Limb Spasticity (limb + spasticity)

Distribution by Scientific Domains

Kinds of Limb Spasticity

  • upper limb spasticity


  • Selected Abstracts


    Intrafusal effects of botulinum toxin in post-stroke upper limb spasticity

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2008
    C. Trompetto
    A previous study in subjects with focal dystonia suggested that the greater and longer-lasting effect induced by botulinum toxin type A (BoNT-A) on the tonic vibration reflex (TVR) than on the maximal M-wave (M-max) might be the physiological marker of the toxin's action at the level of intrafusal muscle fibres. With this approach, we investigated the possible effect of BoNT-A on fusimotor synapses in eight patients with post-stroke spasticity (four with no residual motor capacity before treatment and four with partially spared muscle strength and residual motor capacity). TVR and M-max were recorded from the wrist and finger flexor muscles before treatment and at 1, 4 and 7 months afterwards. The TVR reduction was greater than the M-max reduction and remained fairly constant over time only in the subjects with a residual motor capacity before the treatment. This pilot study suggests that some degree of strength and active movement is necessary for the action of BoNT-A on intrafusal fibres. [source]


    Botulinum neurotoxins for post-stroke spasticity in adults: A systematic review,,

    MOVEMENT DISORDERS, Issue 6 2009
    Antonio Emanuele Elia MD
    Abstract The aim of this systematic review was to determine whether botulinum neurotoxin (BoNT) reduce spasticity or improve function in adult patients after stroke. Eleven double-blind randomized placebo-controlled trials met inclusion criteria. They encompassed 782 patients, 767 (98%) of whom received BoNT/A, and 15 (2%) BoNT/B. Most studies used the Ashworth scale as primary outcome measure. Differences between treated and control groups were assessed as categorical or continuous comparisons. The overall effect on upper limb spasticity was in favor of BoNT/A. A significantly higher number of patients had a reduction of upper limb spasticity at 4-week and 8-week evaluations in the treatment group compared with placebo. Mean changes in joint spasticity revealed improvement 3 to 6 weeks and 9 to 12 weeks after treatment. There were insufficient data to establish BoNT/A efficacy on lower limb spasticity or the effect of BoNT/B on the upper and lower limbs. Because of inconsistency and heterogeneity of the available data, it was not possible to perform a meta-analysis on disability and patients' reported outcomes. There was an overlapping safety profile between the treatment and the placebo groups. BoNT/A reduces upper limb spasticity in patients post-stroke, but the improvement in functional ability remains to be established. This gap needs to be filled by new studies to assess the effect of BoNT in the context of multidisciplinary patient management. © 2009 Movement Disorder Society [source]


    Efficacy and safety of NT 201 for upper limb spasticity of various etiologies , a randomized parallel-group study

    ACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010
    M. Barnes
    Barnes M, Schnitzler A, Medeiros L, Aguilar M, Lehnert-Batar A, Minnasch P. Efficacy and safety of NT 201 for upper limb spasticity of various etiologies , a randomized parallel-group study. Acta Neurol Scand: 2010: 122: 295,302. © 2010 John Wiley & Sons A/S. Objective,,, To assess efficacy and safety of two dilutions of botulinum neurotoxin type A NT 201 (Xeomin®) in patients with upper limb spasticity of diverse etiology. Methods,,, Changes in functional disability and muscle tone from baseline to week 4 after NT 201 treatment. Results,,, One hundred ninety-two patients with stroke, brain injury, multiple sclerosis, or cerebral palsy were randomized to either 50 or 20 U/ml NT 201 dilutions. The maximum total NT 201 dose was 495 units. Four weeks post-injection, a , 1-point reduction was observed on the Disability Assessment Scale in 57.1%, and on the Ashworth scale in , 62.2% of patients. The 20 U/ml NT 201 dilution was non-inferior to the 50 U/ml NT 201 dilution. Global improvement was rated high by patients (80.2%) and investigators (89.0%). Conclusions,,, NT 201 improved functional disability and muscle tone and was well tolerated in patients with upper limb spasticity of diverse etiology in both dilutions. [source]


