Introduction The Hoffmann reflex (H reflex) is one of the most studied reflexes in human neurophysiological literature. Detection of the H reflex is useful in the diagnosis of early polyneuropathy, S1 radiculopathy, early GBS, tibial neuropathy and sciatica, and sacral plexopathy. The H reflex is also used as a tool to measure the excitability of the nervous components of the arc, regardless of the sensitivity of the sensory organs. The monosynaptic nature of reflex circuits makes H-reflex an attractive tool for clinical neurophysiology and research. Objective The objective is to create reference data of soleus H-reflex latency in an adult population from a tertiary care center in India. Materials and methods Seven hundred eighty-four healthy volunteers underwent a physical examination and brief electrophysiological examination before elicitation of the soleus H reflex of both lower extremities using standard techniques. Reference values ​​are expressed as mean ± standard deviation as well as the third and 97th percentiles for latency as the dependent variable. Results The study population included 346 (44.1%) women and 438 (55.9%) men. The men were aged 40.46 ± 14.76 years, and the women were aged 41.63 ± 13.49 years. The average weight of the men was 73.32 ± 10.28 kilograms, and the women were 62.91 ± 7.46 kilograms. The average height of the men was 172.06 ± 4.22 cm, and the women were 159.12 ± 2.42 cm. The third and 97th percentiles for H-reflex latency on the right side were 22.86 ms to 34.22 ms and on the left side were 22.86 ms to 35.39 ms. The average right tibial H latency and left tibial H latency were 28.18 ± 2.59 ms and 28.14 ± 2.70 ms, respectively. Conclusion A sizable subject population was used to provide reference data for this study. Because of the huge sample size and nearly appropriate coverage of different age groups, reference ranges have been established for various age, height, and BMI groups.

OBJECTIVE: Motor neuron pool activity is high in spasticity. The effect of inhibitory kinesiotaping (KT) on spasticity is unclear. The aim of this study is to investigate the effect of inhibitory KT on spasticity after stroke.
METHODS: Fifty stroke patients with ankle plantarflexor spasticity were randomised to intervention (27) and control (23) groups. Inhibitory KT was applied to the triceps surae muscle in the intervention group and sham KT to the Achilles tendon in the control group. Inhibitory and sham KT were applied for 72 h with a combined conventional rehabilitation programme. Spasticity was assessed at baseline and 72 h after KT using three instruments: Modified Ashworth Scale (MAS), Homosynaptic Post-Activation Depression (HPAD) reflecting the level of motor neuron pool activity, and joint torque as a measure of resistance to passive ankle dorsiflexion.
RESULTS: The baseline MAS score, HPAD levels and dorsiflexion torque of the two groups were not significantly different. The change in MAS score was -3.7 ± 17.5 (p = 0.180) in the intervention group and 3.6 ± 33.3 (p = 0.655) in the control group. The change in dorsiflexion torque was -0.3 ± 16.1 kg m (p = 0.539) in the intervention group and 8.0 ± 24.1 kg m (p = 0.167) in the control group. The change in mean HPAD was 8.7 ± 34.7 (p = 0.911) in the intervention group and 10.1 ± 41.6 (p = 0.609) in the control group.
CONCLUSIONS: The present study showed that inhibitory KT has no antispastic effect in stroke patients.

Considering the growing interest in clinical applications of neuromodulation, assessing effects of various modulatory approaches is increasingly important. Monosynaptic spinal reflexes undergo depression following repeated activation, offering a means to quantify neuromodulatory influences. Following spinal cord injury (SCI), changes in reflex modulation are associated with spasticity and impaired motor control. To assess disrupted reflex modulation, low-frequency depression (LFD) of Hoffman (H)-reflex excitability is examined, wherein the amplitudes of conditioned reflexes are compared to an unconditioned control reflex. Alternatively, some studies utilize paired-pulse depression (PPD) in place of the extended LFD train. While both protocols induce similar amounts of H-reflex depression in neurologically intact individuals, this may not be the case for persons with neuropathology. We compared the H-reflex depression elicited by PPD and by trains of 3-10 pulses to an 11-pulse LFD protocol in persons with incomplete SCI. The amount of depression produced by PPD was less than an 11-pulse train (mean difference = 0.137). When compared to the 11-pulse train, the 5-pulse train had a Pearson\'s correlation coefficient (R) of 0.905 and a coefficient of determination (R2) of 0.818. Therefore, a 5-pulse train for assessing LFD elicits modulation similar to the 11-pulse train and thus we recommend its use in lieu of longer trains.

