Postganglionic sympathetic neurons, but not locus coeruleus optostimulation, activates neuromuscular transmission in the adult mouse in vivo.

Recent work demonstrated that sympathetic neurons innervate the skeletal muscle near the neuromuscular junction (NMJ), and muscle sympathectomy and sympathomimetic agents strongly influence motoneuron synaptic vesicle release ex vivo. Moreover, reports attest that the pontine nucleus locus coeruleus (LC) projects to preganglionic sympathetic neurons and regulates human mobility and skeletal muscle physiology. Thus, we hypothesized that peripheral and central sympathetic neurons projecting directly or indirectly to the skeletal muscle regulate NMJ transmission. The aim of this study was to define the specific neuronal groups in the peripheral and central nervous systems that account for such regulation in adult mice in vivo by using optogenetics and NMJ transmission recordings in 3-5-month-old, male and female ChR2(H134R/EYFP)/TH-Cre mice. After detecting ChR2(H134R)/EYFP fluorescence in the paravertebral ganglia and LC neurons, we tested whether optostimulating the plantar nerve near the lumbricalis muscle or LC neurons effectively modulates motor nerve terminal synaptic vesicle release in living mice. Nerve optostimulation increased motor synaptic vesicle release in vitro and in vivo, while the presynaptic adrenoceptor blockers propranolol (ß1/ß2) and atenolol (ß1) prevented this outcome. The effect is primarily presynaptic since miniature end-plate potential (MEPP) kinetics remained statistically unmodified after stimulation. In contrast, optostimulation of LC neurons did not regulate NMJ transmission. In summary, we conclude that postganglionic sympathetic neurons, but not LC neurons, increased NMJ transmission by acting on presynaptic ß1-adrenergic receptors in vivo.

Diabetic distal symmetric polyneuropathy: effect of low-intensity laser therapy.

Low-intensity laser therapy (LILT) has been considered as a treatment modality in diabetic distal symmetric polyneuropathy (DSP). The aim of this study is to determine the effectiveness of LILT on DSP. We examined 107 subjects with type 2 diabetes for detection of DSP using the Michigan Neuropathy Screening Instrument (MNSI). Seventeen subjects were eligible to be enrolled in the study. Nerve conduction studies (NCS) were performed in all eligible subjects as an objective method to confirm neuropathy. The participants received LILT three times a week for ten sessions. NCSs were reevaluated after completion of the treatment. The absolute changes in NCS parameters were considered to establish the effectiveness of the treatment. Baseline demographics were similar in all participants. The mean differences of NCV parameters were considered for comparison. At the end of the study, the subjects showed a significant increase in neural potential amplitudes (p < 0.05). This study clearly demonstrated a significant positive effect of LILT on improvement of nerve conduction velocity on diabetic distal symmetric polyneuropathy (DSP). This finding supports the therapeutic potential of LILT in DSP.

Effect of spinal transcutaneous direct current stimulation on somatosensory evoked potentials in humans.

OBJECTIVE: Invasive stimulation of the spinal cord is used to treat a number of pathological conditions. Aiming to modulate human spinal cord function non-invasively, we evaluated whether transcutaneous direct current (DC) stimulation induces long-lasting changes in conduction along the sensory spinal pathways. METHODS: Somatosensory evoked potentials (SEPs) by posterior tibial nerve and by median nerve stimulation were recorded, before, at current offset and at 20 min after transcutaneous anodal or cathodal DC stimulation over the thoracic spinal cord (2.5 mA, 15 min) in a group of 12 healthy subjects. RESULTS: Whereas both polarities left the spinal (N22) and the cortical potentials (P39) unchanged, anodal transcutaneous spinal DC stimulation decreased significantly by about 25% the amplitude of the cervico-medullary component of posterior tibial nerve SEPs (P30) for at least 20 min. Thoracic transcutaneous spinal cord stimulation left median nerve SEPs unchanged. CONCLUSIONS: Transcutaneous DC stimulation over the thoracic spinal cord induces changes in conduction along human lemniscal pathway that persist after stimulation ends. SIGNIFICANCE: Our results support the use of transcutaneous DC stimulation as a novel tool for non-invasive spinal neuromodulation. Because the method is non-expensive and simple, it can be tested in patients with disorders presently treated with invasive procedures.

