H-rex

Alpha Motor Neuron

The α-motor neurons are the largest neurons in the spinal cord, with myelinated axons that exit the spinal cord through the ventral roots and travel in peripheral nerves to innervate muscles.

From: Fundamental Neuroscience (Fourth Edition), 2013

Related terms:

Gamma Motor Neuron

Motor Neuron

Stretch Reflex

Interneuron

Muscle Spindle

Skeletal Muscle

Axon

Reflex

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Functional Neural Transplantation III

Peter H. Chipman, ... Victor F. Rafuse, in Progress in Brain Research, 2012

Abstract

Alpha motor neurons (also known as lower or skeletal motor neurons) have been studied extensively for over 100 years. Motor neurons control the contraction of skeletal muscles and thus are the final common pathway in the nervous system responsible for motor behavior. Muscles become paralyzed when their innervating motor neurons die because of injury or disease. Motor neuron diseases (MNDs), such as Amyotrophic Lateral Sclerosis, progressively destroy motor neurons until those inflicted succumb to the illness due to respiratory failure. One strategy being explored to study and treat muscle paralysis due to motor neuron loss involves deriving surrogate motor neurons from pluripotent stem cells. Guided by decades of research on the development of the spinal cord, recent advances in neurobiology have shown that functional motor neurons can be derived from mouse and human embryonic stem (ES) cells. Furthermore, ES cell-derived motor neurons restore motor behavior when transplanted into animal models of motor dysfunction. The recent discovery that mouse and human motor neurons can be derived from induced pluripotent stem (iPS) cells (i.e., somatic cells converted to pluripotency) has set the stage for the development of patient-specific therapies designed to treat movement disorders. Indeed, there is now hope within the scientific community that motor neurons derived from pluripotent stem cells will be used to treat MNDs through cell transplantation and/or to screen molecules that will prevent motor neuron death. In this chapter, we review the journey that led to the generation of motor neurons from ES and iPS cells, how stem cell-derived motor neurons have been used to treat/study motor dysfunction, and where the technology will likely lead to in the future.

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Neuromotor Control of Speech

Wanda G. Webb PhD, CCC-SLP, in Neurology for the Speech-Language Pathologist (Sixth Edition), 2017

Alpha Motor Neurons

The alpha motor neuron (AMN) innervates the main fibers that cause muscle contraction. These fibers lie within the muscle and are called extrafusal fibers. Figure 6-6 illustrates the structure of a muscle fiber including the input from the AMN. The axon of each AMN branches to supply the fibers. An axon may supply only a few fibers, as in the case of a small muscle with precisely controlled contraction, or it may control several hundred fibers, as in the case of large muscles with strong, crude movements. This fact is consistent with what you saw on the homunculus illustrated in Figure 2-7. The oral musculature involved in speech and swallowing requires a much larger area on the motor strip because the innervation and control of these muscles requires the involvement of a vastly larger number of neurons to allow fine and precise motor control for these acts.

The alpha motor neuron supplies the trophic, or nutritional, factors, which direct differentiation of muscle fibers and keep the muscle healthy. These substances are called myotrophic factors. The motor neuron also supplies the acetylcholine that stimulates contraction of muscle.

Three types of extrafusal fibers can be differentiated in skeletal muscle. All muscles contain all three types of fibers, but all muscle fibers in one motor unit are of the same type. The type is determined by the myotrophic influences of the innervating neuron. The first of the three types of fibers are slow twitch (type I) fibers that contract slowly and are resistant to fatigue. These fibers predominate in sustaining postural activities, including standing. Fast twitch fibers (type IIx in humans) contract faster but fatigue more rapidly. They exert a more powerful force and are primarily found in superficial muscles. An intermediate fiber (Type IIA) has properties between the other two types in terms of speed of contraction and amount of force; it is considered a fast twitch fiber, however.

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Spinal Motor Neurons: Properties

H. Hultborn, B. Fedirchuk, in Encyclopedia of Neuroscience, 2009

Motor Neuronal Plasticity Following Training or Disuse

Do α-motor neurons, like muscle fibers, adapt to long-lasting increases or decreases in activity? There is much evidence to support the idea that motor activity and motor learning indeed involve neuronal plasticity at both the spinal and supraspinal levels of the central nervous system. However, it is only during the last several years that changes in the properties of α-motor neuron themselves in response to altered levels of physical activity have been directly assessed. The present evidence originates from experiments in which rats were subjected to forced endurance training or spontaneous running in exercise wheels to increase the motor activity or were subjected to body-weight support (i.e., suspension of the hindlimbs) for a couple of weeks to reduce the motor activity. Only a few examples of the described changes are mentioned here. With increased motor activity, the slow motor neurons showed more negative resting membrane potential as well as firing threshold. It was proposed that these changes may prevent depolarization, accommodation, and firing adaptation during prolonged activity. During inactivity, the resting membrane potential and firing threshold became more depolarized. The motor neurons become less excitable and more prone to accommodation and frequency adaptation. The signals mediating the adaptation of these (and other) motor neuron properties are not known at this time. However, it has been proposed that increased levels of neurotrophins originating from the exercised muscle, or other neurotrophic factors released by afferent activity, may induce appropriate changes in motor neuronal gene expression.

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Motor Control, Peripheral

N. Goyal, DA. Chad, in Encyclopedia of the Neurological Sciences (Second Edition), 2014

Sensory Neurons and the Simple Reflex Arc

The alpha motor neurons are influenced not only by upper motor neurons in the motor cortex and motor control neurons in the brainstem but also by sensory inputs from the periphery. In fact, the peripheral pathway that serves as the foundation for the generation of spontaneous muscle contraction in the resting state (also known as muscle tone) is the simple reflex arc. It is composed of a sensory or afferent limb (the heavily myelinated axon originating in the muscle spindle (known as Ia afferent fiber, the largest among all nerve fibers) whose unipolar cell body resides in the sensory or dorsal root ganglia); and a motor or efferent limb (the myelinated axon extending from the lower motor neuron). The afferent limb directly stimulates the efferent lower motor neuron via a single synapse; hence, the reflex arc is designated monosynaptic (Figure 9). The specialized unipolar structure of the sensory neuron cell body allows for its axon to bifurcate after leaving the cell body: one process passes to the muscle spindle in the periphery, whereas the other travels into the spinal cord to make its monosynaptic contact with the lower motor neuron.

