensity increments. Our results are in contrast to prior studies of brain activities to brief frequency changes showing cortical tonotopic organization. Significance: These results suggest that intensity and frequency discrimination employ distinct central processes. © 2008 International Federation of Clinical Neurophysiology.

Objective: Transtympanic electrocochleography (ECochG) was recorded bilaterally in children and adults with auditory neuropathy (AN) to evaluate receptor and neural generators. Methods: Test stimuli were clicks from 60 to 120 dB p.e. SPL. Measures obtained from eight AN subjects were compared to 16 normally hearing children. Results: Receptor cochlear microphonics (CMs) in AN were of normal or enhanced amplitude. Neural compound action potentials (CAPs) and receptor summating potentials (SPs) were identified in five AN ears. ECochG potentials in those ears without CAPs were of negative polarity and of normal or prolonged duration. We used adaptation to rapid stimulus rates to distinguish whether the generators of the negative potentials were of neural or receptor origin. Adaptation in controls resulted in amplitude reduction of CAP twice that of SP without affecting the duration of ECochG potentials. In seven AN ears without CAP and with prolonged negative potential, adaptation was accompanied by reduction of both amplitude and duration of the negative potential to control values consistent with neural generation. In four ears without CAP and with normal duration potentials, adaptation was without effect consistent with receptor generation. In five AN ears with CAP, there was reduction in amplitude of CAP and SP as controls but with a significant decrease in response duration. Conclusions: Three patterns of cochlear potentials were identified in AN: (1) presence of receptor SP without CAP consistent with pre-synaptic disorder of inner hair cells; (2) presence of both SP and CAP consistent with post-synaptic disorder of proximal auditory nerve; (3) presence of prolonged neural potentials without a CAP consistent with post-synaptic disorder of nerve terminals. Significance: Cochlear potential measures may identify pre- and post-synaptic disorders of inner hair cells and auditory nerves in AN. © 2008 International Federation of Clinical Neurophysiology.

Objective: We examined auditory cortical potentials in normal hearing subjects to spectral changes in continuous low and high frequency pure tones. Methods: Cortical potentials were recorded to increments of frequency from continuous 250 or 4000 Hz tones. The magnitude of change was random and varied from 0% to 50% above the base frequency. Results: Potentials consisted of N100, P200 and a slow negative wave (SN). N100 amplitude, latency and dipole magnitude with frequency increments were significantly greater for low compared to high frequencies. Dipole amplitudes were greater in the right than left hemisphere for both base frequencies. The SN amplitude to frequency changes between 4% and 50% was not significantly related to the magnitude of spectral change. Conclusions: Modulation of N100 amplitude and latency elicited by spectral change is more pronounced with low compared to high frequencies. Significance: These data provide electrophysiological evidence that central processing of spectral changes in the cortex differs for low and high frequencies. Some of these differences may be related to both temporal- and spectral-based coding at the auditory periphery. Central representation of frequency change may be related to the different temporal windows of integration across frequencies.

The term auditory neuropathy (Starr, A. et al., 1996) was first used to describe a hearing disorder due to altered function of the auditory nerve in the presence of preserved functions of cochlear outer hair cells (OHCs; Starr, A. et al., 1991). The hearing loss has specific features reflecting impairment of auditory temporal processes that are typically unaffected with sensory outer hair disturbances (Zeng, F. G. et al., 1999). The disorder has also been referred to as type I afferent neuron dysfunction (Berlin, C. I. et al., 1993), auditory neuropathy/auditory dys-synchrony (Berlin, C. I. et al., 2003), and neural hearing loss (Rapin, I. and Gravel, J., 2003). We now know that dysfunction of the auditory nerve, having quite similar clinical features, accompanies a variety of disorders acting on the nerve, the inner hair cell, and/or their synapse. We will refer to the disorder as auditory neuropathy and emphasize whenever possible the site(s) of involvement in the auditory periphery. We will review how the varieties of auditory neuropathy are identified, the special psychoacoustic features of the hearing loss, candidate pathophysiological mechanisms, and cochlear and auditory nerve pathologies. We will introduce recent advances in knowledge of molecular organization of cochlear inner hair cell synapses and auditory nerve that suggest some mechanisms likely to be involved in auditory nerve dysfunction.

