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Journal articles on the topic 'Amyotrophic lateral sclerosis – Treatment – Australia'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Urbi, Berzenn, Simon Broadley, Richard Bedlack, Ethan Russo, and Arman Sabet. "Study protocol for a randomised, double-blind, placebo-controlled study evaluating the Efficacy of cannabis-based Medicine Extract in slowing the disease pRogression of Amyotrophic Lateral sclerosis or motor neurone Disease: the EMERALD trial." BMJ Open 9, no. 11 (November 2019): e029449. http://dx.doi.org/10.1136/bmjopen-2019-029449.

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IntroductionAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no known cure and with an average life expectancy of 3–5 years post diagnosis. The use of complementary medicine such as medicinal cannabis in search for a potential treatment or cure is common in ALS. Preclinical studies have demonstrated the efficacy of cannabinoids in extending the survival and slowing of disease progression in animal models with ALS. There are anecdotal reports of cannabis slowing disease progression in persons with ALS (pALS) and that cannabis alleviated the symptoms of spasticity and pain. However, a clinical trial in pALS with these objectives has not been conducted.Methods and analysisThe Efficacy of cannabis-based Medicine Extract in slowing the disease pRogression of Amyotrophic Lateral sclerosis or motor neurone Disease trial is a randomised, double-blind, placebo-controlled cannabis trial in pALS conducted at the Gold Coast University Hospital, Australia. The investigational product will be a cannabis-based medicine extract (CBME) supplied by CannTrust Inc., Canada, with a high-cannabidiol-low-tetrahydrocannabinol concentration. A total of 30 pALS with probable or definite ALS diagnosis based on the El Escorial criteria, with a symptom duration of <2 years, age between 25 and 75years and with at least 70% forced vital capacity (FVC) will be treated for 6 months. The primary objective of the study is to evaluate the efficacy of CBME compared with placebo in slowing the disease progression measured by differences in mean ALS Functional Rating Scale-Revised and FVC score between the groups at the end of treatment. The secondary objectives are to evaluate the safety and tolerability of CBME by summarising adverse events, the effects of CBME on spasticity, pain, weight loss and quality of life assessed by the differences in mean Numeric Rating Scale for spasticity and Numeric Rating Scale for pain, percentage of total weight loss and ALS specific quality of life-Revised questionnaire.Ethics and disseminationThe study has been approved by the local Institutional Review Board. The results of this study will be published in a peer-reviewed journal.Trial registration numberNCT03690791

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Vucic, Steve, Matthew C. Kiernan, Parvathi Menon, William Huynh, Austin Rynders, Karen S. Ho, Robert Glanzman, and Michael T. Hotchkin. "Study protocol of RESCUE-ALS: A Phase 2, randomised, double-blind, placebo-controlled study in early symptomatic amyotrophic lateral sclerosis patients to assess bioenergetic catalysis with CNM-Au8 as a mechanism to slow disease progression." BMJ Open 11, no. 1 (January 2021): e041479. http://dx.doi.org/10.1136/bmjopen-2020-041479.

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IntroductionAmyotrophic lateral sclerosis (ALS) is an adult-onset, progressive and universally fatal neurodegenerative disorder. In Europe, Australia and Canada, riluzole is the only approved therapeutic agent for the treatment of ALS, while in the USA, riluzole and edaravone have been approved by the Food and Drug Administration (FDA) . Neither riluzole nor edaravone treatment has resulted in substantial disease-modifying effects. There is, therefore, an urgent need for drugs that result in safe and effective treatment. Here, we present the design and rationale for the phase 2 RESCUE-ALS study, investigating the novel nanocatalytic drug, CNM-Au8, as a therapeutic intervention that enhances the metabolic and energetic capacity of motor neurones. CNM-Au8 is an aqueous suspension of clean-surfaced, faceted gold nanocrystals that have extraordinary catalytic capabilities, that enhance efficiencies of key metabolic reactions, while simultaneously reducing levels of reactive oxygen species. This trial utilises a novel design by employing motor unit number index (MUNIX), measured by electromyography, as a quantitative measure of lower motor neurone loss and as an early marker of ALS disease progression.Methods and analysisThis is a multicentre, randomised, double-blind, parallel group, placebo-controlled study of the efficacy, safety, pharmacokinetics and pharmacodynamics of CNM-Au8 in ALS patients. Patients will be randomised 1:1 to either receive 30 mg of CNM-Au8 once daily or matching placebo over a 36-week double-blind treatment period. Efficacy will be assessed as the change in motor neurone loss as measured by electromyography (eg, MUNIX, the primary endpoint; and secondary endpoints including MScanFit, motor unit size index, Split Hand Index, Neurophysiology Index). Exploratory endpoints include standard clinical and quality of life assessments.Ethics and disseminationRESCUE-ALS was approved by the Western Sydney Local Health District Human Research Ethics Committee (Ethics Ref: 2019/ETH12107). Results of the study will be submitted for publication in a peer-reviewed journal.Trial registration numberNCT04098406