With regard to the sensory innervation of the muscle spindle, the large-diameter myelinated axon (Ia) pierces the capsule of the spindle, loses its myelin sheath, and becomes a naked axon that winds spirally around the equatorial regions of the nuclear bag or chain portions of the intrafusal fibers (Figure 10). A slightly smaller diameter myelinated axon, arising from a smaller dorsal root ganglion neuron, also pierces the muscle spindle capsule, loses its myelin sheath, and forms a naked axon that branches terminally and ends as varicosities, resembling a spray of flowers. These endings are situated mainly on the nuclear chain fibers and some distance away from the equatorial region.

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The Somatic Nervous System

Javier Cuevas, in xPharm: The Comprehensive Pharmacology Reference, 2007

The neuromuscular junction

Each alpha motoneuron innervates a motor unit, which is a population of muscle fibers. Although the number of muscle fibers innervated by a single motoneuron varies depending on the size and function of the muscle, there are about 150 muscle fibers per motor unit. While each muscle fiber receives input from a single motor neuron, motor units usually overlap such that 10–15 fibers from one motor unit are adjacent to similar bundles of a second motor unit. This permits motor units to work in unison and to contract in support of each other. Shown in Fig. 5A is a representation of four muscle fibers receiving innervation from a single motor neuron. Upon reaching the muscle fiber, the axon of the motoneuron divides into multiple terminal nerve twigs (Fig. 5B and 5D), all of which form synaptic contacts with the muscle fiber (Fig. 5C and 5E). These synaptic contacts are physically supported by both the basement membrane and overlapping Schwann cells (Fig. 5B and 5C). The presence of three cell types (neuron, glial and muscle) in the neuromuscular junction led to the term tripartite synapse.

Fig. 5. The motor unit and motor endplate. A: A single motoneuron innervates multiple muscle fibers forming a motor unit. B: Enlargement from (A) showing multiple synaptic contacts between a motoneuron and a single muscle fiber. C: Enlargement from (B) showing regions where synaptic activity occurs. Reprinted from Clinical Neuroanatomy and Related Neuroscience, from Fitzgerald, Copyright 2001, with permission from Elsevier. D: A methylene blue-stained muscle preparation showing several nerve twigs (T) branching from a single axon and innervating multiple muscle fibers. There is a bulbous swelling (the motor endplate, MEP) at the end of each twig at the site of connection with the muscle. E: Electron micrograph of a motor endplate showing the cell membrane of the muscle fiber arranged into a series of deep folds (junctional folds, JF) beneath which the sarcoplasm (S) contains numerous mitochondria (M). In the terminal swelling of the motor axon, neurosecretory granules (G), containing acetylcholine (ACh) and mitochondria are abundant. The terminal swelling of the axon is separated from the muscle cell membrane by a gap of 30–50 nm (the synaptic cleft, C), which includes the external lamina of the muscle. Reprinted from Human Histology,Stevens, Copyright 1996, with permission from Elsevier.

The synaptic contact between a motor neuron and skeletal muscle, or neuromuscular junction, is a highly specialized structure called the motor endplate (Fig. 5E). Neurosecretory vesicles that contain ACh are abundant on the presynaptic terminus of the motor axon. The synaptic cleft separating the neuron and nerve fiber at the motor endplate is 30–50 nm. The postsynaptic membrane of the muscle fiber contains numerous folds called junctional folds, and the apex of these junctional folds (membrane closes to the presynaptic terminus) exhibits pronounced optical density. These optically dense regions contain clusters of nicotinic acetylcholine receptors and associated proteins.

Depicted in Fig. 6 are some of the key molecules/components involved in structural organization and neurotransmission at the neuromuscular junction. The synaptic vesicles of the motor nerve terminal are released when an action potential reaches the presynaptic terminus. Activation of postsynaptic nicotinic receptors results in depolarization of the muscle fiber. If this depolarization is of sufficient magnitude, an action potential is evoked in the muscle fiber, and the resulting calcium influx and calcium release from intracellular stores activate the contraction machinery of the cell. Some of the proteins listed in Fig. 6 are also involved in antibody-mediated (autoimmune) or genetic disorders affecting motor control. For example, autoantibodies directed against nicotinic acetylcholine receptors on the skeletal muscle give rise to myasthenia gravis.

Fig. 6. Key components of neurotransmission at the neuromuscular junction. The synthesis of acetylcholine (ACh) is catalyzed by choline acetyl transferase (CHAT), after which the neurotransmitter is accumulated in synaptic vesicles, and released when an action potential reaches the nerve terminus and evokes calcium entry through voltage-gated calcium channels (VGCC). Upon release the ACh diffuses across the synaptic cleft and activates nicotinic ACh receptors (nAChRs) on the postsynaptic membrane. The nAChRs are clustered on the top of the junctional folds. Molecules that contribute to this clustering are and rapsyn. The clustering of nAChRs by these molecules is triggered by neural agrin (not shown). The depolarization initiated by ion flux through nAChRs activates voltage-gated sodium channels (VGNaCs) localized at the bottom of the folds and ultimately leads to elevation of intracellular calcium concentrations and muscle contraction. The action of ACh is terminated by the action of acetylcholinesterase, which is tethered in the synaptic basement membrane. Repolarization of the motor nerve terminal and the muscle fiber is mediated by opening of voltage-gated potassium channels (VGKCs) on the plasma membrane of both cells (only shown on motoneuron here). (Reproduced from (McConville and Vincent (2002)).

A variety of drugs exert their effects by influencing neurotransmission at the neuromuscular junction (Table 2).

Table 2. Drugs acting at the neuromuscular junction.

Site of actionAgent TypeDrug NamePresynapticBotulinum toxinPostsynapticDepolarizing Blocking Agents (nAChR agonist)SuccinylcholineNon-Depolarizing Blocking Agents (nAChR antagonists)MetocurinePancuroniumTubocurarineCholinesterase InhibitorsEchothiophateEdrophoniumMalathionNeostigminePhysostigmineSarinSoman

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The Somatic Nervous System☆

J. Cuevas, in Reference Module in Biomedical Sciences, 2015

The Neuromuscular Junction

Each α motor neuron innervates a population of muscle fibers termed a motor unit. The number of muscle fibers innervated by a single motoneuron varies depending on the size and function of the muscle, but averages about 150 muscle fibers per motor unit. While each muscle fiber receives input from a single motor neuron, motor units usually overlap whereby 10–15 fibers from one motor unit are adjacent to similar bundles of a second motor unit. This phenomenon permits motor units to work in unison and to contract in support of each other. Figure 5a shows a representation of four muscle fibers receiving innervation from a single motor neuron. Upon reaching the muscle fiber, the axon of the motoneuron divides into multiple terminal nerve twigs (Figure 5b and d), all of which form synaptic contacts with the muscle fiber (Figure 5c and e). These synaptic contacts are physically supported by both the basement membrane and overlapping Schwann cells (Figure 5b and c). The presence of three cell types (neuron, glial and muscle) in the neuromuscular junction led to the term tripartite synapse.

