Masticatory muscle activity during maximum voluntary clench in different research diagnostic criteria for temporomandibular disorders (RDC/TMD) groups

The research diagnostic criteria for temporomandibular disorders (RDC/TMD) are used for the classification of patients with temporomandibular disorders (TMD). Surface electromyography of the right and left masseter and temporalis muscles was performed during Maximum teeth clenching in 103 TMD patients subdivided according to the RDC/TMD into 3 non-overlapping groups: (a) 25 myogenous; (b) 61 arthrogenous; and (c) 17 psycogenous patients. Thirty-two control subjects matched for sex and age were also measured. During clenching, standardized total muscle activities (electromyographic potentials over time) significantly differed: 131.7 mu V/mu V s % in the normal subjects, 117.6 mu V/mu V s % in the myogenous patients, 105.3 mu V/mu V s % in the arthrogenous patients, 88.7 mu V/mu V s % in the psycogenous patients (p < 0.001, analysis of covariance). Symmetry in the temporalis muscles was larger in normal subjects (86.3%) and in myogenous patients (84.9%) than in arthrogenous (82.7%), and psycogenous patients (80.5%) (p=0.041). No differences were found for masseter muscle symmetry and torque coefficient (p>0.05). Surface electromyography of the masticatory muscles allowed an objective discrimination among different RDC/TMD subgroups. This evaluation could assist conventional clinical assessments. (C) 2007 Elsevier Ltd. All rights reserved.

Alterations in ciliary neurotrophic factor signaling in rapsyn deficient mice

Rapsyn is a key molecule involved in the formation of postsynaptic specializations at the neuromuscular junction, in its absence there are both pre- and post-synaptic deficits including failure to cluster acety]choline receptors. Recently we have documented increases in both nerve-muscle branching and numbers of motoneurons, suggesting alterations in skeletal muscle derived trophic support for motoneurons. The aim of the present study was to evaluate the contribution of target derived trophic factors to increases in motoneuron branching and number, in rapsyn deficient mice that had their postsynaptic specializations disrupted, We have used reverse transcription-polymerase chain reaction and Western blot to document the expression of known trophic factors and their receptors in muscle, during the period of synapse formation in rapsyn deficient mouse embryos. We found that the mRNA levels for ciliary neurotrophic factor (CNTF) was decreased in the rapsyn deficient muscles compared with litter mate controls although those for NGF, BDNF, NT-3 and TGF-beta2 did not differ. We found that both the mRNA and the protein expression for suppressor of cytokine signaling 3 (SOCS3) decreased although janus kinase 2 (JAK2) did not change in the rapsyn deficient muscles compared with litter mate controls. These results suggest that failure to form postsynaptic specializations in rapsyn deficient mice has altered the CNTF cytokine signaling pathway within skeletal muscle, the target for motoneurons. This alteration may in part, account for the increased muscle nerve branching and motoneuron survival seen in rapsyn deficient mice. (C) 2001 Wiley-Liss, Inc.

Mid-thoracic tenderness: a comparison of pressure pain threshold between spinal regions, in asymptomatic subjects

Palpation for tenderness forms an important part of the manual therapy assessment for musculoskeletal dysfunction, In conjunction with other testing procedures it assists in establishing the clinical diagnosis. Tenderness in the thoracic spine has been reported in the literature as a clinical feature in musculoskeletal conditions where pain and dysfunction are located primarily in the upper quadrant. This study aimed to establish whether pressure pain thresholds (PPTs) of the mid-thoracic region of asymptomatic subjects were naturally lower than those of the cervical and lumbar areas. A within-subject study design was used to examine PPT at four spinal levels C6, T4, T6, and L4 in 50 asymptomatic volunteers. Results showed significant (P < 0.001) regional differences. PPT values increased in a caudal direction. The cervical region had the lowest PPT scores, that is was the most tender. Values increased in the thoracic region and were highest in the lumbar region. This study contributes to the normative data on spinal PPT values and demonstrates that mid-thoracic tenderness relative to the cervical spine is not a normal finding in asymptomatic subjects. (C) 2001 Harcourt Publishers Ltd.

