Our study covered a 5-year period, and included all patients within a well-defined area who developed seizures after age 60 years. The dominant cause of seizures was a previous stroke, accounting for 32% of all cases. Tumors accounted for 14%, and the cause of seizures remained unknown in 25%. Seizures were recurrent in greater than 80% of patients with first seizure greater than 6 months after stroke. Fifteen of 21 patients with tumors had metastatic tumors. Of the six patients with primary brain tumors, five had malignant gliomas and one had a meningioma. We conclude that epilepsy with onset after age 60 years is more often symptomatic than is epilepsy in younger patients; since seizures were the first sign of a central nervous system (CNS) disease in half of the patients with brain tumors, careful investigation is necessary to reach a correct diagnosis.

The incidence of epilepsy in persons greater than or equal to 60 years was studied during a 5-year period in an urban area. The incidence of patients with definite epilepsy was 77 new cases per year per 100,000 citizens greater than 60 years of age, with a significant excess of male patients. Generalized and partial seizures each accounted for about half of the seizures, but the majority of patients experienced generalization at least once. Of 163 patients with onset of epilepsy during the study period, 152 could manage in their own home, but 97 of these required permanent home help. Marital status, dementia, and focal neurological signs, but not age, influenced patients' social function. A group of patients of the same age with established epilepsy before the study period managed as well or even better, indicating that epilepsy did not significantly influence social function. For both groups, too many patients as compared with the population at risk were economically inactive at the time of admission. Judging from patients' previous occupation, it seems as if patients predominantly came from the lower social classes, indicating that occupational risks may be of ethiological importance.

Thirteen out of 18 young out-patients with simple schizophrenia under neuroleptic treatment completed a double-blind cross-over trial with Madopar [L-Dopa + benserazid (a peripheral decarboxylase inhibitor)] and placebo. Nine patients were given 900 mg L-Dopa + 225 mg benserazid daily, 1 patient received 600 mg L-Dopa + 150 mg benserazid, and 3 patients, 300 mg L-Dopa + 75 mg benserazid. In these doses, L-Dopa was effective against emotional withdrawal, blunted affect, tendency to isolation and apathy, without inducing or aggravating productive, accessory symptoms. The activity score, according to the specific activity-withdrawal scale, was significantly increased (P less than 0.05), whereas the total BPRS score (Brief Psychiatric Rating Scale) was slightly, but significantly reduced (P less than 0.05). In cases where L-Dopa had to be limited to 600 and 300 mg daily, a tendency to anxiety, distortion of thinking, and a sense of unreality were observed, depending on the dose of L-Dopa. In no case were gastrointestinal, cardiovascular or neurological side-effects observed.

Thyroid function, the clinical occurrence of goitre and ultrasonically determined thyroid gland volume were investigated in 23 patients with phenytoin- and 28 patients with carbamazepine-treated convulsive disorders and compared with matched healthy controls. In the phenytoin treated group median thyroid volume was 26 ml (range 14-57 ml) compared to 17 ml (range 8-41 ml) in the controls (P less than 0.01). Ten patients and four controls had a goitre (NS). Median serum T4 and FT4I levels were reduced, serum TSH level increased and serum T3, T3RU, FT3I and thyroglobulin levels unaltered compared with the controls. In the carbamazepine treated group median thyroid volume was 25 ml (range 13-66 ml) compared to 16 ml (range 9-44 ml) in the controls (P less than 0.01). Thirteen patients and three controls had a goitre (P less than 0.02). Median serum T4, FT4I and FT3I levels were reduced, serum thyroglobulin increased and serum T3, T3RU and TSH levels unaltered compared with the controls. The increase in thyroid size is probably a compensatory mechanism due to the low free thyroid hormones in serum caused by an increased hepatic degradation of thyroid hormones by phenytoin and carbamazepine.