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Bibliografias temáticas / Myoclonies

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Literatura científica selecionada sobre o tema "Myoclonies"

Autor: Grafiati

Publicado: 8 de fevereiro de 2025

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Artigos de revistas sobre o assunto "Myoclonies"

1

Borg, M. "Myoclonies". EMC - Neurologie 2, n.º 2 (janeiro de 2005): 1–19. http://dx.doi.org/10.1016/s0246-0378(05)21708-6.

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Borg, M. "Myoclonies". EMC - Neurologie 9, n.º 3 (julho de 2012): 1–21. http://dx.doi.org/10.1016/s0246-0378(12)57572-x.

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Borg, M. "Myoclonies". EMC - Neurologie 2, n.º 2 (maio de 2005): 105–32. http://dx.doi.org/10.1016/j.emcn.2004.10.004.

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4

Auvin, S., P. Derambure, F. Cassim e L. Vallée. "Myoclonies et myoclonies épileptiques : orientation diagnostique et connaissances physiopathologiques". Revue Neurologique 164, n.º 1 (janeiro de 2008): 3–11. http://dx.doi.org/10.1016/j.neurol.2007.12.001.

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Rey, M. "Sommeil et myoclonies". Médecine du Sommeil 3, n.º 10 (dezembro de 2006): 50–52. http://dx.doi.org/10.1016/s1769-4493(06)70087-5.

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Genton, P., M. Bureau, C. Dravet e R. Guerrini. "Les myoclonies épileptiques". Neurophysiologie Clinique/Clinical Neurophysiology 28, n.º 4 (setembro de 1998): 374–75. http://dx.doi.org/10.1016/s0987-7053(98)80134-2.

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Cassim, F., P. Derambure, JL Bourriez, L. Defebvre, A. Destée e JD Guieu. "Myoclonies négatives d’origine corticale". Neurophysiologie Clinique/Clinical Neurophysiology 28, n.º 4 (setembro de 1998): 375. http://dx.doi.org/10.1016/s0987-7053(98)80135-4.

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Touchon, J., M. Miloudi, W. Camu e F. Tarodo. "Myoclonies d’action observées chez l’enfant". Neurophysiologie Clinique/Clinical Neurophysiology 28, n.º 4 (setembro de 1998): 376–77. http://dx.doi.org/10.1016/s0987-7053(98)80138-x.

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Goossens, D., M. Guatterie, M. Barat e M. de Séze. "Myoclonies vélo-pharyngées et dysphagie". Annales de Réadaptation et de Médecine Physique 47, n.º 1 (fevereiro de 2004): 13–19. http://dx.doi.org/10.1016/j.annrmp.2003.07.002.

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Vanrenterghem, B., E. Bakhache, R. Azar e J. B. Campagne. "Myoclonies et agitation psychomotrice sous péfloxacine". Réanimation Urgences 5, n.º 2 (janeiro de 1996): 117–18. http://dx.doi.org/10.1016/s1164-6756(96)80162-9.

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Teses / dissertações sobre o assunto "Myoclonies"

1

BEN, HADJALI BEN KHALIFA JAMEL. "Les myoclonies squelettiques". Lille 2, 1991. http://www.theses.fr/1991LIL2M234.

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Lantéri-Minet, Michel. "Traitement et pathogenie des myoclonies post-hypoxiques : etude prospective de l'effet du piracetam". Nice, 1991. http://www.theses.fr/1991NICE6829.

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GRANDSIRE, DIDIER. "Les myoclonies neonatales benignes du sommeil : un diagnostic differentiel des convulsions du nouveau-ne". Amiens, 1990. http://www.theses.fr/1990AMIEM082.

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Vellieux, Geoffroy. "Syndrome de Lance-Adams : étude translationnelle de l’homme à l’animal". Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS432.

