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Libros sobre el tema "Motoneurones"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 7 de julio de 2024

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1

O'Donovan, Michael J. y Mélanie Falgairolle, eds. Vertebrate Motoneurons. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07167-6.

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2

Imaharu, Nakano y Hirano Asao 1926-, eds. Amyotrophic lateral sclerosis: Progress and perspectives in basic research and clinical application : proceedings of the 11th Tokyo Metropolitan Institute for Neuroscience (TMIN) International Symposium, Tokyo, October 25-27, 1995. Amsterdam: Elsevier Science, 1996.

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3

A, Wernig, ed. Plasticity of motoneuronal connections. Amsterdam: Elsevier, 1991.

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4

Stewart, Bryan A. Synaptic plasticity in a regenerated crayfish phasic motoneuron. Ottawa: National Library of Canada, 1992.

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5

Krammer, Eva B., Martin F. Lischka, Thomas P. Egger, Maria Riedl y Helmut Gruber. The Motoneuronal Organization of the Spinal Accessory Nuclear Complex. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-662-10362-3.

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6

1944-, Krammer E. B., ed. The Motoneuronal organization of the spinal accessory nuclear complex. Berlin: Springer-Verlag, 1987.

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7

Orth, Peter M. R. Phosphorylation-dependent plasticity at synapses of a crayfish phasic motoneuron. Ottawa: National Library of Canada, 2002.

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8

Patel, Varsha. Neuromuscular synaptic differentiation of a crab motoneuron in four separate muscles. Ottawa: National Library of Canada, 1996.

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9

Hirji, Rahim. Structure of regenerated synaptic connections of allotransplanted phasic motoneurons on a tonic muscle in crayfish. Ottawa: National Library of Canada, 1999.

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10

Campbell, Jessica J. An investigation into factors affecting motoneuron regeneration in the rat sciatic nerve. Ottawa: National Library of Canada, 1990.

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11

Coulthard, Rosalind Jane. The roles of motoneurons and their muscle targets in synaptogenesis during regeneration of a foreign transplant. Ottawa: National Library of Canada, 1998.

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12

Ju, William Young-Ho. Characterization and manipulation of the reactive astrocyte response following axotomy-induced motoneuronal injury and death. Ottawa: National Library of Canada, 1994.

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13

C, Williams A., ed. Motor neuron disease. London: New York, 1994.

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14

R, Dimitrijevic Milan y Eccles, John C. Sir, 1903-, eds. Upper motor neuron functions and dysfunctions. Basel: Karger, 1985.

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15

Takao, Kumazawa, Kruger Lawrence y Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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16

Falgairolle, Melanie y Michael O'Donovan. Vertebrate Motoneurons. Springer International Publishing AG, 2022.

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17

Burke, David y James Howells. The motor unit. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0002.

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The motor unit represent the final output of the motor system. Each consists of a motoneuron, its axon, neuromuscular junctions, and muscle fibres innervated by that axon. The discharge of a motor unit can be followed by recording its electromyographic signature, the motor unit action potential. Motoneurons are not passive responders to the excitatory and inhibitory influences on them from descending and segmental sources. Their properties can change, e.g. due to descending monoaminergic pathways, which can alter their responses to other inputs (changing ‘reflex gain’). Contraction strength depends on the number of active motor units, their discharge rate, and whether the innervated muscle fibres are slow-twitch producing low force, but resistant to fatigue, fast-twitch producing more force, but susceptible to fatigue, or intermediate fast-twitch fatigue-resistant. These properties are imposed by the parent motoneurons, and the innervated muscle fibres have different histochemical profiles (oxidative, glycolytic, or oxidative-glycolytic, respectively).
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18

Bawa, Parveen N. S., Maria Piotrkiewicz y Annie Schmied, eds. Mechanisms underlying firing in healthy and sick human motoneurons. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-592-3.

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19

The Motoneurone and Its Muscle Fibres (Monographs of the Physiological Society). Oxford University Press, USA, 2006.

