Mikhal Gafni

The depression of the auditory nerve-brain-stem evoked response in hypoxaemia — mechanism and site of effect ☆

During severe hypoxaemia in the cat the ABR was depressed in 2 different patterns: if mean arterial blood pressure (MAP) was maintained then all other evoked potentials (EPs--somatosensory and visual) remained. If MAP was not maintained, all of these EPs were depressed. This study sought to document these different patterns of ABR depression and to ascertain their mechanisms. When MAP fell, the ABR loss began with the later waves and progressed to the earlier waves. These are signs of a central brain lesion. The hypoxaemia, detrimental to normal function of the cardiovascular system, leads to depression of MAP, to a fall in cerebral perfusion pressure and blood flow, to cerebral ischaemia and ABR loss. On the other hand, when MAP was maintained, severe hypoxaemia was accompanied by a depression of all of the ABR waves at the same time. The cochlear microphonic potential was also simultaneously depressed. These are signs of a peripheral, cochlear effect similar to the demonstrated depression of the positive endocochlear resting potential of the scala media and of the cochlear microphonic potential during hypoxaemia. This leads to interference with the cochlear transduction mechanism so that all of the auditory evoked potentials, including the ABR, are simultaneously depressed. These results lead to the suggestion that the ABR abnormalities seen in patients who suffered a hypoxic (anoxic) insult or an ischaemic episode (prolonged interpeak latencies, loss of later waves and finally all waves absent or only the first wave remaining) is always due to ischaemia even when the initial insult was hypoxic.

Auditory nerve-brain stem potentials in man and cat under hypoxic and hypercapnic conditions.

In order to study the effects of hypoxic and hypercapnic respiratory gas mixtures on brain activity, the auditory nerve brain stem evoked potentials (ABP) were recorded in 6 human volunteers and in 12 cats while they were breathing various gas mixtures. In humans, no effect of gas mixtures containing 9-13% O2 or 7.5-10% CO2 was observed on the wave form, latency and amplitude of the ABP. The cats were exposed to up to 25% CO2 and down to 5.5% O2 or to combined hypoxic and hypercapnic gas mixtures for up to 45 min while recording ABP and monitoring CO2 and O2 in the respired gases, arterial blood gas levels, pH, arterial blood pressure, body temperature and EEG. The extremes of pH were 6.68 and 7.46. The EEG was depressed or became isoelectric during hypercapnia. In general, the wave form, amplitude and latencies of the ABP waves were not much affected by these conditions. Loss of ABP was observed only when the animal was ventilated with about 5% O2 and this was secondary to and following cardiac failure and depressed arterial blood pressure, presumably leading to brain ischaemia. Thus, even though the cortex (EEG) is depressed, the brain stem seems to be resistant to these alterations in the blood gases in spite of the relatively higher rates of metabolism reported for the brain stem auditory structures.

Auditory nerve-brain stem evoked potentials in cats during manipulation of the cerebral perfusion pressure

In order to study the effects of various degrees of cerebral ischemia on the auditory nerve-brain stem evoked potentials (BAEP), the cerebral perfusion pressure (CPP), defined as the difference between mean arterial blood pressure (MAP) and intracranial pressure (ICP), was systemically manipulated in anesthetized, paralyzed and ventilated cats. The CPP was varied by decreasing MAP, either by hemorrhage or by the infusion of a vasodilating drug, and elevating ICP by infusion of mock CSF into the cisterna magna, or by MAP depression and ICP elevation simultaneously. Even though the lower limit of adequate CPP is considered to be 40 mm Hg, the EEG became isoelectric at an average CPP of 24 mm Hg and the BAEP became isoelectric at an average CPP of 7 mm Hg. These extremely low CPP values of 7-24 mm Hg are far below the range of autoregulation of cerebral blood flow (CBF) so that the brain stem auditory pathway is still capable of generating its electrical response (BAEP) at very low CBF. This is paradoxical since these same regions of the brain have been shown to have the highest levels or regional metabolism as shown by their very high local cerebral blood flow and local glucose utilization.

Persistence of auditory nerve response and absence of brain-stem response in severe cerebral ischaemia.

