scholarly journals Experimental myofascial trigger point creation in rodents

2019 ◽  
Vol 126 (1) ◽  
pp. 160-169 ◽  
Author(s):  
Ramon Margalef ◽  
Marc Sisquella ◽  
Marc Bosque ◽  
Clara Romeu ◽  
Orlando Mayoral ◽  
...  
Keyword(s):  
Muscle Pain ◽  
Structural Changes ◽  
Myofascial Pain ◽  
Ex Vivo ◽  
Trigger Point ◽  
Clinical Signs ◽  
Trigger Points ◽  
Diaphragm Muscle ◽  
Needle Stimulation

Myofascial pain syndrome is one of the most common forms of muscle pain. In this syndrome, pain is originated by the so-called trigger points, which consists of a set of palpable contraction knots in the muscle. It has been proposed that a high, spontaneous neurotransmission may be involved in the generation of these contraction knots. To confirm this hypothesis, we exposed mouse muscles to an anticholinesterasic agent to increase the neurotransmision in the synaptic cleft in two different conditions, in vivo and ex vivo experiments. Using intracellular recordings, a sharp increase in the spontaneous neurotransmission in the levator auris longus muscle and a lower increase in the diaphragm muscle could be seen. Likewise, electromyography recordings reveal an elevated endplate noise in gastrocnemius muscle of treated animals. These changes are associated with structural changes such as abundant neuromuscular contracted zones observed by rhodaminated α-bungarotoxin and the presence of abundant glycosaminoglycans around the contraction knots, as shown by Alcian PAS staining. In a second set of experiments, we aimed at demonstrating that the increases in the neurotransmission reproduced most of the clinical signs associated to a trigger point. We exposed rats to the anticholinesterase agent neostigmine, and 30 min afterward we observed the presence of palpable taut bands, the echocardiographic presence of contraction knots, and local twitch responses upon needle stimulation. In summary, we demonstrated that increased neurotransmission induced trigger points in both rats and mice, as evidenced by glycosaminoglycans around the contraction zones as a novel hallmark of this pathology.NEW & NOTEWORTHY In rodents, when neostigmine was injected subcutaneously, the neuromuscular neurotransmission increased, and several changes can be observed: an elevated endplate noise compared with normal endplate noise, as evidenced by electromyographyc recording; many muscular fibers with contraction knots (narrower sarcomeres and locally thickened muscle fiber) surrounded by infiltration of connective tissue like glycosaminoglycans molecules; and palpable taut bands and local twitch responses upon needle stimulation. Several of these signs are also observed in humans with muscle pain.

scholarly journals Dry needling in situations with varying degrees of muscle tone: an ex vivo study

2019 ◽  
Vol 02 (02) ◽  
pp. 113-113
Author(s):  
Margalef R. ◽  
Bosque M. ◽  
Santafé MM
Keyword(s):  
Myofascial Pain ◽  
Muscle Tone ◽  
Ex Vivo ◽  
Muscle Tension ◽  
Muscle Fibers ◽  
Optimal Solution ◽  
Trigger Points ◽  
Dry Needling ◽  
Myofascial Trigger Points

Abstract Introduction Numerous studies support the fact that myofascial trigger points are responsible for the clinical findings in myofascial pain syndrome, therefore it is reasonable to believe that the destruction of the same via dry needling may be an optimal solution. However, this technique has not been assessed in relation to muscle tone. Methods The experiments were performed with the levator auris longus (LAL) muscle of Swiss adult mice. The muscles, once extracted from the animal, were maintained ex vivo using normal oxygenated Ringer solution. Once these were extracted, they were extended upon a Sylgard® surface, maintained in vivo at all times. In these conditions, 15 insertions were performed with dry needling needles (0.25 mm X 25mm; AguPunt) in the attempt to avoid repeating needling on the same site. Different degrees of muscle tone were obtained as follows (from lesser to greater tone): healthy animals; animal model of myofascial trigger points (PGM); muscles which, once extracted were treated with ClK 30 mM and ClCa2 5mM; formaldehyde. Immediately after treatment, the muscles were dyed with methylene blue. Results The muscle fibers of healthy muscles are mostly pushed aside by the needle, practically without injury. Muscles with MTrPs are more injured than healthy muscles because of the use of dry needling, albeit only partially. The tone acquired with ClK and ClCa2 is more powerful and generalized, therefore, dry needling creates a greater injury. Lastly, formaldehyde provokes a powerful increase of muscle tension, however the injury produced by dry needling is not so noteworthy, due to the fact that the muscle fibers fixed with formaldehyde are extremely resistant. Conclusions Dry needling is a technique which, overall, provokes limited lesions, independent of the muscle tone.