Evaluating reciprocal inhibition of the thigh muscles is important to investigate the neural circuits of locomotor behaviors. However, measurements of reciprocal inhibition of thigh muscles using spinal reflex, such as H-reflex, have never been systematically established owing to methodological limitations. The present study aimed to clarify the existence of reciprocal inhibition in the thigh muscles using transcutaneous spinal cord stimulation (tSCS). Twenty able-bodied male individuals were enrolled. We evoked spinal reflex from the biceps femoris muscle (BF) by tSCS on the lumber posterior root. We examined whether the tSCS-evoked BF reflex was reciprocally inhibited by the following conditionings: (1) single-pulse electrical stimulation on the femoral nerve innervating the rectus femoris muscle (RF) at various inter-stimulus intervals in the resting condition; (2) voluntary contraction of the RF; and (3) vibration stimulus on the RF. The BF reflex was significantly inhibited when the conditioning electrical stimulation was delivered at 10 and 20 ms prior to tSCS, during voluntary contraction of the RF, and during vibration on the RF. These data suggested a piece of evidence of the existence of reciprocal inhibition from the RF to the BF muscle in humans and highlighted the utility of methods for evaluating reciprocal inhibition of the thigh muscles using tSCS.

Although recent studies in nonhuman primates have provided evidence that transcranial magnetic stimulation (TMS) activates cells within the reticular formation, it remains unclear whether descending brain stem projections contribute to the generation of TMS-induced motor evoked potentials (MEPs) in skeletal muscles. We compared MEPs in muscles with extensive direct corticomotoneuronal input (first dorsal interosseous) versus a prominent role in postural control (gastrocnemius) to determine whether the amplitudes of early and late MEPs were differentially modulated by cortical suppression. Suprathreshold TMS was applied with and without a preceding suprathreshold TMS pulse at two interstimulus intervals (50 and 80 ms). H reflexes in target muscles were also tested with and without TMS conditioning. Early and late gastrocnemius MEPs were differentially modulated by cortical inhibition, the amplitude of the early MEP being significantly reduced by cortical suppression and the late MEP facilitated. The amplitude of H reflexes in the gastrocnemius was reduced within the cortical silent period. Early MEPs in the first dorsal interosseous were also reduced during the silent period, but late MEPs were unaffected. Independent modulation of early and late MEPs in the gastrocnemius muscle supports the idea that the MEP is generated by multiple descending pathways. Suppression of the early MEP is consistent with transmission along the fast-conducting corticospinal tract, whereas facilitation of the late MEP suggests transmission along a corticofugal, potentially cortico-reticulospinal, pathway. Accordingly, differences in late MEP modulation between the first dorsal interosseous and gastrocnemius reflect an increased role of corticofugal pathways in the control of postural muscles.NEW & NOTEWORTHY Early and late portions of the response to transcranial magnetic stimulation (TMS) in a lower limb postural muscle are modulated independently by cortical suppression, late motor evoked potentials (MEPs) being facilitated during cortical inhibition. These results suggest a cortico-brain stem transmission pathway for late portions of the TMS-induced MEP.

