Database : MEDLINE
Search on : Muscle and Rigidity [Words]
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[PMID]: 29272080
[Au] Autor:Shamloo A; Mehrafrooz B
[Ad] Address:Department of Mechanical Engineering, Sharif University of Technology, Tehran, Iran.
[Ti] Title:Nanomechanics of actin filament: A molecular dynamics simulation.
[So] Source:Cytoskeleton (Hoboken);75(3):118-130, 2018 Mar.
[Is] ISSN:1949-3592
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Actin is known as the most abundant essentially protein in eukaryotic cells. Actin plays a crucial role in many cellular processes involving mechanical forces such as cell motility, adhesion, muscle contraction, and intracellular transport. However, little is known about the mechanical properties of this protein when subjected to mechanical forces in cellular processes. In this article, a series of large-scale molecular dynamics simulations are carried out to elucidate nanomechanical behavior such as elastic and viscoelastic properties of a single actin filament. Here, we used two individual methods namely, all-atoms and coarse-grained molecular dynamics, to evaluate elastic properties of a single actin filament. In the other word, based on Brownian motions of the filament and using the principle of the equipartition theorem, in aqueous solution, tensile stiffness, torsional rigidity, and bending rigidity of the single actin filament are studied. The results revealed that increasing the sampling window time leads to convergence of obtained mechanical properties to the experimental values. Moreover, in order to investigate viscoelastic properties of a single actin filament, constant force steered molecular dynamics method is used to apply different external tensile loads and perform five individual creep tests on the molecule. The strain-time response of the filament for each creep test is obtained. Based on the Kelvin-Voigt model, the results reveal that a single actin filament shows a nonlinear viscoelastic behavior, with a Young's modulus of 2.85 GPa, a viscosity of 4.06 GPa.ns, and a relaxation time in the range of 1.42 ns which were measured here for the first time at the single filament level. The findings of this article suggest that molecular dynamics simulations could also be a useful tool for investigating the mechanical behavior of bio-nanomaterials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1002/cm.21429

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[PMID]: 29516782
[Au] Autor:Jaffar J; Yang SH; Kim SY; Kim HW; Faiz A; Chrzanowski W; Burgess JK
[Ti] Title:Greater cellular stiffness in fibroblasts from patients with idiopathic pulmonary fibrosis.
[So] Source:Am J Physiol Lung Cell Mol Physiol;, 2018 Mar 08.
[Is] ISSN:1522-1504
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Idiopathic pulmonary fibrosis (IPF) is a lethal lung disease involving degenerative breathing capacity. Fibrotic disease is driven by dysregulation in mechanical forces at the organ, tissue and cellular level. While it is known that, in certain pathologies, diseased cells are stiffer than healthy cells, it is not known if fibroblasts derived from patients with IPF are stiffer than their normal counterparts. Using IPF patient-derived cell cultures, we measured the stiffness of individual lung fibroblasts via high-resolution force maps using atomic force microscopy. Fibroblasts from patients with IPF were stiffer and had an augmented cytoskeletal response to TGFß1 compared to fibroblasts from donors without IPF. The results from this novel study indicate that the increased stiffness of lung fibroblasts of IPF patients may contribute to the increased rigidity of fibrotic lung tissue.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1152/ajplung.00030.2018

  3 / 5298 MEDLINE  
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[PMID]: 29253290
[Au] Autor:Ying GY; Yao Y; Shen F; Wu ZY; Chen CM; Zhu YJ
[Ad] Address:Department of Neurosurgery, Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.
[Ti] Title:Percutaneous Endoscopic Removal of Cervical Foraminal Schwannoma via Interlaminar Approach: A Case Report.
[So] Source:Oper Neurosurg (Hagerstown);14(1):1-5, 2018 Jan 01.
[Is] ISSN:2332-4260
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND IMPORTANCE: Cervical foraminal schwannomas commonly originate from spinal nerves that pass through the intervertebral foramen of the cervical vertebrae. Because of the proximity of this type of tumor to the vertebral artery and spinal nerves, surgical management remains a major challenge. Conventional open spine surgery usually requires the removal of the articular process and is supplemented by a simultaneous posterolateral spine fusion surgery. To decrease the associated risks of surgical complications by further reducing invasiveness, percutaneous spinal endoscopy may be used for resection of foraminal spinal neoplasm. CLINICAL PRESENTATION: A 52-yr-old female who presented with neck pains with duration of 1 yr was admitted to our hospital. Physical examination revealed moderate rigidity in the neck and grade 5 muscle strength in both upper and lower limbs. Preoperative magnetic resonance imaging (MRI) scans demonstrated a left-sided lesion at the C3-C4 intervertebral foraminal area. Under C-arm fluoroscopy navigation and neuromonitoring, the endoscope was properly positioned on the same side of the tumor, and a small part of the left C3 inferior and C4 superior lamina were first removed by an endoscopic drill to enlarge the interlaminar space. Next, through an endoscopic working canal, the left intervertebral ligamentum flavum was removed to fully expose the tumor. The tumor mass was finally resected in a piecemeal approach. Postoperative MRI confirmed complete tumor resection. CONCLUSION: This is the first case report of a total removal of a cervical foraminal schwannoma with a percutaneous spinal endoscopic procedure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1093/ons/opx088

