Ipsilateral Sural Nerve Research Articles

The role of sural nerve reflexes during drop-landing in subjects with and without chronic ankle instability

The purpose of this study was to investigate the functional role of cutaneous reflexes during a single-leg drop-landing task among healthy, neurologically intact adults, and to identify whether individuals with chronic ankle instability (CAI) demonstrate altered reflexes and subsequent ankle kinematics. All subjects were physically active adults and were categorized as control (n = 10, Male = 6, Female = 4) or CAI (n = 9, Male = 4, Female = 5) depending on whether they scored a 0 or ≥ 11 on the Identification of Functional Ankle Instability questionnaire, respectively. Subjects performed 30-40 single-leg drop-landing trials from a platform set to the height of their tibial tuberosity. Muscle activity of four lower leg muscles was collected via surface electromyography, while ankle kinematics were recorded via an electrogoniometer. Non-noxious stimulations were elicited randomly to the ipsilateral sural nerve at two unique phases of the drop-landing task (takeoff and landing). Unstimulated and stimulated trials were used to calculate middle latency reflex amplitudes (80-120ms) and net ankle kinematics (140-220ms) post-stimulation. Mixed-factor ANOVAs were used to identify significant reflexes within groups and differences in reflex amplitudes between groups. Unlike the CAI group, the control group experienced significant facilitation of the Peroneus Longus (PL) and inhibition of the Lateral Gastrocnemius (LG) when stimulated at takeoff, resulting in eversion immediately prior to landing. When stimulated at landing, the control group experienced significantly more inhibition of the PL compared to the CAI group (p = 0.019). These results suggest lower neural excitability for individuals with CAI, which may predispose them to recurrent injury during similar functional tasks.

Age-related outcome of facial reanimation surgery using cross face nerve graft and gracilis free functional muscle transfer-A retrospective cohort study.

Free functional muscle transfer has become the criterion standard for the treatment of long-standing flaccid facial paralysis. Clinical experience suggests that a two-stage approach using a cross-face nerve graft (CFNG) as a donor nerve for free functional muscle transfers (FFMT) is less successful in older patients when compared to the pediatric population. However, clear data and scientific evidence are still rare. This study examines the age-related outcome of CFNG-driven FFMT. Twenty-eight patients with a mean age of 20.73 years (ranging 5-51 years) who received two-stage facial reanimation with CFNG-driven gracilis FFMT at our institution from 1998 to 2019 were included. The ipsilateral sural nerve was used as CFNG. After 12 months, the ipsilateral gracilis muscle was used as FFMT. Patients were distributed equally into three cohorts according to their age. We assessed facial symmetry before and after facial reanimation measuring the angle between the interpupillary and the intermodiolar line (pupillo-modiolar angle). Additionally, the commissure height was measured using the Emotrics software. The mean follow-up of the pediatric, young adults and the middle-aged cohort was 29.5± 7.3, 24.9± 6.3, and 25.5± 12.4months, respectively. One patient suffered flap loss due to flap ischemia. Four patients suffered insufficient innervation of the FFMT. Otherwise no major complication occurred. The likelihood of successful innervation of the FFMT was significantly higher in patients younger than 31 years (100% vs. 50%; p= .003). Smiling facial symmetry (pupillo-modiolar angle) significantly improved in the pediatric cohort (5-16 years; 8.68° ± 0.69° to 1.48° ± 0.67°; p< .001) and the young adults' cohort (17-30 years; 11.55° ± 1.95° to 4.62° ± 1.08°; p= .005), but improved only slightly in the middle-aged cohort (31-51 years; 11.77° ± 1.16° to 9.4° ± 1.8° p= .27). The postoperative smiling symmetry showed a significant correlation with increasing age (r= .62, p< .001). The smiling commissure height deviation significantly improved in the pediatric cohort (5-16 years; 6.5-2.3 mm; p= .006) and the postoperative result was significantly better than the middle-aged group (31-51 years; 2.3 vs. 7.5 mm; p= .02). The outcome of CFNG-driven gracilis FFMT is age-related. Static as well as dynamic facial symmetry after two-stage facial reanimation was best in the pediatric and young adult population. For older patients, other approaches like the nerve-to-masseter-driven FFMT should be considered.

Toward Assessing the Functional Connectivity of Spinal Neurons.

