Anomalous Innervations

David C. Preston MD , in Electromyography and Neuromuscular Disorders , 2021

Routine Median Motor Report: Increased Compound Muscle Action Potential Amplitude Proximally

The third case in which an MGA should be suspected is during routine median motor studies, when the median-to-ulnar cross-over innervates i of the ulnar-innervated thenar muscles (i.e., adductor pollicis or deep head of the flexor pollicis brevis) (Fig. vii.six). With this type of MGA, routine ulnar motor studies, recording the abductor digiti minimi, are normal. However, during routine median motor studies, recording the thenar muscles, a characteristic pattern is seen: the CMAP amplitude is college stimulating the median nerve at the antecubital fossa than stimulating at the wrist (Fig. vii.7), unlike the usual pattern of a higher-amplitude CMAP with distal stimulation. The differential diagnosis of this pattern is:

•

Submaximal stimulation of the median nervus at the wrist

•

Excessive stimulation of the median nerve at the antecubital fossa resulting in co-stimulation of the ulnar nervus

•

An MGA with cross-over fibers innervating the thenar muscles

To demonstrate that an MGA is present, the examiner must then stimulate the ulnar nerve at the wrist and below-elbow siteswhile recording the thenar muscles. Commonly, ulnar stimulation at the wrist, recording thenar muscles, evokes a thenar CMAP, commonly with an initial positive deflection. This CMAP reflects the normal ulnar-innervated muscles in the thenar eminence. If no MGA is present, subsequent stimulation of the ulnar nerve at the beneath-elbow site will evoke a CMAP potential with a similar shape and amplitude. If an MGA is present, the CMAP amplitude volition exist substantially lower, stimulating the ulnar nerve at the beneath-elbow site, than at the wrist. This is because stimulation at the below-elbow site is above the cross-over, and, therefore, the cross-over fibers exercise not contribute to the CMAP. The difference in amplitude between these two potentials approximates the contribution of the cross-over fibers.

Muscle Wrinkle; Overview

D.B. DiCapua , in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Excitation–Contraction–Relaxation Cycle

The muscle action potential triggers a sequence of deportment that ultimately results in the contraction and relaxation of the muscle cobweb. This sequence is chosen the excitation–contraction–relaxation bike. An early on step in this cycle is the release of stored calcium from an intracellular membrane circuitous called the sarcoplasmic reticulum (SR). This is mediated through the activation of a specialized membrane poly peptide complex that binds the drug dihydropyridine and has been called the dihydropyridine receptor (DHPR). The DHPR is a tetrameric complex located in the sarcolemmal membrane of the T tubules at the junctional region between the T tubules and the terminal cisternae of the SR. Each DHPR is believed to represent a functional unit in the transduction of sarcolemmal depolarization and sarcoplasmic calcium release. The transmembrane portions of the DHPR establish the voltage-sensitive elements and are believed to change conformation in response to depolarization, similar to the voltage-gated channels described previously. Although the DHPR has also been shown to take the properties of a slowly activating, voltage-sensitive, calcium channel in vitro, entry of extracellular calcium is not required for either point detection or transmission. It has been shown that a cytoplasmic loop portion of the DHPR is the critical element for transmission of the external membrane depolarization to the intracellular SR calcium release channels.

The SR calcium release channels consist of four identical monomers that bind a constitute alkaloid ryanodine and therefore take been called ryanodine receptors (RyRs). These channels are located in the SR, with a cloverleaf pattern of poly peptide constituents forming a central pore that branches in four radially arranged canals. Interestingly, although each tetrad of DHPRs faces 1 RyR at the junctional region with the T tubules, this only accounts for half of the RyRs, and it is not known how the rest of these channels are activated.

On the cytoplasmic face up of the SR, the calcium release channels are associated with several small proteins whose functions are non every bit clear. Calsequestrin is a low-affinity, calcium-binding protein in the SR membrane, which enables the SR to maintain an extraordinary amount of calcium ions. Another minor protein, triadin, anchors calsequestrin in the membrane and provides a straight link between calsequestrin and the RyRs. A small-scale cytoplasmic protein that binds the immunosuppressive drug FK506, called FK506-binding protein (FKBP), has been establish to stabilize the total calcium conductance of the RyRs. In addition, the activity of the RyRs is modulated by several endogenous cytoplasmic factors, adenosine triphosphate (ATP), Mg2+, H+, inorganic phosphate, and unlike phosphorylation states of the RyR, but the most of import appears to be a very potent inhibitory association with Mg2+.

