Electroencephalography and clinical neurophysiology
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Electroencephalogr Clin Neurophysiol · Aug 1998
Clinical TrialNeurophysiological monitoring of pharmacological manipulation in acute organophosphate (OP) poisoning. The effects of pralidoxime, magnesium sulphate and pancuronium.
The neuromuscular transmission failure in acute organophosphate (OP) poisoning occurs because of the irreversible inactivation of the enzyme acetylcholinesterase located in the neuromuscular junction, and is distinguished neuroelectrophysiologically by single electrical stimulus-induced repetitive responses and either a decremental or a decrement-increment response upon high-rate repetitive nerve stimulation (RNS). Understandably, the administration of pharmacological agents with actions at different sites in the neuromuscular junction would alter the neuroelectrophysiological findings in acute OP poisoning. ⋯ While the administration of all 3 agents-- pralidoxime, magnesium sulphate and pancuronium-- resulted in the reversion of the neuroelectrophysiological defects, only pralidoxime is contended to be therapeutically useful. The therapeutic benefit due to its administration is limited by a short duration of action, and hence it is recommended that it should be administered for a longer period of time under neuroelectrophysiolgical guidance.
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Electroencephalogr Clin Neurophysiol · Aug 1998
Latency of changes in spinal motoneuron excitability evoked by transcranial magnetic brain stimulation in spinal cord injured individuals.
To examine the basis for delay in the excitatory effects of transcranial magnetic stimulation (TMS) of motor cortex on motoneuron pools of muscles left partially-paralyzed by traumatic spinal cord injury (SCI). ⋯ The results suggest that motor conduction slowing after traumatic SCI most likely occurs across the population of the descending tract axons mediating the TMS-evoked motor responses.