Figure 5. The motor unit and motor endplate. (a) A single motoneuron innervates multiple muscle fibers forming a motor unit. (b) Enlargement from (a) showing multiple synaptic contacts between a motoneuron and a single muscle fiber. (c) Enlargement from (b) showing regions where synaptic activity occurs. (Fitzgerald: Clinical Neuroanatomy and Related Neuroscience Figure 8.2). (d) A methylene blue-stained muscle preparation showing several nerve twigs (T) branching from a single axon and innervating multiple muscle fibers. There is a bulbous swelling (the motor endplate, MEP) at the end of each twig at the site of connection with the muscle. (e) Electron micrograph of a motor endplate showing the cell membrane of the muscle fiber thrown into a series of deep folds (junctional folds, JF) beneath which the sarcoplasm (S) contains numerous mitochondria (M). In the terminal swelling of the motor axon, neurosecretory granules (G), containing the transmitter substance acetylcholine (ACh), and mitochondria are abundant. The terminal swelling of the axon is separated from the muscle cell membrane by a gap of 30–50 nm (the synaptic cleft, C), which includes the external lamina of the muscle.

The synaptic contact between a motor neuron and skeletal muscle, or neuromuscular junction, is a highly specialized structure called the motor endplate. Figure 5e shows an electron micrograph of a motor endplate. On the presynaptic terminus of the motor axon neurosecretory vesicles that contain ACh are abundant. The synaptic cleft separating the neuron and nerve fiber at the motor endplate is 30–50 nm. The postsynaptic membrane of the muscle fiber contains numerous folds called junctional folds, and the apex of these junctional folds (membrane closes to the presynaptic terminus) exhibits pronounced optical density. These optically dense regions contain clusters of nicotinic ACh receptors and associated proteins.

Figure 6 depicts some of the key molecules/components involved in structural organization and neurotransmission at the neuromuscular junction. The synaptic vesicles of the motor nerve terminal are released when an action potential reaches the presynaptic terminus. Activation of postsynaptic nicotinic receptors results in depolarization of the muscle fiber. If this depolarization is of sufficient magnitude, an action potential will be evoked in the muscle fiber, and the resulting calcium influx and calcium release from intracellular stores will activate the contraction machinery of the cell. Some of the proteins listed in Figure 6 are also involved in antibody-mediated (autoimmune) or genetic disorders affecting motor control. For example, autoantibodies directed against nicotinic ACh receptors on the muscle give rise to myasthenia gravis.

Figure 6. Key component of neurotransmission at the neuromuscular junction: ACh is synthesized by choline acetyl transferase (CHAT), taken up into synaptic vesicles, and released when an action potential reaches the nerve terminus and evokes calcium entry through voltage-gated calcium channels (VGCC). ACh diffuses across the synaptic cleft and activates nicotinic ACh receptors (nAChRs) on the postsynaptic membrane. nAChRs are clustered on the top of the junctional folds. Two molecules that contribute to this clustering are muscle-specific kinase (MuSK) and rapsyn. The clustering of nAChRs by these molecules is triggered by neural agrin (not shown in this diagram). The depolarization initiated by ion flux through nAChRs activates voltage-gated sodium channels (VGNaCs) localized at the bottom of the folds and ultimately leads to elevation of intracellular calcium concentrations and muscle contraction. The action of ACh is terminated by its hydrolysis by AChesterase (AChE), which is tethered in the synaptic basement membrane. Repolarization of the motor nerve terminal and the muscle fiber is mediated by opening of voltage-gated potassium channels (VGKCs) that are found on the plasma membrane of both cells (only shown on motoneuron here).

Figure 1 from McConville J, Vincent A., Diseases of the neuromuscular junction. Curr Opin Pharmacol. 2002.

A variety of drugs exert their effects by influencing neurotransmission at the neuromuscular junction. Table 2 lists some of these agents and categorizes them as presynaptic or postsynaptic, based on their site of action. More information of these cholinergic synapses is provided in Neurotransmitters and Their Life Cycles and Neurotransmission.

Table 2. Drugs acting at the neuromuscular junction

Site of actionAgent typeDrug namePresynapticBotulinum toxinPostsynapticDepolarizing blocking agents (nAChR agonist)SuccinylcholineNon-depolarizing blocking agents (nAChR antagonists)Atracurium cisatracurium doxacurium

Mivacurium pancuronium

Pipecuronium

Tubocurarine

VecuroniumCholinesterase inhibitorsEchothiophate

Edrophonium

Malathion (malaoxona)

Neostigmine

Physostigmine

Sarin

Soman

aActive metabolite.

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Peripheral Nervous System

Andrei V. Krassioukov, in Encyclopedia of the Human Brain, 2002

V.C.2.a Neuromuscular Junctions in Skeletal Muscles

A single α motor neuron (located within the ventral horn of the spinal cord; see Fig. 1), with the muscle fibers that it innervates, is defined as the motor unit. As soon as the large myelinated axon of an α motor neuron enters a skeletal muscle, it branches many times. Each small branch terminates on muscle fibers at the motor end plate or neuromuscular junction (Fig. 11). The plasma membrane of the axon terminal (axolemma) is separated by the synaptic cleft (gap of 20–50 nm) from the plasma membrane of the muscle fiber (sarcolemma). The surface area of sarcolemma (postsynaptic membrane) at a motor end plate is thrown into numerous folds. These serve to increase the contact area of muscle to the naked axon (presynaptic membrane). The neurotransmitter, acetylcholine, is released from synaptic vesicles into the synaptic cleft when a nerve impulse reaches the motor end plate. Once the acetylcholine is released, it will stimulate receptor sites on the postsynaptic muscular membrane, causing the contraction of skeletal muscle fibers. The acetylcholine remains in contact with the postsynaptic membrane for a very short period of time (about 1 msec), and it is rapidly inactivated by the enzyme acetylcholinesterase (AChE). Acetylcholinesterase hydrolyzes acetylcholine into acetic acid and choline. The choline is taken up by the presynaptic terminals for the synthesis of new molecules of acetylcholine.

