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Gulaev, E. V., and V. V. Lin’kov. "Clinical and functional characteristics of intraoperative motor evoked potentials monitoring in microdiscectomy." Kazan medical journal 97, no. 3 (June 15, 2016): 371–76. http://dx.doi.org/10.17750/kmj2016-371.
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Aim. To assess motor evoked potentials parameters in a complex of intraoperative neurophysiological monitoring at the time of discectomy for a herniated intervertebral disc under general anesthesia, to determine their dependence on age, sex, height.Methods. Intraoperative motor evoked potentials monitoring during microdiscectomy under inhalational anesthesia was conducted in 43 patients for the herniated disc at L4-L5 or L5-S1 levels. In all patients, the herniated disc diagnosis was confirmed by the magnetic resonance imaging data. Monitoring was performed using the «Neuro-IOM» device («Neurosoft», Russia). Latency and amplitude of muscle response for m. abductor hallucis and m. tibialis anterior were analyzed.Results.. The obtained data suggest that the motor evoked potentials allow to objectify the presence of motor disorders, which persist at the end of microdiscectomy. The data on the relationship between latency of muscles responses on the side of radiculopathy and the healthy side with patients’ age, body height and weight are obtained. The motor evoked potentials amplitude had a direct correlation with the patients’ body weight. Increase in latency of transcranial motor evoked potentials on the side of the clinical motor fall-out compared with the healthy limb was defined. Due to the expressed variability of motor evoked potentials responses amplitude under general anesthesia, significant differences for a given parameter were not obtained.Conclusion. There is relationship between latency of motor evoked potentials and patients’ age, body height and weight; an increase in the latency of transcranial motor evoked potentials on the side of the clinical motor fall-out compared with the healthy limb was revealed.
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Kallioniemi, Elisa, Minna Pitkänen, Laura Säisänen, and Petro Julkunen. "Onset Latency of Motor Evoked Potentials in Motor Cortical Mapping with Neuronavigated Transcranial Magnetic Stimulation." Open Neurology Journal 9, no. 1 (July 31, 2015): 62–69. http://dx.doi.org/10.2174/1874205x01509010062.
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Cortical motor mapping in pre-surgical applications can be performed using motor evoked potential (MEP) amplitudes evoked with neuronavigated transcranial magnetic stimulation. The MEP latency, which is a more stable parameter than the MEP amplitude, has not so far been utilized in motor mapping. The latency, however, may provide information about the stress in damaged motor pathways, e.g. compression by tumors, which cannot be observed from the MEP amplitudes. Thus, inclusion of this parameter could add valuable information to the presently used technique of MEP amplitude mapping. In this study, the functional cortical representations of first dorsal interosseous (FDI), abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles were mapped in both hemispheres of ten healthy righthanded volunteers. The cortical muscle representations were evaluated by the area and centre of gravity (CoG) by using MEP amplitudes and latencies. As expected, the latency and amplitude CoGs were congruent and were located in the centre of the maps but in a few subjects, instead of a single centre, several loci with short latencies were observed. In conclusion, MEP latencies may be useful in distinguishing the cortical representation areas with the most direct pathways from those pathways with prolonged latencies. However, the potential of latency mapping to identify stressed motor tract connections at the subcortical level will need to be verified in future studies with patients.
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Linden, R. Dean, Yi-Ping Zhang, Darlene A. Burke, Matthew A. Hunt, John E. Harpring, and Christopher B. Shields. "Magnetic motor evoked potential monitoring in the rat." Journal of Neurosurgery: Spine 91, no. 2 (October 1999): 205–10. http://dx.doi.org/10.3171/spi.1999.91.2.0205.
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Object. The authors conducted a study to provide an objective electrophysiological assessment of descending motor pathways in rats, which may become a means for predicting outcome in spinal cord injury research. Methods. Transcranial magnetic motor evoked potentials (TMMEPs) were recorded under various conditions in awake, nonanesthetized, restrained rats. Normative data were collected to determine the reproducibility of the model and to evaluate the effect of changing the stimulus intensity on the evoked signals. In addition, an experiment was performed to determine if the TMMEPs produced were the result of auditory startle response (ASR) potentials elicited by the sound generated by the movement of the copper coil inside its casing during magnetic stimulation. Transcranial magnetic motor evoked potentials were elicited after magnetic stimulation. At 100% stimulus intensity, the mean forelimb onset latency was 4.2 ± 0.39 msec, and the amplitude was 9.16 ± 3.44 mV. The hindlimb onset latency was 6.5 ± 0.47 msec, and the amplitude was 11.47 ± 5.25 mV. As the stimulus intensity was decreased, the TMMEP onset latency increased and the response amplitude decreased. The ASR potentials were shown to have longer latencies, smaller amplitudes, and were more variable than those of the TMMEPs. Conclusions. These experiments demonstrate that TMMEPs can be recorded in awake, nonanesthetized rats. The evoked signals were easy to elicit and reproduce. This paper introduces noninvasive TMMEPs as a new technique for monitoring the physiological integrity of the rat spinal cord.
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Kombos, Theodoros, Olaf Suess, Öczan Ciklatekerlio, and Mario Brock. "Monitoring of intraoperative motor evoked potentials to increase the safety of surgery in and around the motor cortex." Journal of Neurosurgery 95, no. 4 (October 2001): 608–14. http://dx.doi.org/10.3171/jns.2001.95.4.0608.
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Object. The repetitive application of high-frequency anodal monopolar stimulation during surgery in or near the motor cortex allows a qualitative and quantitative evaluation of motor evoked potentials (MEPs). Using this method, motor pathways and motor function can be continuously monitored during surgery. Methods. In this prospective study, 70 patients underwent MEP monitoring during surgery performed in the central region. All procedures were performed after general anesthesia had been induced without the aid of muscle relaxants. The motor pathways were monitored during the entire surgical procedure by repetitive high-frequency anodal monopolar stimulation (frequency 400–500 Hz; train 7–10 pulses; impulse duration 0.2–0.7 msec; and stimulation intensity 16.9 ± 7.76 mA). The MEPs were continuously evaluated to assess their latency, potential duration, and amplitude. Recorded alterations in these parameters were subsequently correlated with surgical maneuvers and with postoperative neurological deterioration. The monitoring parameters (latency, potential duration, and amplitude) had a broad interindividual range of variation. A correlation between individual intraoperative changes in the potentials and surgical maneuvers or postoperative neurological deterioration was observed in eight cases. A spontaneous shift in latency greater than 15% or a sudden reduction in the amplitude of the potential greater than 80% was considered a warning criterion. In all cases in which there was an irreversible change in latency or a complete loss of potentials were observed, there was postoperative neurological deterioration. Conclusions. Improved surgical safety can be achieved using intraoperative neurophysiological monitoring procedures. Repetitive stimulation of the motor cortex proved to be a reliable method for monitoring subcortical motor pathways. Changes in MEP latency and MEP amplitude served as warning criteria during surgery and possessed prognostic value.
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Bala, Endrit, Daniel I. Sessler, Dileep R. Nair, Robert McLain, Jarrod E. Dalton, and Ehab Farag. "Motor and Somatosensory Evoked Potentials Are Well Maintained in Patients Given Dexmedetomidine during Spine Surgery." Anesthesiology 109, no. 3 (September 1, 2008): 417–25. http://dx.doi.org/10.1097/aln.0b013e318182a467.
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Background Many commonly used anesthetic agents produce a dose-dependent amplitude reduction and latency prolongation of evoked responses, which may impair diagnosis of intraoperative spinal cord injury. Dexmedetomidine is increasingly used as an adjunct for general anesthesia. Therefore, the authors tested the hypothesis that dexmedetomidine does not have a clinically important effect on somatosensory and transcranial motor evoked responses. Methods Thirty-seven patients were enrolled and underwent spinal surgery with instrumentation during desflurane and remifentanil anesthesia with dexmedetomidine as an anesthetic adjunct. Upper- and lower-extremity transcranial motor evoked potentials and somatosensory evoked potentials were recorded during four defined periods: baseline without dexmedetomidine; two periods with dexmedetomidine (0.3 and 0.6 ng/ml), in a randomly determined order; and a final period 1 h after drug discontinuation. The primary outcomes were amplitude and latency of P37/N20, and amplitude, area under the curve, and voltage threshold for transcranial motor evoked potential stimulation. Results Of the total, data from 30 patients were evaluated. Use of dexmedetomidine, as an anesthetic adjunct, did not have an effect on the latency or amplitude of sensory evoked potentials greater than was prespecified as clinically relevant, and though the authors were unable to claim equivalence on the amplitude of transcranial motor evoked responses due to variability, recordings were made throughout the study in all patients. Conclusion Use of dexmedetomidine as an anesthetic adjunct at target plasma concentrations up to 0.6 ng/ml does not change somatosensory or motor evoked potential responses during complex spine surgery by any clinically significant amount.
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Shine, Timothy S. J., Barry A. Harrison, Martin L. De Ruyter, Julia E. Crook, Michael Heckman, Jasper R. Daube, Wolf H. Stapelfeldt, et al. "Motor and Somatosensory Evoked Potentials." Anesthesiology 108, no. 4 (April 1, 2008): 580–87. http://dx.doi.org/10.1097/aln.0b013e318168d921.
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Background Paraplegia is a devastating complication for patients undergoing repair of thoracoabdominal aortic aneurysms. A monitor to detect spinal cord ischemia is necessary if anesthesiologists are to intervene to protect the spinal cord during aortic aneurysm clamping. Methods The medical records of 60 patients who underwent thoracoabdominal aortic aneurysm repair with regional lumbar epidural cooling with evoked potential monitoring were reviewed. The authors analyzed latency and amplitude of motor evoked potentials, somatosensory evoked potentials, and H reflexes before cooling and clamping, after cooling and before clamping, during clamping, and after release of aortic cross clamp. Results Twenty minutes after the aortic cross clamp was placed, motor evoked potentials had 88% sensitivity and 65% specificity in predicting spinal cord ischemia. The negative predictive value of motor evoked potentials at 20 min after aortic cross clamping was 96%. Conclusions Rapid loss of motor evoked potentials or H reflexes after application of the aortic cross clamp identifies a subgroup of patients who are at high risk of developing spinal cord ischemia and in whom aggressive anesthetic and surgical interventions may be justified.
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Bernard, Jean-Marc, Yann Pereon, Guillemette Fayet, and Pierre Guiheneuc. "Effects of Isoflurane and Desflurane on Neurogenic Motor- and Somatosensory-evoked Potential Monitoring for Scoliosis Surgery." Anesthesiology 85, no. 5 (November 1, 1996): 1013–19. http://dx.doi.org/10.1097/00000542-199611000-00008.
