Characteristics of the tonic stretch reflex in spastic spinal cord and head-injured patients

Spasticity is a known sequelae of spinal cord injury and head injury. We sought to examine whether there were any significant differences in the characteristics or underlying mechanisms of spasticity in these two groups in the chronic period which may be related to the level of injury of the neuraxis. The response to vibration applied to the muscle, or the tonic vibratory reflex, has been shown to be related to the degree of spasticity, and was therefore studied along with phasic reflexes and passive movements. These studies were carried out on cooperative, stabilized patients who were otherwise healthy, 5 with head injuries, and 5 with spinal cord injuries. The patients were examined in a supine position while surface EMG recordings were made of quadriceps and triceps surae muscles bilaterally. Tendon jerk responses, passive and volitional movements, and responses to a powerful vibratory stimulator were measured. In both head injury and spinal cord injury patient groups, a large EMG response was elicited by passive maneuvers, and tendon jerks were exaggerated. The tonic vibratory response, previously shown to be dependent upon brain influence, was present in both groups. These observations suggest that similar suprasegmental mechanisms may be responsible for hypertonia in both head-injured and spinal cord-injured patients.     

Spinal reflexes and coactivation of ankle muscles during a submaximal fatiguing contraction.

This study examined the involvement of spinal mechanisms in the control of coactivation during a sustained contraction of the ankle dorsiflexors at 50% of maximal voluntary contraction. Changes in the surface electromyogram (EMG) of the tibialis anterior and of two antagonist muscles, the soleus and lateral gastrocnemius, were investigated during and after the fatigue task. Concurrently, the compound action potential (M-wave) and the Hoffmann reflex of the soleus and lateral gastrocnemius were recorded. The results showed that the torque of the ankle dorsiflexors and the average EMG of the tibialis anterior during maximal voluntary contraction declined by 40.9 +/- 17.7% (mean +/- SD; P < 0.01) and 37.0 +/- 19.9% (P < 0.01), respectively, at task failure. During the submaximal fatiguing contraction, the average EMG of both the agonist and antagonist muscles increased, leading to a nearly constant ratio at the end of the contraction when normalized to postfatigue values. In contrast to the monotonic increase in average EMG of the antagonist muscles, the excitability of their spinal reflex pathways exhibited a biphasic modulation. The amplitude of the Hoffman reflexes in the soleus and lateral gastrocnemius increased to 147.5 +/- 52.9% (P < 0.05) and 166.7 +/- 74.9% (P < 0.01), respectively, during the first 20% of the contraction and then subsequently declined to 66.3 +/- 44.8 and 74.4 +/- 44.2% of their initial values. In conclusion, the results show that antagonist coactivation did not contribute to task failure. The different changes in voluntary EMG activity and spinal reflex excitability in the antagonist muscles during the fatiguing contraction support the concept that the level of coactivation is controlled by supraspinal rather than spinal mechanisms. The findings indicate, however, that antagonist coactivation cannot simply be mediated by a central descending "common drive" to the motor neuron pools of the agonist-antagonist muscle pairs. Rather, they suggest a more subtle regulation of the drive, possibly through presynaptic mechanisms, to the motoneurons that innervate the antagonist muscles.     

Functional consequences of motor unit recruitment order reversals following spinal cord transection in cat

Motoneuron recruitment order determinations were made for acute, 2-week chronic, and 3-month chronic spinal cats by comparing cutaneous nerve stimulation thresholds for evoking single unit tibialis anterior (TA) electromyogram (EMG) spikes of different sizes. Recruitment order was largely ( approximately 80%) orderly (small spikes recruited at lower stimulus intensities than large spikes) in acute and 3-month chronic spinal animals. However, in 2-week chronic spinal animals recruitment order was reversed, with large units more often recruited at lower stimulus intensities than small units ( approximately 65%). Morphological analyses of TA muscle fibers suggested that fiber size changes were unlikely to account for the dramatic alterations in recruitment order results of the 2-week chronic spinal animals. Additional studies suggested that the recruitment order reversal in the 2-week chronic animals coincided with an enhanced reflex neural output (increased recruitment or reflex gain) for the flexion reflex which compensated for disuse atrophy related decreases in flexor muscle force generation capability in these animals. The data from 2-week chronic spinal animals represent a functionally significant example of deviation from the normal size principle of motoneuron recruitment order as the corresponding reflex gain increases can enhance the rapidity of motor function recovery (standing, locomotion) following spinal injury.     