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Le syndrome de Lance-Adams est une pathologie neurologie chronique très handicapante rencontrée chez les survivants d'anoxie cérébrale. Il est caractérisé essentiellement par des myoclonies positives, d'action, multifocales ou généralisées, et des myoclonies négatives. Les mécanismes sous-tendant les myoclonies de cette pathologie sont peu connus. De multiples hypothèses ont été proposées depuis la description initiale de ce syndrome. L'étude multimodale d'une large cohorte de patients avec un syndrome de Lance-Adams a montré que les myoclonies sont générées dans le cortex cérébral, en particulier le cortex moteur (ou sensorimoteur). L'observation de l'histoire clinique de certains patients a par ailleurs permis de proposer, avec succès, une nouvelle approche thérapeutique par électroconvulsivothérapies à une patiente pharmacorésistante. Une revue extensive de la littérature a permis de faire émerger une vue d'ensemble et intégrée de cette pathologie et de mieux délimiter le profil de patients. Enfin, nous avons essayé, par différentes approches, de développer un nouveau modèle murin de myoclonies post-anoxiques, sans succès. Une amélioration de cette préparation expérimentale permettrait la réalisation de multiples explorations, notamment immunohistochimiques et électrophysiologiques, afin de mieux comprendre les mécanismes cellulaires et de réseaux à l'origine des myoclonies du syndrome de Lance-Adams
Lance-Adams syndrome is a post-anoxic disabling chronic neurological disorder. The main clinical features are action-induced multifocal or generalized positive myoclonus, and negative myoclonus. The underlying mechanisms of this disorder are poorly understood. Multiple hypotheses have been proposed since the initial description of this syndrome. The multimodal analysis of a large cohort of patients with Lance-Adams syndrome demonstrated that myoclonus originates in the cerebral cortex, particularly in the motor (or sensorimotor) cortex. Additionally, careful observation of the natural history of patients led to the successful proposal of a new therapeutic approach using electroconvulsive therapy in a pharmacoresistant patient. An extensive literature review provided an integrated overview of this pathology and helped better define the patient profile. Lastly, through various approaches, we attempted to develop a new murine model of post-anoxic myoclonus, without success. An improvement in this experimental preparation would allow for multiple explorations, particularly immunohistochemical and electrophysiological studies, to better understand the cellular and network mechanisms underlying the myoclonus in Lance-Adams syndrome

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Carr, Jonathan. "Familial adult myoclonus epilepsy : a clinical, neurophysiological and genetic study of a familial form of myoclonic epilepsy". Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/1201.