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3

Eisen, Andrew, and Markus Weber. "Treatment of Amyotrophic Lateral Sclerosis." Drugs & Aging 14, no. 3 (1999): 173–96. http://dx.doi.org/10.2165/00002512-199914030-00003.

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4

Färkkilä, M. A., M. V. Iivanainen, L. Bergström, R. O. Roine, R. Laaksonen, M.-L. Niemi, and K. Cantell. "Interferon treatment in amyotrophic lateral sclerosis." Acta Neurologica Scandinavica 69, S98 (January 29, 2009): 184–85. http://dx.doi.org/10.1111/j.1600-0404.1984.tb02429.x.

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5

Mandrioli, Jessica, Roberto D’Amico, Elisabetta Zucchi, Annalisa Gessani, Nicola Fini, Antonio Fasano, Claudia Caponnetto, et al. "Rapamycin treatment for amyotrophic lateral sclerosis." Medicine 97, no. 24 (June 2018): e11119. http://dx.doi.org/10.1097/md.0000000000011119.

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6

Simpson, Ericka P. "Antioxidant treatment for amyotrophic lateral sclerosis." Lancet Neurology 4, no. 5 (May 2005): 266. http://dx.doi.org/10.1016/s1474-4422(05)70052-1.

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7

Benditt, Joshua O., and Louis Boitano. "Respiratory Treatment of Amyotrophic Lateral Sclerosis." Physical Medicine and Rehabilitation Clinics of North America 19, no. 3 (August 2008): 559–72. http://dx.doi.org/10.1016/j.pmr.2008.02.007.

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8

Cwik, Valerie A. "Pharmaceutical Treatment of Amyotrophic Lateral Sclerosis." Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders 10, no. 2 (June 2000): 11–16. http://dx.doi.org/10.1044/nnsld10.2.11.

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9

Li, Lian, Jie Liu, and Hua She. "Targeting Macrophage for the Treatment of Amyotrophic Lateral Sclerosis." CNS & Neurological Disorders - Drug Targets 18, no. 5 (September 23, 2019): 366–71. http://dx.doi.org/10.2174/1871527318666190409103831.

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Background & Objective: Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that specifically affects motor neurons in the brain and in the spinal cord. Patients with amyotrophic lateral sclerosis usually die from respiratory failure within 3 to 5 years from when the symptoms first appear. Currently, there is no cure for amyotrophic lateral sclerosis. Accumulating evidence suggests that dismantling of neuromuscular junction is an early event in the pathogenesis of amyotrophic lateral sclerosis. Conclusion: It is starting to realized that macrophage malfunction contributes to the disruption of neuromuscular junction. Modulation of macrophage activation states may stabilize neuromuscular junction and provide protection against motor neuron degeneration in amyotrophic lateral sclerosis.

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10

Marcus, Revital. "What Is Amyotrophic Lateral Sclerosis?" JAMA 328, no. 24 (December 27, 2022): 2466. http://dx.doi.org/10.1001/jama.2022.19305.

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11

Tysnes, O. B. "Treatment of sialorrhea in amyotrophic lateral sclerosis." Acta Neurologica Scandinavica 117, s188 (May 2008): 77–81. http://dx.doi.org/10.1111/j.1600-0404.2008.01037.x.

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12

Mazzini, Letizia, Katia Mareschi, Ivana Ferrero, Elena Vassallo, Giuseppe Oliveri, Nicola Nasuelli, Gaia Donata Oggioni, Lucia Testa, and Franca Fagioli. "Stem cell treatment in Amyotrophic Lateral Sclerosis." Journal of the Neurological Sciences 265, no. 1-2 (February 2008): 78–83. http://dx.doi.org/10.1016/j.jns.2007.05.016.

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13

Voitenkov, Vladislav B., and E. V. Ekusheva. "Pain in amyotrophic lateral sclerosis." Journal of Clinical Practice 10, no. 2 (August 17, 2019): 66–73. http://dx.doi.org/10.17816/clinpract10266-73.

