Bibliografías temáticas / Lance et Adams, Syndrome de

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Literatura académica sobre el tema "Lance et Adams, Syndrome de"

Autor: Grafiati
Publicado: 8 de febrero de 2025

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Artículos de revistas sobre el tema "Lance et Adams, Syndrome de"

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Liron, L., M. Chambost, P. Depierre, D. Peillon y C. Combe. "Efficacité de l'acide valproïque sur les myoclonies d'action postanoxiques (syndrome de Lance et Adams)". Annales Françaises d'Anesthésie et de Réanimation 17, n.º 10 (enero de 1998): 1247–49. http://dx.doi.org/10.1016/s0750-7658(99)80033-1.

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Lanteri-Minet, M., P. Bedoucha, M. H. Mahagne, Cl Desnuelle y M. Chatel. "Pathogénie et traitement du syndrome de Lance et Adams Étude de trois cas avec effet à long-terme du piracetam". La Revue de Médecine Interne 13, n.º 7 (diciembre de 1992): S515. http://dx.doi.org/10.1016/s0248-8663(05)81094-x.

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Shin, Jun-Hwa, Jong Moon Park, A. Ram Kim, Hee Suk Shin, Eun Shin Lee, Min-Kyun Oh y Chul Ho Yoon. "Lance-Adams Syndrome". Annals of Rehabilitation Medicine 36, n.º 4 (2012): 561. http://dx.doi.org/10.5535/arm.2012.36.4.561.

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Lee, Ha Lim y Ju Kang Lee. "Lance-Adams Syndrome". Annals of Rehabilitation Medicine 35, n.º 6 (2011): 939. http://dx.doi.org/10.5535/arm.2011.35.6.939.

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Withanagama, CJ, R. Gamage y HPMC Caldera. "Lance-Adams Syndrome". Galle Medical Journal 17, n.º 1 (29 de mayo de 2012): 53. http://dx.doi.org/10.4038/gmj.v17i1.4363.

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Freund, Brin, Raoul Sutter y Peter W. Kaplan. "Lance-Adams Syndrome in the Pretargeted Temperature Management Era". Clinical EEG and Neuroscience 48, n.º 2 (10 de julio de 2016): 130–38. http://dx.doi.org/10.1177/1550059416643193.

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Acute posthypoxic myoclonus portends a poor prognosis. Another form of posthypoxic myoclonus, Lance-Adams syndrome, is associated with a better outcome. Differentiating these two entities is important in prognostication and guiding further medical intervention. This can be difficult in the acute setting after hypoxic brain injury but the use of neurophysiologic studies may be helpful. In this article, we present a case of a patient who presented after pulseless electrical activity arrest, underwent targeted temperature management and subsequently developed Lance-Adams syndrome. The neurologic and electroencephalographic findings in Lance-Adams syndrome are discussed with an updated review.
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Gudivada, KiranK, Cherian Roy y ManuM K. Varma. "Lance-Adams Syndrome after Cardiac Arrest". Neurology India 70, n.º 1 (2022): 166. http://dx.doi.org/10.4103/0028-3886.338676.

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Guo, Yu, Yan Xiao, Li-Fa Chen, De-Hui Yin y Ruo-Dan Wang. "Lance Adams syndrome: two cases report and literature review". Journal of International Medical Research 50, n.º 2 (febrero de 2022): 030006052110599. http://dx.doi.org/10.1177/03000605211059933.

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Hypoxic myoclonus, also known as Lance Adams syndrome, is a rare syndrome that results from the serious brain damage caused by cerebral hypoxia that often follows cardiopulmonary resuscitation. This current case report describes two patients with post-hypoxic myoclonus, both of whom received cardiopulmonary resuscitation. The neurological symptoms of these two patients were significantly improved by the administration of clonazepam and sodium valproate sustained-release tablets. The report presents a literature review detailing the pathogenesis, diagnosis and treatment of Lance Adams syndrome. The timely diagnosis and treatment of Lance Adams syndrome can significantly improve the quality of life of patients. Valproic acid, clonazepam and other antiepileptic drugs can be used. Whether levetiracetam is effective for cortical myoclonus requires further clinical study.
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Pokryszko-Dragan, Anna. "Anoxic encephalopathy with myoclonus – Lance-Adams syndrome". Family Medicine & Primary Care Review 4 (2015): 338–40. http://dx.doi.org/10.5114/fmpcr/60413.

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Stubblefield, Kassandra, Salman Zahoor, Hasan Sonmezturk, Kevin Haas, Danielle Mattingly y Bassel Abou-Khalil. "Perampanel is effective against Lance-Adams syndrome". Epileptic Disorders 23, n.º 5 (octubre de 2021): 769–71. http://dx.doi.org/10.1684/epd.2021.1329.

