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Rehabilitation after Trauma
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Once the spinal cord has recovered from spinal shock, spasticity is almost universal. Normally, as a muscle is stretched, strong contraction occurs, stimulating a reflex arc. Inhibitory control from the brain via the spinal cord modifies this response in the muscle. In SCI, this inhibitory influence is absent. Even slight stimuli, such as a slight movement of a limb or even touching the skin, can stimulate this reflex arc and lead to powerful muscle contractions: joint stiffness, loss of movement, muscle spasms and contractures. These spasms are very painful and can be powerful enough to throw a patient from their wheelchair. Measures to control spasticity include stretching, postural management and drugs such as Baclofen, Tizanidine and botulinum toxin.
Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Clinical trials with idebenone have demonstrated some benefit for cardiac hypertrophy in Friedreich's patients.37,38 There was a suggestion of possible benefit for neurologic symptoms at higher doses, especially in patients not yet wheelchair bound.39 Clinical trials are currently underway to assess this prospectively. Symptomatic treatment with: Spasticity medication (e.g. baclofen, botulinum toxin).Physiotherapy.Occupational therapy.Podiatry.Speech therapy.Social work.Cardiology consultation: for hypertrophic cardiomyopathy.Pulmonary function.Orthopedic spinal surgery (Harrington's rod); for scoliosis.
Modelling human neurodegeneration using induced pluripotent stem cells
Published in Christine Hauskeller, Arne Manzeschke, Anja Pichl, The Matrix of Stem Cell Research, 2019
Iryna Prots, Beate Winner, Jürgen Winkler
HSP can be classified into two groups: pure and complicated, based on the absence (pure) or presence (complicated) of additional clinical features besides spastic paraparesis, such as ataxia, extrapyramidal signs, peripheral neuropathy, epilepsy, deafness, optic atrophy, pigmentary retinopathy, cognitive impairment, dementia, and severe amyotrophy (reviewed in [Blackstone, 2012; Fink, 2013]). Unfortunately, there are still no medications or therapies which cure or at least halt disease progression in HSP. The existing therapies are only symptomatic and allow the reduction of symptoms of spasticity by the use of muscle relaxants or botulinum toxin (also known as Botox) to help reduce the spasticity locally (reviewed in [Fink, 2013; Soderblom and Blackstone, 2006]). Other symptoms are treated symptomatically – exercise and physical therapies are important. Therapeutic progress relies on the knowledge of the disease mechanisms. Therefore, studying HSP provides an important means, firstly, to understand the specific molecular mechanisms underlying axonal maintenance and degeneration in motor neurons and, secondly, to develop new effective therapies. It is hoped that the stem cell technology detailed in the section below on ‘iPSC as a modelling tool for human neurodegeneration’ will enable detailed investigations of disease mechanisms and thus treatment of HSP as well as PD.
Treatment approaches of stage III and IV pressure injury in people with spinal cord injury: A scoping review
Published in The Journal of Spinal Cord Medicine, 2023
Carina Fähndrich, Armin Gemperli, Michael Baumberger, Marco Bechtiger, Bianca Roth, Dirk J. Schaefer, Reto Wettstein, Anke Scheel-Sailer
Spasticity and contractures are considered risk factors for skin breakdown in people with SCI/D.32,33 Before flap surgery, spasticity control should be optimized since muscle spasms can tear open fresh surgical incisions.3,31 According to two studies, spasticity has to be suppressed with anti-spasm agents to prevent excessive movements.31,34 In addition, surgery, oral pharmacology, muscle blocks with botulinum toxin, nerve blocks with alcohol or phenol, intrathecal baclofen therapy, preliminary flexor tendon releases, casts or intraoperative tenotomy are described.3,9,32 After surgery, spasticity should be controlled with external fixation for a few weeks to prevent tearing of the flap.9,15 Kreutzträger et al. include considerations about spasticity.15 Spasticity control, however, is not explicitly mentioned as a element among the Basel Decubitus Concept.5,11,15
Dry needling for the treatment of muscle spasticity in a patient with multiple sclerosis: a case report
Published in Physiotherapy Theory and Practice, 2022
Maede Khalifeloo, Soofia Naghdi, Noureddin Nakhostin Ansari, Jan Dommerholt, Mohammad Ali Sahraian
Medical and rehabilitation strategies for decreasing spasticity are reported in the literature (Ansari et al., 2015). Pharmacological options have generalized effects on the body and can trigger side effects such as weakness and cognitive problems (Rizzo, Hadjimichael, Preiningerova, and Vollmer, 2004). Rehabilitation strategies used by physical therapists to reduce spasticity may include hydrotherapy, electrical stimulations, vibration, ice therapy, or other interventions (de Sa et al., 2011). Hydrotherapy and ice therapy have temporary effects on muscle spasticity (de Sa et al., 2011). Electrical stimulation did not have an obvious influence on reduction of spasticity in individuals with MS. However, increasing the duration of the application was found to be beneficial to reduce pain and muscle spasm (Miller, Mattison, Paul, and Wood, 2007). Moreover, whole-body vibration has not been found to be effective for spasticity in patients with MS (Schyns et al., 2009).
Repetitive peripheral magnetic stimulation for the assessment of wrist spasticity: reliability, validation and correlation with clinical measures
Published in Disability and Rehabilitation, 2022
Marta Fernandez-Lobera, Merche Morales, Josep Valls-Solé
The study was composed of three phases:Characterization of the movement induced by rPMS in healthy subjects (HS), a group of patients with stroke in their acute phase (AS), who did not show yet any sign of spasticity, and a group of patients with stroke in their chronic phase (CS), who showed clear signs of spasticity. We expected to establish the influence of paresis in the test by comparing the results in AS with those in HS and the influence of spasticity by comparing results in CS with those in HS and in AS.Examination of test-retest reliability in CS.Evaluation of the effects of botulinum neurotoxin type A (BoNT-A) treatment on the characteristics of the movement induced by rPMS in CS patients. This part of the study was aimed at establishing the correlation of the technique with clinical measures of spasticity.