Infrared Thermography – A Tool for Computer Assisted Research in Rehabilitation Medicine

2015 ◽  
Vol 772 ◽  
pp. 603-607
Author(s):  
Marius Cristian Cojocaru ◽  
Ioana Maria Cojocaru ◽  
Nida Alexandra Cojan Carlea ◽  
Delia Cinteza ◽  
Mihai Berteanu
Keyword(s):  
Infrared Thermography ◽  
Muscle Pain ◽  
Myofascial Pain ◽  
Pain Syndrome ◽  
Myofascial Pain Syndrome ◽  
Trigger Points ◽  
Rehabilitation Medicine ◽  
Clinical Findings ◽  
Computer Assisted ◽  
The Central Nervous System

Muscle pain can be elicited by any irritation of the nociceptors in the muscle or central sensitization in the central nervous system and represent a challenge for medical as well as for neurological rehabilitation. The most frequently described muscle pain syndromes are myofascial pain syndrome (MPS) and fibromyalgia syndrome (FMS). The use of infrared thermography in rehabilitation medicine for assessment of musculoskeletal disorders is not well documented in the current literature. This study is focused around MPS due to the more localized manifestations of this syndrome and it’s objective is to asses a correlation between the clinical findings, ultrasound examination and the thermal pattern of trigger points.

Myofascial Pain May Present Clinically as Occipital Neuralgia

Neurosurgery ◽  
1986 ◽  
Vol 19 (4) ◽  
pp. 610-613 ◽  
Author(s):  
Steven B. Graff-Radford ◽  
Bernadette Jaeger ◽  
John L. Reeves
Keyword(s):  
Myofascial Pain ◽  
Clinical Signs ◽  
Signs And Symptoms ◽  
Trigger Points ◽  
Occipital Neuralgia ◽  
Invasive Procedures ◽  
Myofascial Trigger Points ◽  
Surgical Interventions ◽  
Clinical Signs And Symptoms ◽  
Case Presentations

Abstract Three case presentations illustrate that the clinical signs and symptoms of occipital neuralgia may be produced by myofascial pain. Assessment of myofascial trigger points is needed before making a diagnosis of occipital neuralgia. Myofascial trigger points can be effectively treated with minimally invasive procedures, thereby avoiding irreversible surgical interventions.

scholarly journals Peripheral EphrinB1/EphB1 signalling attenuates muscle hyperalgesia in MPS patients and a rat model of taut band-associated persistent muscle pain

2020 ◽  
Vol 16 ◽  
pp. 174480692098407
Author(s):  
Feihong Jin ◽  
Lianying Zhao ◽  
Qiya Hu ◽  
Feng Qi
Keyword(s):  
Muscle Pain ◽  
Rating Scale ◽  
Myofascial Pain ◽  
Trigger Point ◽  
Numerical Rating Scale ◽  
Protein Microarray ◽  
Trapezius Muscle ◽  
Pain Syndrome ◽  
Myofascial Pain Syndrome ◽  
Peripheral Sensitization

Background Myofascial pain syndrome (MPS) is an important clinical condition that is characterized by chronic muscle pain and a myofascial trigger point (MTrP) located in a taut band (TB). Previous studies showed that EphrinB1 was involved in the regulation of pathological pain via EphB1 signalling, but whether EphrinB1-EphB1 plays a role in MTrP is not clear. Methods The present study analysed the levels of p-EphB1/p-EphB2/p-EphB3 in biopsies of MTrPs in the trapezius muscle of 11 MPS patients and seven healthy controls using a protein microarray kit. EphrinB1-Fc was injected intramuscularly to detect EphrinB1s/EphB1s signalling in peripheral sensitization. We applied a blunt strike to the left gastrocnemius muscles (GM) and eccentric exercise for 8 weeks with 4 weeks of recovery to analyse the function of EphrinB1/EphB1 in the muscle pain model. Results P-EphB1, p-EphB2, and p-EphB3 expression was highly increased in human muscles with MTrPs compared to healthy muscle. EphB1 (r = 0.723, n = 11, P < 0.05), EphB2 (r = 0.610, n = 11, P < 0.05), and EphB3 levels (r = 0.670, n = 11, P < 0.05) in the MPS group were significantly correlated with the numerical rating scale (NRS) in the MTrPs. Intramuscular injection of EphrinB1-Fc produces hyperalgesia, which can be partially prevented by pre-treatment with EphB1-Fc. The p-EphB1 contents in MTrPs of MPS animals were significantly higher than that among control animals (P < 0.01). Intramuscular administration of the EphB1 inhibitor EphB1-Fr significantly suppressed mechanical hyperalgesia. Conclusions The present study showed that the increased expression of p-EphB1/p-EphB2/p-EphB3 was related to MTrPs in patients with MPS. This report is the first study to examine the function of EphrinB1-EphB1 signalling in primary muscle afferent neurons in MPS patients and a rat animal model. This pathway may be one of the most important and promising targets for MPS.