Amnestic mild cognitive impairment (MCI) is an isolated episodic memory disorder that has a high likelihood of progressing to Alzheimer's disease. Auditory sensory cortical responses (P50, N100) have been shown to be increased in amplitude in MCI compared to older controls. We tested whether (1) cortical potentials to other sensory modalities (somatosensory and visual) were also affected in MCI and (2) cholinesterase inhibitors (ChEIs), one of the therapies used in this disorder, modulated sensory cortical potentials in MCI. Somatosensory cortical potentials to median nerve stimulation and visual cortical potentials to reversing checkerboard stimulation were recorded from 15 older controls and 15 amnestic MCI subjects (single domain). Results were analyzed as a function of diagnosis (Control, MCI) and ChEIs treatment (Treated MCI, Untreated MCI). Somatosensory and visual potentials did not differ significantly in amplitude in MCI subjects compared to controls. When ChEIs use was considered, somatosensory potentials (N20, P50) but not visual potentials (N70, P100, N150) were of larger amplitude in untreated MCI subjects compared to treated MCI subjects. Three individual MCI subjects showed increased N20 amplitude while off ChEIs compared to while on ChEIs. An enhancement of N20 somatosensory cortical activity occurs in amnestic single-domain MCI and is sensitive to modulation by ChEIs. © 2007 Elsevier B.V. All rights reserved.

Objective To study the effects of duration and intensity of noise that precedes gaps in noise on the N-Complex (N 1a and N 1b ) of Event-Related Potentials (ERPs) to the gaps. Methods ERPs were recorded from 13 normal subjects in response to 20ms gaps in 2–4.5s segments of binaural white noise. Within each segment, the gaps appeared after 500, 1500, 2500 or 4000ms of noise. Noise intensity was either 75, 60 or 45dBnHL. Analysis included waveform peak measurements and intracranial source current density estimations, as well as statistical assessment of the effects of pre-gap noise duration and intensity on N 1a and N 1b and their estimated intracranial source activity. Results The N-Complex was detected at about 100ms under all stimulus conditions. Latencies of N 1a (at ∼90ms) and N 1b (at ∼150ms) were significantly affected by duration of the preceding noise. Both their amplitudes and the latency of N 1b were affected by the preceding noise intensity. Source current density was most prominent, under all stimulus conditions, in the vicinity of the temporo-parietal junction, with the first peak (N 1a ) lateralized to the left hemisphere and the second peak (N 1b ) – to the right. Additional sources with lower current density were more anterior, with a single peak spanning the duration of the N-Complex. Conclusions The N 1a and N 1b of the N-Complex of the ERPs to gaps in noise are affected by both duration and intensity of the pre-gap noise. The minimum noise duration required for the appearance of a double-peaked N-Complex is just under 500ms, depending on noise intensity. N 1a and N 1b of the N-Complex are generated predominantly in opposite temporo-parietal brain areas: N 1a on the left and N 1b on the right. Significance Duration and intensity interact to define the dual peaked N-Complex, signaling the cessation of an ongoing sound.

Perceptual consequences of disrupted auditory nerve activity were systematically studied in 21 subjects who had been clinically diagnosed with auditory neuropathy (AN), a recently defined disorder characterized by normal outer hair cell function but disrupted auditory nerve function. Neurological and electrophysical evidence suggests that disrupted auditory nerve activity is due to desynchronized or reduced neural activity or both. Psychophysical measures showed that the disrupted neural activity has minimal effects on intensity-related perception, such as loudness discrimination, pitch discrimination at high frequencies, and sound localization using interaural level differences. In contrast, the disrupted neural activity significantly impairs timing related perception, such as pitch discrimination at low frequencies, temporal integration, gap detection, temporal modulation detection, backward and forward masking, signal detection in noise, binaural beats, and sound localization using interaural time differences. These perceptual consequences are the opposite of what is typically observed in cochlear-impaired subjects who have impaired intensity perception but relatively normal temporal processing after taking their impaired intensity perception into account. These differences in perceptual consequences between auditory neuropathy and cochlear damage suggest the use of different neural codes in auditory perception: a suboptimal spike count code for intensity processing, a synchronized spike code for temporal processing, and a duplex code for frequency processing. We also proposed two underlying physiological models based on desynchronized and reduced discharge in the auditory nerve to successfully account for the observed neurological and behavioral data. These methods and measures cannot differentiate between these two AN models, but future studies using electric stimulation of the auditory nerve via a cochlear implant might. These results not only show the unique contribution of neural synchrony to sensory perception but also provide guidance for translational research in terms of better diagnosis and management of human communication disorders.