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Background Most techniques used to monitor spinal cord tracts are sensitive to the effects of anesthesia, particularly to volatile anesthetic agents. The aim of this prospective study was to show that evoked potentials recorded from the peripheral nerves after spinal cord stimulation, so-called neurogenic motor evoked potentials, are resistant to clinical concentrations of isoflurane or desflurane, compared with somatosensory-evoked potentials. Methods Twenty-three patients were studied during surgery to correct scoliosis. The background anesthetic consisted of a continuous infusion of propofol. Isoflurane (n = 12) or desflurane (n = 11) were then introduced to achieve 0.5 and 1.0 end-tidal minimum alveolar concentrations (MAC), both in 50% oxygen-nitrous oxide and in 100% oxygen. Somatosensory-evoked potentials were elicited and recorded using a standard method, defining cortical P40 and subcortical P29. Neurogenic motor-evoked potentials were elicited by electric stimulation of the spinal cord via needle electrodes placed by the surgeon in the rostral part of the surgical field. Responses were recorded from needle electrodes inserted in the right and left popliteal spaces close to the sciatic nerve. Stimulus intensity was adjusted to produce a supramaximal response; that is, an unchanged response in amplitude with subsequent increases in stimulus intensity. Measurements were obtained before introducing volatile agents and 20 min after obtaining a stable level of each concentration. Results Isoflurane and desflurane in both 50% oxygen-nitrous oxide and 100% oxygen were associated with a significant decrease in the amplitude and an increase in the latency of the cortical P40, whereas subcortical P29 latency did not vary significantly. Typical neurogenic motor-evoked potentials were obtained in all patients without volatile anesthetic agents, consisting of a biphasic wave, occurring 15 to 18 ms after stimulation, with an amplitude ranging from 1.3 to 4.1 microV. Latency or peak-to-peak amplitude of this wave was not significantly altered with isoflurane and desflurane, either in the presence or in the absence of nitrous oxide. Conclusions Compared with cortical somatosensory-evoked potentials, neurogenic motor-evoked potential signals are well preserved in patients undergoing surgery to correct scoliosis under general anesthesia supplemented with isoflurane or desflurane in concentrations as great as 1 MAC.
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Welch, Joseph F., Patrick J. Argento, Gordon S. Mitchell, and Emily J. Fox. "Reliability of diaphragmatic motor-evoked potentials induced by transcranial magnetic stimulation." Journal of Applied Physiology 129, no. 6 (December 1, 2020): 1393–404. http://dx.doi.org/10.1152/japplphysiol.00486.2020.
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Transcranial magnetic stimulation (TMS) is a noninvasive technique to assess neural impulse conduction along the cortico-diaphragmatic pathway. The reliability of diaphragm motor-evoked potentials (MEP) induced by TMS is unknown. Notwithstanding large variability in MEP amplitude, we found good-to-excellent reproducibility of all MEP characteristics (latency, duration, amplitude, and area) both within- and between-day in healthy adult men and women. Our findings support the use of TMS and surface EMG to assess diaphragm activation in humans.
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Rodionov, Vladimir, Josef Elidan, Meir Nitzan, Mordechai Sela, and Haim Sohmer. "Vertical Plane Short and Middle Latency Vestibular Evoked Potentials in Humans." Annals of Otology, Rhinology & Laryngology 105, no. 1 (January 1996): 43–48. http://dx.doi.org/10.1177/000348949610500107.
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In order to determine whether short and middle latency vestibular evoked potentials (VsEPs) can be recorded in humans in response to angular acceleration stimuli in the vertical plane, a drum, head-holder, and stepper motor were designed to deliver upward acceleration impulses of 10,000°/s2 (1.8° displacement) to the human head. Forehead and mastoid electrodes recorded electrical activity that was filtered, differentially amplified, and averaged in short (12.7 milliseconds) and middle (63.5 milliseconds) latency time frames. Control recordings were used to eliminate various types of artifact. Recordings were conducted in 7 normal subjects and in 4 control patients with congenital, profound hearing loss and absence of caloric responses. Short and middle latency VsEPs with high intrasubject and intersubject consistency were recorded in normal subjects and not in control patients. The middle latency responses were larger in amplitude than the short latency responses. The effects of stimulus intensity and repetition rate on VsEP waveform, latency, and amplitude were studied. Experiments have shown that the responses are not electrical artifact, nor are they contaminated by auditory, somatosensory, or passive eye movement potentials.
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Ohtaki, Shunya, Yukinori Akiyama, Aya Kanno, Shouhei Noshiro, Tomo Hayase, Michiaki Yamakage, and Nobuhiro Mikuni. "The influence of depth of anesthesia on motor evoked potential response during awake craniotomy." Journal of Neurosurgery 126, no. 1 (January 2017): 260–65. http://dx.doi.org/10.3171/2015.11.jns151291.
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OBJECTIVE Motor evoked potentials (MEPs) are a critical indicator for monitoring motor function during neurological surgery. In this study, the influence of depth of anesthesia on MEP response was assessed. METHODS Twenty-eight patients with brain tumors who underwent awake craniotomy were included in this study. From a state of deep anesthesia until the awake state, MEP amplitude and latency were measured using 5-train electrical bipolar stimulations on the same site of the precentral gyrus each minute during the surgery. The depth of anesthesia was evaluated using the bispectral index (BIS). BIS levels were classified into 7 stages: < 40, and from 40 to 100 in groups of 10 each. MEP amplitude and latency of each stage were compared. The deviation of the MEP measurements, which was defined as a fluctuation from the average in every BIS stage, was also considered. RESULTS A total of 865 MEP waves in 28 cases were evaluated in this study. MEP amplitude was increased and latency was decreased in accordance with the increases in BIS level. The average MEP amplitudes in the > 90 BIS level was approximately 10 times higher than those in the < 40 BIS level. Furthermore, the average MEP latencies in the > 90 BIS level were 1.5–3.1 msec shorter than those in the < 60 BIS level. The deviation of measured MEP amplitudes in the > 90 BIS level was significantly stabilized in comparison with that in the < 60 BIS level. CONCLUSIONS MEP amplitude and latency were closely correlated with depth of anesthesia. In addition, the deviation in MEP amplitude was also correlated with depth of anesthesia, which was smaller during awake surgery (high BIS level) than during deep anesthesia. Therefore, MEP measurement would be more reliable in the awake state than under deep anesthesia.
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Dull, S. T., P. E. Konrad, and W. A. Tacker. "Amplitude and latency characteristics of spinal cord motor evoked potentials in the rat." Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section 77, no. 1 (January 1990): 68–76. http://dx.doi.org/10.1016/0168-5597(90)90018-9.
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Jellinek, David, Doreen Jewkes, and Lindsay Symon. "Noninvasive Intraoperative Monitoring of Motor Evoked Potentials under Propofol Anesthesia: Effects of Spinal Surgery on the Amplitude and Latency of Motor Evoked Potentials." Neurosurgery 29, no. 4 (October 1, 1991): 551–57. http://dx.doi.org/10.1227/00006123-199110000-00011.
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Abstract We present the results of intraoperative monitoring of motor evoked potentials from 34 patients undergoing spinal surgery under total anesthesia with intravenously administered propofol. intraoperative recording was performed with transcranial electrical stimulation. Two groups of patients were studied: 1) a control population of 26 patients undergoing lumbar discectomy for prolapsed intervertebral disc, all of whom had normal preoperative motor conduction; and 2) a population of 8 patients undergoing neurosurgical procedures for spinal tumor (5 patients) and spinal arteriovenous malformation (3 patients), all of whom had abnormal preoperative neurological signs and abnormal preoperative motor conduction. In the first group, electromyographic responses were recorded intraoperatively either from the 2nd dorsal interosseous muscle of the hand (5 patients) or from the 1st dorsal interosseous muscle of the foot (21 patients). In the second group, responses were recorded intraoperatively either from the 1st dorsal interosseous muscle of the foot (7 patients) or from the anterior tibial muscle (1 patient). Intraoperative monitoring of motor function was successful in 88.5% of the patients in the control group. Propofol anesthesia caused a reduction in response amplitude to 7% of baseline values obtained from conscious relaxed subjects. Intraoperative monitoring was successful in 87% of the patients in the pathological group. We observed significant changes in both amplitude (>50%) and/or onset latency (>3 ms) from the intraoperative baseline that indicated cither improvement (3 patients) or deterioration (2 patients) in motor conduction within minutes of surgical maneuvers anticipated to alter spinal cord function. Only permanent complete loss of intraoperative motor conduction (1 patient) correlated with a significant change in the postoperative neurological state. We conclude 1) that changes in latency as well as amplitude are useful evaluation criteria of intraoperative motor evoked potentials, and 2) that even in the presence of significant intraoperative deterioration in motor conduction, subsequent recovery of motor conduction toward baseline values during anesthesia is a favorable prognostic sign.
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Kalkman, Cor J., Leon H. Ubags, Henk D. Been, Astrid Swaan, and John C. Drummond. "Improved Amplitude of Myogenic Motor Evoked Responses after Paired Transcranial Electrical Stimulation during Sufentanil/Nitrous Oxide Anesthesia." Anesthesiology 83, no. 2 (August 1, 1995): 270–76. http://dx.doi.org/10.1097/00000542-199508000-00006.
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Background Measurement of motor evoked responses to transcranial stimulation (tc-MER) is a technique for intraoperative monitoring of motor pathways in the brain and spinal cord. However, clinical application of tc-MER monitoring is hampered because most anesthetic techniques severely depress the amplitude of motor evoked responses. Because paired electrical stimuli increase tc-MER responses in awake subjects, we examined their effects in anesthetized patients undergoing surgery. METHODS. Eleven patients whose neurologic condition was normal and who were undergoing spinal or aortic surgery were anesthetized with sufentanil-N20-ketamine. Partial neuromuscular blockade (single-twitch height 25% of baseline) was maintained with vecuronium. Single and paired electrical stimuli were delivered to the scalp, and compound action potentials were recorded from the tibialis anterior muscle. The amplitude and latency of the tc-MERs were measured as the interval between paired stimuli was varied between 0 (single stimulus) and 10 ms. All recordings were completed before spinal manipulation or aortic clamping. Results Median amplitude of the tc-MER after a single stimulus was 106 microV (10th-90th percentiles: 23-1,042 microV), and the latency to onset was 33.2 +/- 1.4 ms (SD). With paired stimuli (interstimulus interval 2-3 ms), tc-MER amplitudes increased to 285 (79-1,605) microV, or 269% of the single-pulse response (P < 0.01). Reproducibility of individual responses increased with paired stimulation. Onset latency decreased to 31.4 +/- 3.2 ms (P < 0.05). Maximum amplitude augmentation was observed with interstimulus intervals between 2 and 5 ms and in patients with low-amplitude responses after single-pulse stimulation. Conclusions Application of paired transcranial electrical stimuli increases amplitudes and reproducibility of tc-MERs during anesthetic-induced depression of the motor system. The effect may represent temporal summation of stimulation at cortical or spinal sites. The results of this study warrant further clinical evaluation of paired transcranial stimulation.