Figure 11. Motor end plate on skeletal muscle. Gold chloride method.

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Strength and Reflexes

John P. Hammerstad, in Textbook of Clinical Neurology (Third Edition), 2007

Gamma Motor Neuron

Like the alpha motor neurons, the gamma motor neurons lie in the ventral horn of the spinal cord interspersed among the alpha motor neurons innervating the same muscle. Gamma motor neurons innervate the intrafusal muscle fibers of a specialized sensory organ, the muscle spindle.11 The muscle spindle consists of a small bag of muscle fibers that lie in parallel with the extrafusal skeletal muscle fibers. Therefore, when the muscle lengthens or shortens, the intrafusal muscle spindle fibers are stretched or relaxed correspondingly. The intrafusal fibers are surrounded by sensory nerve endings that become 1a afferents to the dorsal root ganglion. When the intrafusal fibers are stretched as the muscle is lengthened, the sensory fibers are activated, providing sensory feedback about the degree of lengthening that has occurred. When the muscle contracts and shortens, the intrafusal spindle fibers also shorten. If this were a completely passive system, the intrafusal fibers would relax and the sensory endings would become silent, providing no helpful feedback information about the state of the muscle. To prevent this inefficient circumstance, gamma motor neurons are activated, maintaining tension in the intrafusal fibers to continue to provide precise sensory information.

This phenomenon can be observed experimentally if alpha motor neurons are excited in isolation. When the muscle contracts, there is a pause in volleys from the 1a afferent. When the gamma motor neuron is excited at the same time, the afferent volleys do not pause. This simultaneous activation of alpha and gamma motor neurons during muscle contraction is called alpha‐gamma coactivation; it is an excellent example of sensory motor integration in the nervous system. By this means, innervation of the muscle spindle by an independent system of gamma motor neurons allows the central nervous system to adjust the sensitivity of the spindle and fine‐tune the information it receives (Fig. 15‐9).

Another sensory organ, the Golgi tendon organ, also conveys information about the state of the muscle. The Golgi tendon organs lie in the muscle tendon and, unlike the muscle spindle, are coupled in series with the extrafusal muscle fibers. Therefore, both passive stretch and active contraction of the muscle increase the tension of the tendon and activate the tendon organ receptor. In contrast to the activity of the muscle spindle, which depends on muscle length, the Golgi tendon organ conveys information about muscle tension. Together they convey precise information about the length, tension, velocity, and force of the muscle contraction, thus allowing greater precision of movement.12

Changes in muscle tone, defined as resistance to passive stretch of muscle, are an important feature of diseases of the motor system. At one time, an important component of normal resting muscle tone was thought to be the result of low‐level background alpha‐gamma coactivation. However, more recent studies in fully relaxed individuals indicate that the viscoelastic properties of muscle and tendons account for normal resting tone.13 Common experience indicates that resting muscle tone can vary considerably depending on the state of relaxation of the muscle as well as its viscoelastic properties. Some studies have shown that the passive viscoelastic properties of muscle may contribute to increased tone in patients with chronic spasticity and rigidity, but the most important determinants of pathological alterations in tone are the result of alterations in stretch reflexes.

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Muscle tone and movement

JAMES W. LANCE CBE, MD, FRCP, FRACP, FAA, JAMES G. McLEOD MB, BS, BSc(Med), DPhil(Oxon), FRCP, FRACP, in A Physiological Approach to Clinical Neurology (Third Edition), 1981

Recruitment

Anterior horn cells (alpha, beta and gamma motor neurones) comprise Sherrington's 'final common pathway' of movement. Using the technique of microneurography, Vallbo61 established that alpha motor neurones become active before fusimotor fibres increase the afferent discharge from muscle spindles. The regulation of alpha and gamma motor neurones in parallel was termed 'alpha-gamma linkage' by Granit. The part played by beta motor neurones has yet to be determined. The force of muscle contraction is regulated by the number of motor units active at any one time and by the firing rate of those units. Small motor units are more excitable than large and become active first in reflex or voluntary contractions in cat22 and man15. As voluntary isometric contraction in man increases, additional motor units are recruited, usually in a constant order15,41. The level of force at which motor units are recruited correlates with motor neurone size, axonal conduction velocity and the histochemistry and contraction properties of the innervated muscle fibres. The more-slowly-conducting units increase their firing rate more for each increment of increase in force than the rapidly-conducting units. No evidence has been found for separate tonic or phasic motor units, although smaller units, being of lower threshold, tend to fire tonically in sustaining any weak contraction while units of higher threshold are recruited only with strong contractions. This seems to hold whether a motor unit terminates on type 1 or type 2 muscle fibres with different contraction characteristics13. Even in fast voluntary contractions in man, slow motor units are recruited before fast motor units. The histochemical and functional types of motor units (slow and fast) may well be related, not to any selective usage in either slow or fast voluntary movements in man, but rather to the more frequent activation of smaller neurones according to the size principle8.

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Terms and conditions

H-Reflex

H reflexes provide nerve conduction measurements along the entire length of the nerve, demonstrating abnormalities in neuropathies and radiculopathies.

From: Handbook of Clinical Neurology, 2019

Related terms:

F Wave

Electromyography

Nerve Conduction Study

Radiculopathy

Lesion

Excitability

Stimulation

Spinal Cord

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H-Reflex and F-Response Studies

Morris A. Fisher, in Aminoff's Electrodiagnosis in Clinical Neurology (Sixth Edition), 2012