Several lines of evidence support the following model for the mechanism of coupling excitation and wrinkle proposed past Stephenson et al. Depolarization of the T-tubule membrane triggers conformational changes in the DHPR that, through interaction betwixt cytoplasmic loop portions of the DHPR complex and the FKBP, lead to changes in the RyRs complex that lower its affinity for Mgtwo+ binding. Dissociation of ionic magnesium releases the RyRs from the inhibited state, and sarcoplasmic calcium is released into the cytoplasm. This is accompanied by further Ca2+-activated calcium release that results in a rapid increase in cytoplasmic calcium. Information technology is the interaction of this intracellular calcium with the contractile apparatus that ultimately leads to wrinkle.

Once depolarization, activation, and contraction cease, relaxation of the muscle fiber gain by more than well-understood mechanisms. Relaxation is achieved when the cytoplasmic Ca2+ concentration is decreased to its resting land. This is partially achieved by resequestration of Ca2+ by the sarcoplasmic calcium pump. This membrane protein is widespread in the SR, except at the junctional region with the T tubules, and it couples the active ship of Caii+, against its concentration gradient, with hydrolysis of Mg/ATP. The observed subtract in cytoplasmic calcium concentration, however, precedes full activation of the SR calcium pump, and therefore must likewise be mediated past other cytoplasmic-binding sites. The residue of calcium release and sequestration is modulated by the frequency of sarcoplasmic depolarization. Higher frequencies of nervus action potentials every bit well as pathological depolarization lead to greater calcium release and subsequent wrinkle.

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Office Nerve Conduction Testing

Grant C. Fowler Physician , in Pfenninger and Fowler's Procedures for Master Care , 2020

Differentiating Compound Musculus Action Potential (Motor) and Sensory Nervus Action Potential (Sensory) Responses

Several parameters differentiate CMAP and SNAP. The size of the signal involved is larger with CMAP. The signal is measured in millivolts rather than microvolts for SNAP. Although muscle tin can amplify the indicate in CMAP, noise and other pocket-size artifacts can alter the quality of the reading with SNAP. CMAP can observe pathology in nerve and muscle, whereas SNAP tin identify nervus changes only. The SNAP response is not affected by radiculopathies, whereas CMAP can exist. The sensitivity of aamplitude decrement to axonal loss is very high in SNAP because of the proportional relationship of amplitude to the number of axons in this study. This sensitivity is hard to overcome in CMAP considering of vigorous muscle fiber reinnervation until avant-garde axonal loss occurs. As mentioned earlier, CMAP requires stimulation at two locations to evaluate conduction velocity, whereas SNAP requires only one stimulation site.

Activity Potential of the Fish Heart☆

1000 Vornanen , in Reference Module in Life Sciences, 2017

AP of the Atrio-Ventricular Canal

The atrial muscle AP is conducted to the ventricle via the atrio-ventricular culvert along the myocytes in the inner layer of the canal. Hither, the AP has a similar shape as in the primary pacemaker tissue of the sinoatrial ring. This has several of import implications: (1) the rate of AP upstroke is slower, delaying the conduction of the impulse and allowing adequate filling of the ventricle with claret; (2) the AP does not have stable RMP and therefore myocytes of the atrio-ventricular canal can office as an ancillary pacemaker – this would merely go important if the sino-atrial pacemaker fails or if atrial conduction is blocked for some reason because the pacemaker potential is non every bit steep equally that for the principal pacemaker cells; and (3) atrial tissue is prone to arrhythmias, which could easily propagate to the ventricle and generate detrimental ventricular arrhythmias without the slow conduction of the atrio-ventricular canal.

