Mechanisms of Electrically Induced Damage after Cochlear Implantation

Abstract

This report is the fourth in a series of parametric studies designed to evaluate and define conditions that may produce histological damage by means of electrical stimulation from cochlear prostheses. Earlier studies established damage thresholds for both acute (400 μA rms or 70 μC/cm²0) and chronic (100 μA rms or 15 to 20 μC/cm²0) stimulation with continuous sinusoidal current of 1,000 Hz. In a subsequent study, a tenfold reduction in the stimulation frequency (to 100 Hz) resulted in a 50% reduction in the acute damage threshold (200 μA rms), which was a smaller reduction than anticipated if damage is dependent only on charge density. This finding and the damage patterns observed in the preceding studies suggested that multiple mechanisms are responsible for the sensory and supporting cell degeneration induced by the electrical stimulus. A similar pattern of structural changes has been observed by other investigators after acoustic stimulation of the cochlea, suggesting that common mechanisms may be involved. With electrical stimulation, electrophoretic effects have been implicated; like acoustic trauma, however, mechanical, biochemical, and metabolic processes may also be involved. This investigation was designed to identify and analyze better the damage mechanisms active in acute stimulation. Sixteen normal guinea pigs were implanted and stimulated using an interrupted 1,000-Hz signal at 500 μA for three hours. Duty cycle was reduced to 50% and signal periodicity ranged from 100 to 1,000 ms. After stimulation, the animals were killed and the cochleas examined with the scanning electron microscope for evidence of pathological changes. Despite reduction of the duty cycle to 50% of the exposure duration used in previous acute stimulation experiments, the degree of damage and the damage pattern were similar to those observed with a continuous stimulus. Alteration in the stimulus intervals appeared to have no effect on the degree and type of damage observed. Our data compare favorably to a parallel model of acoustic trauma in which mechanical injury results in similar damage patterns. Based on our observations we suggest that a primary mechanism of acute tissue damage at higher intensities of electrical stimulation is electromechanical.