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In this review, we discuss different aspects of pain syndrome in patients with amyotrophic lateral sclerosis: etiology, incidence, pathophysiology and main clinical features. Also we review the modern approaches to the treatment of pain in amyotrophic lateral sclerosis. Pain is actually not rare in this condition: it appears in 80% of patients, affecting their quality of life and functional activity, leading to the development of depressive and anxiety disorders. Pain in amyotrophic lateral sclerosis is often overlooked by clinicians, since their attention may focus on the motor symptoms of the disease. Thus, a more careful approach is needed to diagnose and treat pain in amyotrophic lateral sclerosis.

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Agnello, Luisa, and Marcello Ciaccio. "Molecular Research on Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 23, no. 20 (October 11, 2022): 12069. http://dx.doi.org/10.3390/ijms232012069.

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15

Fawad, Laiba, and Mehrab Tahir. "Emerging Therapies in Amyotrophic Lateral Sclerosis." Molecular Medicine Communications 2, no. 01 (June 30, 2022): 31–42. http://dx.doi.org/10.55627/mmc.002.001.0041.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the loss of cortical and spinal motor neurons, leading to weakness, muscle atrophy, and, in a substantial number of patients, cognitive impairment. Most patients die within 2 to 5 years of diagnosis. The disease initiates from the death of upper and lower motor neurons leading to a degeneration of motor pathways and the paralytic effects of the disease. The disease has huge economic costs as well. FDA has approved two drugs, riluzole, and edaravone for the treatment of ALS. However, these drugs provide modest benefits in mortality and/or function. Recent developments in the understanding of the underlying pathophysiologic processes that contribute to ALS have led to the development of numerous investigational therapies, with several now in phase 3 trials. This article highlights the epidemiology, pathophysiology, and several current and emerging treatment options for ALS including stem cell therapy.

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Saitoh, Yuji, and Yuji Takahashi. "Riluzole for the treatment of amyotrophic lateral sclerosis." Neurodegenerative Disease Management 10, no. 6 (December 2020): 343–55. http://dx.doi.org/10.2217/nmt-2020-0033.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease caused by the death of motor neurons. Riluzole is a benzothiazole derivative that blocks glutamatergic neurotransmission in the CNS, which is thought to exert neuroprotective effects. Riluzole was approved by the US FDA in 1995 as the first drug to treat ALS. Although riluzole is generally safe and well tolerated in clinical practice, its efficacy in ALS is modest, prolonging tracheostomy-free survival by only 2–3 months. In this article, we will first provide an overview of the ALS field, followed by a discussion of riluzole regarding its physical properties; pharmacology; clinical efficacy in ALS; safety and tolerability; and recommended administration.

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Nabizadeh, Fardin. "Biomaterials in The Treatment of Amyotrophic Lateral Sclerosis." Neurology Letters 1, no. 1 (June 1, 2022): 12–16. http://dx.doi.org/10.52547/nl.1.1.12.

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18

Werdelin, L., G. Boysen, T. S. Jensen, and P. Mogensen. "Immunosuppressive treatment of patients with amyotrophic lateral sclerosis." Acta Neurologica Scandinavica 82, no. 2 (January 29, 2009): 132–34. http://dx.doi.org/10.1111/j.1600-0404.1990.tb01602.x.

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Yoshino, Hiide. "Edaravone for the treatment of amyotrophic lateral sclerosis." Expert Review of Neurotherapeutics 19, no. 3 (February 27, 2019): 185–93. http://dx.doi.org/10.1080/14737175.2019.1581610.

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20

Kuźma-Kozakiewicz, Magdalena. "Edaravone in the treatment of amyotrophic lateral sclerosis." Neurologia i Neurochirurgia Polska 52, no. 2 (March 2018): 124–28. http://dx.doi.org/10.1016/j.pjnns.2018.03.004.

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21

Smith, R. A., S. Melmed, B. Sherman, J. France, T. L. Munsat, and B. W. Festoff. "Recombinant growth hormone treatment of amyotrophic lateral sclerosis." Muscle & Nerve 16, no. 6 (June 1993): 624–33. http://dx.doi.org/10.1002/mus.880160608.

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22

Pozza, Andreza Martinez, Milene Karenine Delamura, Clarissa Ramirez, Nelson Iguimar Valério, Laís Helena Carvalho Marino, and Neuseli Marino Lamari. "Physiotherapeutic conduct in amyotrophic lateral sclerosis." Sao Paulo Medical Journal 124, no. 6 (November 2006): 350–54. http://dx.doi.org/10.1590/s1516-31802006000600011.