Spinal interneurons play a critical role in motor output. A given interneuron may receive convergent input from several different sensory modalities and descending centers and relay this information to just as many targets. Therefore, there is a critical need to quantify populations of spinal interneurons simultaneously. Here, we quantify the functional connectivity of spinal neurons through the concurrent recording of populations of lumbar interneurons and hindlimb motor units in the in vivo cat model during activation of either the ipsilateral sural nerve or contralateral tibial nerve. Two microelectrode arrays were placed into lamina VII, one at L3 and a second at L6/7, while an electrode array was placed on the surface of the exposed muscle. Stimulation of tibial and sural nerves elicited similar changes in the discharge rate of both interneurons and motor units. However, these same neurons showed highly significant differences in prevalence and magnitude of correlated activity underlying these two forms of afferent drive. Activation of the ipsilateral sural nerve resulted in highly correlated activity, particularly at the caudal array. In contrast, the contralateral tibial nerve resulted in less, but more widespread correlated activity at both arrays. These data suggest that the ipsilateral sural nerve has dense projections onto caudal lumbar spinal neurons, while contralateral tibial nerve has a sparse pattern of projections.

The The first report of pure neuritic leprosy with involvement of the anterior femoral cutaneous nerve

We describe the case of a young man, 22 years old, a household contact of leprosy, presenting paresthesia in the right leg and great thickening in the anterior femoral nerve and in the ipsilateral sural nerve. There were no typical dermatological lesions of leprosy. Ultrasonography confirmed the clinical finding. The clinical diagnosis of the disease was established and the patient started multibacillary-multidrug therapy, obtaining improvement of the initial symptomatology.

Thermo-dependence of noxious mechanical heterotopic stimulation-dependent modulation of the spinal dorsal horn response to somatosensory stimulation

Despite the frequent clinical hyper- or hypothermia cases, thermal-dependence of the endogenous pain modulation system at the spinal cord is not well understood. We evaluate spinal dorsal horn neuronal network responses during mechanical heterotopic noxious stimuli (HNS) at three different body temperatures (34; 37 or 40°C) by measuring lumbar cord dorsum potentials activated by electrical stimulation of the ipsilateral sural nerve in adult thiopental anesthetized rats. A noxious clamp was applied randomly to the tail, right hindpaw, right forepaw, muzzle and left forepaw. HNS induced a decrease of the N wave amplitude and duration at 37°C. This effect was reduced at 40°C for both amplitude (-18.2% for 37-40°C; P<0.0005) and duration (-16.4% for 37-40°C; P<0.0001). P wave did not show neither amplitude nor duration changes at neither 3 tested temperatures. Clinical range changes of temperature could modify pain sensation, moreover, hyperthermia increases nociceptive sensory input to dorsal horn, and could exacerbate pain sensation in individuals with fever.

Autologous transplantation with fewer fibers repairs large peripheral nerve defects.

Peripheral nerve injury is a serious disease and its repair is challenging. A cable-style autologous graft is the gold standard for repairing long peripheral nerve defects; however, ensuring that the minimum number of transplanted nerve attains maximum therapeutic effect remains poorly understood. In this study, a rat model of common peroneal nerve defect was established by resecting a 10-mm long right common peroneal nerve. Rats receiving transplantation of the common peroneal nerve in situ were designated as the in situ graft group. Ipsilateral sural nerves (10-30 mm long) were resected to establish the one sural nerve graft group, two sural nerves cable-style nerve graft group and three sural nerves cable-style nerve graft group. Each bundle of the peroneal nerve was 10 mm long. To reduce the barrier effect due to invasion by surrounding tissue and connective-tissue overgrowth between neural stumps, small gap sleeve suture was used in both proximal and distal terminals to allow repair of the injured common peroneal nerve. At three months postoperatively, recovery of nerve function and morphology was observed using osmium tetroxide staining and functional detection. The results showed that the number of regenerated nerve fibers, common peroneal nerve function index, motor nerve conduction velocity, recovery of myodynamia, and wet weight ratios of tibialis anterior muscle were not significantly different among the one sural nerve graft group, two sural nerves cable-style nerve graft group, and three sural nerves cable-style nerve graft group. These data suggest that the repair effect achieved using one sural nerve graft with a lower number of nerve fibers is the same as that achieved using the two sural nerves cable-style nerve graft and three sural nerves cable-style nerve graft. This indicates that according to the 'multiple amplification' phenomenon, one small nerve graft can provide a good therapeutic effect for a large peripheral nerve defect.

