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Journal articles on the topic 'Motor neuron disease'

To see the other types of publications on this topic, follow the link: Motor neuron disease.

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2024

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1

Cork, Linda C. "Hereditary Canine Spinal Muscular Atrophy: An Animal Model of Motor Neuron Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (August 1991): 432–34. http://dx.doi.org/10.1017/s0317167100032613.

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ABSTRACT:Motor neuron diseases selectively produce degeneration and death of motor neurons; the pathogenesis of these disorders and the specificity for this population of neurons are unknown. Hereditary Canine Spinal Muscular Atrophy produces a lower motor neuron disease which is clinically and pathologically similar to human motor neuron disease: motor neurons dysfunction and degenerate. The canine model provides an opportunity to investigate early stages of disease when there are viable motor neurons still present and might be responsive to a variety of therapeutic interventions. The canine disease, like the human disease, is inherited as an autosomal dominant. The extensive canine pedigree of more than 200 characterized individuals permits genetic analysis using syntenic linkage techniques which may identify a marker for the canine trait and provide insights into homologous regions for study in human kindreds.

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2

Kristensen, O., and B. Melgaard. "MOTOR NEURON DISEASE." Acta Neurologica Scandinavica 56, no. 4 (January 29, 2009): 299–308. http://dx.doi.org/10.1111/j.1600-0404.1977.tb01437.x.

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3

Sonoo, Masahiro. "Motor Neuron Disease." Spinal Surgery 25, no. 3 (2011): 234–41. http://dx.doi.org/10.2531/spinalsurg.25.234.

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4

Talbot, Kevin. "Motor neuron disease." Medicine 32, no. 11 (November 2004): 105–7. http://dx.doi.org/10.1383/medc.32.11.105.53361.

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5

Mills, K. R. "Motor neuron disease." Brain 118, no. 4 (1995): 971–82. http://dx.doi.org/10.1093/brain/118.4.971.

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6

Liveson, Jay. "Motor Neuron Disease." New England Journal of Medicine 334, no. 18 (May 2, 1996): 1203. http://dx.doi.org/10.1056/nejm199605023341818.

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7

Mitchell, J. D. "Motor neuron disease." Neuromuscular Disorders 6, no. 2 (March 1996): 141. http://dx.doi.org/10.1016/s0960-8966(96)90024-3.

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8

Leigh, P. N., and K. Ray-Chaudhuri. "Motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 57, no. 8 (August 1, 1994): 886–96. http://dx.doi.org/10.1136/jnnp.57.8.886.

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9

Westarp, M. E., and H. H. Kornhuber. "Motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 58, no. 2 (February 1, 1995): 269. http://dx.doi.org/10.1136/jnnp.58.2.269.

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10

Dimachkie, Mazen M., and Richard J. Barohn. "Motor Neuron Disease." Neurologic Clinics 33, no. 4 (November 2015): i. http://dx.doi.org/10.1016/s0733-8619(15)00090-0.

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11

Jackson, Carlayne E., and Jeffrey Rosenfeld. "Motor Neuron Disease." Physical Medicine and Rehabilitation Clinics of North America 12, no. 2 (May 2001): 335–52. http://dx.doi.org/10.1016/s1047-9651(18)30073-1.

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12

Dimachkie, Mazen M., and Richard J. Barohn. "Motor Neuron Disease." Neurologic Clinics 33, no. 4 (November 2015): xiii—xiv. http://dx.doi.org/10.1016/j.ncl.2015.09.001.

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13

Laing, Nigel G., Frank L. Mastaglia, and B. A. Kakulas. "Motor Neuron Disease." Trends in Neurosciences 17, no. 11 (January 1994): 505. http://dx.doi.org/10.1016/0166-2236(94)90145-7.

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14

Griffin, John W. "Motor neuron disease." Trends in Neurosciences 18, no. 11 (November 1995): 513–14. http://dx.doi.org/10.1016/0166-2236(95)90053-5.

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15

Kernich, Catherine A. "Motor Neuron Disease." Neurologist 15, no. 1 (January 2009): 49–50. http://dx.doi.org/10.1097/nrl.0b013e31818fb5a2.