Interaction of slow cortical rhythm with somatosensory information processing in urethane-anesthetized rats.

Slow cortical rhythm (SCR) is a rhythmic alteration of active (hypopolarized), and silent (hyperpolarized) epochs in cortical cells. SCR was found to influence sensory information processing in various models, but these studies yielded inconsistent results. We examined sensory processing in anesthetized rats during SCR by recording multiple unit activity (MUA) and evoked field potentials (eFPs). Evoked field potentials as well as spontaneous FP changes around spontaneous activations were analyzed by subsequent current source density (CSD) analysis. MUA responses and eFPs were recorded from the hindlimb area (HL) of the somatosensory cortex (SI) to electrical stimuli of the tibial nerve during active and silent states, respectively. Stimulus-associated MUA above the ongoing background activity did not differ significantly in active vs. silent states. Short-latency (<50 ms) eFP responses consisted of a sequence of deep-negative and deep-positive waves. Parameters of the first negative deflection were similar in both states. Stimulation in the silent state occasionally induced 500-700 ms long spindles in the alpha range (10-16 Hz). Spindles were never observed in responses to active state stimulation. CSD analysis showed moderately different cortical sink-source patterns when the stimulus was applied during active vs. silent state. Sinks first appeared in layer IV, V and VI, corresponding sources were in layer I/II, V and VI. Stronger activation appeared in the infraganular layers in the case of active state. CSD of spontaneous FPs revealed some sequential activation pattern in the cortex when strongest and earlier sink appeared in layer III during active states.

Dissociated effects of quiet stance on standard and high-frequency (600 Hz) lower limb somatosensory evoked potentials.

OBJECTIVE: To verify whether standing can modulate somatosensory input from lower limb to the cortex. Somatosensory afferents have been evaluated not only by means of somatosensory evoked potentials recorded by means of classical wide-bandpass filtering (standard SEPs), but also by high-frequency somatosensory evoked potentials (HF-SEPs), which probably play a role in the processing of rapid adaptive changes. METHODS: Eight healthy subjects underwent right posterior tibial nerve (PTN) stimulation in two different conditions (standing and lying supine). Standard SEPs reflecting the activity of both subcortical and cortical generators further underwent digital filtering (300-800 Hz), in order to enhance HF-SEP components. RESULTS: Stance significantly reduces the P40 cortical component of standard SEPs. By contrast, HF-SEPs did not show any significant change between the two conditions. CONCLUSIONS: The lack of any gating effect on HF-SEPs lends further substance to the hypothesis that HF-SEPs play a pivotal role in the processing of somatosensory inputs related to rapid adaptive changes. SIGNIFICANCE: Our data confirm that standard and HF-SEPs reflect two distinct mechanisms with strongly different functional significance. Further studies are needed to definitively establish whether this dissociation is merely caused by the activation of anatomically different neuronal pools, or by the involvement of distinct functional mechanisms.

Short-latency crossed inhibitory responses in extensor muscles during locomotion in the cat.

During locomotion, contacting an obstacle generates a coordinated response involving flexion of the stimulated leg and activation of extensors contralaterally to ensure adequate support and forward progression. Activation of motoneurons innervating contralateral muscles (i.e., crossed extensor reflex) has always been described as an excitation, but the present paper shows that excitatory responses during locomotion are almost always preceded by a short period of inhibition. Data from seven cats chronically implanted with bipolar electrodes to record electromyography (EMG) of several hindlimb muscles bilaterally were used. A stimulating cuff electrode placed around the left tibial and left superficial peroneal nerves at the level of the ankle in five and two cats, respectively, evoked cutaneous reflexes during locomotion. During locomotion, short-latency ( approximately 13 ms) inhibitory responses were frequently observed in extensors of the right leg (i.e., contralateral to the stimulation), such as gluteus medius and triceps surae muscles, which were followed by excitatory responses ( approximately 25 ms). Burst durations of the left sartorius (Srt), a hip flexor, and ankle extensors of the right leg increased concomitantly in the mid- to late-flexion phases of locomotion with nerve stimulation. Moreover, the onset and offset of Srt and ankle extensor bursts bilaterally were altered in specific phases of the step cycle. Short-latency crossed inhibition in ankle extensors appears to be an integral component of cutaneous reflex pathways in intact cats during locomotion, which could be important in synchronizing EMG bursts in muscles of both legs.