Objective: To define both auditory nerve and cochlear receptor functions in subjects with auditory neuropathy (AN). Design: We tested 33 AN subjects (66 ears) and compared them with 21 healthy subjects (28 ears). In AN subjects, the average pure-tone (1, 2, and 4 kHz) threshold loss was 57 dB HL. Click stimuli were used to elicit transient evoked otoacoustic emissions (TEOAEs), cochlear microphonics (CMs), and auditory brain stem responses (ABRs). Both cochlear and ABR potentials were recorded from surface electrodes (vertex-ipsilateral mastoid) using averaging procedures. The amplitudes and latencies of CMs and ABRs and the amplitude of the TEOAEs were analyzed. Results: CM amplitudes recorded from normal ears decreased as a function of subject age. CMs recorded from AN subjects fell within the normal age-adjusted range in 60% of the subjects and were >2 SEEs (standard error of estimate) above the age-adjusted normal regression in 40% of the subjects. TEOAEs were absent in 19 (30%) AN ears (bilaterally in eight, and unilaterally in three subjects) and were present in 44 ears. In AN subjects, correlations among CM amplitude, TEOAE amplitude, and pure-tone average thresholds were not significantly related. CM amplitudes were not significantly different whether TEOAEs or ABRs were present or absent. The ABR was present in 21% of AN subjects and consisted of a low-amplitude Wave V without a preceding Wave I. Measures of CM amplitude and PTA hearing loss were not significantly different in those AN ears with a preserved ABR compared with ears with absent ABRs. Summating potentials to transient click stimuli were of small amplitude (

Objective : To use transcranial magnetic stimulation (TMS) to define motor cortical excitability in chronic fatigue syndrome (CFS) subjects during a repetitive, bilateral finger movement task. Methods : A total of 14 CFS patients were tested and compared with 14 age-matched healthy control subjects. TMS of the motor cortex (5% above threshold) was used to elicit motor evoked potentials (MEPs). Subjects performed regular (3–4/s) repetitive bilateral opening–closing movements of the index finger onto the thumb. MEPs of the first dorsal interosseus (FDI) were measured before, immediately following exercise periods of 30, 60 and 90 s, and after 15 min of rest. Results : Performance, defined by rate of movement, was significantly slower in CFS subjects (3.5/s) than in controls (4.0/s) independent of the hand measured. The rate, however, was not significantly affected by the exercise duration for either group. The threshold of TMS to evoke MEPs from the FDI muscle was significantly higher in CFS than in control subjects, independent of the hemisphere tested. A transient post-exercise facilitation of MEP amplitudes immediately after the exercise periods was present in controls independent of the hemisphere tested, but was absent in CFS subjects. A delayed facilitation of MEPs after 15–30 min of rest was restricted to the non-dominant hemisphere in controls; delayed facilitation was absent in CFS subjects. Conclusions : Individuals with CFS do not show the normal fluctuations of motor cortical excitability that accompany and follow non-fatiguing repetitive bimanual finger movements.

