Since Schmid (115) and Kruse (74) reported on osteopathies occurring after antiepileptic treatment in children, there have been numerous publications concerning the influence of antiepileptics on mineral metabolism in the bones. The investigators' results range from slight anomalies of the plasma levels of calcium, phosphate, alkaline phosphatase, parathormone and 25-hydroxycholecalciferol to severe bone alterations. In the majority of cases, the severe pictures occurred in retarded, neurologically abnormal, institutionalised children who were treated with a high-dose combination of several antiepileptics for epilepsy which was difficult to treat. The first case reports from adults were published by Dent et al. (26). These patients had also been treated since their early youth with an antiepileptic combination. They displayed fractures and suffered from bone pain and muscular weakness. The good response of the rachitic bone alterations to vitamin D treatment both in children and in adults indicated vitamin D deficiency. These reports prompted systematic investigations on the influence of antiepileptics on bone metabolism in numerous hospitals and outpatient departments. According to the available literature, it can be stated that antiepileptic therapy can lead to shifts in calcium and phosphate metabolism and to a raised activity of serum alkaline phosphatase. In studies comprising control groups, the patient treated with anticonvulsants more frequently displayed variations of clinical laboratory parameters. The frequent observation of vitamin D hypovitaminosis led to the assumption that alterations in vitamin D metabolism by enzyme induction are the cause of the disorders in calcium and vitamin D metabolism. This hypothesis was frequently contradicted in recent years after hypocalcaemia and alterations in the mineral content of the bone after antiepileptic therapy had been reported irrespective of the vitamin D level. Besides a restricted intestinal calcium absorption, an influence of antiepileptics on the hormones regulating calcium and phosphate metabolism was found. Thus, a multifactorial genesis of the disorders in bone mineral balance must be assumed. The fact that the vast majority of outpatients with long-term anticonvulsant therapy do not display any disorders of bone metabolism indicate that there are individually different compensation capabilities (possibly of genetic origin). According to the literature, the probability that adults will develop osteomalacia under antiepileptic therapy is associated with the joint presence of various risk factors.(ABSTRACT TRUNCATED AT 400 WORDS)