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Cellular Physiology of Skeletal, Cardiac, and Smooth Muscle

Walter F. Boron MD, PhD , in Medical Physiology , 2017

Action potentials of smooth muscles may be brief or prolonged

Although activeness potentials initiate wrinkle in both skeletal and cardiac muscle, diverse changes in membrane potential (5 thousand) can either initiate or modulate wrinkle in smooth-muscle cells. Action potentials that are similar to those seen in skeletal muscle are observed in unitary polish muscle and in some multiunit muscles. Like cardiac muscle cells, some smooth-muscle cells exhibit prolonged activity potentials that are characterized past a prominent plateau stage. All the same other smooth-muscle cells cannot generate action potentials at all. In these cells,V yard changes in a graded fashion (seepp. 174–176) rather than in the all-or-none style of activity potentials. The stimuli that produce agraded response ofFive m include many circulating and local humoral factors as well equally mechanical stimuli such as stretching of the cell. These gradedFive chiliad changes may exist either hyperpolarizing or depolarizing; they sum temporally likewise as spatially. If the summation of graded depolarizations bringsV yard above threshold, activity potentials will fire in electrically excitable smoothen-muscle cells.

Action potentials —characteristic responses of unitary (visceral) polish muscle—typically have a slower upstroke and longer duration (up to ~100 ms) than practice skeletal muscle action potentials (~two ms). The action potential in a smooth-muscle cell tin be a uncomplicated spike, a spike followed by a plateau, or a series of spikes on tiptop of slow waves of V m (Fig. 9-14A ). In any case, the depolarizing phase of the activeness potential reflects opening of 50-type voltage-gated Catwo+ channels. The initial inward Caii+ current further depolarizes the prison cell and thereby causes still more voltage-gated Catwo+ channels to open in positive-feedback fashion. Thus, some smooth-musculus cells showroom the same type of regenerative all-or-none depolarization that is seen in skeletal muscle. However, the rate of ascent of the action potential in smooth musculus is typically slower because Cav channels (seepp. 190–193) open more slowly than practise Nav channels (run intopp. 187–189) of skeletal and cardiac muscle. Repolarization of the smooth-muscle jail cell is besides relatively wearisome considering L-type Cav Ca2+ channels showroom prolonged openings and inactivate slowly. In improver, the slow repolarization reflects the delayed activation of voltage-gated Thousand+ channels and, in many cases, Ca2+-activated Thousand+ channels, which depend on pregnant superlative of [Ca2+]i.

Some smoothen-muscle cells as well express fast voltage-gated Na+ channels. However, these channels practice not appear to exist necessary for generating an action potential simply rather contribute to a greater charge per unit of depolarization and thus the activation of voltage-gated Catwo+ channels.

Skeletal Muscle Excitability

Nicholas Sperelakis , ... Hugo Gonzalez-Serratos , in Cell Physiology Source Volume (Fourth Edition), 2012

VI Mechanisms of Repolarization

The skeletal musculus AP is terminated past 3 processes: turn-on of yard K, turn-off of g Na and influx of Cl− ions. The turn-on of the V-dependent K+ conductance (thousand Yard) (the delayed rectifier) (see Fig. 42.3) acts to bring Due eastm towards EM (about −98   mV), since the membrane potential at any time is determined primarily past the ratio of g Na/g K. This type of thou K channel is activated by depolarization and turned off by repolarization. Therefore, this thousand K aqueduct is cocky-limiting, in that it turns itself off as the membrane is repolarized past its activity.

In addition to the g K turn-on, plough-off of g Na occurs (run across Fig. 42.3) (contributing to repolarization) for 2 reasons: (i) spontaneous inactivation of fast Na+ channels that had been activated, i.e. closing of their I-gate (inactivation τ of 1–three   ms) and (2) reversible shifting of activated channels directly back to the resting state (deactivation), considering of the rapid repolarization that is occurring due to the g One thousand increment (Fig. 42.five). Theoretically, it would be possible to have an AP that would repolarize (but more slowly) even if in that location were no g K mechanism, considering the g Na channels would spontaneously inactivate and so the g Na /gK ratio and Eone thousand would be more slowly restored to their original resting values.