Objective : To study activity of auditory cortex reflected by the N100 and P200 components of the auditory evoked potentials during memorization and scanning of short-term memory stores. Methods : In a MEMORY task subjects classified a probe digit either as a member or not a member of a previously presented list of digits that varied in size from one, 3, 5 and 7 items. For comparison, subjects in a NUMBER task listened to a list of digits as in the MEMORY task but determined only whether the probe digit as odd or even . Evoked potentials to the presentation list and to probes were recorded from scalp electrodes and separately averaged for both tasks. The components peaking at approximately 100 ms (N100) and 200 ms (P200) that reflect activity of primary auditory cortex were identified and peak amplitudes and latencies were measured. Results : For presentation set items, the amplitude of N100 was affected by set size in the MEMORY but not in the NUMBER task; N100 was larger for the one item set than for the 3, 5, and 7 item sets. P200 increased in amplitude in a linear manner for both the MEMORY and NUMBER tasks. For probe items, N100 but not P200 amplitude decreased in a linear manner as the number of items in the presentation set increased in the MEMORY but not in the NUMBER task. The linear change of N100 amplitude during memory scanning was particular to in-set but not to out-of-set probes. The amplitudes of both N100 and P200 were almost twice as large in probe digits than in the digits in the presentation set in both the MEMORY and NUMBER tasks. Conclusion : Auditory sensory cortical activity in humans during an auditory short-term memory task shows dynamic changes during both memorization and memory scanning.

Premovement, sensory, and cognitive brain potentials were recorded from patients with Chronic Fatigue Syndrome (CFS) in four tasks: i) target detection, ii) short-term memory, iii) self-paced movement, and iv) expectancy and reaction time (CNV). Accuracy and reaction times (RTs) were recorded for tasks i, ii, and iv. Results from CFS patients were compared to a group of healthy normals. Reaction times were slower for CFS patients in target detection and significantly slower in the short-term memory task compared to normals. In target detection, the amplitude of a premovement readiness potential beginning several hundred milliseconds prior to stimulus onset was reduced in CFS, whereas the poststimulus sensory (N100) and cognitive brain potentials (P300) did not differ in amplitude or latency. In the memory task, a negative potential related to memory load was smaller in CFS than normals. The potentials to self-paced movements and to expectancy and RT (CNV) were not different between groups. The findings in CFS of slowed RTs and reduced premovement-related potentials suggest that central motor mechanisms accompanying motor response preparation were impaired in CFS for some tasks. In contrast, measures of neural processes related to both sensory encoding (N100) and to stimulus classification (P300) were normal in CFS.

To define mechanisms accounting for transient deafness in three children (two siblings, ages 3 and 6, and an unrelated child, age 15) when they become febrile.Audiometric tests (pure-tone audiometry, speech and sentence comprehension), tympanometry, middle ear muscle reflex thresholds, otoacoustic emissions (OAEs), and electrophysiological methods (auditory brain stem responses [ABRs], sensory evoked potentials, peripheral nerve conduction velocities) were used to test the children when they were afebrile and febrile.ABRs, when afebrile, were abnormal with a profound delay of the IV-V and absence of waves I-III. The ABR in one of the children, tested when febrile, showed no ABR components. Measures of cochlear receptor function using OAEs were normal in both febrile and afebrile states. Cochlear microphonic potentials were present in the three children, and a summating potential was likely present in two. When afebrile, there was a mild threshold elevation for all frequencies in the 15-yr-old and a mild elevation of thresholds for just low frequencies in the two siblings. Speech comprehension in quiet was normal but impaired in noise. One of the siblings tested when febrile had a profound elevation (80 dB) of pure-tone thresholds and speech comprehension was absent. Acoustic reflexes subserving middle ear muscles and olivocochlear bundle were absent when febrile and when afebrile. No other peripheral or cranial nerve abnormalities were found in any of the children. Sensory nerve action potentials from median nerve in one of the children showed no abnormalities on warming of the hand to 39 degrees C.These children have an auditory neuropathy manifested by a disorder of auditory nerve function in the presence of normal cochlear outer hair cell functions. They develop a conduction block of the auditory nerves when their core body temperature rises due, most likely, to a demyelinating disorder of the auditory nerve. The auditory neuropathy in the two affected siblings is likely to be inherited as a recessive disorder.

