Effect of Pyritinol on EEG and SSEP in Comatose Patients in the Acute Phase of Intensive Care Therapy

Abstract

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)

Guidelines for Quality Management of Apallic Syndrome / Vegetative State

“…EEG shows the typical sleep-wake cycles. Computerized EEG analysis and pharmaco-EEG were demonstrated to provide some prognostic information when the arousal effect obeyed as desynchronization with shifting of the power spectra to faster frequency bands may proceed clinical restoration of consciousness for weeks and even months (on class II evidence A [2,16,131,138,147]). Somatosensory evoked potentials have been proposed as acceptable predictor of output in the early phase of coma and AS with a higher predictive value above 90% compared to EEG reactivity in two thirds comparable to GCS (class 2 evidence) [17].…”

“…The senior author has used successfully amphetamine for arousal of comatose and AS individuals between 1965 and 1990 when it was no longer licensed in Germany so that is was replaced by weaker amphetamine drugs [166]. The effect of pyritinol is attributable to a pyritinol-induced release of acetylcholine at the synapses within the mesencephalic structures and to an increased cortical postsynaptic reaction of the cholinergic system [131,147]. In [63], von Wild reported for the first time on the unexpected neurobehavioral arousal effect Botulinum toxin A application for the treatment of central neurogenic spasticity in 5 out of 12 subjects who were in full state AS for several weeks and months secondary to severe TBI or stroke, despite intensive early neurorehabilitation interventions.…”