Spinal Cord Transection Significantly Influences nNOS-IR in Neuronal Circuitry that Underlies the Tail-Flick Reflex Activity

Aim Spinal cord transection interrupts supraspinal input and leads to the development of prominent spasticity. In this study, we investigated the effect of rat spinal cord transection performed at low thoracic level on changes in (i) neuronal nitric oxide synthase immunoreactivity (nNOS-IR), and (ii) the level of neuronal nitric oxide synthase (nNOS) protein in the neuronal circuitry that underlies tail-flick reflex. Methods nNOS-IR was detected by immunohistochemistry and the level of nNOS protein was determined by the Western blot analysis. The tail-flick reflex was tested by a noxious thermal stimulus delivered to the tail of experimental animals. After surgery, experimental animals survived for 7 days. Results A significant increase in the level of nNOS protein was found 1 week after thoracic transection in the L2–L6 segments. Immunohistochemical analysis discovered that this increase may be a result of (1) a high nNOS-IR in a large number of axons, located predominantly in the dorsal columns (DCs) of lower lumbosacral segments, and (2) a slight increase of density in nNOS-IR in motoneurons. On the other hand the number of nNOS-IR neurons in the superficial dorsal horn and in area surrounded the central canal (CC) was greatly reduced. The tail-flick response was immediate in animals after spinal transection, while control rats responded to thermal stimulus with a slight delay. However, the tail-flick latency in experimental animals was significantly higher than in control. Conclusion These data indicate that transection of the spinal cord significantly influences nNOS-IR in neuronal circuitry that underlies the tail-flick reflex activity.     

Combinational spinal GAD65 gene delivery and systemic GABA-mimetic treatment for modulation of spasticity

Background

Loss of GABA-mediated pre-synaptic inhibition after spinal injury plays a key role in the progressive increase in spinal reflexes and the appearance of spasticity. Clinical studies show that the use of baclofen (GABA_B receptor agonist), while effective in modulating spasticity is associated with major side effects such as general sedation and progressive tolerance development. The goal of the present study was to assess if a combined therapy composed of spinal segment-specific upregulation of GAD65 (glutamate decarboxylase) gene once combined with systemic treatment with tiagabine (GABA uptake inhibitor) will lead to an antispasticity effect and whether such an effect will only be present in GAD65 gene over-expressing spinal segments.

Methods/Principal Findings

Adult Sprague-Dawley (SD) rats were exposed to transient spinal ischemia (10 min) to induce muscle spasticity. Animals then received lumbar injection of HIV1-CMV-GAD65 lentivirus (LVs) targeting ventral α-motoneuronal pools. At 2–3 weeks after lentivirus delivery animals were treated systemically with tiagabine (4, 10, 20 or 40 mg/kg or vehicle) and the degree of spasticity response measured. In a separate experiment the expression of GAD65 gene after spinal parenchymal delivery of GAD65-lentivirus in naive minipigs was studied. Spastic SD rats receiving spinal injections of the GAD65 gene and treated with systemic tiagabine showed potent and tiagabine-dose-dependent alleviation of spasticity. Neither treatment alone (i.e., GAD65-LVs injection only or tiagabine treatment only) had any significant antispasticity effect nor had any detectable side effect. Measured antispasticity effect correlated with increase in spinal parenchymal GABA synthesis and was restricted to spinal segments overexpressing GAD65 gene.

Conclusions/Significance

These data show that treatment with orally bioavailable GABA-mimetic drugs if combined with spinal-segment-specific GAD65 gene overexpression can represent a novel and highly effective anti-spasticity treatment which is associated with minimal side effects and is restricted to GAD65-gene over-expressing spinal segments.     