Brain potentials were recorded from 12 normal subjects engaged in an auditory target detection task (target stimulus probability of 0.2, stimulus rate of 1 every 2 sec) when instructions were (1) to press a response button with the thumb of the dominant hand to each target or (2) to keep a mental count of each target. A pre-stimulus slow negative potential was identified before every stimulus except non-targets immediately after targets. The amplitude of the pre-stimulus negativity was significantly affected by task instructions and was up to 4 times larger during the button press than the mental count condition. In contrast, the amplitudes and latencies of the event-related components (N100, P200, N200 and P300), when slow potentials were removed by filtering, were not different as a function of press or count instructions. The immediately preceding stimulus sequence affected both the amplitude and onset latency of the pre-stimulus negativity; both measures increased as the number of preceding non-targets increased. The amplitude of the pre-stimulus negative shift to targets also increased significantly as RT speed decreased. The major portion of the pre-stimulus negative potential is considered a readiness potential (RP) reflecting preparations to make a motor response. The amplitude of the RP during the target detection task did not significantly lateralize in contrast to the RP accompanying self-paced movements. © 1995.

Auditory‐evoked potentials were recorded from normal hearing subjects in response to voiced and unvoiced phonemes (e.g., “ta” vs “da”). The negative component generated by primary auditory cortex (N100) is markedly reduced in amplitude to unvoiced compared to voiced signals. The effects of the initial consonants' intensity, duration, and proximity to the vowel were defined. It is the initial unvoiced 10–20 ms portion that is responsible for the attenuation of the vowel‐evoked N100 component. This attenuation persists even when the consonant is attenuated 20 dB relative to the vowel's intensity; the attenuation persists with as much as a 150‐ms silent period inserted between the consonant and vowel. “Noise masking” as the basis for the unvoiced consonants ability to attenuate vowel evoked potentials were evaluated using a brief noise burst to mask tone evoked potentials; there was little similarity between the two paradigms suggesting that noise masking is not the mechanism accounting for the effects. The ...

Slow brain potentials were recorded from normal male and female subjects during a tone discrimination task presented in the CNV interval. Compared to a control condition, CNV averages derived from monopolar scalp sites (Cz, F3, F4, T3, and T4) indicated a substantial increase in the amplitude of the potentials during the tone situation. Other CNV features observed included (1) a decline in the slow wave corresponding with a perceptual judgment about the tones, and (2) asymmetries in the CNV that may have been related to differential hemispheric processing of the tone task. The results are discussed in terms of attention, decision processes, and lateral asymmetries.

An emitted potential paradigm was used to investigate P3 scalp potentials in a group of older individuals (M = 66.8 years) and a group of younger persons (M = 22.0 years). Since no physical stimulus is necessary to elicit an emitted potential, an age comparison of P3 can be made which does not depend on normal sensory transmission channels. Both traditional and latency corrected averages to missing auditory clicks were analyzed from electrodes placed over midline frontal, central, and parietal locations. Results indicated that while the scalp distribution of emitted potentials was similar for both age groups, amplitudes at Pz and Cz were significantly smaller in the older group. Latency corrected potentials indicated similar trends but did not reach significant levels. No group differences were seen for N2 or P3 latencies for either traditional or corrected averages. The findings support age differences in the amplitudes of the P3 component and suggest that when P3 is not synchronized with a sensory event, latencies in this component may not be sensitive to age differences.

Age and sex differences in the brainstem auditory evoked response (BAER) were investigated in older (60 to 79 yrs), middle-aged (40 to 59 years), and young (20 to 39 yrs) individuals. Within each age group the number of males (N = 10) and females (N = 10) were divided equally. Scalp potentials were recorded from the vertex to clicks presented at 60, 70, and 80 dB(SL) for stimulus rates of 5, 10, and 15 clicks/sec. Results indicated that older adults had longer latencies at Wave III than either middle-aged or young adults. Age effects were also found for Waves I, II, and IV but were restricted to the lowest intensity and were more evident in older males than females. Significant sex effects showed that the females in each group had shorter Wave IV and V latencies than males. The results suggest that age affects neural propagation at the level of the olivary complex (Wave III) and that BAER latencies are also influenced by the sex of the individual.

