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Published: 4 June 2021
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1

Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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2

Leigh, P. N., and Michael Swash, eds. Motor Neuron Disease. London: Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-1871-8.

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Talbot, Kevin. Motor neuron disease. Oxford: Oxford University Press, 2008.

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4

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

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5

L, Mancini Raffaele, ed. Motor neuron disease research progress. New York: Nova Biomedical Books, 2008.

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6

Orrell, Richard William. Genetics of motor neuron disease. Manchester: University of Manchester, 1996.

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7

Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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8

Talbot, Kevin. Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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9

Motor neuron disease: A practical manual. Oxford: Oxford University Press, 2010.

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10

Motor neuron diseases: Causes, classification, and treatments. Hauppauge, N.Y: Nova Science Publishers, 2011.

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11

The voice in my head is perfect. UK: Cloister House, 2012.

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12

Waging a War against Motor Neuron Disease: On the Frontier of Translational Research for Lou Gehrig's Disease. Saarbrücken: VDM Verlag Dr. Müller, 2009.

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13

Talbot, Paul Richard. Single photon emission computed tomography in the investigation of non-Alzheimer lobar atrophy and motor neuron disease. Manchester: University of Manchester, 1996.

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14

Turner, Martin R. Motor neuron disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0232.

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Motor neuron disease (MND) is characterized by progressive muscular weakness due to simultaneous degeneration of lower and upper motor neurons (L/UMNs). Involvement of LMNs, arising from the anterior horns of the spinal cord and brainstem, leads to secondary wasting as a result of muscle denervation. Involvement of the UMNs of the motor cortex and corticospinal tract results in spasticity. In ~85% of cases, there is clear clinical involvement of both, and the condition is termed ‘amyotrophic lateral sclerosis’ (ALS; a term often used synonymously with MND). In ~13% of cases, there may be only LMN signs apparent, in which case the condition is termed ‘progressive muscular atrophy’, although such cases have a natural history that is to largely identical to that of ALS. In a very small group of patients (~2%), there are only UMN signs for at least the first 4 years, in which case the condition is termed ‘primary lateral sclerosis’; such cases have a uniformly slower progression. There is clinical, neuropathological, and genetic overlap between MND and some forms of frontotemporal dementia.
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15

Thakore, Nimish, and Erik P. Pioro. Types of Motor Neuron Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0022.

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Disorders of lower motor neurons (LMNs, or anterior horn cells) and upper motor neurons (UMNs), jointly termed motor neuron disorders (MNDs), are diverse and numerous. The prototypical MND, namely amyotrophic lateral sclerosis (ALS), a relentlessly progressive lethal disorder of adults, is the subject of another section and will not be discussed further here. Other MNDs include spinal muscular atrophy (SMA), of which there are four types: Kennedy’s disease, Brown-Violetto-Van Laere, and Fazio-Londe syndromes, lower motor neuron disorders as part of neurodegenerations and secondary motor neuron disease as part of malignancy, radiation and infection.
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16

Talbot, Kevin, Martin R. Turner, Rachael Marsden, and Rachel Botell. Motor Neuron Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199547364.001.1.

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Written and designed to provide comprehensive, easily accessible advice for all healthcare professionals involved in the care of patients with this challenging condition, this resource addresses the entire care pathway from presentation to diagnosis to symptom management and end of life issues.
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17

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Disorders of peripheral nerves and motor neuron disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0007.

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This chapter discusses the clinical features and evidence-based drug treatment regimens of polyneuropathies (Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, paraproteinaemic neuropathies, and vasculitic neuropathies), mononeuropathies (Bell’s palsy), systemic conditions with peripheral nerve involvement (Sjögren’s and sarcoidosis), and motor neuron disease (MND).
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18

Kaplan, Tamara, and Tracey Milligan. Motor Neuron Disease (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0018.

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The video in this chapter explores motor neuron disease, including amytrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). It discusses the signs of upper motor neuron (UMN) and lower motor neuron (LMN) pathology, as well as Kennedy disease.
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19

Bromberg, Mark, ed. Motor Neuron Disease in Adults. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199783113.001.0001.

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20

Shaw, Pamela. The motor neurone disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0524.

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The motor neurone diseases are a group of disorders in which there is selective loss of function of upper and/or lower motor neurones in the motor cortex, brainstem, and spinal cord resulting in impairment in the nervous system control of voluntary movement. The term ‘motor neurone disease’, often abbreviated to ‘MND’, is used differently in different countries. In the United Kingdom it is used as an umbrella term to cover the related group of neurodegenerative disorders including amyotrophic lateral sclerosis, the commonest variant, as well as progressive muscular atrophy, primary lateral sclerosis, and progressive bulbar palsy. However, in many other countries amyotrophic lateral sclerosis, referred to as ALS, has been adopted as the umbrella term for this group of clinical variants of motor system degeneration. There is a tendency now internationally to use the ALS/MND abbreviation to cover this group of conditions. Careful diagnosis within the motor neurone diseases is essential for advising about prognosis, potential genetic implications, and for identifying those with acquired lower motor neurone syndromes who may benefit for the administration of immunomodulatory therapy.
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21

S, Kazandjian Marta, and Communication Independence for the Neurologically Impaired, Inc., eds. Communication and swallowing solutions for the ALS/MND community: A CINI manual. San Diego: Singular Pub. Group, 1997.

