Abstract
Auditory brainstem evoked potentials (ABEP) were recorded from 16 awake cats to obtain 3-Channel Lissajous' Trajectories (3CLTs) using three orthogonal differential electrode configurations (nasion — midline nuchal ridge, left — right mastoids, vertex - midline under the mandible). Potentials, evoked by monaural 80 dBnHL (re. human threshold) clicks, were studied before, and up to 7 weeks after inducing neuronal lesions localized to the cochlear nucleus (CN) or the superior olivary complex (SOC), or myelin lesions localized to the fibers of the trapezoid body connecting these two structures. Neuronal lesions were induced by injection of kainic acid (KA), while myelin lesions were induced by injection of L-alpha-lysophosphatidylcholine (LPC). With CN neuronal lesions the major changes in 3CLT were in the time domain of ‘b’, ‘c’ and ‘d’ (components P2, P3 and P4 of single-channel ABEP). With SOC neuronal lesions the major changes were in ‘c’ and ‘d’ of 3CLT (P3 and P4 of ABEP). With trapezoid body lesions the major change was in ‘c’ (P3 of ABEP). The results are compatible with the peripheral generation of the first ABEP components (P1a and P1b). The second component (P2) is generated by ipsilateral CN neurones and their outputs. The third component (P3) is generated primarily by ipsilateral SOC neurones and their outputs, with the ipsilateral CN providing input. The fourth component (P4) is generated bilaterally by the SOC neurones and their outputs, receiving their inputs from ipsilateral CN. The fifth ABEP component (P5) is generated by structures central to the SOCs and their immediate outputs. Neither focal neuronal nor myelin lesions were sufficient to produce obliteration of any component, consistent with a set of generators for each of the ABEP components, consisting of both cell bodies and their output fibers, that is distributed spatially in the brainstem.
Highlights
Significant (P < 0.001) decreases are marked by -, marginally significant (P < 0.009) increases by +, and decreases by - . while nonsignificance is indicated by an empty cell
Peaks in the ‘Z’ channel are placed under the 3CLT components corresponding in latency
CN - lesion to cochlear nucleus; SOC - lesion to the superior olivary complex; AMP - apex amplitude; LAT - apex latency
Summary
G); five of which were subsequently injected with LPC to the left trapezoid body in the vicinity of SOC, five were injected with KA into the left CN, and five with KA into the left SOC. In addition to these unilateral lesions, one cat was injected with KA to the SOC, ELECTRODE POSlTlON bilaterally. The ‘x’ derivation was not precisely at right angles to the ‘Y’ and ‘Z’ channels and the data were subsequently adjusted mathematically to correct for this discrepancy. The amplified potentials were averaged (12 bit analog-to-digital converter) using 512 addresses and a dwell time of 20 ps per point per channel. Sweeps that included potentials that approached the full range were not included in the average
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