Neurochemical evidence indicates that cognitive impairment in dementia of Alzheimer type (DAT) is related to degeneration of cholinergic neurons in the brain. A pharmacological approach is treatment with a cholinesterase inhibitor such as tetrahydroaminoacridine (THA). THA treatment of 17 patients with DAT was studied with a double-blind crossover design with three types of treatment, THA + lecithin, THA + placebo and placebo + placebo. Each treatment period was 6 weeks with wash out periods of 2 weeks. The treatment was evaluated with clinical ratings, psychometric testing, EEG and regional cerebral blood flow (rCBF) measurements. No significant clinical differences between treatment periods were found in the total sample, but marked individual differences were observed. The patients were subdivided into three outcome groups based on four clinical measures: 6 patients improved (responders), 5 patients were mainly unchanged, and 6 patients showed further deterioration during the trial period of 26 weeks. Pretreatment rCBF in responders differed significantly from that of the deteriorated patients. EEG showed more high frequency activity among responders. Hepatotoxic side effects were observed in several cases. Three subjects showed marked increases of liver enzymes, with normalization following dose reduction. The majority of patients who improved or remained unchanged during the study chose to continue THA treatment in an open trial.

SUMMARYSpontaneous hypoglycaemia was related to treatment with a commonly used neuroleptic drug (haloperidol) in two diabetic patients with organic brain disease. Hypoglycaemia disappeared when the drug was replaced by a dopamine agonist (bromocriptine). Impaired secretion of growth hormone (GH) was demonstrated in both of the patients during haloperidol medication, or a short time thereafter, and a normalized GH response was found when the patients were treated with bromocriptine. Cerebral ventricular dilatation and subnormal cerebral perfusion were demonstrated in both and a partially empty sella in one of the patients. Organic brain disease and possibly additional endocrine abnormalities might have contributed to hypoglycaemia in our patients. The significance of dopamine-related neuroendocrine reactions and of GH in counteracting hypoglycaeniic stimuli is discussed.

SUMMARYEvidence for cerebral B12 deficiency was searched for in 16 patients (age range 54-94 years) with subnormal serum B12 values (