View clinical trials related to Spasticity.
Filter by:Spasticity has been defined as a disorder of the sensorimotor system characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. The treatment goal of spasticity is Medical treatment generally combines physiotherapy with medications, depending on spasticity distribution. Systemic treatments such as oral or intrathecal baclofen are generally considered in case of generalized spasticity, whereas local treatments are considered in case of focal spasticity. Local treatments such as Botulinum Toxin type A, phenol, and alcohol present several advantages, allowing to treat of selected muscles without the risk of sedation. As stated above, they are indicated for focal spasticity but might be helpful even in the presence of generalized spasticity with identified focal goals (Bethoux et al., 2015). In particular, Botulinum Toxin type A (BoNT-A) is considered the gold standard treatment for focal spasticity, showing a level A evidence for spasticity reduction in upper- and lower-limb spasticity (Simpson et al., 2016). However, current evidence is mainly focused on post-stroke spasticity (Franceschini et al., 2014), whereas it is still limited in spasticity as a consequence of other aetiologies, such as spinal cord injury (SCI), traumatic brain injury (TBI), or multiple sclerosis (MS). Interestingly, spasticity is a major concern for the rehabilitation of these patients. The aim of this observational study is the evaluation of the clinical efficacy of BoNT-A in spasticity reduction in patients affected by neurological conditions different from post-stroke spasticity, such as SCI, TBI, and MS.
The aim of the study is to describe the long-term use of abobotulinumtoxinA (Dysport®) in adult subjects affected with upper limb spasticity (ULS) +/- lower limb spasticity (LLS) who received treatment with Dysport® for a minimum of three injections cycles at the Instituto de Medicina Física e Reabilitação do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (IMREA HC FMUSP) in Brazil.
The aim of the study is to describe the long term use of Botulinum Neurotoxin Type A (BoNT-A) in adult subjects affected with upper and/or lower limb spasticity who received treatment with BoNT-A for a minimum of three injections cycles at three Italian centers. The study has a retrospective design and data relating to subjects' injections cycles occurred in the past are collected. Period of observation defined in the protocol is from 2008 to 2018, but it could change for each subject according to the number of injections cycles performed. Time frame for data collection is 12 months from study start.
40 chronic stroke patients with upper limb spasticity will randomly divided into two groups. First group will receive 3 sessions of radial extracorporeal shock wave therapy (rESWT) with one week apart without cessation of current physical therapy, while the second group will continue to receive conventional rehabilitative program. Assessment will be done at baseline, 2 weeks after rESWT and 3 months after rESWT using Modified Ashworth Scale, Fugl Meyer Assessment for hand function and wrist control, motricity index for pinch grip and Hmax/ Mmax amplitude ratio of flexor carpi radialis muscle.
Phase 2/3, randomized, double-blind, placebo-controlled, single-treatment, multicenter trial assessing the efficacy and safety of MYOBLOC for the treatment of lower limb spasticity, in adults followed by an open-label extension safety trial.