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Zhang, Jianmei, Victor Z. Han, Johannes Meek, and Curtis C. Bell. "Granular Cells of the Mormyrid Electrosensory Lobe and Postsynaptic Control Over Presynaptic Spike Occurrence and Amplitude Through an Electrical Synapse." Journal of Neurophysiology 97, no. 3 (March 2007): 2191–203. http://dx.doi.org/10.1152/jn.01262.2006.
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Primary afferent fibers from the electroreceptors of mormyrid electric fish use a latency code to signal the intensity of electrical current evoked by the fish's own electric organ discharge (EOD). The afferent fibers terminate centrally in the deep and superficial granular layers of the electrosensory lobe with morphologically mixed chemical–electrical synapses. The granular cells in these layers seem to decode afferent latency through an interaction between primary afferent input and a corollary discharge input associated with the EOD motor command. We studied the physiology of deep and superficial granular cells in a slice preparation with whole cell patch recording and electrical stimulation of afferent fibers. Afferent stimulation evoked large all-or-none electrical excitatory postsynaptic potentials (EPSPs) and large all or none GABAergic inhibitory postsynaptic potentials (IPSPs) in both superficial and deep granular cells. The amplitudes of the electrical EPSPs depended on postsynaptic membrane potential, with maximum amplitudes at membrane potentials between −65 and −110 mV. Hyperpolarization beyond this level resulted in either the abrupt disappearance of EPSPs, a step-like reduction to a smaller EPSP, or a graded reduction in EPSP amplitude. Depolarization to membrane potentials lower than that yielding a maximum caused a linear decrease in EPSP amplitude, with EPSP amplitude reaching 0 mV at potentials between −55 and −40 mV. We suggest that the dependence of EPSP size on postsynaptic membrane potential is caused by close linkage of pre- and postsynaptic membrane potentials through a high-conductance gap junction. We also suggest that this dependence may result in functionally important nonlinear interactions between synaptic inputs.
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Friedman, William A., Barry L. Kaplan, Arthur L. Day, George W. Sypert, and Michael T. Curran. "Evoked Potential Monitoring during Aneurysm Operation: Observations after Fifty Cases." Neurosurgery 20, no. 5 (May 1, 1987): 678–87. http://dx.doi.org/10.1227/00006123-198705000-00002.
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Abstract Somatosensory or brain stem auditory evoked potentials (EPs) were monitored during 50 aneurysm procedures. Base line EPs were obtained shortly after the induction of general anesthesia and were recorded continuously during operation. Absolute latency, interpeak latency, and cortical EP amplitude were subsequently determined. Statistical analysis confirmed that significant changes in these parameters are routine during aneurysm operation. Arbitrary definitions of abnormal latency and amplitude changes led to an excessive false-positive/false-negative rate. From the time of dural opening to the time of closure, prolongation of central conduction time, decrease in cortical amplitude, or disappearance of the EP was predictive of postoperative sensory or motor deficit in all patients monitored, except those undergoing operation on basilar artery aneurysms. In basilar aneurysm cases, outcome could not be reliably predicted with either EP technique.
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Chabot, Robert, Donald H. York, Clark Watts, and Wendy A. Waugh. "Somatosensory evoked potentials evaluated in normal subjects and spinal cord-injured patients." Journal of Neurosurgery 63, no. 4 (October 1985): 544–51. http://dx.doi.org/10.3171/jns.1985.63.4.0544.
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✓ Somatosensory evoked cortical potentials (SSEP's) were recorded in 27 healthy subjects using tibial and peroneal nerve stimulation with cephalic and non-cephalic references. Four major peaks were present in all recordings. Analysis of these components showed that SSEP's collected after tibial nerve stimulation with non-cephalic reference (linked earlobes) produced the most consistent clearly defined component peaks. Average latency, amplitude, and interpeak latency differences are presented for these SSEP's. Significant correlations were obtained between the height of the individual and the P1, N2, P2, and N3 latencies, and the N3-P1 interpeak latency. These results suggest that reproducible SSEP's can be obtained from tibial nerve stimulation in normal subjects using minimal numbers of stimulus presentations (28 to 64). The SSEP's from 34 patients with varying degrees of spinal cord trauma were compared with the SSEP's from normal subjects. These comparisons involved the P1, N2, P2, and N3 latencies and the interpeak latency values, as well as the amplitude values. Patients with normal sensory and motor neurological examinations could be distinguished from patients showing decreased sensory and motor findings or clinically complete lesions on the basis of peak latency and interpeak latency values. The latter two groups could not be distinguished from one another. In general, all patient groups had SSEP's of lower amplitude than did normal individuals, but the groups could not be distinguished from one another. These results indicate that SSEP's can be a useful clinical tool for differentiation of complete from incomplete spinal cord lesions, but do not invariably predict recovery of function.
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Campos, Agustín, Rafael Barona, Joaquín Escudero, José Montalt, and Manuel Escudero. "Hypoglossal Nerve Conduction Study by Transcranial Magnetic Stimulation in Normal Subjects." Otolaryngology–Head and Neck Surgery 112, no. 4 (April 1995): 520–25. http://dx.doi.org/10.1177/019459989511200403.
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The introduction of transcranial magnetic stimulation has allowed the study of conduction in the proximal portions and central pathways of the cranial nerves. A study is made of cranial nerve XII with transcranial magnetic stimulation at two levels, cortical and cisternal, registering the motor evoked potential by means of surface electrodes in contact with the upper face of the tongue. Motor evoked potentials were constantly observed on cortical stimulation, in a painless, easy, and reproducible way, with mean values of 10.84 ± 1.14 milliseconds (latency) and 7.81 ± 1.14 mV (amplitude). Motor evoked potentials were unconstant and showed reduced amplitues on cisternal stimulation, with mean values of 4.72 ± 0.62 milliseconds and 0.83 ± 1.26 mV. The magnetic stimulation technique allows the study of the entire motor pathway of cranial nerve XII (motor cortex-medulla, motoneuron-muscle). The method is efficient, noninvasive, painless, and easily reproduced, and it comes close to being an ideal clinical conduction study technique for this cranial nerve.
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Kim, Young Suk, Jin Woo Hong, Byung Jo Na, Seong Uk Park, Woo Sang Jung, Sang Kwan Moon, Jung Mi Park, Chang Nam Ko, Ki Ho Cho, and Hyung Sup Bae. "The Effect of Low versus High Frequency Electrical Acupoint Stimulation on Motor Recovery After Ischemic Stroke by Motor Evoked Potentials Study." American Journal of Chinese Medicine 36, no. 01 (January 2008): 45–54. http://dx.doi.org/10.1142/s0192415x08005576.
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Electrical acupoint stimulation (EAS) has been used to treat motor dysfunction of stroke patients with reportedly effective results. When we operate EAS treatment, we can modulate the intensity and frequency of stimulation. The purpose of this study is to evaluate the effect of different frequencies in treating motor dysfunction of ischemic stroke patients with EAS. The subjects of this study were 62 ischemic stroke patients with motor dysfunction in Kyunghee oriental medical center. They have been hospitalized after 1 week to 1 month from onset. They were treated with 2 Hz or 120 Hz EAS for 2 weeks, and had motor evoked potentials (MEPs) tests before and after 2 weeks of EAS treatment. We measured latency, central motor conduction time (CMCT) and amplitude of MEPs. After 2 weeks of treatment, we compared MEPs data of the affected side between the 2 Hz group and the 120 Hz group. The 2 Hz group showed more significant improvement than the 120 Hz group in latency, CMCT and amplitude ( p = 0.008, 0.002, 0.002). In the case of the affected side MEPs data divided by normal side MEPs data, the 2 Hz group also showed higher improvement rate than the 120 Hz group in latency, CMCT and amplitude with significant differences ( p = 0.003, 0.000, 0.008). These results suggest that low frequency EAS activates the central motor conduction system better than high frequency EAS, and EAS with low frequency could be more helpful for motor recovery after ischemic stroke than that with high frequency.
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Nakata, Hiroki, Tadayoshi Miyamoto, Shigehiko Ogoh, Ryusuke Kakigi, and Manabu Shibasaki. "Effects of acute hypoxia on human cognitive processing: a study using ERPs and SEPs." Journal of Applied Physiology 123, no. 5 (November 1, 2017): 1246–55. http://dx.doi.org/10.1152/japplphysiol.00348.2017.
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Although hypoxia has the potential to impair the cognitive function, the effects of acute hypoxia on the high-order brain function (executive and/or inhibitory processing) and somatosensory ascending processing remain unknown. We tested the hypothesis that acute hypoxia impairs both motor executive and inhibitory processing and somatosensory ascending processing. Fifteen healthy subjects performed two sessions ( sessions 1 and 2), consisting of electroencephalographic event-related potentials with somatosensory Go/No-go paradigms and somatosensory-evoked potentials (SEPs) under two conditions (hypoxia and normoxia) on different days. On 1 day, participants breathed room air in the first and second sessions of the experiment; on the other day, participants breathed room air in the first session, and 12% O2 in the second session. Acute hypoxia reduced the peak amplitudes of Go-P300 and No-go-P300, and delayed the peak latency of Go-P300. However, no significant differences were observed in the peak amplitude or latency of N140, behavioral data, or the amplitudes and latencies of individual SEP components between the two conditions. These results suggest that acute hypoxia impaired neural activity in motor executive and inhibitory processing, and delayed higher cognitive processing for motor execution, whereas neural activity in somatosensory processing was not affected by acute hypoxia. NEW & NOTEWORTHY Hypoxia has the potential to impair the cognitive function, but the effects of acute hypoxia on the cognitive function remain debatable. We investigated the effects of acute hypoxia on human cognitive processing using electroencephalographic event-related potentials and somatosensory-evoked potentials. Acute normobaric hypoxia impaired neural activity in motor executive and inhibitory processing, but no significant differences were observed in neural activity in somatosensory processing.
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Li, Qun-Xi, Xiao-Jing Zhao, Xiang-Nan Li, Ai-Jun Fu, Yun-He Zhang, Tong Chen, Tie-Jun Liu, Fu-Xia Zheng, and Jian-Min Li. "Application of intraoperative electrophysiological monitoring in vertebral canal decompression surgery for acute spinal cord injury." Journal of International Medical Research 48, no. 6 (June 2020): 030006052092420. http://dx.doi.org/10.1177/0300060520924205.
