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Intracortical Facilitation (intracortical + facilitation)
Selected AbstractsIntracortical inhibition and facilitation upon awakening from different sleep stages: a transcranial magnetic stimulation studyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004Luigi De Gennaro Abstract Intracortical facilitation and inhibition, as assessed by the paired-pulse transcranial magnetic stimulation technique with a subthreshold conditioning pulse followed by a suprathreshold test pulse, was studied upon awakening from REM and slow-wave sleep (SWS). Ten normal subjects were studied for four consecutive nights. Intracortical facilitation and inhibition were assessed upon awakening from SWS and REM sleep, and during a presleep baseline. Independently of sleep stage at awakening, intracortical inhibition was found at 1,3-ms interstimulus intervals and facilitation at 7,15-ms interstimulus intervals. Motor thresholds were higher in SWS awakenings, with no differences between REM awakenings and wakefulness, while motor evoked potential amplitude to unconditioned stimuli decreased upon REM awakening as compared to the other conditions. REM sleep awakenings showed a significant increase of intracortical facilitation at 10 and 15 ms, while intracortical inhibition was not affected by sleep stage at awakening. While the dissociation between motor thresholds and motor evoked potential amplitudes could be explained by the different excitability of the corticospinal system during SWS and REM sleep, the heightened cortical facilitation upon awakening from REM sleep points to a cortical motor activation during this stage. [source] Altered Motor Cortex Excitability to Magnetic Stimulation in Alcohol Withdrawal SyndromeALCOHOLISM, Issue 4 2010Raffaele Nardone Background:, Alcohol addiction is a complex brain disease caused by alterations in crucial neurotransmitter systems, including gamma-aminobutyric acid (GABA) and glutamate. These disturbances could be revealed by changes in cortical excitability parameters, as assessed by transcranial magnetic stimulation (TMS). This study was aimed to further investigate the complex pathophysiology of alcohol withdrawal syndrome (AWS). Methods:, Motor cortex excitability was examined in 13 subjects with AWS in a mild predelirial state, in 12 chronic alcoholics and in 15 age-matched control subjects, using a range of TMS protocols. Central motor conduction time, resting and active motor threshold, duration of the cortical silent period, short latency intracortical inhibition (SICI), and intracortical facilitation (ICF) to paired TMS were examined. Results:, Intracortical facilitation was significantly increased in the AWS patients when compared with the chronic alcoholics and the control subjects. The other TMS parameters did not differ significantly from the controls. Administration of a single oral dose of the glutamatergic antagonist riluzole in a subgroup of 8 patients significantly reduced ICF; motor threshold and SICI were not affected by riluzole. Conclusion:, Transcranial magnetic stimulation shows a selective increase in intracortical facilitation after ethanol withdrawal. Our findings support the theory that altered glutamatergic receptor function plays an important role in the pathogenesis of human alcohol withdrawal. This study provides further physiological evidence that antiglutamatergic approaches represent an efficacious alternative for treating alcohol withdrawal symptoms. [source] Pregabalin Exerts Oppositional Effects on Different Inhibitory Circuits in Human Motor Cortex: A Double-blind, Placebo-controlled Transcranial Magnetic Stimulation StudyEPILEPSIA, Issue 5 2006Nicolas Lang Summary:,Purpose: To explore acute effects of pregabalin (PGB) on human motor cortex excitability with transcranial magnetic stimulation (TMS). Methods: PGB, 600 mg/day, was orally administered in 19 healthy subjects twice daily in a randomized, double-blind, placebo-controlled crossover design. Several measures of motor cortex excitability were tested with single- and paired-pulse TMS. Results: Mean short-interval intracortical inhibition (SICI) was reduced after PGB (74 ± 7% of unconditioned response) compared with placebo (60 ± 6% of unconditioned response). In contrast, mean long-interval intracortical inhibition (LICI) was increased by PGB (26 ± 4% of unconditioned response) compared with placebo (45 ± 8% of unconditioned response), and mean cortical silent period (CSP) showed an increase from 139 ± 8 ms or 145 ± 8 ms after placebo to 162 ± 7 ms or 161 ± 10 ms after PGB. Motor thresholds, intracortical facilitation, and corticospinal excitability were unaffected. Conclusions: The observed excitability changes with oppositional effects on SICI and LICI or CSP suggest ,-aminobutyric acid (GABA)B -receptor activation. They are markedly distinct from those induced by gabapentin, although