Inter-relationships among anticipatory EMG activity, Hoffmann reflex amplitude and EMG reaction time during voluntary standing movement

In order to understand the process of executing a voluntary standing movement, the parameters latency (AEA-LT), duration (AEA-DUR) and amplitude (AEA-AMP) of the anticipatory electromyographic (EMG) activity (AEA) in the tibialis anterior muscle, Hoffmann (H) reflex amplitude in the soleus muscle (Sol) prior to the onset of EMG activity in that muscle, and EMG reaction time (EMG-RT) were measured during heel raising from the standing position. The following results were obtained: the three parameters of AEA correlated with EMG-RT in each subject; the average values for all nine normal subjects were r = 0.856 for AEA-DUR, r = 0.448 for AEA-LT and r = -0.215 for AEA-AMP; for the group the mean value of AEA-DUR correlated significantly with that of EMG-RT (r = 0.983, P less than 0.01), while no such significant correlation was observed for AEA-LT; the average value of the AEA-DUR in three slower EMG-RT performers (SLOW-PFM) was significantly longer (P less than 0.05) than that in three faster ones (FAST-PFM), while no significant difference in the AEA-LT was observed; and lastly the total area of the anticipatory suppression of the Sol H reflex amplitude in the SLOW-PFM was greater than that in the FAST-PFM. These results suggest that AEA-DUR, representing postural responses, rather than AEA-LT, reflecting cognitive processes, may have had a close link with EMG-RT, and that the increased suppression in Sol H reflex amplitude originated from the increased anticipatory postural requirement, thus bringing about the EMG-RT delay.     

Limiting mechanisms of force production after repetitive dynamic contractions in human triceps surae.

The influence of repetitive dynamic fatiguing contractions on the neuromuscular characteristics of the human triceps surae was investigated in 10 subjects. The load was 50% of the torque produced during a maximal voluntary contraction, and the exercise ended when the ankle range of motion declined to 50% of control. The maximal torque of the triceps surae and the electromyographic (EMG) activities of the soleus and medial gastrocnemius were studied in response to voluntary and electrically induced contractions before and after the fatiguing task and after 5 min of recovery. Reflex activities were also tested by recording the Hoffmann reflex (H reflex) and tendon reflex (T reflex) in the soleus muscle. The results indicated that whereas the maximal voluntary contraction torque, tested in isometric conditions, was reduced to a greater extent (P < 0.05) at 20 degrees of plantar flexion (-33%) compared with the neutral position (-23%) of the ankle joint, the EMG activity of both muscles was not significantly reduced after fatigue. Muscle activation, tested by the interpolated-twitch method or the ratio of the voluntary EMG to the amplitude of the muscle action potential (M-wave), as well as the neuromuscular transmission and sarcolemmal excitation, tested by the M-wave amplitude, did not change significantly after the fatiguing exercise. Although the H and T reflexes declined slightly (10-13%; P < 0.05) after fatigue, these adjustments did not appear to have a direct deleterious effect on muscle activation. In contrast, alterations in the mechanical twitch time course and postactivation potentiation indicated that intracellular Ca(2+)-controlled excitation-contraction coupling processes most likely played a major role in the force decrease after dynamic fatiguing contractions performed for short duration.     

Presynaptic inhibition in humans: a comparison between normal and spastic patients.

During the last 40 years, several studies in man have been devoted to the pathophysiological mechanisms underlying spasticity. Spasticity is characterised by a velocity dependent increase in muscle tone. Many spinal pathways control stretch reflex excitability and a malfunction in any one of them could theoretically produce the exaggeration of the stretch reflex. Delwaide showed that the vibration-induced inhibition of Ia fibres is reduced in spastic patients. However, the relation between a decrease in presynaptic Ia inhibition and the pathophysiology of spasticity has been recently questioned since it was argued that homosynaptic depression (or post-activation depression) also contributes to the vibratory-induced depression of monosynaptic reflexes. This paper is thus devoted to a review of the methods recently developed to study selectively presynaptic Ia inhibition in man and to a reevaluation of the relations between modifications in presynaptic Ia inhibition and spasticity in hemiplegic and spinal spastic patients.     