Plantar cutaneous input modulates differently spinal reflexes in subjects with intact and injured spinal cord.

STUDY DESIGN: Spinal reflex excitability study in sensory-motor incomplete spinal cord-injured (SCI) and spinal intact subjects. OBJECTIVES: To investigate the effects of plantar cutaneous afferent excitation on the soleus H-reflex and flexion reflex in both subject groups while seated. SETTING: Rehabilitation Institute of Chicago and City University of New York, USA. METHODS: The flexion reflex in SCI subjects was elicited by non-nociceptive stimulation of the sural nerve. In normal subjects, it was also elicited via innocuous medial arch foot stimulation. In both cases, reflex responses were recorded from the ipsilateral tibialis anterior muscle. Soleus H-reflexes were elicited and recorded via conventional methods. Both reflexes were conditioned by plantar cutaneous afferent stimulation at conditioning test intervals ranging from 3 to 90 ms. RESULTS: Excitation of plantar cutaneous afferents resulted in facilitation of the soleus H-reflex and late flexion reflex in SCI subjects. In normal subjects, the soleus H-reflex was depressed while the late flexion reflex was absent. The early flexion reflex was irregularly observed in SCI patients, while in normal subjects a bimodal reflex modulation pattern was observed. CONCLUSION: The effects of plantar cutaneous afferents change following a lesion to the spinal cord leading to exaggerated activity in both flexors and extensors. This suggests impaired modulation of the spinal inhibitory mechanisms involved in the reflex modulation. Our findings should be considered in programs aimed to restore sensorimotor function and promote recovery in these patients. SPONSORSHIP: NIH, NICHD, Grant no. 1R03 HD 043951-01 and PSC CUNY Research Award no. 67051-0036.

Evidence for early activation of primary motor cortex and SMA after electrical lower limb stimulation using EEG source reconstruction.

Compared to median nerve somatosensory evoked potentials (SEP), less is known about activity evoked by nerve stimulation of the lower limb. To understand the mechanisms and the physiology of sensor- and motor control it is useful to investigate the sensorimotor functions as revealed by a standardized functional status. Therefore, we investigated SEPs of the lower limb in 6 healthy male volunteers. For each side, tibial and peroneal nerves were stimulated transcutaneously at the fossa poplitea. The tibial nerves were also stimulated further distally at the ankle joint. Source localization was applied to 64-EEG-channel data of the SEPs. In contrast to somatosensory areas, which are activated after median nerve stimulation, we found dipoles adjacent to motor areas near Brodmann area 4 (BA 4) for SEP components P 32/40 and P 54/60 and near the supplementary motor area (SMA) for the N 75/83 component. These sources could reliably be distinguished for each individual subject as well as for the grand mean data set. Our data show that afferent projections from the lower limb mainly reach primary motor areas (BA 4) and only subsequently, with a delay of 40 ms, higher order motor areas such as SMA. We conclude that a focused view on SEP of the lower limb could be a useful tool to investigate pathological states in motor control or peripheral deafferentiation.

Proposal of a new criterion for electrodiagnosis of meralgia paresthetica by evoked potentials.