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Objective This study aimed to evaluate the joint monitoring of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in vertebral canal decompression surgery for acute spinal cord injury. Methods Twenty-four patients, who were admitted to the hospital for the surgical treatment of spinal cord injury with SEP and MEP monitoring, were assigned to the intraoperative monitoring group (group I). In addition, 24 patients who were admitted to the hospital for the surgical treatment of spinal cord injury without SEP or MEP monitoring were assigned to the control group (group C). Results In group I, there were significant changes before and after decompression surgery in the P40 latency and amplitude, and in the latency of MEP in the abductor hallucis brevis (AHB), in patients with improved spinal nerve function following surgery. In contrast, there were no significant differences in the P40 latency or amplitude, or the latency of MEP in the AHB, in patients who showed no improvement after surgery. Conclusion In vertebral canal decompression surgery for acute spinal cord injury, the application of joint MEP and SEP monitoring can timely reflect changes in spinal cord function.
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Ibraheem, Ola, and Mohammad Hassaan. "Cervical Vestibular-Evoked Myogenic Potentials in Sedated Toddlers." International Archives of Otorhinolaryngology 22, no. 03 (March 21, 2017): 197–202. http://dx.doi.org/10.1055/s-0037-1599151.
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Introduction Cervical vestibular-evoked myogenic potentials (cVEMPs) are difficult to test in toddlers who cannot follow instructions or stay calm. Objective Due to the growing need for vestibular testing in very young children as a part of a delayed walking assessment battery, this study aimed to provide a solution to this problem by recording the cVEMPs in toddlers during sedation. Method The cVEMPs measures were assessed in 30 toddlers aged 12 to 36 months with normal motor milestones. They were sedated with chloral hydrate. Then, the head was retracted ∼ 30° backward with a pillow under the shoulders, and turned 45° contralateral to the side of stimulation to put the sternocleidomastoid (SCM) muscle in a state of tension. Results The P13 and N23 waves of the cVEMPs were recordable in all sedated toddlers. The cVEMPs measures resulted in the following: P13 latency of 17.5 ± 1.41 milliseconds, N23 latency of 25.58 ± 2.02 milliseconds, and peak-to-peak amplitude of 15.39 ± 3.45 µV. One-sample t-test revealed statistically significant longer latencies and smaller amplitude of the toddlers' cVEMPs relative to the normative data for adults. Conclusions The difficulty of cVEMPs testing in toddlers can be overcome by sedating them and attaining a position that contracts the SCM muscle. However, the toddlers' recordings revealed delayed latencies and smaller amplitudes than those of adults.
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Poskotinova, L. V., E. V. Krivonogova, N. M. Khasanova, and M. N. Krasnikova. "The Predictability of Motor and Cognitive Impairment According to Brain Asymmetry of Cognitive Evoked Potentials P300 and Features of Symptom Complex in Patients with Parkinson’s Disease." Annals of the Russian academy of medical sciences 71, no. 1 (November 19, 2015): 41–45. http://dx.doi.org/10.15690/vramn519.
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Link the degree of progression of motor and cognitive impairment in Parkinson’s disease and parameters of cognitive evoked potentials brain activity recognized not always unambiguous. This is due to the wide range of differences in amplitude and latency time of evoked potentials in the different leads of electroencephalogram caused functional reorganization of neuronal activity in brain structures in the early stages of the disease. Objective. The aim is to determine the correlation of the cognitive auditory evoked potentials P300 characteristics and symptom features in patients with Parkinson’s disease. Methods. The study involved 60 people, right-handers: 34 people (24 women and 10 men) with a verified diagnosis of Parkinson’s disease and the control group — 26 people (20 women and 6 men). The disease duration, severity of symptoms (Unified Parkinson’s Disease Rating Scale), and stage of the disease (Hoehn, Yahr) were determined, the 15-item Geriatric Depression Scale was used to indicate the depression symptoms. Assessment of the electroencephalogram and auditory evoked potentials P300 was performed by an electroencephalograph «Encephalan» (Medicom, Taganrog, Russia). The minimum amplitude and the maximum latency of P300 in electroencephalogram-leads (F3, F4, C3, C4, P3, P4, F7, F8, T3, T4, T5 and T6) on the right and left sides were determined. Results. A significant positive correlation between the amplitude of evoked potential P300 on the left and duration of Parkinson’s disease was revealed, moreover the severity of disease symptoms such as left-side resting tremors of the hand, left-side muscle tension of the hand and/or foot, rising from a chair without using their hands, posture disorder were established. Conclusion. Marked brain asymmetry in the form of increase of the P300 amplitude on the left side combined with a significant reduction in the P300 amplitude on the right side in contra lateral electroencephalogram-lead indicates unfavorable prognosis in relation to cognitive dysfunction and motor disorders identified with left-sided Parkinson’s disease onset.
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van den Bos, Mehdi A. J., Nimeshan Geevasinga, Parvathi Menon, David Burke, Matthew C. Kiernan, and Steve Vucic. "Physiological processes influencing motor-evoked potential duration with voluntary contraction." Journal of Neurophysiology 117, no. 3 (March 1, 2017): 1156–62. http://dx.doi.org/10.1152/jn.00832.2016.
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Voluntary contraction leads to facilitation of motor-evoked potentials (MEPs) producing greater amplitude, shorter onset latency, and prolonged duration of the electromyography potential. Whereas hyperexcitability of spinal motoneurons and changes in descending corticospinal volleys have been proposed as putative mechanisms for changes in MEP amplitude and onset latency, a contribution of propriospinal interneurons, exerting modulatory effects on α-motoneurons, has been proposed as a potential explanation for prolongation of MEP duration. The aim of the present study is to gain further insight into the physiological processes underlying changes in MEP duration. Transcranial magnetic stimulation (TMS) studies were undertaken on 30 healthy controls, using a 90-mm circular coil, with MEPs recorded at rest and during facilitation, produced by contraction of abductor pollicis brevis. In the same experiment, short interval-intracortical inhibition (SICI) was recorded at rest. Facilitation resulted in a significant prolongation of MEP duration, which increased with stimulus intensity and was accompanied by an increase in MEP amplitude. The main effect (TMS intensity × activation state) was correlated with MEP duration ( F = 10.9, P < 0.001), whereas TMS intensity ( F = 30.5, P < 0.001) and activation state ( F = 125.8, P < 0.001) in isolation were correlated with MEP amplitude. There was a significant inverse relationship between SICI and MEP duration at rest (R2 = 0.141, P = 0.041) and during facilitation (R2 = 0.340, P = 0.001). The present findings suggest that similar physiological processes mediate changes in the facilitated MEP duration and amplitude and that both cortical and nonpropriospinal spinal mechanisms contribute to changes in MEP duration. NEW & NOTEWORTHY Muscle contraction is associated with a significant increase in motor-evoked potential (MEP) duration and amplitude. Whereas the increase in MEP duration was linear, the amplitude increase exhibited a ceiling effect. Importantly, the MEP duration increase strongly correlated with short interval-intracortical inhibition, a biomarker of motor cortical function. This suggests that whereas similar physiological processes contribute to changes in facilitated MEP duration and amplitude, cortical mechanisms appear to contribute to MEP duration changes.
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Kobayashi, Kazuyoshi, Kei Ando, Ryuichi Shinjo, Kenyu Ito, Mikito Tsushima, Masayoshi Morozumi, Satoshi Tanaka, et al. "A new criterion for the alarm point using a combination of waveform amplitude and onset latency in Br(E)-MsEP monitoring in spine surgery." Journal of Neurosurgery: Spine 29, no. 4 (October 2018): 435–41. http://dx.doi.org/10.3171/2018.3.spine171348.
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OBJECTIVEMonitoring of brain evoked muscle-action potentials (Br[E]-MsEPs) is a sensitive method that provides accurate periodic assessment of neurological status. However, occasionally this method gives a relatively high rate of false-positives, and thus hinders surgery. The alarm point is often defined based on a particular decrease in amplitude of a Br(E)-MsEP waveform, but waveform latency has not been widely examined. The purpose of this study was to evaluate onset latency in Br(E)-MsEP monitoring in spinal surgery and to examine the efficacy of an alarm point using a combination of amplitude and latency.METHODSA single-center, retrospective study was performed in 83 patients who underwent spine surgery using intraoperative Br(E)-MsEP monitoring. A total of 1726 muscles in extremities were chosen for monitoring, and acceptable baseline Br(E)-MsEP responses were obtained from 1640 (95%). Onset latency was defined as the period from stimulation until the waveform was detected. Relationships of postoperative motor deficit with onset latency alone and in combination with a decrease in amplitude of ≥ 70% from baseline were examined.RESULTSNine of the 83 patients had postoperative motor deficits. The delay of onset latency compared to the control waveform differed significantly between patients with and without these deficits (1.09% ± 0.06% vs 1.31% ± 0.14%, p < 0.01). In ROC analysis, an intraoperative 15% delay in latency from baseline had a sensitivity of 78% and a specificity of 96% for prediction of postoperative motor deficit. In further ROC analysis, a combination of a decrease in amplitude of ≥ 70% and delay of onset latency of ≥ 10% from baseline had sensitivity of 100%, specificity of 93%, a false positive rate of 7%, a false negative rate of 0%, a positive predictive value of 64%, and a negative predictive value of 100% for this prediction.CONCLUSIONSIn spinal cord monitoring with intraoperative Br(E)-MsEP, an alarm point using a decrease in amplitude of ≥ 70% and delay in onset latency of ≥ 10% from baseline has high specificity that reduces false positive results.
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Graf, Werner, Robert Spencer, Harriet Baker, and Robert Baker. "Excitatory and Inhibitory Vestibular Pathways to the Extraocular Motor Nuclei in Goldfish." Journal of Neurophysiology 77, no. 5 (May 1, 1997): 2765–79. http://dx.doi.org/10.1152/jn.1997.77.5.2765.