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Tesis sobre el tema "Lance et Adams, Syndrome de"

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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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HAWKINS, BERTELOOT LAURENCE. "Le syndrome de bickers et adams : a propos de deux familles". Lille 2, 1992. http://www.theses.fr/1992LIL2M173.

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GABORIAU, VERONIQUE. "Syndrome d'adams et oliver : a propos d'un cas". Nantes, 1994. http://www.theses.fr/1994NANT005M.

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Capítulos de libros sobre el tema "Lance et Adams, Syndrome de"

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Shibasaki, H. "Lance–Adams Syndrome☆". En Reference Module in Neuroscience and Biobehavioral Psychology. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-809324-5.00652-0.

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Shibasaki, H. "Lance–Adams Syndrome". En Encyclopedia of Movement Disorders, 116–19. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00040-x.

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Klewer, Scott E., Raymond B. Runyan, y Robert P. Erickson. "TBX1 and the DiGeorge Syndrome Critical Region". En Inborn Errors Of Development, 862–66. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195306910.003.0093.

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Abstract Congenital cardiovascular malformation is the most common class of birth defects and one of the three most common causes of death in the )rst year of life (Rubin et al., 1985). Abnormal gene dosage is the best understood genetic cause of congenital heart defects (CHDs). The most common genetic cause of CHDs is trisomy-21 (Down syndrome), which affects approximately 1 in 1000 fetuses and is associated with a 40% incidence of cardiac defects (Adams et al., 1981). Inappropriate gene dosage caused by gene deletions is also associated with congenital heart disease. Children with DiGeorge syndrome (DGS) or sequence, who display a recognizable spectrum of craniofacial anomalies, abnormal morphogenesis of the cardiac out%ow tract and great vessels (aorta, subclavian, pulmonary arteries), and thymic and parathyroid defects often have microdeletions of chromosome 22q11 (Driscoll et al., 1993). Identical chromosome 22q11 deletions have been identi)ed in patients with velocardiofacial syndrome (VCFS), conotruncal anomaly face syndrome (CAFS), and isolated CHDs (Goldmuntz et al., 1998). Deletion of this region on chromosome 22, called the “DiGeorge critical region” (DGCR), is the second most common known genetic cause of congenital heart disease (Goodship et al., 1998). The heterogeneous clinical manifestations of these 22q11 deletion syndromes have captured the interest and attention of clinical and molecular geneticists hoping to dissect the genetic basis of this human chromosomal haploinsuf)ciency.
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Francisco, Gerard E. "Pharmacologic Management of Spastic Hypertonia". En Rehabilitation for Traumatic Brain Injury, 271–304. Oxford University PressNew York, NY, 2005. http://dx.doi.org/10.1093/oso/9780195173550.003.0014.

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Abstract Spastic hypertonia is a costly complication of traumatic brain injury (TBI) that contributes to the loss of motor abilities. Along with associated impairments, it results in functional limitations, such as inability to use the hand in daily activities and difficulty with transfers and gait. When severe, it may cause pain and lead to contractures and other permanent deformities. Lance (1980) defined spasticity as “motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.” While this is the most commonly used definition, it does not accurately describe the entire spectrum of motor disorders observed in clinical practice. Indeed, recent investigations suggest that spastic hypertonia may not be the sole cause of these impairments and functional limitations. (Ada et al., 1998; Gracies, 2001; Gracies et al., 2002; Levin et al., 2000; Sgouros & Seri, 2002) Rather, the abnormalities associated with the upper motor neuron syndrome—dystonia, co contraction of agonists and antagonists, clonus, weakness, incoordination—are also believed to play important, if not predominant, roles.
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Actas de conferencias sobre el tema "Lance et Adams, Syndrome de"

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Anis, K. "Post-hypoxic Myoclonus: A Case of Lance Adams Syndrome". En 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.a3542.

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López, E. Lázaro, MM Jalón Urbina, AI Plano Sánchez, A. Rodríguez Ferreras, C. Carriles Fernández, I. Zapico García, L. Velasco Roces y L. Gómez de Segura Iriarte. "DI-096 Refractory lance–adams syndrome: pharmacotherapy management and iatrogenic complications". En 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.343.

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Primera, G., M. Ingemi y K. H. Young. "A Case of Lance- Adams Syndrome Following Peri Arrest and Severe Hypoxia From Opioid Overdose: A Case Report". En 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.a5194.

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Informes sobre el tema "Lance et Adams, Syndrome de"

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

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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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