Cerebral ischaemia, in which the brain-stem components of the ABP were isoelectric, was accompanied by the paradoxical persistence of the compound action potential of the auditory nerve (wave 1). This ischaemia was induced in cats by reducing mean arterial blood pressure and elevating intracranial pressure, resulting in decreased cerebral perfusion pressure (CPP). This is unexpected since the inner ear is supplied by a branch of an intracranial artery. To study this phenomenon, CPP was manipulated and when average CPP was 13.5 mm Hg, only wave 1 remained. In 7 of 9 experiments, clamping of both common carotid arteries did not abolish wave 1. Experiments with radioactive tracers demonstrated a remaining residual blood flow through the inner ear. This remaining auditory nerve response is probably not due to a very low metabolism of the inner ear or to the cochlea being supplied by anastomoses from the middle ear, supplied by the external carotid artery. The residual cochlear blood flow and the persistent wave 1 can probably be explained in the following way: at low CPPs the smaller intracranial blood vessels collapse so that the brain tissue is not perfused, leading to loss of the brain-stem components of the ABP. However, flow still persists in the larger intracranial arteries. This blood preferentially flows to the cochlea since the intracochlear pressure is slightly below the intracranial pressure due to the presence of the oval and round windows. Thus a sufficient blood flow to the cochlea is maintained, with sparing of wave 1.

The source along the basilar membrane of the cochlear microphonic potential recorded by surface electrodes in man

In order to determine the region along the basilar membrane which contributes to the recorded CM, an attempt was made to record CM responses in subjects with normal hearing and in subjects with high frequency cochlear hearing losses (e.g. acoustic trauma). In such cases of high frequency hearing loss, one may assume that damage has occurred to the hair cells in the basal turn of the cochlea. The CM, elicited by one cycle sinusoidal stimuli of various frequencies, intensities, phases, etc., was recorded by means of earlobe and scalp vertex electrodes. The CM recorded in subjects with normal hearing to high frequency sounds showed (besides the previously reported properties of the CM) large amplitudes and short latencies in response to low frequency stimuli. On the other hand, the CM recorded in subjects with high frequency hearing loss were either prolonged in latency and small in amplitude or completely absent. A plot of the relationship between CM lastency to high intensity 500 HZ stimuli stimuli and audiometric hearing loss in 66 ears shows clearly that in those cases in which hearing was normal at frequencies up to about 8 kHZ, CM latency was very short. On the other hand, in those cases in which the high frequency hearing loss progressed to include more and more lower frequencies, CM latency was more prolonged and smaller in amplitude until CM could no longer be observed. These results indicate that the CM recorded in normally hearing subjects from skin electrodes in response to low frequency (500 HZ) stimuli is generated in the basal turn of the cochlea. This finding is probably a consequence of the form of the mechanical response of the basilar membrane (travelling wave) to low frequency stimuli.

The latency of auditory nerve-brainstem responses in sensorineural hearing loss

ZusammenfassungDie Latenz der Hörnervenantwort ist bei Schalleitungsschwerhörigkeit ebenso verlängert wie die der Hirnstammantwort bei den meisten retrocochleären Schwerhörigkeiten. Der Effekt des sensorineuralen Hörverlustes auf die Latenz der Hörnervenantwort ist dagegen nicht klar. Deshalb wurden die Hörnerven-Hirnstammantworten bei Normalhörigen und bei Patienten mit sensorineuraler Schwerhörigkeit im Hochtonbereich untersucht. (75 dB HL clicks). Die durchschnittliche Latenz bei der Gruppe mit mehr als 40 dB Hörverlust ab 4 kHz war nur 0,35 ms länger als bei den Normalhörigen. Dieser Wert ist kleiner als bei den meisten Schalleitungs- und retrocochleären Schwerhörigkeiten.SummaryThe use of auditory nerve-brainstem responses in differential diagnosis of hearing loss is based on several properties of these responses including response latency. The auditory nerve response latency has been shown to be prolonged in conductive hearing loss. The latency of the brainstem responses is also often prolonged in retrocochlear hearing loss. However, the effect of sensorineural hearing losses on auditory nerve response latency is not clear. Several authors report that response latency is prolonged in sensorineural loss, whereas others claim that it is unchanged.To study this, auditory nerve-brainstem responses to 75 dB HL clicks were recorded in normal-hearing subjects and in those with various degrees of high-frequency sensorineural hearing loss. In the more extreme hearing losses, the auditory nerve response could not be seen in the response trace, so the latency of the earlobe positive wave from the region of the inferior colliculus was considered as mirroring auditory nerve response latency, since the time interval between these two waves has been shown to be constant.The average latency of the more severe hearing loss group (more than 40 dB hearing loss at 4 kHz) was found to be only 0.35 ms longer than that of the normal-hearing group. This value is smaller than that seen in most conductive and retrocochlear hearing losses.This result warrants continued use of prolonged auditory nerve response latency (greater than 0.35 ms) as an indicator of conductive hearing loss. Possible explanations for smaller latency prolongation than expected of the auditory nerve response in sensorineural hearing loss are discussed based on the properties of single auditory nerve fibers.