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Amyotrophic Lateral Sclerosis (ALS) is a fatal progressive neurodegenerative disease with multifactorial etiology for which, so far, there is no effective medicinal treatment. However, by means of kinesiotherapy intervention and patient guidance and care, physiotherapy can delay physical functional losses, muscle fatigue and immobility of the joint-muscle system, thereby improving the quality of life. This survey had the aim of reviewing the physiotherapeutic conduct currently used in ALS cases. Monthly monitoring is recommended, with changes in goals and conduct at each stage of the disease, activities to be pursued around the home, and emphasis on stretching, muscle strengthening, posture adequacy and respiratory kinesiotherapy.

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23

Parakh, Sonam, Damian M. Spencer, Mark A. Halloran, Kai Y. Soo, and Julie D. Atkin. "Redox Regulation in Amyotrophic Lateral Sclerosis." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/408681.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results from the death of upper and lower motor neurons. Due to a lack of effective treatment, it is imperative to understand the underlying mechanisms and processes involved in disease progression. Regulations in cellular reduction/oxidation (redox) processes are being increasingly implicated in disease. Here we discuss the possible involvement of redox dysregulation in the pathophysiology of ALS, either as a cause of cellular abnormalities or a consequence. We focus on its possible role in oxidative stress, protein misfolding, glutamate excitotoxicity, lipid peroxidation and cholesterol esterification, mitochondrial dysfunction, impaired axonal transport and neurofilament aggregation, autophagic stress, and endoplasmic reticulum (ER) stress. We also speculate that an ER chaperone protein disulphide isomerase (PDI) could play a key role in this dysregulation. PDI is essential for normal protein folding by oxidation and reduction of disulphide bonds, and hence any disruption to this process may have consequences for motor neurons. Addressing the mechanism underlying redox regulation and dysregulation may therefore help to unravel the molecular mechanism involved in ALS.

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McCluskey, Gavin, Karen E. Morrison, Colette Donaghy, Frederique Rene, William Duddy, and Stephanie Duguez. "Extracellular Vesicles in Amyotrophic Lateral Sclerosis." Life 13, no. 1 (December 31, 2022): 121. http://dx.doi.org/10.3390/life13010121.

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Amyotrophic Lateral Sclerosis is a progressive neurodegenerative disease and is the most common adult motor neuron disease. The disease pathogenesis is complex with the perturbation of multiple pathways proposed, including mitochondrial dysfunction, RNA processing, glutamate excitotoxicity, endoplasmic reticulum stress, protein homeostasis and endosomal transport/extracellular vesicle (EV) secretion. EVs are nanoscopic membrane-bound particles that are released from cells, involved in the intercellular communication of proteins, lipids and genetic material, and there is increasing evidence of their role in ALS. After discussing the biogenesis of EVs, we review their roles in the propagation of pathological proteins in ALS, such as TDP-43, SOD1 and FUS, and their contribution to disease pathology. We also discuss the ALS related genes which are involved in EV formation and vesicular trafficking, before considering the EV protein and RNA dysregulation found in ALS and how these have been investigated as potential biomarkers. Finally, we highlight the potential use of EVs as therapeutic agents in ALS, in particular EVs derived from mesenchymal stem cells and EVs as drug delivery vectors for potential treatment strategies.

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Dorst, Johannes, and Albert C. Ludolph. "Non-invasive ventilation in amyotrophic lateral sclerosis." Therapeutic Advances in Neurological Disorders 12 (January 2019): 175628641985704. http://dx.doi.org/10.1177/1756286419857040.

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Non-invasive ventilation (NIV) has become an important cornerstone of symptomatic treatment in amyotrophic lateral sclerosis (ALS), improving survival and quality of life. In this review, we summarize the most important recent developments and insights, including evidence of efficacy, indication criteria and time of initiation, ventilation parameters and adaptation strategies, treatment of complicating factors, transition from NIV to invasive ventilation, termination of NIV and end-of-life management. Recent publications have questioned former conventions and guideline recommendations, especially with regard to timing and prognostic factors; therefore, a fresh look and re-evaluation of current evidence is needed.

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26

Mahoney, Colin J., and Matthew C. Kiernan. "Expanding the availability of medications for amyotrophic lateral sclerosis in Australia." Medical Journal of Australia 212, no. 4 (January 15, 2020): 189. http://dx.doi.org/10.5694/mja2.50482.

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27

McCann, E. P., K. L. Williams, J. A. Fifita, I. S. Tarr, J. O'Connor, D. B. Rowe, G. A. Nicholson, and I. P. Blair. "The genotype-phenotype landscape of familial amyotrophic lateral sclerosis in Australia." Clinical Genetics 92, no. 3 (March 30, 2017): 259–66. http://dx.doi.org/10.1111/cge.12973.