Disorders of the Peripheral Nervous System

H reflexes are a sensitive test for polyneuropathies and may be abnormal even in mild neuropathies. H reflexes involve conduction in proximal as well as distal fibers. These studies, therefore, can define proximal nerve injury and may be abnormal even when studies of distal function are unremarkable. Absent H reflexes are characteristic of acute inflammatory demyelinating polyneuropathy (Guillain–Barré syndrome). This loss of H reflexes occurs early and may be an isolated finding in patients studied within several days after onset of illness. H reflexes may be abnormal in asymptomatic patients with possible neuropathic dysfunction,30 and in plexopathies and radiculopathies. H reflexes in the forearm flexor muscles may be abnormal with C6 or C7 root injury,31 and calf H reflexes may be abnormal with S1 radiculopathies. H reflexes are affected by injury to either the posterior or anterior roots. Examination of these reflexes therefore can be important in the electrodiagnostic evaluation of radiculopathies by documenting nerve injury, even when needle EMG is unrevealing owing to sparing of the anterior roots. Eliciting the H reflex by direct stimulation of the S1 root may enhance their utility for detecting an S1 radiculopathy.32 Increase in the stimulus threshold has been noted in patients with neurogenic claudication when studied after reproduction of their symptoms with walking.33

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Electromyography and Evoked Potentials

Bernard M. Abrams, Howard J. Waldman, in Practical Management of Pain (Fifth Edition), 2014

Pitfalls and Comments

The H-reflex is somewhat more useful than the F wave, but the main reason for the study is to evaluate patients with suspected S1 radiculopathy whose history or findings on physical examination are suggestive but the EMG is normal.34 Usually, when an absent H-reflex is noted, which suggests a problem with S1 nerve root conduction, an absent or depressed ankle reflex has already been noted on the physical examination, so the study is, for many, redundant. Pitfalls occur when the opposite leg is not studied to show a normal H-reflex as a contrast. If the H-reflex is absent bilaterally, it may reflect more generalized disease, such as peripheral neuropathy. Older patients often do not have good H-reflexes as a normal finding. In addition, a unilaterally absent H-reflex with normal findings on needle EMG does not indicate when the injury occurred; the findings may have been the result of a previous injury.

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Specialized Electrodiagnostic Studies

Bashar Katirji M.D., F.A.C.P., in Electromyography in Clinical Practice (Second Edition), 2007

H Reflex

The H reflex, named after Hoffmann for his original description, is an electrical counterpart of the stretch reflex which is elicited by a mechanical tap. Group 1A sensory fibers constitute the afferent arc which monosynaptically or oligosynaptically activate the alpha motor neurons that in turn generate the efferent arc of the reflex through their motor axons. The H reflex amplitude may be occasionally as high as the M amplitude but it is often lower with the H/M amplitude ratio usually not exceeding 0.75.

The H reflex and F wave can be distinguished by increasing stimulus intensity (see Table 3-1). The H reflex is best elicited by a long-duration stimulus which is submaximal to produce an M response, whereas the F wave requires supramaximal stimulus Also, the F wave can be elicited from any limb muscle while the H reflex is most reproducible with stimulating the tibial nerve while recording the soleus muscle which assess the integrity of the S1 arc reflex and is equivalent to the Achilles reflex (Figure 3-4). Finally, the H reflex latency (and often amplitude) is constant when elicited by the same stimulus intensity, since it reflects activation of the same motor neuron pool.

The H reflex is most useful as an adjunct study in the diagnosis of peripheral polyneuropathy or S1 radiculopathy. The H reflex latency and amplitude is the most sensitive, yet nonspecific, among the nerve conduction studies in the early phases of Guillain-Barré syndrome. The H reflex may be absent in healthy elderly subjects and isolated abnormalities of the H reflex are nondiagnostic since they may reflect pathology anywhere along the reflex arc.

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Clinical Neurophysiology: Basis and Technical Aspects

Nivedita Jerath, Jun Kimura, in Handbook of Clinical Neurology, 2019

Clinical applications

The H reflex provides a measure of nerve conduction along the entire length of the tibial/S1 pathway, providing information along proximal nerve segments, including the plexus and roots (Burke, 2016). Clinical conditions with a depressed ankle reflex, such as polyneuropathy, sciatic neuropathy, or S1 radiculopathy, will show a diminished or absent H reflex. Diabetic polyneuropathy is known to increase the H-reflex latency. Table 15.2 summarizes normal values in healthy adults. In evaluating radiculopathy, a unilateral absent H reflex or a side-to-side latency difference greater than 2.0 ms supports a diagnosis of an S1 radiculopathy (Kimura, 2013).

Table 15.2. H reflex normal valuesa (Kimura, 2013)

Amplitude (mV)bDifference between right and left (mV)Latency to recording Site (ms)bDifference between right and left (ms)2.4 ± 1.41.2 ± 1.229.5 ± 2.40.6 ± 0.4

aMean ± standard deviation.bAmplitude of the evoked response measured from baseline to negative peak; latency measured to the onset of the evoked response.

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H-reflex

J.A. Robichaud, in Encyclopedia of Movement Disorders, 2010

Introduction

The H-reflex can be used to assess changes in motoneuron pool reflex excitability. This reflex, also known as the Hoffmann reflex, is an electrically stimulated reflex that excites the muscle spindles Ia afferents. When electrical stimulation is applied over a nerve, this causes action potentials to be transmitted to the spinal cord where monosynaptic or polysynaptic connections cause motoneurons to reach threshold, thereby, causing the extrafusal muscle to contract. The overall level of reflex excitability may be influenced by excitation of Ib afferents from Golgi tendon organs, group II afferents from muscle spindles, and larger cutaneous afferents. While the H-reflex was originally suggested to be analogous to the tendon jerk, the central timing of the H-reflex is shorter than the tendon response, allowing for the possibility that more spinal processing occurs with the tendon response. Therefore, it is possible that both responses use slightly different pathways, and hence, it may not be appropriate to directly compare these responses.

The H-reflex can be evaluated either through the latency of the response or the reflex size (peak to peak amplitude). While there are established values for the latency of this response (time from stimulus application until initial deflection from baseline), this is not the case for the amplitude. The validity and reliability of the H-reflex amplitude have been evaluated by Crayton and King and Hugon et al. Because of the variability of the amplitude of the H-reflex, one test measurement should consist of the average of at least 5–7 (and up to 20) H-reflex measurements. The amplitude of the H-reflex also exhibits a wide intersubject variability in reflex recording; however, there is small test/retest variability within each subject. Because of this variability, changes in the amplitude of the H-reflex should only be analyzed relative to each subject's baseline H-reflex value.