Levels of gamma-aminobutyric acid in the dorsal grey lumbar spinal cord during the development of experimental spinal spasticity.

Dogs were made paraplegic by complete mid-thoracic spinal cord transection. At one, three, eight, and twelve weeks post-transection the lumbar cord was removed and the dorsal grey matter microdissected from L_2–3 and the content of ?-aminobutyric acid (GABA) determined. An initial decrease in GABA levels was followed by a gradual increase in content which correlated with the progressive development of spinal spasticity. By twelve weeks post-transection, GABA was elevated 68% above controls.     

Intrathecal baclofen withdrawal syndrome- a life-threatening complication of baclofen pump: A case report

Background  

Intrathecal baclofen pump has been used effectively with increasing frequency in patients with severe spasticity, particularly for those patients who are unresponsive to conservative pharmacotherapy or develop intolerable side effects at therapeutic doses of oral baclofen. Drowsiness, nausea, headache, muscle weakness, light-headedness and return of pretreatment spasticity can be caused by intrathecal pump delivering an incorrect dose of baclofen. Intrathecal baclofen withdrawal syndrome is a very rare, potentially life-threatening complication of baclofen pump caused by an abrupt cessation of intrathecal baclofen.     

Spasticity and spastic dystonia: the two faces of velocity-dependent hypertonia

BackgroundSpasticity and spastic dystonia are two separate phenomena of the upper motor neuron syndrome. Spasticity is clinically defined by velocity-dependent hypertonia and tendon jerk hyperreflexia due to the hyper-excitability of the stretch reflex. Spastic dystonia is the inability to relax a muscle leading to a spontaneous tonic contraction. Both spasticity and spastic dystonia are present in patients who are at rest; however, only patients with spasticity are actually able to kept their muscles relaxed prior to muscle stretch. The idea that has inspired the present work is that also in patients with spastic dystonia the stretch reflex is likely to be hyper-excitable. Therefore, velocity-dependent hypertonia could be mediated not only by spasticity, but also by spastic dystonia.MethodsTonic stretch reflexes in the rectus femoris muscle were evoked in 30 patients with multiple sclerosis showing velocity-dependent hypertonia of leg extensors and the habituation of the reflex was studied. Moreover, the capability of relax the muscle prior to muscle stretch (spastic dystonia) was also investigated.ResultsA tonic stretch reflex was evoked in all the enrolled patients. 73% of the patients were able to relax their rectus femoris muscle prior to stretch (spasticity). In the overwhelming majority of these patients, the tonic stretch reflex decreased during repeated stretches. In the remaining 27% of the subjects, the muscle was tonically activated prior to muscle stretch (spastic dystonia). In the patients in whom spastic dystonia progressively increased over the subsequent stretches (50% of the subjects with spastic dystonia), the habituation of the reflex was replaced by a progressive reflex facilitation.DiscussionThis study shows for the first time that velocity-dependent hypertonia can be caused by two distinct phenomena: spasticity and spastic dystonia. The habituation of the tonic stretch reflex, which is a typical feature of spasticity, is replaced by a reflex facilitation in the half of the subject with spastic dystonia. These preliminary findings suggest that differentiating the two types of velocity-dependent muscle hypertonia (spasticity and spastic dystonia) could be clinically relevant.     

Locomotion induced by epidural stimulation in a decerebrated cat after spinal cord injury

The effect of partial and complete spinal cord transection (Th7–Th8) on locomotor activity evoked in decerebrated cats by electrical epidural stimulation (segment L5, 80–100 μA, 0.5 ms at 5 Hz) has been investigated. Transection of dorsal columns did not substantially influence the locomotion. Disruption of the ventral spinal quadrant resulted in deterioration and instability of the locomotor rhythm. Injury to lateral or medial descending motor systems led to redistribution of the tone in antagonist muscles. Locomotion could be evoked by epidural stimulation within 20 h after complete transection of the spinal cord. The restoration of polysynaptic components in EMG responses correlated with recovery of the stepping function. The data obtained confirm that initiation of locomotion under epidural stimulation is caused by direct action on intraspinal systems responsible for locomotor regulation. With intact or partially injured spinal cord, this effect is under the influence of supraspinal motor systems correcting and stabilizing the evoked locomotor pattern.     