both PGB and gabapentin are thought to mediate their function by binding to the ,(2)-, subunit of voltage-gated calcium channels. Conversely, the TMS profile of PGB shows striking similarities with the pattern evoked by the GABA-reuptake inhibitor tiagabine. [source] Afferent-induced facilitation of primary motor cortex excitability in the region controlling hand muscles in humansEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2009H. Devanne Abstract Sensory inputs from cutaneous and limb receptors are known to influence motor cortex network excitability. Although most recent studies have focused on the inhibitory influences of afferent inputs on arm motor responses evoked by transcranial magnetic stimulation (TMS), facilitatory effects are rarely considered. In the present work, we sought to establish how proprioceptive sensory inputs modulate the excitability of the primary motor cortex region controlling certain hand and wrist muscles. Suprathreshold TMS pulses were preceded either by median nerve stimulation (MNS) or index finger stimulation with interstimulus intervals (ISIs) ranging from 20 to 200 ms (with particular focus on 40,80 ms). Motor-evoked potentials recorded in the abductor pollicis brevis (APB), first dorsalis interosseus and extensor carpi radialis muscles were strongly facilitated (by up to 150%) by MNS with ISIs of around 60 ms, whereas digit stimulation had only a weak effect. When MNS was delivered at the interval that evoked the optimal facilitatory effect, the H-reflex amplitude remained unchanged and APB motor responses evoked with transcranial electric stimulation were not increased as compared with TMS. Afferent-induced facilitation and short-latency intracortical inhibition (SICI) and intracortical facilitation (ICF) mechanisms are likely to interact in cortical circuits, as suggested by the strong facilitation observed when MNS was delivered concurrently with ICF and the reduction of SICI following MNS. We conclude that afferent-induced facilitation is a mechanism which probably involves muscle spindle afferents and should be considered when studying sensorimotor integration mechanisms in healthy and disease situations. [source] Intracortical inhibition and facilitation upon awakening from different sleep stages: a transcranial magnetic stimulation studyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004Luigi De Gennaro Abstract Intracortical facilitation and inhibition, as assessed by the paired-pulse transcranial magnetic stimulation technique with a subthreshold conditioning pulse followed by a suprathreshold test pulse, was studied upon awakening from REM and slow-wave sleep (SWS). Ten normal subjects were studied for four consecutive nights. Intracortical facilitation and inhibition were assessed upon awakening from SWS and REM sleep, and during a presleep baseline. Independently of sleep stage at awakening, intracortical inhibition was found at 1,3-ms interstimulus intervals and facilitation at 7,15-ms interstimulus intervals. Motor thresholds were higher in SWS awakenings, with no differences between REM awakenings and wakefulness, while motor evoked potential amplitude to unconditioned stimuli decreased upon REM awakening as compared to the other conditions. REM sleep awakenings showed a significant increase of intracortical facilitation at 10 and 15 ms, while intracortical inhibition was not affected by sleep stage at awakening. While the dissociation between motor thresholds and motor evoked potential amplitudes could be explained by the different excitability of the corticospinal system during SWS and REM sleep, the heightened cortical facilitation upon awakening from REM sleep points to a cortical motor activation during this stage. [source] Altered Motor Cortex Excitability to Magnetic Stimulation in Alcohol Withdrawal SyndromeALCOHOLISM, Issue 4 2010Raffaele Nardone Background:, Alcohol addiction is a complex brain disease caused by alterations in crucial neurotransmitter systems, including gamma-aminobutyric acid (GABA) and glutamate. These disturbances could be revealed by changes in cortical excitability parameters, as assessed by transcranial magnetic stimulation (TMS). This study was aimed to further investigate the complex pathophysiology of alcohol withdrawal syndrome (AWS). Methods:, Motor cortex excitability was examined in 13 subjects with AWS in a mild predelirial state, in 12 chronic alcoholics and in 15 age-matched control subjects, using a range of TMS protocols. Central motor conduction time, resting and active motor threshold, duration of the cortical silent period, short latency intracortical inhibition (SICI), and intracortical facilitation (ICF) to paired TMS were examined. Results:, Intracortical facilitation was significantly increased in the AWS patients when compared with the chronic alcoholics and the control subjects. The other TMS parameters did not differ significantly