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We measured the fluctuations in plasma pyridostigmine concentration from day to day on 3 consecutive days and hour to hour during 1 day in 11 myasthenic patients, by studying their usual dosage regime. Plasma pyridostigmine was measured by gas chromatography/mass spectrometry. The intraindividual day-to-day variation in plasma pyridostigmine levels was small. A highly significant relationship was found between the oral pyridostigmine dose and the area under the plasma concentration/time curve. The bioavailability of oral pyridostigmine was 3.6, estimated by replacing one dose with an intravenous dose amounting to 1/30 of the oral dose. The relatively stable kinetic behavior of pyridostigmine is in contrast to the interpatient variability. in dose requirement, indicating that monitoring of plasma pyridostigmine levels should be reserved for special cases.

Of 1,250 patients with convulsive disorders studied during a 13-year period, 37 had convulsive attacks preceded by severe "stress." Follow-up examinations were done 1 to 12 years later on 36 of these patients and 27 children ( ≤ 20 years of age) of 16 of the 36. Patients were 20 to 50 years old, with twice as many men as women. Families of propositi showed increased incidences of febrile convulsions. Familial disposition to epilepsy was not found. One child had paroxysmal changes on an electroencephalogram only during photostimulation. Lack of sleep was the dominating stress factor; mostly "combination stress" was involved. One patient died, two of 36 developed unprovoked convulsions, and 10 experienced recurrence(s) of stress convulsions. Prophylaxis is avoidance of provoking factors; anticonvulsants apparently did not prevent recurrence. The EEG provided no aid in diagnostic evaluation or prognosis.

• In a study of congenital heart defects (CHD) in 2,461 live-born children of an unselected group of 979 male and 1,093 female epileptics, 18 children with CHD were recorded; eight had epileptic fathers and 10 epileptic mothers. The prevalence of CHD does not differ significantly from that of the background population. Many different CHD types were recorded with no single defect being predominant. Likewise, no association with a specific type of anticonvulsant treatment was noted. The fact that the prevalence of CHD among children of male and female epileptics and of the background population was similar supports the view that antiepileptic treatment is no major factor in the etiology of CHD in the offspring of epileptics.

• Anticonvulsants have been suspected of teratogenicity, with facial clefts being the malformation most frequently associated with maternal anticonvulsant therapy. Paternal epilepsy has also been suggested as a factor in the genesis of birth defects, including facial clefts. An association between epilepsy per se and facial clefts would be reflected in a higher facial cleft prevalence among epileptics, and consequently result in an increase of such malformations among their children. The prevalence of facial clefts was determined in an unselected group of 3,203 epileptic probands: their personal data were cross-matched with a complete file of Danish facial cleft patients born between 1934 and 1977. Eleven epileptic probands had a facial cleft, which is twice the expected number. The increased prevalence of cleft defects among epileptics could partly explain why more of their children have facial clefts.