Paraspinal muscle reflex dynamics

Neuromuscular control of spinal stability may be represented as a control system wherein the paraspinal muscle reflex acts as feedback response to kinetic and kinematic disturbances of the trunk. The influence of preparatory muscle recruitment for the control of spinal stability has been previously examined, but there are few reported studies that characterize paraspinal reflex gain as feedback response. In the current study, the input-output dynamics of paraspinal reflexes were quantified by means of the impulse response function (IRF), with trunk perturbation force representing the input signal and EMG the output signal. Surface EMGs were collected from the trunk muscles in response to a brief anteriorly directed impact force applied to the trunk of healthy participants. Reflex behavior was measured in response to three levels of force impulse, 6.1, 9.2 and 12.0 Ns, and two different levels of external trunk flexion preload, 0 and 110 N anterior force. Reflex EMG was quantifiable in response to 91% of the perturbations. Mean reflex onset latency was 30.7+/-21.3 ms and reflex amplitude increased with perturbation amplitude. Impulse response function gain, G(IRF), was defined as the peak amplitude of the measured IRF and provided a consistent measure of response behavior. EMG reflex amplitude and G(IRF) increased with force impulse. Mean G(IRF) was 2.27+/-1.31% MVC/Ns and demonstrated declining trend with flexion preload. Results agree with a simple systems model of the neuromechanical feedback behavior. The relative contribution of the reflex dynamics to spinal stability must be investigated in future research.     

Modulation of spinal inhibitory reflexes depends on the frequency of transcutaneous electrical nerve stimulation in spastic stroke survivors

Neurophysiological studies in healthy subjects suggest that increased spinal inhibitory reflexes from the tibialis anterior (TA) muscle to the soleus (SOL) muscle might contribute to decreased spasticity. While 50?Hz is an effective frequency for transcutaneous electrical nerve stimulation (TENS) in healthy subjects, in stroke survivors, the effects of TENS on spinal reflex circuits and its appropriate frequency are not well known. We examined the effects of different frequencies of TENS on spinal inhibitory reflexes from the TA to SOL muscle in stroke survivors. Twenty chronic stroke survivors with ankle plantar flexor spasticity received 50-, 100-, or 200-Hz TENS over the deep peroneal nerve (DPN) of the affected lower limb for 30?min. Before and immediately after TENS, reciprocal Ia inhibition (RI) and presynaptic inhibition of the SOL alpha motor neuron (D1 inhibition) were assessed by adjusting the unconditioned H-reflex amplitude. Furthermore, during TENS, the time courses of spinal excitability and spinal inhibitory reflexes were assessed via the H-reflex, RI, and D1 inhibition. None of the TENS protocols affected mean RI, whereas D1 inhibition improved significantly following 200-Hz TENS. In a time-series comparison during TENS, repeated stimulation did not produce significant changes in the H-reflex, RI, or D1 inhibition regardless of frequency. These results suggest that the frequency-dependent effect of TENS on spinal reflexes only becomes apparent when RI and D1 inhibition are measured by adjusting the amplitude of the unconditioned H-reflex. However, 200-Hz TENS led to plasticity of synaptic transmission from the antagonist to spastic muscles in stroke survivors.     

Gravitational force modulates muscle activity during mechanical oscillation of the tibia in humans