FIGURE 42.5. Illustration of the hypothetical states of the fast Na+ channel. The 3 states patterned later the Hodgkin–Huxley view were modified to reflect the fact that in that location is bear witness for three closed states. Equally depicted, in the most closed land (C3), all three g gates (or particles) are in the closed configuration. In the mid-closed land (C2), ii m gates are airtight and one is open. In the to the lowest degree closed state (Ci), i gate is closed and ii are open up. In the resting state, the activation gate (A) is closed and the inactivation gate (I) is open: k = 0, h = one. Depolarization to the threshold activates the channel to the agile land, the A-gate opening rapidly and the I-gate withal beingness open up: m = 1, h = 1. The activated channel spontaneously inactivates to the inactive land due to closure of the I-gate: thousand = I, h = 0. The recovery process on repolarization returns the channel from the inactive state dorsum to the resting country, thus making the aqueduct again available for reactivation. Na+ ion is depicted as being spring to the outer mouth of the channel and poised for entry downwardly its electrochemical gradient when both gates are open. The reaction betwixt the resting country and the active state is readily reversible and there is some reversibility of the other reactions. The fast Na+ channel is blocked by tetrotodoxin (TTX) binding to the outer mouth and plugging it.

In addition, in that location is an important third factor involved in repolarization of the AP in skeletal musculus: the Cl− current (see Fig. 42.ii). The Cl− permeability (P Cl) and conductance (one thousand Cl) are very high in skeletal musculus (and are not strongly 5-dependent). In fact, P Cl of the surface membrane is much higher than P K , the P Cl/P Thou ratio being about three–vii. As discussed in the chapter on RP (see Chapter nine), the Cl− ion is passively distributed, or near so, and thus cannot determine the RP. However, net Cl− movements inwards (hyperpolarizing) or outward (depolarizing) do touch Egrand transiently until re-equilibration occurs and there is no further net move. At the RP, at that place is no internet Cl− current (I Cl), since there is no electrochemical driving force for Cl− (since Em = EastwardCl ). However, during the AP depolarization, there is a larger and larger driving forcefulness for outward I Cl (i.e. Cl− influx), since I Cl = g Cl (Em−E Cl). In other words, the large electric field that was keeping Cl− out (i.e. [Cl−] i << [Cl−] o ) diminishes during the AP and so Cl− ion enters the cobweb. This Cl− entry is hyperpolarizing and so tends to repolarize the membrane more than quickly than would otherwise occur. That is, AP repolarization is sharpened by the Cl− machinery. (Annotation that influx of the negatively-charged Cl− ion is an outward Cl− electric current, which is repolarizing.)

To illustrate farther some of the preceding points on the office of Cl−, when skeletal muscle fibers are placed into Cl−-free Ringer solution (due east.one thousand. methanesulfonate substitution), depolarization and spontaneous APs and twitches occur for a few minutes until most or all of the [Cl−]i is washed out. After equilibration, the resting Due eastm returns to the original value ca. −ninety   mV for frog skeletal muscle and −lxxx   mV for mammalian, conspicuously indicating that Cl− does non determine the RP and that net Cl− efflux produces depolarization. Re-addition of Cl− to the bath produces a rapid big hyperpolarization, e.k. to −120   mV, due to net Cl− influx; the Em then slowly returns to the original value (eastward.g. −xc   mV) as Cl− re-equilibrates, i.e. redistributes itself passively. These aforementioned furnishings occur in cardiac muscle, shine musculus and nerve, but to a lesser extent, considering in these tissues PCl is much lower (e.g. PCl/PG ratio is only about 0.v in vascular smooth muscle).

The importance of the Cl− electric current in repolarization in skeletal muscle fibers is illustrated past one type of myotonia in which an abnormally low PCl causes repetitive APs to occur. Because m Cl is abnormally depression, full membrane conductance Thousandyard is also low. From the relationship between membrane current (Im ) and G1000 (I grand /Gm = Egrand ), it tin be deduced that merely a smaller outward depolarizing membrane current Im is necessary to attain threshold Ethursday for an AP. Since chiliad Cl is abnormally low, the membrane resistance Rm volition exist abnormally high, making the space constant λ larger than normal. Because thousandCl is abnormally depression, the Cl− influx during AP repolarization is much less than normal and so the repolarization process is slowed, thus increasing the duration of the AP. Every bit a issue of the higher up, when depolarization occurs, the AP threshold is easily and quickly reached and the generated APs spread easily along the sarcolemma. These factors make the whole system unstable and oscillations trigger repetitive discharge of APs. That is, the muscle fibers lose their tight control by the motor neurons and so contraction becomes partly involuntary. For example, persons with myotonia observe it difficult to release a handshake or to remove their hand from a drinking glass. There are several causes of myotonia, including genetic abnormalities in ion channels, too as drug-induced conditions. Whatsoever agent that greatly lowers PCl or g Cl volition take the aforementioned consequence. It has been shown that simply decreasing thouCl causes repetitive firing in equivalent excursion models of skeletal muscle fibers. In addition, K+ ions tend to accumulate in the lumen of the T-tubules under normal conditions (run across Section VIII). This aggregating is exaggerated with the prolonged APs and then tends partially to depolarize the fibers and increase their excitability. Some forms of myotonia are produced by abnormal fast Na+ channels; namely, a modest fraction of these channels do not inactivate equally quickly equally usual (i.eastward. their I-gates do non close unremarkably) and and then causes a prolonged small depolarization afterwards the AP and, consequently, a repetitive belch.

