von Wild K, Simons P, Schoeppner H
Neurosurgical Department, Clemenshospital, Westphalian Wilhelms University in Münster, Germany.
Pharmacopsychiatry. 1992 May;25(3):157-65. doi: 10.1055/s-2007-1014398.
The extent and duration of acute disturbances of consciousness depend on the severity and localization of the underlying cerebral dysfunction. The Glasgow Coma Scale (GCS) permits a relevant statement to be made on the course and recovery tendency of functional damage patterns in cerebral, mesencephalic, and brain stem structures. Therapy is directed at exerting a beneficial effect on the disturbed cerebral metabolism by administration of centrally active substances and at utilizing the available reserve plasticity of the brain for any possible recovery of mental performance. The bioavailability and profile of action of pyritinol have been well documented in animal experiments. We have studied the question as to the extent to which the substance influences the depth of coma in patients receiving acute intensive care therapy, and how this can be objectified electrophysiologically in the form of a specific central effect on basal brain structures. In a phase-II pilot study over five days the acute effect of intravenous 60-min. administration of 1,000 mg pyritinol on the depth of coma, the central conduction time (CCT) and the primary complex amplitude (N20/P25) of the SSEP, and on vigilance behavior (spectral edge frequencies and power) was investigated for 90 minutes in each case under intensive-medical steady-state conditions in 10 comatose patients. Because of the differences in the underlying brain damage, the primary depth of coma, age (30-89 years), sex (two female, eight male), as well as previous treatment (surgery, conservative), the significance of the results could not be evaluated by confirmatory statistical analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