We examined 19 subjects with meralgia paresthetica (bilateral in three cases), recording bilateral somatosensory-evoked potentials (SSEPs) after stimulation of the tibial posterior nerve (TPN) and cutaneous stimulation in the region of the lateral femoral cutaneous nerve (LFCN). We calculated the difference between TPN SSEPs and LFCN SSEPs cortical potentials, identifying a temporal parameter that we termed D(SEP). We defined D(SEP) normal values in a control group. D(SEP) evaluation showed good sensitivity and specificity (85.7% and 82.4%, respectively; accuracy, 83.3%) in discriminating affected limbs from unaffected. The main advantage of this method is to disengage from the necessity of contralateral comparison of LFCN recordings, joined with a reduction of interindividual variability of LFCN SSEPs amplitude and latency that often causes a lower sensitivity of other methods. As an interesting consideration, D(SEP) evaluation appears to mark out a possible subclinical involvement of LFCN in the asymptomatic side of patients with meralgia paresthetica.

H-reflex depression by propofol and sevoflurane is dependent on stimulus intensity.

OBJECTIVE: The H-reflex has been widely used to investigate effects of drugs on motoneuron excitability in humans. However, up to now no systematic investigation has been done to examine the effects at different stimulus intensities. Here, the M. soleus recruitment curves were compared under influence of propofol and sevoflurane with control conditions to investigate these stimulus intensity dependent effects. METHODS: The study was performed in 10 volunteers for propofol and sevoflurane each, aged 23-32 years. The M. soleus H-reflex was evoked by stimulation of the tibial nerve. Recruitment curves were gained by increasing the stimulation current stepwise from below the threshold of a minimal H-reflex up to a maximal (m-response. Measurements were performed under the influence of the respective drug (2mg/l propofol, 0.8 vol% sevoflurane) and compared to control measurements before and after drug administration. RESULTS: The relative amount of depression of the H-reflex at high stimulus intensities is for both drugs significantly (p<0.001, Friedman's test) lower than at low stimulus intensities. CONCLUSIONS: Stimulus dependent effects have to be taken into consideration when experimental settings to investigate the effects of drugs on the H-reflex are being designed. According to the size principle of motoneuron excitation, it can also be assumed that under the influence of propofol and sevoflurane larger motoneurons are not depressed in the same amount as smaller motoneurons. SIGNIFICANCE: Different drug effects on the H-reflex at different stimulus intensities are not only of methodological importance, but also indicate different drug effects on motoneurons of different sizes.

Lack of modulation of Ib inhibition during antagonist contraction in spasticity.

OBJECTIVE: To examine the modulation of non-reciprocal group I (Ib) inhibition during tonic contraction of antagonist muscles in patients with spasticity vs normal subjects. METHODS: The authors studied 10 patients with spastic paraplegia due to cervical compression myelopathy and 16 age-matched normal subjects. Ib inhibition to soleus motoneurons was recorded as the change in size of the H-reflex of the soleus, evoked by conditioning stimulus to the nerve innervating the medial gastrocnemius muscle. The extent of inhibition was studied at rest and during tonic contraction of the pretibial muscles of variable strength. RESULTS: In the resting state, the extent of inhibition in the patients did not differ from normal controls. During antagonist contraction, the extent of inhibition increased both in the normal subjects and patients. The increment was smaller in the patients, especially in those with severe spastic gait. The smaller increment in the inhibition was correlated with the time required to walk 10 m in the patients. CONCLUSION: The authors observed a lack of modulation of Ib inhibition during tonic antagonist contraction in patients with spasticity, especially those with gait disturbance. Disturbed central modulation of non-reciprocal (Ib) interneurons may be responsible for spasticity.

Generators and temporal succession of giant somatosensory evoked potentials in cortical reflex myoclonus: epicortical recording from sensorimotor cortex.

OBJECTIVE: To clarify the generator mechanism of giant somatosensory evoked potentials (giant SEPs) and the hyperexcitability of primary somatosensory and motor cortices (SI and MI). METHODS: In a patient with intractable focal seizures manifesting cortical reflex myoclonus of the left foot, giant SEPs to left tibial nerve stimulation were epicortically recorded as a part of presurgical evaluation with subdural electrodes. RESULTS: In the single pulse SEPs, enlarged P1-N1 components were observed at the foot area of the SI and MI (86.5-258.8 microV, respectively), and the peak latencies were always shorter at SI than at MI by 6 ms. Similar findings were obtained for peroneal and sural nerve stimulation. In the paired pulse SEPs, the second response was less suppressed, as compared to other interstimulus intervals (ISIs), with ISIs of 40 and 200 ms both at SI and MI. CONCLUSIONS: In this particular patient, cortical hyperexcitability to somatosensory stimuli seems to originate from SI but subsequently both SI and MI are responsible for the generation of giant SEPs and cortical reflex myoclonus. SIGNIFICANCE: Somatosensory and primary motor cortices both generated enhanced early cortical components of SEPs, most likely by enhancing the latter by the former.

