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Muscle Stiffness (muscle + stiffness)
Selected AbstractsFunctional Electrical Stimulation-Induced Surface Muscle Stiffness Captured by Computer-Controlled TonometryARTIFICIAL ORGANS, Issue 3 2002Dietmar Rafolt Abstract: A new tonometric test system to assess surface stiffness over relaxed and activated calf muscles was developed. The mechanical arrangement consists of a skin indentor driven by a torque motor (galvo-drive) that is rigidly connected to an ankle dynamometer. The indentation depth is measured by a displacement transducer. Software routines for cyclic indentation (recording of stiffness curves), static indentation (sensing of twitch responses), and vibration (skin resonance) were implemented. A visual interface is used to capture surface stiffness during target contractions and during controlled relaxation. For functional electrical stimulation (FES) applications, the software includes a pulse train synthesizer to generate arbitrary stimulation test patterns. The system's performance was tested in FES and voluntary contraction procedures. [source] Electrophysiological studies in a mouse model of Schwartz,Jampel syndrome demonstrate muscle fiber hyperactivity of peripheral nerve originMUSCLE AND NERVE, Issue 1 2009Andoni Echaniz-Laguna MD Abstract Schwartz,Jampel syndrome (SJS) is an autosomal-recessive condition characterized by muscle stiffness and chondrodysplasia. It is due to loss-of-function hypomorphic mutations in the HSPG2 gene that encodes for perlecan, a proteoglycan secreted into the basement membrane. The origin of muscle stiffness in SJS is debated. To resolve this issue, we performed an electrophysiological investigation of an SJS mouse model with a missense mutation in the HSPG2 gene. Compound muscle action potential amplitudes, distal motor latencies, repetitive nerve stimulation tests, and sensory nerve conduction velocities of SJS mice were normal. On electromyography (EMG), neuromyotonic discharges, that is, bursts of motor unit action potentials firing at high rates (120,300 HZ), were constantly observed in SJS mice in all muscles, except in the diaphragm. Neuromyotonic discharges were not influenced by general anesthesia and disappeared with curare administration. They persisted after complete motor nerve section, terminating only with Wallerian degeneration. These results demonstrate that perlecan deficiency in SJS provokes a neuromyotonic syndrome. The findings further suggest a distal axonal localization of the generator of neuromyotonic discharges. SJS should now be considered as an inherited disorder with peripheral nerve hyperexcitability. Muscle Nerve, 2009 [source] Differential diagnosis of myotonic disordersMUSCLE AND NERVE, Issue 3 2008Timothy M. Miller MD Abstract The presence of myotonia and paramyotonia on clinical examination and of myotonic discharges during electrodiagnostic (EDX) studies are important for the diagnosis of certain neuromuscular conditions. The increased muscle activity of myotonia produces muscle stiffness that improves with repeated activity. Paramyotonia produces a similar symptom, but the stiffness paradoxically increases with activity. Myotonic discharges are easily recognized on EDX testing because of the waxing and waning discharges. Myotonic dystrophy and myotonia congenita share both clinical and electrodiagnostic myotonia. Paramyotonia congenita and hyperkalemic periodic paralysis are associated with clinical paramyotonia and electrical myotonia. Acid maltase deficiency often produces myotonic potentials without clinical evidence of myotonia or paramyotonia. The differential diagnosis of these myotonic disorders is discussed. Muscle Nerve, 2007 [source] Physical signs associated with excessive television-game playing and sleep deprivationPEDIATRICS INTERNATIONAL, Issue 6 2001Yusaku Tazawa AbstractBackground: To elucidate significance of physical signs seen in excessive television-game (TVG) players complaining of unexplained persistant symptoms, a cross-sectional cohort study was designed. Methods: A total of 1143 school children, aged between 6 and 