H-reflex Depression Research Articles

Neural interactions between transspinal evoked potentials and muscle spindle afferents in humans

The objective of this study was to establish neural interactions between transspinal evoked potentials (TEPs) and muscle spindle group Ia afferents in healthy humans. Soleus H-reflexes were assessed following transspinal stimulation at conditioning-test (C-T) intervals that ranged from negative to positive 100 ms. TEPs were recorded from the right and left ankle/knee flexor and extensor muscles, and their amplitude was assessed following stimulation of soleus muscle spindle group Ia afferents at similar C-T intervals. Transspinal conditioning stimulation produced a short-latency, long-lasting soleus H-reflex depression. Excitation of muscle spindle group Ia afferents produced depression of ipsilateral ankle TEPs and medium-latency facilitation of the ipsilateral knee TEPs. At specific C-T intervals, the soleus H-reflex and ipsilateral ankle TEPs were summated based on their relative onset and duration. No changes were observed in the contralateral TEPs. These effects were exerted at both peripheral and spinal levels. Both transspinal and muscle spindle group Ia afferent stimulation produce long-lasting depression of the soleus H-reflex and TEPs, respectively. Transspinal stimulation may promote targeted neuromodulation and can be utilized in upper motoneuron lesions to normalize spinal reflex hyper-excitability and alter excitation thresholds of peripheral nerve axons.

Impaired Ability to Suppress Excitability of Antagonist Motoneurons at Onset of Dorsiflexion in Adults with Cerebral Palsy.

We recently showed that impaired gait function in adults with cerebral palsy (CP) is associated with reduced rate of force development in ankle dorsiflexors. Here, we explore potential mechanisms. We investigated the suppression of antagonist excitability, calculated as the amount of soleus H-reflex depression at the onset of ankle dorsiflexion compared to rest, in 24 adults with CP (34.3 years, range 18–57; GMFCS 1.95, range 1–3) and 15 healthy, age-matched controls. Furthermore, the central common drive to dorsiflexor motoneurons during a static contraction in the two groups was examined by coherence analyses. The H-reflex was significantly reduced by 37% at the onset of dorsiflexion compared to rest in healthy adults (P < 0.001) but unchanged in adults with CP (P = 0.91). Also, the adults with CP had significantly less coherence. These findings suggest that the ability to suppress antagonist motoneuronal excitability at movement onset is impaired and that the central common drive during static contractions is reduced in adults with CP.

The Short-Term Effect of Slope Walking on Soleus H-Reflexes in People with Multiple Sclerosis

Downslope walking (DSW) causes H-reflex depression in healthy adults, and thus may hold promise for inducing spinal reflex plasticity in people with Multiple Sclerosis (PwMS). The study purpose was to test the hypothesis that DSW will cause acute depression of spinal excitability in PwMS. Soleus H-reflexes were measured in PwMS (n = 18) before and after 20 min of treadmill walking during three visits. Participants walked on a different slope each visit [level: 0% level walking (LW), upslope: +7.5% treadmill walking with an upslope (USW) or downslope: −7.5% (DSW)]. The soleus Hmax/Mmax ratio was used to measure spinal excitability. Heart rate and ratings of perceived exertion (RPE) were measured during walking. DSW induced the largest change in spinal excitability (a 26.7% reduction in soleus Hmax/Mmax (p = 0.001)), although LW also reduced Hmax/Mmax (-5.3%, p = 0.05). Heart rate (p < 0.001) was lowest for DSW, and RPE for DSW did not exceed “Fairly light”. DSW evokes short-term spinal plasticity in PwMS, while requiring no greater effort than LW. Our results suggest that PwMS retain the capacity for DSW-induced short-term spinal reflex modulation previously found in healthy adults. These results may provide a foundation for further investigation of long-term effects of DSW on spinal reflex plasticity and functional ability in PwMS.

