{'fraction_non_alphanumeric': 0.020713463751438434, 'fraction_numerical': 0.0, 'mean_word_length': 5.796875, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Focal epilepsy: generation and spreading mechanisms in experimental conditions].

This paper describes essential mechanisms underlying focal epileptic activity. Within the centre of an epileptic focus neurons display a characteristic phenomenon - the paroxysmal depolarization shift. This type of activity is partly caused by membrane-intrinsic mechanisms and also by postsynaptic excitation. Burster neurons seem to play a special role in this mechanism. Whereas the centre of an epileptic focus is distinguished by its massive excitation, the immediate surrounding are characterized by massive inhibitory phenomena ("epileptic inhibition"). The transition from interictal to ictal phenomena goes along with the spread of activity to adjacent neocortical areas. Experimental studies give strong evidence that this epileptic spread is dependent on neocortical anatomy.