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16

Swash, M. "Motor neuron disease." Postgraduate Medical Journal 68, no. 801 (July 1, 1992): 533–37. http://dx.doi.org/10.1136/pgmj.68.801.533.

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17

Genc, Baris, Oge Gozutok, Nuran Kocak, and P. Hande Ozdinler. "The Timing and Extent of Motor Neuron Vulnerability in ALS Correlates with Accumulation of Misfolded SOD1 Protein in the Cortex and in the Spinal Cord." Cells 9, no. 2 (February 22, 2020): 502. http://dx.doi.org/10.3390/cells9020502.

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Understanding the cellular and molecular basis of selective vulnerability has been challenging, especially for motor neuron diseases. Developing drugs that improve the health of neurons that display selective vulnerability relies on in vivo cell-based models and quantitative readout measures that translate to patient outcome. We initially developed and characterized UCHL1-eGFP mice, in which motor neurons are labeled with eGFP that is stable and long-lasting. By crossing UCHL1-eGFP to amyotrophic lateral sclerosis (ALS) disease models, we generated ALS mouse models with fluorescently labeled motor neurons. Their examination over time began to reveal the cellular basis of selective vulnerability even within the related motor neuron pools. Accumulation of misfolded SOD1 protein both in the corticospinal and spinal motor neurons over time correlated with the timing and extent of degeneration. This further proved simultaneous degeneration of both upper and lower motor neurons, and the requirement to consider both upper and lower motor neuron populations in drug discovery efforts. Demonstration of the direct correlation between misfolded SOD1 accumulation and motor neuron degeneration in both cortex and spinal cord is important for building cell-based assays in vivo. Our report sets the stage for shifting focus from mice to diseased neurons for drug discovery efforts, especially for motor neuron diseases.

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18

Souza, Paulo Victor Sgobbi de, Wladimir Bocca Vieira de Rezende Pinto, Flávio Moura Rezende Filho, and Acary Souza Bulle Oliveira. "Far beyond the motor neuron: the role of glial cells in amyotrophic lateral sclerosis." Arquivos de Neuro-Psiquiatria 74, no. 10 (October 2016): 849–54. http://dx.doi.org/10.1590/0004-282x20160117.

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ABSTRACT Motor neuron disease is one of the major groups of neurodegenerative diseases, mainly represented by amyotrophic lateral sclerosis. Despite wide genetic and biochemical data regarding its pathophysiological mechanisms, motor neuron disease develops under a complex network of mechanisms not restricted to the unique functions of the alpha motor neurons but which actually involve diverse functions of glial cell interaction. This review aims to expose some of the leading roles of glial cells in the physiological mechanisms of neuron-glial cell interactions and the mechanisms related to motor neuron survival linked to glial cell functions.

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19

Shannon, P., D. Chitayat, K. Chong, C. Dunham, and C. Fallet-Bianco. "Motor neuron disease presenting with fetal akinesia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S1 (May 2018): S4. http://dx.doi.org/10.1017/cjn.2018.44.

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By contrast to infantile spinal muscular atrophy, which usually links to deletions in the SMN genes, fetal onset motor neuron disease is poorly reported. We collected a series of twelve cases of fetal arthrogryposis (16-31 weeks gestational age) with fetal motor neuron disease and excluded infectious diseases, lysosomal storage disease and neuroaxonal dystrophy. Of these twelve, 3 were thought to be ischemic in nature with microvascular alterations and systemic or central nervous system ischemic injury. The remaining 9 all displayed marked reduction in anterior horn motor neurons. Of these 9, four demonstrated mineralised neurons, four demonstrated either neuronal loss or cavitation in the globus pallidus, and in two, degenerating neurons were detectable in the brainstem or globus pallidus. Specific sequencing of SMN1 was performed in 6 of 9 and was reported as normal. Whole exome sequencing was performed in 4 without definitive diagnosis. We conclude that fetal motor neuron disease can be distinguished from ischemic injury, is morphologically heterogeneous, may affect the globus pallidus and is rarely linked to SMN1 mutations.