Acute whole-body vibration increases reciprocal inhibition

Based on previous evidence that whole-body vibration (WBV) affects pathways involved in disynaptic reciprocal inhibition (DRI), the present hypothesis-driven experiment aimed to assess the acute effects of WBV on DRI and co-contraction. DRI from ankle dorsiflexors to plantar flexors was investigated during submaximal dorsiflexion before and after 1 min of WBV. With electromyography, musculus soleus (SOL) H-reflex depression following a conditioning stimulation of the peroneal nerve (1.1x motor threshold for the musculus tibialis anterior, TA) was assessed and co-contraction was calculated. After WBV, DRI was significantly increased (+4%, p < 0.05). SOL (−13%, p < 0.05) and TA (−6%, p < 0.05) activities were significantly reduced; co-contraction tended to be diminished (−8%, p = 0.05). Dorsiflexion torque remained unchanged. After WBV, DRI increased during submaximal isometric contraction in healthy subjects. The simultaneous SOL relaxation and TA contraction indicate that a more economic movement execution is of functional significance for WBV application in clinical and athletic treatment.

Transient Increase in Cortical Excitability Following Static Stretching of Plantar Flexor Muscles.

Spinal excitability in humans is inhibited by both passively holding a static position with the muscle lengthened (static stretching) and by a single non-active lengthening movement. However, whilst immediately after a passive lengthening movement the inhibition persists for several seconds, there seem to be an immediate recovery following static stretching. This result is counter intuitive and could be attributed to methodological procedures. Indeed, differently to what has been done until now, in order to study whether static stretching has a transient effect on the neuromuscular pathway, the procedure should be repeated many times and measurements collected at different time points after stretching. In the present study we repeated 60 times 30 s static stretching of ankle plantar flexors and measured tap reflex (T-reflex), Hoffman reflex (H-reflex), and motor evoked potentials (MEPs) from the Soleus muscle at several time points, starting from immediately after until 30 s following the procedure. T-reflex was strongly inhibited (range 31–91%, p = 0.005) and the inhibition persisted for 30 s showing a slow recovery (r = 0.541, p = 0.037). H-reflex was not affected by the procedure. Stretching increased the size of the MEPs (p < 0.0001), differences at times 0 and 2 s after stretching (p = 0.015 and p = 0.047, respectively). These results confirm that static stretching reduces muscle spindle sensitivity. Moreover it is suggested that post-activation depression of Ia afferents, which is commonly considered the cause of H-reflex depression during both dorsiflexion and static stretching, vanished immediately following stretching or is counteracted by an increased corticospinal excitability.

Changes in H-Reflex Recruitment After Trans-Spinal Direct Current Stimulation With Multiple Electrode Configurations.

Trans-spinal direct current stimulation (tsDCS) is an electro-modulatory tool with possible application in the rehabilitation of spinal cord injury. TsDCS generates a small electric field, aiming to induce lasting, functional neuromodulation in the targeted neuronal networks. Earlier studies have shown significant modulatory effects after application of lumbar tsDCS. However, for clinical application, a better understanding of application specific factors is required. Our goal was to investigate the effect of different electrode configurations using lumbar spinal tsDCS on spinal excitability. We applied tsDCS (2.5 mA, 15 min) in 10 healthy subjects with three different electrode configurations: (1) Anode and cathode placed over vertebra T11, and the posterior left shoulder respectively (LSC-S) (one polarity), and (2) Both electrodes placed in equal distance (ED) (7 cm) above and below vertebra T11, investigated for two polarities (ED-Anodal/Cathodal). The soleus H-Reflex is measured before, during and after tsDCS in either electrode configuration or a sham condition. To account for genetic predispositions in response to direct current stimulation, subject BDNF genotype was assessed. Stimulation in configuration ED-Cathodal induced an amplitude reduction of the H-reflex, 30 min after tsDCS with respect to baseline, whereas none of the other configurations led to significant post intervention effects. BDNF genotype did not correlate with post intervention effects. Furthermore, we failed to replicate effects shown by a previous study, which highlights the need for a better understanding of methodological and subject specific influences on tsDCS outcome. The H-reflex depression after tsDCS (Config. ED-Cathodal) provides new insights and may foster our understanding of the working mechanism of tsDCS.