Assessment of Peripheral Neuropathy Using Measurement of the Current Perception Threshold with the Neurometer® in patients with type 1 diabetes mellitus

ObjectiveThe aim of this study is to evaluate the role of current perception threshold (CPT) measurement in peripheral neuropathy in type 1 diabetic patients by using the Neurometer®, a nerve measuring instrument. Methods52 patients with type 1 diabetes mellitus with a disease duration of less than five years and normal neuropathy symptom score (NSS), neuropathy disability score (NDS) and sensory nerve conduction velocity (SCV), and 40 healthy controls were enrolled in this study. Measurement of CPT using the Neurometer® at 2000, 250 and 5Hz assesses function in the bilateral median nerve and sural nerve in all studied cases. We also evaluated the glycated hemoglobin, microalbuminuria, urinary albumin/creatinine ratio and other metabolism indexes of all patients. ResultsThe CPT of the bilateral median nerve and sural nerve was significantly lower in diabetic patients (P<0.01). Moreover, the number of median nerve injuries in the diabetic group (left side 8/52, right side 8/52) is significantly different from the number of its ipsilateral sural nerve injuries (left side 28/52, right side 22/52) (left side P<0.01, right side P<0.01). By comparing those with DPN and those without DPN in the diabetic group, DPN groups had significantly higher glycated hemoglobin (t=2.518, P<0.05). Using binary logistic regression, high glycated hemoglobin was identified to be an independent risk factor of DPN incidence (OR (95% CI): 1.317 (1.013 −1.712), P<0.05). ConclusionThese data suggest that CPT is useful in early detection of peripheral neuropathy in patients with type 1 diabetes mellitus. Patients with diabetic peripheral neuropathy, the lower limb nerve is more vulnerable than the upper limb nerve. In addition, patients with DPN had higher glycated hemoglobin which is an independent risk factor of DPN.

Habituation behavior of the medium-latency reflex over the anterior tibial muscle after electrical stimulation of the sural nerve

Over human leg muscles, three motor responses (MR) can commonly be elicited, namely short-latency reflex (SLR), medium-latency reflex (MLR), and long-latency reflex (LLR). The MLR is less well understood than SLR and LLR. As the response to subsequent stimuli may be used to characterize central influences of an MR, we were interested, whether the MLR differs from SLR and LLR with respect to its habituation and facilitation behavior. MR were examined over the anterior tibial (TA) muscle at different contraction levels after electrical single or train stimuli (time intervals of 3ms) over the ipsilateral sural nerve. Furthermore, MR were selectively averaged after each of four subsequent stimuli (1Hz, 0.4Hz, trains-of-3). After single stimuli, the peak latency values were 46.2±2.3ms, 88.0±5.8ms (MLR), and 131.7±22.2ms (LLR). All three MR gained similarly strong and significantly in amplitude when up to 10kg of weight was loaded compared with no weight load. After train stimuli, the LLR but not SLR and MLR gained significantly in amplitude as compared with single stimuli. Different to SLR and LLR, the MLR showed significant habituation behavior at a stimulus repetition rate of 1Hz but not of 0.4Hz. Thus, inhibitory interneurons seem to be involved in the MLR pathway.

Endoneurial pathology of the needlestick‐nerve‐injury model of Complex Regional Pain Syndrome, including rats with and without pain behaviors

Current rodent models of neuropathic pain produce pain hypersensitivity in almost all lesioned animals and not all identified experimental effects are pain specific. 18G needlestick-nerve-injury (NNI) to one tibial nerve of outbred Sprague-Dawley rats models the phenotype of Complex Regional Pain Syndrome (CRPS), a post-traumatic neuropathic pain syndrome, leaving roughly half of NNI rats with hyperalgesia. We compared endoneurial data from these divergent endophenotypes searching for pathological changes specifically associated with pain-behaviors. Tibial, sural, and common sciatic nerves from 12 NNI rats plus 10 nerves from sham-operated controls were removed 14 days post-surgery for morphometric analysis. PGP9.5(+) unmyelinated-fibers were quantitated in plantar hindpaw skin. Distal tibial nerves of NNI rats had endoneurial edema, 30% fewer axons, twice as many mast cells, and thicker blood-vessel walls than uninjured tibial nerves. However the only significant difference between nerves from hyperalgesic versus non-hyperalgesic NNI rats was greater endoneurial edema in hyperalgesic rats (p < 0.01). We also discovered significant axonal losses in uninjured ipsilateral sural nerves of NNI rats, demonstrating spread of neuropathy to nearby nerves formerly thought spared. Tibial and sural nerves contralateral to NNI had significant changes in endoneurial blood-vessels. Similar pathological changes have been identified in CRPS-I patients. The current findings suggest that severity of endoneurial vasculopathy and inflammation may correlate better with neuropathic pain behaviors than degree of axonal loss. Spread of pathological changes to nearby ipsilateral and contralateral nerves might potentially contribute to extraterritorial pain in CRPS.

