Opiate-Antagonist Reversal of Neurological Deficits –Experimental and Clinical Studies–
- 1 March 1986
- journal article
- research article
- Published by Wiley in Psychiatry and Clinical Neurosciences
- Vol. 40 (1) , 61-79
- https://doi.org/10.1111/j.1440-1819.1986.tb01613.x
Abstract
The proximal left M1 and the common trunk of A2 were clipped in 12 adult dogs. Naloxone was injected after placing the clips onto 6 dogs. Neither the systemic blood pressure nor the local cerebral blood flow were influenced by naloxone. In another group of 6 dogs with chronic right hemiplegia, naloxone proved passably effective in improving the hemiplegia. Eight patients with neurological deficits of various etiologies were administered levallorpham. The improvement in motor performance and/or elevation of mental activity was observed more or less in all but 2 of the patients. It was considered that the effect of opiate antagonists is based partially on the facilitation of synaptic transmission exaggerated by the arousal response.Keywords
This publication has 24 references indexed in Scilit:
- A double blind trial of naloxone in the treatment of acute stroke.Stroke, 1984
- Opiate antagonists in the treatment of stroke.Stroke, 1984
- Studies of nuclear magnetic resonance imaging and regional cerebral glucose metabolism in acute cerebral ischemia: Possible mechanism of opiate antagonist therapeutic activityLife Sciences, 1983
- Effects of naloxone on systemic and cerebral responses to experimental concussive brain injury in catsJournal of Neurosurgery, 1983
- Neuropeptides and stroke: current status and potential application.Stroke, 1983
- Effect of naloxone on neurologic deficit and cortical blood flow during focal cerebral ischemia in catsLife Sciences, 1982
- Naloxone reversal of ischemic neurologic deficits in baboons is not mediated by systemic effectsLife Sciences, 1982
- Naloxone in the treatment of strokeSurgical Neurology, 1982
- NALOXONE REVERSAL OF NEUROLOGICAL DEFICITThe Lancet, 1982
- Naloxone or TRH fails to improve neurologic deficits in gerbil models of “stroke”Life Sciences, 1982