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I read with interest the short report “Human `memories' can be evoked by stimulation of the lateral temporal cortex after ipsilateral medial temporal lobe resection”, by Moriarity et al.1
The cortical localisation of experiential memory phenomenon was summarised by Penfield and Perot.2
Subsequent to that, Halgren et al3 used implanted depth electrodes to delineate medial temporal structures as a source of experiential phenomenon in patients with temporal lobe seizures. However, their work did not include simultaneous recordings from temporal neocortex and mesial structures. This subsequently was performed by Gloor et al.4
Based on this and a review of the images, there seems to be a fair amount of amygdala still present in this patient. Therefore, it was not surprising that simple seizures, as well as complex seizures, recurred within four months. Specific to the stimulation of the lateral temporal cortex after mesial temporal lobe resection, the anatomical work by Klinger and Gloor,5 along with the axial images, suggests that there was adequate anterior, inferior temporal, and insular cortex connected to residual amygdala to produce the experiential phenomenon on cortical stimulation.
Professor Lehman raises the interesting question of whether participation of the amygdala can account for the auditory hallucinations observed in our patient. He cites two previous studies in which electrical stimulation of the amygdala and hippocampus evoked experiential phenomena such as visceral sensations, déjà vu, and emotions.1, 2 The experiential phenomena reported with stimulation of the amygdala were usually associated with afterdischarges and did not include formed auditory hallucinations. In contrast, we reported formed auditory hallucinations evoked by neocortical stimulation, often without afterdischarges, in a patient who had an extensive medial temporal resection.3 Our study suggests that medial temporal lobe involvement cannot account entirely for evoked auditory hallucinations. While our case does not preclude a contribution from the medial temporal lobe, we think it is more likely that neocortical structures are primarily involved. Further investigation will be required to determine the potential interaction between limbic and neocortical structures in experiential phenomena.4
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