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22

Communication And Swallowing Solutions for the ALS/MND Community: A CINI Manual. Singular, 1996.

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23

de Carvalho, Mamede, and Michael Swash. Neurophysiology in amyotrophic lateral sclerosis and other motor degenerations. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0022.

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Electromyography is critical for the diagnosis of motor neuron disease, as its findings exclude mimicking disorders, and confirm signs of widespread motor unit loss and reinnervation. In chronic conditions the slow disease course allows giant, stable motor unit potentials to appear. In contrast, in amyotrophic lateral sclerosis, the rapid degenerative process is characterized by signs of denervation and unstable motor unit potentials, where motor units become dysfunctional before having time to sustain very large reinnervated motor unit potentials. Fasciculation potentials are observed in both conditions. In amyotrophic lateral sclerosis fasciculation potentials are important supporting electrodiagnostic evidence, permitting earlier diagnosis. Many methods have been developed to quantify and monitor the lower motor neuron pool, but few have been used in clinical trials. Their role as tools to follow interventions or to interpret pathogenesis remains incompletely explored. Electromyography is a sensitive and reliable test in the diagnosis and assessment of motor neuron diseases.
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24

Paganoni, Sabrina, and Nazem Atassi. Upper Motor Neuron Disorders Hereditary Spastic Paraplegia and Primary Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0032.

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Upper motor neuron (UMN) syndromes are a group of rare, degenerative neurological disorders that are classified as either hereditary spastic paraplegia (HSP) or primary lateral sclerosis (PLS). Our understanding of their underlying pathophysiology is unfortunately very limited and has been a significant barrier to the development of disease-modifying treatments. Recent advances in genetics and in vitro and in vivo disease modeling have provided new insights into disease mechanisms and hold the promise to lead to the future development of mechanism-based therapies.
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25

Watson, Max, Caroline Lucas, Andrew Hoy, and Jo Wells. Palliative care in non-malignant neurological disease. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199234356.003.0029.

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This chapter focuses on the symptom management of multiple sclerosis, Parkinson’s disease, multiple system atrophy (MSA), progressive supranuclear palsy (PSP), motor neuron disease, neurological complications of AIDS, Creutzfeldt-Jakob disease (CJD), and useful contacts.
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26

Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.

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Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
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27

Katirji, Bashar. Case 19. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0023.

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Amyotrophic lateral sclerosis is a fatal neurological disorder, classically presenting with signs of upper motor neuron and lower motor neuron degeneration. Several motor neuron disease variants with purely upper or lower motor neuron degeneration exist. These includes primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. The diagnostic criteria, including El-Escorial criteria and its most recent Awaji revision, are not used in clinical practice and for research purposes. This case highlights the clinical features and electrodiagnostic characteristics of amyotrophic lateral sclerosis. The findings on nerve conduction studies and needle electromyography are emphasized in detail. The role of electrodiagnostic studies in the diagnosis of amyotrophic lateral sclerosis is to establish evidence of lower motor neuron degeneration, confirm its diffuse nature, and exclude treatable causes (such as multifocal motor neuropathy and mimickers of motor neuron disease such as chronic myopathies).
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28

W, Kuncl Ralph, ed. Motor neuron disease. London: W.B. Saunders, 2002.

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29

Motor Neuron Disease. Chapman & Hall, 1993.

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30

Rutherford, Kunel, and John L. R. Forsythe. Motor Neuron Disease. Saunders Ltd., 2002.

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31

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

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32

Talbot, Kevin, and Rachael Marsden. Motor Neuron Disease. Oxford University Press, 2008.

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33

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0018.

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Hyperactive deep tendon reflexes area sign of upper motor neuron lesion. They are also commonly seen in normal but tense people. Proper technique of reflexes examination and experience play a major role in eliciting and categorizing deep tendon reflexes. Clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is ALS due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, PLS, HSP, and other causes of myelopathies should be entertained. Jaw clonus often indicates a lesion above the midpontine level. When hyperreflexia is found, it is wise to look for other features of upper motor neuron dysfunction such as positive Babiniski signs and hypertonia.
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34

Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Neurology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0007.

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This chapter provides information on the ageing brain and nervous system, tremor, neuropathic pain/neuralgia, presentation of Parkinson’s disease, management of Parkinson’s disease, diseases masquerading as Parkinson’s disease, epilepsy and its drug treatment, neuroleptic malignant syndrome, motor neuron disease, peripheral neuropathies, subdural haematoma, sleep and insomnia, and other sleep disorders.
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35

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 72-Year-Old Female with Facial Weakness and Droopy Eyelids. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0030.