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Thesis (DMed (Medicine. Internal Medicine))--University of Stellenbosch, 2009.
ENGLISH ABSTRACT: Progressive Myoclonic Epilepsies (PME) are characterized by progressive neurological impairment with myoclonus, seizures and dementia. In contradistinction, Familial Adult Myoclonic Epilepsy (FAME) is characterized by a benign course with rare seizures and cortical tremor. Both conditions have neurophysiological features suggestive of a cortical origin for their myoclonus. This dissertation reports on a novel form of PME. Many of those who were affected had no or minimal progression of their illness, low seizure frequency and were cognitively intact, suggestive of non-progressive disorders linked to the FAME loci. The majority of patients had features of cortical myoclonus, with generalized spike and wave discharges on electroencephalography, enlarged evoked potentials, enhanced C reflexes, and evidence of cortical excitability with magnetic stimulation. However, there was evidence of cerebellar dysfunction both pathologically and on imaging. With regard to similar conditions, dentatorubral pallidoluysian atrophy and Unverricht-Lundborg syndrome were excluded by linkage analysis. Similarly, linkage was not present for either the FAME 1 or FAME 2 loci. This syndrome is both clinically and genetically novel, and has a nosology which is difficult to characterize, in which the condition appears to lie on the spectrum between FAME and PME. The dissociation between the pathological and radiological findings which suggest subcortical dysfunction, and the neurophysiological findings of cortical myoclonus is striking. Review of the literature associated with the neurophysiology of related conditions associated with PME and FAME suggests that: 1. The assumption that generalized forms of myoclonic disorders represent multifocal forms of focal cortical discharges is an oversimplification. 2. The dissociation between initial and later components of the evoked potential is less robust than is generally supposed, and that subcortical inputs may affect later components of the evoked potential. 3. In a high proportion of cases the latency from cortical spike discharge to myoclonic jerk obtained with jerk locked averaging is incompatible with a cortical origin for the spike discharge. 4. The proposal that myoclonus is a form of long latency reflex and that myoclonus represents a reflex arising from subclinical sensory input, is unproven.
AFRIKAANSE OPSOMMING: Progressiewe Miokloniese Epilepsie (PME) word gekenmerk deur progressiewe neurologiese agteruitgang met mioklonus, konvulsies en demensie. Daarenteen word Familiële Volwasse Miokloniese Epilepsie (FAME) gekenmerk deur 'n benigne verloop met ongereelde konvulsies en kortikale tremor. Beide entiteite het neurofisiologiese kenmerke suggestief van 'n kortikale oorsprong vir die mioklonus. Hierdie manuskrip beskryf 'n nuwe vorm van PME. Baie van die aangetaste persone toon geen of min agteruitgang van die siekte oor tyd nie, met 'n lae frekwensie van konvulsies en is kognitief intak, wat suggestief is van 'n nie-progressiewe siekte gekoppel aan die FAME loci. Die oorgrote meerderheid van pasiente het kenmerke van kortikale mioklonus gehad, met algemene spits en boog ontladings op elektroensefalografie, hoë amplitude ontlokte potensiale, versterkte C-reflekse, en tekens van kortikale eksiteerbaarheid met magnetiese stimulasie. Met neurobeelding en patologie was daar egter bewyse van serebellêre disfunksie. Soortgelyke toestande, naamlik dentatorubro-pallidoluysiese atrofie en Unverricht-Lundborg sindroom is uitgeskakel deur middel van koppelingsanalise. Koppeling met die FAME1 of FAME2 loci kon ook nie aangetoon word nie. Die sindroom is beide klinies sowel as geneties nuut en het 'n nosologie wat moeilik gekaraktiseer kan word. Dit wil voorkom of die siekte op 'n spektrum lê tussen FAME en PME. Die dissosiasie tussen die patologiese en radiologiese bevindinge, wat suggestief is van subkortikale disfunksie, en die neurofisiologiese bevindinge van kortikale mioklonus is opmerklik. ’n Oorsig van die literatuur in verband met die neurofisiologie van toestande geassosieer met PME en FAME suggesteer die volgende: 1. Die aanname dat algemene vorme van miokloniese toestande multifokale vorme van fokale kortikale ontladings verteenwoordig, is ’n oorvereenvoudiging. 2. Die dissosiasie tussen inisiële en latere komponente van die ontlokte potensiaal is minder robuust as wat algemeen aanvaar word, en subkortikale invoer mag latere komponente van die ontlokte potensiaal beïnvloed. 3. In ’n groot proporsie van gevalle is die latensie van kortikale spits ontlading tot miokloniese ruk, verkry deur “jerk locked averaging”, nie verenigbaar met met ’n kortikale oorsprong vir die spits ontlading nie. 4. Geen bewyse bestaan vir die teorie dat mioklonus ’n vorm van ’n lang latensie refleks is en dat mioklonus ’n refleks is wat ontstaan uit subkliniese sensoriese invoer nie.

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Lafrenière, Ronald G. "Molecular and genetic studies of progressive myoclonus epilepsy type 1 (EPM1)". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0021/NQ36996.pdf.

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7

Waite, Adrian. "The molecular genetics of myoclonus-dystonia syndrome". Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531805.

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Elmslie, Frances Veryan. "Molecular genetic analysis of juvenile myoclonic epilepsy". Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299535.

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DASSO, MARTIN BRIGITTE. "Encephalopathie myoclonique precoce a bouffees electroencephalographiques periodiques : a propos de trois observations". Toulouse 3, 1988. http://www.theses.fr/1988TOU31062.

