query: where are the upper motor neurons that control skeletal muscles found

pos: Upper motor neuron the most important areas in the frontal lobe. The precentral gyrus is the most posterior gyrus of the frontal lobe and it lies anterior to the central sulcus. The pyramidal cells of the precentral gyrus are also called upper motor neurons. The fibers of the upper motor neurons project out of the precentral gyrus ending in the brainstem, where they will decussate (intersect) within the lower medulla oblongata to form the lateral corticospinal tract on each side of the spinal cord. The fibers that do not decussate will pass through the medulla and continue on to form the anterior corticospinal

pos: Somatic nervous system the efferent somatic nervous system involves a sequence that begins in the upper cell bodies of motor neurons (upper motor neurons) within the precentral gyrus (which approximates the primary motor cortex). Stimuli from the precentral gyrus are transmitted from upper motor neurons and down the corticospinal tract, via axons to control skeletal (voluntary) muscles. These stimuli are conveyed from upper motor neurons through the ventral horn of the spinal cord, and across synapses to be received by the sensory receptors of alpha motor neurons (large lower motor neurons) of the brainstem and spinal cord. Upper motor neurons release a neurotransmitter,

neg: Lower motor neuron Lower motor neuron Lower motor neurons (LMNs) are motor neurons located in either the anterior grey column, anterior nerve roots (spinal lower motor neurons) or the cranial nerve nuclei of the brainstem and cranial nerves with motor function (cranial nerve lower motor neurons). All voluntary movement relies on spinal lower motor neurons, which innervate skeletal muscle fibers and act as a link between upper motor neurons and muscles. Cranial nerve lower motor neurons control movements of the eyes, face and tongue, and contribute to chewing, swallowing and vocalization. Damage to the lower motor neurons can lead to flaccid paralysis, absent

neg: Upper motor neuron tracts. The upper motor neuron descends in the spinal cord to the level of the appropriate spinal nerve root. At this point, the upper motor neuron synapses with the lower motor neuron, each of whose axons innervate a fiber of skeletal muscle. These neurons connect the brain to the appropriate level in the spinal cord, from which point nerve signals continue to the muscles by means of the lower motor neurons. The neurotransmitter glutamate transmits the nerve impulses from upper to lower motor neurons, where it is detected by glutamatergic receptors. Upper motor neurons travel in several neural pathways through

neg: Acetylcholine heart, lungs, upper gastrointestinal tract, and sweat glands. Acetylcholine is the substance the nervous system uses to activate skeletal muscles, a kind of striated muscle. These are the muscles used for all types of voluntary movement, in contrast to smooth muscle tissue, which is involved in a range of involuntary activities such as movement of food through the gastrointestinal tract and constriction of blood vessels. Skeletal muscles are directly controlled by motor neurons located in the spinal cord or, in a few cases, the brainstem. These motor neurons send their axons through motor nerves, from which they emerge to connect

neg: Alpha motor neuron Alpha motor neuron Alpha (α) motor neurons (also called alpha motoneurons), are large, multipolar lower motor neurons of the brainstem and spinal cord. They innervate extrafusal muscle fibers of skeletal muscle and are directly responsible for initiating their contraction. Alpha motor neurons are distinct from gamma motor neurons, which innervate intrafusal muscle fibers of muscle spindles. While their cell bodies are found in the central nervous system (CNS), α motor neurons are also considered part of the somatic nervous system—a branch of the peripheral nervous system (PNS)—because their axons extend into the periphery to innervate skeletal muscles. An alpha motor

neg: Lower motor neuron reflexes in affected areas. Damage to the upper motor neuron causes muscle atrophy with long standing lesion. These findings are in contrast to findings in upper motor neuron lesions. LMNL is indicated by abnormal EMG potentials, fasciculations, paralysis, weakening of muscles, and neurogenic atrophy of skeletal muscle. Bell's Palsy, Bulbar palsy, Poliomyelitis and Amyotrophic lateral sclerosis (ALS) are all pathologies associated with lower motor neuron dysfunction. Lower motor neuron Lower motor neurons (LMNs) are motor neurons located in either the anterior grey column, anterior nerve roots (spinal lower motor neurons) or the cranial nerve nuclei of the brainstem and cranial

neg: Motor neuron categories: Somatic motor neurons originate in the central nervous system, project their axons to skeletal muscles (such as the muscles of the limbs, abdominal, and intercostal muscles), which are involved in locomotion. The three types of these neurons are the "alpha efferent neurons", "beta efferent neurons", and "gamma efferent neurons". They are called efferent to indicate the flow of information from the central nervous system (CNS) to the periphery. In addition to voluntary skeletal muscle contraction, alpha motor neurons also contribute to muscle tone, the continuous force generated by noncontracting muscle to oppose stretching. When a muscle is stretched, sensory

neg: Motor pool (neuroscience) each motor pool is tightly controlled by complex developmental pathways. Distinct skeletal muscles are controlled by groups of individual motor units. Such motor units are made up of a single motor neuron and the muscle fibers that it innervates. Motor neurons are located in the ventral horn of the spinal cord and the brainstem. These neurons innervate skeletal muscle fibers through the propagation of action potentials down their axons (through ventral roots and cranial nerves), and they stimulate skeletal muscle fibers at neuromuscular junctions where they synapse with the motor end plates of muscle fibers. In humans, these axons can

neg: Motor pool (neuroscience) be as long as one meter. Motor neurons themselves fall into three main classes: alpha-motor neurons control extrafusal muscle fibers, meaning that they innervate skeletal muscles leading to movement; gamma-motor neurons innervate intrafusal muscle fibers, controlling the sensitivity of muscle spindles to stretch; beta-motor neurons are capable of synapsing on either type of muscle fiber. Alpha-motor neurons can further be divided into three separate subclasses, distinguished according to the contractile properties of the motor units that they form: fast-twitch fatigable (FF), fast-twitch fatigue-resistant (FR), and slow-twitch fatigue-resistant (S). The composition of a motor pool may consist of multiple classes and

neg: Upper motor neuron syndrome Upper motor neuron syndrome Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion. Following upper motor neuron lesions, affected muscles potentially have many features of altered performance including: Such signs are collectively termed the "upper motor neuron syndrome". Affected muscles typically show multiple signs, with severity depending on the degree of damage and other factors that influence motor control. In neuroanatomical circles, it is often joked, for example, that hemisection of the cervical spinal cord leads to an "upper lower motor neuron syndrome and a lower upper

neg: Upper motor neuron syndrome benefits. Upper motor neuron syndrome Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion. Following upper motor neuron lesions, affected muscles potentially have many features of altered performance including: Such signs are collectively termed the "upper motor neuron syndrome". Affected muscles typically show multiple signs, with severity depending on the degree of damage and other factors that influence motor control. In neuroanatomical circles, it is often joked, for example, that hemisection of the cervical spinal cord leads to an "upper lower motor neuron syndrome and a lower