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Fatigable weakness is the hallmark of myasthenia gravis (MG). It may present with false localizing signs leading to an itinal incorrect diagnosis of a brainstem stroke. MRI scanning of the brain with specific sequences can rule out the diagnosis of stroke. Differential diagnosis of MG may also include also motor neuron disease. Electromyography is very helpful in confirming the diagnosis of motor neuron disease. The two major diseases of the neuromuscular junction are MG and Lambert-Eaton syndrome (LEMS). A table presents the differing characteristics of each. LEMS can be associated with malignancy and MG with thyoma. Laboratory examinations have greatly assisted in differentiating these two conditions. There is specific antibody testing for each condition. Repetitive stimulation and single fiber electromyography also improve diagnostic acumen.
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36

Eisen, Andrew. Motor neurone disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0009.

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In this chapter, the following ten key events in motor neurone disease, also known as amyotrophic lateral sclerosis (ALS), are considered: the first description of ALS by Cruveilhier; discovery of the first SOD1 mutation; use of the ALSFRS (functional rating scale) for determining therapeutic trial outcomes; the contentious issue of establishing the site of onset of ALS; clinical, pathological, and molecular evidence indicating that frontotemporal dementia and ALS are closely related; demonstration that ALS bears some resemblance to the transmissible spongiform encephalopathies; use of Riluzole as the approved therapy for ALS; the major inflammatory component of ALS; a Guamanian disorder that is biochemically and ultrastructurally similar to that of Alzheimer’s disease; and awareness that the true onset of ALS is unknown but certainly precedes clinical onset by years or decades.
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37

Thakore, Nimish J., and Erik P. Pioro. Clinical Presentations, Diagnostic Criteria, and Lab Testing. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0023.

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Amyotrophic lateral sclerosis (ALS) is the protypical motor neuron disease, which is characterized by the simultaneous presence of upper motor neuron (UMN) and lower motor neuron (LMN) signs in the same extremity or in the cranial-bulbar region. UMN signs at spinal levels include spasticity, slowness of motor activation, hyperactive deep tendon reflexes and extensor plantar responses, whereas UMN signs at the cranial level include spastic dysarthia (slow, labored, nasal); slowness of tongue movements, and hyperactive jaw, gag, and facial reflexes. LMN signs at the spinal level include muscle atrophy, fasciculations, and weakness and LMN signs at the cranial level include tongue atrophy and weakness, facial weakness, tongue and facial fasciculations, palatal weakness, weak cough, and dysphonia. ALA is fatal in 2 to 4 years, and the only medication known to prolong tracheostomy-free survival
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38

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0018.

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Hyperactive deep tendon reflexes (DTRs) is a sign of upper motor neuron (UMN) lesions. It is also commonly seen in normal but anxious people. The proper technique of deep tendon reflex examination and experience play a major role in eliciting and categorizing DTRs. Sustained clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is amyotrophic lateral sclerosis (ALS) due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), and other causes of myelopathies should be entertained. Compressive myelopathies are easily excludable by neuroimaging.
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39

Motor Neuron Disease in Adults. Oxford University Press, Incorporated, 2015.

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40

Strong, Michael J. Dementia and Motor Neuron Disease. Informa Healthcare, 2006.

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41

Strong, Michael, ed. Dementia and Motor Neuron Disease. CRC Press, 2006. http://dx.doi.org/10.1201/9780367800161.

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42

Strong, Michael, and Andrew Kertesz, eds. Dementia and Motor Neuron Disease. CRC Press, 2006. http://dx.doi.org/10.1201/b14376.

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43

J, Strong Michael, ed. Dementia and motor neuron disease. Abingdon [England]: Informa UK Ltd., 2006.

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44

Strong, Michael. Dementia and Motor Neuron Disease. Taylor & Francis Group, 2006.

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45

Monani, Umrao R., and Darryl C. De Vivo. Spinal Muscular Atrophy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0033.

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Spinal muscular atrophy (SMA) is a common, inherited, pediatric motor neuron disorder caused by insufficient SMN protein. As of yet, there is no good treatment for the disease. SMA has an incidence of ~1 in 10,000 newborns carrier frequency of 1 in 50, making it the most common inherited cause of infant mortality. Patients with severe SMA, or Werdnig-Hoffman disease, typically manifest weakness during the first 6 months of life. Such patients are so debilitated that they never sit independently, frequently succumbing to the disease before age 2 years. A much milder form of SMA, Kugelberg-Welander disease, with onset after 18 months of age, often during childhood and characterized by prolonged ambulation and a normal life expectancy, was described in 1956. In 1995 mutations in a novel gene, Survival of Motor Neuron 1 (SMN1), were determined to be the specific cause of SMA.
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46

Leigh, P. N. Motor Neuron Disease: Biology and Management. Springer-Verlag Telos, 1995.

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47

Leigh, P. Nigel. Motor Neuron Disease:: Biology and Management. Springer, 1995.

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48

Leigh, P. N., and Michael Swash. Motor Neuron Disease: Biology and Management. Springer London, Limited, 2012.

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49

Nigel, Leigh P., and Swash Michael, eds. Motor neuron disease: Biology and management. London: Springer-Verlag, 1995.

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50

Leigh, P. N. Motor Neuron Disease: Biology And Management. Springer, 2011.

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