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Graf, Werner, Robert Spencer, Harriet Baker, and Robert Baker. Excitatory and inhibitory vestibular pathways to the extraocular motor nuclei in goldfish. J. Neurophysiol. 77: 2765–2779, 1997. Electrophysiological, ultrastructural, and immunohistochemical techniques were utilized to describe the excitatory and inhibitory vestibular innervation of extraocular motor nuclei in the goldfish. In antidromically activated oculomotor motoneurons, electrical stimulation of the intact contralateral vestibular nerve produced short-latency, variable amplitude electrotonic excitatory postsynaptic potentials (EPSPs) at 0.5–0.7 ms followed by chemical EPSPs at 1.0–1.3 ms. Stimulation of the ipsilateral vestibular nerve produced small amplitude membrane hyperpolarizations at a latency of 1.3–1.7 ms in which equilibrium potentials were slightly more negative than resting potentials. The inhibitory postsynaptic potentials (IPSPs) reversed with large amplitudes after the injection of chloride ions suggesting a proximal soma-dendritic location of terminals exhibiting high efficacy inhibitory synaptic conductances. In antidromically identified abducens motoneurons and putative internuclear neurons, electrical stimulation of the contralateral vestibular nerve produced large-amplitude, short-latency electrotonic EPSPs at 0.5 ms followed by chemical depolarizations at 1.2–1.3 ms. Stimulation of the ipsilateral vestibular nerve evoked IPSPs at 1.4 ms that were reversed after injection of current and/or chloride ions. γ-Aminobutyric acid (GABA) antibodies labeled inhibitory neurons in vestibular subdivisions with axons projecting into the ipsilateral medial longitudinal fasciculus (MLF). Putative GABAergic terminals surrounded oculomotor, but not abducens, motoneurons retrogradely labeled with horseradish peroxidase. Hence the spatial distribution of GABAergic neurons and terminals appears highly similar in the vestibuloocular system of goldfish and mammals. Electron microscopy of motoneurons in the oculomotor and abducens nucleus showed axosomatic and axodendritic synaptic endings containing spheroidal synaptic vesicles establishing chemical, presumed excitatory, synaptic contacts with asymmetric pre- and/or postsynaptic membrane specializations. The majority of contacts with spheroidal vesicles displayed gap junctions in which the chemical and electrotonic synapses were either en face to dissimilar or adjacent to one another on the same soma/dendritic profiles. Another separate set of axosomatic synaptic endings, presumed to be inhibitory, contained pleiomorphic synaptic vesicles with symmetric pre- and/or postsynaptic membrane specializations that never included gap junctions. Excitatory and inhibitory synaptic contacts appeared equal in number but were more sparsely distributed along the soma-dendritic profiles of oculomotor as compared with abducens motoneurons. Collectively these data provide evidence for both disynaptic vestibular inhibition and excitation in all subdivisions of the extraocular motor nuclei suggesting the basic vestibulooculomotor blueprint to be conserved among vertebrates. We propose that unique vestibular neurons, transmitters, pathways, and synaptic arborizations are homologous structural traits that have been essentially preserved throughout vertebrate phylogeny by a shared developmental plan.
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Bailey, Aaron Z., Yiqun P. Mi, and Aimee J. Nelson. "Short-latency afferent inhibition in chronic spinal cord injury." Translational Neuroscience 6, no. 1 (January 1, 2015): 235–43. http://dx.doi.org/10.1515/tnsci-2015-0025.
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AbstractBackground: Short-latency afferent inhibition (SAI) results when somatosensory afferent input inhibits the corticospinal output from primary motor cortex (M1). The present study examined SAI in the flexor carpi radialis (FCR) muscle in individuals with spinal cord injury (SCI) and uninjured controls. Methods: Short-latency afferent inhibition (SAI) was evoked by stimulating the median nerve at the elbow at intervals of 15, 20 and 25 ms in advance of a transcranial magnetic stimulation (TMS) pulse over M1. SAI was tested with the FCR at rest and also during ~20% of maximum voluntary contraction. Corticospinal output was assessed through measuring both motor thresholds and motor evoked potential (MEP) recruitment curves. The afferent volley was assessed via the N20-P25 amplitude of the somatosensory evoked potential (SEP) and the amplitude of sensory nerve action potentials (SNAP) recorded over the median nerve at the elbow. Results: SAI is reduced in SCI in both the contracted and non-contracted FCR muscle. MEP recruitment curves and thresholds were decreased in SCI only in the active state and not the resting state. N20-P25 amplitude was similar between groups in both the resting and active states although SNAP was significantly reduced in SCI at rest. Conclusions: We conclude that reduced SAI in SCI is likely attributed to neuroplasticity altering the intrinsic M1 circuitry mediating SAI and/or reduced afferent input traversing a direct thalamocortical route to M1. These data provide a new avenue of research aimed at identifying therapeutic approaches to alter SAI to improve upper limb function in individuals with SCI.
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Huang, Chien Hui, A. Daniel Martin, and Paul W. Davenport. "Effect of inspiratory muscle strength training on inspiratory motor drive and RREP early peak components." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 462–68. http://dx.doi.org/10.1152/japplphysiol.00364.2002.
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This study investigated the effect of inspiratory muscle strength training (IMST) on inspiratory motor drive [mouth occlusion pressure at 0.1 s (P0.1)] and respiratory-related evoked potentials (RREP). It was hypothesized that, if IMST increased inspiratory muscle strength, inspiratory motor drive would decrease. If motor drive were related to the RREP, it was further hypothesized that an IMST-related decrease in drive would change RREP latency and/or amplitude. Twenty-three subjects received IMST at 75% of their maximal inspiratory pressure (Pi max) with the use of a pressure threshold valve. IMST consisted of four sets of six breaths daily for 4 wk. P0.1 and the RREP were recorded before and after IMST. Posttraining, Pi maxincreased significantly by 36.0 ± 2.7%. P0.1decreased significantly by 21.9 ± 5.2%. The increase in Pi max was significantly correlated to the decrease in P0.1. RREP peaks P1a, Nf, P1, and N1 were identified pre- and post-IMST, and there was no difference in either amplitude or latency for those peaks. These results demonstrate that high-intensity IMST significantly increased Pi max, decreased P0.1, but did not change the RREP.
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Ferreri, Florinda, David Ponzo, Taina Hukkanen, Esa Mervaala, Mervi Könönen, Patrizio Pasqualetti, Fabrizio Vecchio, Paolo Maria Rossini, and Sara Määttä. "Human brain cortical correlates of short-latency afferent inhibition: a combined EEG–TMS study." Journal of Neurophysiology 108, no. 1 (July 1, 2012): 314–23. http://dx.doi.org/10.1152/jn.00796.2011.
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When linking in time electrical stimulation of the peripheral nerve with transcranial magnetic stimulation (TMS), the excitability of the motor cortex can be modulated to evoke clear inhibition, as reflected by the amplitude decrement in the motor-evoked potentials (MEPs). This specific property, designated short-latency afferent inhibition (SAI), occurs when the nerve–TMS interstimulus interval (ISI) is approximately 25 ms and is considered to be a corticothalamic phenomenon. The aim of the present study was to use the electroencephalographic (EEG) responses to navigated-TMS coregistration to better characterize the neuronal circuits underlying SAI. The present experimental set included magnetic resonance imaging (MRI)–navigated TMS and 60-channel TMS-compatible EEG devices. TMS-evoked EEG responses and MEPs were analyzed in eight healthy volunteers; ISIs between median nerve and cortical stimulation were determined relative to the latency of the individual N20 component of the somatosensory-evoked potential (SEP) obtained after stimulation of the median nerve. ISIs from the latency of the N20 plus 3 ms and N20 plus 10 ms were investigated. In all experimental conditions, TMS-evoked EEG responses were characterized by a sequence of negative deflections peaking at approximately 7, 44, and 100 ms alternating with positive peaks at approximately 30, 60, and 180 ms post-TMS. Moreover, ISI N20+3 ms modulated both EEG-evoked activity and MEPs. In particular, it inhibited MEP amplitudes, attenuated cortical P60 and N100 responses, and induced motor cortex beta rhythm selective decrement of phase locking. The findings of the present experiment suggest the cortical origin of SAI that could result from the cortico–cortical activation of GABAergic-mediated inhibition onto the corticospinal neurons modulated by cholinergic activation able to reducing intralaminar inhibition and promoting intracolumnar inhibition.
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Garasz, Anna, and Juliusz Huber. "REVIEW ON METHODOLOGY AND INTERPRETATION OF RESULTS OF MOTOR EVOKED POTENTIALS INDUCED WITH MAGNETIC FIELD OR ELECTRICAL STIMULI RECORDED PREOPERATIVELY OR INTRAOPERATIVELY." Issues of Rehabilitation, Orthopaedics, Neurophysiology and Sport Promotion – IRONS, no. 34 (March 2021): 33–42. http://dx.doi.org/10.19271/irons-000131-2021-34.
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Introduction The method of motor evoked potentials recordings induced with magnetic field (MEP) (as part of the differential diagnosis of disease in the musculoskeletal system before the introduction of treatment) and motor evoked potentials induced with electrical stimuli (during intraoperative neuromonitoring) is particularly intensively used among clinical neurophysiology studies in the last twenty years. Aim The aim of the study is to review the practical usefulness of MEP in clinical diagnostics and present the most common examples of the application of this method, the possibility of modifications aimed at increasing non-invasiveness, safety and diagnostic precision. Material and methods The results of pilot tests of different variants of MEP recordings are presented preoperatively from muscles and nerves of the lower extremities in healthy volunteers (N = 10) and patients with disc-root conflicts (N = 15). Results Pilot tests show that in healthy people after oververtebral stimulation with the magnetic field at the lumbar level, the MEP amplitude and latency parameters recorded from nerves compared to those recorded from muscles are characterized by lower values (amplitudes by about 50%, latencies with mean at about 3 ms) and the time duration is increased by approximately 20%. The variability of MEP parameters is similar in patients with disc-root conflict in preoperative diagnostics, even though mean amplitude values from muscles were lower in comparison to healthy control group. Conclusions The MEP recording method from nerves vs. muscles after oververtebral stimulation with the magnetic field at the lumbar level in patients with disc-root conflict is diagnostically essential in cases of visible atrophic changes in muscles with symptoms of slight pathology in the transmission of nerve impulses in motor axons. Keywords: motor evoked potentials, neurophysiological diagnostics, neuromonitoring, methodological modifications
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Sysoev, Yu I., R. T. Chernyakov, R. D. Idiyatullin, K. A. Kroshkina, V. A. Piankova, V. A. Prikhodko, and S. V. Okovitiy. "Changes of Visually Evoked Potentials in Rats after Brain Trauma." Journal Biomed, no. 2 (June 10, 2020): 68–77. http://dx.doi.org/10.33647/2074-5982-16-2-68-77.
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In this study, we compared visually evoked potentials (VEP) in healthy rats and rats following traumatic brain injury. Traumatic brain injury was modelled by the method of controlled cortical impact. The electrical activity of the brain cortex was registered using nichrome electrodes. Responses in primary and secon dary motor cortex areas, as well as in the area of primary sensory cortex over the hippocampus, were evoked by 3 Hz white light fl ashes on the 3rd and 7th day after the operation. The latencies and amplitudes of N1, P2, N2, P3 и N3, as well as the duration and amplitudes of inter-peak intervals, were calculated. It is shown that unilateral traumatic damage of the motor cortex area and underlying regions in rats does not signifi cantly reduce the number of VEP peaks. However, in most of the animals, the N1 component was absent in the area of damage.In comparison with healthy rats, traumatized rats demonstrated an increased latency of N1 and N3 peaks on the 3rd day after the operation followed by their return to normal values on the 7th day. In addition, traumatized rats showed a higher P2 amplitude in regions remote from the traumatized cortex area on the 3rd day; however, the P2 amplitude was lower in the injury area on the 7th day. The obtained results indicate that the registration and analysis of VEP can be used for localizing the traumatized area and to analyse the dynamics of the brain functional state in rats with brain trauma.
