The Experts below are selected from a list of 162 Experts worldwide ranked by ideXlab platform
Markus Kofler - One of the best experts on this subject based on the ideXlab platform.
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Effects of vibration on cutaneous silent period
Experimental Brain Research, 2019Co-Authors: Şenay Aydın, Markus Kofler, Yeliz Bakuy, Ayşegül Gündüz, Meral E. KızıltanAbstract:Suppression of an ongoing muscle contraction following noxious digital stimulation is called cutaneous silent period (CSP) which is under the influence of several physiological factors. In this study, we aimed to evaluate the influence of group Ia afferents on the cutaneous silent period (CSP) by applying 2-min vibration. CSP was obtained from abductor pollicis brevis muscle after stimulating index finger. The recordings were repeated three times—before, during and after vibration—which was applied over the tendon of flexor carpi radialis muscle. Onset latency, duration and magnitude of total CSP, inhibitory phases I1 and I2, and of the long-Loop Reflex were measured and compared. Suppression indices of CSP, I1 and I2 increased significantly during and after vibration, indicating significantly less exteroceptive EMG suppression outlasting the time of vibration. Vibration also caused mild shortening of I2 end latency ( p = 0.048) and I2 duration ( p = 0.019). Our findings indicate that vibration exerts a powerful influence on CSPs and causes reduction in the magnitude of exteroceptive EMG suppression during and after vibration. Although vibration is known to activate Ia afferents, we cannot exclude contribution of other afferents, e.g. mechanoreceptors, as well as pre- or postsynaptic inhibitory effects on ensuing interneurons, or enhanced vibration-related excitatory influence.
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Sensory modulation of voluntary and TMS-induced activation in hand muscles
Experimental Brain Research, 2008Co-Authors: Markus Kofler, Josep Valls-solé, Peter Fuhr, Christian Schindler, Barbara R. Zaccaria, Leopold SaltuariAbstract:Nociceptive suppression of tonic voluntary electromyographic (EMG) activity in human hand muscles (cutaneous silent period, CSP) is in its functional organization consistent with a spinal protective Reflex. Motoneuronal excitability and its modulation may also be investigated by conditioned motor evoked potentials (MEPs). To date, effects of exteroceptive stimuli on tonic EMG and on MEPs have been compared mainly using innocuous stimuli, while noxious stimuli have not been studied in great detail. In ten subjects, we recorded CSPs induced in volitionally activated flexor pollicis brevis muscle (FPB) by noxious digit II (D2) stimulation, and in first dorsal interosseous muscle (FDI) following noxious D2 and digit V (D5) stimulation. Then, transcranial magnetic stimulation (TMS) was used to evoke MEPs in the same hand muscles at rest—conditioned by equal noxious D2 or D5 stimulation and individually delayed—so that the MEPs occurred at times corresponding to immediately before, during, and immediately after the CSP in each subject. Immediately before the CSP, there was no significant difference between nociceptive MEP modulation and tonic EMG modulation in any muscle–finger-combination. In the middle of the CSP, noxious finger stimulation exerted suppression of TMS-induced MEPs in all the three muscle–finger-combinations, but less so as compared to corresponding tonic EMG levels. After the CSP, MEPs remained suppressed when corresponding tonic EMG levels were significantly enhanced. Notably, MEPs were also suppressed in cases when occurring at times corresponding to the excitatory long-Loop Reflex. Incomplete MEP suppression during the CSP may allow for an “emergency grip” even during noxious stimulation. MEP suppression outlasting the CSP is compatible with a “passive” re-synchronization of volitionally activated motor units rather than an “active” Reflex involving recruitment of corticospinal motoneurons. The differences in tonic EMG and MEP modulation favors an effect of noxious digital nerve stimulation on interneurons responsible for presynaptic inhibition rather than a postsynaptic inhibitory effect on the motoneuron pool. The present findings caution against the use of nociceptive MEP modulation at rest to substitute for tonic EMG modulation as tested in CSP studies.
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Tumors localized near the central sulcus may cause increased somatosensory evoked potentials.