The H-Reflex as a Biomarker for Spinal Disinhibition in Painful Diabetic Neuropathy.

Neuropathic pain may arise from multiple mechanisms and locations. Efficacy of current treatments for painful diabetic neuropathy is limited to an unpredictable subset of patients, possibly reflecting diversity of pain generator mechanisms, and there is a lack of targeted treatments for individual patients. This review summarizes preclinical evidence supporting a role for spinal disinhibition in painful diabetic neuropathy, the physiology and pharmacology of rate-dependent depression (RDD) of the spinal H-reflex and the translational potential of using RDD as a biomarker of spinally mediated pain. Impaired RDD occurs in animal models of diabetes and was also detected in diabetic patients with painful vs painless neuropathy. RDD status can be determined using standard neurophysiological equipment. Loss of RDD may provide a clinical biomarker of spinal disinhibition, thereby enabling a personalized medicine approach to selection of current treatment options and enrichment of future clinical trial populations.

Vibration training after chronic spinal cord injury: Evidence for persistent segmental plasticity

H-reflex paired-pulse depression is gradually lost within the first year post-SCI, a process believed to reflect reorganization of segmental interneurons after the loss of normal descending (cortical) inhibition. This reorganization co-varies in time with the development of involuntary spasms and spasticity. The purpose of this study is to determine whether long-term vibration training may initiate the return of H-reflex paired-pulse depression in individuals with chronic, complete SCI. Five men with SCI received twice-weekly vibration training (30Hz, 0.6g) to one lower limb while seated in a wheelchair. The contra-lateral limb served as a within-subject control. Paired-pulse H-reflexes were obtained before, during, and after a session of vibration. Untrained limb H-reflex depression values were comparable to chronic SCI values from previous reports. In contrast, the trained limbs of all 5 participants showed depression values that were within the range of previously-reported Acute SCI and Non-SCI H-reflex depression. The average difference between limbs was 34.98% (p=0.016). This evidence for the return of H-reflex depression suggests that even for people with long-standing SCI, plasticity persists in segmental reflex pathways. The spinal networks involved with the clinical manifestation of spasticity may thus retain adaptive plasticity after long-term SCI. The results of this study indicate that vibration training may hold promise as an anti-spasticity rehabilitation intervention.

Characterization of Involuntary Contractions after Spinal Cord Injury Reveals Associations between Physiological and Self-Reported Measures of Spasticity.

Correlations between physiological, clinical and self-reported assessments of spasticity are often weak. Our aims were to quantify functional, self-reported and physiological indices of spasticity in individuals with thoracic spinal cord injury (SCI; 3 women, 9 men; 19–52 years), and to compare the strength and direction of associations between these measures. The functional measure we introduced involved recording involuntary electromyographic activity during a transfer from wheelchair to bed which is a daily task necessary for function. High soleus (SL) and tibialis anterior (TA) F-wave/M-wave area ratios were the only physiological measures that distinguished injured participants from the uninjured (6 women, 13 men, 19–67 years). Hyporeflexia (decreased SL H/M ratio) was unexpectedly present in older participants after injury. During transfers, the duration and intensity of involuntary electromyographic activity varied across muscles and participants, but coactivity was common. Wide inter-participant variability was seen for self-reported spasm frequency, severity, pain and interference with function, as well as tone (resistance to imposed joint movement). Our recordings of involuntary electromyographic activity during transfers provided evidence of significant associations between physiological and self-reported measures of spasticity. Reduced low frequency H-reflex depression in SL and high F-wave/M-wave area ratios in TA, physiological indicators of reduced inhibition and greater motoneuron excitability, respectively, were associated with long duration SL and biceps femoris (BF) electromyographic activity during transfers. In turn, participants reported high spasm frequency when transfers involved short duration TA EMG, decreased co-activation between SL and TA, as well as between rectus femoris (RF) vs. BF. Thus, the duration of muscle activity and/or the time of agonist-antagonist muscle coactivity may be used by injured individuals to count spasms. Intense electromyographic activity and high tone related closely (possibly from joint stabilization), while intense electromyographic activity in one muscle of an agonist-antagonist pair (especially in TA vs. SL, and RF vs. BF) likely induced joint movement and was associated with severe spasms. These data support the idea that individuals with SCI describe their spasticity by both the duration and intensity of involuntary agonist-antagonist muscle coactivity during everyday tasks.

