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Bücher zum Thema „Myoclonies“

Autor: Grafiati

Veröffentlicht am 8. Februar 2025

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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, Hrsg. 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 und Van Woert Melvin H, Hrsg. Myoclonus. New York: Raven Press, 1986.

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5

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

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6

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

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7

Parker, James N., und 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, Hrsg. 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 und 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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11

Myoclonus: Poems. Thunder Bay, Ont: Emmerson Street Press, 2011.

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12

Andermann, Frederick, und Joseph Roger. Progressive Myoclonus Epilepsies. Butterworth-Heinemann, 2006.

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13

Duncann, J., C. P. Panayiotopoulos, J. Duncan und CP Panayiotopoulos. Eyelid Myoclonia with Absences. John Libbey Eurotext Limited, 1996.

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14

Thompson, Phillip D., Hiroshi Shibasaki und Mark Hallett. The Neurophysiological Basis of Myoclonus. Herausgegeben von Donald L. Schomer und Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0037.

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There are several types of myoclonus, with a variety of classification schemes, and the clinician must determine what type of myoclonus a patient has and what type of neurophysiological assessment can facilitate diagnosis. The electromyographic (EMG) correlate of the myoclonus should be examined, including the response to sensory stimuli (C-reflex). The electroencephalographic (EEG) correlate of the myoclonus should then be examined, possibly including back-averaging from the myoclonus or looking at corticomuscular (EEG–EMG) coherence. The somatosensory evoked response (SEP) should be obtained. Such studies will help determine the myoclonus origin, most commonly cortical or brainstem. One form of cortical myoclonus has the clinical appearance of a tremor (cortical tremor). Brainstem myoclonus includes exaggerated startle (hyperekplexia). Other forms of myoclonus include spinal myoclonus and functional myoclonus, which have their own distinct physiological signature. Several causes of myoclonus are reviewed, including rare types such as Creutzfeldt-Jakob disease and subacute sclerosing panencephalitis.

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15

Schmitz. Juvenile Myoclonic Epilepsy: The Janz Syndrome. Routledge, 2000.

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16

Minassian, Berge A., Giuliano Avanzini und Pasquale Striano. Progressive Myoclonus Epilepsies: State-Of-the-Art. Editions John Libbey Eurotext, 2017.

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17

Frucht, Steven J. Myoclonus: A Physician's Guide (Current Clinical Neurology). Humana Press, 2008.

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18

Chan, Elayne Mai. The molecular genetics of Lafora progressive myoclonus epilepsy. 2005.

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19

Myoclonus and Paroxysmal Dyskinesias (Advances in Neurology, Volumme 89). Lippincott Williams & Wilkins, 2002.

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20

Nita, Dragos A., Miguel A. Cortez, Jose Luis Perez Velazquez und O. Carter Snead. Biological Bases of Symptomatic Generalized Epilepsies in Children. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0040.

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Symptomatic generalized epilepsies represent a group of challenging epilepsy syndromes, most often seen in children, which share the hallmark of a triad encompassing multiple seizure types, electroencephalographical (EEG) evidence of diffuse brain involvement, and dysfunction in the intellectual domain (global developmental delay or mental retardation). SGEs include the early myoclonic encephalopathy, early infantile epileptic encephalopathy (Ohtahara syndrome), West syndrome, epilepsy with myoclonic-astatic seizures, epilepsy with myoclonic absence, Lennox-Gastaut syndrome, and the progressive myoclonic epilepsies. SGEs may arise from various genetic, developmental, or acquired brain pathologies and also can be associated with other cerebral or systemic defects and thus being part of a broader epilepsy syndrome phenotype. SGEs are associated with significant mortality and morbidity and most patients with SGE grow up to have intractable epilepsy, mental retardation, and depend on parents and institutions for the activities of the daily living. The mechanisms of SGE are numerous and heterogeneous and the EEG findings usually reflect the age-related changes as the brain matures.

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21

Noebels, Jeffrey L., Massimo Avoli, Michael A. Rogawski, Annamaria Vezzani und Antonio V. Delgado-Escueta, Hrsg. Jasper's Basic Mechanisms of the Epilepsies. 5. Aufl. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.001.0001.

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Abstract Unverricht-Lundborg disease (ULD; EPM1) is an inherited neurodegenerative disorder characterized by onset at 6–15 years, stimulus-sensitive, action-activated myoclonus, epilepsy, and progressive neurological deterioration. It is caused by biallelic pathogenic variants in the CSTB gene, encoding a cystatin B. The most common of these is an unstable expansion of a dodecamer repeat element in the promoter region of the gene, leading to marked downregulation of CSTB expression. Total loss of CSTB is associated with severe neonatal-onset encephalopathy. A cystatin B–deficient mouse models the EPM1 disease relatively well. Myoclonic seizures, preceded by microglial activation, develop at one month of age and are followed by progressive gray and white matter degeneration and motor problems. CSTB is an inhibitor of cysteine proteases of the cathepsin family showing both nuclear and cytoplasmic localization with partial co-localization with lysosomal markers. CSTB function has been linked to protecting neurons from oxidative damage through an oxidative stress-responsive cystatin B-cathepsin B signaling pathway. In the nucleus CSTB has been shown to participate in regulation of cell cycle, and histone H3 tail proteolytic cleavage. Downstream effects of CSTB dysfunction have also been implicated in apopotosis, microglial dysfunction, inflammation, neurogenesis and synapse physiology. Despite the progress made, the exact disease mechanisms in EPM1 remain elusive. This chapter discusses the clinical features of EPM1 and recent advances in understanding its pathophysiology.

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22

Guerrini, Renzo, Michelle Bureau, Pierre Genton, Antonio V. Delgado-Escueta und Marco T. Medina. Myoclonic Epilepsies: Understanding Its Nature, Diagnosis and Treatment (Advances in Neurology). Lippincott Williams & Wilkins, 2004.