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20

Gruber, Helmut, Eva B. Krammer, Martin F. Bach, Thomas P. Egger y Maria Riedl. The Motoneuronal Organization of the Spinal Accessory Nuclear Complex. Springer, 1987.

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21

Jabre, Joe F., M. D. Binder y M. D. Binder. Mechanisms Underlying the Control of Firing in the Healthy and Sick Motoneurone. Elsevier Science Ltd, 1999.

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22

The control of human upper limb motoneurons: Corticospinal projections and sensor motor interactions. Ottawa: National Library of Canada, 1991.

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23

Vetter, Karolina. Vergleich funktioneller neurophysiologischer Veränderungen und klinischer Symptome der oberen und unteren Motoneurone bei ALS-Patienten. 2011.

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24

Mason, Peggy. From Movement to Action. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0023.

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Tracts descending from motor control centers in the brainstem and cortex target motor interneurons and in select cases motoneurons. The mechanisms and constraints of postural control are elaborated and the effect of body mass on posture discussed. Feed-forward reflexes that maintain posture during standing and other conditions of self-motion are described. The role of descending tracts in postural control and the pathological posturing is described. Pyramidal (corticospinal and corticobulbar) and extrapyramidal control of body and face movements is contrasted. Special emphasis is placed on cortical regions and tracts involved in deliberate control of facial expression; these pathways are contrasted with mechanisms for generating emotional facial expressions. The signs associated with lesions of either motoneurons or motor control centers are clearly detailed. The mechanisms and presentation of cerebral palsy are described. Finally, understanding how pre-motor cortical regions generate actions is used to introduce apraxia, a disorder of action.
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25

Mason, Peggy. The Motor Unit and Orderly Recruitment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0021.

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The physiological, metabolic, and anatomical properties of fast- and slow-twitch skeletal muscle fibers are detailed. How the proportions of different types of muscle fibers in a muscle are matched to the functions of that muscle is described. The important concept of the motor unit consisting of the motoneuron and all the muscle fibers it innervates is introduced. The roles of warm-up, orderly recruitment, and tetanus in determining muscle force are elaborated. Examples of muscle fiber recruitment and de-recruitment during natural movements before and after weight-lifting exercise are presented. The large effects of small changes in motoneuron discharge on resulting muscle tension are discussed in the context of exercise and disease. Differences between extraocular and other skeletal muscles in composition and innervation have clinical implications. Finally, students are introduced to electromyography, a minimally invasive clinical test that can be used to assess motor unit function and reveal fibrillations.
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26

Worden, Mary Kate. The physiological role of proctolin as a cotransmitter of an identified skeletal motoneuron in an insect. 1989.

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27

(Editor), Andrew Eisen y Pamela J. Shaw (Editor), eds. Motor Neuron Disorders and Related Diseases: Handbook of Clinical Neurology (Series Editors: Aminoff, Boller and Swaab) (Handbook of Clinical Neurology). Elsevier, 2007.

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28

Mason, Peggy. Spinal Cord. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0004.

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The spinothalamic and lemniscal pathways carry somatosensory information from the periphery into the brain while the corticospinal pathway carries motor commands from the brain to motoneurons of the spinal cord. Following these pathways through the spinal cord allows the student to infer lesion location from symptoms. To exemplify the clinical importance of sympathetic outputs from thoracic segments, Horner syndrome is described. Similarly, the common problems caused by spinal cord injury on sacral parasympathetic functions are stressed. The contributions of specific spinal segments to breathing, hand and foot dexterity, and micturition are emphasized. Working through the logic of the symptoms caused by spinal hemisection (Brown-Séquard syndrome), pyramidal stroke, and syringomyelia provides the student with a clear framework for understanding spinal function in the clinical context.
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29

Witta, Loeiws. Cause Di Crampi Alle Gambe: Neuropatia Periferica, Malattia Del Fegato, Infezione, Disidratazione, Malattia Del Motoneurone, Tossine, Gravidanza, Crampi Notturni Alle Gambe, Farmaci, Esercizio. Independently Published, 2021.