In myotonia, AP repolarization is slowed and the duration of the AP is increased. Every bit AP duration increases, more than Na+ channels accept time to render to the resting conformation by deactivation or recovery from inactivation (a process which has a time constant of 2–3   ms). This creates a window of instability during AP repolarization. The membrane potential remains depolarized to a higher place threshold, assuasive some Na+ channels to reopen and trigger some other AP. The skeletal muscles accept a large condom factor with respect to the number of Na+ channels in the membrane and as few as 3–five% in the open country tin can trigger an AP. This instability in membrane repolarization is farther enhanced past the high membrane resistance. Without the normal large gCl , only a smaller than normal outward depolarizing electric current is required to reach threshold. Considering of the high membrane resistance Rm , the space constant λ is longer than normal. Consequently, the APs propagate at a faster velocity. These factors human action synergistically to brand the whole arrangement unstable. Consequently, when depolarization occurs, the AP threshold is hands and quickly reached, the generated APs spread fast along the sarcolemma and the membrane is more excitable and susceptible to repetitive discharge of APs.

The loftier thousand Cl in skeletal muscle fibers is due to a large number of voltage-dependent gated Cl− channels, which are outwardly rectifying. The major Cl− channel of skeletal muscle is the ClC-i channel (Steinmeyer et al., 1991), a member of the ClC family of Cl− channels and Cl−/H+ antiporters (Zifarellli and Pusch, 2007). These Cl− channels are located both on the surface sarcolemma and T-rubule membrane in frogs and mammals. Denervation of mammalian fibers causes one thousand Cl to decrease almost to zilch.

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Genetic Disorders of Neuromuscular Development

Juan M. Pascual , in Molecular Neurology, 2007

D. Excitation-Contraction Coupling

The transduction of muscle activity potential to wrinkle relies on molecules that command Ca 2+ release at the T-tubule/ SR junction (Hibberd & Trentham, 1986). 1 poly peptide, an integral component of the T-tubular membrane, is an L-type, dihydropyridine-sensitive, voltage-dependent calcium channel. Some other is the ryanodine receptor (RyR), a large protein associated with the SR membrane in the triad that probably couples conformational changes in the Caii+ aqueduct induced by T-tubular depolarization to Ca2+ release from the SR (come across Figure eleven.three) (Campbell et al., 1987). Skeletal musculus contains a higher density of L-type Ca2+ channels than can be accounted for on the footing of measured voltage-dependent Ca2+ influx because much of the Ca2+ channel protein in the T-tubular membrane does not directly regulate calcium ion movement merely, rather, acts as a voltage transducer that links depolarization of the T-tubular membrane to Ca2+ release through the ryanodine receptor in the SR membrane. The ryanodine receptor thus mediates sarcoplasmic reticulum Caii+ release. This protein, which binds the plant alkaloid ryanodine, is a very big multimer comprised of four subunits (Wagenknecht et al., 1989).