The effect of musculoskeletal pain on motor activity and control

Aberrant movement patterns and postures are obvious to clinicians managing patients with musculoskeletal pain. However, some changes in motor function that occur in the presence of pain are less apparent. Clinical and basic science investigations have provided evidence of the effects of nociception on aspects of motor function. Both increases and decreases in muscle activity have been shown, along with alterations in neuronal control mechanisms, proprioception, and local muscle morphology. Various models have been proposed in an attempt to provide an explanation for some of these changes. These include the vicious cycle and pain adaptation models. Recent research has seen the emergence of a new model in which patterns of muscle activation and recruitment are altered in the presence of pain (neuromuscular activation model). These changes seem to particularly affect the ability of muscles to perform synergistic functions related to maintaining joint stability and control. These changes are believed to persist into the period of chronicity. This review shows current knowledge of the effect of musculoskeletal pain on the motor system and presents the various proposed models, in addition to other shown effects not covered by these models. The relevance of these models to both acute and chronic pain is considered. It is apparent that people experiencing musculoskeletal pain exhibit complex motor responses that may show some variation with the time course of the disorder. (C) 2001 by the American Pain Society.

Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity

Recent findings that spinal manual therapy (SMT) produces concurrent hypoalgesic and sympathoexcitatory effects have led to the proposal that SMT may exert its initial effects by activating descending inhibitory pathways from the dorsal periaqueductal gray area of the midbrain (dPAG). In addition to hypoalgesic and sympathoexcitatory effects, stimulation of the dPAG in animals has been shown to hal e a facilitatory effect on motor activity. This study sought to further investigate the proposal regarding SMT and the FAG by including a test of motor function in addition to the variables previously investigated, Using a condition randomised, placebo-controlled, double blind, repeated measures design, 30 subjects with mid to lon er cervical spine pain of insidious onset participated in the study. The results indicated that the cervical mobilisation technique produced a hypoalgesic effect as revealed by increased pressure pain thresholds on the side of treatment (P = 0.0001) and decreased resting visual analogue scale scores (P = 0.049). The treatment technique also produced a sympathoexcitatory effect with an increase in skin conductance (P < 0.002) and a decrease in skin temperature (P = < 0.02). There was a decrease in superficial neck flexor muscle activity (P < 0.0002) at the lower levels of a staged cranio-cervical flexion test. This could imply facilitation of the deep neck flexor muscles with a decreased need for co-activation of the superficial neck flexors, The combination of all findings,would support the proposal that SMT may, at least initially, exert part of its influence via activation of the PAG, (C) 2000 Harcourt Publishers Ltd.

A revision of Benedenia Diesing, 1858 including a redescription of B-sciaenae (van Beneden, 1856) Odhner, 1905 and recognition of Menziesia Gibson, 1976 (Monogenea : Capsalidae)

