Human auditory evoked potentials during natural sleep: The early components

The auditory brain-stem evoked potential (ABEP) was recorded from 9 female subjects during 1 night of natural sleep. Monaural click stimuli were delivered at a rate of either 11, 41 or 81/sec through a hearing-aid device. The intensity was held constant at 70 dB nHL. In other runs, the intensity was lowered to either 50, 30 or 10 dB, the rate of click presentation being held constant at 81/sec. Tympanic temperature was monitored throughout the recording session. The ABEP was unaltered during any stage of sleep regardless of the rate of presentation or stimulus intensity. Distinct peak V responses were recognizable to within 10 dB of the adult threshold in the sleeping subject. It may be concluded that sleep has no virtually on effect on ABEP morphology.     

Short- and middle-latency auditory evoked potentials in abstinent chronic alcoholics: preliminary findings

Short- and middle-latency auditory evoked potentials (BAEPs and MAEPs) were studied in 15 chronic alcoholic patients after 1 month's abstinence and compared with those of 15 healthy controls, matching the patients pairwise for sex and age. Most of the parameters studied varied more within the alcoholic group than within the control group. The BAEP results agree with previous reports; in the alcoholic group, BAEP peak V was significantly delayed and the inter-peak intervals, III–V and I–V, were lengthened. The latencies of the MAEP components Na and Pa, on the other hand, were significantly shortened. These findings suggest that chronic abusive consumption of alcohol may bring about structural and/or neurochemical alterations at various levels in the auditory pathway.     

Whole-head mapping of middle-latency auditory evoked magnetic fields

We recorded middle-latency auditory evoked magnetic fields from 9 healthy subjects with a 122-channel whole-head SQUID gradiometer. The stimuli were click triplets, 2.5 msec in total duration, delivered alternately to the two ears once every 333 msec. Contralateral clicks elicited P30m responses in 16 and P50m responses in 12 out of 18 hemispheres studied; ipsilateral clicks did so in 7 and 13 hemispheres, respectively. The field patterns were satisfactorily explained by current dipoles in 16 and 4 hemispheres for contra- and ipsilateral P30m, and in 4 and 10 hemispheres for contra- and ipsilateral P50m. The peak latencies of P30m and P50m were not affected by stimulation side. The results show that middle-latency auditory evoked responses receive a strong contribution from auditory cortical structures, and that differences of input latency to cortical auditory areas, evaluated from MLAEF latencies, do not explain the latency differences seen in late auditory evoked fields to contralateral vs. ipsilateral stimulation.     

Median and tibial nerve somatosensory evoked potentials: middle-latency components from the vicinity of the secondary somatosensory cortex in humans

The topography of the middle-latency N110 after radial nerve stimulation suggested a generator in SII. To support this hypothesis, we have tried to identify a homologous component in the tibial nerve SEP (somatosensory evoked potential). Evoked potentials following tibial nerve stimulation (motor+sensory threshold) were recorded with 29 electrodes (bandpass 0.5–500 Hz, sampling rate 1000 Hz). For comparison, the median nerve was stimulated at the wrist. Components were identified as peaks in the global field power (GFP). Map series were generated around GFP peaks and amplitudes were measured from electrodes near map maxima. With median nerve stimulation, we recorded a negativity with a maximum in temporal electrode positions and 106±12 ms peak latency (mean±SD), comparable to the N110 following radial nerve stimulation. After tibial nerve stimulation the latency of a component with the same topography was 131±11 ms (N130). Both N110 and N130 were present ipsi- as well as contralaterally. Amplitudes were significantly higher on the contralateral than the ipsilateral scalp for both median (3.1±2.4 μV vs. 1.7±1.6 μV) and tibial nerve (1.9±1.2 μV vs. 0.6+1 μV). The topography of the N130 can be explained by a generator in the vicinity of SII. The latency difference between median and tibial nerve stimulation is related to the longer conduction distance (cf. N20 and P40). The smaller ipsilateral N130 is consistent with the bilateral body representation in SII.     