Clinical Neurophysiology, 2006Co-Authors: Ivana Stetkarova, Lubor Stejskal, Markus KoflerAbstract:Abstract Objective Median nerve somatosensory evoked potentials (SEPs) may be altered in patients with cerebral tumors. In rare cases cortical responses may be increased, but the significance of this finding remains unclear. Methods We investigated 3 patients in whom an epileptic seizure was the only neurological symptom of a cerebral tumor located near the central sulcus. We studied median nerve SEPs, motor evoked potentials in abductor digiti minimi muscle, and long-Loop Reflexes in abductor pollicis brevis muscle bilaterally. Two patients also underwent intraoperative neurophysiological monitoring. Results All 3 patients presented with enlarged cortical SEPs on the side of the brain tumor. The responses increased further post-operatively, and the enhancement persisted in follow-up examinations up to 6 months after surgical tumor extirpation. Intraoperative monitoring documented a substantial increase of the enlarged potential N20–P22 during tumor removal in one patient, who also presented with an exaggerated long-Loop Reflex on the tumor side. Transcranial magnetic stimulation revealed unremarkable motor evoked potentials in all 3 patients. Conclusions Distinct mechanisms must be considered in order to explain both immediate and long-term changes of neuronal excitability leading to increased cortical SEPs. Significance Hyperexcitability of cortical neurons or insufficient cortical inhibitory mechanisms may be responsible for increased SEPs, which may serve as an epileptic marker in patients suffering from a tumor near the central sulcus.
Francesco Pierelli - One of the best experts on this subject based on the ideXlab platform.
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spinal myoclonus with giant somatosensory evoked potentials and enhanced long Loop Reflex a case report
Functional Neurology, 2004Co-Authors: Mariano Serrao, Patrizio Cardinali, Paolo Rossi, Armando Perrotta, Michaelangelo Bartolo, L Parisi, Francesco PierelliAbstract:: We describe a patient with an ischaemic lesion of the cervical spinal cord who presented with clinical evidence of stimulus-sensitive, multisegmental myoclonic jerks restricted to the truncal and proximal limb muscles and accompanied by electrophysiological features (giant somatosensory evoked potentials and enhanced long-Loop Reflex) of cortical myoclonus. We hypothesize that these features might result from a loss of inhibitory influences on the sensory input to cortical structures: a concomitant contribution of spinal and cortical hyperexcitability seems to have played a crucial role in inducing myoclonus in our patient.
Mikio Nishioka - One of the best experts on this subject based on the ideXlab platform.
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Electrophysiological and pharmacological studies of somatosensory Reflex myoclonus.
Electromyography and clinical neurophysiology, 1992Co-Authors: H Takeuchi, Tetsuo Touge, Yamada A, Miki H, Kazushi Deguchi, Mikio NishiokaAbstract:: Reflex myoclonus displays symptomatological heterogeneity involving the cortical and brain stem types that seem to originate above the spinal cord. Three cases of generalized myoclonus proved to be spontaneous and stimulus-sensitive, and increased with action. Segmental spinal myoclonus was spontaneous, stimulus-sensitive and rhythmical and decreased with action. Two cases of post-anoxic myoclonus seemed to be of the reticular Reflex in which myoclonus was manifested in all muscles, particularly the proximal ones, and for which the EEG showed no spikes preceding myoclonus. The evoked electromyogram showed a long-Loop Reflex (LLR) of high amplitude, with no giant somatosensory evoked potential (SEP). Pharmacological examinations showed that the thyrotropin-releasing hormone (TRH) enhanced the onset of myoclonus, shortened the latency of the LLR and increased its amplitude, but caused no remarkable changes in SEP. These results indicate that TRH stimulates the medullary reticular neuron, thereby enhancing reticular Reflex myoclonus. The myoclonus of a 3rd case was believed to be cortical Reflex myoclonus on the basis of the emergence of giant SEP, increased LLR and the onset of spikes in the EEGs preceding myoclonic jerks, as ascertained by jerk-locked averaging analysis with muscular discharge. Pharmacologically, LLR, SEP and myoclonus showed no definite changes in response to TRH. Segmental myoclonus which seemed to have a spinal origin, showed no giant SEP, enhanced LLR or cortical spikes in the electrophysiological studies. No definite clinical or electrophysiological changes in response to TRH were observed. We believe the TRH administration test may be useful in the differential diagnosis of stimulus-sensitive myoclonus. In addition, the origins and nature of these types of Reflex myoclonus are discussed.
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the long Loop Reflex in spinocerebellar degeneration and motor neuron disease its changes with trh therapy
Electromyography and clinical neurophysiology, 1990Co-Authors: Tetsuo Touge, H Takeuchi, A Yamada, H Miki, Mikio NishiokaAbstract:: This study aimed to define the characteristics of the long Loop Reflex (LLR) in patients with spinocerebellar degeneration (SCD) and motor neuron disease (MND), and observe changes in LLR caused by thyrotropin releasing hormone (TRH), a facilitator of cerebellar and motor neurons. The markers used for LLR were: V1-2 peak Latency (the latency between the V1 and V2 peaks); V2 peak-P24 Latency (the latency between the V2 peak and P24 of a somatosensory evoked potential); V2 Amplitude, and V2 Square (the area of the V2 wave). V1-2 peak Latency was significantly longer, and V2 Amplitude was significantly lower than the control in SCD. We attributed these alterations of the LLR to cerebellar ataxia, since all SCD cases had cerebellar ataxia, and extrapyramidal symptoms were only present in one SCD case; the MND cases with motor neuron disturbance showed no significant difference from the control. TRH injection resulted in an increase in V2 Square and a decrease in V2 peak-P24 Latency in SCD and other neurological disease patients. We regarded these changes as activation of the LLR by TRH. With TRH therapy, activation of the LLR coincided with improvement of cerebellar ataxia in SCD. Symptomatic improvement, however, was not observed and the LLR changes were not stable in MND. These results suggest that TRH-induced activation of LLR is caused by the activation of cerebellar function, and indirectly concerns with upper motor neurons because V2 Square increased in MND without pyramidal tract signs.