scholarly journals Electromechanical and structural alterations in the aging rabbit heart and aorta

2012 ◽  
Vol 302 (8) ◽  
pp. H1625-H1635 ◽  
Author(s):  
Leroy L. Cooper ◽  
Katja E. Odening ◽  
Min-Sig Hwang ◽  
Leonard Chaves ◽  
Lorraine Schofield ◽  
...  
Keyword(s):  
Conduction Velocity ◽  
Structural Changes ◽  
Optical Mapping ◽  
Diastolic Pressure ◽  
Ex Vivo ◽  
Rabbit Model ◽  
Systolic Pressure ◽  
Age Related ◽  
Sheet Structure

Aging increases the risk for arrhythmias and sudden cardiac death (SCD). We aimed at elucidating aging-related electrical, functional, and structural changes in the heart and vasculature that account for this heightened arrhythmogenic risk. Young (5–9 mo) and old (3.5–6 yr) female New Zealand White (NZW) rabbits were subjected to in vivo hemodynamic, electrophysiological, and echocardiographic studies as well as ex vivo optical mapping, high-field magnetic resonance imaging (MRI), and histochemical experiments. Aging increased aortic stiffness (baseline pulse wave velocity: young, 3.54 ± 0.36 vs. old, 4.35 ± 0.28 m/s, P < 0.002) and diastolic (end diastolic pressure-volume relations: 3.28 ± 0.5 vs. 4.95 ± 1.5 mmHg/ml, P < 0.05) and systolic (end systolic pressure-volume relations: 20.56 ± 4.2 vs. 33.14 ± 8.4 mmHg/ml, P < 0.01) myocardial elastances in old rabbits. Electrophysiological and optical mapping studies revealed age-related slowing of ventricular and His-Purkinje conduction (His-to-ventricle interval: 23 ± 2.5 vs. 31.9 ± 2.9 ms, P < 0.0001), altered conduction anisotropy, and a greater inducibility of ventricular fibrillation (VF, 3/12 vs. 7/9, P < 0.05) in old rabbits. Histochemical studies confirmed an aging-related increased fibrosis in the ventricles. MRI showed a deterioration of the free-running Purkinje fiber network in ventricular and septal walls in old hearts as well as aging-related alterations of the myofibrillar orientation and myocardial sheet structure that may account for this slowed conduction velocity. Aging leads to parallel stiffening of the aorta and the heart, including an increase in systolic stiffness and contractility and diastolic stiffness. Increasingly, anisotropic conduction velocity due to fibrosis and altered myofibrillar orientation and myocardial sheet structure may contribute to the pathogenesis of VF in old hearts. The aging rabbit model represents a useful tool for elucidating age-related changes that predispose the aging heart to arrhythmias and SCD.

scholarly journals Ultrasound-Guided Trigger Point Injections in the Cervicothoracic Musculature: A New and Unreported Technique

2008 ◽  
Vol 6;11 (12;6) ◽  
pp. 885-889 ◽  
Author(s):  
Kenneth P. Botwin
Keyword(s):  
Ultrasound Guidance ◽  
Myofascial Pain ◽  
Trigger Point ◽  
Trigger Points ◽  
Target Tissue ◽  
Obese Patients ◽  
Needle Placement ◽  
Ultrasound Guided ◽  
Myofascial Trigger Points ◽  
Point Injection