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[PMID]: 29504479
[Au] Autor:Cho N; Razipour SE; McCain ML
[Ad] Address:1 Laboratory for Living Systems Engineering, Department of Biomedical Engineering, USC Viterbi School of Engineering, University of Southern California, Los Angeles, CA 90089, USA.
[Ti] Title:TGF-ß1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts.
[So] Source:Exp Biol Med (Maywood);:1535370218761628, 2018 Jan 01.
[Is] ISSN:1535-3699
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cardiac fibroblasts and their activated derivatives, myofibroblasts, play a critical role in wound healing after myocardial injury and often contribute to long-term pathological outcomes, such as excessive fibrosis. Thus, defining the microenvironmental factors that regulate the phenotype of cardiac fibroblasts and myofibroblasts could lead to new therapeutic strategies. Both chemical and biomechanical cues have previously been shown to induce myofibroblast differentiation in many organs and species. For example, transforming growth factor beta 1, a cytokine secreted by neutrophils, and rigid extracellular matrix environments have both been shown to promote differentiation. However, the relative contributions of transforming growth factor beta 1 and extracellular matrix rigidity, two hallmark cues in many pathological myocardial microenvironments, to the phenotype of human cardiac fibroblasts are unclear. We hypothesized that transforming growth factor beta 1 and rigid extracellular matrix environments would potentially have a synergistic effect on the differentiation of human cardiac fibroblasts to myofibroblasts. To test this, we seeded primary human adult cardiac fibroblasts onto coverslips coated with polydimethylsiloxane of various elastic moduli, introduced transforming growth factor beta 1, and longitudinally quantified cell phenotype by measuring expression of α-smooth muscle actin, the most robust indicator of myofibroblasts. Our data indicate that, although extracellular matrix rigidity influenced differentiation after one day of transforming growth factor beta 1 treatment, ultimately transforming growth factor beta 1 superseded extracellular matrix rigidity as the primary regulator of myofibroblast differentiation. We also measured expression of POSTN, FAP, and FSP1, proposed secondary indicators of fibroblast/myofibroblast phenotypes. Although these genes partially trended with α-smooth muscle actin expression, they were relatively inconsistent. Finally, we demonstrated that activated myofibroblasts incompletely revert to a fibroblast phenotype after they are re-plated onto new surfaces without transforming growth factor beta 1, suggesting differentiation is partially reversible. Our results provide new insights into how microenvironmental cues affect human cardiac fibroblast differentiation in the context of myocardial pathology, which is important for identifying effective therapeutic targets and dictating supporting cell phenotypes for engineered human cardiac disease models. Impact statement Heart disease is the leading cause of death worldwide. Many forms of heart disease are associated with fibrosis, which increases extracellular matrix (ECM) rigidity and compromises cardiac output. Fibrotic tissue is synthesized primarily by myofibroblasts differentiated from fibroblasts. Thus, defining the cues that regulate myofibroblast differentiation is important for understanding the mechanisms of fibrosis. However, previous studies have focused on non-human cardiac fibroblasts and have not tested combinations of chemical and mechanical cues. We tested the effects of TGF-ß1, a cytokine secreted by immune cells after injury, and ECM rigidity on the differentiation of human cardiac fibroblasts to myofibroblasts. Our results indicate that differentiation is initially influenced by ECM rigidity, but is ultimately superseded by TGF-ß1. This suggests that targeting TGF-ß signaling pathways in cardiac fibroblasts may have therapeutic potential for attenuating fibrosis, even in rigid microenvironments. Additionally, our approach can be leveraged to engineer more precise multi-cellular human cardiac tissue models.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher
[do] DOI:10.1177/1535370218761628