Corrigendum

CorrigendaCorrigendumPublished Online:01 Sep 2011https://doi.org/10.1152/jn.z9k-0931-corr.2011Original articleMoreSectionsPDF (32 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Volume 105, February 2011Stubbs et al. Phase modulation of the short-latency crossed spinal response in the human soleus muscle. J Neurophysiol 105: , 2011; doi:10.1152/jn.00786.2010; http://jn.physiology.org/content/105/2/503.full.We now make the following corrections:In the abstract, the following two sentences have been corrected: “First was ipsilateral tibial nerve (iTN) stimulation at motor threshold (MT), 35% of the maximal peak-to-peak M-wave (M-Max) and 85% M-Max (85M-Max) with stimuli applied at 60%, 70%, 80%, 90%, and 100% of the gait cycle of the ipsilateral leg. Second was ipsilateral sural nerve (SuN) and medial plantar nerve (MpN) stimulation at 1, 2, and 3× perceptual threshold at 90% of the gait cycle.”The running head is now corrected as: “P. W. STUBBS, J. F. NIELSEN, T. SINKJAER, AND N. MRACHACZ-KERSTING.”The affiliations are now corrected as: “1Hammel Neurorehabilitation Hospital and Research Center, Aarhus University, Hammel; 2Center for Sensory-Motor Interaction, Department of Health Science and Technology, Aalborg University, Fredrik Bajers Vej, Aalborg; and 3Danish National Research Foundation, Copenhagen K, Denmark.”This article has no references to display. Download PDF Previous Back to Top FiguresReferencesRelatedInformationRelated ArticlesPhase Modulation of the Short-Latency Crossed Spinal Response in the Human Soleus Muscle 01 Feb 2011Journal of Neurophysiology More from this issue > Volume 106Issue 3September 2011Pages 1600-1600 Copyright & PermissionsCopyright © 2011 the American Physiological Societyhttps://doi.org/10.1152/jn.z9k-0931-corr.2011History Published online 1 September 2011 Published in print 1 September 2011 Metrics

Phase Modulation of the Short-Latency Crossed Spinal Response in the Human Soleus Muscle

Short-latency spinally mediated interlimb reflex pathways were recently reported between the left and right soleus muscles in the human lower-limb during sitting. The aim of the current study was to establish if these pathways were observed during a functional motor task such as human gait and modulated by the gait cycle phase and/or electrical stimulation intensity. The second aim was to elucidate on the afferents involved. Two interventions were investigated. First was ipsilateral tibial nerve (iTN) stimulation at motor threshold (MT), 35% of the maximal peak-to-peak M-wave(M-Max) and 85% M-Max (85M-Max) with stimuli applied at 60%, 70%, 80%, 90%, and 100%of the gait cycle of the ipsilateral leg. Second was ipsilateral sural nerve (SuN) and medial plantar nerve (MpN) stimulation at 1, 2, and 3X perceptual threshold at 90% of the gait cycle [corrected]. The root mean squared (RMS) of the contralateral soleus (cSOL) responses were analyzed in a time window, 40-55 ms (or 45-60 ms for subjects >50 y/o) following iTN stimulation. The most consistent responses occurred at 90 and 100% of the gait cycle at higher stimulation intensities of the iTN. Significantly inhibitory responses (P = 0.006) were reported at 60 versus 80% (P = 0.03), 90% (P = 0.006), and 100% (P = 0.002) and 70 versus 90% (P = 0.02) and 100% (P = 0.009) of the gait cycle at 85M-Max. The responses became more inhibitory with increasing stimulation intensities at 80% (P = 0.01), 90% (P = 0.001), and 100% (P = 0.004) of the gait cycle. Stimulation of the MpN and SuN at all stimulation intensities demonstrated no short-latency responses. Therefore, it is unlikely that afferents within these nerves contribute to the response. This is the first study to show short-latency spinally mediated responses in the cSOL following iTN stimulation, during walking. It provides evidence for a new spinal pathway contributing to motor control and demonstrates that the response likely has functional relevance.

