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the auditory nerve (as can occur with nearby electrocoagulation) can result in a change of CAP waveform. This change in CAP waveform recorded from the vestibulocochlear nerve takes the form of a decrease in amplitude of the negative peak or of total obliteration of this peak so that only a single positive peak remains. Because the negative peak occurs when the volley of neural activity passes under the recording electrode, and the initial positive peak reflects the approaching volley, a decrease in the amplitude of the negative peak indicates partial conduction block in the vestibulocochlear nerve. Likewise, obliteration of the negative peak indicates that the neural volley in the vestibulocochlear nerve approaches the recording electrode but never reaches it, and thus that there is a total conduction block distal to the location of the recording electrode. Such changes in the CAP therefore indicate that the heat from coagulation has blocked neural transmission in a larger or smaller number of vestibulocochlear nerve fibers.

Use of BSAERs in Monitoring Brain Stem Manipulations
Many large acoustic tumors distort the brain stem, and removal of such tumors involves further manipulation of the brain stem. Brain stem manipulations are traditionally detected through their effects on cardiovascular function, but we have found it of value to use BSAERs as well to monitor brain stem manipulations during operations to remove acoustic tumors. In this context, we monitor the BSAER evoked by stimulating the ear contralateral to the tumor. We monitor these BSAERs, and not for instance SSEPs, because the ascending auditory pathway has several nuclei located in the brain stem and it may be assumed that these nuclei are more sensitive to mechanical manipulation of the brain stem than fiber tracts. Monitoring SSEPs is likely to detect changes in the long fiber tract (the medial lemniscus) in the part of the brain stem that is at primary risk for manipulations, but monitoring BSAERs is more likely to lead to detection of more significant changes in the nuclei. There is also reason to and the operation of these systems may keep heart rate and blood pressure within the normal range for some time after changes occur in the brain stem cardiovascular control centers. These mechanisms would thus delay detection of changes in cardiovascular parameters due to brain stem manipulations.
In the patient whose BSAER and cardiovascular function values are shown in Figure 6, there was little change in the latencies of peak III while there were noticeable changes in the latency of peak V of the BSAER. This is in agreement with the assumption that peak III originates mainly from the ipsilateral cochlear nucleus, thus, in this case, from a structure that is located contralateral to the tumor. Peak V is generated by the (contralateral) lateral lemniscus, and is affected by changes in the function of the lateral lemniscus as well as all structures of the ascending auditory pathway located caudal to the lateral lemniscus, such as the trapezoid body located in the center of the brain stem and the superior olivary complex

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