neg: Motor pool (neuroscience) subclasses of motor neurons. Motor pools in the spinal cord are clustered in distinct columns of motor neurons extending over multiple spinal cord segments; although, there is significant overlap. Motor pools that control proximal muscles are generally located medial to the ventral horn, while those that control distal muscles are located laterally. Motor pools that control flexor muscles are located dorsally to the ventral horn while those that control extensor muscles are located ventrally. The number of motor neurons in an individual motor pool is highly variable and can generally be predicted by the level of nuanced control that a

neg: Motor neuron Motor neuron A motor neuron (or motoneuron) is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper motor neurons and lower motor neurons. Axons from upper motor neurons synapse onto interneurons in the spinal cord and occasionally directly onto lower motor neurons. The axons from the lower motor neurons are efferent nerve fibers that carry signals from the

neg: Epigenetics of neurodegenerative diseases is a motor neuron disease that involves neurogeneration. All skeletal muscles in the body are controlled by motor neurons that communicate signals from the brain to the muscle through a neuromuscular junction. When the motor neurons degenerate, the muscles no longer receive signals from the brain and begin to waste away. ALS is characterized by stiff muscles, muscle twitching, and progressive muscle weakness from muscle wasting. The parts of the body affected by early symptoms of ALS depend on which motor neurons in the body are damaged first, usually the limbs. As the disease progresses most patients are unable to

neg: Upper motor neuron Upper motor neuron Upper motor neurons (UMNs) are the main source of voluntary movement. They are found in the brain and carry motor information down the spinal cord to activate the lower motor neurons, which in turn directly signal muscles to contract. They are a type of giant pyramidal cell called "Betz cells" and are found just below the surface of the cerebral cortex within layer V of the primary motor cortex. The cell bodies of "Betz cell" neurons are the largest in the brain, approaching nearly 0.1mm in diameter. The primary motor cortex, or precentral gyrus, is one of

neg: Upper motor neuron contraction/relaxation of a muscle), and an extensor plantar response known as the Babinski sign. Upper motor neuron Upper motor neurons (UMNs) are the main source of voluntary movement. They are found in the brain and carry motor information down the spinal cord to activate the lower motor neurons, which in turn directly signal muscles to contract. They are a type of giant pyramidal cell called "Betz cells" and are found just below the surface of the cerebral cortex within layer V of the primary motor cortex. The cell bodies of "Betz cell" neurons are the largest in the brain, approaching

neg: Premovement neuronal activity purpose of generating specific muscles movements or contractions. Spike-triggered averaging is a way to measure the activity of one cortical motor neuron, on a group of lower motor neurons in the spinal cord. Experimentation confirmed that single upper motor neurons are connected to multiple lower motor neurons. This supports the general conclusion that movements and not individual muscles are controlled by the activity of upper motor neurons. Individual motor neurons were recorded using implanted microelectrodes to record their activity in awake and behaving monkeys. This experimentation provided a way to figure out the correlation between neuronal activity and voluntary movement.

neg: Motor neuron PNS, which synapses onto the muscle. All vertebrate motor neurons are cholinergic, that is, they release the neurotransmitter acetylcholine. Parasympathetic ganglionic neurons are also cholinergic, whereas most sympathetic ganglionic neurons are noradrenergic, that is, they release the neurotransmitter noradrenaline. (see Table) Motor neuron A motor neuron (or motoneuron) is a neuron whose cell body is located in the motor cortex, brainstem or the spinal cord, and whose axon (fiber) projects to the spinal cord or outside of the spinal cord to directly or indirectly control effector organs, mainly muscles and glands. There are two types of motor neuron – upper

neg: Epigenetics of neurodegenerative diseases anterior horn of the spinal cord and brain. Muscles depend on connections to motor neurons and the central nervous system to stimulate muscle maintenance and therefore degeneration of motor neurons and subsequent denervation of muscles lead to loss of muscle control and muscle atrophy. The muscles of the lower extremities are often affected first followed by upper extremities and sometime the muscles of respiration and mastication. In general, proximal muscle are always affected more than distal muscle. Spinal muscular atrophy is linked to genetic mutations in the SMN1 (Survival of Motor Neuron 1) gene. The SMN protein is widely expressed

neg: Beta motor neuron Beta motor neuron Beta motor neurons (β motor neurons), also called beta motoneurons, are a kind of lower motor neuron, along with alpha motor neurons and gamma motor neurons. Beta motor neurons innervate intrafusal fibers of muscle spindles with collaterals to extrafusal fibers - a type of slow twitch fiber. Also, axons of alpha, beta, and gamma motor neurons become myelinated. Moreover, these efferent neurons originate from the anterior grey column of the spinal cord and travel to skeletal muscles. However, the larger diameter alpha motor fibers require higher conduction velocity than beta and gamma. There are two kinds of

neg: Primary motor cortex shortly before reaching the lower motor neurons. Corticomotorneurons are neurons in the primary cortex which project directly to motor neurons in the ventral horn of the spinal cord. Axons of corticomotorneurons terminate on the spinal motor neurons of multiple muscles as well as on spinal interneurons. They are unique to primates and it has been suggested that their function is the adaptive control of the distal extremities (e.g. the hands) including the relatively independent control of individual fingers. Corticomotorneurons have so far only been found in the primary motor cortex and not in secondary motor areas. Branches of the middle

neg: Primary lateral sclerosis Primary lateral sclerosis Primary lateral sclerosis (PLS) is a rare neuromuscular disease characterized by progressive muscle weakness in the voluntary muscles. PLS belongs to a group of disorders known as motor neuron diseases. Motor neuron diseases develop when the nerve cells that control voluntary muscle movement degenerate and die, causing weakness in the muscles they control. PLS only affects upper motor neurons. There is no evidence of the degeneration of spinal motor neurons or muscle wasting (amyotrophy) that occurs in amyotrophic lateral sclerosis (ALS). Onset of PLS usually occurs spontaneously after age 50 and progresses gradually over a number of

neg: Somatic nervous system Somatic nervous system The somatic nervous system (SNS or voluntary nervous system) is the part of the peripheral nervous system associated with the voluntary control of body movements via skeletal muscles. The somatic nervous system consists of afferent nerves or sensory nerves, and efferent nerves or motor nerves. Afferent nerves are responsible for relaying sensation from the body to the central nervous system; efferent nerves are responsible for sending out commands from the CNS to the body, stimulating muscle contraction; they include all the non-sensory neurons connected with skeletal muscles and skin. The "a-" of "afferent" and the "e-" of

neg: Central facial palsy upper motor neurons of the facial nerve. The facial motor nucleus contains ventral and dorsal areas that have lower motor neurons that supply the upper and lower face muscles. When central facial palsy occurs, there are lesions in the corticobulbar tract between the cerebral cortex. Because of these lesions, the facial motor nucleus reduces or destroys input in the ventral division. The ipsilateral input in the dorsal region is preserved. Central facial palsy is often characterized by either hemiparalysis or hemiparesis of the contra-lateral muscles in facial expression. Muscles on the forehead are left intact. Also, most patients have lost