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[PMID]: 29174294
[Au] Autor:Liu H; Jia L; Chen X; Shi L; Xie J
[Ad] Address:Collaborative Innovation Center for Brain Science, Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Medical College of Qingdao University, 266071, China.
[Ti] Title:The Kv7/KCNQ channel blocker XE991 protects nigral dopaminergic neurons in the 6-hydroxydopamine rat model of Parkinson's disease.
[So] Source:Brain Res Bull;137:132-139, 2018 Mar.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The excitability of dopaminergic neurons in the substantia nigra pars compacta (SNc) that supply the striatum with dopamine (DA) determines the function of the nigrostriatal system for motor coordination. We previously showed that 4-pyridinylmethyl-9(10H)-anthracenone (XE991), a specific blocker of Kv7/KCNQ channels, enhanced the excitability of nigral DA neurons and resulted in attenuation of haloperidol-induced catalepsy in a Parkinson's disease (PD) rat model. However, whether XE991 exhibits neuroprotective effects towards DA neuron degeneration remains unknown. The aim of this study was to investigate the effects of Kv7/KCNQ channel blocker, XE991, on 6-hydroxydopamine (6-OHDA)-induced nigral DA neuron degeneration and motor dysfunction. Using immunofluorescence staining and western blotting, we showed that intracerebroventricular administration of XE991 prevented the 6-OHDA-induced decrease in tyrosine hydroxylase (TH)-positive neurons and TH protein expression in the SNc. High-performance liquid chromatography with electrochemical detection (HPLC-ECD) also revealed that XE991 partly restored the levels of DA and its metabolites in the striatum. Moreover, XE991 decreased apomorphine (APO)-induced contralateral rotations, enhanced balance and coordination, and attenuated muscle rigidity in 6-OHDA-treated rats. Importantly, all neuroprotective effects by XE991 were abolished by co-application of Kv7/KCNQ channel opener retigabine and XE991. Thus, Kv7/KCNQ channel inhibition by XE991 can exert neuroprotective effects against 6-OHDA-induced degeneration of the nigrostriatal DA system and motor dysfunction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:In-Data-Review

  6 / 5298 MEDLINE  
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[PMID]: 29390334
[Au] Autor:Lee HD; Chang MC
[Ad] Address:Department of Physical Medicine and Rehabilitation, College of Medicine, Yeungnam University, Namku, Daegu, Republic of Korea.
[Ti] Title:Degeneration of the corticofugal tract from the secondary motor area in a Parkinson's disease patient with limb-kinetic apraxia: A case report.
[So] Source:Medicine (Baltimore);96(50):e9195, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: In this case report, we describe a Parkinson's disease (PD) patient with limb-kinetic apraxia (LKA) in whom degeneration of the corticofugal tract (CFT) from the supplementary motor area (SMA) was observed in diffusion tensor tractography (DTT). PATIENT CONCERNS: A 63-year-old woman presented with a loss of dexterity in both upper extremities, which indicated LKA, and typical PD-related symptoms, including a gait disturbance with a short step, resting tremor in both upper extremities, and rigidity, and these symptoms had been present for 2 years. The F-florinated-N-3-fluoropropyl-2-ß-carboxymethoxy-3-ß-(4-lodophenyl) nortropane positron emission tomography scanning findings were consistent with PD. Based on the clinical symptoms and imaging findings, we diagnosed the patient with PD. In a coin-rotation test that was used to evaluate the severity of the LKA, the patient's results significantly decreased compared to the results of the normal controls. DIAGNOSES: The DTT showed that the CFTs from the SMAs in both hemispheres were partially torn and thinned. The fractional anisotropy values and CFT volumes in both SMAs were >2 standard deviations lower than those of the normal controls. INTERVENTIONS: The patient was treated with an initial dose of 150/37.5 mg/day of levodopa/benserazide, and the dose was gradually increased to 400/100 mg/day. OUTCOMES: After treatment, although the bradykinesia, rigidity, and resting tremor of the patient significantly decreased, the dexterity of the patient's hands did not improve. LESSONS: These observations indicated degeneration of the CFTs from the SMAs in both hemispheres in the patient. This degeneration might have, at least in part, contributed to the patient's LKA. The results of this study suggest that CFT degeneration could be one of the pathological mechanisms underlying LKA in patients with PD.
[Mh] MeSH terms primary: Motor Cortex/pathology
Parkinson Disease/pathology
[Mh] MeSH terms secundary: Anisotropy
Antiparkinson Agents/therapeutic use
Benserazide/therapeutic use
Diffusion Tensor Imaging
Drug Combinations
Female
Humans
Levodopa/therapeutic use
Middle Aged
Motor Cortex/diagnostic imaging
Muscle Rigidity/diagnostic imaging
Muscle Rigidity/drug therapy
Muscle Rigidity/pathology
Muscular Atrophy, Spinal/diagnostic imaging
Muscular Atrophy, Spinal/drug therapy
Muscular Atrophy, Spinal/pathology
Parkinson Disease/diagnostic imaging
Parkinson Disease/drug therapy
Positron-Emission Tomography
Tremor/diagnostic imaging
Tremor/drug therapy
Tremor/pathology
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antiparkinson Agents); 0 (Drug Combinations); 0 (benserazide, levodopa drug combination); 46627O600J (Levodopa); 762OS3ZEJU (Benserazide)
[Em] Entry month:1802
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009195