Benedenia Diesing, 1858, a genus of capsalid (benedeniine) monogeneans, is redefined. The generic diagnosis is amended to include: the path of tendons in the haptor from extrinsic muscles in the body; presence and form of the marginal valve; a penis occupying a penis canal with weakly muscular wall; a weakly muscular accessory gland reservoir proximal to the penis and enclosed by a proximal extension of the wall of the penis canal; male and female genital apertures usually common, rarely separate; vagina with pore usually close to the common genital pore but may open in mid body between the germarium and the common genital pore, or anterior to the common genital pore. A conservative approach is adopted and the generic diagnosis is clarified and broadened to accommodate species that display some variation in reproductive anatomy, especially of the female system. We argue against potential alternative actions such as defining Benedenia strictly to contain species with separate male and female genital apertures and against recognition of a separate genus, Tareenia Hussey, 1986, for species with a vaginal pore anterior to the common genital pore. Under our conception, Benedenia comprises 21 species: B. sciaenae (van Beneden, 1856) Odhner, 1905 (type species); B. acanthopagri (Hussey, 1986) comb. nov.; B. anticavaginata Byrnes, 1986; B. bodiani Yamaguti, 1968; B. elongata (Yamaguti, 1968) Egorova, 1997; B. epinepheli (Yamaguti, 1937) Meserve, 1938; B. hawaiiensis Yamaguti, 1968; B. hendorffi(von Linstow, 1889) Odhner, 1905; B. hoshinai Ogawa, 1984; B. innobilitata Burhnheim Gomes and Varela, 1973: B. jaliscana Bravo-Hollis, 1952; B. lolo Yamaguti, 1968; B. lutjani Whittington and Kearn, 1993: B. monticellii (Parona and Perugia, 1895) Johnston, 1929; B. ovata (Goto, 1894) Johnston. 1929: B. pompatica Burhnheim, Gomes and Varela, 1973; B. rohdei Whittington, Kearn and Beverley-Burton, 1994; B. scari Yamaguti, 1968; B. sekii (Yamaguti, 1937) Meserve, 1938; B, seriolae (Yamaguti, 1934) Meserve, 1938; and B. synagris Yamaguti, 1953. The type species, B. sciaenae, is redescribed based on new material from Australia. No types for this taxon were designated and we have assigned a series of voucher specimens. Tareenia acanthopagri Hussey, 1986 becomes B. acanthopagri (Hussey, 1986) comb. nov. and T. anticavaginata (Byrnes, 1986) Egorova, 1997 and T. lutjani (Whittington and Kearn, 1993) Egorova, 1997 are returned to Benedenia as B. anticavaginata and B. lutjani Benedenia akaisaki Iwata, 1990 is considered a synonym of B. ovata and B. kintoki Iwata, 1990 is considered a synonym of B. elongata. Two species, B, madai Ishii and Sawada, 1938 and B. pagrosomi Ishii and Sawada, 1938, are considered species inquirendae. Based on the redefinition of Benedenia, the diagnosis for the Benedeniinae is amended. Tareenia is synonymized with Benedenia but Menziesia Gibson, 1976 is recognized and its generic diagnosis amended to include: anterior attachment organs tending to form a 'hooded' appearance; prominent anterior gland cells between the pharynx and the anterior margin of the body: long penis, tapering proximally, occupying a penis canal with weakly muscular wall: penis canal and penis describe a sigmoid; accessory gland reservoir dorsal and alongside, or posterior and lateral to, proximal end of the penis and enclosed by a proximal extension of the wall of the penis canal. Under this conception. Menziesia comprises: M. noblei (Menzies. 1946) Gibson, 1976 (type species); M. malaboni (Velasquez. 1982) comb. nov.: M. merinthe (Yamaguti, 1968) Gibson. 1976: M. ovalis (Yamaguti, 1968) Gibson, 1976: and M. sebastodis (Yamaguti, 1934) comb, nov. A key to valid species of Benedenia and Menziesia is provided and a list is presented of published records of undescribed or unattributed species of Benedenia. Some protocols are suggested for preparation of benedeniine material to enhance future taxonomic studies and comparisons. The host-specificity and geographic distribution of species in these revised genera are discussed. The composition of the Capsalidae is discussed and some difficulties in defining and distinguishing between its different subfamilies are considered.

Recent advances in the pathology of alcoholic myopathy

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Victor R. Preedy and Junko Adachi. The presentations were (1) Alcoholic myopathy: Past, present and future, by Timothy J. Peters and Victor R. Preedy; (2) Protein adducts in the type I and II fiber-predominant muscles of the ethanol-fed rat, by Simon Worrall, Seppo Parkkila, and Onni Niemela; (3) Hydroperoxides and changes in alcoholic myopathy, by Junko Adachi, Migiwa Asamo, and Yasuhino Ueno; and (4) A close association between testicular atrophy, muscle atrophy, and the increase in protein catabolism after chronic ethanol administration, by Kunihiko Takeda, Masayoshi Yamauchi, Kazuhiko Sakamoto, Masaru Takagi, Hisato Nakajima, and Gotaro Toda.