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20

Williams, U. E., E. E. Philip-Ephraim, and S. K. Oparah. "Multidisciplinary Interventions in Motor Neuron Disease." Journal of Neurodegenerative Diseases 2014 (November 18, 2014): 1–10. http://dx.doi.org/10.1155/2014/435164.

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Motor neuron disease is a neurodegenerative disease characterized by loss of upper motor neuron in the motor cortex and lower motor neurons in the brain stem and spinal cord. Death occurs 2–4 years after the onset of the disease. A complex interplay of cellular processes such as mitochondrial dysfunction, oxidative stress, excitotoxicity, and impaired axonal transport are proposed pathogenetic processes underlying neuronal cell loss. Currently evidence exists for the use of riluzole as a disease modifying drug; multidisciplinary team care approach to patient management; noninvasive ventilation for respiratory management; botulinum toxin B for sialorrhoea treatment; palliative care throughout the course of the disease; and Modafinil use for fatigue treatment. Further research is needed in management of dysphagia, bronchial secretion, pseudobulbar affect, spasticity, cramps, insomnia, cognitive impairment, and communication in motor neuron disease.

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21

Dr.U.J.JanI, Dr U. J. JanI, Dr Ashwin Patil, Dr Mitesh J. Makawana, Dr KalpeshH Patel, Dr Dignesh Vasava, and Dr TejasChaudhari Dr.TejasChaudhari. "Madras Variant Motor Neuron Disease - A Rare Presentation." International Journal of Scientific Research 3, no. 2 (June 1, 2012): 355–56. http://dx.doi.org/10.15373/22778179/feb2014/114.

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22

Oh, Seong-il, Jin-Sung Park, Jung-Joon Sung, and Seung Hyun Kim. "Clinical Scales Used in Motor Neuron Disease." Journal of the Korean Neurological Association 39, no. 2 Suppl (May 1, 2021): 77–86. http://dx.doi.org/10.17340/jkna.2021.2.22.

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Motor neuron diseases (MND) are heterogeneous spectra of disorders that that primarily affect the motor neurons (MN) resulting in motor nerve and muscle degeneration. The pathophysiological mechanisms of MN cell death are known to be combined with disturbance of proteostasis, ribonucleostasis and exaggerated neuro-inflammation. Amyotrophic lateral sclerosis is the prototypic disease of MND followed by spinal and bulbar muscular atrophy, spinal muscular atrophy, benign focal amyotrophy and other various diseases. Although diverse spectra of these diseases share common symptoms, significant differences are known in their clinical manifestations and their clinical progression. With increasing number of new clinical trials, the importance of selecting appropriate clinical scales for the monitoring of clinical progression in different types of MNDs should be emphasized. The purpose of this review is to illustrate different types of clinical scales and demonstrate how to utilize these in the clinical research field with consensus. With these efforts, we hope to be ready to understand different kinds of clinical scales in MND in participating global standard clinical trials.

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23

Preston, D. C. "Paraneoplastic motor neuron disease." Neurology 40, no. 10 (October 1, 1990): 1638. http://dx.doi.org/10.1212/wnl.40.10.1638.

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24

Evans, B. K., and S. J. Oh. "Paraneoplastic motor neuron disease." Neurology 40, no. 10 (October 1, 1990): 1638. http://dx.doi.org/10.1212/wnl.40.10.1638-a.

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25

Grisold, W., M. Drlicek, and U. Zifko. "Reversible motor neuron disease." Neurology 42, no. 11 (November 1, 1992): 2229. http://dx.doi.org/10.1212/wnl.42.11.2229.

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26

Keppel Hesselink, J. M. "Reversible motor neuron disease." Neurology 42, no. 11 (November 1, 1992): 2229. http://dx.doi.org/10.1212/wnl.42.11.2229-a.

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27

Chad, D., R. B. Layzer, and T. Tucker. "Reversible motor neuron disease." Neurology 42, no. 11 (November 1, 1992): 2230. http://dx.doi.org/10.1212/wnl.42.11.2230.