Event-related auditory evoked potentials and multiple sclerosis

Long latency event-related auditory evoked potentials, particularly the P300 wave, constitute an objective electrophysiological index of cognitive function. For this reason, these potentials have been studied in a series of 101 patients with multiple sclerosis (MS), classified according to McAlpine's criteria into definite, probable and possible cases. The patients were also classified as depressed or non-depressed according to the DSM-III and Research Diagnostic Criteria. They were also subjected to a battery of psychometric tests.In the patient population the N200 and P300 latencies were increased, as were the P200 latencies, when compared with a control population. This electrophysiological pattern had previously been observed in other conditions characterised by subcortical lesions. Partial correlations (at constant disease duration) between the disability score and the cognitive deficit were found to be significant. Patients with an increased P300 latency had a greater disability and the P300 latency was significantly correlated with the duration of the illness.The N200 and P300 latencies were increased in depressed MS subjects, but this increase did not reach the level of significance. Depression was more frequent in the more severely handicapped patients. This suggests that the origin of the depression seen in multiple sclerosis is only partly organic, and that it is one of the factors contributing to the subcortical cognitive deficit in multiple sclerosis.Progressive forms of the disease exhibited the most profound cognitive deficit, and the most marked increase in P300 latency.     

Brain-stem auditory evoked potentials and brain death

BAEP records were obtained from 30 brain-dead patients. Three BAEP patterns were observed: (1) no identifiable waves (73.34%), (2) an isolated bilateral wave I (16.66%) and (3) an isolated unilateral wave I (10%). When wave I was present, it was always significantly delayed. Significant augmentation of wave I amplitude was present bilaterally in one case and unilaterally in another. On the other hand, in serial records from 3 cases wave I latency tended to increase progressively until this component disappeared. During the same period. wave I amplitude fluctuations were observed. A significant negative correlation was found for wave I latency with heart rate and body temperature in 1 case. Two facts might explain the progressive delay and disappearance of wave I in brain-dead patients: a progressive hypoxic-ischaemic dysfunction of the cochlea and the eight nnerve plus hypothermia, often present in brain-dead patients. Then the incidence of wave I preservation reported by different authors in single BAEP records from brain-dead patients might depend on the moment at which the evoked potential study was done in relation to the onset of the clinical state. It is suggested that, although BAEPs provide an objective electrophysiological assessment of brain-stem function, essential for BD diagnosis, this technique could be of no value for this purpose when used in isolation.     

Logarithmic display of auditory evoked potentials

Auditory evoked potentials (AEP) can be simultaneously recorded on-line as a succession of 11 waves, through a single input channel of a mini-computer. Since the response waves differ widely in frequency, a computing routine has been developed to display the whole response pattern in a single picture. Based upon a non-linear samples reduction of the digitized response, this routine allows a logarithmic transformation of the time axis. The method improves the identification of the AEP components and provides an objective estimate of the central auditory pathway for both neurophysiological and neuroclinical studies.     

Topography of middle-latency somatosensory evoked potentials following painful laser stimuli and non-painful electrical stimuli

The aim of this study was to compare cerebral evoked potentials following selective activation of Aβ and Aδ fibers. In 15 healthy subjects, Aβ fibers were activated by electrical stimulation of the left radial nerve at the wrist. Aδ fibers were activated by short painful radian heat pulses, applied to the dorsum of the left hand by a CO₂ laser. Evoked potentials were recorded with 15–27 scalp electrodes, evenly distributed over both hemispheres (bandpass 0.5–200 Hz). The laser-evoked potentials exhibited a component with a mean peak latency of 176 msec (N170). Its scalp topography showed a parieto-temporal maximum contralateral to the stimulus side. In contrast, the subsequent vertex negativity (N240), which appeared about 60 msec later, had a symmetrical scalp distribution. Electrically evoked potentials showed a component at 110 msec (N110), that had a topography similar to the laser-evoked N170. The topographies of the N170 and N110 suggest that they may both be generated in the secondary somatosensory cortex. There was no component in the electrically evoked potential that had a comparable interpeak latency to the following vertex potential: for N60 it was longer, for N110 it was shorter. On the other hand, in the laser-evoked potentials no component could be identified the topography of which corresponded to the primary cortical component N20 following electrical stimulation.     

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.     

Habituation of auditory evoked potentials and emotional state

"Fast" and "slow" habituation of N1 and N1-P2 components of auditory evoked potentials was studied in healthy subjects and in depressed patients. In patients, initially more low amplitudes of N1 and N1-P2 were revealed, as well as slowing down of habituation in the beginning of stimuli series and acceleration to its end (in healthy people--the greatest habituation in the initial part of the series and amplitude increase at its end), the absence of power effect in the component N1 at reaching, in the process of habituation, of the same minimum parameters as in healthy subjects. This points to weakening of dishabituation process parallel with well expressed "slow" habituation in patients and allows to suggest at expressed negative emotions a deficit of attention processes as a result of "internal abstraction".     

