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Critical care, neurology and analgesia
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
In most mammalian muscles, each muscle fibre has a single area of contact with the axon of the motor neurone that supplies it. This specialised structure is the neuromuscular junction, which facilitates transmission of the electrical impulse from the nerve terminal to the motor end plate of the muscle. This is achieved by the transmission of acetylcholine molecules across the 60–100 nanometre synaptic cleft. Acetylcholine binds to receptors on the motor end plate, causing depolarisation and contraction of the muscle fibre. After acetylcholine dissociates from the receptor, it is degraded by acetylcholinesterase into acetate and choline, which is reabsorbed into the nerve terminal for recycling into further acetylcholine [1].
Muscle Physiology and Electromyography
Published in Verna Wright, Eric L. Radin, Mechanics of Human Joints, 2020
The central nervous system (CNS) sends information coded as a wave of depolarization to the muscles via one or more nerves. The depolarization is received at the neurovascular hilum, a small oval area on the surface of the muscle, usually near the origin. As the name implies, the neurovascular hilum is also the entry point for blood into the muscle. The nerve enters the muscle as a series of small branches containing both sensory and motor fibers, all of which are myelinated. Once inside the muscle, the nerves branch further into a plexus that runs through the epimysial and perimysial septa to infiltrate the endomysial spaces. The ramifications of the nerve branch again within the endomysial spaces and are at this level unmyelinated. Each of these final branches is an a motor neuron. The a motor neurons terminate at the motor end plate of the individual muscle fibers (the a motor neuron and the motor end plate are collectively known as the motor unit). The motor end plates of all the fibers are grouped together fairly closely in the central region of the muscle (9).
Myofascial Trigger Point Therapy
Published in David Lesondak, Angeli Maun Akey, Fascia, Function, and Medical Applications, 2020
The etiological definition from the second edition of the Trigger Point Manual by Simons et al. gives several pages to the “integrated trigger point hypothesis”. They begin with electrodiagnostic characteristics emphasizing Electromyography (EMG) findings of noise at the site of the motor endplate area and move on to an ultrasound picture demonstrating the shortened sarcomeres called for in the hypotheses. This was followed up by other ultrasound studies.24–26 Additional input has contributed to an understanding of the biochemical milieu of the trigger point in a series of studies by Jay Shah and colleagues.27–30
Heterogeneity in myasthenia gravis: considerations for disease management
Published in Expert Review of Clinical Immunology, 2021
Amelia Evoli, Gregorio Spagni, Gabriele Monte, Valentina Damato
At the motor end plate, a high concentration of AChRs at the top of junctional folds, facing the sites of neurotransmitter release, is crucial for synapsis efficiency. The AChR is a ligand-gated ion channel made of five subunits with stoichiometry α(2)βεδ in the adult muscle, and α(2)βγδ in the embryonic muscle. Each subunit is a glycosylated peptide comprised of a large extracellular N-terminal domain, four transmembrane regions (M1-M4), two cytoplasmic loops (between M1-M2 and M3-M4) and a short C-terminal extracellular domain. The M2 region of each subunit lines the cation-specific pore [9]. Tyrosine phosphorylation of the β subunit is required for AChR clustering and postsynaptic membrane stabilization [10]. The two acetylcholine-binding sites are between α-δ and α-ε (or γ) subunits (Figure 1(a)).
The role of sugammadex, a novel cyclodextrin compound in modern anesthesia practice: conventional neuromuscular physiology and clinical pharmacology
Published in Expert Review of Clinical Pharmacology, 2019
Alan D. Kaye, Rachel J. Kaye, Elyse M. Cornett, Ivan Urits, Vwaire Orhurhu, Omar Viswanath, Amit Prabhakar
Succinylcholine was first introduced in 1951 and is surprisingly still the only rapid acting depolarizing neuromuscular blocking agent clinically available for use. Its chemical structure mimics two connected acetylcholine molecules. Binding to motor end plate receptors results in a state of persistent depolarization via sodium influx. Muscle fasciculations will arise as a result of this depolarization, which is often observed after intravenous or intramuscular administration. Traditionally, 1.0 mg/kg of succinylcholine has been used for intubation, however, the ED95 of succinylcholine is less than 0.30mg/kg. Therefore, 1.0 mg/kg dose would be 3.5–4 times the ED95. Degradation is accomplished predominantely via plasma cholinesterases. The benefits of succinylcholine administration are often outweighed by its numerous adverse effects. These include but are not limited to hyperkalemia, ocular hypertension, increased intracranial pressure, myalgia, bradycardia, and the possibility for triggering malignant hypertension [2]. The aforementioned make succinylcholine far from an ideal muscle relaxant.
Sensory neurotization of muscle: past, present and future considerations
Published in Journal of Plastic Surgery and Hand Surgery, 2019
Steven D. Kozusko, Alexander J. Kaminsky, Louisa C. Boyd, Petros Konofaos
Sönmez studied motor reinnervation of a denervated muscle by using a sensory nerve and found that some axonal regeneration occurred, muscle experienced only partial atrophy and some reinnervation was obtained on electrophysiologic studies [31]. In their study, they analyzed the effect of the lateral femoral cutaneous nerve (LFCN) on the gluteus maximus muscle in a rat model. Their histological analysis showed that axonal regenerations were present distal to the coaptation zones, indicating axons reached the gluteus maximus muscle through the LFCN. Scanning electron microscopic findings depicted only partial muscle atrophy, meaning that sensory reinnervation inhibited total atrophy. Li et al. [17,22] found that with sensory nerve protection, the ultrastructure and cross-sectional area of the target muscle, as well as areas postsynaptic to the motor endplate were preserved. In their rat model, they found that muscle fiber architecture was preserved with both sensory and mixed nerve neurotization. Superior results were demonstrated with mixed nerve neurotization than purely sensory. This study also showed that early innervation with sensory or a mixed nerve led to better functional recovery following native nerve reinnervation [22].