Abstracts

Mismatch-negativity (MMN) is an auditory event-related potential (ERP) produced by a deviant stimuli that occurs infrequenty among standard stimuli. MMN is thought to reflect the activation of an automatic change-detector system that compares new auditory input with a short-term memory trace generated by the previous auditory stimuli. MMN in human has been demonstrated from several cortical sites, but not to our knowledge from hippocampus or amygdala. This is surprising, given that these limbic structures are so essential for learning and memory functions. We could obtain MMN from these temporomesial structures using intracranial electrodes in adult patients undergoing presurgical evaluation for epilepsy surgery. 4 adults with intractable temporal lobe seizures (age 32-48 years) had each 2-4 stereotactically implanted 6-contact depth-electrodes at amygdalo-hippocampal complex. The electrodes were implanted via lateral approach and their exact anatomical localizations were confirmed by MRI and CT in situ. After the post hoc anatomical localization of the depth-electrodes, the presence of MMN could be studied from 6 hippocampi and 5 amygdalas (i.e., the electrode tips were exactly within amygdalo-hippocampal complex). The most mesial depth-electrode contacts were chosen for the MMN analysis with the MMN latency range of 120-250 ms, as well as with the P300 range of 250-500 ms. We analyzed possible statistically significant differences between the ERPs to deviant and standard tones. A definite MMN within 120-250 ms latency range could be recorded from 4/6 hippocampi and 3/5 amygdalas. MMN was also detected within 250-500 ms latency range in 3/6 hippocampi and 2/5 amygdalas, respectively. In only one patient the hippocampal MMN resembled typical scalp-recorded MMN. In all, the MMN decreased from the deepest contacts towards the cortex, suggesting a local maximum of MMN at the amygdalo-hippocampal complex. Our data implicates that a local and early (120-500 ms post-stimuli) automatic electrophysiological change-detector system exists within the amygdalo-hippocampal complex. This data is the first to demonstrate that also these temporomesial structures are activated and involved in mismatch detection, and is in line with recent sensory mismatch fMRI studies. Other sensory stimuli might also produce MMN in the same structures, possibly thus revealing a common function for hippocampus and amygdala in early sensory stimulus detection.