Modulation of H-Reflex Depression with Paired-Pulse Stimulation in Healthy Active Humans.

Depression of the Hoffman reflex (H-reflex) is used to examine spinal control mechanisms during exercise, fatigue, and vibration and in response to training. H-reflex depression protocols frequently use trains of stimuli; this is time-consuming and prevents instantaneous assessment of motor neuronal excitability. The purpose of this study was to determine if paired-pulse H-reflex depression is reproducible and whether paired-pulse stimulation adequately estimates the depression induced by the more traditional ten-pulse train. H-reflexes were elicited via ten-pulse trains at 0.1, 0.2, 1, 2, and 5 Hz in ten neurologically intact individuals on two separate days. We measured the depression elicited by the second pulse (H2) and the mean depression elicited by pulses 2–10 (Hmean). H2 was consistent at all frequencies on both days (r2 = 0.97, p < 0.05, and ICC(3,1) = 0.81). H2 did not differ from Hmean (p > 0.05). The results indicate that paired-pulse H-reflex depression has high between-day reliability and yields depression estimates that are comparable to those obtained via ten-pulse trains. Paired-pulse H-reflex depression may be especially useful for studies that require rapid assessment of motor neuronal excitability, such as during exercise, fatigue, and vibration, or to establish recovery curves following inhibition.

Walking duration and slope steepness determine the effect of downslope walking on the soleus H-reflex pathway

The purpose of this study was to determine if the effect of downslope walking (DSW) on spinal excitability depends on walking duration and slope steepness, and if findings from the soleus (Sol) generalize to the tibialis anterior (TA). Sol and TA Hmax and Mmax were measured before and after four DSW doses (time/slope, min/%) on separate days (10/-15, 20/-15, 10/-25, 20/-25, n=14), and one 20-min bout of level walking (LW, n=12), always at 2.5 mph. Heart rate (HR) and ratings of perceived exertion (RPE) were measured during walking. DSW for all doses except 10/-15 caused greater Sol Hmax/Mmax depression than LW (p≤0.02), and 20/-25 caused greater Hmax/Mmax depression than 10/-15 (p≤0.01). TA H-reflex curves were substantially smaller than Sol H-reflex curves, and this study was unable to detect an effect of LW or DSW on TA Hmax/Mmax. Although HR and RPE were significantly higher during DSW at −25% than at −15% slope, group HR and RPE nevertheless peaked at relatively low values of 101.4±14.2 bpm and 12.6±2.3, respectively. In conclusion, DSW duration and slope steepness interact to determine the magnitude of Sol H-reflex depression, but these effects do not generalize to the TA.

Dynamic Fatigue Does Not Alter Soleus H-Reflexes Conditioned by Homonymous or Heteronymous Pathways.

H-reflex depression (diminution of amplitude after a conditioning stimulus) is mediated presynaptically and therefore can help distinguish central versus peripheral mechanisms of fatigue. We examined the effects of a dynamic exercise protocol on H-reflex depression using two conditioning methods: homonymous conditioning (paired-pulse tibial nerve stimulation); and heteronymous conditioning (common peroneal nerve stimulation). Ten subjects performed dynamic contractions of the soleus muscle through 30° ankle range of motion. The concentric phase required a target force of 10% of maximum voluntary isometric contraction (MVIC) and the eccentric phase force target was 80% MVIC. Fatigue persisted for >20 min after cessation of the exercise. Compared with prefatigue values, the dynamic fatigue protocol did not increase presynaptic inhibition after either homonymous or heteronymous conditioning. Peak to peak amplitude of unconditioned H-reflexes was likewise unchanged despite a long term depression of muscle force (long duration fatigue). These results suggest that persistent fatigue after dynamic exercise is attributed to muscle changes and not altered spinal mechanisms.