Phasic modulation of corticomotor excitability during passive movement of the upper limb: effects of movement frequency and muscle specificity

Modulations in the excitability of spinal reflex pathways during passive rhythmic movements of the lower limb have been demonstrated by a number of previous studies [4]. Less emphasis has been placed on the role of supraspinal pathways during passive movement, and on tasks involving the upper limb. In the present study, transcranial magnetic stimulation (TMS) was delivered to subjects while undergoing passive flexion-extension movements of the contralateral wrist. Motor evoked potentials (MEPs) of flexor carpi radialis (FCR) and abductor pollicus brevis (APB) muscles were recorded. Stimuli were delivered in eight phases of the movement cycle during three different frequencies of movement. Evidence of marked modulations in pathway excitability was found in the MEP amplitudes of the FCR muscle, with responses inhibited and facilitated from static values in the extension and flexion phases, respectively. The results indicated that at higher frequencies of movement there was greater modulation in pathway excitability. Paired-pulse TMS (sub-threshold conditioning) at short interstimulus intervals revealed modulations in the extent of inhibition in MEP amplitude at high movement frequencies. In the APE muscle, there was some evidence of phasic modulations of response amplitude, although the effects were less marked than those observed in FCR. It is speculated that these modulatory effects are mediated via Ia afferent pathways and arise as a consequence of the induced forearm muscle shortening and lengthening. Although the level at which this input influences the corticomotoneuronal pathway is difficult to discern, a contribution from cortical regions is suggested. (C) 2001 Published by Elsevier Science B.V.

Neural adaptations to resistance training - Implications for movement control

It has long been believed that resistance training is accompanied by changes within the nervous system that play an important role in the development of strength. Many elements of the nervous system exhibit the potential for adaptation in response to resistance training, including supraspinal centres, descending neural tracts, spinal circuitry and the motor end plate connections between motoneurons and muscle fibres. Yet the specific sites of adaptation along the neuraxis have seldom been identified experimentally, and much of the evidence for neural adaptations following resistance training remains indirect. As a consequence of this current lack of knowledge, there exists uncertainty regarding the manner in which resistance training impacts upon the control and execution of functional movements. We aim to demonstrate that resistance training is likely to cause adaptations to many neural elements that are involved in the control of movement, and is therefore likely to affect movement execution during a wide range of tasks. We review a small number of experiments that provide evidence that resistance training affects the way in which muscles that have been engaged during training are recruited during related movement tasks. The concepts addressed in this article represent an important new approach to research on the effects of resistance training. They are also of considerable practical importance, since most individuals perform resistance training in the expectation that it will enhance their performance in-related functional tasks.

Neural influences on sprint running - Training adaptations and acute responses

Performance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint performance. An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest reflex has been reported to be lower in athletes trained for explosive events compared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sensitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indicative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint-trained athletes. Fatigue of neural origin both during and following sprint exercise has implications with respect to optimising training frequency and volume. Research suggests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage. Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance.

