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Hypertonia is seen in 85% of people with Multiple Sclerosis (pwMS) resulting in disability and functional restrictions. Hypertonia can be caused by increases in passive stiffness and enhanced stretch reflexes (spasticity) and is frequently managed clinically using passive stretches. However, the optimal parameters of stretching such as the applied torque and stretch duration remain unclear. During commonly prescribed ankle plantarflexor stretches pwMS produced higher torques when standing in a weight bearing position compared to stretches applied using the upper limbs. Stretches could be held for 120 seconds on average and stretch duration was mainly limited by fatigue. People with higher disability tended to favour more supported stretching positions. The effects of stretching for either 30 or 10 minutes using a customised motor at three torque levels covering the range that MS participants could produce was investigated. Compared to the 10 minute stretch, greater reductions in passive stiffness and greater increases in range of movement (ROM) were seen immediately following the 30 minute stretch with the effects being sustained for the 30 minute post stretch period. Higher levels of applied torque resulted in a greater change in ROM however; there was no effect of applied torque on passive stiffness. Stretch reflex mediated stiffness was unaffected by the stretching intervention and showed transient post stretch increases. Ultrasonography was used to investigate changes in muscle–tendon length and strain in pwMS and controls and following stretching. PwMS showed evidence of stiffer muscles and increased tendon length at baseline compared to controls. Following a 10 minute stretch overall muscle length did not increase in pwMS, although increases in strain in the musculotendinous junction region were observed suggesting that more proximal regions of the muscle was likely to have contributed significantly to overall stiffness. This work highlights that stretch duration and levels of applied torque are critical factors in determining the effectiveness of stretches. The pathological mechanisms underlying hypertonia at a molecular and structural level and the effects of stretching on components of the musculo-tendinous structure and on functional ability should be ascertained.

No description available.

This study deals with the effects of botulinum toxin A treatment on pathological muscular hyperactivity in a group of 53 children. The thesis objective was to evaluat eeffect of botulinum toxin on muscle tone, range of movement and motor performance of the patient. The theoretical part summarizes the knowledge about this theme, characterizes the term spasticity and an impact of botulinum toxin on abnormal muscular hyperactivity. The practical part evaluates the effect of botulinum toxin in two groups of patients. The first group consists of 14 children, who were tested before and at least one month after botulinum toxin application. Clinical assessment involved range of movement measurement, the evaluation of spasticity with Modified Ashworth scale, Global Assesment of Spasticity Scale (GSA), assessment of motor performance with the use of GMFM test and Functional Independence Meassure for children WeeFIM and summarized physical therapeutic methods used in treatment of patients before and after the application. The second group consists of 39 patients who administered the GSA survey forms within a period of one month. The results confirmed positive effect of botulinum toxin treatment on reduction of spasticity, increasing of range of movement and improvement of motor performance of children. Powered by...

This study has brought an overview of botulinum toxin and its influence on the human muscles, especially on spastic muscles. In the practical part is resumed experience with botulinum toxin A therapy in children with cerebral palsy. There were observed two groups. Group A (n=9) was measured before and after therapy. Patients in group B (n=24) filled out a table of the global spasticity scale, which they returned by mail. All the patients improved after the treatment. Powered by TCPDF (www.tcpdf.org)