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Turco, Claudia V., Jenin El-Sayes, Hunter J. Fassett, Robert Chen, and Aimee J. Nelson. "Modulation of long-latency afferent inhibition by the amplitude of sensory afferent volley." Journal of Neurophysiology 118, no. 1 (July 1, 2017): 610–18. http://dx.doi.org/10.1152/jn.00118.2017.
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Long-latency afferent inhibition (LAI) is the inhibition of the transcranial magnetic stimulation (TMS) motor-evoked potentials (MEP) by the sensory afferent volley following electrical stimulation of a peripheral nerve. It is unknown how the activation of sensory afferent fibers relates to the magnitude of LAI. This study investigated the relationship between LAI and the sensory nerve action potentials (SNAP) from the median nerve (MN) and the digital nerves (DN) of the second digit. LAI was obtained by delivering nerve stimulation 200 ms before a TMS pulse delivered over the motor cortex. Experiment 1 assessed the magnitude of LAI following stimulation of the contralateral MN or DN using nerve stimulus intensities relative to the maximum SNAP (SNAPmax) of that nerve and two TMS intensities (0.5- and 1-mV MEP). Results indicate that MN LAI is maximal at ~50% SNAPmax, when presumably all sensory afferents are recruited for TMS of 0.5-mV MEP. For DN, LAI appears at ~50% SNAPmax and does not increase with further recruitment of sensory afferents. Experiment 2 investigated the magnitude of LAI following ipsilateral nerve stimulation at intensities relative to SNAPmax. Results show minimal LAI evoked by ipsilateral MN and no LAI following ipsilateral DN stimulation. Implications for future studies investigating LAI include adjusting nerve stimulation to 50% SNAPmax to obtain maximal LAI. Additionally, MN LAI can be used as a marker for neurological disease or injury by using a nerve stimulation intensity that can evoke a depth of LAI capable of increasing or decreasing. NEW & NOTEWORTHY This is the first investigation of the relationship between long-latency afferent inhibition (LAI) and the sensory afferent volley. Differences exist between median and digital nerve LAI. For the median nerve, LAI increases until all sensory fibers are presumably recruited. In contrast, digital nerve LAI does not increase with the recruitment of additional sensory fibers but rather is present when a given volume of sensory afferent fibers is recruited (~50% of maximum sensory nerve action potential). This novel data provide practical guidelines and contribute to our understanding of the mechanisms underlying LAI.
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Slavutskaya, Maria, and Valerii V. Shulgovskii. "Presaccadic Brain Potentials in Conditions of Covert Attention Orienting." Spanish Journal of Psychology 10, no. 2 (November 2007): 277–84. http://dx.doi.org/10.1017/s1138741600006545.
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Twelve healthy subjects underwent investigation of averaged (electroencephalogram) EEG potentials during preparation for motor activity and in the latent period (LP) of visually evoked saccades by presentation of stimuli using Posner's (1980) design of “cost-benefit.” It has been shown that covert spatial attention orientation leads to an increase in amplitude and decrease in latency of presaccadic initiation potential peaks within the saccadic latent period (LP) (P-100, N –50). Processes of covert orientation of attention during the interstimulus interval period of anticipation of the target stimulus correlate with the increase of slow negativity of fronto-parietal-temporal localization. Spatial-temporal changes of presaccadic potentials are evidence of the fact that orientation of attention during motor preparation and saccadic initiation is reflected in intensification of fronto-parietal networks of saccadic control and attention, activating the fronto-medio-thalamic and thalamo-parietal modulating systems.
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Seo, Bo-Kyung, Gudrun Sartory, Bernhard Kis, Norbert Scherbaum, and Bernhard W. Müller. "Intensity Dependence of Auditory Evoked Potentials (IDAP) in Adult Attention Deficit/Hyperactivity (ADHD) Disorder." Journal of Psychophysiology 28, no. 2 (April 1, 2014): 63–72. http://dx.doi.org/10.1027/0269-8803/a000111.
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Intensity-dependent auditory evoked potentials (IDAP) were shown to be increased in highly impulsive individuals. As impulsivity is one of the core symptoms of attention deficit/hyperactivity disorder (ADHD), patients with ADHD were expected to exhibit an enhanced IDAP. Twenty-five ADHD patients taking methylphenidate and 21 healthy control participants were given diagnostic questionnaires including the Barratt Impulsivity Scale and IDAP was assessed with five-tone intensities. Amplitude, latency, and intensity slope of the N1, P2, and N1/P2 were determined. Contrary to our hypothesis, there was no significant group difference with regard to N1 amplitude and ADHD patients exhibited significantly lower P2 amplitude at high intensity and a flatter N1/P2 slope of the stimulus intensity function than healthy controls. Motor impulsivity, a subscale of the Barratt impulsivity scale, showed a significantly negative correlation with P2 amplitude within the ADHD group. The unexpected results could be due to the effect of methylphenidate.
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Jellinek, David, Michael Platt, Doreen Jewkes, and Lindsay Symon. "Effects of Nitrous Oxide on Motor Evoked Potentials Recorded from Skeletal Muscle in Patients under Total Anesthesia with Intravenously Administered Propofol." Neurosurgery 29, no. 4 (October 1, 1991): 558–62. http://dx.doi.org/10.1227/00006123-199110000-00012.
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Abstract The effect of nitrous oxide (N2O) on motor evoked potentials (MEPs) recorded from human subjects under total intravenous anesthesia with propofol (2,6-diisopropylphenol) was studied. MEPs were recorded from the 1st dorsal interosseous muscle of the foot in nine subjects; in two of these, simultaneous recordings were made from the 2nd dorsal interosseous muscle of the hand and from the deltoid muscle. Single transcranial electrical stimuli were used in recording the MEPs. The effects of N2O were studied at concentrations from 20 to 70%. Increasing concentrations of N2O caused a progressive increase in onset latency and a fall in the peak-to-peak amplitude of the MEPs recorded from the foot. Latency values showed a significant increase above the baseline at concentrations of N2O greater than 20% (Pvalues, 0.05-0.005). The response amplitude showed a significant decrease from the baseline at concentrations of N2O greater than 50% (P values, 0.05-0.005). The 2nd dorsal interosseous muscle of the hand demonstrated a pattern of sensitivity to N2O similar to that of the 1 st dorsal interosseous muscle of the foot. The onset latency and initial peak-to-peak amplitude of the deltoid muscle were insensitive to N2O at the concentrations used. We conclude that N2O can be used as an anesthetic adjunct without a significant deleterious effect on MEPs during intraoperative monitoring in patients under propofol anesthesia, providing concentrations are maintained below 50%.
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Raux, Mathieu, Haiqun Xie, Thomas Similowski, and Lisa Koski. "Facilitatory conditioning of the supplementary motor area in humans enhances the corticophrenic responsiveness to transcranial magnetic stimulation." Journal of Applied Physiology 108, no. 1 (January 2010): 39–46. http://dx.doi.org/10.1152/japplphysiol.91454.2008.
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Inspiratory loading in awake humans is associated with electroencephalographic signs of supplementary motor area (SMA) activation. To provide evidence for a functional connection between SMA and the diaphragm representation in the primary motor cortex (M1DIA), we tested the hypothesis that modulating SMA activity using repetitive transcranial magnetic stimulation (rTMS) would alter M1DIA excitability. Amplitude and latency of diaphragm motor evoked potentials (MEPDIA), evoked through single pulse M1DIA stimulation, before and up to 16 min after SMA stimulation, were taken as indicators of M1DIA excitability. MEPs from the first dorsal interosseous muscle (FDI, MEPFDI) served as a control. Four SMA conditioning sessions were performed in random order at 1-wk intervals. Two aimed at increasing SMA activity (5 and 10 Hz, both at 110% of FDI active motor threshold; referred to as 5Hz and 10Hz, respectively), and two aimed at decreasing it (1 Hz either at 110% of FDI active or resting motor threshold, referred to as aMT or rMT, respectively). The 5Hz protocol increased MEPDIA and MEPFDI amplitudes with a maximum 11–16 min poststimulation ( P = 0.04 and P = 0.02, respectively). The 10Hz protocol increased MEPFDI amplitude with a similar time course ( P = 0.03) but did not increase MEPDIA amplitude ( P = 0.32). Both aMT and rMT failed to decrease MEPDIA or MEPFDI amplitudes ( P = 0.23 and P = 0.90, respectively, for diaphragm and P = 0.48 and P = 0.14 for FDI). MEPDIA and MEPFDI latencies were unaffected by rTMS. These results demonstrate that 5-Hz rTMS over the SMA can increase the excitability of M1DIA. These observations are consistent with the hypothesis of a functional connection between SMA and M1DIA.
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Fisicaro, Francesco, Giuseppe Lanza, Carmela Cinzia D’Agate, Raffaele Ferri, Mariagiovanna Cantone, Luca Falzone, Giovanni Pennisi, Rita Bella, and Manuela Pennisi. "Intracortical and Intercortical Motor Disinhibition to Transcranial Magnetic Stimulation in Newly Diagnosed Celiac Disease Patients." Nutrients 13, no. 5 (May 1, 2021): 1530. http://dx.doi.org/10.3390/nu13051530.
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Background: Celiac disease (CD) may present or be complicated by neurological and neuropsychiatric manifestations. Transcranial magnetic stimulation (TMS) probes brain excitability non-invasively, also preclinically. We previously demonstrated an intracortical motor disinhibition and hyperfacilitation in de novo CD patients, which revert back after a long-term gluten-free diet (GFD). In this cross-sectional study, we explored the interhemispheric excitability by transcallosal inhibition, which has never been investigated in CD. Methods: A total of 15 right-handed de novo, neurologically asymptomatic, CD patients and 15 age-matched healthy controls were screened for cognitive and depressive symptoms to the Montreal Cognitive Assessment (MoCA) and the 17-item Hamilton Depression Rating Scale (HDRS), respectively. TMS consisted of resting motor threshold, amplitude, latency, and duration of the motor evoked potentials, duration and latency of the contralateral silent period (cSP). Transcallosal inhibition was evaluated as duration and latency of the ipsilateral silent period (iSP). Results: MoCA and HDRS scored significantly worse in patients. The iSP and cSP were significantly shorter in duration in patients, with a positive correlation between the MoCA and iSP. Conclusions: An intracortical and interhemispheric motor disinhibition was observed in CD, suggesting the involvement of GABA-mediated cortical and callosal circuitries. Further studies correlating clinical, TMS, and neuroimaging data are needed.
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Rampil, Ira J., and Bryan S. King. "Volatile Anesthetics Depress Spinal Motor Neurons." Anesthesiology 85, no. 1 (July 1, 1996): 129–34. http://dx.doi.org/10.1097/00000542-199607000-00018.