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28

Freischmidt, Axel, Kathrin Müller, Lisa Zondler, Patrick Weydt, Alexander E. Volk, Anže Lošdorfer Božič, Michael Walter, et al. "Serum microRNAs in patients with genetic amyotrophic lateral sclerosis and pre-manifest mutation carriers." Brain 137, no. 11 (September 5, 2014): 2938–50. http://dx.doi.org/10.1093/brain/awu249.

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Abstract Knowledge about the nature of pathomolecular alterations preceding onset of symptoms in amyotrophic lateral sclerosis is largely lacking. It could not only pave the way for the discovery of valuable therapeutic targets but might also govern future concepts of pre-manifest disease modifying treatments. MicroRNAs are central regulators of transcriptome plasticity and participate in pathogenic cascades and/or mirror cellular adaptation to insults. We obtained comprehensive expression profiles of microRNAs in the serum of patients with familial amyotrophic lateral sclerosis, asymptomatic mutation carriers and healthy control subjects. We observed a strikingly homogenous microRNA profile in patients with familial amyotrophic lateral sclerosis that was largely independent from the underlying disease gene. Moreover, we identified 24 significantly downregulated microRNAs in pre-manifest amyotrophic lateral sclerosis mutation carriers up to two decades or more before the estimated time window of disease onset; 91.7% of the downregulated microRNAs in mutation carriers overlapped with the patients with familial amyotrophic lateral sclerosis. Bioinformatic analysis revealed a consensus sequence motif present in the vast majority of downregulated microRNAs identified in this study. Our data thus suggest specific common denominators regarding molecular pathogenesis of different amyotrophic lateral sclerosis genes. We describe the earliest pathomolecular alterations in amyotrophic lateral sclerosis mutation carriers known to date, which provide a basis for the discovery of novel therapeutic targets and strongly argue for studies evaluating presymptomatic disease-modifying treatment in amyotrophic lateral sclerosis.

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McGeer, Edith G., and Patrick L. McGeer. "Pharmacologic Approaches to the Treatment of Amyotrophic Lateral Sclerosis." BioDrugs 19, no. 1 (2005): 31–37. http://dx.doi.org/10.2165/00063030-200519010-00004.

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Aoki, Yoshitsugu, Andrew GL Douglas, and Matthew JA Wood. "Oligonucleotide therapies: the future of amyotrophic lateral sclerosis treatment?" Neurodegenerative Disease Management 5, no. 2 (April 2015): 93–95. http://dx.doi.org/10.2217/nmt.15.4.

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31

Henahan, Sean. "Riluzole: the first effective treatment for amyotrophic lateral sclerosis." Inpharma Weekly &NA;, no. 989 (June 1995): 9–10. http://dx.doi.org/10.2165/00128413-199509890-00017.

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32

Seibold, Heidi, Achim Zeileis, and Torsten Hothorn. "Individual treatment effect prediction for amyotrophic lateral sclerosis patients." Statistical Methods in Medical Research 27, no. 10 (February 21, 2017): 3104–25. http://dx.doi.org/10.1177/0962280217693034.

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A treatment for a complicated disease might be helpful for some but not all patients, which makes predicting the treatment effect for new patients important yet challenging. Here we develop a method for predicting the treatment effect based on patient characteristics and use it for predicting the effect of the only drug (Riluzole) approved for treating amyotrophic lateral sclerosis. Our proposed method of model-based random forests detects similarities in the treatment effect among patients and on this basis computes personalised models for new patients. The entire procedure focuses on a base model, which usually contains the treatment indicator as a single covariate and takes the survival time or a health or treatment success measurement as primary outcome. This base model is used both to grow the model-based trees within the forest, in which the patient characteristics that interact with the treatment are split variables, and to compute the personalised models, in which the similarity measurements enter as weights. We applied the personalised models using data from several clinical trials for amyotrophic lateral sclerosis from the Pooled Resource Open–Access Clinical Trials database. Our results indicate that some amyotrophic lateral sclerosis patients benefit more from the drug Riluzole than others. Our method allows gradually shifting from stratified medicine to personalised medicine and can also be used in assessing the treatment effect for other diseases studied in a clinical trial.