Mechanical oscillation (vibration) is an osteogenic stimulus for bone in animal models and may hold promise as an anti-osteoporosis measure in humans with spinal cord injury (SCI). However, the level of reflex induced muscle contractions associated with various loads (g force) during limb segment oscillation is uncertain. The purpose of this study was to determine whether certain gravitational loads (g forces) at a fixed oscillation frequency (30 Hz) increases muscle reflex activity in individuals with and without SCI. Nine healthy subjects and two individuals with SCI sat with their hip and knee joints at 90° and the foot secured on an oscillation platform. Vertical mechanical oscillations were introduced at 0.3, 0.6, 1.2, 3 and 5g force for 20 s at 30 Hz. Non-SCI subjects received the oscillation with and without a 5% MVC background contraction. Peak soleus and tibialis anterior (TA) EMG were normalized to M-max. Soleus and TA EMG were <2.5% of M-max in both SCI and non-SCI subjects. The greatest EMG occurred at the highest acceleration (5g). Low magnitude mechanical oscillation, shown to enhance bone anabolism in animal models, did not elicit high levels of reflex muscle activity in individuals with and without SCI. These findings support the g force modulated background muscle activity during fixed frequency vibration. The magnitude of muscle activity was low and likely does not influence the load during fixed frequency oscillation of the tibia.     

Down-Regulation of KCC2 Expression and Phosphorylation in Motoneurons,and Increases the Number of in Primary Afferent Projections to Motoneurons in Mice with Post-Stroke Spasticity

Spasticity obstructs motor function recovery post-stroke, and has been reported to occur in spinal cord injury and electrophysiological studies. The purpose of the present study was to assess spinal cord circuit spasticity in post-stroke mice. At 3, 7, 21, and 42 d after photothrombotic ischemic cortical injury in C57BL/6J mice, we observed decreased rate-dependent depression (RDD) of the Hoffmann reflex (H reflex) in the affected forelimb of mice compared with the limbs of sham mice and the non-affected forelimb. This finding suggests a hyper-excitable stretch reflex in the affected forelimb. We then performed immunohistochemical and western blot analyses to examine the expression of the potassium-chloride cotransporter 2 (KCC2) and phosphorylation of the KCC2 serine residue, 940 (S940), since this is the main chloride extruder that affects neuronal excitability. We also performed immunohistochemical analyses on the number of vesicular glutamate transporter 1 (vGluT1)-positive boutons to count the number of Ia afferent fibers that connect to motoneurons. Western bolts revealed that, compared with sham mice, experimental mice had significantly reduced KCC2 expression at 7 d post-stroke, and dephosphorylated S940 at 3 and 7 d post-stroke in motoneuron plasma membranes. We also observed a lower density of KCC2-positive areas in the plasma membrane of motoneurons at 3 and 7 d post-stroke. However, western blot and immunohistochemical analyses revealed that there were no differences between groups 21 and 42 d post-stroke, respectively. In addition, at 7 and 42 d post-stroke, experimental mice exhibited a significant increase in vGluT1 boutons compared with sham mice. Our findings suggest that both the down-regulation of KCC2 and increases in Ia afferent fibers are involved in post-stroke spasticity.     

Suppression of detrusor-sphincter dysynergia by GABA-receptor activation in the lumbosacral spinal cord in spinal cord-injured rats

We investigated the effects of intrathecal application of GABAA- or GABAB-receptor agonists on detrusor-sphincter dyssynergia (DSD) in spinal cord transection (SCT) rats. Adult female Sprague-Dawley rats were used. At 4 wk after Th9-10 SCT, simultaneous recordings of intravesical pressure and urethral pressure were performed under an awake condition to examine the effect of intrathecal application of GABAA and GABAB agonists (muscimol and baclofen, respectively) or GABAA and GABAB antagonists (bicuculline and saclofen, respectively) at the level of L6-S1 spinal cord. In spinal-intact rats, the effects of bicuculline and saclofen on bladder and urethral activity were also examined. During urethral pressure measurements, DSD characterized by urethral pressure increases during isovolumetric bladder contractions were observed in 95% of SCT rats. However, after intrathecal application of muscimol or baclofen, urethral pressure showed urethral relaxation during isovolumetric bladder contractions. The effective dose to induce inhibition of urethral activity was lower compared with the dose that inhibited bladder contractions. The effect of muscimol and baclofen was antagonized by intrathecal bicuculline and saclofen, respectively. In spinal-intact rats, intrathecal application of bicuculline induced DSD-like changes. These results indicate that GABAA- and GABAB-receptor activation in the spinal cord exerts the inhibitory effects on DSD after SCT. Decreased activation of GABAA receptors due to hypofunction of GABAergic mechanisms in the spinal cord might be responsible, at least in part, for the development of DSD after SCT.     

