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Deformities of the spastic upper limb result frequently from the association of spasticity, muscle contracture and muscle imbalance between strong spastic muscles and weak non-spastic muscles. This study was designed to evaluate the feasibility of combining selective neurectomy of the usual spastic and strong muscles together with transfer of their motor nerves to the usual weak muscles, to improve wrist and fingers motion while decreasing spasticity.Twenty upper limbs from fresh frozen human cadavers were dissected. All motor branches of the radial and median nerve for the forearm muscles were identified. We attempted all possible end-to-end nerve transfers between the usually strong "donor" motor branches, namely FCR and PT, and the usually weak "recipient" motor branches (ERCL, ECRB, PIN, AIN). The PT had two nerve branches in 80%, thus allowing selective neurectomy. The proximal PT branch could be anastomosed end-to-end in 45% (AIN) to 85% (ECRL) of cases with the potential recipient branches. The distal PT branch could be anastomosed end to end to all potential recipient nerves. The FCR had a single branch in all cases. End-to-end anastomosis was possible in 90% for the ECRL and in 100% for all other recipient branches, but sacrificed all FCR innervation, ruling out hyperselective neurectomy. Selective neurectomies can be associated with distal nerve transfers at the forearm level in selected cases. The motor nerve to the PT is the best donor for nerve transfer combined with selective neurectomy, transferred to the ECRL, ECRB, PIN or AIN.

International audience; The objective of this case report is to illustrate the problem's diagnosis of a CIDP revealing a associated disease. The patient had initially a sensory CIDP wich respond to prednisone. After 2 years, he worsened with motor deficit, pain and atypical skin's lesions. The diagnosis of POEMS syndrome was made only in the fourth research of monoclonal gammopathy. A specific treatment was realised but too late and a important motor deficit with axonal loss unfortunately persisted.

International audience; Effects of electrical stimulation of ulnar and median nerves at wrist level were investigated in post-stimulus time histograms (PSTHs) of single motor units from both flexors and extensors in human arm and forearm. Stimulation of ulnar nerve produced late (mean extra time-after monosynaptic group Ia excitation-10.7 +/- 0.1 ms) high-threshold (>1.2 x motor threshold, MT) excitation, which was not reproduced by purely cutaneous stimulation, in all the investigated motor nuclei except in Extensor Carpi Radialis. Stimulation of median nerve, and of the skin of fingers II and III (at palmar side level), produced short latency inhibition (mean extra time 3.8 +/- 0.3 ms), which was most often truncated or followed by late excitation (mean extra time 11.8 +/- 0.3 ms); both effects were of low threshold (0.8 x MT). Short latency inhibition was very strong, and late excitation was rare and weak in almost all the investigated motor units except in those supplying flexors in forearm, in which the main effect was the late facilitation (stronger than in other motoneurones). Since extra time was not more than 13 ms, it is suggested that the late effects may be mediated through spinal pathways, at least during their 3-5 first ms. Based on the electrophysiological results and on the anatomical characteristics of ulnar and median nerves, it is assumed that ulnar-induced late high-threshold peak in PSTHs might reflect group II excitation in spinal motoneurones, and median-induced modifications in motor unit discharge, mainly cutaneous control of motoneurone discharge. Since the central delay of median-induced inhibition is longer the more caudal the motoneurone, inhibitory propriospinal-like interneurones are supposed to mediate cutaneous inhibitory control from hand upon muscles in arm and forearm. Potential roles of proprioceptive and cutaneous control from hand to more proximal musculature, provided by ulnar and median nerve, respectively, during precise hand movements are discussed.

International audience; Repetitive pairing of a peripheral stimulation with a magnetic transcortical stimulation (PAS) is widely used to induce plastic changes in the human motor cortex noninvasively. Based on the contrast between PAS-induced increase of corticospinal excitability and absence of PAS-induced increase of the spinal F wave size, it has been generally accepted that PAS-induced plasticity is cortical in origin. Here, instead of F waves, we used H reflex recruitment curves to assess spinal excitability, and we demonstrate that PAS induces parallel changes in cortical and spinal excitability.

