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Results for “Muscle Rigidity”

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At least 757 records · Page 42Linked to original sources
PubMedDate not supplied

A case of malignant hyperthermia during epidural analgesia.

Malignant hyperthermia syndrome developed during epidural analgesia in 25-year-old female to be operated on for haemorrhoidal varices. After premedication with diazepam and atropine epidural analgesia was started with lidocaine 300 mg and bupivacaine 50 mg. Signs and symptoms of malignant hyperthermia syndrome appeared 30 min. later, with muscle rigidity, hyperpyrexia 41.5degrees C, and loss of consciousness. Treatment alleviating the syndrome was applied as indicated in this complication. Full recovery was obtained.

Adult↗
PubMed1997

Botulinum toxin A improves muscle spasms and rigidity in stiff-person syndrome.

We studied the effect of botulinum toxin A (BTA) on painful muscular spasms and rigidity in two bedridden patients with clinical, electrophysiologic, and immunologic evidence of stiff-person syndrome. We injected BTA or saline solution into several limb muscles with both the rater and patient blinded to the order of the injections. A physician, unaware of the treatment order, used an objective rating scale for rigidity and spasm frequency scale and independently assessed the treatment results. BTA administration significantly reduced rigidity and stopped the spasms in all limbs. Following BTA injection on one side, the spasm frequency decreased bilaterally possibly because of the spread of hematogenous toxin.

Botulinum Toxins, Type A↗
PubMed1979

[Early patient mobilization after apoplectic stroke].

Principles of individualized functional mechanotherapy in the early post-hemorrhagic period are briefly presented. This therapy makes it possible to prevent or to alleviate complications specific for cerebral hemorrhage (rigidity of the muscles in the humoral region, development of contractures of the joints and pathological models of movements, unfavourable influence of the psychic syndrome developing after organic affections of the brain). While giving the therapy it is recommended to take into consideration the pathophysiological conditions present by the beginning of the development of the motor activity. Principal rules for the individualized functional mechanotherapy are formulated.

Cerebral Hemorrhage↗
PubMedDate not supplied

[The effect of cryo- and cryoelectrotherapy on neuromuscular function in coxarthrosis patients].

Cryotherapy (CT) and cryoelectrotherapy (CET) in combination with therapeutic exercise were assessed for neuromuscular effects in patients with coxarthritis and necrosis of caput femoris. The above complex is found effective in reducing the rigidity of the muscles and joints, in attenuation of functional contractures. It increases muscle strength nearby the affected joints. The best results were achieved with CET. Single CT and CET procedures increase the amplitude of muscular bioelectrical activity at maximal muscular tension, the highest effect being observed at the sites of the direct exposure. Marked analgetic activity of the physical factors was confirmed by electroneuromyographic findings.

Combined Modality Therapy↗
PubMed1998

Muscle thick filaments are rigid coupled tubules, not flexible ropes.

Understanding the structures of thick filaments and their relation to muscle contraction has been an important problem in muscle biology. The flexural rigidity of natural thick filaments isolated from Caenorhabditis elegans as determined by statistical analysis of their electron microscopic images shows that they are considerably more rigid (persistence length=263 microm) than similarly analyzed synthetic actin filaments (6 microm) or duplex DNA (0.05 microm), which are known to be helical ropes. Indeed, cores of C. elegans thick filaments, having only 11% of the mass per unit length of intact thick filaments, are quite rigid (85 microm) compared with the thick filaments. Cores comprise the backbones of the thick filaments and are composed of tubules containing seven subfilaments cross-linked by non-myosin proteins. Microtubules reconstituted from tubulin and microtubule-associated proteins are nearly as rigid (55 microm) as the cores. We propose a model of coupled tubules as the structural basis for the observed rigidity of natural thick filaments and other linear structures such as microtubules. A similar model was recently presented for microtubules [Felgner et al., 1997]. This coupled tubule model may also explain the differences in flexural rigidity between natural rabbit skeletal muscle thick filaments (27 microm) or synthetic thick filaments reconstituted from myosin and myosin binding protein C (36 microm) and those reconstituted from purified myosin (9 microm). The more flexible myosin structures may be helical ropes like F-actin or DNA, whereas the more rigid muscle or synthetic thick filaments which contain myosin and myosin binding protein C may be constructed of subfilaments coupled into tubules as in C. elegans cores. The observed thick filament rigidity is necessary for the incompressibility and lack of flexure observed with thick filaments in contracting skeletal muscle.