neg: Premovement neuronal activity It was found that the force generated by contracting muscles changed as a function of the firing rate of upper motor neurons. The firing rates of the active neurons often change prior to movements involving very small forces. This suggests that, the primary motor cortex contributes to the initial phase of the recruitment of lower motor neurons, involved in the generation of finely controlled movements. Approximately 65% of the neurons in the pre-motor cortex are responsible for conditional "closed-loop" motor tasks. In experimentation using monkeys, when they were trained to reach in different directions, depending on the specified visual cue,

neg: Targeted reinnervation process multiple control signals. The requirement to transplant multiple nerves into a muscle region originated from a hypothesis that hyper-reinnervation, by which an excessive amount of motor neurons transferred to a muscle, can increase the reinnervation of muscle fibers hence improving the recovery of paralyzed muscles. The hypothesis was tested on rat skeletal muscles and the result indicated that hyper-reinnervated muscles recovered more muscle mass and strength and more number of motor units were formed. The first surgical patient was a bilateral shoulder disarticulation amputee. Both arms were entirely amputated at the shoulder level, with only the shoulder blades remaining.

neg: Motor neuron muscle and smooth muscles of the viscera ( the muscles of the arteries): they synapse onto neurons located in ganglia of the autonomic nervous system (sympathetic and parasympathetic), located in the peripheral nervous system (PNS), which themselves directly innervate visceral muscles (and also some gland cells). In consequence, the motor command of skeletal and branchial muscles is "monosynaptic" involving only one motor neuron, either "somatic" or "branchial", which synapses onto the muscle. Comparatively, the command of visceral muscles is "disynaptic" involving two neurons: the "general visceral motor neuron", located in the CNS, synapses onto a ganglionic neuron, located in the

neg: Spinal muscular atrophy death of motor neuron cells in the anterior horn of spinal cord and the brain. Muscles that depend on these motor neurons for neural input now have decreased innervation (also called denervation), and therefore have decreased input from the central nervous system (CNS). Decreased impulse transmission through the motor neurons leads to decreased contractile activity of the denervated muscle. Consequently, denervated muscles undergo progressive atrophy (waste away). Muscles of lower extremities are usually affected first, followed by muscles of upper extremities, spine and neck and, in more severe cases, pulmonary and mastication muscles. Proximal muscles are always affected earlier and

neg: Facial motor nucleus a dorsal and ventral region, with neurons in the dorsal region innervating muscles of the upper face and neurons in the ventral region innervating muscles of the lower face. Because it innervates muscles derived from pharyngeal arches, the facial motor nucleus is considered part of the special visceral efferent (SVE) cell column, which also includes the trigeminal motor nucleus, nucleus ambiguus, and (arguably) the spinal accessory nucleus. Like all lower motor neurons, cells of the facial motor nucleus receive cortical input from the primary motor cortex in the frontal lobe of the brain. Upper motor neurons of the cortex send

neg: Anterior grey column Anterior grey column The anterior grey column (also called the anterior cornu, anterior horn of spinal cord or ventral horn) is the front column of grey matter in the spinal cord. It is one of the three grey columns. The anterior grey column contains motor neurons that affect the skeletal muscles while the posterior grey column receives information regarding touch and sensation. The anterior grey column is the column where the cell bodies of alpha motor neurons are located. The anterior grey column, directed forward, is broad and of a rounded or quadrangular shape. Its posterior part is termed the

neg: Gamma motor neuron motor neurons. Although muscles can be in a relaxed state, muscles have a general resting level of tension. This is termed muscle tone and is maintained by the motor neurons innervating the muscle. Its purpose is to maintain posture and assist in quicker movements, since if muscles were completely loose, then more neuronal firing would need to take place. The amount of tension in the muscles depends primarily on the resting level discharge of alpha motor neurons, mainly the Ia spindle afferents. Gamma motor neurons are also involved through their action on intrafusal muscle fibers. The intrafusal muscle fibers control

neg: Alpha motor neuron neuron and the muscle fibers it innervates is a motor unit. A motor neuron pool contains the cell bodies of all the alpha motor neurons involved in contracting a single muscle. Alpha motor neurons (α-MNs) innervating the head and neck are found in the brainstem; the remaining α-MNs innervate the rest of the body and are found in the spinal cord. There are more α-MNs in the spinal cord than in the brainstem, as the number of α-MNs is directly proportional to the amount of fine motor control in that muscle. For example, the muscles of a single finger have

neg: Premovement neuronal activity with premovement for both types of stimuli. A subcortical loop exists within the brain linking upper motor neurons originating in the primary motor and pre-motor cortices and the brainstem, with the basal ganglia. These upper motor neurons eventually initiate movement by controlling the activity of lower motor neurons, located in the brainstem and spinal cord, and project out to innervate the muscles in the body. Upper motor neurons also modulate activity of local circuit neurons, whose synapses are a large input to these lower motor neurons, in turn affecting subsequent movement. Thus, the basal ganglia indirectly influence movement via regulation

neg: Topographic map (neuroanatomy) the motor cortex travels through Betz cells down the corticospinal tract through upper motor neurons, terminating at the anterior horn of the grey matter where lower motor neurons transmit the signal to peripheral motor neurons and, finally, the voluntary muscles. There are several instances of movements that do not require the participation of topographic maps, or even the participation of the brain. One instance would be (as already stated) in some reflexes. Reflexes usually are mediated at the level of the spinal cord through reflex arcs. In humans, mono-, oligo-, and poly-synaptic reflex arcs, propriospinal interneuron systems, and internuncial gray

neg: Brain to extract the relevant features, and integrated with signals coming from other sensory systems. Motor systems are areas of the brain that are involved in initiating body movements, that is, in activating muscles. Except for the muscles that control the eye, which are driven by nuclei in the midbrain, all the voluntary muscles in the body are directly innervated by motor neurons in the spinal cord and hindbrain. Spinal motor neurons are controlled both by neural circuits intrinsic to the spinal cord, and by inputs that descend from the brain. The intrinsic spinal circuits implement many reflex responses, and contain

neg: Corticobulbar tract addition endings in these motor neurons, fibers of the corticobulbar tract also end in the sensory nuclei of the brainstem including gracile nucleus, cuneate nucleus, solitary nucleus, and all trigeminal nuclei. The corticobulbar tract is composed of the upper motor neurons of the cranial nerves. The muscles of the face, head and neck are controlled by the corticobulbar system, which terminates on motor neurons within brainstem motor nuclei. This is in contrast to the corticospinal tract in which the cerebral cortex connects to spinal motor neurons, and thereby controls movement of the torso, upper and lower limbs. Fibers that end