Several methods, which evaluate H-reflex amplitude changes, have been used to assess spinal reflex excitability. One method assesses the percentage change of the test H-reflex amplitude in comparison to a control (baseline) H-reflex amplitude. However, this method of analysis requires an understanding of how changes in stimulus intensity can influence the amplitude of the H-reflex. At low stimulation intensities, Ia afferents are activated first which causes activation of the muscle's motoneurons eliciting a small amplitude H-reflex. As stimulation intensity further increases, the amplitude of the H-reflex increases which activates alpha motoneurons, and the direct muscle response (M-wave) is now observed. As the stimulation intensity further increases, the amplitude of the H-reflex becomes progressively larger up to a critical point, after which the amplitude of the H-reflex becomes progressively smaller until the H-reflex is no longer present. Therefore, test H-reflex alterations elicited by a given conditioning stimulus depend not only on the conditioning volley, but also on the amplitude of the control H-reflex. This aspect of H-reflex recruitment makes it difficult to determine the 'true' amount of reflex facilitation or inhibition. For instance, a small control H-reflex could result in a large amount of facilitation, while a larger control H-reflex would result in a smaller amount of facilitation. Therefore, using percentage change may make it difficult to estimate the real amount of either facilitation or inhibition of the motoneuron pool.

The H/M ratio, which is the ratio of the size of the H-reflex to the size of the M-wave, is an alternate method of analyzing changes in motoneuron reflex excitability. The H/M ratio represents the percentage of the motoneuron pool that may be considered to be active at any particular time. The maximum M-wave represents 100% of the activity of the specified muscle's motoneuron pool. The H/M ratio allows a quantification of the percentage of the active motoneuron pool. This interpretation enhances the ability to compare changes in the H-reflex between subjects. Crone and colleagues established that regardless of differences in the maximum H-reflex, the change in sensitivity to facilitation followed the same pattern as long as the control reflex sizes are explored.

The H-reflex recovery curve, which is a variation of the H-reflex, can also be used to assess motoneuron pool reflex excitability. The recovery curve is elicited by stimulating a nerve with paired stimuli at intervals from 1 ms to 10 s. The magnitude of the recovery curve at a given interstimulus interval refers to the percentage ratio of the test H-reflex amplitude to the unconditioned H-reflex amplitude, with these amplitudes being plotted as a function of the intervals between the reflexes. The recovery curve in healthy subjects consists of several phases. The first phase occurs with interstimulus intervals from 3 to 10 ms with the test reflex varying in size with simulation intensity. Next, there is an inhibition phase which is then followed by a facilitatory phase which occurs at stimulus intervals between 50 and 400 ms (peaks at 200–300 ms). Finally there is another inhibition phase which can last from 5 to 10 s.

In addition to changes in motoneuron reflex excitability, changes in the H-reflex have also been used to evaluate reciprocal Ia inhibition, Ib inhibition/facilitation, and presynaptic inhibition. Reciprocal Ia inhibition is evaluated by using a test H-reflex and a conditioning response (paired stimulus paradigm). The H-reflex is elicited with a low intensity stimulus (designed to stimulate primarily the muscle spindle Ia afferents) supplying the antagonist muscle. If the antagonist stimulation is given at the appropriate time, the test H-reflex in the agonist can be inhibited. Ib inhibition/facilitation is also assessed using a paired stimulus paradigm. However, unlike Ia inhibition, Ib inhibition/facilitation can be measured in the antagonist or synergists muscles acting at different joints within a limb. Finally, several techniques have been established whereby the H-reflex can be used to assess presynaptic inhibition. One method assesses H-reflex amplitude changes after vibration has been applied to either the tested muscle or a different muscle. In this method, the amount of inhibition is assessed by analyzing the amplitude change between the amplitude of the H-reflex prior to, and then after vibration. Presynaptic inhibition can also be assessed while testing for reciprocal inhibition between extensors and flexors in the forearm. Finally, Hultborn and colleagues showed a more difficult, but more specific method of analyzing presynaptic inhibition. In this method, the amount of H-reflex facilitation in one muscle is assessed while a monosynaptic heteronymous Ia volley is being applied to another muscle.

H-reflex changes have been evaluated in individuals with neurological disorders. It is known that slowing down of the H-reflex latency can be detected long before nerve degeneration in hereditary and acquired demyelinating neuropathies are observed. However, the scientific and clinical implication related to changes in the H-reflex amplitude is not as clear. For instance, Angel and Hoffmann observed that the Hmax/Mmax ratio was higher in individuals with spasticity. In contrast, other studies have concluded that changes in the Hmax/Mmax ratio were not a good measurement tool to quantify changes in spasticity. The literature is also mixed regarding the H-reflex changes when assessing rigidity. While no difference was shown in the H-reflex recovery curve when Parkinson's disease (PD) subjects with rigidity were compared to healthy subjects, other studies showed that rigid PD subjects exhibited an abnormal H-reflex recovery curve. Along this line, changes in the H-reflex behavior correlated with the level of rigidity in PD subjects. Studies are also mixed regarding changes in presynaptic inhibition in individuals with neurological disorders. While studies have shown a decrease in presynaptic inhibition in subjects with upper motoneuron lesions, others researchers have shown no change in presynaptic inhibition in the same type of subjects. While changes in the amplitude of the H-reflex can be used to measure several different parameters related to changes in spinal reflex excitability, it is clear that more research is needed in order to determine the clinical relevance of H-reflex changes in individuals with neurological disorders.

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General principles

Timothy R. Dillingham, in Interventional Spine, 2008

H-reflexes

H-reflexes have commonly been used to determine whether a radiculopathy demonstrates S1 involvement.7 It is a monosynaptic reflex that is an S1-mediated response and can differentiate to some extent L5 from S1 radiculopathy. Many researchers have evaluated their sensitivity and specificity with respect to lumbosacral radiculopathies and generally found a range of sensitivities from 32% to 88%.7–12 However, many of these studies suffered from lack of a control group, imprecise inclusion criteria, or small sample sizes.

Marin et al.12 prospectively examined the H-reflex and the extensor digitorum brevis reflex in 53 normals, 17 patients with L5, and 18 patients with S1 radiculopathy. Patients included in the study had all of the following: (1) radiating low back pain into the leg, (2) reduced sensation or weakness or positive straight leg raise test, and (3) either EMG evidence of radiculopathy or structural causes of radiculopathy on magnetic resonance imaging (MRI) or computed tomography (CT) imaging. The maximal (2 SD) value for the H-reflex side-to-side latency difference was 1.8 ms as derived from the normal group. They analyzed the sensitivity of the H-reflex for side-to-side differences greater than 1.8 ms or a unilaterally absent H-reflex on the affected side. The H-reflex only demonstrated a 50% sensitivity for S1 radiculopathy, 6% for L5 radiculopathy, but had a 91% specificity. Amplitudes were not assessed in this study. These results suggest that the H-reflex has a low sensitivity for S1 root level involvement.