Animals↗
PubMed2005

Extracellular matrix rigidity governs smooth muscle cell motility in a biphasic fashion.

Increasing evidence suggests that mechanical cues inherent to the extracellular matrix (ECM) may be equally as critical as its chemical identity in regulating cell behavior. We hypothesized that the mechanical properties of the ECM directly regulate the motility of vascular smooth muscle cells (SMCs) and tested this hypothesis using polyacrylamide substrates with tunable mechanical properties. Quantification of the migration speed on uniformly compliant hydrogels spanning a range of stiffnesses (Young's moduli values from 1.0 to 308 kPa for acrylamide/bisacrylamide ratios between 5/0.1% and 15/1.2%, respectively) revealed a biphasic dependence on substrate compliance, suggesting the existence of an optimal substrate stiffness capable of supporting maximal migration. The value of this optimal stiffness shifted depending on the concentration of ECM protein covalently attached to the substrate. Specifically, on substrates presenting a theoretical density of 0.8 microg/cm(2) fibronectin, the maximum speed of 0.74 +/- 0.09 microm/min was achieved on a 51.9 kPa gel; on substrates presenting a theoretical density of 8.0 microg/cm(2) fibronectin, the maximum speed of 0.72 +/- 0.06 microm/min occurred on a softer 21.6 kPa gel. Pre-treatment of cells with Y27632, an inhibitor of the Rho/Rho-kinase (ROCK) pathway, reduced these observed maxima to values comparable to those on non-optimal stiffnesses. In parallel, quantification of TritonX-insoluble vinculin via Western blotting, coupled with qualitative fluorescent microscopy, revealed that the formation of focal adhesions and actin stress fibers also depends on ECM stiffness. Combined, these data suggest that the mechanical properties of the underlying ECM regulate Rho-mediated contractility in SMCs by disrupting a presumptive cell-ECM force balance, which in turn regulates cytoskeletal assembly and ultimately, cell migration.

Acrylic Resins↗
PubMed1986

[Phenibut potentiation of the therapeutic action of antiparkinson agents].

It was observed in experiments on mice that the central action of phenibut (beta-phenyl-gamma-aminobutyric acid) diminished after destruction of brain dopaminergic neurons by 6-hydroxydopamine and after pretreatment with the dopamine receptor blocker haloperidol which suggests the dopaminergic component in the action of phenibut. In 13 of 16 patients receiving long-term treatment with antiparkinsonic drugs, addition of phenibut (0.25 g thrice daily for 10 days) resulted in marked clinical improvement with a significant increase of motor activity, as well as diminution of both rigidity and tremor. Follow-up showed a significant lowering of muscle tone of rigid muscles, augmentation of their strength and amplitude of movements. In 8 patients receiving phenibut without antiparkinsonic drugs the results were negligible.

Adult↗
PubMed1991

Stiff-person syndrome: an autoimmune disease.

Stiff-person syndrome (SPS) is characterized by progressive, usually symmetric rigidity of the axial muscles with superimposed painful spasms precipitated by tactile stimuli, passive stretch, volitional movement of affected or unaffected muscles, startling noises, and emotional stimuli. Electromyography demonstrates continuous normal motor unit potentials in the affected muscles. Both the rigidity and the spasms are relieved by sleep, general anesthesia, myoneural blockade, peripheral nerve blockade, and partially by diazepam. Evidence for an autoimmune etiology of SPS includes its association with other autoimmune diseases and autoantibodies and the presence of antibodies against glutamic acid decarboxylase (GAD) in the cerebrospinal fluid (CSF) of many affected patients. We describe two patients with this syndrome who had GAD antibodies in both CSF and serum. Partial relief of the symptoms in these patients by corticosteroid therapy provides additional evidence of an autoimmune etiology of SPS and of the role of immunotherapy in its treatment.

Autoantibodies↗