Effigy eleven.3. Putative arrangement of triad proteins in skeletal muscle. Each dihydropyridine receptor (DHPR)/voltage sensor consists of four homologous repeats, and four such DHPR are clustered together in a diamond-shaped arrangement (a tetrad) apposing four ryanodine receptor (RyR1) monomers that together role equally a single Ca2+-release channel. The intracellular loop between repeats II and Three of each DHPR is thought to activate physically in some style the adjacent RyR monomers. A 12 kDa FK 506-binding protein (FKBP 12) is associated tightly with each RyR1 monomer and may regulate interactions both within and between adjacent RyR. Calsequestrin is the principal Ca2+-binding poly peptide in the sarcoplasmic reticulum (SR) and possibly regulates the RyR. Triadin is another poly peptide tightly associated with the RyR and has been suggested to mediate interactions with both the DHPR and calsequestrin.

 From: Lamb (2000). Copyright © 2000

Activation of the ryanodine receptor complex is coupled to events at the T-tubular membrane by direct mechanical linkage through a conformational modify in the dihydropyridine receptor protein. After improvidence toward the myofibrils, Ca2+ reuptake in the sarcoplasmic reticulum allows the relaxation of muscle and the maintenance of a low resting intracellular Catwo+ concentration by means of ATP-dependent Ca2+ pumps (SERCA) located in the SR membrane. The energy released upon ATP hydrolysis is utilized here for the concentrative uptake of Ca2+ into the SR vesicle through a phosphorylated enzyme intermediate. Other SR proteins assist in Ca2+ uptake and storage: phospholamban is expressed in cardiac musculus and irksome myofibers, where phosphorylation participates in the control of Catwo+-ATPase and Catwo+-uptake activity. Another protein, calsequestrin, contains numerous depression-affinity Caii+-binding sites and is nowadays in the lumen of the SR, participating in Catwo+ storage. Fast myofibers incorporate a soluble Ca2+-binding protein, parvalbumin, which is structurally related to troponin-C. Parvalbumin may also regulate the Ca2+ concentration in the initial stages of relaxation to facilitate rapid contraction.

Several genetic disorders of the developing neuromuscular system are described in the following sections according to the predominant disease locus: motor neuron, nerve, neuromuscular junction, and musculus (see Table eleven.1). Several diseases are covered in other sections of this book and are noted simply briefly in this chapter.

Table 11.one. Genetic Disorders of Neuromuscular Development

I

Motor neuron diseases

Spinal muscular atrophy

Other motor neuron diseases

II

Disorders of nerve

Congenital neuropathies

Charcot-Marie-Tooth diseases *

Riley-24-hour interval syndrome

Neuroaxonal dystrophy

Genetic neuropathies associated with encephalopathy

3

Disorders of the neuromuscular junction

Congenital myasthenic syndromes

Choline acetyl transferase deficiency

Acetylcholine receptor deficiency

Rapsyn deficiency

Tedious aqueduct syndrome

Fast channel syndrome

Acetylcholinesterase deficiency

4

Disorders of muscle

Congenital muscular dystrophies

Laminin α-2 deficiency

Fukuyama muscular dystrophy

Walker-Warburg syndrome

Musculus-Eye-Encephalon illness

Merosin-scarce muscular dystrophy

Congenital myopathies

Primal core disease *

Myotubular myopathy

Nemaline myopathy

Desmin myopathy

Structural myopathies

Dystrophynopathies

Duchenne muscular dystrophy

Sarcoglycanopathies

Calpainopathy

Dysferlinopathy

Caveolinopathy

Emery-Dreifuss dystrophy

Bethlem myopathy

Facioscapulohumeral dystrophy

Metabolic myopathies

Disorders of fatty acid oxidation

Carnitine transporter deficiency

Carnitine palmitoyltransferase deficiencies

Acyl-CoA dehydrogenase deficiencies

Glycogenoses

Acid maltase deficiency

Debrancher enzyme deficiency

Brancher enzyme deficiency

Myophosphorylase deficiency

Glycolytic defects

Phosphofructokinase deficiency

Myoadenylate deaminase deficiency

Disorders of musculus excitability

Hyperkalemic periodic paralysis and paramyotonia congenita

Hypokalemic periodic paralysis

Andersen syndrome

Myotonic dystrophy

Congenital myotonia

Malignant hyperthermia

Brody illness

*
Disorders covered in other capacity.