Background: Myofascial pain is defined as pain that originates from myofascial trigger points in skeletal muscle. It is prevalent in regional musculoskeletal pain syndromes, either alone or in combination with other pain generators. The myofascial pain syndrome is one of the largest groups of under diagnosed and under treated medical problems encountered in clinical practice. Trigger points are commonly seen in patients with myofascial pain which is responsible for localized pain in the affected muscles as well as referred pain patterns. Correct needle placement in a myofascial trigger point is vital to prevent complications and improve efficacy of the trigger point injection to help reduce or relieve myofascial pain. In obese patients, these injections may not reach the target tissue. In the cervicothoracic spine, a misguided or misplaced injection can result in a pneumothorax. Here, we describe an ultrasound-guided trigger point injection technique to avoid this potential pitfall. Office based ultrasound-guided injection techniques for musculoskeletal disorders have been described in the literature with regard to tendon, bursa, cystic, and joint pathologies. For the interventionalist, utilizing ultrasound yields multiple advantages technically and practically, including observation of needle placement in real-time, ability to perform dynamic studies, the possibility of diagnosing musculoskeletal pathologies, avoidance of radiation exposure, reduced overall cost, and portability of equipment within the office setting. To our knowledge, the use of ultrasound guidance in performing trigger point injection in the cervicothoracic area, particularly in obese patients, has not been previously reported. Methods: A palpable trigger point in the cervicothoracic musculature was localized and marked by indenting the skin with the tip of a plastic needle cover. The skin was then sterile prepped. Then, using an ultrasound machine with sterile coupling gel and a sterile latex free transducer cover, the musculature in the cervicothoracic spine where the palpable trigger point was detected was visualized. Then utilizing direct live ultrasound guidance, a 25-gauge 1.5 inch needle connected to a 3 mL syringe was placed into the muscle at the exact location of the presumed trigger point. This guidance helps confirm needle placement in muscle tissue and not in an adipose tissue or any other non-musculature structure. Results: The technique is simple to be performed by a pain management specialist who has ultrasound system training. Conclusion: Ultrasound-guided trigger point injections may help confirm proper needle placement within the cervicothoracic musculature. The use of ultrasound-guided trigger point injections in the cervicothoracic musculature may also reduce the potential for a pneumothorax by an improperly placed injection. Key words: Trigger point injection, myofascial pain, ultrasound

scholarly journals Ex vivo and in vivo study of Kowa HA-2 applanation tonometer in the measurement of intraocular pressure in cats

2017 ◽  
Vol 38 (6) ◽  
pp. 3647
Author(s):  
Claudia Lizandra Ricci ◽  
Rogério Giuffrida ◽  
Glaucia Prada Kanashiro ◽  
Hilidia Stephania Rufino Belezzi ◽  
Carolina De Carvalho Bacarin ◽  
...  
Keyword(s):  
Intraocular Pressure ◽  
Ex Vivo ◽  
Clinical Signs ◽  
In Vivo Study ◽  
Eye Drops ◽  
Significant Difference ◽  
Applanation Tonometer ◽  
Ex Vivo Study ◽  
Healthy Eyes

The objective of this study was to evaluate the use of the Kowa HA-2 applanation tonometer in measuring intraocular pressure (IOP) in cats. Ten healthy eyes were used in an ex vivo study in which the calibration curve for manometry vs. tonometry was determined by artificially raising the IOP in 5 mmHg increments up to 60 mmHg (10-60 mmHg). Both eyes of 10 anesthetized cats were studiedin vivo to compare manometry vs. tonometry. In the ambulatory study, 78 healthy eyes, 7 eyes with glaucoma and 20 eyes with uveitis were evaluated by tonometry, which was performed with topical anesthesia and 1% fluorescein eye drops for the formation of fluorescein semicircles. The correlation coefficient (r²) between the manometer and the Kowa HA-2 tonometer was 0.993 and the linear regression equation was y = 0.0915x + 0.0878 in the ex-vivo study. In the in vivo study, the IOP values (mean±SD, in mmHg) in manometry were 15.6 ± 1.1(14.0 – 17.5) and in tonometry were 15.5 ± 1.2(13.5 – 17.2), with no significant difference (P > 0.05) between manometry and tonometry. In ambulatory study, using the Kowa HA-2 tonometer, the IOP values (mean±SD, in mmHg) were 15.0 ± 1.5 (11.8 – 18.3) for the healthy eyes, 38.4 ± 8.1(29.6 – 53.7) for glaucomatous eyes and 10.4 ± 2.0(5.3 – 12.2) for eyes with uveitis. There was a strong correlation and accuracy between the IOP values with the manometry and the Kowa HA-2 tonometer. In the ambulatorystudy the IOP values obtained with the tonometer were compatible for animals with healthy eyes and with clinical signs of glaucoma and uveitis. We conclude that the Kowa HA-2 tonometer can be used in the measurement of IOP in cats, since it is a practical and accurate method in this species.

scholarly journals Sympathetic Overactivity in CKD Disrupts Buffering of Neurotransmission by Endothelium-Derived Hyperpolarizing Factor and Enhances Vasoconstriction