neg: Post-polio syndrome activates. Poliovirus attacks specific neurons in the brainstem and the anterior horn cells of the spinal cord, generally resulting in the death of a substantial fraction of the motor neurons controlling skeletal muscles. In an effort to compensate for the loss of these neurons, surviving motor neurons sprout new nerve terminals to the orphaned muscle fibers. The result is some recovery of movement and the development of enlarged motor units. The neural fatigue theory proposes that the enlargement of the motor neuron fibers places added metabolic stress on the nerve cell body to nourish the additional fibers. After years of

neg: Spinal cord be divided into two different groups: the lateral corticospinal tract and the anterior cortical spinal tract. The lateral tract contains upper motor neuronal axons which synapse on dorsal lateral (DL) lower motor neurons. The DL neurons are involved in distal limb control. Therefore, these DL neurons are found specifically only in the cervical and lumbosacral enlargements within the spinal cord. There is no decussation in the lateral corticospinal tract after the decussation at the medullary pyramids. The anterior corticospinal tract descends ipsilaterally in the anterior column, where the axons emerge and either synapse on lower ventromedial (VM) motor neurons in

neg: Hyporeflexia Hyporeflexia Hyporeflexia refers to below normal or absent reflexes (areflexia). It can be detected through the use of a reflex hammer. It is the opposite of hyperreflexia. Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from spinal cord to muscle), whereas hyperreflexia is often attributed to upper motor neuron lesions (along the long, motor tracts from the brain). The upper motor neurons are thought to inhibit the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons (including alpha and gamma motor fibers) and appurtenant interneurons. Therefore,

neg: Hyporeflexia drowsiness, dyspnea, and hyporeflexia). Diseases associated with hyporeflexia include Hyporeflexia Hyporeflexia refers to below normal or absent reflexes (areflexia). It can be detected through the use of a reflex hammer. It is the opposite of hyperreflexia. Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from spinal cord to muscle), whereas hyperreflexia is often attributed to upper motor neuron lesions (along the long, motor tracts from the brain). The upper motor neurons are thought to inhibit the reflex arc, which is formed by sensory neurons from intrafusal fibers of muscles, lower motor neurons (including

neg: Motor cortex the muscle force. Each point in motor cortex controls a muscle or a small group of related muscles. This description is only partly correct. Most neurons in the motor cortex that project to the spinal cord synapse on interneuron circuitry in the spinal cord, not directly onto motor neurons. One suggestion is that the direct, cortico-motoneuronal projections are a specialization that allows for the fine control of the fingers. The view that each point in motor cortex controls a muscle or a limited set of related muscles was debated over the entire history of research on the motor cortex, and

neg: Spinal cord the ventral horn ipsilaterally or descussate at the anterior white commissure where they synapse on VM lower motor neurons contralaterally . The tectospinal, vestibulospinal and reticulospinal descend ipsilaterally in the anterior column but do not synapse across the anterior white commissure. Rather, they only synapse on VM lower motor neurons ipsilaterally. The VM lower motor neurons control the large, postural muscles of the axial skeleton. These lower motor neurons, unlike those of the DL, are located in the ventral horn all the way throughout the spinal cord. Proprioceptive information in the body travels up the spinal cord via three tracks.

neg: Renshaw cell proximal muscles of the hand and foot do not have homonymous inhibition. Heteronymous inhibition has been found to be dominant in the leg compared to the arm, where antagonist muscles work simultaneously. (It must also be noted that Renshaw cells are activated by gamma motor neurons, but to a lesser extent). The Renshaw cells not only synapse with homonymous and heteronymous nerves, but also with the Ia interneurones, which are stimulated by the Ia afferents from the same muscle group activated by the motor neurons, which have an inhibitory effect on the antagonist muscle group. This “recurrent facilitation” causes reduced

neg: Alternating hemiplegia Alternating hemiplegia Alternating hemiplegia is a form of hemiplegia that has an ipsilateral and contralateral presentation in different parts of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the

neg: Alpha motor neuron horn of the spinal cord. Amyotropic lateral sclerosis likewise is associated with the selective loss of motor neurons. Paralysis is one of the most pronounced effects of damage to α-MNs. Because α-MNs provide the only voluntary innervation to extrafusal muscle fibers, losing α-MNs effectively severs the connection between the brainstem and spinal cord and the muscles they innervate. Without this connection, voluntary and involuntary (reflex) muscle control is impossible. Voluntary muscle control is lost because α-MNs relay voluntary signals from upper motor neurons to muscle fibers. Loss of involuntary control results from interruption of reflex circuits such as the tonic

neg: Pyramidal tracts Pyramidal tracts The pyramidal tracts include both the corticobulbar tract and the corticospinal tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem ("corticobulbar") or spinal cord ("corticospinal") and are involved in the control of motor functions of the body. The corticobulbar tract conducts impulses from the brain to the cranial nerves. These nerves control the muscles of the face and neck and are involved in facial expression, mastication, swallowing, and other functions. The corticospinal tract conducts impulses from the brain to the spinal cord.

neg: Facial motor nucleus axons that descend through the internal capsule and synapse on neurons in the facial motor nucleus. This pathway from the cortex to the brainstem is called the corticobulbar tract. The neurons in the dorsal aspect of the facial motor nucleus receive inputs from both sides of the cortex, while those in the ventral aspect mainly receive contralateral inputs (i.e. from the opposite side of the cortex). The result is that both sides of the brain control the muscles of the upper face, while the right side of the brain controls the lower left side of the face, and the left

neg: Pyramidal tracts the cruz cerebri (pedunculotomy). In National Lampoon's European Vacation, the Griswold family was asked about the pyramidal tracts on the game show "Pig in a Poke". Pyramidal tracts The pyramidal tracts include both the corticobulbar tract and the corticospinal tract. These are aggregations of efferent nerve fibers from the upper motor neurons that travel from the cerebral cortex and terminate either in the brainstem ("corticobulbar") or spinal cord ("corticospinal") and are involved in the control of motor functions of the body. The corticobulbar tract conducts impulses from the brain to the cranial nerves. These nerves control the muscles of the

neg: Central nervous system disease vessel ruptures, causing blood to leak to the brain. If the brain cannot get enough oxygen and blood, brain cells can die, leading to permanent damage. The spinal cord transmits sensory reception from the peripheral nervous system. It also conducts motor information to the body's skeletal muscles, cardiac muscles, smooth muscles, and glands. There are 31 pairs of spinal nerves along the spinal cord, all of which consist of both sensory and motor neurons. The spinal cord is protected by vertebrae and connects the peripheral nervous system to the brain, and it acts as a "minor" coordinating center. The brain

neg: Spinal interneuron into the contralateral spinal cord. At that location, the interneuron excites the alpha motor neurons that innervate the extensor muscles of the opposite leg. This allows for balance and body posture to be maintained. Spinal interneuron A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord. The grey column of the spinal cord appears to have groups of small neurons, often referred

