Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle Rigidity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources

Clinical analysis of akinesia.

Symptoms called akinesia in movement are analysed and classified into three groups. The first is that secondary to existence of marked rigidity of muscles and the second is that due to striatal dopamine deficiency, which simply be interpreted as "lack of movement". The third is freezing or festination in quick repetitive movement especially in gait, speech and handwriting, for which 1-Dopa therapy has no influence. Specific difficulty in the latter condition is found in the rhythm formation of repetitive movements when repetition is over 2 Hz, which the author named "hastening phenomenon converging into 5 Hz". However, the neural mechanism and pathology under the third group of akinesia is still not known. In most of the parkinsonian patients, it is considered that all three groups of akinesia are mixed together with variety of grade. Careful observations on the changes of clinical pictures through the course of 1-Dopa therapy and of stereotaxic surgery provided the analysis of so-called akinesia as described.

Dopamine↗

Unequal mitotic sister chromatid exchange and different length of Y chromosomes.

There is wide variation in the length of the Y chromosome. In the same individual the length varies continuously and is normally distributed. We describe a boy with borderline mental retardation, gross and fine motor coordination difficulty, muscle rigidity, ptosis, clinodactyly, and a Y chromosome of different lengths in two separate cell populations. The most probable explanation of the cytogenetic finding is a mitotic unequal sister chromatid exchange of the Y chromosome.

Adolescent↗

Induction of physical dependence on and tolerance to ethanol in rats fed a new nutritionally complete and balanced liquid diet.

Rats offered a nutritionally balanced and complete liquid diet containing 35% of energy as ethanol, 12% as fat, 21% as protein, and the balance as carbohydrate consumed greater than 9 g/kg ethanol after 10 days. Rats displayed signs of physical dependence and tolerance while showing a net gain in weight. Physical dependence was indicated by severe intensity of the following signs during withdrawal from ethanol: Muscle rigidity; tail tremors; caudal tremors; and general tremors. Severity of these signs reached a maximum intensity by 19 h after withdrawal of ethanol. Tolerance was exhibited by chronically treated rats as measured by significantly reduced time off the belt after 7 days. Concentrations of ethanol in blood were documented on selected mornings and were observed to increase. These data suggest that physical dependence and tolerance can be induced through voluntary consumption of ethanol by rats and without nutritional compromises or weight loss.

Alcoholism↗

Polarization of tryptophan fluorescence measurements in muscle. A re-evaluation.

The degree of polarization of the intrinsic tryptophan fluorscence of glycerinated simgle muscle fibres or fibre bundles (rabbit psoas or dorsal longitudinal muscle of Lethocerus maximus) was measured: a) With sufficiently high (15 mM) ATP concentration or when an ATP regenerating system was used no difference in the degree of polarization of a contracting and a relaxed muscle was detected, whereas a distinct difference was detected between the relaxed and the rigor state. In contrast a distinct difference between the relaxed and contracting state was obtained at low ATP concentrations (5 mM). This difference is interpreted to be caused by an ATP-free core (rigor core) in the centre of the fibre. b) No change in the polarization degree was detected after a rapid release of the contracting muscle. c) In rigor state no difference in the degree of polarization of the tryptophan fluorescence was observed in the presence or absence of AMPPNP (concentration 0.5 mM). These findings and the lack of difference between the polarization degree of the contracting and the relaxed muscle is interpreted to indicate that the polarization degree of the tryptophan fluorescence is not sensitive to the orientation of the cross bridges, or that the cross bridges do not rotate.

Adenosine Triphosphate↗

Cross-bridge behavior in rigor muscle.

Properties of the rigor state in muscle can be explained by a simple cross-bridge model, of the type which has been suggested for active muscle, in which detachment of cross-bridges by ATP is excluded. Two attached cross-bridge states, with distinct force vs. distortion relationships, are required, in addition to a detached state, but the attached cross-bridge states in rigor muscle appear to differ significantly from the attached cross-bridge states in active muscle. The stability of the rigor force maintained in muscle under isometric conditions does not require exceptional stability of the attached cross-bridges, if the positions in which attachment of cross-bridges is allowed are limited so that the attachment of cross-bridges in positions which have minimum free energy is excluded. This explanation of the stability of the rigor state may also be applicable to the maintenance of stable rigor waves on flagella.