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The Biology, Limits, and Promotion of Peripheral Nerve Regeneration in Rats and Humans

Tessa Gordon , in Nerves and Nerve Injuries, 2015

Magnitude and Fourth dimension Grade of Recovery of Nervus and Targets Afterwards Nervus Injuries and Surgical Repair

Chronic recordings of evoked nervus and muscle action potentials and of musculus tension before and after nerve injuries provide a continuous record of the condition of the nerves proximal to an injury site during nervus regeneration and musculus reinnervation ( Figure 61.7a) (Davis et al., 1978). Moreover, recordings tin be made in a cat that is awake during locomotion. These recordings provide the information to compute the amplitude of motor and sensory signals during walking. These signals rapidly decline later on the transection and resuture of the motor nerve to triceps surae muscles (Effigy 61.7b and d) (Gordon, Hoffer, Jhamandas, & Stein, 1980). The rapid decline in sensory potentials (Effigy 61.7d) reflects the loss of sensory input from denervated sense organs in the muscles, whereas the more gradual pass up in the motor potentials (Figure 61.7b) results from stripping sensory nerve contacts on the axotomized motoneurons (Mendell, Munson, & Scott, 1976). The motor and sensory signals return and increase in amplitude as nerves reinnervate muscle and the contractile forces of the reinnervated muscles increase with an exponential fourth dimension course to preoperative values (Effigy 61.7c) (Davis et al., 1978). The recovery of axon potential amplitudes begins when regenerating fretfulness make contact with denervated musculus, recover their amplitude and, hence, their size paralleling the muscle recovery (cf Effigy 61.7c and east) (Gordon & Stein, 1982b).

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Beefcake AND PHYSIOLOGY OF THE ANORECTUM

Philip H. Gordon Physician FRCS(C), FACS , in Current Therapy in Colon and Rectal Surgery (Second Edition), 2005

Single-Fiber Electromyography

An fifty-fifty more than sophisticated technique identifies the muscle action potential from a single musculus cobweb. The technique provides a means of assessing innervation and reinnervation of the skeletal muscle under investigation. An cess can be made quantitatively using the fiber density that represents the mean of a number of musculus fibers in 1 motor unit inside the uptake expanse of the electrode averaged from 20 different electrode positions. A raised fiber density may exist used as an index of collateral sprouting and reinnervation of muscle fibers within the muscle and is evidence of denervation.

In the past the most useful clinical application of electromyography was sphincter mapping of incontinent patients. At present other techniques such every bit endoanal sonography and endoanal magnetic resonance imaging seem to be more authentic for the detection of sphincter defects. Furthermore, the latter techniques obviate the need for the painful insertion of a needle at several locations effectually the anal canal. Jost and colleagues reported on the use of surface versus needle electrodes in the determination of motor conduction fourth dimension to the external anal sphincter. They compared surface electrodes with needle electrodes and believe the surface electrodes are preferable.

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Nerve Conduction and Needle Electromyography

JUN KIMURA , in Peripheral Neuropathy (Fourth Edition), 2005

SUMMARY

Electromyographic studies analyze spontaneous and voluntarily activated muscle action potentials extracellularly. Following brief injury potentials coincident with the insertion of the needle, a relaxed normal muscle remains electrically silent except for the end-plate activities. Several types of spontaneous discharges all signal diseases of the nervus or muscle, although they carry different clinical implications. Both fibrillation potentials and positive sharp waves represent spontaneous excitation of individual muscle fibers. The circuitous repetitive discharges comprise high-frequency spikes derived from multiple muscle fibers, which belch sequentially, maintaining a stock-still order.

In conventional electromyography, isolated discharges of a single motor unit, the smallest functional element of volitional contraction, give rise to motor unit potentials. Structural or functional disturbances of the motor unit seen in diseases of the nerve or musculus atomic number 82 to alterations of waveform and discharge patterns of their electrical signals. The study of motor unit potentials provides data useful in elucidating the nature of the illness. Certain characteristics of such abnormalities may propose a detail pathologic process.

As a clinical tool, electromyography serves best simply if the examiner conducts the study and interprets the results in lite of the patient's history, physical exam, and other diagnostic findings. In fact, the study constitutes an extension of the physical exam, rather than an independent laboratory test. Therefore, it is most useful if performed past a physician thoroughly familiar with the patient's clinical findings with the aim to bear witness or disprove the diagnostic impression.

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