Home About us Contact
|
Home About us Contact | ||
|
|
||
Median Nerve Stimulation (median + nerve_stimulation)
Selected AbstractsAfferent-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] Difference in somatosensory evoked fields elicited by mechanical and electrical stimulations: Elucidation of the human homunculus by a noninvasive methodHUMAN BRAIN MAPPING, Issue 4 2005Ken Inoue Abstract We recently recorded somatosensory evoked fields (SEFs) elicited by compressing the glabrous skin of the finger and decompressing it by using a photosensor trigger. In that study, the equivalent current dipoles (ECDs) for these evoked fields appeared to be physiologically similar to the ECDs of P30m in median nerve stimulation. We sought to determine the relations of evoked fields elicited by mechanically stimulating the glabrous skin of the great toe and those of electrically produced P40m. We studied SEFs elicited by mechanical and electrical stimulations from the median and tibial nerves. The orientations of dipoles from the mechanical stimulations were from anterior-to-posterior, similar to the orientations of dipoles for P30m. The direction of the dipole around the peak of N20m from median nerve electrical stimulation was opposite to these directions. The orientations of dipoles around the peak of P40m by tibial nerve stimulation were transverse, whereas those by the compression and decompression stimulation of the toe were directed from anterior-to-posterior. The concordance of the orientations in ECDs for evoked fields elicited by mechanical and electrical stimulations suggests that the ECDs of P40m are physiologically similar to those of P30m but not to those of N20m. The discrepancy in orientations in ECDs for evoked field elicited by these stimulations in the lower extremity suggests that electrical and compression stimulations elicit evoked fields responding to fast surface rubbing stimuli and/or stimuli to the muscle and joint. Hum. Brain Mapping 24:274,283, 2005. © 2005 Wiley-Liss, Inc. [source] Timing and connectivity in the human somatosensory cortex from single trial mass electrical activityHUMAN BRAIN MAPPING, Issue 4 2002Andreas A. Ioannides Abstract Parallel-distributed processing is ubiquitous in the brain but often ignored by experimental designs and methods of analysis, which presuppose sequential and stereotypical brain activations. We introduce here a methodology that can effectively deal with sequential and distributed activity. Regional brain activations elicited by electrical median nerve stimulation are identified in tomographic estimates extracted from single trial magnetoencephalographic signals. Habituation is identified in both primary somatosensory cortex (SI) and secondary somatosensory cortex (SII), often interrupted by resurgence of strong activations. Pattern analysis is used to identify single trials with homogeneous regional brain activations. Common activity patterns with well-defined connectivity are identified within each homogeneous group of single trials across the subjects studied. On the contralateral side one encounters distinct sets of single trials following identical stimuli. We observe in one set of trials sequential activation from SI to SII and insula with onset of SII at 60 msec, whereas in the other set simultaneous early co-activations of the same two areas. Hum. Brain Mapping 15:231,246, 2002. © 2002 Wiley-Liss, Inc. [source] Dopamine agonists restore cortical plasticity in patients with idiopathic restless legs syndrome,MOVEMENT DISORDERS, Issue 5 2009Vincenzo Rizzo MD Abstract In the present work, we aimed at assessing whether patients with idiopathic restless legs syndrome (RLS) showed alterations of sensory-motor plasticity, an indirect probe for motor learning, within the motor cortex (M1). Previous findings suggest that learning in human M1 occurs through LTP-like mechanisms. To test our hypothesis, we employed the paired associative stimulation (PAS) protocol by transcranial magnetic stimulation (TMS), which is able to induce LTP-like effects in the motor cortex of normal subjects. Twelve patients with idiopathic RLS and 10 age- and sex-matched control subjects were recruited. PAS protocol consisted of 0.05 Hz electrical median nerve stimulation (90 stimuli), paired with 0.05 Hz TMS (90 stimuli) over the hot spot for stimulating the abductor pollicis brevis (APB) muscle given 25 milliseconds after the onset of the electrical stimulus. Corticospinal excitability recorded in APB muscle, as indexed by MEP obtained after single stimulus, was tested before and up to 30 minutes after PAS protocol. Eight of 12 patients were studied before and after 4 weeks of dopaminergic treatment. PAS protocol increased significantly corticospinal excitability as long as 30 minutes in healthy subjects. On the contrary, PAS protocol did not change the amplitude of MEPs in patients with idiopathic RLS without treatment. PAS associative plasticity was restored after 4 weeks of dopaminergic treatment. Our data demonstrated that associative sensory-motor plasticity, an indirect probe for motor learning, is impaired in idiopathic RLS patients but may be reverted to normal after dopaminergic treatment. © 2008 Movement Disorder Society [source] Impaired heteronymous somatosensory motor cortical inhibition in dystoniaMOVEMENT DISORDERS, Issue 11 2003Laura Bertolasi MD Abstract A typical pathophysiological abnormality in dystonia is cocontraction of antagonist muscles, with impaired reciprocal inhibitory mechanisms in the spinal cord. Recent experimental data have shown that inhibitory interactions between antagonist muscles have also a parallel control at the level of the sensorimotor cortex. The aim of this work was to study heteronymous effects of a median nerve stimulus on the corticospinal projections to forearm muscles in dystonia. We used the technique of antagonist cortical inhibition, which assesses the conditioning effect of median nerve afferent input on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) in ipsilateral forearm extensor muscles at rest. Nine healthy subjects and 10 patients with torsion dystonia participated in the study. MEPs and somatosensory evoked potentials were normal in patients. In healthy subjects, median nerve stimulation at 15- to 18-msec intervals inhibited the test MEPs in forearm extensors. In dystonic patients, median nerve stimulation delivered at the same conditioning,test intervals elicited significantly less inhibition of the test MEP. On the whole, these data suggest an impaired sensory,motor integration in dystonia and, more specifically, the decreased antagonistic cortical inhibition could suggest that functional interactions between antagonist muscles are primarily impaired at the cortical level. © 2003 Movement Disorder Society [source] Somatosensory disinhibition in dystoniaMOVEMENT DISORDERS, Issue 4 2001Emma Frasson MD Abstract Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease. © 2001 Movement Disorder Society. [source] Effect of acute hyperglycaemia on sensory processing in diabetic autonomic neuropathyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2010Jens B. Frøkjær Eur J Clin Invest 2010; 40 (10): 883,886 Abstract Background, Acute hyperglycaemia is known to increase gastrointestinal (GI) sensitivity in healthy subjects and may contribute to the increased prevalence of GI symptoms in diabetes patients. The aim of this study was to evaluate the effect of acute hyperglycaemia on perception and brain responses to painful visceral and somatic stimuli in diabetic patients. Materials and methods, The sensitivity and evoked brain potentials (EPs) to electrical oesophageal and median nerve stimulations were assessed in 14 type-1 diabetes patients with autonomic neuropathy and GI symptoms using a hyperinsulinaemic clamp at 6 and 15 mM. Results, No differences between the normo- and hyperglycaemic conditions were found in sensitivity to both oesophageal (P = 0·72) and median nerve (P = 0·66) stimulations. The latencies and amplitudes of EPs did not differ between the normo- and hyperglycaemic conditions following oesophageal (P = 0·53 and 0·57) and median nerve (P = 0·78 and 0·52) stimulations. Conclusions, Acute hyperglycaemia itself does not contribute to the sensations in patients with longstanding diabetes and autonomic neuropathy. Any potential sensory effects of acute hyperglycaemia can likely be blurred by the neuropathic-like changes in the sensory nervous system. [source] | |||||||||||||