neg: Golgi tendon reflex Golgi tendon reflex The Golgi tendon reflex is a normal component of the reflex arc of the peripheral nervous system. In a Golgi tendon reflex, skeletal muscle contraction causes the antagonist muscle to simultaneously lengthen and relax. This reflex is also called the inverse myotatic reflex, because it is the inverse of the stretch reflex. Though muscle tension is increasing during the contraction, alpha motor neurons in the spinal cord supplying the muscle are inhibited. However, antagonistic muscles are activated. The Golgi tendon reflex operates as a protective feedback mechanism to control the tension of an active muscle by causing

neg: Neural coding the population of neurons codes the signal for the motion. This particular population code is referred to as population vector coding. This particular study divided the field of motor physiologists between Evarts' "upper motor neuron" group, which followed the hypothesis that motor cortex neurons contributed to control of single muscles, and the Georgopoulos group studying the representation of movement directions in cortex. The Johns Hopkins University Neural Encoding laboratory led by Murray Sachs and Eric Young developed place-time population codes, termed the Averaged-Localized-Synchronized-Response (ALSR) code for neural representation of auditory acoustic stimuli. This exploits both the place or tuning within

neg: Premovement neuronal activity in the post central gyrus. Experimentation via intra-cortical micro-stimulation brought about a more detailed understanding of motor maps. By injecting current via a sharpened tip of a microelectrode into the cortex, the upper motor neurons in layer 5, which project to lower motor neurons can be stimulated. These neurons are associated with the neurons in the spinal cord, and thus stimulating specific movements which occur in specified muscular regions rather than stimulating specific muscles which produce those movements. Neuron connections in the motor map are linked for the purpose of generating specific movements. These connections are not linked for the

neg: Gamma motor neuron directly adjust the lengthening or shortening of muscles. However, their role is important in keeping muscle spindles taut, thereby allowing the continued firing of alpha neurons, leading to muscle contraction. These neurons also play a role in adjusting the sensitivity of muscle spindles. The presence of myelination in gamma motor neurons allows a conduction velocity of 4 to 24 meters per second, significantly faster than with non-myelinated axons but slower than in alpha motor neurons. Muscle spindles are the sensory receptors located within muscles that allow communication to the spinal cord and brain with information of where the body is

neg: Axonotmesis Motor fibers injuries may involve lower motor neurons, sympathetic fibers, and or both. Assessment items include: In assessment, sensory-motor defects may be mild, moderate, or severe. Damage to motor fibers results in paralysis of the muscles. Nervous plexus injuries create more signs and symptoms from sensory-motor problems (such as brachial plexus injuries). In these cases, the prognosis depends on the amount of damage and the degree of functional impairment. Electromyography (EMG) is a medical test performed to evaluate and record the electrical activity (electromyogram) produced by skeletal muscles using an instrument called electromyograph. In axonotmesis, EMG changes (2 to 3

neg: Human musculoskeletal system Only skeletal and smooth muscles are part of the musculoskeletal system and only the skeletal muscles can move the body. Cardiac muscles are found in the heart and are used only to circulate blood; like the smooth muscles, these muscles are not under conscious control. Skeletal muscles are attached to bones and arranged in opposing groups around joints. Muscles are innervated, to communicate nervous energy to, by nerves, which conduct electrical currents from the central nervous system and cause the muscles to contract. In mammals, when a muscle contracts, a series of reactions occur. Muscle contraction is stimulated by the

neg: Alpha motor neuron lower limbs: these α-MNs form large cell columns that contribute to the cervical and lumbar enlargements of the spinal cord. In addition to receiving neurotrophic factors from muscles, α-MNs also secrete a number of trophic factors to support the muscle fibers they innervate. Reduced levels of trophic factors contributes to the muscle atrophy that follows an α-MN lesion. Like other neurons, lower motor neurons have both afferent (incoming) and efferent (outgoing) connections. Alpha motor neurons receive input from a number of sources, including upper motor neurons, sensory neurons, and interneurons. The primary output of α-MNs is to extrafusal muscle fibers.

neg: Tumefactive multiple sclerosis neoplasm with symptoms such as headaches, aphasia, and/ or seizures.[13] There are some differences with normal MS symptoms. Spasticity is not as in tumefactive cases, because it standard MS it is caused by demyelination or inflammation in the motor areas of the brain or the spinal cord. This upper motor neuron syndrome appears when motor control of skeletal muscles is affected due to damage to the efferent motor pathways. Spasticity is an involuntary muscle movement like an exaggerated stretch reflex, which is when a muscle overcompensates and contracts too much in response to the muscle being stretched. It is believed

neg: Central facial palsy Central facial palsy Central facial palsy (colloquially referred to as central seven) is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve. The facial motor nucleus has dorsal and ventral divisions that contain lower motor neurons supplying the muscles of the upper and lower face, respectively. The dorsal division receives bilateral upper motor neuron input (i.e. from both sides of the brain) while the ventral division receives only contralateral input (i.e. from the opposite side of the

neg: Anterior grey column and West Nile virus. The anterior grey column is the target for some spasmolytic medications. Norepinephrine release here, (as induced by cyclobenzaprine) reduces spasms by innervation (reducing nerve activity) of alpha motor neurons via interaction with gamma fibers. Anterior grey column The anterior grey column (also called the anterior cornu, anterior horn of spinal cord or ventral horn) is the front column of grey matter in the spinal cord. It is one of the three grey columns. The anterior grey column contains motor neurons that affect the skeletal muscles while the posterior grey column receives information regarding touch and sensation.

neg: Extrafusal muscle fiber Extrafusal muscle fiber Extrafusal muscle fibers are the skeletal standard muscle fibers that are innervated by alpha motor neurons and generate tension by contracting, thereby allowing for skeletal movement. They make up the large mass of skeletal muscle tissue and are attached to bone by fibrous tissue extensions (tendons). Each alpha motor neuron and the extrafusal muscle fibers innervated by it make up a motor unit. The connection between the alpha motor neuron and the extrafusal muscle fiber is a neuromuscular junction, where the neuron's signal, the action potential, is transduced to the muscle fiber by the neurotransmitter acetylcholine. Extrafusal

neg: Intrafusal muscle fiber endings. Both ends of these fibers contract but the central region only stretches and does not contract. They are innervated by gamma motor neurons and beta motor neurons. It is by the sensory information from these two intrafusal fiber types that an individual is able to judge the position of their muscle, and the rate at which it is changing. Intrafusal muscle fibers are not to be confused with extrafusal muscle fibers, which contract, generating skeletal movement and are innervated by alpha motor neurons. Intrafusal muscle fiber Intrafusal muscle fibers are skeletal muscle fibers that serve as specialized sensory organs

neg: Primary motor cortex code by which neurons in the primate motor cortex control the spinal cord, and thus movement, remains debated. Some specific progress in understanding how motor cortex causes movement has also been made in the rodent model. The rodent motor cortex, like the monkey motor cortex, may contain subregions that emphasize different common types of actions. For example, one region appears to emphasize the rhythmic control of whisking. Neurons in this region project to a specific subcortical nucleus in which a pattern generator coordinates the cyclic rhythm of the whiskers. This nucleus then projects to the muscles that control the whiskers.

