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PURPOSE: The most commonly used method for the clinical evaluation of spasticity is the modified Ashworth scale (MAS), which is subjective. In this regard, the spasticity assessment through the tonic stretch reflex threshold, which is an objective method, has emerged as an alternative. It is based on the value of the dynamic stretch reflex threshold, which is measured at different stretch velocities. However, by this definition, it is not possible to define the speed at which passive stretches should be performed during evaluation. OBJECTIVE: This study aimed to evaluate whether the speed-variation sequence used to acquire the dynamic stretch reflex threshold influences the tonic stretch reflex threshold (TSRT) and, consequently, the estimation of spasticity by this method. METHODS: Three forms of stretching-variation speed were adopted, i.e., increasing, decreasing, and randomised. The study was performed using 10 post-stroke patients. RESULTS AND CONCLUSIONS: The results showed that the stretch protocols were not all the same and that the method of increasing was most suitable for performing manual passive stretches to evaluate TSRT in these patients. Another analysis was the correlation between MAS and tonic stretch reflex threshold; a weak correlation was observed between the increasing and decreasing methods, and moderate correlation was observed between the random methods. Implications for Rehabilitation We demonstrated that the protocol of execution of passive stretches influences in the measurement of the tonic stretch reflex threshold (TSRT). We recommend the method of increasing velocity for performing manual passive stretches. We also build software with a reliable biological data acquisition system, which makes acquisition and processing of data in real time. In this way, the TSRT is a promising quantitative measure to assess post-stroke spasticity, calculated automatically. We also we provided the use of portable instruments to facilitate the assessment of spasticity in clinical practice.

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Purpose We propose a visual myofeedback protocol as a coadjuvant therapy to standard rehabilitation of post-stroke spastic patients. We also argue in favor of the tonic stretch reflex threshold (TSRT) as a more sensitive unit for quantifying subtle changes in the spastic response that may be induced by biofeedback training. Method Sixteen volunteers with ischaemic stroke were divided into an experimental group (EG), subjected to myofeedback training in parallel with conventional physical therapy and a control group (CG), receiving only conventional physical therapy. The EG subjects underwent a six-week myofeedback training, with two sessions weekly. Both groups followed the same treatment schedule for physical therapy. The TSRTs of the volunteers' spastic muscles were assessed before the beginning of the experimental protocol and 3 weeks after it ended. Results Both groups showed some degree of improvement in the level of spasticity when the final TSRT values were compared to the initial values. However, the percentage of improvement (after-before) of the experimental group (38.59%) was significantly higher than that in the control group (18.58%). Conclusion The myofeedback training provided a significant contribution to conventional treatment, allowing for a better improvement of the spastic condition. Implications for rehabilitation Biofeedback is an effective means of improving motor control of post-stroke spastic patients. The Tonic Stretch Reflex Threshold is a more sensitive quantitative measure to assess upper-limb post-stroke spasticity. Spastic patients who participate in myofeedback training along with physical therapy can improve faster then those who participate only in traditional physical therapy rehabilitation protocols.

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We propose a new method for detecting the onset of the stretch reflex response for assessment of spasticity based on the Tonic Stretch Reflex Threshold (TSRT). Our strategy relies on a three-stage approach to detect the onset of the reflex EMG activity: (i) Reduction of baseline activity by means of Empirical Mode Decomposition; (ii) Extraction of the complex envelope of the EMG signal by means of Hilbert Transform (HT) and; iii) A double threshold decision rule. Simulated and real EMG data were used to evaluate and compare our method (TSRT-EHD) against three other popular methods described in the literature to assess TSRT ('Kim', 'Ferreira' and 'Blanchette'). Four different groups of signals containing simulated evoked stretch reflex EMG activities were generated: groups A and B without spontaneous EMG activity at rest and signal-to-noise ratio (SNR) of 10dB and 20dB respectively; groups C and D with spontaneous EMG activity at rest, as observed frequently in spastic muscles, and SNR of 10dB and 20dB respectively. The results with simulated data showed a significantly higher accuracy of TSRT-EHD for detecting the onset of the reflex EMG activity in groups C and D when compared to the other methods. Analyses using real data from five post stroke spastic subjects demonstrated that the TSRTs generated by each method were dramatically different from one another. Nevertheless, only TSRT-EHD provided valid measures across all subjects.

