Books: 'Neuromuscular development'

1

Fondazione Pierfranco e Luisa Mariani. Postgraduate Course. Neuromuscular diseases during development. London: John Libbey, 1997.

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2

David, Evered, and Whelan Julie, eds. Plasticity of the neuromuscular system. Chichester: Wiley, 1988.

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3

McGraw, Myrtle B. The neuromuscular maturation of the human infant. London: Mac Keith Press, 1989.

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4

Budnik, Vivian. The fly neuromuscular junction: Structure and function. 2nd ed. San Diego, Calif: Elsevier/Academic Press, 2006.

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5

Vivian, Budnik, and Ruiz-Cãnada Catalina, eds. The Fly neuromuscular junction: Structure and function. 2nd ed. San Diego, Calif: Elsevier/Academic Press, 2006.

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6

W, Winlow, and McCrohan C. R, eds. Growth and plasticity of neural connections. Manchester, UK: Manchester University Press, 1987.

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7

Standring, Janette. The development and evaluation of a muscle strength and functional assessment protocol foruse in the management of patients with neuromuscular diseases. Manchester: University of Manchester, 1994.

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8

Yi, Su-rang. Noe sonsang hwanja ŭi undong mabi chaehwal chʻiryo pʻŭrogŭraem i naejang toen hyudaeyong sinʼgyŏng kŭnyuk chŏnʼgi chagŭkki ŭi kaebal mit sangpʻumhwa =: Development of pre-programmed portable neuromuscular electrical stimulator (PPP-NMES) for rehabilitation of motor dysfunction due to brain injury. [Seoul]: Pogŏn Pokchibu, 2007.

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9

Meade, Vickie. Partners in movement: A family-centered approach to pediatric kinesiology. San Antonio, Tx: Therapy Skill Builders, 1998.

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10

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

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11

M, Kelly Alan, and Blau Helen M, eds. Neuromuscular development and disease. New York: Raven Press, 1992.

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12

Comelio, F., F. Cornelio, G. Lanzi, and E. Fedrizzi. Neuromuscular Diseases During Development. John Libbey Eurotext Limited, 1997.

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13

Takahashi, Masanori P., and Tsuyoshi Matsumura. Myotonic Dystrophy: Disease Mechanism, Current Management and Therapeutic Development. Springer, 2018.

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14

Takahashi, Masanori P., and Tsuyoshi Matsumura. Myotonic Dystrophy: Disease Mechanism, Current Management and Therapeutic Development. Springer, 2018.

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15

Kuwabara, Satoshi. Neuromuscular junction disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0014.

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Ten seminal papers on disorders of the neuromuscular junction are described, covering historical aspects, recent advances in immunological, biological, and genetic researches, and future perspectives. Early descriptions of myasthenia gravis (MG) date back to the seventeenth century, and MG acquired its name in the nineteenth century. The first symptomatic treatment with cholinesterase inhibitors was reported in 1934, leading to the development of modern immunological therapies. Following the discovery of anti-MuSK (muscle-specific tyrosine kinase) antibody in 2001, MG is currently classified into three categories: AChR-positive, MuSK-positive, and dual-seronegative. Lambert-Eaton myasthenic syndrome was recognized in 1956, followed by the discovery of antibodies to voltage-gated calcium channels in the pre-synaptic membrane, facilitating diagnosis and improving the understanding of the pathophysiological mechanisms. Since the late twentieth century, many types of congenital myasthenic syndromes with pre-synaptic, synaptic, and post-synaptic defects have been identified, and a classification based on molecular genetics is in evolution.

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16

Hunter, Jennifer M., and Thomas Fuchs-Buder. Neuromuscular blockade and reversal. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0016.

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Over the past 70 years since the introduction of d-tubocurarine, the search for an ideal neuromuscular blocking agent has led to the development of the depolarizing drug, succinylcholine (suxamethonium), with its rapid onset of action and plasma metabolism, and a series of non-depolarizing agents of which there are two groups: benzylisoquinoliniums (e.g. atracurium, cisatracurium and mivacurium) and aminosteroidal agents (e.g. pancuronium, vecuronium and rocuronium). The need to monitor neuromuscular block perioperatively to ensure the appropriate dose of any neuromuscular blocking drug is given has led to the development of several nerve stimulation techniques. Particularly useful clinically are the train-of-four twitch response, double-burst stimulation, and the post-tetanic count. Their benefits and limitations are considered in this chapter. The most suitable equipment to monitor neuromuscular block and the appropriate anatomical sites for stimulation are discussed. To prevent residual block with its pathophysiological consequences such as upper airway and pharyngeal dysfunction and potential respiratory failure at the end of surgery, antagonizing agents are used. These are of two types: anticholinesterases such as neostigmine and edrophonium, and the γ‎-cyclodextrin, sugammadex. The pharmacodynamics and pharmacokinetics of neuromuscular blocking drugs and their antagonists are altered by the extremes of age, obesity, and several disease states including renal and hepatic failure, neuromuscular disorders, and critical illness. The altered response to all these drugs in these pathologies, which is related to their metabolism and excretion, is considered in detail, together with their other side-effects including the particular disadvantages to the use of succinylcholine.