neg: Henneman's size principle and only using fatigable fibers when high forces are needed. It also permits fine control of force at all levels of output. Before Henneman’s size principle, it was known that neurons varied greatly in size; however, the functional significance of this was not yet known. Henneman's early papers on the motor units of the cat soleus and gastrocnemius muscles found that the diameter of a motor nerve fiber relates to number of muscle fibers it innervates; in other words, the size of the motor unit is proportional to the amount of muscle fibers it innervates. The evidence in previous studies

neg: Spinal muscular atrophy Spinal muscular atrophy Spinal muscular atrophy (SMA) is a rare neuromuscular disorder characterised by loss of lower motor neurons and progressive muscle wasting, often leading to early death. The disorder is caused by a genetic defect in the "SMN1" gene, which encodes SMN, a protein widely expressed in all eukaryotic cells (that is, cells with nuclei, including human cells) and necessary for survival of motor neurons. Lower levels of the protein results in loss of function of neuronal cells in the anterior horn of the spinal cord and subsequent system-wide atrophy of skeletal muscles. Spinal muscular atrophy manifests in various

neg: Motor pool (neuroscience) type neurons being generally spared. Further, motor pools controlling facial muscles (including those of the eye) and voluntary excretory muscles are spared. Motor neuron degeneration caused by ageing similarly affects FF types but not S types; ageing also seems to spare ocular motor pools. These similar patterns of neurodegeneration in three different diseases have led researchers to speculate that slow-twitch motor neurons, along with motor pools of the eyes and excretory muscles, have intrinsic neuroprotective properties that are not disease-specific. Research is currently being conducted to discover a possible molecular basis for neuroprotection in these cell types. Motor pool (neuroscience)

neg: Exhalation This is referred to as the corticospinal pathway or ascending respiratory pathway. The pathway of the electrical signal starts in the motor cortex, goes to the spinal cord, and then to the respiratory muscles. The spinal neurons connect directly to the respiratory muscles. Initiation of voluntary contraction and relaxation of the internal and external internal costals has been shown to take place in the superior portion of the primary motor cortex. Posterior to the location of thoracic control (within the superior portion of the primary motor cortex) is the center for diaphragm control. Studies indicate that there are numerous other

neg: Alternating hemiplegia majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve

neg: Nucleus ambiguus Nucleus ambiguus The nucleus ambiguus (literally "ambiguous nucleus") is a group of large motor neurons, situated deep in the medullary reticular formation named by Jacob Clarke. The nucleus ambiguus contains the cell bodies of nerves that innervate the muscles of the soft palate, pharynx, and larynx which are strongly associated with speech and swallowing. As well as motor neurons, the nucleus ambiguus in its "external formation" contains cholinergic preganglionic parasympathetic neurons for the heart. It is a region of histologically disparate cells located just dorsal (posterior) to the inferior olivary nucleus in the lateral portion of the upper (rostral) medulla.

neg: Motor nerve both sensory and motor nerves called mixed nerves. Motor nerve fibers transduce signals from the CNS to peripheral neurons of proximal muscle tissue. Motor nerve axon terminals innervate skeletal and smooth muscle, as they are heavily involved in muscle control. Motor nerves tend to be rich in Acetylcholine vesicles because the motor nerve, a bundle of motor nerve axons that deliver motor signals and signal for movement and motor control. Calcium vesicles reside in the axon terminals of the motor nerve bundles. The high calcium concentration outside of presynaptic motor nerves increases the size of EPPs (End-Plate potentials). Within motor

neg: Motor neuron of a muscle fiber to a neurotransmitter can only be excitatory, in other words, contractile. Muscle relaxation and inhibition of muscle contraction in vertebrates is obtained only by inhibition of the motor neuron itself. This is how muscle relaxants work by acting on the motor neurons that innervate muscles (by decreasing their electrophysiological activity) or on cholinergic neuromuscular junctions, rather than on the muscles themselves. These are also known as "branchial motor neurons", which are involved in facial expression, mastication, phonation, and swallowing. Associated cranial nerves are the oculomotor, abducens, trochlear, and hypoglossal nerves. These motor neurons indirectly innervate cardiac

neg: Motor control shown that the open loop control can be adapted to different disease conditions and can therefore be used to extract signatures of different motor disorders by varying the cost functional governing the system. A core motor control issue is coordinating the various components of the motor system to act in unison to produce movement. The motor system is highly complex, composed of many interacting parts at many different organizational levels Peripheral neurons receive input from the central nervous system and innervate the muscles. In turn, muscles generate forces which actuate joints. Getting the pieces to work together is a challenging

neg: Premovement neuronal activity of the activity of the upper motor neurons, which ultimately determine activity of the lower motor neurons. The basal ganglia include groups of motor nuclei located deep within the cerebral hemispheres, including the corpus striatum, which contains two nuclei named the caudate and putamen, and also the pallidum, which contains the globus pallidus and substantia nigra pars reticulate. The corpus striatum is the main input center of the basal ganglia, specifically upper neurons of motor areas in the frontal lobe that control eye movement link to neurons in the caudate, while upper neurons from pre-motor and motor cortices in the

neg: Multifocal motor neuropathy Multifocal motor neuropathy Multifocal motor neuropathy (MMN) is a progressively worsening condition where muscles in the extremities gradually weaken. The disorder, a pure motor neuropathy syndrome, is sometimes mistaken for amyotrophic lateral sclerosis (ALS) because of the similarity in the clinical picture, especially if muscle fasciculations are present. MMN is thought to be autoimmune. It was first described in the mid-1980s. Unlike ALS which affects both upper and lower motor neuron pathways, MMN involves only the lower motor neuron pathway and specifically, the peripheral nerves emanating from the lower motor neurons. Definitive diagnosis is often difficult, and many MMN patients

neg: Upper motor neuron syndrome are occurring. Elements of assessment will include analysis of posture, active movement, muscle strength, movement control and coordination, and endurance, as well as muscle tone and spasticity. Impaired muscles typically demonstrate a loss of selective movement, including a loss of eccentric control (decreased ability to actively lengthen); this decreased active lengthening of a muscle is a key factor that limits motor control. While multiple muscles in a limb are usually affected in the Upper Motor Neuron Syndrome, there is usually an imbalance of muscle activity (muscle tone), such that there is a stronger pull on one side of a joint,