    New potent and selective inhibitors of anandamide reuptake with antispastic activity in a mouse model of multiple sclerosis

    BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006
    Alessia Ligresti
    We previously reported that the compound O-2093 is a selective inhibitor of the reuptake of the endocannabinoid anandamide (AEA). We have now re-examined the activity of O-2093 in vivo and synthesized four structural analogs (O-2247, O-2248, O-3246, and O-3262), whose activity was assessed in: (a) binding assays carried out with membranes from cells overexpressing the human CB1 and CB2 receptors; (b) assays of transient receptor potential of the vanilloid type-1 (TRPV1) channel functional activity (measurement of [Ca2+]i); (c) [14C]AEA cellular uptake and hydrolysis assays in rat basophilic leukaemia (RBL-2H3) cells; (d) the mouse ,tetrad' tests (analgesia on a hot plate, immobility on a ,ring', rectal hypothermia and hypolocomotion in an open field); and (e) the limb spasticity test in chronic relapsing experimental allergic encephalomyelitis (CREAE) mice, a model of multiple sclerosis (MS). O-2093, either synthesized by us or commercially available, was inactive in the ,tetrad' up to a 20 mg kg,1 dose (i.v.). Like O-2093, the other four compounds exhibited low affinity in CB1 (Ki from 1.3 to >10 ,M) and CB2 binding assays (1.310 ,M), very low potency as fatty acid amide hydrolase (FAAH) inhibitors (IC50>25 ,M) and were inactive in the ,tetrad' up to a 30 mg kg,1 dose (i.v.). While O-2247 and O-2248 were poor inhibitors of [14C]AEA cellular uptake (IC50>40 ,M), O-3246 and O-3262 were quite potent in this assay. O-3246, which exhibits only a very subtle structural difference with O-2093, is the most potent inhibitor of AEA uptake reported in vitro under our experimental conditions (IC50=1.4 ,M) and is 12-fold more potent than O-2093. When injected intravenously O-3246 and O-3262, again like O-2093 and unlike O-2247 and O-2248, significantly inhibited limb spasticity in mice with CREAE. These data confirm the potential utility of selective AEA uptake inhibitors as anti-spasticity drugs in MS and, given the very subtle chemical differences between potent and weak inhibitors of uptake, support further the existence of a specific mechanism for this process. British Journal of Pharmacology (2006) 147, 83,91. doi:10.1038/sj.bjp.0706418 [source]


    Functional changes of the cortical motor system in hereditary spastic paraparesis

    ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009
    B. Koritnik
    Background,,, Hereditary spastic paraparesis (HSP) is a heterogeneous group of disorders characterized by progressive bilateral lower limb spasticity. Functional imaging studies in patients with corticospinal tract involvement have shown reorganization of motor circuitry. Our study investigates functional changes in sensorimotor brain areas in patients with HSP. Methods,,, Twelve subjects with HSP and 12 healthy subjects were studied. Functional magnetic resonance imaging (fMRI) was used to measure brain activation during right-hand finger tapping. Image analysis was performed using general linear model and regions of interest (ROI)-based approach. Weighted laterality indices (wLI) and anterior/posterior indicies (wAI and wPI) were calculated for predefined ROIs. Results and discussion,,, Comparing patients and controls at the same finger-tapping rate (1.8 Hz), there was increased fMRI activation in patients' bilateral posterior parietal cortex and left primary sensorimotor cortex. No differences were found when comparing patients and controls at 80% of their individual maximum tapping rates. wLI of the primary sensorimotor cortex was significantly lower in patients. Subjects with HSP also showed a relative increase in the activation of the posterior parietal and premotor areas compared with that of the primary sensorimotor cortex. Our findings demonstrate an altered pattern of cortical activation in subjects with HSP during motor task. The increased activation probably reflects reorganization of the cortical motor system. [source]