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The long Loop Reflex in spinocerebellar degeneration and motor neuron disease ― its changes with TRH therapy
Electromyography and clinical neurophysiology, 1990Co-Authors: Tetsuo Touge, H Takeuchi, Yamada A, Miki H, Mikio NishiokaAbstract:: This study aimed to define the characteristics of the long Loop Reflex (LLR) in patients with spinocerebellar degeneration (SCD) and motor neuron disease (MND), and observe changes in LLR caused by thyrotropin releasing hormone (TRH), a facilitator of cerebellar and motor neurons. The markers used for LLR were: V1-2 peak Latency (the latency between the V1 and V2 peaks); V2 peak-P24 Latency (the latency between the V2 peak and P24 of a somatosensory evoked potential); V2 Amplitude, and V2 Square (the area of the V2 wave). V1-2 peak Latency was significantly longer, and V2 Amplitude was significantly lower than the control in SCD. We attributed these alterations of the LLR to cerebellar ataxia, since all SCD cases had cerebellar ataxia, and extrapyramidal symptoms were only present in one SCD case; the MND cases with motor neuron disturbance showed no significant difference from the control. TRH injection resulted in an increase in V2 Square and a decrease in V2 peak-P24 Latency in SCD and other neurological disease patients. We regarded these changes as activation of the LLR by TRH. With TRH therapy, activation of the LLR coincided with improvement of cerebellar ataxia in SCD. Symptomatic improvement, however, was not observed and the LLR changes were not stable in MND. These results suggest that TRH-induced activation of LLR is caused by the activation of cerebellar function, and indirectly concerns with upper motor neurons because V2 Square increased in MND without pyramidal tract signs.
Meral E. Kızıltan - One of the best experts on this subject based on the ideXlab platform.
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Effects of vibration on cutaneous silent period
Experimental Brain Research, 2019Co-Authors: Şenay Aydın, Markus Kofler, Yeliz Bakuy, Ayşegül Gündüz, Meral E. KızıltanAbstract:Suppression of an ongoing muscle contraction following noxious digital stimulation is called cutaneous silent period (CSP) which is under the influence of several physiological factors. In this study, we aimed to evaluate the influence of group Ia afferents on the cutaneous silent period (CSP) by applying 2-min vibration. CSP was obtained from abductor pollicis brevis muscle after stimulating index finger. The recordings were repeated three times—before, during and after vibration—which was applied over the tendon of flexor carpi radialis muscle. Onset latency, duration and magnitude of total CSP, inhibitory phases I1 and I2, and of the long-Loop Reflex were measured and compared. Suppression indices of CSP, I1 and I2 increased significantly during and after vibration, indicating significantly less exteroceptive EMG suppression outlasting the time of vibration. Vibration also caused mild shortening of I2 end latency ( p = 0.048) and I2 duration ( p = 0.019). Our findings indicate that vibration exerts a powerful influence on CSPs and causes reduction in the magnitude of exteroceptive EMG suppression during and after vibration. Although vibration is known to activate Ia afferents, we cannot exclude contribution of other afferents, e.g. mechanoreceptors, as well as pre- or postsynaptic inhibitory effects on ensuing interneurons, or enhanced vibration-related excitatory influence.
Mariano Serrao - One of the best experts on this subject based on the ideXlab platform.
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spinal myoclonus with giant somatosensory evoked potentials and enhanced long Loop Reflex a case report
Functional Neurology, 2004Co-Authors: Mariano Serrao, Patrizio Cardinali, Paolo Rossi, Armando Perrotta, Michaelangelo Bartolo, L Parisi, Francesco PierelliAbstract:: We describe a patient with an ischaemic lesion of the cervical spinal cord who presented with clinical evidence of stimulus-sensitive, multisegmental myoclonic jerks restricted to the truncal and proximal limb muscles and accompanied by electrophysiological features (giant somatosensory evoked potentials and enhanced long-Loop Reflex) of cortical myoclonus. We hypothesize that these features might result from a loss of inhibitory influences on the sensory input to cortical structures: a concomitant contribution of spinal and cortical hyperexcitability seems to have played a crucial role in inducing myoclonus in our patient.