Inflammatory synaptopathy is a prominent pathogenic mechanism in multiple sclerosis (MS) and in its mouse model, which can cause excitotoxic damage by long-lasting excessive synaptic excitation and, consequentially, drives disease progression by leading to motor and cognitive deficits. As synaptopathy occurs early during the disease course and is potentially reversible, it represents an appealing therapeutic target in MS. Although reliable biomarkers of MS synaptopathy are still missing, recent researches highlighted miR-142-3p as a possible candidate. Indeed, miR-142-3p has been described to promote the IL-1beta-dependent synaptopathy by downregulating GLAST/EAAT1, a crucial glial transporter involved in glutamate homeostasis. Furthermore, mir-142-3p has been suggested as a putative negative MS prognostic factor and a target of current MS disease modifying therapies. The hypothesis of this study is that miR-142-3p represents a good biomarker for excitotoxic synaptopathy to predict MS course, and, possibly, treatment efficacy at individual level, including both pharmacological strategies and non-pharmacological interventions, like therapeutic transcranial magnetic stimulation (TMS) to ameliorate MS spasticity. To this aim, the role of miR-142-3p in MS synaptopathy, its potential impact on the efficacy of disease-modifying treatments currently used in MS therapy as well as the influence of genetic variants (SNPs) of miR-142-3p and GLAST/EAAT1 coding genes on the responsiveness to therapeutic TMS, will be further investigated in the study. By validating miR-142-3p as potential biomarker of synaptopathy, it is expect to improve MS prognosis and personalized therapies. Patients with MS, who will undergo neurological assessment, conventional brain MRI scan, and CSF and blood withdrawal for diagnostic and clinical reasons at the Neurology Unit of IRCCS INM-Neuromed will be enrolled in the study. Neurophysiological, biochemical and genetic parameters together with lower limb spasticity will be evaluated. Subjects, who will undergo blood sampling and/or lumbar puncture for clinical suspicions, later on not confirmed, will be recruited as control group. A subgroup of MS patients showing lower limb spasticity will be included in a two-week repetitive TMS stimulation protocol (iTBS) to correlate the patient responsiveness to this non-pharmacological treatment with MS-significant SNPs of both miR-142-3p and GLAST/EAAT1 coding genes.
The investigators aim to determine if dry needling technique in a non myofascial trigger point area generate the same changes in spasticity, function and pain responses as with dry needling in a myofascial trigger point area.
Study hypothesis: The DNHS technique, performed via one session of deep dry needling of myofascial trigger points applied to the biceps brachii, brachialis, flexor digitorum superficialis, flexor digitorum profundus, triceps brachii, extensor digitorum and adductor pollicis muscle is effective for decreasing spasticity and muscle stiffness (both of which are components of hypertonia) as well as for improving the upper limb function of the previously described muscles in patients with chronic cerebral vascular accident (CVA), assessed both post-intervention and after 15 days. General aims To analyse the immediate therapeutic effect of the DNHS technique and the effect at 15 days follow-up, for the following variables: - Spasticity - Muscle stiffness - Upper limb function - Patient perceived quality of life Materials and methods Population: patients from the province of Zaragoza (Spain) diagnosed with a haemorrhagic or ischemic CVA by a neurologist. Recruitment strategy: recruitment will take place via the Stroke Association in Aragon (AIDA) [Aragon Stroke Association] in the province of Zaragoza, Spain, seeing as the greater proportion of patients who have suffered a stroke and are in the chronic stage of the illness go to this centre to receive treatment. Thus, this avoids patients having to travel elsewhere for the study. Furthermore, in the case of patients who wish to participate in the study after having received information via third persons or via other means and who are not members of the Association or do not attend the centre on a regular basis, the Association AIDA has offered to allow these people to attend for free, making its facilities available and supporting the development of this study.
The purpose of this study is to evaluate if it is possible to use a new 3D imaging method to guide Botulinum neurotoxin (BTX) injection for muscle spasticity management after stroke. This imaging method is called three dimensional innervation zone imaging, or 3DIZI.
Involuntary muscle activity, often called spasticity, is a common problem following spinal cord injury (SCI) that can make it hard to move. Many things can cause spasticity including: muscle stretch, movement, or it can happen for no reason, and it is often described as an uncontrolled muscle spasm or feeling of stiffness. Drugs are typically used to treat spasticity, but they often have side effects, like muscle weakness, which can add to movement problems. Rehabilitation therapies offer alternatives to drugs for treating involuntary muscle activity, and rehabilitation can also improve daily function and quality of life. These benefits may be greater when several rehabilitation therapies are used together. Walking ability can be improved with a type of therapy called "locomotor training". This type of therapy may also have the benefit of decreasing spasticity. When locomotor training (LT) is combined with electrical stimulation, the benefits of training may be increased. In this study, investigators will use a kind of stimulation called transcutaneous spinal cord stimulation ("TSS") to stimulate participants' spinal cord nerves during locomotor training.