Phenylephrine Suppresses the Pain Modulation of Diffuse Noxious Inhibitory Control in Rats

Diffuse noxious inhibitory control (DNIC) is a phenomenon whereby wide dynamic range neurons are selectively and powerfully inhibited through the central nervous system by noxious stimuli heterotopically applied to a body area distant from their excitatory receptive fields. Previous work has shown that systemic administration of an alpha1-adrenoceptor agonist, phenylephrine (PE), blocked the DNIC. We hypothesized that descending inhibitory pathways mediate the DNIC mechanism and that the neural network of the DNIC loop exists in the middle brainstem, likely in a more rostral part than formerly assumed, possibly the nucleus raphe magnus (RMg). The aim of this study was to determine whether DNIC is directly modulated by PE when administered close to the RMg. The experiments were performed on anesthetized male Sprague-Dawley rats. For administration of different drugs close to the RMg, the tip of a 33-gauge cannula was placed into an area close to the RMg as determined using the atlas of Paxinos and Watson. Single square-wave electrical stimuli were applied to the digits of the left hindpaw. The C-fiber reflex response elicited by electrical stimulation within the receptive field of the ipsilateral sural nerve was recorded from the biceps femoris muscle in the absence and presence of noxious tail immersion in warm water at 50 degrees C. The DNIC effect was calculated from a recorded electromyogram as the "inhibition rate." Saline (0.05 microL) or PE (0.05 microg/0.05 microL) was microinjected close to the RMg through the cannula. The C-fiber reflex evoked by electromyographic activity was recorded the same way. The inhibition rate of the C-fiber reflex was compared before and after administration of drugs. A paired t test was used for statistical comparison between same drug administration groups, and 1-way analysis of variance and Bonferroni multiple comparison were used for statistical analysis between different drugs. At the end of all experiments, the tissue-contacting end of the cannula tip was cauterized with an electric current to localize the drug administration site. The brain was removed, sliced in coronal sections, and stained with hematoxylin and eosin. The C-fiber reflex inhibited by noxious thermal stimuli (DNIC) was significantly blocked after the injection of PE close to the RMg. Direct administration of PE close to the RMg inhibited DNIC, thereby affecting and modulating the intrinsic pain inhibition system. These findings suggest that the RMg may be involved in the regulation of DNIC.

Short-Latency Crossed Inhibitory Responses in the Human Soleus Muscle

Even though interlimb coordination is critical in bipedal locomotion, the role of muscle afferent mediated feedback is unknown. The aim of this study was to establish if ipsilateral muscle generated afferent feedback can influence contralateral muscle activation patterns in the human lower limb and to elucidate the mechanisms involved. The effect of ipsilateral tibial nerve stimulation on contralateral soleus (cSOL) responses were quantified. Three interventions were investigated, 1) electrical stimulation applied to the tibial nerve at stimulation intensities from 0 to 100% of maximal M-wave (M-max) with the cSOL contracted from 5 to 15% of maximal voluntary contraction (MVC) and 15 to 30% MVC, 2) ispsilateral tibial nerve stimulation at 75% M-max prior to, during, and following the application of ischemia to the ipsilateral thigh. 3) Electrical stimulation applied to the ipsilateral sural (SuN) and medial plantar nerves at stimulation intensities from 1 to 3 times perceptual threshold. A short-latency depression in the cSOL electromyogram (EMG; onset: 37-41 ms) was observed following ipsilateral tibial nerve stimulation. The magnitude of this depression increased (P = 0.0005 and P = 0.000001) with increasing stimulus intensities. Ischemia delayed the time of the minimum of the cSOL depression (P = 0.04). SuN and medial plantar nerve stimulation evoked a longer latency depression [average; 91.2 ms (SuN); 142 ms (medial plantar nerve)] and therefore do not contribute to the response. This is the first study to demonstrate a short-latency depression in the cSOL following ipsilateral tibial nerve stimulation. Due to its short latency, the response is spinally mediated. The involvement of crossed spinal interneurons receiving input from low-threshold muscle afferents is discussed.