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Background Depression of spinal alpha-motor neurons apparently plays a role in the surgical immobility induced by isoflurane. Using the noninvasive technique of F-wave analysis, the authors tested the hypothesis that depressed motor neuron excitability is an effect common to other clinically relevant inhaled anesthetics. Methods The authors measured F-wave amplitude in rats anesthetized with desflurane, enflurane, halothane, or sevoflurane. Each animal received one anesthetic at five equipotent anesthetic concentrations (0.6, 0.8, 1.2, and 1.6 minimum alveolar concentration [MAC] and 0.8 MAC with 65% N2O). F waves were detected as late potentials in electromyographic responses evoked in the intrinsic muscles of the hind paw after monopolar stimulation of the ipsilateral posterior tibial nerve. Results All tested inhaled anesthetics depressed F-wave amplitude but not M-wave (orthodromic, early muscle activation) amplitude, and increased M-F latency in a dose-dependent manner. At 1.0 MAC, the estimated F/M ratio was 70 +/- 13% SD of that at baseline (0.6 MAC). Nitrous oxide added to 0.8 MAC of the potent vapors depressed F/M ratio by 63 +/- 17%. Conclusions All anesthetics tested appeared to depress the excitability of spinal motor neurons. This effect may contribute to surgical immobility, and its magnitude is comparable at equipotent concentrations of agents. The authors hypothesize that this effect is due to hyperpolarization, although, currently, there is insufficient information to discriminate between pre- and postsynaptic mechanisms.
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Calancie, B., M. Nordin, U. Wallin, and K. E. Hagbarth. "Motor-unit responses in human wrist flexor and extensor muscles to transcranial cortical stimuli." Journal of Neurophysiology 58, no. 5 (November 1, 1987): 1168–85. http://dx.doi.org/10.1152/jn.1987.58.5.1168.
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1. Transcranial cortical stimuli (TCCS) were used to elicit motor responses in contralateral wrist flexor and extensor muscles of healthy adult subjects. The motor responses were assessed by surface EMG recordings, by needle recordings of single motor-unit discharges, and by measurements of wrist twitch force. Our main aim was to analyze the single-unit events underlying those changes in latency, amplitude, and duration of the compound EMG responses, which could be induced by voluntary preactivation of target muscles and by changes in stimulation strength. 2. Different stimulus strengths were tested with and without background contractions in the flexor or extensor muscles. For each test (consisting of a series of 20 stimuli) the compound EMG responses were averaged and displayed together with the averaged wrist force signals. Responses of individual flexor and extensor motor units were displayed in raster diagrams and peristimulus time histograms. For units exhibiting a background firing, the mean background interdischarge interval was calculated and compared with the subsequent poststimulus intervals. 3. In relaxed muscles, a shortening of onset latency of evoked compound EMG responses was observed when raising stimulation strength. A similar latency reduction was not seen in any of the single-unit recordings. This would be consistent with the size principle of motoneuron recruitment. 4. A shortening of onset latency of evoked EMG potentials was observed also as a result of a voluntary preactivation. Such latency shifts, which were seen also in single-unit recordings, might be attributed to variations in the time required for D and I wave temporal summation at the anterior horn cell. 5. When raising stimulation strength or when adding voluntary background contraction, the evoked compound EMG potential grew not only in amplitude but also in duration, as later peaks of activity were added to the initial ones. Under optimal conditions (strong stimulus + background contraction), the period of excitation (termed E1) had an onset latency of approximately 15 ms and a duration of approximately 35 ms and was similar for wrist flexor and extensor muscles. 6. We never saw the same flexor or extensor unit fire more than once during the E1 period. For units preactivated by a background contraction, the stimulus-triggered impulse exhibited latency shifts, which, to a large extent, depended on the timing of the stimulus in relation to a preceding background discharge and which could be influenced by a change in stimulation strength.(ABSTRACT TRUNCATED AT 400 WORDS)
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Painter, Rhys, Alan Pearce, Mohamad Rostami, Ashlyn Frazer, and Dawson Kidgell. "Determining the Corticospinal and Neuromuscular Responses Following a Warm-Up Protocol." Journal of Science and Medicine 2, no. 2 (June 10, 2020): 1–12. http://dx.doi.org/10.37714/josam.v2i2.45.
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Background: The effect of warming-up prior to exercise on increased neuromuscular transmission speed remains largely untested. Objective: This study used transcranial magnetic stimulation (TMS) and peripheral nerve stimulation (PNS) to quantify neuromuscular transmission along the corticospinal tract (CST) before and after a warm-up protocol of the elbow flexors. Method: Using a single-group, pre-test-post-test design, 30 participants (20 male; 10 female; mean age 26.3 ± 7.4 years) completed four sets of bicep curls that aimed to increase heart rate (HR) and biceps brachii (BB) muscle temperature by a minimum of 40 beats per minute (bpm) and 1°C, respectively. Single-pulse TMS was applied to the primary motor cortex, and over the cervical and thoracic (C7-T1) areas of the spine to quantify motor evoked potentials (MEPs) and spinal evoked potentials (SEPs), respectively. Central motor conduction time (CMCT) was determined by calculating the difference in latency time of the onset of MEPs and SEPs. Peripheral motor conduction time (PMCT) was calculated following stimuli from Erb’s point to the onset of the maximal compound muscle action potential twitch (MMAX latency). MMAX time to peak twitch was also measured. MMAX amplitude was used to normalize the MEP to quantify corticospinal excitability. Results: Following the warm-up, significant increases in mean heart rate (44.8 ± 11.7 bpm; P < 0.001) and muscle temperature (1.4 ± 0.6°C; P < 0.001) were observed. No changes were seen in corticospinal excitability (P = 0.39), CMCT (P = 0.09), or MMAX latency (P = 0.24). However, MMAX time to peak twitch was significantly reduced (P = 0.003). Conclusion: This study has shown that exercise-based warm-ups improve neuromuscular conduction velocity via thermoregulatory processes that result in the onset of muscle contraction being more rapid, but not as a result of changes in the efficacy of neural transmission along the CST.
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Sloan, T., J. Rogers, and H. Sloan. "CMAP ONSET LATENCY AND AMPLITUDE ARE NOT INTERRELATED DURING MULTIPULSE TRANSCRANIAL MOTOR EVOKED POTENTIALS IN THE ISOFLURANE ANESTHETIZED BABOON." Journal of Neurosurgical Anesthesiology 9, no. 4 (October 1997): 396. http://dx.doi.org/10.1097/00008506-199710000-00085.
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Bonnard, Mireille, Mickael Camus, Jozina de Graaf, and Jean Pailhous. "Direct Evidence for a Binding between Cognitive and Motor Functions in Humans: A TMS Study." Journal of Cognitive Neuroscience 15, no. 8 (November 1, 2003): 1207–16. http://dx.doi.org/10.1162/089892903322598157.
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During voluntary motor actions, the cortico-spinal (CS) excitability is known to be modulated, on the one hand by cognitive (intention-related) processes and, on the other hand, by motor (performance-related) processes. Here, we studied the way these processes interact in the tuning of CS excitability during voluntary wrist movement. We used transcranial magnetic stimulation (TMS) both as a reliable tool for quantifying the CS excitability, through the motor-evoked potentials (MEPs), and as a central perturbation evoking a movement (because the stimulation intensity was above threshold) with subjects instructed to prepare (without changing their muscle activation) either to “let go” or to “resist” to this evoked movement. We studied the simultaneous evolution of both the motor performance and the MEPs in the wrist flexor and extensor, separately for the successful trials (on average, 66% of the trials whatever the condition) and the unsuccessful trials; this allowed us to dissociate the intentionand performance-related processes. To their great surprise, subjects were found able to cognitively prepare themselves to resist a TMS-induced central perturbation; they all reported an important cognitive effort on the evoked movement. Moreover, because TMS only evoked short-latency MEPs (and no long-latency components), the amplitude of these short-latency MEPs was found to be related in a continuous way to the actual movement whatever the prior intention. These results demonstrate that prior intention allows an anticipatory modulation of the CS excitability, which is not only selective (as already known) but also efficient, giving the intended motor behavior a real chance to be realized. This constitutes a direct evidence of the role of the CS excitability in the binding between cognitive and motor processes in humans.
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Xu, Wen, Demin Han, Lizhen Hou, Li Zhang, and Gongwei Zhao. "Value of Laryngeal Electromyography in Diagnosis of Vocal Fold Immobility." Annals of Otology, Rhinology & Laryngology 116, no. 8 (August 2007): 576–81. http://dx.doi.org/10.1177/000348940711600804.
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Objectives: We sought to determine the value of laryngeal electromyography (LEMG) and evoked LEMG in the diagnosis of vocal fold immobility. Methods: We analyzed 110 cases of vocal fold immobility by their clinical manifestations and LEMG characteristics, including spontaneous potential activity, motor unit potential measurement, recruitment pattern analysis, and evoked LEMG signals. Results: With LEMG, we identified 87 patients with neuropathic laryngeal injuries. Neurogenic vocal fold immobility showed a wide variety of abnormal activity. Fibrillation potentials and positive sharp waves were found in patients with laryngeal nerve injuries. For laryngeal paralysis, there was no reaction with LEMG and evoked LEMG. For incomplete laryngeal paralysis, decreased evoked LEMG signals were also seen with delayed latency (thyroarytenoid muscle, 2.2 ± 1.0 ms, p < 01; posterior cricoarytenoid muscle, 2.4 ± 1.0 ms, p < .05) and lower amplitude (thyroarytenoid muscle, 0.9 ± 0.7 mV, p < .05; posterior cricoarytenoid muscle, 1.2 ± 1.0 mV, p < .01). Nineteen patients with vocal fold mechanical limitations generally had normal LEMG and evoked LEMG signals. Four patients with neoplastic infiltration of the laryngeal muscles demonstrated abnormal LEMG signals but nearly normal evoked LEMG signals. Conclusions: We conclude that LEMG and evoked LEMG behavior plays a crucial role in the diagnosis of vocal fold immobility. The decreased recruitment activities on LEMG and the decreased evoked LEMG signals with longer latency and lower amplitude reflect the severity of neuropathic laryngeal injury.
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Goldberg, J., W. Colmers, J. Edstrom, and K. Lukowiak. "Suppression of sensory to motor synaptic transmission and narrowing of the sensory neurone action potential by arginine vasotocin in Aplysia californica." Journal of Experimental Biology 128, no. 1 (March 1, 1987): 47–62. http://dx.doi.org/10.1242/jeb.128.1.47.
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The vertebrate neurohypophysial peptide arginine vasotocin (AVT), which may be endogenous to the Aplysia central nervous system, was tested for its effect on sensory to motor neurone synaptic transmission. In the semi-intact preparation, superfusion of AVT (10(−6) moll-1) over the abdominal ganglion decreased the amplitude of both the gill withdrawal reflex and the short-latency excitatory postsynaptic potentials (EPSPs) evoked in gill and siphon motor neurones by single action potentials elicited in sensory neurones. AVT slowed the rate of rise of the EPSP, enhanced the rate of homosynaptic depression, and reversibly decreased the duration of the action potential of mechanosensory neurones in isolated, perfused abdominal and pleural ganglia. Frequency-dependent prolongation of action potentials of pleural sensory cells was also decreased by application of AVT. Because this peptide has been shown to modulate the gill withdrawal reflex and its subsequent habituation, the hypothesis that AVT plays a physiological role in the expression of the suppressed behavioural state is proposed. In addition, it is proposed that modulation of the reflex by AVT occurs in part by shortening the duration of the sensory neurone action potential.