Plastic changes in spinal synaptic transmission following botulinum toxin A in post-stroke spastic patients

The therapeutic effects of intramuscular injections of botulinum toxin-type A on spasticity can be largely explained by its blocking action at the neuromuscular junction. BTx-A is assumed also to have a central action by affecting the functional organization of the CNS. The objective was to assess its action on spinal motor networks by investigating the post-activation depression (post-AD) of the soleus H-reflex in post-stroke patients. Post-AD that is a presynaptic mechanism controlling the synaptic efficacy of Ia-motoneuron transmission is involved in the pathophysiology of spasticity. Eight chronic hemiplegic post-stroke patients presenting lower limb spasticity and requiring BTx-A injection in ankle extensor muscle. Post-AD of soleus H-reflex assessed as frequency-related depression of H-reflex was investigated before and 3, 6 and 12 weeks after BTx-A injections in triceps surae. Post-AD was quantified as the ratio between H-reflex amplitude at 0.5 Hz and at 0.1 Hz. Post-AD of soleus H-reflex, which is reduced on the paretic leg, was affected 3 weeks after BTx-A injection. Depending on the residual motor capacity of the post-stroke patients, post-AD was either restored in patients with preserved voluntary motor control or further reduced in patients with no residual voluntary control. Botulinum toxin treatment induces synaptic plasticity at the Ia-motoneuron synapse in post-stroke paretic patients, which suggests that the effectiveness of BTx-A in post-stroke rehabilitation might be partly due to its central effects.

Restoration of post-activation depression of the H-reflex by treadmill exercise in aged rats

The purpose of this study was to evaluate the effects of aging and chronic physical activity on the postactivation depression of the Hoffman reflex (H-reflex). The maximal amplitude H wave/maximal amplitude M wave ratio was measured, and the rate-sensitive depression of the H-reflex was assessed. Measurements were performed on sedentary rats aged of 3, 6, 12, and 20 months and on animals aged of 12 and 20 months performing an incremental treadmill exercise protocol during the last eight weeks preceding the recordings. At the end of the experiment, the muscle mass and/or body mass ratio was calculated. Results indicated that the H-reflex depression of the tibialis anterior and soleus muscles were present until age of 6 and 12 months, respectively. For the tibialis anterior muscle, results also pointed out a decrease in the relative muscle mass with age and that the exercise allowed to restore the rate-sensitive depression of the H-reflex and to increase the relative muscle mass in comparison with sedentary animals. These findings clearly demonstrate that neural alteration of the spinal cord is prevented by activity in aged rats.

Cholecalciferol (vitamin D3) improves functional recovery when delivered during the acute phase after a spinal cord trauma

In a previous study, based on a rat model of thoracic spinal cord compression, we demonstrated that cholecalciferol (Vitamin D3), delivered at the dose of 200IU/kg/day, significantly improved ventilatory frequency and spasticity. In order to confirm the restorative potential of vitamin D, we performed a new study, using a rat model of left cervical hemisection (C2). From Day 1 or Day 7, animals received, during three months, a weekly oral bolus of either cholecalciferol, at the dose of 500IU/kg/day, or vehicle, namely triglycerides. Rats were assessed every month, using a ladder test for sensori-locomotor ability and neuromuscular capacity. Three months after injury, H-reflex was recorded from left extensor digitorum muscle in order to measure the reflexivity of the sub-lesional region. Ventilatory frequency was also monitored during an electrically induced muscle fatigue of the hindlimb known to enhance muscle metaboreflex and increase respiratory rate. After recording the phrenic nerve activity, ipsilateral to the lesion, during spontaneous breathing, animals were artificially ventilated while paralyzed with a neuromuscular blocking agent and then the brainstem respiratory centres were provoked to maximal output by temporarily stopping the ventilator. Spinal cords were immunostained with an anti-neurofilament antibody to evaluate axon numbers. We show here that vitamin D-treated animals display i) an enhanced locomotor activity, ii) an improved breathing when hindlimb muscle was electrically stimulated to induce fatigue, iii) an H-reflex depression similar to control animals, iv) a phrenic nerve activity response to a temporary asphyxial stress and v) a non significant decreased number of axons in the proximal stump when compared with the Sham group. This new set of data confirms that vitamin D is a potent molecule that could be tested in clinical trials assessing functional recovery in para-/tetra-plegic patients, shortly after a trauma.