The averaged evoked potential to brief tones was compared for 10 young and 10 elderly female subjects. The amplitudes of the sensory components (P1, N1 and P2) were not affected by an infrequent change in pitch of the tones or instructing subjects to count or ignore them; but overall the elderly had a larger P1 and smaller P2 amplitude and a difference in the scalp distribution of P2. Repetition of the tones produced a decrement in these sensory components and a differential one for young and old subjects A slow potential complex consisting of components N2, P3 and SW appeared to changes in tone pitch and became more pronounced when attention was directed to the tones. Overall smaller SPs for oder subjects were interpreted as evidence for a change with age in the cortical representation of the orienting response. Topographical analysis of SPs indicated diminished activity in frontal (Fz) electrodes for elderly persons, suggestive of an enhanced aging process in the frontal cortices.

Event-related potentials (ERPs) were recorded during a visual discrimination task from nine elderly individuals (mean=68.1 years), diagnosed as having major depressive disorder, and nine age-matched controls (mean=68.0 years). During the task, subjects pressed a switch to targets (the number 9) and ignored background (the number 6) and novel stimuli (random designs). Novel and target stimuli were both interspersed infrequently in the sequence of background stimuli. Scalp electrical activity was recorded from midline frontal (Fz), central (Cz), and parietal (Pz) sites. Depressives were characterized by lengthened response times and increased number of errors across the session. Speed of response was also found to vary directly with clinical status. Additionally, ERP correlates of depression in the elderly were found: N1 was more prolonged for target than non-target stimuli in the depressed group; P2 was larger for all conditions; N2 was uniformly small across the scalp, whereas the controls showed small N2 amplitudes only at Fz; large P3s appeared in trials following the novel stimuli in the depressed but not in the control group. These results are interpreted in terms of the symptomatology associated with depression (i.e., distractability, impaired short-term memory or concentration, indecisiveness) and possible age-related changes in the ERP scalp distribution.

Sex differences in the amplitudes and latencies of the auditory brain stem potential (BAEP) were investigated using 3 levels of intensity and 3 stimulus presentation rates. The females displayed consistently larger BAEPs for waves IV, V, VI, VII than the males. The only latency differences which reached significance over all the intensities and rates occurred for wave V. The females showed significantly shorter wave V latencies than the males. Since hearing losses and individually determined click thresholds were comparable between the two groups tested, the exact sources of the uneven distribution of amplitude and latency effects are in question. Differences in the relative distances of the anatomical generators are considered in accounting for the sex differences. Because the precise origin of the sex differences cannot be stated with certainty at this time, attempts to develop normative data for the BAEP should consider the possible influences of sex differences.

Cerebral potentials evoked by items presented for memorization in a memory-scanning task were recorded from subjects ranging in age from 18 to 86 years old. Subjects were divided into younger (average age = 29 years) and older groups (average age = 66 years). Both verbal (digits) and non-verbal (musical notes) stimuli were used. Digits were presented in the auditory as well as the visual modality, and notes were presented acoustically. Potentials are described in terms of their scalp distribution, latency, and amplitude and are compared between the young and old subjects. Potentials evoked by the memorized items consisted of a positive (P50-90), negative (N100-150), positive (P185-225) sequence in the first 250 msec following stimulus onset. A sustained potential shift then followed whose amplitude differed with the items being memorized. The shift was positive in the parietal region being largest (5 μV) with verbal items presented visually and slightly smaller (3 μV) with non-verbal auditory stimuli (the notes); in contrast, verbal auditory digits were not associated with a detectable sustained parietal potential shift. In the frontal recordings there was a sustained potential shift accompanying all stimulus types, which was more negative in the young subjects. The amplitude of these sustained potential shifts differed as a function of the position of the item in the memorized set. These results provide electrophysiological evidence of brain activity during memorization that varies with the items being processed as well as differing between young and old subjects. © 1989.