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[PMID]: 29422510
[Au] Autor:Zhu W; Kim BC; Wang M; Huang J; Isak A; Bexiga NM; Monticone R; Ha T; Lakatta EG; An SS
[Ad] Address:Department of Environmental Health and Engineering, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 21205, USA.
[Ti] Title:TGFß1 reinforces arterial aging in the vascular smooth muscle cell through a long-range regulation of the cytoskeletal stiffness.
[So] Source:Sci Rep;8(1):2668, 2018 Feb 08.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Here we report exquisitely distinct material properties of primary vascular smooth muscle (VSM) cells isolated from the thoracic aorta of adult (8 months) vs. aged (30 months) F344XBN rats. Individual VSM cells derived from the aged animals showed a tense internal network of the actin cytoskeleton (CSK), exhibiting increased stiffness (elastic) and frictional (loss) moduli than those derived from the adult animals over a wide frequency range of the imposed oscillatory deformation. This discrete mechanical response was long-lived in culture and persistent across a physiological range of matrix rigidity. Strikingly, the pro-fibrotic transforming growth factor ß1 (TGFß1) emerged as a specific modifier of age-associated VSM stiffening in vitro. TGFß1 reinforced the mechanical phenotype of arterial aging in VSM cells on multiple time and length scales through clustering of mechanosensitive α ß and α ß integrins. Taken together, these studies identify a novel nodal point for the long-range regulation of VSM stiffness and serve as a proof-of-concept that the broad-based inhibition of TGFß1 expression, or TGFß1 signal transduction in VSM, may be a useful therapeutic approach to mitigate the pathologic progression of central arterial wall stiffening associated with aging.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:In-Data-Review
[do] DOI:10.1038/s41598-018-20763-w

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[PMID]: 29396114
[Au] Autor:Pandey P; Hawkes W; Hu J; Megone WV; Gautrot J; Anilkumar N; Zhang M; Hirvonen L; Cox S; Ehler E; Hone J; Sheetz M; Iskratsch T
[Ad] Address:Randall Centre for Cell and Molecular Biophysics, King's College London, SE1 1UL London, UK; Institute of Bioengineering and School of Engineering and Materials Science, Queen Mary University of London, E1 4NS London, UK.
[Ti] Title:Cardiomyocytes Sense Matrix Rigidity through a Combination of Muscle and Non-muscle Myosin Contractions.
[So] Source:Dev Cell;44(3):326-336.e3, 2018 Feb 05.
[Is] ISSN:1878-1551
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mechanical properties are cues for many biological processes in health or disease. In the heart, changes to the extracellular matrix composition and cross-linking result in stiffening of the cellular microenvironment during development. Moreover, myocardial infarction and cardiomyopathies lead to fibrosis and a stiffer environment, affecting cardiomyocyte behavior. Here, we identify that single cardiomyocyte adhesions sense simultaneous (fast oscillating) cardiac and (slow) non-muscle myosin contractions. Together, these lead to oscillating tension on the mechanosensitive adaptor protein talin on substrates with a stiffness of healthy adult heart tissue, compared with no tension on embryonic heart stiffness and continuous stretching on fibrotic stiffness. Moreover, we show that activation of PKC leads to the induction of cardiomyocyte hypertrophy in a stiffness-dependent way, through activation of non-muscle myosin. Finally, PKC and non-muscle myosin are upregulated at the costameres in heart disease, indicating aberrant mechanosensing as a contributing factor to long-term remodeling and heart failure.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:In-Data-Review