11-years-old, and their parents were included in the study. Questionnaires were sent to guardians asking the number of hours that their children watched TV, TVG, and slept. All children were examined to check for three physical signs, black rings in the skin under the eye (BR), muscle stiffness in the shoulder (MS), and displacement of the scapula associated with muscle stiffness in the shoulder (DS/MS) by inspection and palpitation. Results: The three signs, BR, MS and DS/MS, were present in 165 (14.4%), 229 (20.0%) and 72 (6.2%) children, respectively. Boys had greater frequencies of two signs than girls (BR, 19.6%vs 8.9%, P<0.01; MS, 26.1%vs 13.6%, P<0.01), respectively. Boys spent more time on TVG playing than girls (1.1±0.7 h/day vs 0.4±0.6 h/day, P<0.0001), respectively. Excessive TVG players, who spent , 1 h/day for TVG had greater frequencies of two signs, BR and MS, than those of non-TVG-players (18.9%vs 13.0%, P<0.05; 25.6%vs 14.4%, P<0.01), respectively. The TVG playing time correlated with two signs, BR (P=0.0143) and MS (P=0.0048). Furthermore, sleep deprivation related to three signs, BR (P=0.0078), MS (P<0.0001) and DS/MS (P=0.0290). Conclusions: Excessive TVG playing links to the occurrence of BR and MS. Other factors, which cause sleep deprivation, may underlie in the occurrence of the three signs. The amount of time spent on TVG playing should be regulated to < 1.0 h/day. [source] A freezing-like posture to pictures of mutilationPSYCHOPHYSIOLOGY, Issue 3 2005Tatiana M. Azevedo Abstract Postural sway and heart rate were recorded in young men viewing emotionally engaging pictures. It was hypothesized that they would show a human analog of "freezing" behavior (i.e., immobility and heart rate deceleration) when confronted with a sustained block of unpleasant (mutilation) images, relative to their response to pleasant/arousing (sport action) or neutral (objects) pictures. Volunteers stood on a stabilometric platform during picture viewing. Significantly reduced body sway was recorded during the unpleasant pictures, along with increased mean power frequency (indexing muscle stiffness). Heart rate during unpleasant pictures also showed the expected greater deceleration. This pattern resembles the "freezing" and "fear bradycardia" seen in many species when confronted with threatening stimuli, mediated by neural circuits that promote defensive survival. [source] Mechanical and neural stretch responses of the human soleus muscle at different walking speedsTHE JOURNAL OF PHYSIOLOGY, Issue 13 2009Neil J. Cronin During human walking, a sudden trip may elicit a Ia afferent fibre mediated short latency stretch reflex. The aim of this study was to investigate soleus (SOL) muscle mechanical behaviour in response to dorsiflexion perturbations, and to relate this behaviour to short latency stretch reflex responses. Twelve healthy subjects walked on a treadmill with the left leg attached to an actuator capable of rapidly dorsiflexing the ankle joint. Ultrasound was used to measure fascicle lengths in SOL during walking, and surface electromyography (EMG) was used to record muscle activation. Dorsiflexion perturbations of 6 deg were applied during mid-stance at walking speeds of 3, 4 and 5 km h,1. At each walking speed, perturbations were delivered at three different velocities (slow: ,170 deg s,1, mid: ,230 deg s,1, fast: ,280 deg s,1). At 5 km h,1, fascicle stretch amplitude was 34,40% smaller and fascicle stretch velocity 22,28% slower than at 3 km h,1 in response to a constant amplitude perturbation, whilst stretch reflex amplitudes were unchanged. Changes in fascicle stretch parameters can be attributed to an increase in muscle stiffness at faster walking speeds. As stretch velocity is a potent stimulus to muscle spindles, a decrease in the velocity of fascicle stretch at faster walking speeds would be expected to decrease spindle afferent feedback and thus stretch reflex amplitudes, which did not occur. It is therefore postulated that other mechanisms, such as altered fusimotor drive, reduced pre-synaptic inhibition and/or increased descending excitatory input, acted to maintain motoneurone