Baclofen blocks LES relaxation and crural diaphragm inhibition by esophageal and gastric distension in cats

Esophageal distension and transient lower esophageal sphincter (LES) relaxation (TLESR) are accompanied by simultaneous relaxation of the LES and inhibition of crural diaphragm. Recent studies indicate that baclofen decreases the frequency of TLESR; however, its effect on the crural diaphragm is not known. We evaluated the effects of baclofen on LES relaxation and crural diaphragm inhibition induced by gastric distension and esophageal distension in cats. Five adult cats underwent surgical implantation of wire electrodes into the crural and costal diaphragm for measurement of their EMG activity, respectively. One week after the surgery, animals were lightly sedated and recordings were performed using a manometry catheter equipped with a 2.5-cm balloon. The effects of baclofen (10 micromol/kg iv) on the graded esophageal distension and gastric distension-induced LES and crural diaphragm responses were studied. Distension of the esophagus and stomach induces relaxation of the LES and inhibition of the crural diaphragm, simultaneously. Baclofen blocks both the esophageal and the gastric distension-induced relaxation of the LES and inhibition of the crural diaphragm. The magnitude of response to baclofen was significantly larger for the crural diaphragm inhibition than for the LES relaxation. Baclofen, a GABA(B) receptor agonist, blocks the reflex inhibitory pathway to the LES and crural diaphragm. The reflex inhibitory pathway to the crural diaphragm is more sensitive to blockade by baclofen than the reflex LES inhibitory pathway.     

Beneficial effects of footbaths in controlling spasticity after stroke

Footbaths are considered to provide beneficial thermal therapy for post-stroke patients with spasticity, but their anti-spastic effects have not been investigated comprehensively. The present study aimed to evaluate alterations in motor-neuron excitability using F-wave parameters in post-stroke patients with spastic hemiplegia. Subjects’ legs below the knee joint were immersed in water at 41°C and F-wave recordings were made over the abductor hallucis muscle before, immediately after, and 30 min after thermal treatment. Antidromic stimulation was performed on the tibial nerve at the ankle. Measurements included F-wave amplitude, F-wave/M-response ratio, changes in modified Ashworth scale (MAS), body temperature and surface-skin temperature. The mean values of both F-wave parameters were higher on the affected side before footbath treatment. In post-stroke patients, the mean values of F-wave parameters were significantly reduced after footbath treatment (P < 0.01). The anti-spastic effects of footbath treatment were indicated by decreased F-wave parameters, in parallel with decreases in MAS. Body temperature was significantly increased both immediately after, and 30 min following footbath treatment in both groups, which appeared to play an important role in decreased spasticity. Surface-skin temperature increased immediately after footbath treatment in both groups and returned to baseline 30 min later. These findings demonstrate that the use of footbaths is an effective nonpharmacological anti-spastic treatment that might facilitate stroke rehabilitation.     

Role of afferent input in muscle atrophy.

It is well known that soleus muscle of rat atrophies following spaceflight or hindlimb suspension (Ohira et al., 1992). It is, further, reported that the electromyogram (EMG) of soleus muscle disappears immediately in response to unloading by exposure to actual micro-g environment (Kawano et al., 2002; Leterme and Falempin, 1998) and by hindlimb suspension of rats (Alford et al., 1987; Ohira et al., 2000). However, the EMG level is increased gradually to the control level following 7-10 days of continuous hindlimb suspension (Alford et al., 1987; Ohira, 2000), while muscle atrophy is progressing (Winiarski et al., 1987). We previously reported that reduction of the EMG level of rat soleus in response to actual micro-g environment, created by a parabolic flight of a jet airplane, was closely associated with a decrease of the afferent input recorded at the L5 segmental level of spinal cord (Kawano et al., 2002). However, it is still unclear how the EMG level of soleus muscle adapts to unloading condition. The current study was performed to investigate the responses of soleus EMG and both afferent and efferent neurogram at the L5 segmental level of spinal cord to acute (20 seconds) and chronic (14 days) unloading.