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VAUGIN-BOULANGER, VERONIQUE. "Effets indesirables des nouvelles quinolones". Clermont-Ferrand 1, 1989. http://www.theses.fr/1989CLF13005.

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Mais fontes

Livros sobre o assunto "Myoclonies"

1

National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison. Myoclonus. Bethesda, Maryland: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 2012.

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2

National Institutes of Health (U.S.). Myoclonus. Bethesda, Maryland: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 2012.

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3

National Institute of Neurological Disorders and Stroke (U.S.). Office of Communications and Public Liaison, ed. Myoclonus. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 2000.

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4

1933-, Fahn Stanley, Marsden C. David e Van Woert Melvin H, eds. Myoclonus. New York: Raven Press, 1986.

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5

1960-, Schmitz Bettina, e Sander Thomas 1956-, eds. Juvenile myoclonic epilepsy: The Janz syndrome. Petersfield, UK: Wrightson Biomedical Pub., 2000.

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6

S, Duncan J., e Panayotopoulos C. P, eds. Eyelid myoclonia with absences. London: John Libbey, 1996.

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7

Parker, James N., e Philip M. Parker. The official patient's sourcebook on opsoclonus myoclonus. San Diego, Calif: Icon Health Publications, 2002.

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8

Stanley, Fahn, ed. Negative motor phenomena. Philadelphia: Lippincott-Raven, 1995.

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9

Myoclonus. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 2000.

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10

Moeller, Friederike, Ronit M. Pressler e J. Helen Cross. Genetic generalized epilepsy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0027.

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This chapter provides an overview of generalized epilepsies (GGE), which comprises a group of epilepsy syndromes of presumed genetic origin. They are classified into several syndromes according to their age, depending on clinical manifestation and associated electroencephalogram (EEG) features. The chapter introduces the concept of GGE before addressing different GGE syndromes, describing their clinical presentation, EEG features, treatment, prognosis, and underlying genetics. The following GGE syndromes are discussed in order of their age of onset—myoclonic astatic epilepsy, childhood absence epilepsy, epilepsy with myoclonic absences, eyelid myoclonia with absences, juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic seizures on awakening. This is followed by an overview on pathophysiological mechanisms underlying GGE.

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Capítulos de livros sobre o assunto "Myoclonies"

1

Lo, Steven E., e Steven J. Frucht. "Myoclonus". In Hyperkinetic Movement Disorders, 113–44. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60327-120-2_5.

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Hohler, Anna DePold, e Marcus Ponce de Leon. "Myoclonus". In Encyclopedia of Clinical Neuropsychology, 2322–23. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_470.

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Caviness, John N., e Daniel D. Truong. "Myoclonus". In International Neurology, 179–83. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch46.

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Hohler, Anna DePold, e Marcus Ponce de Leon. "Myoclonus". In Encyclopedia of Clinical Neuropsychology, 1. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_470-2.

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Caviness, John N., e Daniel D. Truong. "Myoclonus". In International Neurology, 210–13. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch53.

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Caviness, John N. "Myoclonus". In Parkinson’s Disease and Movement Disorders, 339–50. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-410-8_27.

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Imam, Ibrahim. "Myoclonus". In 700 Essential Neurology Checklists, 30–31. New York: CRC Press, 2021. http://dx.doi.org/10.1201/9781003221258-13.

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Rana, Abdul Qayyum, e Peter Hedera. "Myoclonus". In Differential Diagnosis of Movement Disorders in Clinical Practice, 95–106. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01607-8_5.

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Hu, Shu-Ching, Steven J. Frucht e Hiroshi Shibasaki. "Myoclonus". In Therapeutics of Parkinson's Disease and Other Movement Disorders, 363–70. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470713990.ch24.

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Hohler, Anna DePold, e Marcus Ponce de Leon. "Myoclonus". In Encyclopedia of Clinical Neuropsychology, 1700. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_470.