Analysis of auditory nerve-brainstem responses (ABR) in neonates and very young infants

ZusammenfassungDie Antwort von Hörnerv und Hirnstamm auf Clickreize wurde bei 26 normalen Kindern in der Neugeborenenzeit und dann im Alter von 3 Monaten abgeleitet. Untersucht wurden Latenz und Amplitude der Antwort des Hörnervs, Amplitude der Hirnstammantwort aus der Gegend der unteren vier Hügel, das Verhältnis der Amplitude dieser zwei Wellen zueinander und das Zeitintervall zwischen diesen beiden Reizantworten (Hirnstammübertragungszeit). Die Antwort des Hörnervs ist beim Neugeborenen im Vergleich zum Erwachsenen nur gering verlängert und verkürzt sich leicht bis zum 3. Lebensmonat. Die Latenz der Hörnervenantwort ist bei Neugeborenen nur 0,3 ms länger als beim Erwachsenen. Die Hirnstammübertragungszeit ist beim Neugeborenen am längsten und beim 3 Monate alten Kind deutlich kürzer.SummaryAuditory nerve-brainstem responses (ABR) to click stimuli were recorded in 26 normal infants when they were neonates and again in the same infants when they were 3 months old. The cochlear microphonic potential was also recorded in several of the neonates. The following response parameters were studied: latency and amplitude of the auditory nerve response, amplitude of the brainstem response elicited from the region of the inferior colliculus, the ratio of the amplitudes of these two waves and brainstem transmission time (BTT): the time interval between these two responses. It was found that the auditory nerve response is only slightly prolonged in neonates with respect to adults and shortens by a small amount from birth to the age of 3 months. The latency of the auditory nerve response in neonates is only about 0.3 ms longer than in adults. BTT is longest in neonates and shortens significantly in 3-month-old infants.

Patterns of Auditory Nerve and Brainstem-Evoked Responses (ABR) in different types of peripheral hearing loss

ZusammenfassungAbleitung der akustisch evozierten Hirnstammpotentiale bei verschiedenen Arten des peripheren Hörverlustes (Schallempfindung, Schalleitung, kombiniert). Die Auswertung der erzielten Resultate läßt die Möglichkeit erkennen, die Art des peripheren Hörverlustes durch Korrelation der Latenzzeit und der elektrophysiologischen Schwellen zu bestimmen.SummaryAuditory brainstem response (ABR) recordings were made in different types of peripheral hearing loss (sensorineural, conductive, and mixed). Scatter diagrams were constructed by plotting different expressions of the hearing loss (audiometric and electrophysiologic) against the obtained wave latencies and for these two sets of variables, correlation coefficients and the parameters of the regression equation were calculated. Consideration is given to the possibility of diagnosing the type of peripheral hearing loss by correlating wave latencies and the electrophysiologic (ABR) threshold.

The persistence of somatosensory and auditory pathway evoked potentials in severe hypoglycemia in the cat

In a previous study it was shown that during severe insulin-induced hypoglycemia in rats and cats (0.38 mmol/l, i.e., 6.8 mg% and 0.8 mmol/l, i.e., 14 mg% respectively) with isoelectric EEG, the latency and amplitude of the auditory nerve-brain-stem evoked responses were not affected. In the present study on cats, the above evoked responses were complemented by recording in addition the cortical auditory evoked potential and the peripheral, brain-stem and cortical components of the somatosensory evoked potentials. Each of these evoked potentials remained in the presence of 0.75 mmol/l glucose in plasma. The persistence of the somatosensory cortical evoked potential was unexpected since two other groups have reported the disappearance of this potential during hypoglycemia. The types of neuronal activity which can still be recorded in severe hypoglycemia are probably generated by neuronal structures with lower metabolic demands such as axons and oligosynaptic pathways, surviving on the consumption of endogenous substrates with compensatory elevation of local cerebral blood flow.

Auditory nerve and brainstem-evoked responses before and after middle ear corrective surgery

ZusammenfassungBei zwei Patientengruppen — Mittelohrerguß und Otosklerose — wurden die akustisch evozierten Potentiale von Hörnerv und Hirnstamm vor und nach den chirurgischen Eingriffen abgeleitet. Die Aussagemöglichkeiten der Registrierung zur Feststellung der Hörbesserung (Schwelle und Latenz) nach Einlage eines Drainageröhrchens und nach Stapesplastik werden aufgezeigt.SummaryAuditory brainstem response (ABR) recordings were made in two groups of middle ear pathology — middle ear effusion and otospongiosis before and after rehabilitation surgery. The ability of ABR recordings to quantify the hearing improvement (threshold and latency) after insertion of ventilating tubes and after stapedioplasty is demonstrated.