H-reflexes may be useful to identify subtle S1 radiculopathy, yet there are a number of shortcomings related to these responses. They can be normal with radiculopathies12 and, because they are mediated over such a long physiological pathway, they can be abnormal due to polyneuropathy, sciatic neuropathy, or plexopathy.7 They are most useful in the assessment for polyneuropathy.

In order to interpret a latency or amplitude value and render a judgment as to the probability that it is abnormal, precise population-based normative values encompassing a large age range of normal subjects must be available for comparison of these nerve conduction findings. Falco et al.13 demonstrated in a group of healthy elderly subjects (60–88 years old) that the tibial H-reflex was present and recorded bilaterally in 92%. Most elderly are expected to have normal H-reflex studies and, when abnormalities are found in these persons, the electrodiagnostician should critically evaluate these findings and the clinical scenario before attributing H-reflex abnormalities to the aging process.

In patients with upper limb symptoms suggestive of cervical radiculopathy, H-reflexes and F-waves are not useful in diagnosis but rather help exclude polyneuropathy as an underlying cause of symptoms. One study by Miller and colleagues14 examined the H-reflexes in the upper limb in a set of patients defined by a combination of clinical criteria (no imaging or EMG studies) as having definite or probable cervical radiculopathy. They tested the H-reflex for the FCR, the ECR, the APB, and the biceps heteronymous reflex. The later reflex is derived by stimulating the median nerve in the cubital fossa and recording over the biceps brachii muscle, averaging 40–100 trials. These reflex studies had a 72% sensitivity overall for the group with 100% for the subset of patients with definite cervical radiculopathy. In contrast, needle EMG demonstrated 90% sensitivity for the definite group. Although these findings suggest a possible role for these upper limb H-reflexes, they are highly specialized, time consuming, and difficult to consistently elicit. They may have a role in sensory radiculopathies where needle EMG will not be positive and imaging findings are equivocal. Further studies are necessary to clarify whether the findings of Miller et al.14 can be duplicated at other centers.

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Electromyography and Nerve Conduction Velocity

Bernard Abrams, in Pain Management, 2007

H-Reflex

Definition of the H-Reflex

The H-reflex or "Hoffmann reflex" is obtained by electrode stimulation of the posterior tibial nerve in the popliteal space—at a slow rate with long duration—submaximal electrical shock, and recorded with surface electrodes over the gastrocnemius-soleus complex. The impulse travels up the sensory fibers to the spinal cord, synapses with the alpha motor neuron and returns down the motor fibers to the calf muscle. H-reflex latencies are long, in the 40 to 45 msec range. They are mostly carried out in the S1 root distribution and cannot be recorded consistently from other muscles. To determine a delay or an asymmetry, the opposite leg should always be studied for comparison.26–29

The H-reflex is somewhat more useful than the F-wave, but the main reason for this study is in the work-up of a suspected S1 radiculopathy, in which the history and/or physical examination is suggestive, but the EMG is normal.30 In most cases, when an absent H-reflex is found, suggesting a problem with S1 conduction, an absent or depressed ankle reflex has already been seen in the physical examination, so the study is, for many, redundant.

Pitfalls occur when the opposite leg is not studied to show a normal H-reflex as a contrast. If the H-reflex is bilaterally absent, it may reflect a generalized disease—for example, peripheral neuropathy. Older patients do not have good H-reflexes as a rule and this may be a normal finding. In addition, a unilaterally absent H-reflex with a normal needle EMG examination does not indicate when the injury occurred. It could be the result of a previous remote injury.

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Late Responses

David C. Preston MD, Barbara E. Shapiro MD, PhD, in Electromyography and Neuromuscular Disorders (Third Edition), 2013

H Reflex

The H reflex derives its name from Paul Hoffmann, who first evoked the response in 1918. The H response is distinctly different from the F response in that it is a true reflex with a sensory afferent, a synapse, and a motor efferent segment. Likewise, several other properties differentiate the H and F responses (Table 4–1). Unlike the F response that can be elicited from all motor nerves, the distribution of the H reflex is much more limited. In newborns, H reflexes are widely present in motor nerves, but beyond the age of two, they can only be routinely elicited by stimulating the tibial nerve in the popliteal fossa and recording the gastroc–soleus muscle. Although there are techniques for obtaining an H reflex from the femoral nerve recording the quadriceps muscle and from the median nerve recording the flexor carpi radialis muscle, both of these have significant limitations.

The circuitry of the H reflex involves the Ia muscle spindles as sensory afferents and the alpha motor neurons and their axons as efferents (Figure 4–8). If a low submaximal stimulus with a long duration pulse is applied to a nerve, it is possible to relatively selectively activate the Ia fibers. Several adjustments must be made to the EMG machine to record an H reflex, similar to those made for the F response. The gain must be increased initially to 200 to 500 µV. The typical H reflex latency is approximately 30 ms, so the sweep speed must be increased to 10 ms. Most important, the stimulus duration must be increased to 1 ms in order to selectively stimulate the Ia fibers. The recording montage consists of G1 placed over the soleus and G2, the reference electrode, placed over the Achilles tendon (Figure 4–9). Although the H reflex can be recorded over any portion of the gastrocnemius and soleus muscles, the optimal location that yields the largest H reflex has been studied. If one draws a line from the popliteal fossa posteriorly to the Achilles tendon where the medial malleolus flares out and then divides that line into eight equal parts, the optimal location is at the fifth or sixth segment distally, over the soleus (Figure 4–10). This location is approximately two to three fingerbreadths distal to where the soleus meets the two bellies of the gastrocnemius. The tibial nerve is stimulated in the popliteal fossa, with the cathode placed proximally and beginning at very low stimulus intensities. One should stimulate at a rate no faster than once every 2 seconds (0.5 Hz) in order to avoid the effects of a previous stimulus on a subsequent response. As the current is slowly increased, an H reflex (which usually is triphasic) first appears at a latency of 25 to 34 ms. H reflexes are routinely recorded with the muscle at rest. If an H reflex cannot be elicited, having the patient slightly plantar flex the ankle can be used to enhance the H reflex. If that is not helpful, the Jendrassik maneuver, as described earlier for the F response, can be used to prime the anterior horn cells. As the stimulus intensity is slowly increased, the H reflex continues to increase in amplitude and decrease in latency. As the stimulus intensity is increased further, a direct motor (M) potential appears along with the H reflex. As the stimulus intensity is increased still further, the M potential grows in size and the H reflex decreases in size.

