SHORT-LATENCY AUDITORY EVOKED POTENTIALS IN THE MONKEY

Abstract

The short latency auditory evoked potentials (SLAEP), recorded during the first few milliseconds following a brief acoustic stimulus, are believed to originate in the subcortical structures of the auditory pathways. The SLAEP have many clinical uses, and may help localize brainstem lesions, providing the generators of the components are known.;Source hypotheses based on studies in nonprimate experimental animals must be applied with caution to the interpretation of the human SLAEP, because of differences in the SLAEP waveforms and difficulties in identifying precise component homologies. Comparisons of abnormal SLAEP with human neuropathology are useful, but the spatial limits of the physiologic effects of human neuropathology are rarely clear-cut. This thesis consists of a study of the SLAEP in a primate, the monkey.;Following a 100 (mu)sec monaural click stimulus, up to nine positive waves can be identified in the monkey SLAEP recorded at the vertex referred to the ipsilateral mastoid. Some components are more clearly identified with other electrode positions. The monkey SLAEP waveform is highly consistent within and across subjects. SLAEP from anesthetized monkeys display the same components at longer latencies, due to the lowered body temperature. The surface topography of the SLAEP, the SLAEP to binaural stimulation, and the effects of varying the interstimulus interval, stimulus intensity, stimulus polarity, and stimulus duration, are described. For clicks as wide as 1000 (mu)sec, the SLAEP is a response to the onset of the stimulus, regardless of its polarity.;The homologies between the monkey and human SLAEP are defined based on waveshape, surface topography, and parametric studies. Waves 2 and 4, the two monkey SLAEP components which do not correspond to one of the seven positive peaks in the human SLAEP, correspond to negative troughs seen between human waves I, II, and III. The differences reflect the geometries of the head and generators; waves 2 and 4 are negative peaks in some of the monkey SLAEP.;The sources of the monkey SLAEP are determined from electrocochleographic and depth pass recordings. Many of the SLAEP components have multiple sources, and do not reflect only the initial activity at each level of the auditory pathways. They derive from the cochlear summating potentials and action potentials; postsynaptic potentials recorded within brainstem nuclei do not contribute significantly to the far-field SLAEP waveform.;The major identified sources for each of the monkey SLAEP components (with its human homologue in parentheses) are as follows: Wave 1b: Cochlear summating potential. Wave 1c (I): N1 eighth nerve compound action potential in the distal eighth nerve. Wave 2 (IN): Depolarizations corresponding to N1 in the proximal eighth nerve and the axon terminals in the cochlear nucleus. Wave 3 (II): N2 eighth nerve compound action potential in the distal eighth nerve; initial, and largest, outflow burst of activity from the cochlear nucleus. Wave 4 (IIN): Depolarizations corresponding to N2 in the proximal eighth nerve and the axon terminals: activity in second-order auditory fibers ascending in the lateral lemnisci. Wave 5 (III): Outflow from the ipsilateral superior olivary complex; activity in second-order auditory fibers ascending in the contralateral lateral lemniscus. Wave 6 (IV): Outflow from the contralateral superior olivary complex and nucleus of the lateral lemniscus, and the ipsilateral inferior colliculus. Wave 7 (V): Outflow from both nuclei of the lateral lemniscus, from the ipsilateral superior olivary complex, and from both medial geniculate nuclei. Waves 8 and 9 (VI and VII): Outflow from both medial geniculate nuclei propagating in the auditory radiations.;The implied sources for the SLAEP components in man are compared with the published data correlating human SLAEP abnormalities with known neuropathology, and are in good agreement.