Topography of spinal neurons active during hindlimb withdrawal reflexes in the decerebrate cat.

There exists a spatial organization of receptive fields and a modular organization of the flexion withdrawal reflex system. However, the three dimensional location and organization of interneurons interposed in flexion reflex pathways has not been systematically examined. We determined the anatomical locations of spinal neurons involved in the hindlimb flexion withdrawal reflex using expression of the immediate early gene c-fos and the corresponding FOS protein. The flexion withdrawal reflex was evoked in decerebrate cats via stimulation of the tibial or superficial peroneal nerve. Animals that received stimulation had significantly larger numbers of cells expressing FOS-like immunoreactivity (42.7+/-2.3 cells/section, mean+/-standard error of the mean) than operated unstimulated controls (18.6+/-1.4 cells/section). Compared with controls, cells expressing FOS-like immunoreactivity were located predominantly on the ipsilateral side, in laminae IV-VI, at L6 and rostral L7 segments, and between 20% and 60% of the distance from the midline to the lateral border of the ventral gray matter. Labeled neurons resulting from tibial nerve stimulation were medial to neurons labeled following superficial peroneal nerve stimulation in laminae I-VI, but not VII. The mean mediolateral positions of labeled neurons from both nerves shifted medially as the transverse plane in which they were viewed was moved from rostral to caudal and as the coronal plane in which they were viewed was moved from dorsal to ventral. The mediolateral separation between populations of labeled cells was consistent with primary afferent projections and the location of reflex encoders. This topographical segregation corresponding to different afferent inputs is a possible anatomical substrate for a modular organization of the flexion withdrawal reflex system.

Predictive model of muscle fatigue after spinal cord injury in humans.

The fatigability of paralyzed muscle limits its ability to deliver physiological loads to paralyzed extremities during repetitive electrical stimulation. The purposes of this study were to determine the reliability of measuring paralyzed muscle fatigue and to develop a model to predict the temporal changes in muscle fatigue that occur after spinal cord injury (SCI). Thirty-four subjects underwent soleus fatigue testing with a modified Burke electrical stimulation fatigue protocol. The between-day reliability of this protocol was high (intraclass correlation, 0.96). We fit the fatigue index (FI) data to a quadratic-linear segmental polynomial model. FI declined rapidly (0.3854 per year) for the first 1.7 years, and more slowly (0.01 per year) thereafter. The rapid decline of FI immediately after SCI implies that a "window of opportunity" exists for the clinician if the goal is to prevent these changes. Understanding the timing of change in muscle endurance properties (and, therefore, load-generating capacity) after SCI may assist clinicians when developing therapeutic interventions to maintain musculoskeletal integrity.

Evaluation of Na+/K+ pump function following repetitive activity in mouse peripheral nerve.

After conduction of prolonged trains of impulses the increased Na+/K+ pump activity leads to hyperpolarization. The aim of this study was to develop a mouse model to investigate the Na+/K+ pump function in peripheral nerve by measuring the decrease in excitability during activity-dependent hyperpolarization. Acute electrophysiological investigations were carried out in seven adult mice. Nerve excitability was evaluated by tracking the change in threshold current after 5 min of 100 Hz stimulation of the tibial nerve at ankle. We developed a threshold tracking system that allowed us to follow several excitability measures simultaneously from the evoked plantar compound muscle action potential (CMAP) and sciatic compound nerve action potential (CNAP). Three minutes after repetitive supramaximal stimulation maximal CMAP and CNAP amplitudes recovered but the threshold was increased approximately 40% for motor axons approximately 34% for axons generating CNAP. The threshold recovered with a rate of 3.8%/minute that was similar for nerve and motor responses. By tracking the effect of polarizing currents we found evidence of activity dependent hyperpolarization, and our data suggest that the observed threshold change after repetitive stimulation of the mouse tibial nerve is an indicator of the Na+/K+ pump function in vivo. Evaluation of activity-dependent hyperpolarization may be an important indicator of axonal ability to cope with Na+ load.