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Trabalhos de conferências sobre o assunto "Myoclonies"

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Boushila, Ibtissem, Mouna Sahnoun, Sawssan Daoud, Mariem Dammak, Chokri Mhiri e Fathi Kallel. "Potential of brain MRI in the diagnosis of Juvenile Myoclonic Epilepsy: An overview". In 2024 IEEE 7th International Conference on Advanced Technologies, Signal and Image Processing (ATSIP), 524–29. IEEE, 2024. http://dx.doi.org/10.1109/atsip62566.2024.10639007.

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2

José, Yasmim, Lunízia Mariano, Lucas de Moraes, Lilian Goulart, Júlio Moreira, Pedro Pozzobon e Luiz Eduardo Betting. "Myoclonic nonconvulsive status epilepticus as a differential diagnosis in intensive care patients". In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.663.

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Case report: Analyzed the case of three patients with myoclonus in an intensive care setting, all with heart failure with reduced ejection fraction (HFrEF), admitted due to decompensation of the cardiac disease resulting from infectious conditions and the need for moderate to high doses of dobutamine. One of the patients had a concomitant ischemic stroke in border territory. During hospitalization, they presented negative myoclonus in the trunk and lower limbs, an electroencephalogram was performed where in two of the three cases, a generalized epileptiform disorder and electroclinical seizures were diagnosed. The resolution of nonconvulsive status epilepticus (NCSE) of the myoclonic type in the three was obtained after the introduction and titration of valproic acid, infectious control and, in two of the cases, the association of clobazam was necessary. Discussion: The NCSE common to the three patients was the myoclonic one. The etiologies, in the context of critically ill patients, can be multifactorial, such as: ischemic stroke, hypoxia/anoxia, metabolic infectious disorders and induced by drugs, such as dobutamine. The electroclinical classification helps in the management and prognosis of these patients. The initial treatment performed in the three cases was a combination of intravenous benzodiazepine to abort the NCSE and antiseizure medications: that did not induce coma, with good response, in addition to correction of the subjacente cause. Conclusion: The presence of myoclonus in intensive care patients should be quickly investigated. It is important to carry out the differential diagnosis with NCSE and identify comorbidities. The recognition and adequate treatment of this often multifactorial condition is fundamental for the prognosis.

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3

Santos, Maria do Carmo Vasconcelos, Mariana Moreira Soares de Sa, Emanuelle Ferreira Barreto, Aline Cursio Moraes, Roberta Kelly Netto Vinte Guimarães e Antonio Pereira Gomes Neto. "Progressive myoclonic epilepsy: case report". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.688.

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Context: Progressive myoclonic epilepsy (PMS) begins in childhood or during adolescence, being a heterogeneous group of symptomatic progressive progressive generalized epilepsy. Composed of cortical myoclonus, multiple epileptic seizures, delayed or regressed neuropsychomotor development and cerebellar manifestations. Genetics is heterogeneous with a similar clinical presentation, which makes etiological definition difficult. Report a clinical case of generalized epilepsy, myoclonus, cerebellar condition and severe mental impairment. Analysis of medical records of a patient at Santa Casa de Belo Horizonte. Case report: MVPP, 17 years old, previously healthy, adopted son, normal neuropsychomotor development, first generalized tonic-clonic seizure at 8 years old, recurrence at 12 years old, being initiated by Valproato and Clobazam. In 2018 there was a worsening of the crises, perceived myoclonus, added Lamotrigine and Oxcarbazepine. EEG with continuous diffuse epileptic activity of subclinical epilepticus status and unchanged skull MRI. In 2019 he started with gait ataxia, balance changes, dysarthria, dysmetria, cognitive decline, loss of functionality and refractoriness to treatment. Valproate reduced and oxcarbazepine suspended. Video- EEG with ictal pattern of generalized wave polyspicle. Deteriorated cerebellar condition with extensive propaedeutic without alterations. There was no feasibility of genetic testing at the time. Methylprednisolone pulse therapy with partial improvement. Unsuccessful attempt to levetiracetam due to psychotic symptom. He presented lowering of the sensorium, bronchoaspiration and orotracheal intubation. He evolved with myoclonic status, adjusted for anti-crisis drugs, midazolam, thiopental, tracheostomy and gastrostomy. He maintained super- refractory status, being opted for callosotomy. He died within weeks of the procedure. Conclusion: The early diagnosis of PMS is a challenge, and its evolution is usually debilitating, with a poor prognosis and scarce specific treatment. Whenever possible, a genetic study is needed to define an etiological diagnosis.