from the controls. Administration of a single oral dose of the glutamatergic antagonist riluzole in a subgroup of 8 patients significantly reduced ICF; motor threshold and SICI were not affected by riluzole. Conclusion:, Transcranial magnetic stimulation shows a selective increase in intracortical facilitation after ethanol withdrawal. Our findings support the theory that altered glutamatergic receptor function plays an important role in the pathogenesis of human alcohol withdrawal. This study provides further physiological evidence that antiglutamatergic approaches represent an efficacious alternative for treating alcohol withdrawal symptoms. [source] Decreased cortical inhibition and yet cerebellar pathology in ,familial cortical myoclonic tremor with epilepsy'MOVEMENT DISORDERS, Issue 16 2007Anne-Fleur van Rootselaar MD Abstract Cortical hyperexcitability is a feature of "familial cortical myoclonic tremor with epilepsy" (FCMTE). However, neuropathological investigations in a single FCMTE patient showed isolated cerebellar pathology. Pathological investigations in a second FCMTE patient, reported here, confirmed cerebellar Purkinje cell degeneration and a normal sensorimotor cortex. Subsequently, we sought to explore the nature of cerebellar and motor system pathophysiology in FCMTE. Eye movement recordings and transcranial magnetic stimulation performed in six related FCMTE patients showed impaired saccades and smooth pursuit and downbeat nystagmus upon hyperventilation, as in patients with spinocerebellar ataxia type 6. In FCMTE patients short-interval intracortical inhibition (SICI) was significantly reduced. Resting motor threshold, recruitment curve, silent period, and intracortical facilitation were normal. The neuropathological and ocular motor abnormalities indicate cerebellar involvement in FCMTE patients. Decreased SICI is compatible with intracortical GABAA -ergic dysfunction. Cerebellar and intracortical functional changes could result from a common mechanism such as a channelopathy. Alternatively, decreased cortical inhibition may be caused by dysfunction of the cerebello-thalamo-cortical loop as a result of primary cerebellar pathology. © 2007 Movement Disorder Society [source] Theta burst stimulation induces after-effects on contralateral primary motor cortex excitability in humansTHE JOURNAL OF PHYSIOLOGY, Issue 18 2008A. Suppa Interhemispheric interactions between the primary motor cortices (M1) have been described with a variety of TMS methods. Here we give a detailed description of the interhemispheric interactions of a period of theta burst simulation (TBS), a rapid method of producing long lasting after-effects on the excitability of the stimulated M1. A total of 18 right handed healthy subjects participated. In most experiments, continuous and intermittent TBS (cTBS and iTBS) were delivered over the right M1 using a coil orientated to induce antero-posterior followed by postero-anterior (AP,PA) currents in the brain. The intensity of stimulation was 80% of active motor threshold (AMT), and a total of 600 pulses were applied. The effects on the amplitude of motor evoked potentials (MEPs), short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated in the left and right M1 before and at three different times after TBS. We also tested long-interval intracortical inhibition (LICI) in right M1 and interhemispheric inhibition (IHI) from right to left M1. Finally, to explore the effect of different polarities of cTBS over dominant and non-dominant hemisphere we delivered AP,PA and postero-anterior followed by antero-posterior (PA,AP) cTBS over either right or left M1 and tested MEPs in both hemispheres. In the stimulated hemisphere, cTBS reduced MEPs and SICI whereas iTBS increased MEPs and SICI. In the non-stimulated hemisphere cTBS increased MEPs and reduced SICI, while iTBS reduced MEPs and increased SICI. There were no effects on ICF, LICI or IHI. Although both AP,PA cTBS and PA,AP cTBS reduced MEPs in the stimulated M1, the former increased MEPs from non-stimulated M1 whereas the latter did not. There was no difference in the effect of cTBS on the dominant or non-dominant hemisphere. [source] Intracortical modulation of cortical-bulbar responses for the masseter muscleTHE JOURNAL OF PHYSIOLOGY, Issue 14 2008Enzo Ortu Short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated in the masseter muscles of 12 subjects and the cortical silent period (SP) in nine subjects. Motor evoked potentials (MEPs) were recorded from contralateral (cMM) and ipsilateral (iMM) masseters, activated at 10% of maximal voluntary contraction (MVC). Interstimulus intervals (ISIs) were 2 and 3 ms for SICI, 10 and 15 ms for ICF. TMS of the left masseteric cortex induced MEPs that were larger in the cMM than the iMM; stimulation of right masseteric cortex produced a similar asymmetry in response amplitude. SICI was only observed using a CS intensity