Effects of irradiation on nerve graft vasculature.

Increasing doses of therapeutic irradiation are known to impair nerve regeneration after grafting. One possible factor is the effect of irradiation on the endoneurial vasculature. This study investigates the effects of postoperative irradiation on the size, number, and cross-sectional area of endoneurial vessels in the rat posterior tibial nerve graft model. Sixty-five Sprague-Dawley rats underwent 1.5-cm interposition grafts to the tibial nerve. Postoperatively, they were assigned to one of five groups. The animals in Group 1 were unirradiated controls. Groups 2 to 5 received postoperative irradiation in the amounts of 46, 66, 86, and 106 Gy, respectively. One hundred and twenty days after grafting, sections of the proximal, grafted, and distal nerve were harvested and analyzed with digital morphometry. Statistical analysis of the average vessel area, number of vessels, and total vascular area was performed. The grafted segments of Groups 4 and 5 and the distal segments of all irradiated groups showed a statistically significant decrease in the number of vessels, compared to controls. The average size of the vessel was smaller in the proximal segment of the irradiated groups, compared to controls. There was no difference in size in either the grafted or distal segments of the irradiated groups, compared to controls. The observed changes in the endoneurial vasculature resulted from both the action of regeneration and the effects of irradiation. The irradiation effects appear to be dose-dependent.

A new approach to estimation of the number of central synapse(s) included in the H-reflex.

BACKGROUND: Among the main clinical applications of the H-reflex are the evaluation of the S1 nerve root conductivity such as radiculopathy and measurement of the excitability of the spinal motoneurons in neurological conditions. An attempt has been made to reduce the pathway over which H-reflex can be obtained in a hope to localize a lesion to the S1 nerve root, so the S1 central loop has been suggested. The main goal of this study is the estimation of the H-reflex number of synapse(s) for better understanding of the physiology of this practical reflex. METHODS: Forty healthy adult volunteers (22 males, 18 females) with the mean age of (37.7 +/- 10.2) years participated in this study. They were positioned comfortably in the prone position, with their feet off the edge of the plinth. Recording electrodes were positioned at the mid point of a line connecting the mid popliteal crease to the proximal flare of the medial malleolus. Stimulation was applied at the tibial nerve in the popliteal fossa and H, F and M waves were recorded. Without any change in the location of the recording electrodes, a monopolar needle was inserted as cathode at a point 1 cm medial to the posterior superior iliac spine, perpendicular to the frontal plane. The anode electrode was placed over the anterior superior iliac spine, and then M and H waves of the central loop were recorded. After processing the data, sacral cord conduction delay was determined by this formula: sacral cord conduction delay = central loop of H-reflex - (delays of the proximal motor and sensory fibers in the central loop). RESULTS: The central loop of H-reflex was (6.77 +/- 0.28) msec and the sacral cord conduction delay was (1.09 +/- 0.06) msec. CONCLUSION: The sacral cord conduction time was estimated to be about 1.09 msec in this study and because at least 1 msec is required to transmit the signal across the synapse between the sensory ending and the motor cell, so this estimated time was sufficient for only one central synapse in this reflex.

Multimodal electrophysiologic follow-up study in 3 mutated but presymptomatic members of a spinocerebellar ataxia type 1 (SCA1) family.