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30

Murray, E. Lee y Veda V. Vedanarayanan. Neuromuscular Disorders. Editado por Karl E. Misulis y E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0021.

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The hospital neurologist may encounter neuromuscular disorders as known chronic conditions that are exacerbated by a hospital stay, be the principal reason for admission, or develop during a prolonged hospitalization. This chapter details the presentation, diagnosis, and management of conditions affecting the peripheral nerves and neuromuscular junction, such as myasthenia gravis, Lambert-Eaton (myasthenic) syndrome, botulism, and tick paralysis; as well as muscular weakness from various causes such as rhabdomyolysis, critical illness neuromyopathy, inflammatory myopathies, muscular dystrophies, periodic paralysis, and metabolic and endocrine myopathies. Also discussed are motoneuron degeneration, including amyotrophic lateral sclerosis and progressive muscle atrophy, and neuromuscular respiratory failure.
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31

Mason, Peggy. Introduction to the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0001.

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The primary regions and principal functions of the central nervous system are introduced through the story of Jean-Dominique Bauby who became locked in after suffering a brainstem stroke. Bauby blinked out his story of locked-in syndrome one letter at a time. The primary deficit of locked-in syndrome is in voluntary movement because pathways from the brain to motoneurons in the brainstem and spinal cord are interrupted. Perception is also disturbed as pathways responsible for transforming sensory stimuli into conscious awareness are interrupted as they ascend through the brainstem into the forebrain. Homeostasis, through which the brain keeps the body alive, is also adversely affected in locked-in syndrome because it depends on the brain, spinal cord and autonomic nervous system. Abstract functions such as memory, language, and emotion depend fully on the forebrain and are intact in locked-in syndrome, as clearly evidenced by Bauby’s eloquent words.
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32

Mason, Peggy. Gaze Control. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0019.

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In addition to serving perception, gaze acts as a powerful social signal and mode of communication. Gaze is altered in several psychiatric diseases and impaired by a variety of central and peripheral lesions. Eye movements that serve to stabilize gaze include the vestibuloocular reflex (VOR) and fixation, whereas eye movements that shift gaze include saccades, cancellation of the VOR, and smooth pursuit. The pontine horizontal gaze center and midbrain vertical gaze center connect to extraocular motoneurons and mediate all eye movements. Neural circuits involved in generating the VOR, horizontal saccades and saccade modulation are described in detail. Nystagmus consequent to unilateral labyrinthine damage is explained. Other forms of nystagmus including the optokinetic response are introduced. The role of internuclear interneurons in coordinating horizontal saccades and their failure in internuclear ophthalmalplegia are detailed. Finally, the mechanisms involved in fixation and smooth pursuit are briefly presented.
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33

Mason, Peggy. Reflexes and Gait. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0022.

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The importance of proprioception to motor function is revealed by the dramatic story of Ian Waterman, a man who lost function in all proprioceptive and tactile spinal afferents. The circuitry of the stretch reflex, termed the deep tendon reflex in clinical circles, is described in detail. In this context, the student is introduced to load, muscle spindles, Ia afferents, α‎- and γ‎- motoneurons, and α‎- γ‎ coactivation. The concept of physiological extensors and flexors is useful for understanding the role of reflexes in normal and abnormal postures. The logic and utility of reflex testing is fully explained and the Ib and nociceptive withdrawal reflexes briefly introduced. Primitive reflexes and their modulation across development and in response to stroke or disease are presented. In a final segment, movements produced by central pattern generators and refined by reflexes are illustrated by a close examination of human gait across the life cycle.
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34

Williams, A. C. Motor Neuron Disease. Chapman & Hall, 1993.

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35

(Editor), John Eccles y Milan R. Dimitrijevic (Editor), eds. Upper Motor Neuron Functions and Dysfunctions. S. Karger AG (Switzerland), 1985.

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36

(Editor), T. Kumazawa, L. Kruger (Editor) y K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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