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28

Divers, T. J., A. Lahunta, H. F. Hintz, R. C. Riis, C. A. Jackson, and H. O. Mohammed. "Equine motor neuron disease." Equine Veterinary Education 13, no. 2 (April 2001): 63–67. http://dx.doi.org/10.1111/j.2042-3292.2001.tb01887.x.

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29

Wijnberg, I. D. "Equine motor neuron disease." Equine Veterinary Education 18, no. 3 (January 5, 2010): 126–29. http://dx.doi.org/10.1111/j.2042-3292.2006.tb00430.x.

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30

Vrbová, Gerta, Linda Greensmith, and Katarzyna Sieradzan. "Motor neuron disease model." Nature 360, no. 6401 (November 1992): 216. http://dx.doi.org/10.1038/360216b0.

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31

Tsai, Ching-Piao, Hsu-Hua Ho, Der-Jen Yen, Vinchi Wang, Kong-Ping Lin, Kwong-Kum Liao, and Zin-An Wu. "Reversible Motor Neuron Disease." European Neurology 33, no. 5 (1993): 387–89. http://dx.doi.org/10.1159/000116977.

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32

Hahn, C., I. Mayhew, and M. Shepherd. "Equine motor neuron disease." Veterinary Record 132, no. 7 (February 13, 1993): 172. http://dx.doi.org/10.1136/vr.132.7.172.

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33

Proudman, C., D. Knottenbelt, and G. Edwards. "Equine motor neuron disease." Veterinary Record 132, no. 8 (February 20, 1993): 198–99. http://dx.doi.org/10.1136/vr.132.8.198.

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34

Prendergast, M., H. Bassett, and J. Cummings. "Equine motor neuron disease." Veterinary Record 135, no. 17 (October 22, 1994): 416. http://dx.doi.org/10.1136/vr.135.17.416-a.

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35

Polak, A. "Assessing motor neuron disease." QJM 95, no. 2 (February 1, 2002): 125. http://dx.doi.org/10.1093/qjmed/95.2.125.

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36

Kacem, I., C. Gnaichia, Y. Hizem, L. Sellami, M. Ben Djebara, A. Gargouri-Berrechid, and R. Gouider. "Paraneoplastic motor neuron disease." Journal of the Neurological Sciences 333 (October 2013): e634. http://dx.doi.org/10.1016/j.jns.2013.07.2201.

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37

Vishnu, Venugopalan Y., Manish Modi, Sudesh Prabhakar, Anil Bhansali, and Manoj Kumar Goyal. "“A” motor neuron disease." Journal of the Neurological Sciences 336, no. 1-2 (January 2014): 251–53. http://dx.doi.org/10.1016/j.jns.2013.10.003.

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38

Divers, Thomas J., Hussni O. Mohammed, and John F. Cummings. "Equine Motor Neuron Disease." Veterinary Clinics of North America: Equine Practice 13, no. 1 (April 1997): 97–105. http://dx.doi.org/10.1016/s0749-0739(17)30258-4.

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39

Divers, Thomas J. "Equine motor neuron disease." Journal of Equine Veterinary Science 25, no. 5 (May 2005): 238. http://dx.doi.org/10.1016/j.jevs.2005.04.010.

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40

Chopra, Aarti, Ravi Kumar, and Girendra Kumar Gautam. "A review: Management of motor neuron diseases." IP Indian Journal of Neurosciences 7, no. 4 (January 15, 2022): 292–94. http://dx.doi.org/10.18231/j.ijn.2021.053.

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Motor neuron diseases are a group of chronic sporadic and hereditary neurological disorders characterized by progressive degeneration of motor neurons. These might affect the upper motor neurons, lower motor neurons, or both. The prognosis of the motor neuron disease depends upon the age at onset and the area of the central nervous system affected. Amyotrophic lateral sclerosis (ALS) has been documented to be fatal within three years of onset. This activity focuses on amyotrophic lateral sclerosis as the prototype of MND, which affects both the upper and the lower motor neurons and discusses the role of inter-professional team in the differential diagnosis, evaluation, treatment, and prognostication. It also discusses various other phenotypes of MND with an emphasis on their distinguishing features in requisite detail.