Taxometric analysis of biceps femoris EMG following electrocutaneous stimulation over the sural nerve: Determining the latent structure of the nociceptive flexion reflex (NFR)

The nociceptive flexion reflex (NFR) is a polysynaptic withdrawal reflex typically assessed from biceps femoris electromyogram (EMG) following noxious stimulation of the ipsilateral sural nerve. Electrophysiological evidence suggests the reflex is elicited following the activation of small diameter A-delta afferents. As a result, the NFR is assumed to be a categorically distinct construct that emerges from EMG activity only following nociceptor activation. Despite the widespread use of the NFR in pain research, there has been little attempt to verify the latent structure of the NFR. The present study used “coherent cut kinetics” taxometric analyses to examine whether the latent structure of biceps femoris EMG reflects the taxonic structure that would be predicted from electrophysiological evidence. To achieve this end, preliminary analyses first compared different methods of scoring NFR magnitude. Results suggested the presence of a taxon in the covariance of biceps femoris EMG and stimulus intensity that is likely to be the NFR. Furthermore, preliminary analyses suggested the best method of scoring NFR magnitude was using Cohen's d. Implications of these results are discussed.

Experimental study of polarity in reversing cable nerve grafts.

To evaluate the effect of cable nerve graft polarity, the bilateral common peroneal nerves in 12 rabbits were excised to create 20-mm nerve gaps. These gaps were repaired with cable grafts using three strands of 20-mm ipsilateral sural nerves. In the left leg, the sural nerves were grafted with the original orientation. In the right leg, the nerve graft polarity was reversed 180 degrees. Six months later, motor conduction velocities were evaluated, and the bilateral anterior tibial muscles and extensor digitorum longus muscles were measured. The nerves were harvested and analyzed histologically. Motor conduction velocity was 37.4+/-4.1 m/s in the reversed group, and 36.6+/-5.5 m/s in the control group. The weight of the muscles was 7.2+/-0.8 g in the reversed orientation, and 7.0+/-1.0 g in the original orientation. None of the differences was statistically significant. Histologically, the axon counts and the axonal density distal to the nerve graft also showed no differences between groups. The sural nerves used did not have a major branch and their diameter was almost the same throughout its length. Reversing nerve graft polarity of a cable graft did not affect nerve regeneration electrophysiologically or histologically.

Electrical stimulation of the sural nerve partially compensates effects of central fatigue.

Depression of motor evoked potentials (MEPs) following transcranial magnetic stimulation (TMS) may be a sign of central motor fatigue. Abnormal fatigue can be observed in MS patients. We have examined whether post-exercise MEP depression can be compensated by application of sensory stimuli prior to TMS. We studied 15 healthy volunteers (aged 21 to 28 years) who were required to perform an exercise protocol of ankle dorsiflexion until force fell below 66% of maximum force. MEPs were recorded from the right tibialis anterior muscle. Prior to TMS, electrical stimuli were applied to the ipsilateral sural nerve with an individual interstimulus interval between 50 to 80 ms. MEP areas decreased after exercise. When a sensory stimulus was administered MEPs did not change. We conclude that the effects of central fatigue may be--at least partially compensated--by application of sensory stimuli. Sensory stimulation (e.g. by implantation of a neurostimulator) might be a useful therapy for abnormal central fatigue.

Effects of somatosensory input on central fatigue: a pilot study

Objective: Depression of motor evoked potentials (MEPs) following transcranial magnetic stimulation (TMS) may be a sign of central motor fatigue. As a pilot study, we have examined whether post-exercise MEP depression can be compensated by application of sensory stimuli prior to TMS.Methods: We studied 15 healthy volunteers (aged 21–28 years) who were required to perform an exercise protocol of ankle dorsiflexion until force fell below 66% of maximum force. MEPs were recorded from the right tibialis anterior muscle. Prior to TMS, electrical stimuli were applied to the ipsilateral sural nerve with an individual interstimulus interval between 50 and 80 ms.Results: MEP areas decreased after exercise. When a sensory stimulus was administered MEPs did not change.Conclusion: We conclude that the effects of central fatigue may be influenced by application of sensory stimuli.