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Presynaptic inhibition (PSI) has been shown to modulate several neuronal pathways of functional relevance by selectively gating the connections between sensory inputs and spinal motoneurons, thereby regulating the contribution of the stretch reflex circuitry to the ongoing motor activity. In this study, we investigated whether a differential regulation of Ia afferent inflow by PSI may be associated with the performance of two types of plantarflexion sensoriomotor tasks. The subjects (in a seated position) controlled either: 1) the force level exerted by the foot against a rigid restraint (force task, FT); or 2) the angular position of the ankle when sustaining inertial loads (position task, PT) that required the same level of muscle activation observed in FT. Subjects were instructed to maintain their force/position at target levels set at ~10% of maximum isometric voluntary contraction for FT and 90° for PT, while visual feedback of the corresponding force/position signals were provided. Unconditioned H-reflexes (i.e. control reflexes) and H-reflexes conditioned by electrical pulses applied to the common peroneal nerve with conditioning-to-test intervals of 21 ms and 100 ms (corresponding to D1 and D2 inhibitions, respectively) were evoked in a random fashion. A significant main effect for the type of the motor task (FT vs PT) (p = 0.005, η2p = 0.603) indicated that PTs were undertaken with lower levels of Ia PSI converging onto the soleus motoneuron pool. Additionally, a significant interaction between the type of inhibition (D1 vs D2) and the type of motor task (FT vs PT) (p = 0.038, η2p = 0.395) indicated that D1 inhibition was associated with a significant reduction in PSI levels from TF to TP (p = 0.001, η2p = 0.731), whereas no significant difference between the tasks was observed for D2 inhibition (p = 0.078, η2p = 0.305). These results suggest that D1 and D2 inhibitions of the soleus H-reflex are differentially modulated during the performance of plantarflexion FT and PT. The reduced level of ongoing PSI during PT suggests that, in comparison to FT, there is a larger reliance on inputs from muscle spindles primary afferents when the neuromuscular system is required to maintain position-controlled plantarflexion contractions.

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Mechanically evoked reflexes have been postulated to be less sensitive to presynaptic inhibition (PSI) than the H-reflex. This has implications on investigations of spinal cord neurophysiology that are based on the T-reflex. Preceding studies have shown an enhanced effect of PSI on the H-reflex when a train of ~10 conditioning stimuli at 1 Hz was applied to the nerve of the antagonist muscle. The main questions to be addressed in the present study are if indeed T-reflexes are less sensitive to PSI and whether (and to what extent and by what possible mechanisms) the effect of low frequency conditioning, found previously for the H-reflex, can be reproduced on T-reflexes from the soleus muscle. We explored two different conditioning-to-test (C-T) intervals: 15 and 100 ms (corresponding to D1 and D2 inhibitions, respectively). Test stimuli consisted of either electrical pulses applied to the posterior tibial nerve to elicit H-reflexes or mechanical percussion to the Achilles tendon to elicit T-reflexes. The 1 Hz train of conditioning electrical stimuli delivered to the common peroneal nerve induced a stronger effect of PSI as compared to a single conditioning pulse, for both reflexes (T and H), regardless of C-T-intervals. Moreover, the conditioning train of pulses (with respect to a single conditioning pulse) was proportionally more effective for T-reflexes as compared to H-reflexes (irrespective of the C-T interval), which might be associated with the differential contingent of Ia afferents activated by mechanical and electrical test stimuli. A conceivable explanation for the enhanced PSI effect in response to a train of stimuli is the occurrence of homosynaptic depression at synapses on inhibitory interneurons interposed within the PSI pathway. The present results add to the discussion of the sensitivity of the stretch reflex pathway to PSI and its functional role.

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Chronic arthritis (CA) is a common clinical entity associated with persistent pain and limited response to opioid analgesic therapy. However, it is unknown whether these features of CA change depending on its stage of evolution. To address this, in a well-established animal model of CA we studied the time course of electromyographic responses to electrical stimulation of C fibers (C-reflex), pain-like behavior as a response to mechanical nociceptive stimulation, and the inhibition of both responses by a prototypic opioid analgesic, morphine. To induce CA, rats received a single injection of complete Freund's adjuvant into the ankle joint and the C-reflex responses to electrical stimuli or the nociceptive response to paw pressure test were studied 2, 4 or 6 weeks later. The C-reflexes evoked by threshold and supra-threshold electrical stimulation exhibited progressive increases together with enhancement of the nociceptive behavior to mechanical stimulation during induction of monoarthritis. Notably, while systemic morphine produced antinociceptive effects upon both experimental approaches, the effects were markedly reduced during the early stages of CA but enhanced at later stages. These data indicate that C-reflex and pain-like responses evolve in parallel, and are inhibited by morphine in a stage-dependent manner through the induction of CA. The present results may contribute to explain the enhanced pain response and variable analgesic efficacy of opioids that characterize arthritic pain in humans.

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Autosomal recessive cerebellar ataxias are a heterogeneous group of neurological disorders. In 1981, a neurological entity comprised by early onset progressive cerebellar ataxia, dysarthria, pyramidal weakness of the limbs and retained or increased upper limb reflexes and knee jerks was described. This disorder is known as early onset cerebellar ataxia with retained tendon reflexes. In this article, we aimed to call attention for the diagnosis of early onset cerebellar ataxia with retained tendon reflexes as the second most common cause of autosomal recessive cerebellar ataxias, after Friedreich ataxia, and also to perform a clinical spectrum study of this syndrome. In this data, 12 patients from different families met all clinical features for early onset cerebellar ataxia with retained tendon reflexes. Dysarthria and cerebellar atrophy were the most common features in our sample. It is uncertain, however, whether early onset cerebellar ataxia with retained tendon reflexes is a homogeneous disease or a group of phenotypically similar syndromes represented by different genetic entities. Further molecular studies are required to provide definitive answers to the questions that remain regarding early onset cerebellar ataxia with retained tendon reflexes.

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