2020 ◽  
Vol 31 (10) ◽  
pp. 2312-2325
Author(s):  
Wei Cao ◽  
Liling Wu ◽  
Xiaodong Zhang ◽  
Jing Zhou ◽  
Jian Wang ◽  
...  
Keyword(s):  
Gap Junction ◽  
Vascular Resistance ◽  
Connexin 43 ◽  
Structural Changes ◽  
Ex Vivo ◽  
Resistance Arteries ◽  
Cx43 Expression ◽  
Neurovascular Transmission

BackgroundHypertension commonly complicates CKD. Vascular smooth muscle cells (VSMCs) of resistance arteries receive signals from the sympathetic nervous system that induce an endothelial cell (EC)–dependent anticontractile response that moderates vasoconstriction. However, the specific role of this pathway in the enhanced vasoconstriction in CKD is unknown.MethodsA mouse model of CKD hypertension generated with 5/6-nephrectomy (5/6Nx) was used to investigate the hypothesis that an impaired anticontractile mechanism enhances sympathetic vasoconstriction. In vivo, ex vivo (isolated mesenteric resistance arteries), and in vitro (VSMC and EC coculture) models demonstrated neurovascular transmission and its contribution to vascular resistance.ResultsBy 4 weeks, 5/6Nx mice (versus sham) had augmented increases in mesenteric vascular resistance and mean arterial pressure with carotid artery occlusion, accompanied by decreased connexin 43 (Cx43) expression at myoendothelial junctions (MEJs), impaired gap junction function, decreased EC-dependent hyperpolarization (EDH), and enhanced contractions. Exposure of VSMCs to NE for 24 hours in a vascular cell coculture decreased MEJ Cx43 expression and MEJ gap junction function. These changes preceded vascular structural changes evident only at week 8. Inhibition of central sympathetic outflow or transfection of Cx43 normalized neurovascular transmission and vasoconstriction in 5/6Nx mice.Conclusions5/6Nx mice have enhanced neurovascular transmission and vasoconstriction from an impaired EDH anticontractile component before vascular structural changes. These neurovascular changes depend on an enhanced sympathetic discharge that impairs the expression of Cx43 in gap junctions at MEJs, thereby interrupting EDH responses that normally moderate vascular tone. Dysregulation of neurovascular transmission may contribute to the development of hypertension in CKD.

scholarly journals Reduced force of diaphragm muscle fibers in patients with chronic thromboembolic pulmonary hypertension

2016 ◽  
Vol 311 (1) ◽  
pp. L20-L28 ◽  
Author(s):  
Emmy Manders ◽  
Peter I. Bonta ◽  
Jaap J. Kloek ◽  
Petr Symersky ◽  
Harm-Jan Bogaard ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Muscle Fiber ◽  
Ex Vivo ◽  
Muscle Fibers ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Inspiratory Muscle ◽  
Force Generation ◽  
Diaphragm Muscle ◽  
Fast Twitch

Patients with pulmonary hypertension (PH) suffer from inspiratory muscle weakness. However, the pathophysiology of inspiratory muscle dysfunction in PH is unknown. We hypothesized that weakness of the diaphragm, the main inspiratory muscle, is an important contributor to inspiratory muscle dysfunction in PH patients. Our objective was to combine ex vivo diaphragm muscle fiber contractility measurements with measures of in vivo inspiratory muscle function in chronic thromboembolic pulmonary hypertension (CTEPH) patients. To assess diaphragm muscle contractility, function was studied in vivo by maximum inspiratory pressure (MIP) and ex vivo in diaphragm biopsies of the same CTEPH patients ( N = 13) obtained during pulmonary endarterectomy. Patients undergoing elective lung surgery served as controls ( N = 15). Muscle fiber cross-sectional area (CSA) was determined in cryosections and contractility in permeabilized muscle fibers. Diaphragm muscle fiber CSA was not significantly different between control and CTEPH patients in both slow-twitch and fast-twitch fibers. Maximal force-generating capacity was significantly lower in slow-twitch muscle fibers of CTEPH patients, whereas no difference was observed in fast-twitch muscle fibers. The maximal force of diaphragm muscle fibers correlated significantly with MIP. The calcium sensitivity of force generation was significantly reduced in fast-twitch muscle fibers of CTEPH patients, resulting in a ∼40% reduction of submaximal force generation. The fast skeletal troponin activator CK-2066260 (5 μM) restored submaximal force generation to levels exceeding those observed in control subjects. In conclusion, diaphragm muscle fiber contractility is hampered in CTEPH patients and contributes to the reduced function of the inspiratory muscles in CTEPH patients.

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