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Muscle Spindles, Golgi Tendon Organs and Spinal Reflexes
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The Golgi tendon organ is an encapsulated receptor found near the muscle-tendon junction that responds to changes in tension in its muscle fascicle. It is covered by a capsule which is continuous with the connective tissue of the muscle or tendon. The afferent nerves are group Ib axons which branch over several fascicles. An increase in tension in the muscle fascicle increases the frequency of impulses in the Ib afferent nerves. The Golgi tendon body is more sensitive to active muscle tension than passive stretching of the muscle.
Sensory contributions to control
Published in Andrea Utley, Motor Control, Learning and Development, 2018
The Golgi tendon organ is another type of proprioceptor or stretch receptor found in skeletal muscle, which provides information about changes in muscle tension. Golgi tendon organs are located at the junction of tendon and skeletal muscle and are formed from the terminals of Ib afferent fibers. The sensory endings of Golgi tendon organs are arranged in series with the muscle, in contrast to the parallel arrangement of the muscle spindles. Because of their arrangement, Golgi tendon organs can be activated by either muscle stretch or muscle contraction, with the latter being a more effective stimulus. The actual stimulus that activates the Golgi tendon organ is the force that develops in the tendon containing the Golgi tendon organ. Thus, the difference between a muscle spindle and a Golgi tendon organ is that the latter signals force, while the former signals muscle length and the rate of change in muscle length. The job of the Golgi tendon organ is to act as a brake against excessive contractions by inhibiting the motor neurons in the spinal cord.
Nerve
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Mike Fox, Caroline Hing, Sam Heaton, Rolfe Birch
Deep sensation from muscles, ligaments, tendons and joints occurs via free nerve endings and receptors, such as the following: Muscle spindles: consist of intrafusal nuclear bag fibres and nuclear chain fibres within the muscle itself. Innervated by myelinated afferent sensory Aα fibres and efferent motor Aγ fibres.Golgi tendon organs: activated by stretch and important in proprioception. They sense maintained tension in muscle and send impulses to the cerebellum and the cortex. Located at musculocutaneous junctions, they consist of small bundles of tendon fibres enclosed in a capsule of concentric cytoplasmic sheets. The capsule is pierced by Aα nerve fibres that divide and wrap around the tendon fasciculi. They are slowly adapting and the firing rate is proportionate to tension. They play a crucial part in the inverse stretch reflex during the application of acute traction in fracture reduction, whereby a prolonged constant stretch leads to relaxation of muscle contraction, allowing manipulation of the displaced fracture fragments.Paciniform receptors: lamellated receptors. Smaller than Pacinian corpuscles. Rapidly adapting low-threshold mechanoreceptors found in joint capsules. Supplied by myelinated Aα afferent fibres.
Finger Force Matching and Verbal Reports: Testing Predictions of the Iso-Perceptual Manifold Concept
Published in Journal of Motor Behavior, 2021
Cristian Cuadra, Rick Gilmore, Mark L. Latash
Imagine that you co-contract muscles acting about a joint without moving that joint and without looking at it. You will have veridical perception of motionless joint despite the fact that all relevant afferent and efferent signals change. In particular, obviously, there will be changes in signals to and from alpha-motoneurons that innervate the activated muscles. In addition, signals from muscle spindles will change because of changes in signals from gamma-motoneurons due to the phenomenon of alpha-gamma coactivation. Signals from Golgi tendon organs will change with muscle force. Signals from articular receptors will change with joint capsule tension. Given all these changes, stability of the joint position percept is non-trivial, suggesting that these changes are constrained to a manifold in a respective afferent-efferent space—the IPM.
Management of Muscle Spasticity in Children with Cerebral Palsy by Means of Extracorporeal Shockwave Therapy: A Systematic Review of the Literature
Published in Developmental Neurorehabilitation, 2021
Bruno Corrado, Carla Di Luise, Clemente Servodio Iammarrone
None of the selected studies could definitively identify the mechanisms by which shock waves achieved spasticity reduction in children with CP. However, in light of the most recent findings, we assume that ESWT mainly acts through two different pathways: 1) by temporarily reducing the hyperexcitability of the stretch reflexes and 2) by modifying the intrinsic stiffness of spastic muscles. The first effect is probably achieved via different mechanisms such as enhanced production of NO, interference with the segmental reflex arc, and a direct effect on Golgi tendon organs. The possibility of shock waves producing changes in the intrinsic mechanical properties of muscle is supported by the evidence that ESWT stimulates healing and regeneration of injured skeletal muscle.53 It is reasonable to assume that reduction in hyperexcitability of the stretch reflexes is the basis for the short-term effect of EWST, while the changes in intrinsic muscle properties are the basis for the long-term effect of ESWT on muscle spasticity.
The evidence for prolonged muscle stretching in ankle joint management in upper motor neuron lesions: considerations for rehabilitation – a systematic review
Published in Topics in Stroke Rehabilitation, 2019
Stretching can help prevent complications following UMN lesions that can be explained by the neurophysiological effects, the effects of viscoelastical properties, stiffness and ROM, and preventing contractures.15 The neurophysiological effects of stretching on spasticity showed that such effect may be best explained by a change in the excitability of motor neurons within the spastic muscle.16,17 Spasticity develops when an imbalance occurs in the excitatory and inhibitory input to alpha motor neurons (αMN) and more specifically from the loss of inhibition of motor neurons. In response to muscle tension, afferents from the Golgi tendon organs are normally influenced by corticospinal fibers that causes its associated muscle to relax (inhibition) and thereby assists in regulating muscle contraction force.18 Such inhibition is easily demonstrated in healthy subjects but failed to produce on the paretic side in UMN lesion patients.19 In case of spasticity, there is greater increase in excitability of spinal neural function during muscle stretching because of short-latency autogenic inhibition (IB inhibition)20 Ib afferent inhibitory neurons are not fired under short stretching durations. Therefore, UMN lesion patients require longer durations of continuous stretching of the affected hypertonic muscle to fire the Ib inhibitory neurons.21 With regard to viscoelastical properties, even though studies have methodological limitations,15 Some studies showed that stretching reduced the viscoelastic components of the ankle joint muscles.11,22