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41

Dengler, Reinhard. "Detection of upper motor neuron signs in motor neuron disease." Clinical Neurophysiology 119 (October 2008): S144. http://dx.doi.org/10.1016/s1388-2457(08)60520-9.

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42

Winder, Toni R., and Roland N. Auer. "Sensory Neuron Degeneration in Familial Kugelberg-Welander Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 16, no. 1 (February 1989): 67–70. http://dx.doi.org/10.1017/s0317167100028535.

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ABSTRACT:A 53 year old man developed symptoms of motor neuron disease in childhood. There was a family history of a similar disorder and it was felt to represent a form of Kugelberg-Welander disease. In addition to the motor deficits, sensory abnormalities in his legs were documented during life. Autopsy revealed anterior horn cell loss throughout the length of the spinal cord, with preservation of the phrenic nucleus. The lumbar dorsal root ganglia showed active degeneration of sensory neurons, with nuclear changes exceeding cytoplasmic ones. The fasciculus gracilis showed Wallerian degeneration. The findings provide direct evidence that sensory neurons can degenerate in some forms of motor neuron disease, and that the “demyelination” or “degeneration” of posterior columns sometimes seen in the various forms of motor neuron disease may actually be secondary to cell body disease in the dorsal root ganglia.

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43

Barone, Cassandra, and Xin Qi. "Altered Metabolism in Motor Neuron Diseases: Mechanism and Potential Therapeutic Target." Cells 12, no. 11 (June 2, 2023): 1536. http://dx.doi.org/10.3390/cells12111536.

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(Motor Neuron Diseases (MND) are neurological disorders characterized by a loss of varying motor neurons resulting in decreased physical capabilities. Current research is focused on hindering disease progression by determining causes of motor neuron death. Metabolic malfunction has been proposed as a promising topic when targeting motor neuron loss. Alterations in metabolism have also been noted at the neuromuscular junction (NMJ) and skeletal muscle tissue, emphasizing the importance of a cohesive system. Finding metabolism changes consistent throughout both neurons and skeletal muscle tissue could pose as a target for therapeutic intervention. This review will focus on metabolic deficits reported in MNDs and propose potential therapeutic targets for future intervention.

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44

Emmanuel, Ezunu Okechukwu, Akpekpe John, Yusuf Yakub, Oputa Nonye Lawciana, Adoga Esther Atuaje, Ezunu Ngozi Esther, Ogbutor Udoji Godsday, and Mrs Ijeoma Anieto. "Motor Neuron Disease with Descending Paralysis in a 55-Year-old African Man: A Review of the Pattern of Presentation." International Journal of Research and Innovation in Social Science VII, no. VIII (2023): 1603–12. http://dx.doi.org/10.47772/ijriss.2023.7925.

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Motor neuron diseases (MNDs) are neurodegenerative disorders that are distinguished by muscle wasting and loss of muscle strength following the gradual deterioration and death of Motor Neurons. Amyotrophic lateral sclerosis (ALS) is the commonest among MNDs. These diseases are untreatable, with limited disease-modifying therapy options. There is a paucity of research on MNDs in Sub-Saharan Africa, particularly, molecular and genetic-based studies are deficient. We present a case report of a 55-year-old African with a descending form of paralysis of Motor Neuron disease

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45

Carrasco, Dario I., Mark M. Rich, Qingbo Wang, Timothy C. Cope, and Martin J. Pinter. "Activity-Driven Synaptic and Axonal Degeneration in Canine Motor Neuron Disease." Journal of Neurophysiology 92, no. 2 (August 2004): 1175–81. http://dx.doi.org/10.1152/jn.00157.2004.

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The role of neuronal activity in the pathogenesis of neurodegenerative disease is largely unknown. In this study, we examined the effects of increasing motor neuron activity on the pathogenesis of a canine version of inherited motor neuron disease (hereditary canine spinal muscular atrophy). Activity of motor neurons innervating the ankle extensor muscle medial gastrocnemius (MG) was increased by denervating close synergist muscles. In affected animals, 4 wk of synergist denervation accelerated loss of motor-unit function relative to control muscles and decreased motor axon conduction velocities. Slowing of axon conduction was greatest in the most distal portions of motor axons. Morphological analysis of neuromuscular junctions (NMJs) showed that these functional changes were associated with increased loss of intact innervation and with the appearance of significant motor axon and motor terminal sprouting. These effects were not observed in the MG muscles of age-matched, normal animals with synergist denervation for 5 wk. The results indicate that motor neuron action potential activity is a major contributing factor to the loss of motor-unit function and degeneration in inherited canine motor neuron disease.