Introduction Cerebral palsy (CP) is a neurodevelopmental condition that results from an injury to a developing brain. Children with CP fail to execute precise, well-coordinated movements, and excessive muscular co-contraction or co-activation is a prominent attribute of CP. The normal reciprocal relationship between agonists and antagonists during voluntary movements is altered in patients with CP. H-reflex, which is often regarded as the electrical equivalent of the spinal stretch reflex, can be used to examine the overall reflex arc, including the Ia sensory afferent strength and the spinal motoneuron excitability state. Furthermore, neuromodulatory influence of vibration on H-reflex has been found, which has been increasingly investigated to ascertain its potential use as an intervention in patients with increased spinal reflex excitability. Our goal was to identify the brain mechanism underlying the motor deficits by studying Soleus H-reflex changes during voluntary movement (dorsiflexion) and also to determine the role of vibration in H-reflex modulation in children with spastic CP. Methods Soleus H-reflex was recorded in 12 children with spastic CP (10-16 years) and 15 age-matched controls. Recordings were obtained at rest, during dorsiflexion, and during vibratory stimulation for each subject. H-responses (Hmax amplitudes and Hmax-to-Mmax ratio) were compared among the controls and the cases (CP), for the experiments performed, by the Wilcoxon signed-rank test. The recruitment curves depicting the distribution of mean H-response amplitudes with stimulus intensity increment, for dorsiflexion and vibration were compared among controls and cases by the two-sample Kolmogorov-Smirnov (KS) test. p-value <0.05 was considered as statistically significant. Results Hmax amplitudes and the Hmax-to-Mmax ratio increased (15 % and 12.2 % increment, respectively) from the resting values in the children with CP (p<0.05), while controls exhibited a decrease (reduction of 62% and 57 %, respectively) during dorsiflexion (p<0.05). Vibratory stimulation produced a decreasing trend in H-response measures in both the groups. There was about 15 % and 16 % reduction respectively among children with CP while that of 24 % and 21 % respectively among the controls. The differences in the recruitment curves (distribution of average H-response amplitudes with stimulation intensity) recorded during dorsiflexion and vibration experiments among controls compared with those with CP were found to be statistically significant by the two-sample KS test (p<0.0001). Conclusion The failure of H-reflex suppression during voluntary antagonist muscle activation suggests the presence of impaired reciprocal inhibition in spastic CP. The relatively modest H-response reduction caused by vibratory stimulation in children with CP provides limited evidence of vibratory regulation of the H-reflex in CP. More research into the mechanisms driving motor abnormalities in children with CP is needed, which could aid in therapy planning.

We are studying the mechanisms of H-reflex operant conditioning, a simple form of learning. Modelling studies in the literature and our previous data suggested that changes in the axon initial segment (AIS) might contribute. To explore this, we used blinded quantitative histological and immunohistochemical methods to study in adult rats the impact of H-reflex conditioning on the AIS of the spinal motoneuron that produces the reflex. Successful, but not unsuccessful, H-reflex up-conditioning was associated with greater AIS length and distance from soma; greater length correlated with greater H-reflex increase. Modelling studies in the literature suggest that these increases may increase motoneuron excitability, supporting the hypothesis that they may contribute to H-reflex increase. Up-conditioning did not affect AIS ankyrin G (AnkG) immunoreactivity (IR), p-p38 protein kinase IR, or GABAergic terminals. Successful, but not unsuccessful, H-reflex down-conditioning was associated with more GABAergic terminals on the AIS, weaker AnkG-IR, and stronger p-p38-IR. More GABAergic terminals and weaker AnkG-IR correlated with greater H-reflex decrease. These changes might potentially contribute to the positive shift in motoneuron firing threshold underlying H-reflex decrease; they are consistent with modelling suggesting that sodium channel change may be responsible. H-reflex down-conditioning did not affect AIS dimensions. This evidence that AIS plasticity is associated with and might contribute to H-reflex conditioning adds to evidence that motor learning involves both spinal and brain plasticity, and both neuronal and synaptic plasticity. AIS properties of spinal motoneurons are likely to reflect the combined influence of all the motor skills that share these motoneurons. KEY POINTS: Neuronal action potentials normally begin in the axon initial segment (AIS). AIS plasticity affects neuronal excitability in development and disease. Whether it does so in learning is unknown. Operant conditioning of a spinal reflex, a simple learning model, changes the rat spinal motoneuron AIS. Successful, but not unsuccessful, H-reflex up-conditioning is associated with greater AIS length and distance from soma. Successful, but not unsuccessful, down-conditioning is associated with more AIS GABAergic terminals, less ankyrin G, and more p-p38 protein kinase. The associations between AIS plasticity and successful H-reflex conditioning are consistent with those between AIS plasticity and functional changes in development and disease, and with those predicted by modelling studies in the literature. Motor learning changes neurons and synapses in spinal cord and brain. Because spinal motoneurons are the final common pathway for behaviour, their AIS properties probably reflect the combined impact of all the behaviours that use these motoneurons.