Adenosine Triphosphate↗

Ultrastructure of the syndrome of continuous muscle fibre activity.

The ultrastructure of muscle and the myoneural junction of a man of 60 suffering from the syndrome of continuous muscle fibre activity was studied. This syndrome is manifested by disturbances of walking, muscle weakness, permanent muscle contractions and involuntary movements. The myoneural junction was hypertrophied and showed ramifications of the secondary clefts. The presynaptic nerve ending contained no synaptic vesicles. The relationship of these findings to the disease is discussed.

Gait↗

Inhibition of tension development and actomyosin ATPase activity in barnacle muscle by the Ca2+-indicator dye antipyrylazo III.

We have investigated the effects of the Ca2+-indicator dye antipyrylazo III on: (1) tension development in myofibrillar preparations from barnacle depressor muscle; and (2) actomyosin ATPase activity in myofibrils/native actomyosin isolated from barnacle muscle and in actomyosin hybrids prepared from pure (unregulated) rabbit F-actin and purified barnacle myosin. In all solutions, pCa was either heavily buffered with suitable [CaEGTA]/[EGTA] and/or measured with a calcium-electrode so as to offset the appreciable Ca2+-buffering effects of the dyes. Antipyrylazo III produced a rapid, reversible and concentration-dependent inhibition of: (1) tension development by isolated barnacle myofibrils; (2) calcium-regulated ATPase activity in barnacle myofibrils and native actomyosin; and (3) calcium-independent actin-activated ATPase activity in hybrid actomyosins prepared from purified barnacle myosin and rabbit actin. This latter observation indicated that the inhibitory effect of the dye on calcium-regulated tension and ATPase in intact myofibrils is due to specific repression of active crossbridge formation rather than modification of calcium-regulatory mechanisms. The hypothesis that antipyrylazo III specifically represses active crossbridge formation was supported by the observation that the dye had no effect on rigor tension development. Specific and saturable binding of the dye to these myofibrils was characterized by a maximum capacity of 1.3 mumol dye g-1 myofibrillar protein, consistent with a calculated 1 dye: 1 myosin stoichiometry. These various biological effects were observed with both commercially available antipyrylazo III and highly purified dye preparations. Preliminary studies using myofibrillar preparations from rabbit psoas muscle, guinea-pig portal vein smooth muscle, and scallop adductor muscle have indicated that contractile function in these muscle types does not appear to be inhibited by antipyrylazo III.

Actins↗

Crossbridge kinetics in chemically skinned rabbit psoas fibres when the actin-myosin lattice spacing is altered by dextran T-500.

The actin-myosin lattice spacing of chemically skinned rabbit psoas fibres was osmotically altered by dextran T500, and the transient kinetic response of tension arising from maximally cycling cross-bridges was measured by sinusoidal length perturbations. The lattice spacing was estimated from the width of the fibres measured under a light microscope. As the dextran concentration was increased, the widths during both relaxation and Ca-activation decreased monotonically. The tension increased to a maximum at 7% dextran, and decreased again at further increases in dextran. Dynamic modulus (stiffness) increased monotonically with compression by dextran; this increase is primarily due to the elastic modulus. The rate constants slightly decreased between 0% and 4% dextran, then decreased rapidly at higher concentrations. The rate of oscillatory work output stayed approximately constant between 0% and 4% dextran, and sharply decreased at higher concentrations. Apparently, two independent effects occur as the lattice is compressed by dextran: (1) a compensation for the spacing change through an increase in tension and a decrease in the rate constants (this takes place at low dextran concentrations); and (2) an alteration of the crossbridge kinetics by grossly decreasing both the tension and the rate constants (at high dextran concentrations). The first effect is interpreted as a decrease in the detachment rate, while the second effect is interpreted as a decrease in the rate of the 'power stroke' reaction.

Actins↗

The effect of the ATP analogue AMPPNP on the structure of crossbridges in vertebrate skeletal muscles: X-ray diffraction and mechanical studies.