Individuals with stroke have neuromuscular weakness or paralysis on one side of the body caused by some muscles disengaging and overexciting other muscles. Hyperextension of the knee joint and complete lack of plantar flexion of the ankle joint are common symptoms of stroke. This thesis encompasses the simulation of hemiparetic function using both a knee orthosis with variable impedance, specifically in terms of stiffness and damping, and the Proprioception Interference Apparatus. The section regarding the knee orthosis with variable impedance focuses on the creation and implementation of a small, lightweight, and adjustable orthotic device to be positioned around the knee of an able-bodied person to simulate hemiparetic gait. Force and range of motion data from able-bodied subjects fitted with the orthosis, inducing hemiparetic gait, was collected using the Computer Assisted Rehabilitation ENvironment (CAREN) system. The four parameters that the design focused on are damping, catch, hysteresis, and stiffness. The main goal of the project was to discern whether this device could be utilized as a viable research instrument to simulate hemiparetic gait. It was hypothesized that the device has the potential to be utilized in the future as a research device to be used on able-bodied persons to study asymmetries in gait and eventually quantify the Modified Ashworth Scale. It was also believed that it could serve as a possible rehabilitation device for people with stroke since it has been designed to induce larger knee flexion as an after effect. However, this would require the proper clinical evaluation and experimentation procedures to be successfully concluded. A comparison between how the dominant leg was affected by the orthosis and how the non-dominant leg was affected was investigated as well. The results show that the device affected the velocities, knee angles, and force profiles of the subject’s gait. The second section involving the Proprioception Interference Apparatus involved the creation and implementation of a haptic apparatus that utilizes vibration as well as transcutaneous electrical nerve stimulation (TENS) in various combinations with and without visual feedback to induce a proprioceptive illusion around the knee joint, as if a subject has a version of hemiparesis. The main goal of the project was to discern whether a device of relatively the same design could be utilized as a viable research instrument to simulate stroke-like balance in able-bodied subjects. Comparison between how the root mean square (RMS) values of each marker location, the average of the standard deviations of the forces, and RMS of the center of pressure affected the various conditions was investigated as well. It was hypothesized and concluded that the RMS values and average of the standard deviations when subjects had no visual feedback would have a significant difference from when they had visual feedback. It was also hypothesized that Proprioceptive Interference Apparatus (PIA) would have a significant effect on the RMS and standard deviation values since it was meant to disrupt the motor control function of the knee, however, this was proved false after data analysis. It was also surmised that the application of the TENS had more of an effect on the RMS and standard deviation values, whether it was used on its own or in combination with the vibrations, than the vibration stimulation alone. However, once again, this was not statistically significant.

Spinal cord injury (SCI) is a debilitating condition that disrupts the communication between the brain and the spinal cord. Several studies have sought to determine how to revive dormant spinal circuits caudal to the lesion to restore movements in paralyzed patients. So far, recovery levels in human patients have been modest at best. In contrast, animal models of SCI exhibit more recovery of lost function. Recovery of lost function could arise from structural changes in spinal circuits following spinal cord injury. Previous work from our lab has identified dI3 interneurons as a spinal neuron population central to the recovery of locomotor function in spinalized mice. We seek to determine the changes in the circuitry of dI3 interneurons and motoneurons following SCI in adult mice. After a complete transection of the spinal cord at T9-T11 level in transgenic Isl1:YFP mice and subsequent treadmill training at various time points of recovery following surgery, we examined changes in three key circuits involving dI3 interneurons and motoneurons: 1) Sensory inputs from proprioceptive and cutaneous afferents, 2) GABAergic inputs onto sensory afferents (GABApre), 3) Central excitatory glutamatergic synapses from spinal neurons onto dI3 INs and motoneurons. Furthermore, we examined the possible role of treadmill training on changes in synaptic connectivity to dI3 interneurons and motoneurons. Our data suggests that sensory inputs from the periphery labelled by VGLUT1⁺ to dI3 interneurons decrease transiently or only at later stages after injury, whereas levels of VGLUT1⁺ remain the same for motoneurons after injury. Levels of central excitatory inputs labelled by VGLUT2⁺ to dI3 INs and MNs may show transient increases but fall below levels seen in sham-operated mice after a period of time. Levels of GABApre boutons onto the VGLUT1⁺ sensory afferents that project onto to dI3 INs and MNs can rise shortly after SCI, but those increases do not persist. However, levels of these GABApre boutons onto VGLUT1⁺ inputs never fell below levels observed in sham-operated mice. For some synaptic inputs studied, levels were higher in spinal cord-injured animals that received treadmill training, but these increases were observed only at some time points. Changes in spinal circuitry could be maladaptive. For example, spasticity is a common consequence of SCI, disrupting motor function and resulting in significant discomfort. Spasticity may arise from maladaptive changes in spinal circuits. Current models of hindlimb spasticity are lacking, hindering the study of mechanisms or treatments of spasticity. Therefore, we have generated a novel mouse model of SCI-related spasticity that utilizes optogenetics to activate a subset of cutaneous VGLUT2⁺ sensory afferents to produce reliable incidences of hindlimb spasticity. To examine the efficacy of this optogenetic spasticity model, a T9-T10 complete transection injury was performed in Isl1-Vglut2ᒼᵃᵗᒼʰ mice, followed by the implantation of EMG electrodes into the left and right gastrocnemius and tibialis anterior muscles. Beginning at 9 days post-injury, EMG recordings were performed during episodic optogenetic stimulation. During each recording session, an optic fiber coupled to a 470nm wavelength LED was used to deliver light pulses to the palmar surface of each hindpaw. The results of these recordings demonstrated significant increases in the amplitude of EMG responses to the light stimulus from 2 weeks post-injury to 5 weeks post-injury, indicating hyperreflexia. Interestingly, this hyperreflexia was significantly greater in the female cohort in comparison to the males. Incidences of prolonged involuntary muscle contraction and clonus were also detected through EMG and visual observation during the testing period, supporting the presence of spasticity. Overall, the results in my thesis suggest remodelling of spinal circuits involving spinal interneurons that have previously been implicated in the recovery of locomotor function after spinal cord injury in mice. In addition, we have developed an optogenetic mouse model that appears to reliably elicit spasticity in SCI mice and may be valuable for the study of SCI-related limb spasticity mechanisms due to the maladaptive changes within the spinal cord.