Reversal of cardiovascular remodelling with candesart

Cardiovascular remodelling, defined as ventricular and vascular hypertrophy together with fibrosis, characterises hypertension following inhibition of the production of the endogenous vasodilator, nitric oxide (NO). This study has determined whether the cardiovascular remodelling following chronic NO synthase inhibition can e reversed by administration of the selective angiotensin II AT(1)-receptor antagonist, candesartan. Male Wistar rats were treated with L-nitroarginine methyl ester (L-NAME, 400 mg/l in drinking water) for eight weeks and with candesartan cilexetil (2 mg/kg/day by oral gavage) for the last four weeks. L-NAME-treated rats became hypertensive with systolic blood pressure increasing from 110 +/- 4 mmHg (control) to 170 +/- 10 mmHg. Rats developed left ventricular hypertrophy (control 1.70 +/- 0.06; L-NAME 2.10 +/- 0.04 mg/kg body wt) with markedly increased deposition of perivascular and interstitial collagen. Candesartan returned blood pressure, left ventricular weights and collagen deposition to control values. Echo cardiographic assessment showed concentric hypertrophy with an increased fractional shortening; this was reversed by candesartan treatment. Heart failure was not evident. In the isolated Langendorff heart, diastolic stiffness increased in L-NAME-treated rats while the rate of increase in pressure (+dP/dt) increased after eight weeks only; candesartan reduced collagen deposition and normalised +dP/dt. In isolated left ventricular papillary muscles, the potency (negative log EC50) of noradrenaline as a positive inotropic compound was unchanged, (control 6.56 +/- 0.14); maximal increase in force before ectopic beats was reduced from 5.0 +/- 0.4 mN to 2.0 +/- 0.2 mN. Noradrenaline potency as a vasoconstrictor in thoracic aortic rings was unchanged, but maximal contraction was markedly reduced from 25.2 +/- 2.0 mN to 3.0 +/- 0.3 mN; this was partially reversed by candesartan treatment. Thus, chronic inhibition of NO production with L-NAME induces hypertension, hypertrophy and fibrosis with increased toxicity and significant decreases in vascular responses to noradrenaline. These changes were at least partially reversible by treatment with candesartan, implying a significant role of AT(1)-receptors in L-NAME-induced cardiovascular changes.

Postural control of the trunk in response to lateral support surface translations during trunk movement and loading

The postural response to translation of the support surface may be influenced by the performance of an ongoing voluntary task. This study was designed to test this proposal by applying lateral perturbations while subjects handled a load in the frontal plane. Measurements were made of medio-lateral displacement of the centre of pressure, angular displacement of the trunk and thigh in the frontal plane and intra-abdominal pressure. Subjects were translated randomly to the left and right in a variety of conditions that involved standing either quietly or with a 5 kg load in their left hand, which they were required either to hold statically or to lift or lower. The results indicate that when the perturbation occurred towards the loaded left side the subjects were able to return their centre of pressure, trunk and thigh rapidly and accurately to the initial position. However, when the perturbation occurred towards the right (away from the load) this correction was delayed and associated with multiple changes in direction of movement, suggesting decreased efficiency of the postural response. This reduced efficiency can be explained by a conflict between the motor commands for the ongoing voluntary task and the postural response, and/or by the mechanical effect of the asymmetrical addition of load to the trunk.

Reversal of cardiac and renal fibrosis by pirfenidone and spironolactone in streptozotocin-diabetic rats

1 Fibrosis leads to chronic impairment of cardiac and renal function and thus reversal of existing fibrosis may improve function and survival. This project has determined whether pirfenidone, a new antifibrotic compound, and spironolactone, an aldosterone antagonist, reverse both deposition of the major extracellular matrix proteins, collagen and fibronectin, and functional changes in the streptozotocin(STZ)-diabetic rat. 2 Streptozotocin (65 mg kg(-1) i.v.)-treated rats given pirfenidone (5-methyl-1-phenyl-2-[1H]-pyridone; approximately-200 mg kg(-1) day(-1) as 0.2-2g l(-1) drinking water) or spironolactone (50 mg kg(-1) day(-1) s.c.) for 4 weeks starting 4 weeks after STZ showed no attenuation of the increased blood glucose concentrations and increased food and water intakes which characterize diabetes in this model. 3 STZ-treatment increased perivascular and interstitial collagen deposition in the left ventricle and kidney, and surrounding the aorta. Cardiac, renal and plasma fibronectin concentrations increased in STZ-diabetic rats. Passive diastolic stiffness increased in isolated hearts from STZ-diabetic rats. Both pirfenidone and spironolactone treatment attenuated these increases without normalizing the decreased + dP/dt(max) of STZ-diabetic hearts. 4 Left ventricular papillary muscles from STZ-treated rats showed decreased maximal positive inotropic responses to noradrenaline, EMD 57033 (calcium sensitizer) and calcium chloride; this was not reversed by pirfenidone or spironolactone treatment. STZ-treatment transiently decreased GFR and urine flow rates in isolated perfused kidneys; pirfenidone but not spironolactone prevented the return to control values. 5 Thus, short-term pirfenidone and spironolactone treatment reversed cardiac and renal fibrosis and attenuated the increased diastolic stiffness without normalizing cardiac contractility or renal function in STZ-diabetic rats.

