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Persistence of auditory nerve response and absence of brain-stem response in severe cerebral ischaemia
Insights
During cerebral ischemia, the auditory nerve
Area of Science:
- Neuroscience
- Auditory Physiology
- Cerebrovascular Physiology
Background:
- Cerebral ischemia causes widespread brain dysfunction.
- The auditory nerve's compound action potential (wave 1) unexpectedly persists during severe cerebral ischemia.
- The inner ear's blood supply originates from intracranial arteries.
Purpose of the Study:
- Investigate the paradoxical persistence of auditory nerve wave 1 during cerebral ischemia.
- Determine the mechanisms preserving cochlear blood flow under low cerebral perfusion pressure (CPP).
Main Methods:
- Induced cerebral ischemia in cats by manipulating mean arterial blood pressure and intracranial pressure.
- Measured cerebral perfusion pressure (CPP) and auditory brainstem response (ABR).
- Utilized radioactive tracers to assess inner ear blood flow and performed carotid artery clamping.
Main Results:
- Auditory nerve wave 1 persisted even when brainstem auditory evoked potentials (BAEPs) became isoelectric due to low CPP (average 13.5 mm Hg).
- Clamping carotid arteries did not abolish wave 1 in most cases, indicating an alternative blood supply.
- Radioactive tracer experiments confirmed residual blood flow to the inner ear.
Conclusions:
- A residual blood flow mechanism preserves cochlear function during cerebral ischemia.
- Larger intracranial arteries maintain flow to the cochlea preferentially due to pressure gradients, sparing auditory nerve wave 1.
- This phenomenon is not explained by low cochlear metabolism or external carotid artery anastomoses.
Abstract:
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.