Brain potentials accompanying the classification of probe items as being members of previously presented list were recorded from subjects ranging in age from 18 to 86 years old. A group of older subjects (averave age = 66 years) was compared to a younger group (average age = 29 years). The items tested were verbal (digits) and non-verbal (musical notes). Digits were presented in the auditory and visual modalities, and notes were presented acoustically. Reaction times (RTs) and performance accuracy were computed. Potentials are described in terms of scalp distribution, latency and amplitude as a function of the type of stimulus (verbal/non-verbal, auditory/visual) and age group (younger/older). Evoked potentials to target notes in an auditory target-detection ('odd-ball') task were also recorded for comparison with the memory tasks. Potentials evoked by probes consisted of a sequence of sensory components in the first 250 msec followed by a cognitive component that was positive in polarity and sustained in duration (approximately 700 msec labeled P3), consisting of an earlier frontal component, P3a (mean latency: younger = 385 msec, older = 406 msec), and a large (15 μV) and later parietal constituent, P3b (mean latency: younger = 574 msec, older = 630 msec). The frontal derivation of the younger subjects showed a sustained negative bias of the wave forms in the latency range of 200-500 msec (P2 to P3) compared to the older subjects. Reaction times were longer in older subjects than in younger subjects for all stimulus types and set sizes. For the potentials evoked by the probes the younger group had consistently larger late parietal components (P3b) than the older group, whereas the late frontal potentials (P3a) were larger for the older than younger subjects. Except for visual stimuli, the latencies of the parietal sustained potentials were not influenced by subject age in contrast to the uniform changes in RT for all stimulus types. Significant amplitude and latency effects on the parietal sustained potentials accompanied the different stimulus types and memorized-set sizes which were similar for the two age groups. These results suggest that the effects of aging on short-term memory are primarily on response selection, as evidenced by RT slowing with aging, and not on memory-scanning processes as evidenced by the similarity of the latency measures of the accompanying brain potentials between the two age groups. © 1989.

The lateral distribution of the CNV was investigated during conditions that required normal male and female subjects to vocalize simple English words in a CNV paradigm. In addition to a non-verbal or comparison condition (Tone-Clicks/Button Press), two word conditions presented stimulus words in either S1 or S2 positions (Word-Tone/Speak; Tone-Word/Speak) and a third condition required a one-word association to the stimulus words (Word-Tone/Speak Association). Monopolar scalp activity was collected from sites that included a location approximating Broca's speech area on the left hemisphere, a homologous comparison site on the right hemisphere, frontal sites (F3, F4) and the vertex (Cz). Although several subjects showed some asymmetrical activity in some of the word conditions, amplitude measures based on CNV averages indicated no consistent lateralization effects over the left hemisphere prior to word vocalizaiton. Negative pretrial shifting was suspected in those conditions in which words appeared as S1 signals.

Six Ss observed the afterimages of 11 flash-produced stimulus targets; they reported fading, regeneration, and image breakdown similar to results reported for stabilization studies employing contact lenses and afterimage techniques.

Peak latency variation and the temporal interrelationships of the auditory event-related potential were investigated in 12 normal adults (ages 28-42). Measures of variation were based on both conventional averages and single trials. Estimates of N1, P2, N2 and P3 latencies were made on a trial-by-trial basis to target stimuli recorded from Fz, Cz and Pz scalp locations. Results showed that single-trial latency variability of the auditory ERP differed both among the various components and between subjects. Larger standard deviations were measured for the later N2 and P3 components than the earlier N1 and P2 components. Regression analyses between various component latencies indicated a strong covarying relationship between N2 and P3, with N2 accounting for up to 61% of the variance of P3 latency at Pz. Earlier N1 and P2 components added little to the overall prediction of either P3 or N2. For the other components, P2 accounted for 9-16% of the variance of N2, while N1 accounted for approximately 1% of the variance of N2; N1 accounted for 8-10% of the latency variation of P2. The correlations between single-trial peak latencies and RTs were positive but of low magnitude. The highest correlations between peak latency and RT were found for N2 (r = 0.33) and P3 (r = 0.24). The low correlations between the single-trial latencies of N1 and P3 suggest that the processes reflected by these components are independent and support a distinction between the earlier and the later components of the ERP. The close temporal coupling between N2 and P3 suggests that N2 may reflect cognitive properties in common to P3 in stimulus evaluation processes. © 1986.

Visual event-related potentials were recorded from a group of 10 normal subjects while they judged the proximity of two letters of the alphabet. Subjects viewed singly the letters A, D, G, L, N, T, W and Z and indicated by button press whether the letter displayed occured before or after the comparison letter M. Reaction times to close letters (L and N) were longer than ordinally more distant letters (A, D, G, T, W, Z). A late parietally positive potential of approximately 475 ms covaried in latency amplitude with these judgments. Late potentials were delayed in latency and reduced in amplitude to close letter (L and N) judgments compared to the other letters. The results suggest that mental processes, such as alphabetic distance judgments, may be usefully studied by examining their associated event-related potentials. © 1988.