UNASSIGNED: Myofascial trigger points (MTrPs) are the main cause of myofascial pain syndrome (MPS), and patients with MPS also have symptoms of sympathetic abnormalities. Consequently, this study aimed to investigate the potential relationship between MTrPs and sympathetic nerves.
UNASSIGNED: Twenty-four seven-week-old male rats were randomly divided into four groups (six rats every group). Groups I and II were kept in normal condition (n=12), and groups III and IV underwent MTrPs modelling (n=12). After successful MTrPs modelling, differences in sympathetic outcomes between the MTrPs groups (III and IV) and non-MTrPs groups (I and II) were observed. Sympathetic blockade was then applied to groups III and I (n=12). Data were collected on peak inversion spontaneous potentials (PISPs) and the H-reflex-evoked electromyography during spontaneous discharge at the MTrPs before and after sympathetic blockade.
UNASSIGNED: Systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate were significantly higher in the MTrPs group than in the non-MTrPs group (P<0.05). Compared with group I, group III had the PISPs potential lower wave amplitude, shorter duration and amplitude-to-duration ratio, and lower H latency and latency difference H-M (P<0.05). Compared with group IV, group III had the PISPs potential lower wave amplitude, duration, amplitude-to-duration ratio, M-wave latency, H maximum wave amplitude, and maximal wave amplitude ratio H/M (P<0.05). The changes before and after sympathetic blockade in the MTrPs group were significant, and the amplitude, duration, and amplitude-to-duration ratio of the PISPs potentials were lower after the blockade (P<0.05).
UNASSIGNED: MTrPs and sympathetic nerves interact with each other forming a specific relationship. MTrPs sensitize sympathetic nerves, and sympathetic nerve abnormalities affect local muscle myoelectric hyperactivity, leading to MTrPs. This finding is instructive for the clinical management of sympathetic disorders.

Operant conditioning of neural activation has been researched for decades in humans and animals. Many theories suggest two parallel learning processes, implicit and explicit. The degree to which feedback affects these processes individually remains to be fully understood and may contribute to a large percentage of non-learners. Our goal is to determine the explicit decision-making processes in response to feedback representing an operant conditioning environment. We developed a simulated operant conditioning environment based on a feedback model of spinal reflex excitability, one of the simplest forms of neural operant conditioning. We isolated the perception of the feedback signal from self-regulation of an explicit unskilled visuomotor task, enabling us to quantitatively examine feedback strategy. Our hypothesis was that feedback type, biological variability, and reward threshold affect operant conditioning performance and operant strategy. Healthy individuals (N = 41) were instructed to play a web application game using keyboard inputs to rotate a virtual knob representative of an operant strategy. The goal was to align the knob with a hidden target. Participants were asked to \"down-condition\" the amplitude of the virtual feedback signal, which was achieved by placing the knob as close as possible to the hidden target. We varied feedback type (knowledge of performance, knowledge of results), biological variability (low, high), and reward threshold (easy, moderate, difficult) in a factorial design. Parameters were extracted from real operant conditioning data. Our main outcomes were the feedback signal amplitude (performance) and the mean change in dial position (operant strategy). We observed that performance was modulated by variability, while operant strategy was modulated by feedback type. These results show complex relations between fundamental feedback parameters and provide the principles for optimizing neural operant conditioning for non-responders.

This study investigates the effects of varying loading conditions on excitability in neural pathways and gait dynamics. We focussed on evaluating the magnitude of the Hoffman reflex (H-reflex), a neurophysiological measure representing the capability to activate motor neurons and the timing and placement of the foot during walking. We hypothesized that weight manipulation would alter H-reflex magnitude, footfall and lower body kinematics. Twenty healthy participants were recruited and subjected to various weight-loading conditions. The H-reflex, evoked by stimulating the tibial nerve, was assessed from the dominant leg during walking. Gait was evaluated under five conditions: body weight, 20% and 40% additional body weight, and 20% and 40% reduced body weight (via a harness). Participants walked barefoot on a treadmill under each condition, and the timing of electrical stimulation was set during the stance phase shortly after the heel strike. Results show that different weight-loading conditions significantly impact the timing and placement of the foot and gait stability. Weight reduction led to a 25% decrease in double limb support time and an 11% narrowing of step width, while weight addition resulted in an increase of 9% in step width compared to body weight condition. Furthermore, swing time variability was higher for both the extreme weight conditions, while the H-reflex reduced to about 45% between the extreme conditions. Finally, the H-reflex showed significant main effects on variability of both stance and swing phases, indicating that muscle-motor excitability might serve as feedback for enhanced regulation of gait dynamics under challenging conditions.