Objective : To record somatosensory evoked potentials (SEPs) to median nerve stimulation by chronically implanted electrodes in the parieto-rolandic opercular area of 9 epileptic patients, in order to evaluate whether somatosensory evoked responses could be generated in the second somatosensory area (SII) earlier than 40 ms after stimulus. Methods : Nine patients (4 males, 5 females) with drug-resistant partial epileptic seizures were investigated using stereotactically implanted electrodes in the parietal cortex, posterior to vertical anterior commissure plane and in the frontal opercular region rostral to vertical anterior commissure (VAC). Results : The main finding of this study is the recording of an early somatosensory evoked potential, (N30op), by chronically implanted electrodes in the SII area of 8 epileptic patients. In 3 patients where SEPs were performed after ipsilateral median nerve (MN) stimulation, a N30op was recorded 5.8±2 ms later than contralateral one. Conclusions : This is the first report of early SEPs recorded by electrodes implanted in SII area. The N30op potential, even if less consistent than later potentials, confirmed the important role of the SII area in the early processing of somatosensory inputs.

Objectives : To investigate the possible contribution of the second somatosensory (SII) area in the generation of the N60 somatosensory evoked potential (SEP). Methods : In 7 epileptic patients and in 6 healthy subjects scalp SEPs were recorded by 19 electrodes placed according to the 10–20 system. All epileptic patients but one were also investigated using depth electrodes chronically implanted in the parieto-rolandic opercular cortex. Scalp SEPs underwent brain electrical source analysis. Results : In both epileptic patients and healthy subjects, scalp recordings showed two middle-latency components clearly distinguishable on the basis of latency and scalp distribution: a fronto-central N60 potential contralateral to stimulation and a later bilateral temporal N70 response. SEP dipolar source modelling showed that a contralateral perisylvian dipole was activated in the scalp N70 latency range whereas separate perirolandic and frontal sources were activated at the scalp N60 latency. Depth electrodes recorded a biphasic N60/P90 response in the parieto-rolandic opercular regions contra- and ipsilateral to stimulation. Conclusions : Two different middle-latency SEP components N60 and N70 can be distinguished by topographic analysis and source modelling of scalp recordings , the sources of which are located in the fronto-central cortex contralateral to stimulation and in the supra-sylvian cortex on both sides, respectively. The source location of the scalp N70 in the SII area is strongly supported by its spatio-temporal similarities with SEPs directly recorded in the supra-sylvian opercular cortex.

International audience; Median nerve somatosensory-evoked potentials (SEPs) have been recorded using intracortical electrodes stereotactically implanted in the frontal lobe of eight epileptic patients in order to assess the waveforms, latencies and surface-to-depth distributions of somatosensory responses generated in the anterior subdivision of supplementary motor areas (SMAs), the so-called pre-SMA. Intracortical responses were analysed in two latency ranges: 0--50 ms and 50--150 ms after stimulus. In all patients, we recorded in the first 50 ms after stimulus two positive P14 and P20 potentials followed by a N30 negativity. In the hemisphere contralateral to stimulation, the P20--N30 potentials showed a clear amplitude decrease from the outer to the inner aspect of the frontal lobe with minimal amplitudes in the pre-SMA. In the hemisphere ipsilateral to stimulus, P20 and N30 amplitudes were decreasing from mesial to lateral frontal cortex. In the 50--150 ms latency range, contacts implanted in the pre-SMA recorded a negative potential in the 60--70 ms latency range which, in five patients, was followed by a positive response peaking 80--110 ms after stimulus. These potentials were not picked up by more superficial contacts. We conclude that no early SEP is generated in pre-SMA in the first 50 ms after stimulation, while some potentials peaking in the 60--100 ms after stimulus are likely to originate from this cortical area. The latency of the pre-SMA responses recorded in our patients supports the hypothesis that the pre-SMA does not receive short-latency somatosensory inputs via direct thalamocortical projections. More probably the pre-SMA receives somatosensory inputs mediated by a polysynaptic transcortical transmission through functionally secondary motor and somatosensory areas.