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Sloan, Tod, James Rogers, and Heather Sloan. "A471 CMAP ONSET LATENCY AND AMPLITUDE ARE NOT INTERRELATED DURING MULTIPULSE TRANSCRANIAL MOTOR EVOKED POTENTIALS IN THE ISOFLURANE ANESTHETIZED BABOON." Anesthesiology 87, Supplement (September 1997): 471A. http://dx.doi.org/10.1097/00000542-199709001-00471.
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Bertrand, Henri Georges Michel Justin, Joseph Adam Middleton, Stuart Nicolas Baker, Isabel Glover, and Paul Andrew Flecknell. "Influence of alphaxalone on motor somatosensory evoked potentials in a female rhesus macaque (Macaca mulatta)." Laboratory Animals 55, no. 4 (February 9, 2021): 363–66. http://dx.doi.org/10.1177/0023677221990706.
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This communication reports the effect of alphaxalone on motor somatosensory evoked potential (SEPs) in a rhesus macaque. The animal was deeply anaesthetised with an infusion of ketamine, medetomidine, midazolam and alfentanil. The median nerve was stimulated, and SEPs were recorded from the motor cortex. The successive administration of three doses of alphaxalone (0.5, 1 and 2 mg/kg) induced an increase of the latency time and a decrease of the amplitude of the SEPs. However, the structure of the waveforms was conserved, and hence alphaxalone might represent a suitable general anaesthetic option in neuroscience research as well as veterinary or human medicine.
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Ghaly, Ramsis F., James L. Stone, Walter J. Levy, Peter Roccaforte, and Edward B. Brunner. "The Effect of Etomidate on Motor Evoked Potentials Induced by Transcranial Magnetic Stimulation in the Monkey." Neurosurgery 27, no. 6 (December 1, 1990): 936–42. http://dx.doi.org/10.1227/00006123-199012000-00012.
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Abstract Etomidate (ET) is a known hypnotic agent in neuroanesthesia. This study was designed to examine the reliability of motor evoked potentials (MEPs) after transcranial magnetic stimulation in monkeys anesthetized intravenously with ET. The ET regimen was as follows: an initial dose (0.5 mg/kg) followed by 13 doses (0.2 mg/kg every 6-12 min; mean, 8.0 ± 1.3 min). The total dose administered was 3.1 mg/kg. The magnetic coil was placed over the MEP scalp stimulation region. Evoked electromyographic responses were recorded from the contralateral abductor pollicis brevis (APB) and abductor hallucis (AH) muscles of the fore- and hindlimbs, respectively. Reproducible MEP responses were consistently recorded while the animal was under total ET anesthesia. The coil demography was altered and the MEP scalp topography was moderately reduced by ET injections. Significant threshold elevation was noted after a total dose of 1.7 mg/kg for APB responses and 0.5 mg/kg for AH responses (P < 0.05). Marked prolongation of latency was observed after a dose of 0.5 mg/kg for APB MEPs and 2.5 mg/kg for AH MEPs (P < 0.05). MEP amplitude responses showed marked variability. Repeated doses of ET produced a mean threshold rise of 14 to 28% for the APB and 19 to 29% for the AH. The mean latency delay was 5 to 11% for the APB and 0.5 to 8% for the AH, while the mean amplitude depression was 24 to 59% for the APB and 15 to 50% for the AH. Apparent seizure activity or abnormalities in behavior and feeding were not noted over a 1-year period. We conclude that monitoring of MEPs induced by transcranial magnetic stimulation under ET anesthesia is feasible. Clear MEP responses can be maintained under ET anesthesia. ET caused alterations in MEPs induced by transcranial magnetic stimulation, and awareness of such changes is important. Further investigation in humans is recommended.
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Вокина, Vera Vokina, Якимова, Natalya Yakimova, Соседова, Larisa Sosedova, Лизарев, and Aleksandr Lizarev. "Influence of acute hypoxIa In late gestatIon perIod on the development of toluene neurotoxIc effect In adult albIno rats." Бюллетень Восточно-Сибирского научного центра Сибирского отделения Российской академии медицинских наук 1, no. 5 (December 6, 2016): 96–99. http://dx.doi.org/10.12737/23400.
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The aim of the present investigation is to estimate the role of prenatal hypoxia in toluene neurotoxic effect in adult rats. Toluene-induced behavioral and electroencephalographic manifestations were investigated in animals with normal and abnormal embryonic development. To simulate prenatal hypoxia, we gave subcutaneous injections of sodium nitrite to pregnant female rats in a dose of 50mg/kg on the 18–19th day of gestation. At the age of 3months the males from the offspring were exposed to toluene inhalation (560mg/m3, 4w eeks, 4h/day, 5days/week). After toluene inhalation exposure we estimated rats’ individual behavior by plus maze test and visual and auditory evoked potentials (VEPs and AEPs). Toluene reduced P2N2 interpeak amplitude of VEPs compared with control rats without any latency change. We found out that toluene exposure of rats with acute prenatal hypoxia in late gestation had led to inhibition of motor activity and a statistically significant increase in latency of VEP’s N1, AEP’s P3 and N1P2 interpeak amplitude of AEP in comparison with all remained groups. Thus, these results show that prenatal hypoxic damage to the central nervous system is an aggravating factor in toluene intoxication in rats.
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Bazley, Faith A., Charles Hu, Anil Maybhate, Amir Pourmorteza, Nikta Pashai, Nitish V. Thakor, Candace L. Kerr, and Angelo H. All. "Electrophysiological evaluation of sensory and motor pathways after incomplete unilateral spinal cord contusion." Journal of Neurosurgery: Spine 16, no. 4 (April 2012): 414–23. http://dx.doi.org/10.3171/2012.1.spine11684.
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Object Unilateral contusions represent an increasingly popular model for studying the pathways and recovery mechanisms of spinal cord injury (SCI). Current studies rely heavily on motor behavior scoring and histological evidence to make assessments. Electrophysiology represents one way to reliably quantify the functionality of motor pathways. The authors sought to quantify the functional integrity of the bilateral motor and sensory pathways following unilateral SCI by using measurements of motor and somatosensory evoked potentials (MEPs and SSEPs, respectively). Methods Eighteen rats were randomly divided into 3 groups receiving a mild unilateral contusion, a mild midline contusion, or a laminectomy only (control). Contusions were induced at T-8 using a MASCIS impactor. Electrophysiological analysis, motor behavior scoring, and histological quantifications were then performed to identify relationships among pathway conductivity, motor function, and tissue preservation. Results Hindlimb MEPs ipsilateral to the injury showed recovery by Day 28 after injury and corresponded to approximately 61% of spared corticospinal tract (CST) tissue. In contrast, MEPs of the midline-injured group did not recover, and correspondingly > 90% of the CST tissue was damaged. Somatosensory evoked potentials showed only a moderate reduction in amplitude, with no difference in latency for the pathways ipsilateral to injury. Furthermore, these SSEPs were significantly better than those of the midline-injured rats for the same amount of white matter damage. Conclusions Motor evoked potential recovery corresponded to the amount of spared CST in unilateral and midline injuries, but motor behavior consistently recovered independent of MEPs. These data support the idea that spared contralateral pathways aid in reducing the functional deficits of injured ipsilateral pathways and further support the idea of CNS plasticity.
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Cantone, Mariagiovanna, Giuseppe Lanza, Alice Le Pira, Rita Barone, Giovanni Pennisi, Rita Bella, Manuela Pennisi, and Agata Fiumara. "Adjunct Diagnostic Value of Transcranial Magnetic Stimulation in Mucopolysaccharidosis-Related Cervical Myelopathy: A Pilot Study." Brain Sciences 9, no. 8 (August 14, 2019): 200. http://dx.doi.org/10.3390/brainsci9080200.
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Background: Cervical myelopathy (CM) is a common cause of morbidity and disability in patients with mucopolysaccharidosis (MPS) and, therefore, early detection is crucial for the best surgical intervention and follow-up. Transcranial magnetic stimulation (TMS) non-invasively evaluates the conduction through the cortico-spinal tract, also allowing preclinical diagnosis and monitoring. Methods: Motor evoked potentials (MEPs) to TMS were recorded in a group of eight patients with MPS-related CM. Responses were obtained during mild tonic muscular activation by means of a circular coil held on the “hot spot” of the first dorsal interosseous and tibialis anterior muscles, bilaterally. The motor latency by cervical or lumbar magnetic stimulation was subtracted from the MEP cortical latency to obtain the central motor conduction time. The MEP amplitude from peak to peak to cortical stimulation and the interside difference of each measure were also calculated. Results: TMS revealed abnormal findings from both upper and lower limbs compatible with axonal damage and demyelination in six of them. Notably, a subclinical cervical spinal disease was detected before the occurrence of an overt CM in two patients, whereas TMS signs compatible with a CM of variable degree persisted despite surgery in all treated subjects. Conclusions: TMS can be viewed as an adjunct diagnostic test pending further rigorous investigations.
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Sivaramakrishnan, Anjali, and Sangeetha Madhavan. "Stimulus Intensity Affects Variability of Motor Evoked Responses of the Non-Paretic, but Not Paretic Tibialis Anterior Muscle in Stroke." Brain Sciences 10, no. 5 (May 15, 2020): 297. http://dx.doi.org/10.3390/brainsci10050297.
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Background: Transcranial magnetic stimulus induced motor evoked potentials (MEPs) are quantified either with a single suprathreshold stimulus or using a stimulus response curve. Here, we explored variability in MEPs influenced by different stimulus intensities for the tibialis anterior muscle in stroke. Methods: MEPs for the paretic and non-paretic tibialis anterior (TA) muscle representations were collected from 26 participants with stroke at seven intensities. Variability of MEP parameters was examined with coefficients of variation (CV). Results: CV for the non-paretic TA MEP amplitude and area was significantly lower at 130% and 140% active motor threshold (AMT). CV for the paretic TA MEP amplitude and area did not vary with intensity. CV of MEP latency decreased with higher intensities for both muscles. CV of the silent period decreased with higher intensity for the non-paretic TA, but was in reverse for the paretic TA. Conclusion: We recommend a stimulus intensity of greater than 130% AMT to reduce variability for the non-paretic TA. The stimulus intensity did not affect the MEP variability of the paretic TA. Variability of MEPs is affected by intensity and side tested (paretic and non-paretic), suggesting careful selection of experimental parameters for testing.