The effect of chlormadinone acetate (24 mg/day) upon the plasma levels of pituitary gonadotropins and gonadal hormones on the number of generalized convulsions and spike EEG density was investigated in a group of epileptic children with intractable seizures and with clinical signs suggestive of hyperandrogenism. In each case, the effect of chlormadinone was evaluated in relation to hormonal levels and seizures observed during a control period and under the effect of placebo as follows: Control (PC)-Chlormadinone acetate (PCL1)-Placebo (PP)-Chlormadinone acetate (PCL2). In a male child (4MS), the number of convulsive attacks observed in the control period (26/month) was reduced during PCL1 (2/month) increased during PP (12/month) and was reduced again during PCL2 (0/month). Spike EEG density showed a parallel course to the clinical attacks. In this case, control levels of testosterone were markedly elevated (40 ng/ml) and were decreased during PCL1 to 4.0 increased again during PP to 34.0 and decreased again during PCL2 to 1.2 ng/ml. Plasma levels of pituitary gonadotropins were unchanged throughout the entire period of study. In other cases, neither the number of epileptic attacks nor spike EEG density were apparently affected by this regime and plasma levels of pituitary gonadotropins and gonadal hormones were also unmodified. These results suggest that a latent state of hyperandrogenism may be detected in some epileptic patients with intractable seizures and that chlormadinone may reduce convulsive attacks in these patients, probably by decreasing testosterone plasma levels.
PIP: The effect of chlormadinone acetate (24 mg/day) upon the plasma levels of pituitary gonadotropins and gonadal hormones on the number of generalized convulsions and spike EEG density was studied in a group of epileptic children with intractable seizures and with clinical signs suggestive of hyperandrogenism. In each case, the effect of chlormadino ne was evaluated in relation to hormone levels and seizures observed during a control period and under the effect of placebo, as follows: Control (PC); Chlormadinone acetate (PCL1); Placebo (PP); Chlormadinone acetate (PCL2). In a male child, the number of convulsive attacks observed in the control period (26/month) was reduced during PCL1 (2/month), increased during PP (12/month) and reduced again during PCL2 (0/month). Spike EEG density showed a parallel course to the clinical attacks. In this case, control testosterone levels were markedly high (40 ng/ml) and decreased during PCL1 to 4.0, increased again during PP to 34.0 and decreased again during PCL2 to 1.2 ng/ml. Plasma levels of pituitary gonadotropins were unchanged during the entire period of study. In other cases, neither the number of epileptic attacks nor spik e EEG density were apparently affected by this treatment and plasma levels of pituitary gonadotropins and gonadal hormones were also unchanged. These findings suggest that a latent state of hyperandrogenism may be detected in some epileptic patients with intractable seizures and that chlormadinone may reduce convulsive attacks in these patients, probably by decreasing plasma testosterone levels.