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17

Deep Tissue Massage Treatment: A Handbook of Neuromuscular Therapy (Mosby's Massage Career Development). Mosby, 2006.

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18

Gerovasili, Vasiliki, and Serafim N. Nanas. Neuromuscular Electrical Stimulation: A New Therapeutic and Rehabilitation Strategy in the ICU. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0044.

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Many critically ill patients undergo a period of immobilization with detrimental effects on skeletal muscle, effects which seem most pronounced in the first days of critical illness. Diagnosis of intensive care unit muscle weakness (ICUAW) is often made after discontinuation of sedation when significant nerve and/or muscle damage may already have occurred. Recently, there has been interest in early mobilization during the acute phase of critical illness, with the goal of preventing ICUAW. Neuromuscular electrical stimulation (NEMS) is an alternative form of exercise that has been successfully used in patients with advanced chronic obstructive pulmonary disease (COPD) and chronic heart failure. NEMS is a rehabilitation tool that can be used in critically ill, sedated patients, does not require patient cooperation, and is therefore a promising intervention to prevent muscle dysfunction in the critically ill. When applied early during the course of critical illness, NEMS can preserve muscle morphology and function. Available evidence suggests that NEMS may have a preventive role in the development of ICUAW and could even contribute to a shorter duration of weaning from mechanical ventilation. Studies are needed to evaluate the long-term effect of NEMS and to explore NEMS settings and delivery characteristics most appropriate for different subgroups of critically ill patients.

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19

(Editor), Vivian Budnik, and Catalina Ruiz-Canada (Editor), eds. The Fly Neuromuscular Junction: Structure and Function, Volume 75: Second Edition (International Review of Neurobiology) (International Review of Neurobiology). Academic Press, 2006.

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20

(Editor), Vivian Budnik, and Catalina Ruiz-Canada (Editor), eds. The Fly Neuromuscular Junction: Structure and Function, Volume 75: Second Edition (International Review of Neurobiology) (International Review of Neurobiology). 2nd ed. Academic Press, 2006.

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21

Mcgraw. Neuromuscular Maturation Infnt (Classics in Developmental Medicine). MacKeith Press, 1993.

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22

Camilleri, Michael. Mayo Clinic Illustrated Textbook of Neurogastroenterology. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197512104.001.0001.

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Mayo Clinic Illustrated Textbook of Neurogastroenterology reflects experience covering the spectrum and maturation of the field of gastrointestinal motility— from studies of exotic patterns of myoelectric recordings in research laboratories to a clinical discipline with major advances in the clinical management of thousands of patients seen by gastroenterologists, primary care physicians, surgeons, or neurologists. Development of the specialty has been characterized by advances in imaging, developments of methods to measure diverse motor and sensory functions from the stomach to the anorectum, introduction of genetic testing, and a plethora of novel pharmacologic and interventional therapies that have revolutionized its practice. The book covers the spectrum of neurogastroenterologic disorders: from those that are associated with genetic and molecular disorders, through disturbances of the extrinsic neural control or the enteric neuromuscular apparatus, to dysfunction associated with disorders of the gut-brain axis; it reflects a desire to pass on clinical and mechanistic insights and advances in therapies that are relevant to a diverse spectrum of clinicians or clinicians in training who care for the estimated 40% of patients presenting to gastroenterologists with symptoms suggestive of disorders of stomach, intestinal, colonic, or anorectal function.

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23

Sandra, Hall, and Oregon Health Sciences University. Crippled Children's Division., eds. Selected articles on feeding children who have a neuromuscular disorder. Portland, OR: Crippled Children's Division - University Affiliated Program, Child Development and Rehabilitation Center, Oregon Health Sciences University, 1987.

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24

Stålberg, Erik. Electromyography. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0007.

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Electromyography (EMG) has been used since the 1940s in the diagnosis of neuromuscular disorders. It has particularly developed with the advent of computers and recording equipment with integrated software. This has made methods of analysis fast, robust, and precise, helping to deal with increasing numbers of patients. Indications have changed dynamically over the years, with the development of new EMG methods themselves and complementary methods used in this field for diagnosis such as histochemistry, genetics, and imaging techniques. This chapter focuses mainly on the routine methods based on recordings with concentric or monopolar needle electrodes, but will also briefly review some of the other EMG methods. There is an increasing understanding of the relationship between the generators (muscle fibres) and the recorded signal that helps interpretation of the recordings. The parameters used for quantitation of the EMG signal are discussed. The findings in pathological conditions are discussed and some practical hints on EMG studies given.

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25

McGraw, Myrtle B. The Neuromuscular Maturation of the Human Infant (Classics in Developmental Medicine (Mac Keith Press)). Cambridge University Press, 1991.