Obtaining the H reflexes on a rastered trace, which can be superimposed once all the responses are obtained, may be helpful in determining the minimal latency, which is generally also associated with the largest amplitude. It is best to place the latency marker on the H reflex at the point where it departs from the baseline, which most often is a positive (i.e., downward) deflection. At supramaximal stimulation, the H reflex disappears, and the M potential is seen followed by an F response, which has now replaced the H reflex. The explanation for these events is as follows. Initially, with very low stimulation, the H reflex appears without the M potential (Figure 4–11) because only the Ia afferents are selectively stimulated at low stimulus intensities. As the Ia afferents are stimulated, the sensory action potential travels orthodromically to the spinal cord, across the synapse, creating a motor potential that travels orthodromically down the motor nerve to the muscle, in turn creating the H reflex. The motor axons have not been directly stimulated at this point; therefore, there is no M potential. As the stimulus intensity is increased, both the Ia afferents and the motor axons are directly stimulated. At this point, the orthodromically traveling motor action potentials create the M potential, but the motor action potentials also travel antidromically toward the spinal cord (Figure 4–8). These antidromically traveling potentials collide with the orthodromically traveling H reflex potentials, resulting in a decrease in the size of the H reflex. At supramaximal stimulation, both the Ia afferents and the motor axons are stimulated at high levels, and there is greater collision proximally of the descending H reflex. The H reflex then disappears, often replaced by the F response, and the M potential increases in size.

Typically the H reflex with the shortest latency is measured and compared with a set of normal controls for height (Figures 4–12 and 4–13). Comparison with the contralateral side is more useful in assessing a unilateral lesion; any difference of more than 1.5 ms is considered significant. Of course, both H reflexes must be acquired using the same distance for the stimulating and recording electrodes, in order for a side-to-side difference to be considered significant. In addition, the maximal amplitude of the H response (often measured peak to peak) can be compared with the maximal amplitude of the M potential (measured peak to peak) to calculate an H/M ratio (Table 4–1), see below.

The H reflex can be useful in a couple of situations. First, the response is the electrical correlate of the S1 tendon ankle reflex. If the ankle reflex is present clinically, an H reflex should always be present. If the ankle reflex is absent, however, an H reflex may still be present in some cases. Any lesion that might decrease the ankle reflex might also prolong the H reflex. Thus, one may see a prolonged H reflex in polyneuropathy, proximal tibial and sciatic neuropathy, lumbosacral plexopathy, and lesions of the S1 nerve root. One should keep in mind that bilaterally absent H reflexes in the elderly are not necessarily abnormal, and correlate with the common clinical finding of absent ankle reflexes in a significant number of elderly patients. In addition, the H/M ratio is a crude assessment of anterior horn cell excitability. The H/M ratio often increases in upper motor neuron lesions. Likewise, the presence of H reflexes in other muscles in an adult should suggest a central disorder.

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Operant Conditioning of Reflexes

J.R. Wolpaw, X.Y. Chen, in Encyclopedia of Neuroscience, 2009

The Complex Spinal Cord Plasticity Accompanying Reflex Conditioning

H-reflex conditioning is associated with plasticity at multiple sites in the spinal cord. Downconditioning produces a positive shift in motor neuron firing threshold and a reduction in axonal conduction velocity. These two changes together suggest that a positive shift in sodium channel activation voltage occurs throughout the motor neuron soma and axon. As illustrated in Figure 3(a), the change in threshold can account in large part for the smaller reflex. Although activity-dependent synaptic plasticity is often assumed to be the basis of learning, the shift in motor neuron threshold produced by down-conditioning seems to be an example of neuronally based (as opposed to synaptically based) learning. The threshold change could also account for the decrease in motor neuron axonal conduction velocity that is associated with H-reflex down-conditioning (Figure 3(b)). In addition to this neuronal plasticity, H-reflex conditioning modifies Ia afferent motor neuron synapses and several other populations of synaptic terminals on the motor neuron. The effects on GABAergic terminals are particularly striking (Figure 3(c)). Conditioning probably changes spinal cord interneurons as well, either those in di- or trisynaptic pathways that can contribute to the H-reflex and/or those that convey descending influence to the motor neuron. At present, it is most likely that up-conditioning is due to change in oligosynaptic primary afferent input to the motor neuron. Thus, down-conditioning and up-conditioning are probably not mirror images of each other but rather have different mechanisms. In addition to this complex plasticity in the spinal cord ipsilateral to the conditioned reflex, H-reflex conditioning also causes plasticity in the contralateral spinal cord. The precise location and nature of this contralateral plasticity are as yet unknown.

Figure 3. Examples of the multisite spinal cord plasticity underlying H-reflex conditioning. (a) Motor neurons on the conditioned side of H-reflex (HR) down-conditioned animals have more positive firing thresholds and slightly smaller Ia excitatory postsynaptic potentials (EPSPs). Together, these two findings can explain why the H-reflex becomes smaller. (b) Distributions of soleus motor neuron axonal conduction velocities in unconditioned (solid) and down-conditioned (dashed) rats. Down-conditioning has a comparable effect in monkeys. The more positive motor neuron firing threshold can explain this drop in conduction velocity. (c) Soleus motor neurons (dashed lines) from an unconditioned rat (top) and a down-conditioned rat (bottom), with arrows pointing to γ-aminobutyricacidergic (GABAergic) terminals on the somatic membrane. GABAergic terminals are detected by glutamic acid decarboxylase (GAD67) immunoreactivity. After down-conditioning, soleus motor neurons have more GABAergic terminals, and these terminals are more densely labeled and occupy more of the somatic membrane. (a) Modified from Carp JS, Chen XY, Sheikh H, and Wolpaw JR (2001) Operant conditioning of rat H-reflex affects motoneuron axonal conduction velocity. Experimental Brain Research 136: 269–273. (b) Modified from Carp JS, Chen XY, Sheikh H, and Wolpaw JR (2001) Operant conditioning of rat H-reflex affects motoneuron axonal conduction velocity. Experimental Brain Research 136: 269–273.

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