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46

Sassani, Matilde, James Alix, Kathleen Baster, Mara Cercignani, Pamela Shaw, and Thomas Jenkins. "176 Motor fatigability in motor neuron disease." Journal of Neurology, Neurosurgery & Psychiatry 93, no. 9 (August 12, 2022): e2.136. http://dx.doi.org/10.1136/jnnp-2022-abn2.220.

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This study aimed to quantify, characterise and localise motor fatigue in people with motor neuron disease (MND) using a combination of clinical assessments, neurophysiology and muscle phosphorus-31 magnetic resonance spectroscopy (31P-MRS).We quantified fatigability using the fatigue index (FI) in twenty patients and 10 healthy controls. F-wave amplitudes, motor unit number index (MUNIX) and 31P-MRS were acquired pre- and post-maximal voluntary contraction to investigate fatigability at different sites of the motor system (spinal cord, peripheral nerve and muscle, respectively). Between-group differences and associations were assessed using regression models.There were no between-group differences in FI (p=0.115). MUNIX (p=0.008) and f-wave amplitude (p=0.024) declined significantly post-contraction in controls, but not in patients (MUNIX p=0.284, f-wave p=0.264). FI was associated with resting intracellular magnesium (R=0.869, p=0.001, FDR-corrected) in controls, but not patients. Resting magnesium and post-contraction MUNIX decrease were associated with greater fatigue in controls. A decrease in post-contraction f-wave amplitude was associated with greater fatigue in patients, after accounting for denervation (MUNIX) and magnesium.There is a differential response to fatigue in MND compared to healthy controls. Fatigability appears related to spinal excitability (f-waves) in patients, whereas peripheral (MUNIX) and muscular (magnesium) components predominate in healthy controls.

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47

Gizzi, M., A. DiRocco, M. Sivak, and B. Cohen. "Ocular motor function in motor neuron disease." Neurology 42, no. 5 (May 1, 1992): 1037. http://dx.doi.org/10.1212/wnl.42.5.1037.

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48

Hugon, J., M. Lubeau, F. Tabaraud, F. Chazot, J. M. Vallat, and M. Dumas. "Central motor conduction in motor neuron disease." Annals of Neurology 22, no. 4 (October 1987): 544–46. http://dx.doi.org/10.1002/ana.410220417.

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49

Wokke, JohnH J. "Diseases that masquerade as motor neuron disease." Lancet 347, no. 9012 (May 1996): 1347–48. http://dx.doi.org/10.1016/s0140-6736(96)91005-3.

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50

Shell, L. G., B. S. Jortner, and M. S. Leib. "Familial Motor Neuron Disease in Rottweiler Dogs: Neuropathologic Studies." Veterinary Pathology 24, no. 2 (March 1987): 135–39. http://dx.doi.org/10.1177/030098588702400206.

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Two 6-week-old female Rottweiler littermates were evaluated for regurgitation, diminished growth, progressive ataxia, and pelvic limb weakness. Clinical examination indicated a progressive, diffuse, lower motor neuron disorder and megaesophagus. The pups were killed at 6 and 8 weeks of age. Lesions included central chromatolysis and swelling of the perikarya in many large motor neurons in the ventral gray matter of the spinal cord. Some involvement of red, oculomotor, trigeminal motor, and ambiguus nuclei of the brainstem was noted. Ultrastructurally, chromatolytic neurons had excess neurofilaments, and an increase in and enlargement of Golgi complexes. Wallerian-like degeneration was prominent in neuropil of spinal cord and in peripheral nerve. Clinical, histological, and ultrastructural findings were consistent with a progressive motor neuron disease.

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