Adenylylimidodiphosphate (AMPPNP), a nonhydrolysable analogue of ATP, has been used to arrest the crossbridge cycle of muscular contraction in one of its hypothetical intermediate states. Whole frog sartorius muscles were chemically demembranated, and it was found possible to cycle such skinned muscles reversibly between the relaxed and rigor states. The effect of binding of AMPPNP on the structure and spatial arrangement of the crossbridges of such muscles was studied using low-angle X-ray diffraction, with simultaneous recording of the mechanical effects, starting from the rigor state. Saturating concentrations of MgAMPPNP produce a characteristic decrease of about 50% in the original rigor isometric tension with a concomitant increase in muscle length by 0.13%. The equatorial X-ray diffraction pattern is modified in the following way: the lattice dimensions and the intensity of the (10) equatorial reflection do not change, while the intensity of the (11) equatorial reflection increases slightly. These observations of very small equatorial changes could be explained by assuming that in these muscles (as distinct from others such as rabbit psoas) the analogue does not produce a significant degree of detachment of crossbridges; that is, there are only AMPPNP-modified attached ones. The changes in the meridional X-ray diffraction pattern are more pronounced: the meridional reflection at 14.5 nm decreases in intensity, and the meridional reflection at 7.2 nm increases considerably: the intensity of all the actin-based off-meridional layer-lines decreases. There are no signs of the characteristic relaxed layer-lines, and the changes in the layer-line intensities are probably due to there being a single population of AMPPNP-modified attached crossbridges, rather than a mixture of attached and detached crossbridges. Thus the AMPPNP X-ray pattern, both equatorially and meridionally, is somewhat similar to the rigor one, indicating that most of the crossbridges remain attached. On the other hand, the fact that there are some changes in the layer-line intensities of the AMPPNP frog pattern, without the appearance of any signs of a relaxed equatorial pattern, indicates that the attached crossbridges are in a structural state that is different from rigor, one is not seeing, apparently, simply a mixture of rigor and relaxed states. Our tentative interpretation of this result is that there may be a structural change in the crossbridge near to the junction with S2, with less significant changes occurring in the parts of the crossbridge close to actin.

Adenosine Triphosphate↗

The process of muscle relaxation by the combined action of MgAMPPNP and ethylene glycol.

Insect flight muscle fibres were relaxed by the combined action of MgAMPPNP and ethylene glycol, as measured by the stiffness of the fibres. Relaxation occurred over a small range of glycol concentration. Addition of Ca2+ raised the glycol required for relaxation. The speed at which the stiffness measurement was made did not influence the glycol concentration at which relaxation occurred. Glycol in excess of that needed to relax the muscle caused a slight rise in high-frequency stiffness. Removal of the glycol restored the rigor stiffness. Under glycol-relaxed conditions, much of the AMPPNP bound in muscle fibres was retained during cold-chase (elution of [3H] AMPPNP by nonradioactive AMPPNP); the intensity ratio of the inner equatorial X-ray diffraction peaks rose upon glycol relaxation to a value slightly below that characteristic of natural relaxation. The results are interpreted in terms of cooperative attachment of the crossbridges to actin.

Adenosine Triphosphate↗

Stiff man syndrome: neurophysiological findings in eight patients.

The neurophysiological findings in eight patients with the stiff man syndrome (SMS), including four of six tested with autoantibodies against glutamic acid decarboxylase, are presented. Neurophysiological findings did not make it possible to discriminate between patients with and those without autoimmunity against GABAergic neurons. Investigation of mono- and polysynaptic reflexes revealed abnormal results in a variable number of SMS patients, the abnormalities largely corresponding to those seen in spastic paresis. A stereotyped motor response to electrical stimulation of peripheral nerves was recorded from the trunk muscles of all patients investigated. This response was termed spasmodic reflex myoclonus and consisted of a sequence of 1-3 synchronous myoclonic bursts, 60-70 ms after median nerve stimulation, followed by a tonic decrescendo activity over a number of seconds. The recruitment order of muscles along the neuraxis in spasmodic reflex myoclonus suggested that the latter was generated in the spinal cord and conveyed via propriospinal tracts. It is thought that spasmodic reflex myoclonus may serve not only as a diagnostic tool, but also as a key to understanding some aspects of the pathophysiology of both spasms and stiffness in SMS. It is speculated that stiffness is a fragment of spasms, both being generated by common neuronal mechanisms tentatively ascribed to interneurons in the spinal grey matter.