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Panzica, Ferruccio, Giulia Varotto, Laura Canafoglia, Davide Rossi Sebastiano, Elisa Visani e Silvana Franceschetti. "EEG-EMG coherence estimated using time-varying autoregressive models in movement-activated myoclonus in patients with progressive myoclonic epilepsies." In 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5626652.

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Franklin, Gustavo L., Eli Paula Bacheladenski, Danielle C. B. Rodrigues e Ana C. S. Crippa. "Myoclonic-chorea in PURA syndrome". In SBN Conference 2022. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1774648.

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Korajkic, Nadja, Jillian Cameron e John Archer. "3164 Unilateral post-hypoxic myoclonus". In ANZAN Annual Scientific Meeting 2024 Abstracts, A48.2—A48. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/bmjno-2024-anzan.135.

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7

Nijsen, Tamara M. E., Ronald M. Aarts, Johan B. A. M. Arends e Pierre J. M. Cluitmans. "Model for arm movements during myoclonic seizures". In 2007 29th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2007. http://dx.doi.org/10.1109/iembs.2007.4352607.

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Krzeminski, Dominik, Naoki Masuda, Khalid Hamandi, Krish Singh e Jiaxiang Zhang. "MEG energy landscape abnormalities in juvenile myoclonic epilepsy". In 2019 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2019. http://dx.doi.org/10.32470/ccn.2019.1256-0.

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Goker, I., M. B. Baslo, M. Ertas e Y. Ulgen. "Motor unit territories in juvenile myoclonic epilepsy patients". In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5334552.

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10

Asghar, A., B. J. Barnes, A. Aburahma, S. Khan, G. Primera e N. Ravikumar. "Post-hypoxic Myoclonus: A Tale of Two Minds". In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1746.

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Relatórios de organizações sobre o assunto "Myoclonies"

1

Shijani, Seyed Mohammad Malakooti, Sina Neshat, Hossein Shayestehyekta e Milad Gorgani. Lance-Adams syndrome; what we know now. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, novembro de 2022. http://dx.doi.org/10.37766/inplasy2022.11.0025.

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Resumo:

Review question / Objective: 1. In Lance-Adams syndrome, what is the effect of current therapeutic management on improving patients' condition compared with the control group? 2. Are EEG, Brain CT, MRI, and brain SPECT more accurate in diagnosing Lance-Adams syndrome? 3. Does Early diagnosis and treatment influence the quality of life in patients with Lance-Adams syndrome? 4. Are patients with abnormal cortical discharge or cerebellum brain stem and thalamus cortical circuit or neurotransmitter imbalance at higher risk for/of Lance-Adams syndrome compared with patients without these symptoms? Condition being studied: LAS is a group of clinical symptoms; The primary manifestation is action myoclonus which can occur as generalized, focal, or multifocal repeated myoclonic motor movement myoclonus. In some patients, sensory stimuli can trigger myoclonus. Furthermore, negative myoclonus can impair posture and cause falls in the lower extremities.

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2

Wang, Huanliang, Kangda Zhang, Linyu Wang, Danxu Zhang e Zhihua Zhang. Effectiveness comparisons of various drug interventions the prevention of Etomidate-Induced myoclonus: a Bayesian network meta‑analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, setembro de 2021. http://dx.doi.org/10.37766/inplasy2021.9.0087.

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3

Yang, Zonghui, Jia Guo e Fenglian Shan. COVID-19-mediated neurologic symptoms of syndromes such as ataxia and myoclonus: a Meta-Analysis of Case Series. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, novembro de 2023. http://dx.doi.org/10.37766/inplasy2023.11.0050.

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