The effects of distraction on the contingent negative variation (CNV) were investigated in a group of 11 elderly (mean = 72.2 years) and a group of 12 young (mean = 23.3 years) subjects. Scalp electrical activity was recorded from midline sites at frontal, central, and parietal locations. Three experimental conditions included Recall, No Recall, and Control situations. In the Recall, or distraction condition, spoken consonant-vowel-consonant (CVC) letters were presented concurrently with the CNV signal interval and were recalled by the subjects after each trial. The No Recall condition was similar to the Recall task except that subjects were not required to repeat the CVSs. The Control condition presented a standard S1 - S2 CNV situation without CVCs. Amplitudes of the CNV, reaction times (RTs), and heart rate (HR) served as indices of distraction. The effects of distraction for both age groups indicated reduced CNVs, lengthened RTs, and elevated HRs. However, a significant age by electrode interaction revealed that while CNV amplitudes at central and parietal sites were comparable between age groups, amplitudes at the frontal placement were consistently reduced in the elderly compared to the young in all conditions. The finding of diminished frontal activity, as measured by the CNV, suggests a process of selective cortical aging and possible cellular loss which may be linked to performance deficits.

Auditory event-related potentials (ERPs) were investigated in 15 demented (12 presumed Alzheimer's, 3 cerebrovascular), 8 depressed, and 15 normal older, and 12 normal young, subjects. Both latencies from conventional averages and latency variability measures from single trials were derived for the N100, P200, N200, and P300 components of the ERP recorded from Fz, Cz and Pz scalp placements in a task requiring detection of an infrequent target tone among a series of frequent non-target tones. The P300 component most consistently separated the groups. Demented subjects had longer P300 latencies and greater P300 latency variability than both control groups and the depressed group. Age differences were observed for P300 latency, but not for P300 latency variability. Amplitudes were not significantly different among the groups. Reaction times (RTs) to the targets were longest for the demented subjects and shortest for the young controls, with the depressed and normal older control groups falling in between. Correlations between RT and P300 latency from single trials did not differentiate the groups. Using regression analysis to evaluate the deviation of P300 latency and latency variability for the patients from the predicted values for normal controls, no misclassifications of depressed patients occurred, but only 27% of the demented individuals were correctly classified using P300 variability, and 13% using P300 latency. These findings indicate that ERP measures using the "oddball" target detection paradigm were useful in describing group differences, but were not sufficiently sensitive to be used in differentiating demented persons on an individual basis for clinical diagnosis. © 1988.

Event-related potentials were measured in normal young subjects during a memory-scanning paradigm modified from one proposed by Sternberg. The stimuli used were verbal (digits) and non-verbal (musical notes) with the verbal stimuli and notes presented acoustically and the verbal stimuli also presented visually. In this paradigm each set of stimuli was presented for memorization, and then, after a 2 sec interval, a probe item appeared and was identified by the subject as belonging or not belonging to the memorized set. Memorized set sizes of 1, 3 and 5 items were studied. The potentials are described in terms of scalp distribution, latency and amplitude, and are compared with behavioral descriptors of performance (accuracy and reaction time). These potentials are also compared with those evoked by an auditory target-detection task ('odd-ball' paradigm) in the same subject at the same session. The potentials evoked by the probe stimuli consisted of a positive (P50-90), negative (N100-150), positive (P185-225) sequence in the first 250 msec, followed by a later, long-lasting (approximately 700 msec) positive component (labeled P3). This positivity consisted of an earlier component (latency of approximately 350-400 msec) with a frontal distribution, followed by a larger and later parietal component. The amplitude of the frontal component and the latency of the parietal component varied with the number of items in the memorized set differently from behavioral reaction times. Stimulus modality also affected both the amplitude and latency of the sustained parietal positive potential. Memory processes associated with the P3 complex in the 'odd-ball' task and the long-lasting positivity in the memory-scanning task are discussed. © 1989.