neg: Upper motor neuron syndrome motor neuron syndrome". The saying refers to lower motor neuron symptoms in the upper extremity (arm) and upper motor neurons symptoms in the lower extremity (leg). Health professionals' understanding of impairments in muscles after an upper motor neuron lesion has progressed considerably in recent decades. However, a diagnosis of "spasticity" is still often used interchangeably with upper motor neuron syndrome, and it is not unusual to see patients labeled as spastic who demonstrate an array of UMN findings. Spasticity is an exaggerated stretch reflex, which means that a muscle has a reflex contraction when stretched, and that this contraction is

neg: Aging movement control Aging movement control Normal aging movement control in humans is about the changes in the muscles, motor neurons, nerves, sensory functions, gait, fatigue, visual and manual responses, in men and women as they get older but who do not have neurological, muscular (atrophy, dystrophy...) or neuromuscular disorder. With aging, neuromuscular movements are impaired, though with training or practice, some aspects may be prevented. For voluntary force production, action potentials occur in the cortex. They propagate in the spinal cord, the motor neurons and the set of muscle fibers they innervate. This results in a twitch which properties are driven by

neg: Hypertonia by upper motor neuron lesions which may result from injury, disease, or conditions that involve damage to the central nervous system. The lack of or decrease in upper motor neuron function leads to loss of inhibition with resultant hyperactivity of lower motor neurons. Different patterns of muscle weakness or hyperactivity can occur based on the location of the lesion, causing a multitude of neurological symptoms, including spasticity, rigidity, or dystonia. Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles, shock-like contractions of all or part of a group of muscles, and abnormal muscle tone. It is seen

neg: Alpha motor neuron spontaneous, involuntary muscle contractions. Diseases that impair signaling between α-MNs and extrafusal muscle fibers, namely diseases of the neuromuscular junction have similar signs to those that occur with α-MN disease. For example, myasthenia gravis is an autoimmune disease that prevents signaling across the neuromuscular junction, which results in functional denervation of muscle. Alpha motor neuron Alpha (α) motor neurons (also called alpha motoneurons), are large, multipolar lower motor neurons of the brainstem and spinal cord. They innervate extrafusal muscle fibers of skeletal muscle and are directly responsible for initiating their contraction. Alpha motor neurons are distinct from gamma motor neurons,

neg: Muscle contraction same. In contrast, a muscle contraction is isotonic if muscle tension remains the same throughout the contraction. If the muscle length shortens, the contraction is concentric; if the muscle length lengthens, the contraction is eccentric. In natural movements that underlie locomotor activity, muscle contractions are multifaceted as they are able to produce changes in length and tension in a time-varying manner. Therefore, neither length nor tension is likely to remain the same in muscles that contract during locomotor activity. In vertebrates, skeletal muscle contractions are neurogenic as they require synaptic input from motor neurons to produce muscle contractions. A single

neg: Skeletal muscle individuals can voluntarily produce this rumbling sound by contracting the tensor tympani muscle of the middle ear. The rumbling sound can also be heard when the neck or jaw muscles are highly tensed. Skeletal muscle fiber-type phenotype in adult animals is regulated by several independent signaling pathways. These include pathways involved with the Ras/mitogen-activated protein kinase (MAPK) pathway, calcineurin, calcium/calmodulin-dependent protein kinase IV, and the peroxisome proliferator γ coactivator 1 (PGC-1). The Ras/MAPK signaling pathway links the motor neurons and signaling systems, coupling excitation and transcription regulation to promote the nerve-dependent induction of the slow program in regenerating muscle. Calcineurin,

neg: Extrafusal muscle fiber muscle fibers are not to be confused with intrafusal muscle fibers, which are innervated by sensory nerve endings in central noncontractile parts and by gamma motor neurons in contractile ends and thus serve as a sensory proprioceptor. Extrafusal muscle fibers can be generated in vitro (in a dish) from pluripotent stem cells through directed differentiation. This allows study of their formation and physiology. Extrafusal muscle fiber Extrafusal muscle fibers are the skeletal standard muscle fibers that are innervated by alpha motor neurons and generate tension by contracting, thereby allowing for skeletal movement. They make up the large mass of skeletal

neg: Motor nerve types. Beta motor neurons innervate intrafusal fibers of muscle spindles. These nerves are responsible for signaling slow twitch muscle fibers. Gamma motor neurons, unlike alpha motor neurons, are not directly involved in muscle contraction. The nerves associated with these neurons do not send signals that directly adjust the shortening or lengthening of muscle fibers. However, these nerves are important in keeping muscle spindles taut. Motor neural degeneration is the progressive weakening of neural tissues and connections in the nervous system. Muscles begin to weaken as there are no longer any motor nerves or pathways that allows for muscle innervation. Motor

neg: Primary motor cortex body is cleanly segregated. Yet it is not a map of individuated muscles or even individuated body parts. The map contains considerable overlap. This overlap increases in more anterior regions of the primary motor cortex. One of the main goals in the history of work on the motor cortex was to determine just how much the different body parts are overlapped or segregated in the motor cortex. Researchers who addressed this issue found that the map of the hand, arm, and shoulder contained extensive overlap. Studies that map the precise functional connectivity from cortical neurons to muscles show that even

neg: Gamma motor neuron beta motor neurons and gamma motor neurons. Because beta motor neurons innervate extrafusal as well as intrafusal muscle fibers, they are more specifically named skeletofusimotor neurons. Gamma motor neurons are the efferent (sending signals away from the central nervous system) part of the fusimotor system, whereas muscle spindles are the afferent part, as they send signals relaying information from muscles toward the spinal cord and brain. Gamma bias is gamma motor neurons' consistent level of activity. Smaller neurons require a smaller amount of excitatory input to reach its threshold compared to larger neurons. Therefore, gamma motor neurons (smaller in size

neg: Respiratory tract exhaled through the lower respiratory tract and then the upper, to complete the process of breathing. Unlike the trachea and bronchi, the upper airway is a collapsible, compliant tube. As such, it has to be able to withstand suction pressures generated by the rhythmic contraction of the diaphragm that sucks air into the lungs. This is accomplished by the rhythmic contraction of upper airway muscles, such as the genioglossus (tongue) and the hyoid muscles. In addition to rhythmic innervation from the respiratory center in the medulla oblongata, the motor neurons controlling the muscles also receive tonic innervation that sets a

neg: Epigenetics of neurodegenerative diseases walk or use their arms and eventually develop difficulty speaking, swallowing and breathing. Most patients retain cognitive function and sensory neurons are generally unaffected. Patients are often diagnosed after the age of 40 and the median survival time from onset to death is around 3–4 years. In the final stages, patients can lose voluntary control of eye muscles and often die of respiratory failure or pneumonia as a result of degeneration of the motor neurons and muscles required for breathing. Currently there is no cure for ALS, only treatments that may prolong life. To date, multiple genes and proteins have

