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.     

Evoked potential changes in cats following injection of an extract from the venom sac of the oriental hornet (Vespa orientalis)

Venom sac extract from the hornet Vespa orientalis was injected (via the subclavian artery) into cats and its effects on evoked potentials in two different sensory pathways (auditory and somatosensory) was investigated. A comparison was made between the venom sac extract from adult hornets and that from young (0-24 hr of age) hornets. There was a bimodal change in blood pressure, a hypothermic effect and a decrease in amplitude of the last waves of the auditory and somato sensory pathways when venom sac extract of adult hornets was injected. Venom sac extract from young hornet workers had the same influence on the blood pressure, did not affect thermoregulation and the effect on the auditory and somato sensory pathways were less consistent. Adult venom sac extract had mainly a central effect whilst the venom sac extract from young hornets (in larger doses) affected the central and/or peripheral nervous system. The central effects could be interpreted as due to opening of the blood-brain barrier by the venom.     

Salicylate ototoxicity and its implications for cochlear microphonic potential generation

Salicylic acid causes a reversible sensori-neural hearing loss. Its ototoxicity is probably related to its effect on prestin, the motor protein of the outer hair cells. In order to gain further insight into the mechanism and implications of its ototoxicity, auditory nerve brainstem evoked responses, compound action potentials of the auditory nerve, distortion product otoacoustic emissions, and cochlear microphonic potentials (CM) and vestibular evoked potentials were recorded before and after systemic salicylate administration. These responses were depressed, except for the CM and the vestibular evoked potential. This result and additional considerations provide evidence that the extracellularly recorded CM does not represent the summation of intracellular outer hair cell receptor potentials. It is possible that the CM reflects an early stage of mechano-electrical transduction by the outer hair cells, before the activation of the cochlear amplifier and the later stages of transduction.     

How are the inner hair cells and auditory nerve fibers activated without the mediation of the outer hair cells and the cochlear amplifier?

The present study was designed to assess whether, in the presence of a depression of the cochlear amplifier i.e. a sensorineural hearing loss (SNHL), the inner hair cells (IHCs) require the presence of a normal endocochlear potential for transduction. An SNHL was induced by injecting salicylic acid (which binds to the motor protein prestin in the outer hair cells), and then furosemide (which depresses the endocochlear potential) was injected. Furosemide did not cause an additional elevation of the threshold of the auditory nerve brainstem evoked response (ABR) over that induced by the salicylic acid injection. Exposure to noise was also used to induce a SNHL in other mice, and then furosemide was injected. Here too furosemide did not cause an additional ABR threshold elevation over that induced by the noise. These results show that the IHCs (and the auditory nerve) can be excited in the presence of a SNHL (i.e. without the cochlear amplifier) and in the absence of an endocochlear potential. Possible mechanisms of excitation in such a state are discussed.     

Mutual cancellation between tones presented by air conduction, by bone conduction and by non-osseous (soft tissue) bone conduction

Auditory sensation can be elicited not only by air conducted (AC) sound or bone conducted (BC) sound, but also by stimulation of soft tissue (STC) sites on the head and neck relatively distant from deeply underlying bone. Tone stimulation by paired combinations of AC with BC (mastoid) and/or with soft tissue conduction produce the same pitch sensation, mutual masking and beats. The present study was designed to determine whether they can also cancel each other. The study was conducted on ten normal hearing subjects. Tones at 2 kHz were presented in paired combinations by AC (insert earphone), by BC (bone vibrator) at the mastoid, and by the same bone vibrator to several STC sites; e.g. the neck, the sterno-cleido-mastoid muscle, the eye, and under the chin, shifting the phases between the pairs. Subjects reported changes in loudness and cancellation. The phase for cancellation differed across subjects. Neck muscle manipulations (changes in head position) led to alterations in the phase at which cancellation was reported. Cancellation was also achieved between pairs of tones to two STC sites. The differing phases for cancellation across subjects and the change in phase accompanying different head positions may be due to the different acoustic impedances of the several tissues in the head and neck. A major component of auditory stimulation by STC may not induce actual skull bone vibrations and may not involve bulk fluid volume displacements.     

Salicylic acid injection before noise exposure reduces permanent threshold shift

The permanent threshold shift (PTS) following exposure to intense noise may be due to the noise-induced excessive vibrations in the cochlea or to the generation of elevated levels of reactive oxygen species. Thus, it is possible that the resulting PTS may be reduced if the cochlear amplifier could be temporarily depressed beginningjust before the onset of the noise and continuing during the noise exposure or if antioxidant drugs were administered. These possibilities were assessed in mice by administering a single injection of salicylic acid (an antioxidant drug which also reversibly depresses the motor protein prestin of the cochlear amplifier) just before, and in other mice, just after, 3.5 h of 113-dB SPL broadband noise exposure. The PTS in the mice injected with salicylic acid just before the noise exposure was significantly smaller than that in mice exposed to the same noise without salicylic acid. The PTS in the latter was not significantly different from that in mice who received the drug just after the noise. Thus a single injection of salicylic acid, just before a noise exposure, can protect the ear from a noise-induced hearing loss.     

Neonatal auditory brain-stem response threshold and latency: 1 hour to 5 months.

Auditory brain-stem evoked responses were recorded in normal neonates and infants ranging in age from less than 1 h to 5.5 months. The average threshold in neonates 0-5 h old was 29 dB greater than that in adults, reaching the adult threshold range within 2 weeks. The latency of wave I in 0-5 h neonates was 1.81 msec and reached the adult range within 2 weeks. The V-I interpeak latency in 0-5 h neonates was 5.3 msec and did not reach adult values within the period of this study.     

Multi-modality evoked potentials in hypoxaemia

The auditory nerve-brain-stem evoked response (ABR) has been shown to be insensitive to hypoxic inspiratory gas mixtures which severely depress the EEG. In order to determine the relative sensitivities of additional brain regions and pathways to hypoxaemia, anaesthetized paralysed cats were ventilated with various gas mixtures while recording the evoked responses of the auditory, somatosensory (including peripheral nerve, brain-stem and primary cortical components), visual and vestibular systems. Arterial blood pressure was maintained by dopamine infusion and pH was corrected with bicarbonate. Hypoxic gas mixtures (6-7% O2) presented for 60 min, causing severe hypoxaemia (paO2 20-30 mm Hg; O2 saturation 25-50%), were without effect on the somatosensory, vestibular and visual EPs while the auditory evoked potentials (ABR and cortical components) were depressed. However, if arterial blood pressure was allowed to fall, all of the evoked potentials became severely depressed and isoelectric. These results and others indicate that the cortical components are qualitatively similar to the more peripheral evoked potentials. The resistance of these evoked potentials to controlled hypoxaemia is probably due to their generation by oligosynaptic pathways and to a compensatory switch to anaerobic metabolism and to an elevation of cerebral blood flow.