Phase-dependent modulation of soleus H-reflex and post-activation depression during elliptical trainer and treadmill walking in humans

Phase-dependent modulation of soleus H-reflex and post-activation depression during elliptical trainer and treadmill walking in humans

Post-activation Depression Is Modulated By Electrical Stimulation Frequency In Individuals With Spinal Cord Injury

People with chronic spinal cord injury (SCI) lose the ability to suppress the H-reflex when it is elicited repetitively, a process known as post-activation depression. The loss of H-reflex depression is believed to be one adaptation that contributes to spasticity. Electrical stimulation of paralyzed muscle has many known benefits including reducing spasticity; however, the mechanism that causes changes in muscle spasticity has not been clearly delineated. In this study we examine the mechanism, post-activation depression, after electrical stimulation of paralyzed muscles. Importantly, we assess whether frequency of neuromuscular electrical stimulation (NMES) affects post-activation depression. PURPOSE: To determine the effect of 1-Hz and 5-Hz NMES on post-activation depression in individuals with complete quadriplegia and paraplegia. METHODS: Nine individuals with SCI (5 quadriplegics & 4 paraplegics) participated in this study. Each participant received 1-Hz and 5-Hz NMES on two different days. NMES was applied to the bilateral quadriceps and hamstring muscles for 20 minutes at an intensity of 50% of maximum. Soleus H reflex was elicited by doublets before, 0 min, 10 min, and 30 min after NMES. Repeated measures ANOVAs were used to compare differences across 2 protocols, 4 time points, and 2 groups. RESULTS: The amplitude of the first H reflex during the H-reflex doublet was not affected by either 1-Hz or 5-Hz NMES (all P > 0.51). In addition, 5-Hz NMES decreased post-activation depression for at least 30 minutes (all P < 0.007), whereas 1-Hz NMES did not change post-activation depression at any time points after NMES (all p > 0.769). Furthermore, following 5-Hz NMES, there was a trend (P = 0.051) that people with quadriplegia showed a significant disinhibition at 0 (P = 0.004) and 10 min (P = 0.016) post; while people with paraplegia showed a significant disinhibition at 10 (P = 0.016) and 30 min (P = 0.011) post. CONCLUSIONS: 5-Hz, but not 1-Hz NMES applied to the bilateral quadriceps and hamstring muscles diminished post-activation depression of soleus H reflex in people with SCI. These findings suggest that 1-Hz stimulation would induce less spasticity in people with SCI. Supported By NIH Grant RO1-HD-062507 and VA Grant 1-01RX000149-01

Characteristics of preceding Ia activity on postactivation depression in health and disease.