The objective was to determine the progression of nervous system involvement in spinocerebellar ataxia type 1 (SCA1). Three presymptomatic members of an Italian SCA1 family underwent molecular analysis and showed the SCA1 mutation. They were defined as "at risk/mutated" individuals. A clinical and electrophysiologic 7-9 year follow-up was performed. The Inherited Ataxia Progression Scale was used for clinical staging. Sensory and motor conduction velocities, somatosensory evoked potentials and transcranial magnetic stimulation were performed at least three times in each subject. Clinical examination showed the early corticospinal pathway involvement. Electrophysiologic investigations confirmed that at the asymptomatic stage only magnetic motor cortex stimulation was abnormal and rapidly worsened with time. Somatosensory pathway studies showed a later involvement and a light sensory-motor neuropathy was the last electrophysiologic abnormality to be recognised. These data confirm that SCA1 phenotype is characterised by early and prevalent pyramidal tract involvement and that peripheral neuropathy is a late and moderate complication.

Inhibition from the plantar nerve to soleus muscle during the stance phase of walking.

The purpose of this study is to investigate the effect and the circuit from the branch of tibial (plantar) nerve to soleus muscle and its modulation during walking in humans. Stimulation of the plantar nerve produced short latency inhibition of soleus EMG activity and the H-reflex in humans. The threshold of afferent fibers was lower than that of motor fibers. This inhibition did not converge to disynaptic reciprocal Ia inhibition nor did inhibition from the cutaneous nerve of the big toe, but to Ib inhibition from the medial gastrocnemius nerve. The inhibitory pathway from the plantar nerve therefore is considered to include Ib inhibitory interneurones. Modulation of the inhibition was investigated during walking. Less EMG depression after plantar nerve stimulation occurred in the stance phase of walking than for tonic or dynamic plantar flexion at similar background EMG activity level. The inhibition of the soleus H-reflex after plantar nerve stimulation was also decreased during the stance phase. For investigating the influence of load on the inhibition from the plantar nerve, more EMG depression occurred in the stance phase with body unloading. Similar findings were observed in Ib inhibition from the medial gastrocnemius nerve, but not in disynaptic reciprocal Ia inhibition to soleus muscle. It is concluded that transmission of inhibition from the plantar nerve to soleus muscle is modulated during walking. It would minimize this inhibition during the stance phase of walking and might enhance soleus muscle activity via this reflex pathway for the support of weight.

Interlimb reflex activity after spinal cord injury in man: strengthening response patterns are consistent with ongoing synaptic plasticity.

OBJECTIVE: Previous reports from our laboratory have described short-latency contractions in muscles of the distal upper limb following stimulation of lower limb nerves or skin in persons with injury to the cervical spinal cord. It takes 6 or more months for interlimb reflexes (ILR) to appear following acute spinal cord injury (SCI), suggesting they might be due to new synaptic interconnections between lower limb sensory afferents and motoneurons in the cervical enlargement. In this study, we asked if once formed, the strength of these synaptic connections increased over time, a finding that would be consistent with the above hypothesis. METHODS: We studied persons with sub-acute and/or chronic cervical SCI. ILR were elicited by brief trains of electrical pulses applied to the skin overlying the tibial nerve at the back of the knee. Responses were quantified based on their presence or absence in different upper limb muscles. We also generated peri-stimulus time histograms for single motor unit response latency, probability, and peak duration. Comparisons of these parameters were made in subjects at sub-acute versus chronic stages post-injury. RESULTS: In persons with sub-acute SCI, the probability of seeing ILR in a given muscle of the forearm or hand was low at first, but increased substantially over the next 1-2 years. Motor unit responses at this sub-acute stage had a prolonged and variable latency, with a lower absolute response probability, compared to findings from subjects with chronic (i.e. stable) SCI. CONCLUSIONS: Our findings demonstrate that interlimb reflex activity, once established after SCI, shows signs of strengthening synaptic contacts between afferent and efferent components, consistent with ongoing synaptic plasticity. SIGNIFICANCE: Neurons within the adult human spinal cord caudal to a lesion site are not static, but appear to be capable of developing novel-yet highly efficacious-synaptic contacts following trauma-induced partial denervation. In this case, such contacts between ascending afferents and cervical motoneurons do not appear to provide any functional benefit to the subject. In fact their presence may limit the regenerative effort of supraspinal pathways which originally innervated these motoneurons, should effort in animal models to promote regeneration across the lesion epicenter be successfully translated to humans with chronic SCI.