Limbic event-related potentials to words and pictures in the presurgical evaluation of temporal lobe epilepsy.

We recorded limbic event-related potentials (ERPs) with intrahippocampal depth electrodes in a more demanding verbal and an easier pictorial continuous recognition task in patients undergoing presurgical evaluations of their medical refractory mesial temporal lobe epilepsies (MTLE). In all cases depth electrodes were implanted because non-invasive studies could not demonstrate unilateral seizure-onset unequivocally. For the present study we only considered 24 patients who eventually were found to suffer from unilateral MTLE, in whom hippocampal sclerosis (HS) was confirmed histologically, and who were seizure-free post-operatively. We found that the rhinal anterior medial temporal lobe N400 (AMTL-N400) to first presentations of words but not to pictures was reduced in amplitude on the side of seizure origin. Our data suggest that limbic ERPs to words are more sensitive to the epileptogenic process than those to pictures. Thus, if limbic ERPs are recorded as part of invasive presurgical evaluations, verbal instead of pictorial recognition paradigms should be employed.

Intracranially recorded memory-related potentials reveal higher posterior than anterior hippocampal involvement in verbal encoding and retrieval.

The human hippocampus is essential for both encoding and recollection, but it remains controversial whether there is a functionally different involvement of anterior versus posterior parts of the hippocampus in these memory processes. In the present study, we examined encoding and retrieval processes via intrahippocampal recordings in 27 patients with unilateral temporal lobe epilepsy. Multicontact depth electrodes were implanted along the longitudinal axis of the hippocampus as part of the presurgical evaluation. In a continuous word recognition test, subjects had to indicate whether words were new or already presented. Recognized old words, as compared to new words, resulted in a larger P600 component, as well as in a larger late negative component (LNC, 600-900 msec). In addition, subsequently remembered words elicited a larger positivity (400 to 900 msec) than later forgotten words. We found differences concerning the distribution along the hippocampus for the LNC old-new effect, reflecting successful retrieval, as well as for the subsequent memory effect, reflecting successful encoding. Both effects were larger the further posterior an electrode was located in the hippocampus. Findings are suggestive for a predominant posterior hippocampal involvement in both verbal encoding and retrieval.

Towards a functional topography of sensory gating areas: invasive P50 recording and electrical stimulation mapping in epilepsy surgery candidates.

The filtering of sensory information, also referred to as "sensory gating", is impaired in various neuropsychiatric diseases. In the auditory domain, sensory gating is investigated mainly as a response decrease of the auditory evoked potential component P50 from one click to the second in a double-click paradigm. In order to relate deficient sensory gating to anatomy, it is essential to identify the cortical structures involved in the generation of P50. However, the exact cerebral topography of P50 gating remains largely unknown. In a group of 17 patients with drug-resistant focal epilepsy, P50 was recorded invasively via subdural electrodes, and the topography of functionally indispensable ("eloquent") cortices was obtained by electrical stimulation mapping. These eloquent areas were involved in language, motor, and sensory functions. P50 could be identified in 13 patients in either temporal (n=8) or midfrontal sites (n=5). There were six occurrences (in five patients) of overlap of sites with maximal P50 responses and eloquent areas. Those were auditory (n=1), supplementary sensorimotor (n=3), primary motor (n=1), and supplementary negative motor (n=1). Results suggest that the early stage of sensory gating already involves a top-down modulation of sensory input by frontal areas.

Subdural recordings of the mismatch negativity (MMN) in patients with focal epilepsy.

Mismatch negativity (MMN) is elicited by discernible changes in an otherwise regular stream of auditory stimulation and reflects a pre-attentive detection mechanism. In the current study, auditory evoked potentials were recorded intracranially and electrode contacts sensitive for stimulus deviance were selected in order to further elucidate the contribution of different brain areas to MMN generation. Data were obtained from patients with frontal and temporal lobe epilepsy undergoing a presurgical evaluation by subdural and depth electrodes. In 13 of 29 patients under investigation an intracranial MMN could be observed, while in four other patients a response recovery of the N100 was revealed, mimicking an MMN. Most electrodes with an MMN signal were located in or close to the superior temporal lobe. In two patients an MMN was observed at electrode contacts over the lateral inferior frontal cortex and in one patient at a frontal interhemispheric electrode strip, giving evidence for a participation of the frontal gyrus in MMN generation. Current findings have, however, to be interpreted with caution owing to the placement and limited extension of the used electrode arrays.

Short-term habituation of the intracranially recorded auditory evoked potentials P50 and N100.

At an interstimulus interval (ISI) of 500-ms stimulus repetition leads to a strong decrease in cortical response. The functional foundation of this response suppression (or sensory gating) is yet not fully understood. Experiments on short-term habituation using the same stimulus material as sensory gating experiments and same ISI might help to elucidate the mechanisms behind the P50 suppression. Event-related potentials were recorded intracranially in epileptic patients undergoing presurgical evaluation with subdural and depth electrodes. Stimulus material consisted of trains of six clicks, with the last stimulus deviating in pitch and duration. P50 and N100 were calculated for each stimulus in the train separately and compared by analysis of variance (ANOVA). A highly significant amplitude reduction was found from the 1st to 2nd stimulus for both P50 and N100. From the 2nd to 5th stimulus no further amplitude decrease was observable. The deviating 6th stimulus led to a response recovery of both components, but the P50 elicited by the 6th stimulus was still smaller than the P50 of the 1st stimulus. Current results indicate that the P50 suppression as investigated in sensory gating experiments seems to be completed after the 2nd stimulus.