Yes / Background: Cerebral Palsy (CP) is the most common childhood disorder affecting four percent of children born in the UK. It is common for children with CP to have reduced range of movement (ROM) due to spasticity and contractures. Stretching is commonly used in physiotherapy programmes to manage this. Aim: This critical review aims to evaluate the evidence base behind the use of stretching for children with CP. Methods: A systematic literature search of AMED, CINAHL, MEDLINE and Cochrane Library Trials was conducted. Returned searches were assessed against strict criteria according to a predefined PICOS (Population, Intervention, Comparison, Outcome, Study). These studies were then critically appraised to assess the validity, reliability and clinical relevance. Findings: There is evidence supporting the use of stretching in children with CP. However there is also some evidence to suggest very little or no positive change. All of the included studies have methodological limitations, which questions the validity of the results. Conclusions/Recommendations: The research suggests some positive outcomes for the use of stretching in CP, studies that did not find positive outcomes found no adverse effects; however further research in the area is required to validate the effectiveness of stretching to maintain ROM in children with CP.

The prevalence of spasticity after first-ever stroke is approximately 20%, but there are no data on the prevalence of disabling spasticity.The reported prevalence of pain after stroke varies between 19% and 74%, whether pain is associated with spasticity is not known. Until now, there is no health economic analysis of patients with spasticity after stroke. Methods: Two groups of patients were studied. Cohort I was a cross-sectional survey. A representative sample of 140 patients was investigated 1 year after their first-ever stroke. Spasticity was defined as ≥ 1 score on the modified Ashworth scale, disabling spasticity was defined as spasticity having such an impact that intervention, e.g. intensive physiotherapy, orthoses or pharmacological treatment, should be offered. Pain was assesed with the Visual Analogue Scale. All direct costs during one year were identified and converted into Purchasing Power Parities US dollar (PPP$). Cohort II was a prospective cohort study. Forty-nine patients were examined at day 2–10, at one month, and at six months after their first-ever stroke. Assessment and definitions were similar as for cohort I. Results: Spasticity occurs within 1 month and disabling spasticity occur within 6 months. After one year, the prevalence of spasticity was 17% and that of  disabling spasticity 4%. Disabling spasticity was more frequent in the upper extremity. There was an independent effect of severe upper extremity paresis (OR 22, CI 3.9–125) and age below 65 years (OR 9.5, CI 1.5–60). The prevalence of stroke-related pain was 21% after one year. Stroke-related pain was associated with paresis (OR 3.1, 95% CI 1.2–7.7), sensory disturbance (OR 3.1, 95% CI 1.1–8.9) and depression (OR 4.1, 95% CI 1.4–13), but not with spasticity as an independent variable. The majority of the direct costs for one year (78%) were associated with hospitalization, whereas 20% was associated with municipality services. Only 1% of all direct costs were related to primary health care and 1% to medication. The mean (median, inter-quartile range) direct cost for stroke patients with spasticity was PPP$ 84 195 (72 116, 53 707) compared to PPP$ 21 842 (12 385, 17 484) for stroke patients without spasticity (P < 0.001).

Studies suggest that deficits in central regulation of stretch reflex thresholds (SRT) underlie both spasticity and other disorders of motor control. We investigated intra- and inter-evaluator reliability to quantify spasticity based on tonic SRT (TSRT) and the relationship between TSRT and Modified Ashworth Scale (MAS, clinical assessment of resistance to stretch). Spasticity was evaluated in 20 subjects with chronic stroke-related spasticity in two different days, by three evaluators. Twenty different velocity-dependent dynamic SRT (angle where biceps brachii EMG signal increased for a given velocity of stretch) were recorded. TSRT (excitability of motoneurons at 0°/sec) was then computed. Spasticity was also estimated with MAS. Reliability was moderately good for subjects with moderately high spasticity (intra--evaluator: 0.46 to 0.68, inter--evaluator: 0.53 to 0.68). There was no correlation between TSRT and MAS since they measure different phenomena. TSRT is a promising new measure of spasticity. Further improvements for its quantification are suggested.