{'fraction_non_alphanumeric': 0.014373716632443531, 'fraction_numerical': 0.0, 'mean_word_length': 5.863849765258216, '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}}
Therapeutic concentration of antiepileptic drugs and the severity of epileptogenesis.

In sodium valproate monotherapy for generalized seizures and carbamazepine for partial seizures, it was found in a within-patient follow-up study that the effect-developing concentrations which were sufficient to suppress the clinical seizures were significantly higher than the effect-sustaining concentrations by which longstanding suppression was maintained. There was a delayed onset of therapeutic effect which worked to suppress the clinical and electrographic seizure manifestations, and the length of the delay depended on the nature of the epilepsy. In animal experiments, the possibility that the severity of epilepsy may become milder as a consequence of successful pharmacotherapy was reconfirmed in amygdaloid-kindled cats on chronic medication in place of kindling animals on acute prophylactic medication. Only when the established generalized seizures were completely suppressed, was the generalized seizure triggering threshold evidently elevated. Since epilepsy is a long-standing condition lasting for years to decades, short-spanned cross-sectional observations are often misleading. Whatever relationship might exist between the blood levels of antiepileptic drugs and the paroxysmal discharges in the EEG, the severity of epileptogenesis as well as the longitudinal time course must always be taken into consideration in the drug treatment of epilepsy.