T B Sloan1, R Erian. 1. Department of Anesthesiology, University of Texas Health Science Center, San Antonio 78284-7838.
Abstract
BACKGROUND: Neuromuscular blockade (NMB) is a frequent component of anesthetic techniques used during surgery in which monitoring of the nervous system is desirable. Because NMB should affect the evoked muscle response to transcranial magnetic stimulation (tcMMEP), their relationship in a primate model was characterized. METHODS: Transcranial magnetic stimulation was characterized during NMB using an infusion of vecuronium in ten adult cynomologous monkeys during anesthesia with a continuous ketamine infusion. Neuromuscular blockade was measured by peak-to-peak amplitude of the evoked muscular activity (compound muscle action potential [m-response]) of the thenar muscles and mechanical muscle action (ratio of the fourth to first peak in the train of four [TOF]) after direct stimulation of the median nerve. Neuromuscular blockade was increased incrementally to complete block and then allowed to decrease until complete resolution of measurable block. Transcranial magnetic stimulation was assessed by measuring the onset latency (time from stimulation to beginning response) and amplitude of the thenar EMG response. Cortical stimulation was accomplished using a Cadwell MES-10 magnetic stimulator at 80% of full output (1.6 Tesla). RESULTS: The tcMMEP, m-response amplitude, and mechanical muscle action, unblocked, were reduced with increasing NMB. Transcranial magnetic stimulation amplitude was more variable than was onset latency. Transcranial magnetic stimulation amplitude reduction from the baseline value did not achieve statistical significance until the m-response amplitude was reduced to 0.2 of baseline or until the TOF ratio was reduced to 0.1. Transcranial magnetic stimulation onset latency prolongation from baseline was not significantly affected by declining TOF ratios, but was prolonged when the m-response declined to 0.1 of baseline. CONCLUSIONS: This study indicates that tcMMEP onset latency is not significantly affected by NMB if the degree of blockade in the muscles used for tcMMEP monitoring is not extreme (greater than 0.2 of baseline by m-response amplitude or a TOF ratio of 0.1 or greater). If monitoring of tcMMEP amplitude is desired, partial neuromuscular blockade may be acceptable. However, amplitude reduction may occur during partial NMB. Maintenance of a constant degree of NMB is suggested to minimize amplitude fluctuations.
BACKGROUND:Neuromuscular blockade (NMB) is a frequent component of anesthetic techniques used during surgery in which monitoring of the nervous system is desirable. Because NMB should affect the evoked muscle response to transcranial magnetic stimulation (tcMMEP), their relationship in a primate model was characterized. METHODS: Transcranial magnetic stimulation was characterized during NMB using an infusion of vecuronium in ten adult cynomologous monkeys during anesthesia with a continuous ketamine infusion. Neuromuscular blockade was measured by peak-to-peak amplitude of the evoked muscular activity (compound muscle action potential [m-response]) of the thenar muscles and mechanical muscle action (ratio of the fourth to first peak in the train of four [TOF]) after direct stimulation of the median nerve. Neuromuscular blockade was increased incrementally to complete block and then allowed to decrease until complete resolution of measurable block. Transcranial magnetic stimulation was assessed by measuring the onset latency (time from stimulation to beginning response) and amplitude of the thenar EMG response. Cortical stimulation was accomplished using a Cadwell MES-10 magnetic stimulator at 80% of full output (1.6 Tesla). RESULTS: The tcMMEP, m-response amplitude, and mechanical muscle action, unblocked, were reduced with increasing NMB. Transcranial magnetic stimulation amplitude was more variable than was onset latency. Transcranial magnetic stimulation amplitude reduction from the baseline value did not achieve statistical significance until the m-response amplitude was reduced to 0.2 of baseline or until the TOF ratio was reduced to 0.1. Transcranial magnetic stimulation onset latency prolongation from baseline was not significantly affected by declining TOF ratios, but was prolonged when the m-response declined to 0.1 of baseline. CONCLUSIONS: This study indicates that tcMMEP onset latency is not significantly affected by NMB if the degree of blockade in the muscles used for tcMMEP monitoring is not extreme (greater than 0.2 of baseline by m-response amplitude or a TOF ratio of 0.1 or greater). If monitoring of tcMMEP amplitude is desired, partial neuromuscular blockade may be acceptable. However, amplitude reduction may occur during partial NMB. Maintenance of a constant degree of NMB is suggested to minimize amplitude fluctuations.