Three-channel Lissajous' trajectory of the binaural interaction components in human auditory brain-stem evoked potentials

The 3-channel Lissajous' trajectory (3-CLT) of the binaural interaction components (BI) in auditory brain-stem evoked potentials (ABEPs) was derived from 17 normally hearing adults by subtracting the response to binaural clicks (B) from the algebraic sum of monaural responses (L + R). ABEPs were recorded in response to 65 dB nHL, alternating polarity clicks, presented at a rate of 11/sec. A normative set of BI 3-CLT measures was calculated and compared with the corresponding measures of simultaneously recorded, single-channel vertex-left mastoid and vertex-neck derivations of BI and of ABEP L+R and B. 3-CLT measures included: apex latency, amplitude and orientation, as well as planar segment duration and orientation.The results showed 3 apices and associated planar segments (“Bd_II,” “Be” and “Bf”) in the 3-CLT of BI which corresponded in latency to the vertex-mastoid and vertex-neck peaks IIIn, V and VI of ABEP L + R and B. These apices corresponded in latency and orientation to apices of the 3-CLT of ABEP L + R and ABEP B. This correspondence suggests generators of the BI components between the trapezoid body and the inferior colliculus output. Durations of BI planar segments were approximately 1.0 msec. Apex amplitudes of BI 3-CLT were larger than the respective peak amplitudes of the vertex-mastoid and vertex-neck recorded BI, while their intersubject variabilities were comparable.     

Physiology-based modeling of cortical auditory evoked potentials

Evoked potentials are the transient electrical responses caused by changes in the brain following stimuli. This work uses a physiology-based continuum model of neuronal activity in the human brain to calculate theoretical cortical auditory evoked potentials (CAEPs) from the model’s linearized response. These are fitted to experimental data, allowing the fitted parameters to be related to brain physiology. This approach yields excellent fits to CAEP data, which can then be compared to fits of EEG spectra. It is shown that the differences between resting eyes-open EEG and standard CAEPs can be explained by changes in the physiology of populations of neurons in corticothalamic pathways, with notable similarities to certain aspects of slow-wave sleep. This pilot study demonstrates the ability of our model-based fitting method to provide information on the underlying physiology of the brain that is not available using standard methods.     

Stimulus-dependent oscillations and evoked potentials in chinchilla auditory cortex

Besides the intensity and frequency of an auditory stimulus, the length of time that precedes the stimulation is an important factor that determines the magnitude of early evoked neural responses in the auditory cortex. Here we used chinchillas to demonstrate that the length of the silent period before the presentation of an auditory stimulus is a critical factor that modifies late oscillatory responses in the auditory cortex. We used tetrodes to record local-field potential (LFP) signals from the left auditory cortex of ten animals while they were stimulated with clicks, tones or noise bursts delivered at different rates and intensity levels. We found that the incidence of oscillatory activity in the auditory cortex of anesthetized chinchillas is dependent on the period of silence before stimulation and on the intensity of the auditory stimulus. In 62.5% of the recordings sites we found stimulus-related oscillations at around 8-20 Hz. Stimulus-induced oscillations were largest and consistent when stimuli were preceded by 5 s of silence and they were absent when preceded by less than 500 ms of silence. These results demonstrate that the period of silence preceding the stimulus presentation and the stimulus intensity are critical factors for the presence of these oscillations.     

Age-dependent amplitude variation of brain-stem auditory evoked potentials

Normative amplitude values of brain-stem auditory evoked potential (BAEP) components are given for normally hearing subjects at 1, 10, 30, 50 and 70 years of age, with an intragroup age variation of only ±6 months. Under these circumstances amplitude standard deviations decreased to less than 20% of the mean values. In contrast with the reduced evolution of latency with age, BAEP amplitude (for components I–V) undergoes a greater oscillation during ontogeny. With the exception of component I, it increased markedly from 1 year to 10 years of age and decreased thereafter constantly up to 50 years, with a mean rate of 10 nV yearly. The decrease slowed down between 50 and 70 years. The amplitude differences between the subgroups are highly significant statistically (P < 0.01). Possible reasons for these changes are discussed.