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Spinal Cord and Reflexes
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The Renshaw cell (Figure 1.5) is an inhibitory interneuron that has been studied quite intensively. Originally, Renshaw cells were shown to be excited by branches of axons of motoneurons within the gray matter of the spinal cord (Figure 1.5). These branches are known as recurrent collaterals. It has since been established that Renshaw cells also receive sensory inputs, mainly from segmental sensory fibers, as well as inputs from other interneurons and descending systems. A Renshaw cell may be contacted by more than one α-motoneuron axon collateral and may synapse on multiple α-motoneurons and γ-motoneurons, in the same motoneuron pool, or in the motoneuron pools of synergist muscles. The inhibitory feedback connection to the same, or homonymous, motoneuron pool is referred to as homonymous recurrent inhibition, whereas the inhibition of motor neuron pools of other muscles is referred to as heteronymous recurrent inhibition. Figure 11.5 illustrates these two types of inhibition.
Motor Function and ControlDescending Tracts
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
A reflex can be defined as an automatic or involuntary stereotype response to a stimulus mediated by a receptor, an afferent and efferent pathway and an effector organ. The reflex pathway generally consists of a receptor and an afferent neuron and is integrated by interneurons in the spinal cord. The final common efferent path is a motor neuron to the effector organ. Spinal cord ventral horn motor neurons may be either α motor neurons (14 μm in diameter and rapid conduction velocity) or γ motor neurons (5 μm in diameter and slower conduction velocity). There are also interneurons, which are highly excitable and may have high spontaneous firing rates. The Renshaw cell is a special interneuron that receives collateral branches of motor neuron axons. The Renshaw cell provides inhibitory connections with the same or neighbouring motor neurons via its own axons.
The Spinal Cord and the Spinal Canal
Published in Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand, Pediatric Regional Anesthesia, 2019
Bernard J. Dalens, Jean-Pierre Monnet, Yves Harmand
Basically, these neurons consist of alpha and gamma motor neurons. Another type of neuron, the Renshaw cells, have been (physiologically) identified in the ventral horns: these synapse with alpha motor neurons, from which they receive some recurrent axonal collaterals.
Strychnine, old still actual poison: description of poisoning cases reported to French Poison Control Centers over the past thirteen years
Published in Toxin Reviews, 2022
Camille Paradis, Denis Dondia, Audrey Nardon, Ingrid Blanc-Brisset, Arnaud Courtois, Jules-Antoine Vaucel, Magali Labadie
In the gray matter of the spinal cord, Renshaw cells function as inhibitory interneurons associated with an alpha motor neuron. Renshaw cells receive excitatory collaterals from the alpha motor neurone and thus, upon excitation, could release glycine to the alpha motor neurone in order to exert an inhibitory feedback and prevent alpha motor neurone firing. Strychnine is a potent antagonist of glycine receptors thus acting as an inhibitor of an inhibitory signal. This results in a motor disturbance characterized by an increase in muscle tone, associated with muscular hyperactivity. Clinical symptoms of poisoning appear suddenly and rapidly after ingestion, and begin with painful muscle contractures spontaneous or triggered by even the slightest stimulus, trismus, an opisthotonus (a position which the whole body is arched backward in hyperextension) and generalized convulsions for the severe forms. Importantly, during the course of poisoning, consciousness is retained. The clinical picture is complicated by major acidosis and rhabdomyolysis. Death occurs due to the paralysis of respiratory muscles or a cardiac arrest (Baud and Garnier 2017).
Relationship between subarachnoid and central canal hemorrhage and spasticity: A first experimental study
Published in The Journal of Spinal Cord Medicine, 2021
Selim Kayaci, Mehmet Dumlu Aydin, Baris Ozoner, Tayfun Cakir, Orhan Bas, Sare Sipal
Previous experimental data have shown that harmful processes caused by spinal ischemia cause the loss of inhibitor interneurons in the spinal segments.22 Renshaw cells are the most well-known of these inhibitor interneurons. The inhibition of these cells is most important in the pathophysiology of spasticity. Renshaw cells receive input from the collateral axions of the motor neurons and they inhibit the motor neurons once stimulated. They can effectively control the activation of all motor units of a muscle.23 The main transmitter in the synapsis between these cells and their target neurons is glycine (with strychnine as the antagonist).24 Neurons in the spinal cord that secrete these neurotransmitters that regulate muscle tone cannot secrete these neurotransmitters as they present with ischemic damage. As a result, the reflex arc is disrupted, and spasticity is exacerbated as inhibition will be disabled in the neurochemical pathway that regulates muscle tone via excitation mechanisms. In this study, we believe that the Renshaw cells that are a part of the neural network in the GM of the spinal cord lost their function in animals with induced spinal SAH and this plays an important role in spasticity.
Comparison of transcutaneous electrical nerve stimulation (TENS) and functional electrical stimulation (FES) for spasticity in spinal cord injury - A pilot randomized cross-over trial
Published in The Journal of Spinal Cord Medicine, 2018
Anjali Sivaramakrishnan, John M. Solomon, Natarajan Manikandan
Similar to TENS, FES also reduced spasticity in MAS scores of hip adductors, and knee extensors up to four hours post application. We stimulated the spastic muscle, based on a previous study32 which showed better reduction of spasticity compared to antagonist and dermatome stimulation. It is hypothesized that recurrent inhibition of the spastic muscle via the Renshaw cell may account for the reduction in tone.18 The Renshaw cell has a negative feedback loop to the alpha motor neuron i.e. recurrent inhibition,18 which is thought to be reduced in patients with spasticity. Electrical stimulation of the agonist muscle is theorized to increase the recurrent inhibition to the alpha motoneuron, and consequently to the agonist muscle thus reducing spasticity.41,42 Our findings are in consensus with previous studies which have utilized other forms of FES. Granat et al.43 investigated the role of a FES gait program in rehabilitation of patients with incomplete SCI and found a reduction in quadriceps spasticity. Rayegani et al.44 also found a significant reduction in spasticity with electrical passive cycling in veterans with SCI.