output as walking speed increased, preventing a decrease in short latency reflex amplitudes. [source] The effects of experimental muscle and skin pain on the static stretch sensitivity of human muscle spindles in relaxed leg musclesTHE JOURNAL OF PHYSIOLOGY, Issue 11 2008Ingvars Birznieks Animal studies have shown that noxious inputs onto ,-motoneurons can cause an increase in the activity of muscle spindles, and it has been proposed that this causes a fusimotor-driven increase in muscle stiffness that is believed to underlie many chronic pain syndromes. To test whether experimental pain also acts on the fusimotor system in humans, unitary recordings were made from 19 spindle afferents (12 Ia, 7 II) located in the ankle and toe extensors or peronei muscles of awake human subjects. Muscle pain was induced by bolus intramuscular injection of 0.5 ml 5% hypertonic saline into tibialis anterior (TA); skin pain was induced by 0.2 ml injection into the overlying skin. Changes in fusimotor drive to the muscle spindles were inferred from changes in the mean discharge frequency and discharge variability of spindle endings in relaxed muscle. During muscle pain no afferents increased their discharge activity: seven afferents (5 Ia, 2 II) showed a decrease and six (4 Ia, 2 II) afferents were not affected. During skin pain of 13 afferents discharge rate increased in one (Ia) and decreased in two (1 Ia, 1 II). On average, the overall discharge rate decreased during muscle pain by 6.1% (P < 0.05; Wilcoxon), but remained essentially the same during skin pain. There was no detectable correlation between subjective pain level and the small change in discharge rate of muscle spindles. Irrespective of the type of pain, discharge variability parameters were not influenced (P > 0.05; Wilcoxon). We conclude that, contrary to the ,vicious cycle' hypothesis, acute activation of muscle or skin nociceptors does not cause a reflex increase in fusimotor drive in humans. Rather, our results are more aligned with the pain adaptation model, based on clinical studies predicting pain-induced reductions of agonist muscle activity. [source] Whole-body high-field MRI shows no skeletal muscle degeneration in young patients with recessive myotonia congenitaACTA NEUROLOGICA SCANDINAVICA, Issue 2 2010C. Kornblum Kornblum C, Lutterbey GG, Czermin B, Reimann J, von Kleist-Retzow J-C, Jurkat-Rott K, Wattjes MP. Whole-body high-field MRI shows no skeletal muscle degeneration in young patients with recessive myotonia congenita. Acta Neurol Scand: 2010: 121: 131,135. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Background,,, Muscle magnetic resonance imaging (MRI) is the most sensitive method in the detection of dystrophic and non-dystrophic abnormalities within striated muscles. We hypothesized that in severe myotonia congenita type Becker muscle stiffness, prolonged transient weakness and muscle hypertrophy might finally result in morphologic skeletal muscle alterations reflected by MRI signal changes. Aim of the study,,, To assess dystrophic and/or non-dystrophic alterations such as fatty or connective tissue replacement and muscle edema in patients with severe recessive myotonia congenita. Methods,,, We studied three seriously affected patients with myotonia congenita type Becker using multisequence whole-body high-field MRI. All patients had molecular genetic testing of the muscle chloride channel gene (CLCN1). Results,,, Molecular genetic analyses demonstrated recessive CLCN1 mutations in all patients. Two related patients were compound heterozygous for two novel CLCN1 mutations, Q160H and L657P. None of the patients showed skeletal muscle signal changes indicative of fatty muscle degeneration or edema. Two patients showed muscle bulk hypertrophy of thighs and calves in line with the clinical appearance. Conclusions,,, We conclude that (i) chloride channel dysfunction alone does not result in skeletal muscle morphologic changes even in advanced stages of myotonia congenita, and (ii) MRI skeletal muscle alterations in myotonic dystrophy must be clear consequences of the dystrophic disease process. [source] | ||||||||||