Effect of chronic morphine treatment on alpha(2)-adrenoceptor mediated autoinhibition of transmitter release from sympathetic varicosities of the mouse vas deferens

1 The effect of chronic morphine treatment (CMT) on sympathetic innervation of the mouse vas deferens and on alpha (2)-adrenoceptor mediated autoinhibition has been examined using intracellular recording of excitatory junction potentials (EJPs) and histochemistry. 2 In chronically saline treated (CST) preparations. morphine (1 muM) and the alpha (2)-adrenoceptor agonist (clonidine, 1 muM) decreased the mean amplitude of EJPs evoked with 0.03 Hz stimulation by 81+/-8% (n=16) and 92+/-6% (n=7) respectively. In CMT preparations, morphine (1 muM) and clonidine (1 muM) decreased mean EJP amplitude by 68+/-8% (n = 7) and 79+/-8% (n = 7) respectively. 3 When stimulating the sympathetic axons at 0.03 Hz. the mean EJP amplitude recorded from smooth muscles acutely withdrawn from CMT was four times greater than for CST smooth muscles (40.7+/-3.8 mV, n = 7 compared with 9.9+/-0.3 mV, n = 7). 4 Part of the increase in mean EJP amplitude following CMT was produced by a 31% increase in the density of sympathetic axons and varicosities innervating the smooth muscle. 5 Results from the present study indicate that the effectiveness of alpha (2)-adrenocrptor mediated autoinhibition is only slightly reduced in CMT preparations. Most of the cross tolerance which develops between morphine, clonidine and alpha (2)-adrenoceptor mediated autoinhibition occurs as a consequence of increased efficacy of neuromuscular transmission which is produced by an increase in the probability of transmitter release and an increase in the density of sympathetic innervation.

Effect of aestivation on muscle characteristics and locomotor performance in the Green-striped burrowing frog, Cyclorana alboguttata

The Green-striped burrowing frog. Cyclorana alboguttata survives extended drought periods by burrowing underground and aestivating. These frogs remain immobile within cocoons of shed skin and Mucus during aestivation and emerge from their burrows upon heavy rains to feed and reproduce. Extended periods of immobilisation in mammals typically result in muscle atrophy and a decrease in muscle performance. We examined the effect of aestivation and hence prolonged immobilisation, on skeletal Muscle mass. in vitro muscle performance, and locomotor performance in C. alboguttata. Frogs were aestivated in soil for 3 months and were compared with control animals that remained active, were fed, and had a continual supply of water. Compared to the controls, the wet mass of the gastrocnemius. sartorius, gracilus major. semimembranosus. peroneus, extensor cruris, tibialis posticus and tibialis anticus longus of aestivators remained unchanged indicating no muscle atrophy. The in-vitro performance characteristics of the gastroenemius muscle were maintained and burst swimming speed Was Unaffected, requiring no recovery from the extended period of immobilisation associated with aestivation. This preservation of muscle size, contractile condition and locomotor performance through aestivation enables C. alboguttata to compress their life history into unpredictable windows of opportunity, whenever heavy rains occur.