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Nijeweme-D'hollosy, Wendy Oude, Emile P. F. Janssen, Rianne M. H. A. Huis In ‘T Veld, Jos Spoelstra, Miriam M. R. Vollenbroek-Hutten, and Hermie J. Hermens. "Tele-treatment of patients with amyotrophic lateral sclerosis (ALS)." Journal of Telemedicine and Telecare 12, no. 1_suppl (July 2006): 31–34. http://dx.doi.org/10.1258/135763306777978434.

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Dorst, Johannes, Albert C. Ludolph, and Annemarie Huebers. "Disease-modifying and symptomatic treatment of amyotrophic lateral sclerosis." Therapeutic Advances in Neurological Disorders 11 (October 9, 2017): 175628561773473. http://dx.doi.org/10.1177/1756285617734734.

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35

Lechtzin, Noah, Jeffery Rothstein, Lora Clawson, Gregory B. Diette, and Charles M. Wiener. "Amyotrophic lateral sclerosis: evaluation and treatment of respiratory impairment." Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders 3, no. 1 (January 2002): 5–13. http://dx.doi.org/10.1080/146608202317576480.

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Jackson, Mandy, Jerònia Lladó, and Jeffrey D. Rothstein. "Therapeutic developments in the treatment of amyotrophic lateral sclerosis." Expert Opinion on Investigational Drugs 11, no. 10 (October 2002): 1343–64. http://dx.doi.org/10.1517/13543784.11.10.1343.

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Shefner, Jeremy M. "Creatine as a Potential Treatment for Amyotrophic Lateral Sclerosis." Progress in Neurotherapeutics and Neuropsychopharmacology 1, no. 1 (January 2006): 79–90. http://dx.doi.org/10.1017/s174823210500008x.

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Kast, Richard E., and Eric Lewin Altschuler. "Consideration of acamprosate for treatment of amyotrophic lateral sclerosis." Medical Hypotheses 69, no. 4 (January 2007): 836–37. http://dx.doi.org/10.1016/j.mehy.2007.01.072.

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39

Pongratz, D. "Treatment of psychiatric symptoms in amyotrophic lateral sclerosis (ALS)." European Neuropsychopharmacology 10 (September 2000): 116–17. http://dx.doi.org/10.1016/s0924-977x(00)80011-5.

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40

Aisen, M. L., D. Sevilla, G. Gibson, H. Kutt, A. Blau, L. Edelstein, J. Hatch, and J. Blass. "3,4-Diaminopyridine as a treatment for amyotrophic lateral sclerosis." Journal of the Neurological Sciences 129, no. 1 (March 1995): 21–24. http://dx.doi.org/10.1016/0022-510x(94)00225-d.

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41

Khademullah, C. Sahara, Afif J. Aqrabawi, Kara M. Place, Zahra Dargaei, Xinyi Liang, Jessica C. Pressey, Simon Bedard, et al. "Cortical interneuron-mediated inhibition delays the onset of amyotrophic lateral sclerosis." Brain 143, no. 3 (March 1, 2020): 800–810. http://dx.doi.org/10.1093/brain/awaa034.

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Abstract Amyotrophic lateral sclerosis is a fatal disease resulting from motor neuron degeneration in the cortex and spinal cord. Cortical hyperexcitability is a hallmark feature of amyotrophic lateral sclerosis and is accompanied by decreased intracortical inhibition. Using electrophysiological patch-clamp recordings, we revealed parvalbumin interneurons to be hypoactive in the late pre-symptomatic SOD1*G93A mouse model of amyotrophic lateral sclerosis. We discovered that using adeno-associated virus-mediated delivery of chemogenetic technology targeted to increase the activity of the interneurons within layer 5 of the primary motor cortex, we were able to rescue intracortical inhibition and reduce pyramidal neuron hyperexcitability. Increasing the activity of interneurons in the layer 5 of the primary motor cortex was effective in delaying the onset of amyotrophic lateral sclerosis-associated motor deficits, slowing symptom progression, preserving neuronal populations, and increasing the lifespan of SOD1*G93A mice. Taken together, this study provides novel insights into the pathogenesis and treatment of amyotrophic lateral sclerosis.

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42

Heo, Gi-yoon, Hee-kyung Kang, Min-hwa Kim, Irang Nam, Mariah Kim, So-yeon Kim, So-jung Park, et al. "A Case Report on a Patient with Amyotrophic Lateral Sclerosis Treated with Korean Medicine." Journal of Internal Korean Medicine 43, no. 5 (October 30, 2022): 891–900. http://dx.doi.org/10.22246/jikm.2022.43.5.891.