Previous activation of the soleus Ia afferents causes a depression in the amplitude of the H-reflex. This mechanism is referred to as postactivation depression (PAD) and is suggested to be presynaptically mediated. With the use of a paired reflex depression paradigm (eliciting two H-reflexes with conditioning-test intervals from 80 ms to 300 ms), PAD was examined in a group of healthy individuals and a group of hemiplegic patients. Healthy individuals showed substantial depression of the test H-reflex at all intervals. Although the patient group showed substantially less depression at all intervals, increasing the interval between the two reflexes sharply reduced the depression. In a separate experiment, we varied the size of the conditioning H-reflex against a constant test H-reflex. In healthy individuals, by increasing the size of the conditioning H-reflex, the amplitude of the test H-reflex exponentially decreased. In the patient group, however, this pattern was dependent on the conditioning-test interval; increasing the size of the conditioning H-reflex caused an exponential decrease in the size of the test reflex at intervals shorter than 150 ms. This pattern was similar to that of healthy individuals. However, conducting the same protocol at a longer interval (300 ms) in these patients resulted in an abnormal pattern (instead of an exponential decrease in the size of the test reflex, exaggerated responses were observed). Fisher discriminant analysis suggested that these two patterns (which differed only in the timing between the two stimuli) were substantially different from each other. Therefore, it is suggested that the abnormal pattern of PAD in hemiplegic stroke patients could be a contributing factor for the pathophysiology of spasticity.

Locomotor training improves reciprocal and nonreciprocal inhibitory control of soleus motoneurons in human spinal cord injury.

Pathologic reorganization of spinal networks and activity-dependent plasticity are common neuronal adaptations after spinal cord injury (SCI) in humans. In this work, we examined changes of reciprocal Ia and nonreciprocal Ib inhibition after locomotor training in 16 people with chronic SCI. The soleus H-reflex depression following common peroneal nerve (CPN) and medial gastrocnemius (MG) nerve stimulation at short conditioning-test (C-T) intervals was assessed before and after training in the seated position and during stepping. The conditioned H reflexes were normalized to the unconditioned H reflex recorded during seated. During stepping, both H reflexes were normalized to the maximal M wave evoked at each bin of the step cycle. In the seated position, locomotor training replaced reciprocal facilitation with reciprocal inhibition in all subjects, and Ib facilitation was replaced by Ib inhibition in 13 out of 14 subjects. During stepping, reciprocal inhibition was decreased at early stance and increased at midswing in American Spinal Injury Association Impairment Scale C (AIS C) and was decreased at midstance and midswing phases in AIS D after training. Ib inhibition was decreased at early swing and increased at late swing in AIS C and was decreased at early stance phase in AIS D after training. The results of this study support that locomotor training alters postsynaptic actions of Ia and Ib inhibitory interneurons on soleus motoneurons at rest and during stepping and that such changes occur in cases with limited or absent supraspinal inputs.

Plastic changes in spinal synaptic transmission following botulinum toxin A in patients with post-stroke spasticity.

The therapeutic effects of intramuscular injections of botulinum toxin-type A on spasticity can largely be explained by its blocking action at the neuromuscular junction. Botulinum toxin-type A is also thought to have a central action on the functional organization of the central nervous system. This study assessed the action of botulinum toxin-type A on spinal motor networks by investigating post-activation depression of the soleus H-reflex in post-stroke patients. Post-activation depression, a presynaptic mechanism controlling the synaptic efficacy of Ia-motoneuron transmission, is involved in the pathophysiology of spasticity. Eight patients with chronic hemiplegia post-stroke presenting with lower limb spasticity and requiring botulinum toxin-type A injection in the ankle extensor muscle. Post-activation depression of soleus H-reflex assessed as frequency-related depression of H-reflex was investigated before and 3, 6 and 12 weeks after botulinum toxin-type A injections in the triceps surae. Post-activation depression was quantified as the ratio between H-reflex amplitude at 0.5 and 0.1 Hz. Post-activation depression of soleus H-reflex, which is reduced on the paretic leg, was affected 3 weeks after botulinum toxin-type A injection. Depending on the residual motor capacity of the post-stroke patients, post-activation depression was either restored in patients with preserved voluntary motor control or further reduced in patients with no residual voluntary control. Botulinum toxin treatment induces synaptic plasticity at the Ia-motoneuron synapse in post-stroke paretic patients, which suggests that the effectiveness of botulinum toxin-type A in post-stroke rehabilitation might be partly due to its central effects.