Electromyography↗

Tissue oxygen measurement and 31P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia.

Muscle tissue oxygen tension was measured by a polarographic oxygen fine-needle probe, and inorganic phosphate and creatine phosphate spectra were recorded using magnetic resonance spectroscopy in patients with chronic low back pain and in patients with fibromyalgia. Results were compared with healthy controls. The tissue oxygen tension was markedly higher in those with tense muscles than in normal subjects. Magnetic resonance spectra for inorganic phosphate were higher in patients demonstrating muscle contraction, and intracellular pH was shifted in the alkaline direction in cases with increased muscle tension. Results show that hypoxia is not the result of increased muscle tension, as was thought previously, but results from oversupply of oxygen demanded by the muscle, leading to increased capillary perfusion and rising oxygen tension.

Adult↗

Actin filament organization and myosin head labelling patterns in vertebrate skeletal muscles in the rigor and weak binding states.

The structures of vertebrate skeletal muscles (particularly from frog and fish) in the rigor state are analysed in terms of the concept of target areas on actin filaments. Assuming that 100% of the heads are to be attached to actin in rigor, then satisfactory qualitative low-resolution modelling of observed X-ray diffraction data is obtained if the outer ends of these myosin heads can move axially (total range about 200A) and azimuthally (total range less than 60 degrees) from their original lattice sites on the myosin filament surface to attach in defined target areas on the actin filaments. On this basis, each actin target area comprises about four actin monomers along one of the two long-pitched helical strands of the actin filament (about 200 A) or an azimuthal range of actin binding sites of about 100 degrees around the thin filament axis. If myosin heads simply label in a non-specific way the nearest actin monomers to them, as could occur with non-specific transient attachment in a 'weak binding' state, then the predicted X-ray diffraction pattern would comprise layer lines at the same axial spacings (orders of 429 A) as those seen in patterns from resting muscle. It is shown that actin target areas in vertebrate skeletal muscles are probably arranged on an approximate 62 (right-handed) helix of pitch (P) of about 720 A, subunit translation P/6 and near repeat P/2. Troponin position need not be considered in defining the labelling pattern of cross-bridges on this 62 helix of target areas; the target areas appear to be defined solely by the azimuthal position of the actin binding sites. The distribution of actin filament labelling patterns could be regular in fish muscle which has a 'crystalline' A-band, but will be irregular in higher vertebrate muscles such as frog sartorius muscle.

Actin Cytoskeleton↗

The influence of ionic strength upon relaxation from rigor induced by flash photolysis of caged-ATP in skinned murine skeletal muscle fibres.

The influence of ionic strength upon relaxation kinetics from rigor in skinned murine extensor digitorum longus (EDL) skeletal muscle fibres was examined using photolysis of caged-ATP at low Ca2+. The ionic strength was adjusted with either KMeSO3 or ethylene glycolbis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid, dipotassium salt (K2EGTA) in the range of tau /2 = 65-215mM, or I.E. 49-194mM, where I.E. denotes ionic equivalent. Following rigor development at a tau /2 of 165-215mM (I.E. 144-194mM), the liberation of approximately 0.5mM ATP resulted in an initial 6-to 10-ms detachment phase with a decline in force of approximately 10-20% followed by a 10-to 30-ms reattachment with up to a 60% increase compared to the corresponding rigor level and a final detachment leading to complete relaxation. Interestingly, when similar ATP concentrations were liberated at lower ionic strengths between a tau /2 of 65mM and 110mM (I.E. 60-100mM), the initial detachment phase was shortened and force decreased by only approximately 5-10%, while the following reattachment phase was lengthened and led to an increased steady-state force of approximately 20-80% without final relaxation. ATP-induced detachment and subsequent reattachment were mainly determined by the currently present ionic strength and were relatively independent of the preceding rigor state which had been developed at higher or lower ionic strengths. The effects of phosphate and apyrase on the force transient suggest that reattachment of ADP- binding crossbridges may contribute to the increase in tension at high and even more at low ionic strengths. The study shows that the kinetics of initial fast relaxation and subsequent redevelopment of force following flash photolysis of similar ATP concentrations are markedly modified by the ionic strength in the narrow range of between 65mM and 215mM.

Adenosine Triphosphate↗