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Purpose: The purpose of this paper is to report the improvement of a patient with amyotrophic lateral sclerosis after long-term combined Korean medical treatment.Methods: A patient diagnosed with amyotrophic lateral sclerosis was treated with herbal medicine, acupuncture, pharmacopuncture, moxibustion, and rehabilitation for four separate hospital stays. To evaluate their respiratory discomfort and limb weakness, we used Manual Muscle Testing, the Pulmonary Function Test, and the Korean Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised.Results: The weakness of the muscles of the lower extremities and respiratory function was improved.Conclusion: We consider that combined Korean medicine treatments might be an effective treatment for muscle weakness and respiratory discomfort of amyotrophic lateral sclerosis. To verify the effectiveness of these treatments, further research is required.

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Chieia, Marco A., Acary S. B. Oliveira, Helga C. A. Silva, and Alberto Alain Gabbai. "Amyotrophic lateral sclerosis: considerations on diagnostic criteria." Arquivos de Neuro-Psiquiatria 68, no. 6 (December 2010): 837–42. http://dx.doi.org/10.1590/s0004-282x2010000600002.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder, compromising the motor neuron, characterized by progressive muscle weakness, with reserved prognosis. The diagnosis is based on inclusion and exclusion clinical criteria, since there is no specific confirmation test. The objective of this research is to critically examine the main diagnosis instrument - El Escorial revisited, from the World Federation of Neurology (1998). Of the 540 patients with initial ALS diagnosis, either probable or definite, seen at UNIFESP-EPM, 190 underwent thorough investigation, following regular clinical and therapeutic treatment for over two years. Thirty patients (15.78%) had their diagnosis completely changed. The false-positive diagnoses were related to: early age, clinical presentation of symmetry, weakness greater than atrophy, symptomatic exacerbation. In addition, three patients with myasthenia gravis developed framework for ALS, suggesting the post-synaptic disability as a sign of early disease.

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K, Ambika, Arundhathi K, and Lekshmi G. Krishna. "AN AYURVEDIC CASE REPORT ON AMYOTROPHIC LATERAL SCLEROSIS." International Ayurvedic Medical Journal 9, no. 11 (November 15, 2021): 2903–8. http://dx.doi.org/10.46607/iamj4409112021.

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Amyotrophic Lateral Sclerosis (ALS) is a common and most severe type of Motor Neuron Disease. It is characterized by progressive skeletal muscle weakness, wasting and fasciculations. Survival is for 3-5 years, and the death is from respiratory paralysis. The incidence of ALS is between 0.6 and 3.8 per 100000 persons per year. Males are predominantly affected. Here is a case report of 45yrs old male who presented with complaints of difficulty in walking since 3years, with an insidious asymmetric onset of weakness of bilateral lower limbs with wasting and fasciculations. In Ayurveda, the case was symptomatologically diagnosed as Mamsa Sosha, which occurs as the result of obstruction of Snayu and Rakthadhamanis (Mamsavaha srotomoolas). The assessment was done using ALSFRS-R Scale. The treatment was aimed at improving the quality of life and also decreasing the rate of disease progression. The treatment principle adopted was Srothosodhana (Ama- Avaranaghna cikitsa) and Brimhana. Promising results were obtained after treatment. Keywords: ALS, MND, Ayurveda, Avaranaghna cikitsa, Mamsa Sosha, Mamsa Kshaya

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Govindarajan, Raghav, Alexis Peters, and Tejas Mehta. "Clinical Experience of Edaravone in Amyotrophic Lateral Sclerosis." RRNMF Neuromuscular Journal 1, no. 2 (June 9, 2020): 3–6. http://dx.doi.org/10.17161/rrnmf.v1i2.13554.

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Objective: To describe clinical experience with edaravone in ALS over a period of 12 months Methods:The current study retrospectively investigated characteristics in a group of patients (n=31) with ALS who underwent edaravone treatment. Information including age, gender, race, and site of onset of symptoms were collected for all patients. Adverse events with edaravone therapy was documented where available. Results:The average age of the patients observed was 62.09 years, with 18 males and 13 females. 18 patients had limb onset, 12 bulbar onset, and 1 diaphragmatic onset. 7 of the 31 patients discontinued treatment at the end of one year. The average age of patients who discontinued edaravone was 65.71 years, of whom which 3 had limb onset, 3 bulbar onset, and 1 diaphragmatic onset. No perceived benefit, port complications, systemic bacteremia, and development of atrial fibrillation were documented as reasons for discontinuation of therapy.Conclusion: Edaravone is well tolerated in ALS patients at the end of one year. Lack of perceived benefit and port related complications are common reasons for discontinuation of treatment

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Zerecero-Morcksharpe, Marquelle, and Elisa García-Vences. "Clinical advances in multiple sclerosis and amyotrophic lateral sclerosis treatment: A review." Proceedings of Scientific Research Universidad Anáhuac. Multidisciplinary Journal of Healthcare 1, no. 2 (August 6, 2021): 58–69. http://dx.doi.org/10.36105/psrua.2021v1n2.06.