The effect of denervated muscle and Schwann cells on axon collateral sprouting

The effects of denervated muscle and Schwann cells on collateral sprouting from peripheral nerve were studied in the peroneal and tibial nerves of 48 Sprague-Dawley rats. Three groups were prepared. In group MSW (muscle-Schwann cell-window), the peroneal nerves were transected 3 mm below the sciatic bifurcation. The proximal stumps were sealed in a blocked tube to prevent regeneration and the distal stumps were implanted into denervated muscle cells that were wrapped around the ipsilateral tibial nerve, which had a window of perineurium resected. Schwann cells from the ipsilateral sural nerve were implanted into the muscle. Group MS (muscle-Schwann cell) was similar to group MSW, except that the tibial nerve perineurium was kept intact. In group MW (muscle-window), the muscle was prepared without Schwann cells and the tibial nerve perineurium was windowed. S-100 immunostain was used to identify the Schwann cells surviving 1 week after transplantation. After 16 weeks of regeneration, horseradish peroxidase tracer was used to label motor neurons and sensory neurons reinnervating the peroneal nerve. Myelinated axons of the reinnervated peroneal nerves were quantified with the Bioquant OS/2 computer system (R&M Biometrics, Nashville, TN). A mean of 169 motor neurons in group MSW, 64 in group MW, and 26 in group MS reinnervated the peroneal nerve. In the dorsal root ganglion, the mean number of labeled sensory neurons was 1,283 in group MSW, 947 in group MS, and 615 in group MW. The mean number of myelinated axons in the reinnervated peroneal nerve was 1,659 in group MSW, 359 in group MS, and 348 in group MW. Reinnervated anterolateral compartment muscles in group MSW were significantly heavier than those in group MS or MW. This study demonstrates that the transplantation of denervated muscle and Schwann cells promotes motor and sensory nerve collateral sprouting through a perineurial window.

Clinical use of polysynaptic flexion reflexes in the management of spasticity with intrathecal baclofen

The aim of this study was to evaluate the clinical usefulness of lower limb flexion reflexes (FR) in the assessment of spinal excitability responsible for spontaneous or induced spasms. FR were recorded on the short head of biceps femoris, after electrical stimulation of the ipsilateral sural nerve at the ankle, in 17 spastic patients selected for chronic intrathecal administration of baclofen. The results obtained before and after treatment were compared with clinical scores commonly used to assess spasticity (Ashworth and spasm scores). Before intrathecal baclofen 15 17 patients (88%) had pathologically enhanced flexor in the lower limbs, which were associated to clinical spasms. Reflex enhancement was accompanied in 47% of cases by abnormal decrease of reflex threshold. No significant correlation appeared between the magnitude or threshold of FR in control conditions and either the hypertonia (Ashworth scale) or the number of clinical spasms per unit of time. Intrathecal baclofen attenuated flexor reflex amplitude and increased reflex threshold in all patients. Our results suggest that FR investigate the intrinsic features of the spasms (threshold, intensity and duration) not assessed clinically, and that therefore the information gathered from FR recordings is not redundant with, and adds significantly to, that obtained by clinical scales. In our experience, FR recordings appeared to be a useful tool for quantifying the benefit of antispastic treatment and might be used as an ancillary indicator to determine the minimal effective dose of intrathecal baclofen.

Inhibition of a somatic nociceptive reflex by gastric distention in humans

Background/Aims: The spinal nociceptive RIII reflex, an exteroceptive cutaneous-muscular flexion reflex, is powerfully and specifically inhibited by painful heterotopic somatic stimuli. The aim of the present study was to evaluate the effects of nonpainful and painful visceral stimuli on this reflex.Methods: In nine healthy volunteers, the effects of five levels of gastric distention were tested on the RIII reflex, recorded from the biceps femoris, and elicited by electrical stimulation of the ipsilateral sural nerve. Distentions were performed by means of a balloon that was placed in the proximal part of the stomach and connected to an electronic barostat. The sensations evoked by gastric distention were scored using a graded (0–6) questionnaire. Results: The 200- and 400-mL distention levels elicited no significant modifications of the RIII reflex; the 600-, 800-, and 1000-mL levels inhibited the RIII reflex by 25%, 35%, and 55%, respectively. The magnitude of this inhibition correlated significantly (P < 0.0001) with both the level of distention and the intensity of visceral perception. Conclusions: Gastric distention produces volume-dependent inhibition of the somatic RIII reflex in humans. This model may provide an interesting tool for objective and quantitative evaluation of normal and disturbed visceral sensations in humans.