of 70% AMT and was equal in both cMM and iMM. SICI was stronger at higher TS intensities, was abolished by muscle activation greater than 10% MVC, and was unaffected by coil orientation changes. Control experiments confirmed that SICI was not contaminated by any inhibitory peripheral reflexes. However, ICF could not be obtained because it was masked by bilateral reflex depression of masseter EMG caused by auditory input from the coil discharge. The SP was bilateral and symmetric; its duration ranged from 35 to 70 ms depending on TS intensity and coil orientation. We conclude that SICI is present in the cortical representation of masseter muscles. The similarity of SICI in cMM and iMM suggests either that a single pool of inhibitory interneurons controls ipsi- and contralateral corticotrigeminal projections or that inhibition is directed to bilaterally projecting corticotrigeminal fibres. Finally, the corticotrigeminal projection seems to be weakly influenced by inhibitory interneurons mediating the cortical SP. [source] Paired-pulse transcranial magnetic stimulation protocol applied to visual cortex of anaesthetized cat: effects on visually evoked single-unit activityTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Vera Moliadze In this study, we tested the paired-pulse transcranial magnetic stimulation (ppTMS) protocol , a conditioning stimulus (CS) given at variable intervals prior to a test stimulus (TS) , for visually evoked single-unit activity in cat primary visual cortex. We defined the TS as being supra-threshold when it caused a significant increase or decrease in the visually evoked activity. By systematically varying the interstimulus interval (ISI) between 2 and 30 ms and the strength of CS within the range 15,130% of TS, we found a clear dependence of the ppTMS effect on CS strength but little relation to ISI. The CS effect was strongest with an ISI of 3 ms and steadily declined for longer ISIs. A switch from enhancement of intracortical inhibition at short ISIs (2,5 ms, SICI) to intracortical facilitation (ICF) at longer ISIs (7,30 ms), as demonstrated for human motor cortex, was not evident. Whether the CS caused facilitation or suppression of the TS effect mainly depended on the strength of CS and the polarity of the TS effect: within a range of 60,130% a positive correlation between ppTMS and TS effect was evident, resulting in a stronger facilitation if the TS caused facilitation of visual activity, and more suppression if the TS was suppressive by itself. The correlation inverted when CS was reduced to 15,30%. The ppTMS effect was not simply the sum of the CS and TS effect, it was much smaller at weak CS strength (15,50%) but stronger than the sum of CS and TS effects at CS strength 60,100%. Differences in the physiological state between sensory and motor cortices and the interactions of paired synaptic inputs are discussed as possible reasons for the partly different effects of ppTMS in cat visual cortex and human motor cortex. [source] Mechanisms of motor-evoked potential facilitation following prolonged dual peripheral and central stimulation in humansTHE JOURNAL OF PHYSIOLOGY, Issue 2 2001M. C. Ridding 1Repetitive electrical peripheral nerve or muscle stimulation can induce a lasting increase in the excitability of the corticomotor projection. By pairing peripheral stimulation with transcranial magnetic brain stimulation it is possible to shorten the duration of stimulation needed to induce this effect. This ability to induce excitability changes in the motor cortex may be of significance for the rehabilitation of brain-injured patients. The mechanisms responsible for the increases in excitability have not been investigated thoroughly. 2Using two paired transcranial magnetic stimuli protocols we investigated the excitability of intracortical inhibitory and excitatory systems before and following a period of repetitive dual muscle and brain stimulation. The dual stimulation consisted of motor point stimulation of first dorsal interosseous (FDI; 10 Hz trains of 1 ms square waves for 500 ms) delivered at one train every 10 s, paired with single transcranial magnetic stimulation given 25 ms after the onset of the train. 3Following 30 min of dual stimulation, motor-evoked potentials (MEPs) were significantly increased in amplitude. During this period of MEP facilitation there was no significant difference in the level of intracortical inhibition. There was, however, a significant increase in the intracortical facilitation demonstrated with paired magnetic stimuli. The increase in facilitation was seen only at short interstimulus intervals (0.8-2.0 ms). These intervals comprised a peak in the time course of facilitation, which is thought to reflect I wave interaction within the motor cortex. 4The relevance of this finding to the MEP facilitation seen following dual peripheral and central stimulation is discussed. [source] |