neg: Sam Schmidt Paralysis Foundation region of the brain that controls voluntary movement, send their axons through the corticospinal tract to connect with motor neurons in the spinal cord. The spinal motor neurons project out of the cord to the correct muscles via the ventral root. These connections control conscious movements like writing and running. Information also flows in the opposite direction, resulting in involuntary movement. Sensory neurons provide feedback to the brain via the dorsal root. Some of the sensory information is conveyed directly to lower motor neurons before it reaches the brain, resulting in involuntary or reflex movements. The remaining sensory information travels

neg: Grey column spinal cord, is part of the sympathetic nervous system and receives input from brain stem, organs, and hypothalamus. The lateral column is only present in the thoracic region and upper lumbar segments. The lateral grey column contains neurons supplying nerves to the muscles of the limbs, preganglionic cell bodies of the autonomic nervous system and sensory relay neurons. Neurons in the anterior column have been shown to be affected by amyotrophic lateral sclerosis (ALS). The number of large alpha motor neurons and medium gamma motor neurons was greatly reduced and the number of small neurons was either slightly or greatly

neg: Motor neuron disease to individual articles for the diagnostic methods used in each individual motor neuron disease. There are no known curative treatments for the majority of motor neuron disorders. Please refer to the articles on individual disorders for more details. The table below lists life expectancy for patients who are diagnosed with MND. Motor neuron disease Motor neuron diseases (MNDs) are a group of neurodegenerative disorders that selectively affect motor neurons, the cells which control voluntary muscles of the body. Commonly, the following disorders are counted among motor neuron diseases: The term “motor neuron disease” sometimes refers to ALS, but in this

neg: Microexpression In E.I. attunement is an unconscious synchrony that guides empathy, and report. attunement relies heavily on nonverbal communication. Looping is where facial expressions can elicit involuntary behavior, In the research motor mimicry there shows neurons that pick up on facial expressions and communicate with motor neurons responsible for muscles in the face to display the same facial expression. Thus displaying a smile may elicit a micro expression of a smile on someone who is trying to remain neutral in their expression. Through fMRI we can see the area where these Mirror neurons are located lights up when you show the

neg: Grey column manner as the muscles they innervate. Alpha motor neurons innervate extrafusal muscle fibers that generate force at neuromuscular junctions at the start of muscle contraction. They have large cell bodies and receive proprioceptive input. They have been shown to reduce in population, but not in size with age. Damage to these cell bodies can lead to severe muscle weakness and loss of reflexes. Gamma motor neurons innervate intrafusal muscle fibers that control the sensitivity of muscle spindles to stretch. They have smaller cell bodies than alpha motor neurons and do not receive proprioceptive input. They have been shown to reduce

neg: Halteres afferents originating from the forewing were also shown to converge in the same regions. Not every specific target for the haltere afferents have been determined, but a few connections between motor neurons known to be involved in wing steering control and particular haltere sensory fields have been identified, particularly one synapse between the haltere nerve and a wing steering motor neuron known as mnb1. Flies use indirect flight muscles to accomplish wing movement, and the beating haltere movements are driven by the same group of muscles (see dynamics section). In addition to the indirect flight muscles which are responsible for

neg: Aging movement control and old adults seemed to use these resources to improve their cognitive performance under dual-task conditions. Aging movement control Normal aging movement control in humans is about the changes in the muscles, motor neurons, nerves, sensory functions, gait, fatigue, visual and manual responses, in men and women as they get older but who do not have neurological, muscular (atrophy, dystrophy...) or neuromuscular disorder. With aging, neuromuscular movements are impaired, though with training or practice, some aspects may be prevented. For voluntary force production, action potentials occur in the cortex. They propagate in the spinal cord, the motor neurons and the

neg: Nervous system target is a set of spinal interneurons that project to motor neurons controlling the arm muscles. The interneurons excite the motor neurons, and if the excitation is strong enough, some of the motor neurons generate action potentials, which travel down their axons to the point where they make excitatory synaptic contacts with muscle cells. The excitatory signals induce contraction of the muscle cells, which causes the joint angles in the arm to change, pulling the arm away. In reality, this straightforward schema is subject to numerous complications. Although for the simplest reflexes there are short neural paths from sensory neuron

neg: Esophagus The esophagus is innervated by the vagus nerve and the cervical and thoracic sympathetic trunk. The vagus nerve has a parasympathetic function, supplying the muscles of the esophagus and stimulating glandular contraction. Two sets of nerve fibers travel in the vagus nerve to supply the muscles. The upper striated muscle, and upper esophageal sphincter, are supplied by neurons with bodies in the nucleus ambiguus, whereas fibers that supply the smooth muscle and lower esophageal sphincter have bodies situated in the dorsal motor nucleus. The vagus nerve plays the primary role in initiating peristalsis. The sympathetic trunk has a sympathetic function.

neg: Motor pool (neuroscience) Motor pool (neuroscience) A motor pool consists of all individual motor neurons that innervate a single muscle. Each individual muscle fiber is innervated by only one motor neuron, but one motor neuron may innervate several muscle fibers. This distinction is physiologically significant because the size of a given motor pool determines the activity of the muscle it innervates: for example, muscles responsible for finer movements are innervated by motor pools consisting of higher numbers of individual motor neurons. Motor pools are also distinguished by the different classes of motor neurons that they contain. The size, composition, and anatomical location of

neg: Amyotrophic lateral sclerosis can be classified a few different ways: by how fast the disease progresses (slow vs fast progressors), by whether it is inherited or sporadic, and by where it starts. In about 25% of cases, muscles in the face, mouth, and throat are affected first, because motor neurons in the part of the brain stem called the medulla oblongata (formerly called the "bulb") start to die first along with lower motor neurons. This form is called "bulbar onset". In about 5% of cases muscles in the trunk of the body are affected first. In most cases the disease spreads and affects

neg: Neuroeffector junction Neuroeffector junction A neuroeffector junction is a site where a motor neuron releases a neurotransmitter to affect a target—non-neuronal—cell. This junction functions like a synapse. However, unlike most neurons, somatic efferent motor neurons innervate skeletal muscle, and are always excitatory. Visceral efferent neurons innervate smooth muscle, cardiac muscle, and glands, and have the ability to be either excitatory or inhibitory in function. Neuroeffector junctions are known as neuromuscular junctions when the target cell is a muscle fiber. Non-synaptic transmission is characteristic of autonomic neuroeffector junctions. The structure of the autonomic neuromuscular junction consists of several essential features including that: the

neg: Neuroeffector junction afferents and ICC-IM within the stomach wall (Fig. 5) and their absence in mutant animals that lack ICC-IM also supports a role for ICC-IM as possible integrators for in-series stretch-dependent changes in this organ. Neuroeffector junction A neuroeffector junction is a site where a motor neuron releases a neurotransmitter to affect a target—non-neuronal—cell. This junction functions like a synapse. However, unlike most neurons, somatic efferent motor neurons innervate skeletal muscle, and are always excitatory. Visceral efferent neurons innervate smooth muscle, cardiac muscle, and glands, and have the ability to be either excitatory or inhibitory in function. Neuroeffector junctions are known