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Neurodegenerative diseases are clinical manifestations that depend on the anatomy and function of the affected areas. Amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS) are some of these diseases, but they are also autoimmune and their etiology makes treatments limited and of little therapeutic efficacy. Currently, some clinical research advances can be pillars for the development of new treatments for these diseases. Therefore, the objective of this review is to describe the latest clinical advances in ALS and MS as well as their results in clinical recovery in randomized clinical trials, meta-analyzes, and full-text systematic reviews conducted in humans and rats, published in English and Spanish in the last 5 years, using PubMed, SciELO, and Cochrane. For clinical trials to be included, they had to provide a detailed breakdown of randomization methods, diagnostic criteria, intervention details, and efficacy evaluation. The results show that, so far, available medications, like riluzole and edaravone for ALS and fingolimod, dimethyl fumarate, and IFN β-1b for MS, only prolong the life of the patient. Among these drugs are also glutamate neurotransmitter antagonists, immunomodulators and even antioxidants; each of them showed significant improvement in the reviewed trials. Similarly, other non-pharmaceutical treatments, as the 600-mg dose of curcumin in the diet for ALS, showed improvement of the patients’ conditions. Regarding MS, more studies should be carried out on autotransplantation with adiposederived mesenchymal stem cells (AdMSCs) to investigate the potential therapeutic benefit of this technique in phases prior to secondary-progressive (SPMS).

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Vucic, Steve, Henk-Jan Westeneng, Ammar Al-Chalabi, Leonard H. Van Den Berg, Paul Talman, and Matthew C. Kiernan. "Amyotrophic lateral sclerosis as a multi-step process: an Australia population study." Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 20, no. 7-8 (July 8, 2019): 532–37. http://dx.doi.org/10.1080/21678421.2018.1556697.

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Koberskaya, N. N., D. A. Grishina, and N. N. Yakhno. "Syndrome amyotrophic lateral sclerosis — Alz heimer's dementia." Russian neurological journal 26, no. 2 (May 29, 2021): 17–24. http://dx.doi.org/10.30629/2658-7947-2021-26-2-17-24.

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Recently, there is more and more evidence of the presence of a cognitive defect of varying severity in the clinical picture of ALS. A rare form of the disease is the amyotrophic lateral sclerosis (ALS) — dementia complex, characterized by a combination of dementia (usually frontotemporal) with ALS symptoms. The profile of cognitive deficit in ALS includes impairment of executive functions, memory, speech and visual-spatial disorders. A literature review on this problem is presented with a description of the clinical observation of ALS–dementia syndrome (frontal variant of possible Alzheimer’s disease). A patient with a reliable diagnosis of ALS showed rapidly progressive cognitive impairments in the form of hippocampal memory impairments, speech, visual-spatial impairments, and defective executive functions, accompanied by behavioral changes (apathy, decreased criticism). Magnetic resonance imaging of the brain revealed significant atrophy of the hippocampus, frontal lobe cortex, and left temporal lobe. In the literature, there are practically no descriptions of patients with a clinical picture of a combination of AD and ALS. Difficulties in diagnosing this condition are discussed. The relationship between these neurodegenerative diseases is discussed. The presented literature data and the presented clinical observation confi rm the expediency of studying cognitive functions in patients with suspected or signifi cant ALS, on the one hand, and analysis of the state of the central and peripheral neurons in patients with neuropsychiatric disorders of the frontotemporal type, on the other hand, which can be useful for diagnostics and treatment and rehabilitation measures.

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Clemente, Simonetta. "Amyotrophic Lateral Sclerosis Treatment with Ultramicronized Palmitoylethanolamide: A Case Report." CNS & Neurological Disorders - Drug Targets 11, no. 7 (December 1, 2012): 933–36. http://dx.doi.org/10.2174/1871527311201070933.

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Riemenschneider, Karina A., Dallas A. Forshew, and Robert G. Miller. "Multidisciplinary clinics: optimizing treatment for patients with amyotrophic lateral sclerosis." Neurodegenerative Disease Management 3, no. 2 (April 2013): 157–67. http://dx.doi.org/10.2217/nmt.13.7.

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