  9 / 5298 MEDLINE  
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Clinical Trials Registry
Clinical Trials Registry
Clinical Trials Registry
Clinical Trials Registry
Clinical Trials Registry
Clinical Trials Registry
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[PMID]: 29424169
[Au] Autor:Wang YJ; Li CH; Lin SH; Wang YZ
[Ad] Address:Department of Joint Surgery, Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong, China; yjwang730715@163.com.
[Ti] Title:[Clinical efficiency and activity range of stiff knee by total knee arthroplasty].
[So] Source:Zhongguo Gu Shang;30(6):508-512, 2017 Jun 25.
[Is] ISSN:1003-0034
[Cp] Country of publication:China
[La] Language:chi
[Ab] Abstract:OBJECTIVE: To observe clinical effect and influencing factor of total knee arthroplasty (TKA) for the treatment of stiff knee. METHODS: From January 2010 to October 2014, 20 patients(25 knees) with stiff knee were treated with TKA. Among them, including 2 males(3 knees) and 18 females(22 knees), aged from 55 to 78 years old with an average of(64.5± 4.9) years old, the courses of disease ranged from 5 to 21 years with an average 8.3 years. Preoperative and postoperative HSS (hospital for special surgery knee score) score, activity range and complications were observed and compared. RESULTS: All patients were followed up from 12 to 69 months with an average of 35.3 months. Ten patients occurred complications after operation. HSS score was improved from 32.36±12.31 preoperatively to 80.70±18.52 postoperatively, and had statistical difference between two groups;7 knees obtained excellent results, 15 knees good and 3 knees moderate. Activity range was improved from(39.4±5.3)°preoperatively to (92.5±11.2)° at the latest follow up. CONCLUSIONS: Total knee arthroplasty for stiffness knees is feasible and could obtain satisfied activity range and function.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180209
[Lr] Last revision date:180209
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Process
[do] DOI:10.3969/j.issn.1003-0034.2017.06.005

  10 / 5298 MEDLINE  
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Chung, Tae Mo
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[PMID]: 29423615
[Au] Autor:Dressler D; Bhidayasiri R; Bohlega S; Chana P; Chien HF; Chung TM; Colosimo C; Ebke M; Fedoroff K; Frank B; Kaji R; Kanovsky P; Koçer S; Micheli F; Orlova O; Paus S; Pirtosek Z; Relja M; Rosales RL; Sagástegui-Rodríguez JA; Schoenle PW; Shahidi GA; Timerbaeva S; Walter U; Saberi FA
[Ad] Address:Head of Movement Disorders Section, Department of Neurology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany. dressler.dirk@mh-hannover.de.
[Ti] Title:Defining spasticity: a new approach considering current movement disorders terminology and botulinum toxin therapy.
[So] Source:J Neurol;, 2018 Feb 08.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Spasticity is a symptom occurring in many neurological conditions including stroke, multiple sclerosis, hypoxic brain damage, traumatic brain injury, tumours and heredodegenerative diseases. It affects large numbers of patients and may cause major disability. So far, spasticity has merely been described as part of the upper motor neurone syndrome or defined in a narrowed neurophysiological sense. This consensus organised by IAB-Interdisciplinary Working Group Movement Disorders wants to provide a brief and practical new definition of spasticity-for the first time-based on its various forms of muscle hyperactivity as described in the current movement disorders terminology. We propose the following new definition system: Spasticity describes involuntary muscle hyperactivity in the presence of central paresis. The involuntary muscle hyperactivity can consist of various forms of muscle hyperactivity: spasticity sensu strictu describes involuntary muscle hyperactivity triggered by rapid passive joint movements, rigidity involuntary muscle hyperactivity triggered by slow passive joint movements, dystonia spontaneous involuntary muscle hyperactivity and spasms complex involuntary movements usually triggered by sensory or acoustic stimuli. Spasticity can be described by a documentation system grouped along clinical picture (axis 1), aetiology (axis 2), localisation (axis 3) and additional central nervous system deficits (axis 4). Our new definition allows distinction of spasticity components accessible to BT therapy and those inaccessible. The documentation sheet presented provides essential information for planning of BT therapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180209
[Lr] Last revision date:180209
[St] Status:Publisher
[do] DOI:10.1007/s00415-018-8759-1


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