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26

Jones, R. M. Recent Developments in Muscle Relaxation. Royal Society of Medicine, 1988.

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27

M, Jones R., Payne J. P. 1922-, and Royal Society of Medicine Services (Great Britain), eds. Recent developments in muscle relaxation: Atracurium in perspective. London: Royal Society of Medicine Services, 1988.

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28

Leung, Doris G. Other Proven and Putative Autoimmune Disorders of the Peripheral Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0098.

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Myasthenia gravis is in most cases an autoimmune disorder of the neuromuscular junction in which antibodies are directed at nicotinic acetylcholine receptors or other synaptic proteins, such as the MusK protein that is involved in the formation of the formation and maturation of the motor endplate. Less commonly, myasthenia gravis can result from antibodies directed to presynaptic calcium channels as a side effect of paraneoplastic antibodies (Lambert-Eaton syndrome) or from a developmental paucity of acetylcholine receptors in the neonatal form of the disease. Treatment is usually a combination of aceetylcoholinesterase inhibitors such as pyridostigmine to prolong the life of acetylcholine released at the neuromuscular junction and/or drugs such as corticosteroids aimed at reducing inflammation.

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29

Goode, Jamie A., and Gregory R. Bock. Growth Factors As Drugs for Neurological and Sensory Disorders. Wiley & Sons, Incorporated, John, 2008.

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30

Symposium, CIBA Foundation, Jamie A. Goode, and Gregory R. Bock. Growth Factors as Drugs for Neurological and Sensory Disorders. Wiley & Sons, Limited, John, 2007.

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31

Meade, Vickie, and T. V. Meade. Partners in Movement: A Family-Centered Approach to Pediatric Kinesiology. Academic Press, 1999.

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32

Meade, Vickie. Partners in Movement: A Family-Centered Approach to Pediatric Kinesiology. Therapy Skill Builders, 1999.

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33

Meade, Vickie, and T. V. Meade. Partners in Movement: A Family-Centered Approach to Pediatric Kinesiology. Academic Press, 1999.

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34

Misra, V. Peter, and Santiago Catania. EMG-guided botulinum toxin therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0026.

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This chapter explains the mechanism by which botulinum neurotoxin (BoNT) causes its neuromuscular paralytic effects, and reviews the developments that led these effects to be harnessed therapeutically. It specifically focuses upon the conditions of dystonia and spasticity. Within the spectrum of these diseases, it discusses those situations where BoNT injections are the treatment of choice. The very accurate targeting of BoNT into specific muscles in many situations is both desirable and crucial in some situations BoNT’s therapeutic neuroparalytic effect may need to be restricted to a single muscle fascicle.. In some cases, an inaccurately placed injection may be associated with unacceptable side effects. In order to achieve accuracy of BoNT injection delivery, intramuscular injections of BoNT aided by electromyography (EMG) guidance allows the very accurate targeting of specific muscles. The practical aspects related to the preparation of BoNT for injection and the methodology and techniques for injecting using EMG guidance are discussed. The importance of good anatomical knowledge and the relevant EMG techniques to target individual muscles are highlighted and applied to injection of muscles in different body areas. Finally, certain diagnostic neurophysiological tests, which may be useful for the management of some neurological conditions that are treated by BoNT are briefly discussed.

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35

McKenzie, Alistair G. The history of anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0031.

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Even though ether was prepared in 1540 and nitrous oxide in 1774, it was not until the 1840s that these agents were used to induce anaesthesia to enable painless surgery. Modern inhalation anaesthesia has evolved from the public demonstration of ether anaesthesia by William Morton at the Massachusetts General Hospital, Boston, United States, on 16 October 1846. In the United Kingdom, from 1847 John Snow applied scientific principles to develop safer anaesthetic practice. Newer and safer agents have replaced ether in most countries. Successful intravenous anaesthesia began with chloral hydrate in 1874; progress was hesitant until the wide acceptance of thiopental from 1934—in turn superseded by propofol from 1985. Regional anaesthesia has evolved from the first use of the local anaesthetic, cocaine, to enable awake eye surgery by Carl Koller in 1884. This progressed to nerve blocks, spinal and epidural anaesthesia with a high degree of sophistication, through provision of better and safer local anaesthetics: lidocaine and bupivacaine. The introduction of neuromuscular blocking agents into anaesthetic practice began with the use of curare by Griffith and Johnson in Montreal in 1942. Muscle relaxation became a component of ‘balanced anaesthesia’—necessitating advances in airway management, including tracheal intubation and safe mechanical ventilation of the lungs. The modern anaesthetic workstation for inhalation anaesthesia has evolved from the early anaesthetic machines over 100 years. Of all the advances in anaesthesia during the past 50 years, developments in monitoring techniques—particularly pulse oximetry and capnography—have probably made the greatest contribution to patient safety. Anaesthetists have embraced enhanced postoperative recovery.

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36

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

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Books on the topic 'Neuromuscular development'

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