Abstract
The anatomical and physiological origins of the middle-latency auditory evoked potential (MLAEP) are not well understood. The present investigation was conducted to determine whether the MLAEP derives its origins in part from the anterior temporal lobe. Twelve subjects with intractable seizures were evaluated with the MLAEP pre and post excision of the anterior-mesial temporal lobe (ATL) unilaterally. In our study, component Pa latency was unaffected by the ATL. The Na latency and the Na/Pa amplitude showed significant increases after ATL. The results we interpreted as being consistent with currently held beliefs regarding the origins of Pa. The changes in Na latency and Na/Pa amplitude are hypothesized to reflect a loss of the modulating influence of the cortex on the subcortical generators of Na.
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