Brainstem auditory evoked potentials in the rabbit.

Eight white New Zealand rabbits were submitted to auditory stimulation in order to obtain normative BAEP parameters. A monaural alternating 0.1 ms click stimulation at 20 Hz, 90 dB was used. Two series of 1000 responses were averaged (10 ms time-base, 160-3000 Hz band-pass) and highly reproducible peaks were obtained. Peaks P1, P2, P3, P4 were obtained in all ipsilateral recordings, whereas peak P5 was detectable in only 6 animals. In contralateral recordings P1 was absent and the following peaks were similar to those of ipsilateral recordings. Normative values of absolute and interpeak latencies, peak amplitudes and amplitude ratios were obtained. The procedure was repeated 24 hours after basal recordings and measures of test-retest variability were obtained.     

Brainstem auditory evoked potentials (BAEPs), pathology of wave IV

In a group of 134 consecutive patients with brainstem symptomatology wave IV was bilaterally absent in 69%. Bilateral absence of this wave can be considered as a normal state. Only absence of wave IV on one side with its presence on the other side was appraised as pathologic. Asymmetries of the latency and amplitude could not be taken into consideration because of the lack of normative data for this wave. Computer tomography showed in our pathologic cases lesions in the pons, oblongata and cerebellum. The clinical semiology was extensive and multiform pointing in 84% to a pontine origin, in 16% to a lesion of the midbrain or oblongata. A possible lesion of the pons was in accordance with its functional anatomy as well as with the supposed origin of wave IV (superior olivar complex, lateral lemniscal nucleus). In 62% of cases the pathology of wave IV was present without impairment of auditory functions. The pathology of wave IV was considered as little sensitive and little specific.     

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.     

The human fetal auditory evoked potential

The brain-stem auditory evoked potential (BAEP), a sensitive test of the functional status of the neonatal brain, has not been studied in utero since no practical technique for human fetal recording is available. We have developed a simple recording technique which allows continuous monitoring of the fetal AEP during labor. Waves I, III and V of the fetal brain-stem AEP have been consistently identified. Wave form morphology, interpeak latencies, and latency-intensity relations are similar to postnatal recordings. Middle latency potentials have also been recorded, with wave forms that correspond to the neonatal middle latency AEP.     

Temperature responses following ventilation of the fetal sheep in utero

The mammalian fetus produces significant quantities of heat. This passes to the mother principally through the placenta and to a lesser extent via a pathway comprising the skin, amniotic fluid, and uterine wall. To assess the importance of the lesser pathway, temperature responses were recorded in 7 near-term fetal sheep after intrauterine ventilation with oxygen, after snaring the umbilical cord to block the placental route, and following fetal death. Four distinguishing characteristics of responses were observed: fetal temperature rose 0.10 +/- 0.03 (SEM) degrees C after oxygenation; it rose progressively an additional 0.9 +/- 0.1 degrees C during the 90-min interval after cord snaring; amniotic fluid temperature rose slowly until it was about midway between fetal and maternal temperature; and after fetal death, fetal amniotic fluid temperatures fell slowly. In a simple mathematical model with constant parameters these results could not be explained fully. It was necessary to assume that heat production rose with increased oxygenation and elevated body temperature and that ventilation increased heat transfer through the amniotic fluid, as would occur if chest wall movement were stirring the fluid. Using the model, the value for heat conductance from fetal skin to amniotic fluid was estimated to be 10.5 watts degrees C-1 under basal conditions.     

Almitrine inhibits breathing movements in fetal sheep in utero

Whilst hypoxia stimulates fetal peripheral chemoreceptors, fetal breathing movements do not increase as hypoxia also has central effects. We wondered whether specific stimulation of the arterial chemoreceptors by almitrine would produce a stimulation of fetal breathing movements. When almitrine was given to 5 intact and 3 peripherally-chemodenervated fetal sheep in utero, fetal breathing movements rapidly ceased for 1-12 h. There was also a decrease in the amount of time spent in low voltage electrocortical activity. The effects of almitrine are therefore similar to those of hypoxia, and are independent of the peripheral chemoreceptors. Thus it may be a valuable tool in the study of the control of fetal breathing.     

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.     

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.     

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.     

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.     

Metabolic and hormonal responses to cooling the fetal sheep in utero

The metabolic and hormonal effects of cooling 10 fetal sheep in utero (115-142 days of gestation) for 2h were studied. The fetal core temperature fell by 2.81 +/- 0.14 degrees C while the maternal temperature fell 0.86 +/- 0.15 degrees C. This hypothermia caused a significant rise in the fetal and maternal plasma glucose concentrations (P less than 0.001) and a fall in the fetal insulin concentrations (P less than 0.01). The fetal plasma lactate and cortisol concentrations rose rapidly (P less than 0.01) while the growth hormone fell (P less than 0.01) and remained low until cooling ceased when a rapid rebound occurred. There was no significant change in any of the fetal iodothyronines and no elevation of nonesterified free fatty acid concentrations, in contrast to the rapid rise (P less than 0.01) which occurred when newborn lambs were cooled. These observations demonstrate that appropriate glucose, insulin, lactate and cortisol responses to hypothermia have differentiated by 120 days of gestation. However, neither a thyroid hormone response nor an elevation in free fatty acid levels was observed. Thus not all components of the thermogenic response to hypothermia can be demonstrated in the late gestation fetail sheep in utero.     

Intensity dependence of auditory evoked potentials in behaving cats

The intensity dependence of auditory evoked potentials (AEPs) recorded epidurally over the primary (AI) and secondary (AII) areas of the auditory cortex was studied in behaving cats during wakefulness, sleep and anesthesia. Four kHz tones of 50, 60, 70, and 80 dB SPL, presented in random order every 2 ± 0.2 s by a bone conductor, elicited clear changes of the AEP amplitudes with increasing stimulus intensity, but individual components displayed different responses curves. AEP components from the AI region showed saturation of their amplitude with stimulus intensity (P13, P34) or no amplitude increase (N19), while amplitude and intensity were linearly related in the AII area. The intensity dependence of the first positive component (P12/P13) was consistently stronger for the AEP recorded from the AI than from the AII area, while later components exhibited no difference between AI and AII. During slow wave sleep, the intensity dependence of this first positive component increased in the two areas, while that of later components decreased. Pentobarbital anesthesia abolished almost all later components and depressed the intensity dependence of the first positive component both in the AI and AII area. These results indicate that (1) clear intensity dependence of AEP exists in the cat auditory cortex and (2) this intensity dependence, especially that of the first positive AEP component, shares functional similarities to the human augmenting/reducing phenomenon in the auditory modality concerning regional differences and sleep-waking cycle.     

Age-related changes in human middle latency auditory evoked potentials

We recorded middle latency auditory evoked potentials (MAEPs) in young (20–40 years) and elderly (60–80 years) subjects with normal hearing. The Pa component was prolonged in latency and markedly enhanced in amplitude in the elderly subjects. No changes were found in Na, or in the binaural interaction of the MAEP. Differences in Pa amplitude and latency were not due exclusively to changes in auditory thresholds, since they were not duplicated by changes in stimulus intensity, and persisted when MAEPs from selected young and old subjects were compared at similar SPL levels. The enhancement of Pa amplitude appears to reflect age-related central modifications in auditory processing.