[Valve of symptomatic therapy with memantine in cerebral coma. I. Correlation with coma stages and EEG spectral patterns]

1.3-Dimethyl-5-aminoadamantane (DMAA, D-145, memantine, Memantine) was used in a group of 45 patients of both sexes in our intensive care ward for the purpose of symptomatic therapy. The patients included in the study had been suffering from obtuse craniocerebral trauma and post-traumatic cerebrovascular complications. We evaluated only those cases in which the initial duration of the coma had been not less than 3 days. The mean treatment period was 9.5 days and the observation was continued over an average of 25 days. The clinical course was recorded on the basis of Frowein's coma classification introduced by the European Association of Neurosurgical Societies. In addition, we observed the development of any cerebroorganic psychosyndrome or the emergence of an apallic syndrome. As expected, apart from individual exceptions, a regression of the coma stages 1 to 3 was observed in the course of the observation period. The significant improvement of coma stages 2 and 3 already during the treatment with memantine should be emphasized. There was a transient increase in the category-1 coma group and in the patients with cerebro-organic psychosyndromes. In correlation with the development of the clinical course, an increase significant at the 5% confidence level was found in the documentation of the EEG spectral patterns in the "normal findings/slight over-all change" evaluation, as opposed to a significant reduction of the "moderate/pronounced over-all change" EEG finding (same confidence limit). The tolerance of memantine was generally graded as very good to good. No side effects that would have led to discontinuation of the treatment were observed, and in particular there was no impairment of the blood coagulation or of the metabolic activity of the liver cells. In long-term cerebro-electric check-ups it was found that no spasm potentials are produced at the doses used here, nor was there any promotion of the propagation of epileptic attack patterns when these had been present.