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23

Binnie, Colin D. Tranient Disorders in Adults and Children, Including the Epilepsies Myoclonus, Hypoxic. Elsevier - Health Sciences Division, 2012.

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24

Jonas, Sherri. Connecting the Dots: Palatal Myoclonus, Glossopharyngeal Neuralgia, Eagle Syndrome, Lyme Disease. BookBaby, 2019.

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25

Publications, ICON Health. Myoclonus - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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26

Diebold, K. Die Erblichen Myoklonisch-Epileptisch-Dementiellen Kernsyndrome: Progressive Myoklonusepilepsien-Dyssynergia Cerebellaris Myoclonica-Myoklonische ... ... der Psychiatrie). Springer, 2012.

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27

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson und David Ledingham. Drugs causing neurological disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0018.

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This chapter describes concise lists of common drug causes of neurological symptoms (cerebellar syndrome, chorea, dystonia, myoclonus, myopathy, peripheral neuropathy, posterior reversible encephalopathy syndrome (PRES), tremors, tics, and seizures).

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28

Human upper limb cutaneous reflexes: Studies in normal subjects and in patients with myoclonus. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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29

Misulis, Karl E., und E. Lee Murray. Hypoxic-Ischemic Encephalopathy. Herausgegeben von Karl E. Misulis und E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0014.

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Hypoxic-ischemic encephalopathy (HIE) is one of the most common reasons for hospital neurology consultation. The reasons for neurologic consultations are usually medical management, evaluation and management of myoclonus and seizure activity, and prognosis.

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30

Hain, Richard D. W., und Satbir Singh Jassal. Neurological symptoms. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198745457.003.0012.

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This chapter covers a range of neurological symptoms commonly encountered in paediatric palliative care. This includes epilepsy, seizures, spasticity, myoclonus, chorea, dystonia, and akathisia. For most of these conditions, both definitions and details of management are provided.

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31

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson und David Ledingham. Hyperkinetic movement disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0010.

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This chapter discusses the clinical features and evidence-based pharmacological management of tremor, dystonia (focal, generalized, and dopa-responsive dystonia), tics and Tourette’s syndrome, chorea (Huntington’s disease (HD) and Sydenham’s chorea), ballism and athetosis, myoclonus, and restless legs syndrome (RLS).

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32

Publications, ICON Health. The Official Patient's Sourcebook on Myoclonus: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2004.

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33

Fang, John Y., und David A. Isaacs. Movement Disorders. Herausgegeben von Karl E. Misulis und E. Lee Murray. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190259419.003.0023.

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Abnormal movements are a common reason for hospital neurology consultation. Tremor and myoclonus are the most common abnormal movements seen in the inpatient setting. Medications and metabolic disturbances are the most common identified etiologies. Equally important, drug withdrawal can result in abnormal movements.

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34

Publications, ICON Health. The Official Patient's Sourcebook on Opsoclonus Myoclonus: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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35

Ghatora, Kiran. Adventures of Lily and Leo : Exploring Myoclonic Epilepsy: A Journey of Resilience, Advocacy, and Embracing Differences. Lulu Press, Inc., 2023.

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36

Kessler, Sudha Kilaru. The Ketogenic Diet and Related Therapies in “Novel” Situations. Herausgegeben von Eric H. Kossoff. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0008.

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The ketogenic diet (KD) is often considered as a treatment option for medication-resistant focal epilepsies and symptomatic generalized epilepsies, but is perhaps less commonly considered for idiopathic generalized epilepsies. The evidence for the use of the KD in two common idiopathic generalized epilepsy syndromes, childhood absence epilepsy and juvenile myoclonic epilepsy, is presented here.

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37

Andrade, Danielle Molinari de. Assessment of TAT-PTD in the transduction of cystatin B for protein replacement therapy in Unverricht-Lundborg progressive myoclonous epilepsy. 2004.

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38

Diebold, K. Die Erblichen Myoklonisch-Epileptisch-dementiellen Kernsyndrome: Progressive Myoklonusepilepsien-Dyssynergia Cerebellaris Myoclonica-Myoklonische Varianten der Drei Nachinfantilen Formen der Amaurotischen Idiotie. Springer London, Limited, 2013.

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39

Fox, Susan H. Delayed and Often Persistent. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0021.

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Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.

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40

Newsome, Scott D. Other Proven and Putative Autoimmune Disorders of the CNS. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0092.

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Antiglutamic acid decarboxylase (GAD)-associated disorders are a group of rare neuroimmunological disorders that encompass an expanding spectrum of neurological syndromes. The pathophysiology of these disorders is not well understood, although the presence of very high levels of antibodies to GAD is indicative of immunological dysfunction. The most well-known disease within this class of disorders is stiff-person syndrome (SPS), which often manifests as painful spasms, stiffness/rigidity in axial and limb musculature, and increased lumbar lordosis. Other anti-GAD-associated disorders include isolated cerebellar ataxia, progressive encephalopathy with rigidity and myoclonus (PERM), and encephalitis. Treatment depends on the severity of disease, ranging from symptomatic to immunomodulating/immunosuppressant therapies.

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41

Youngblood, Mark W., und Hal Blumenfeld. Biological Basis of Primary Generalized Epilepsies—Pathophysiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0037.

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The primary generalized epilepsies include a heterogeneous group of seizures including absence, myoclonic, and generalized tonic-clonic seizures that are not strictly localized on EEG and not secondary to another disorder. The seizures are often associated with a loss of consciousness and may present with motor manifestations, including convulsions and arrest of respiration. Generalized spike-and-wave discharges on electroencephalogram are a uniting feature, and this pattern of activity is a direct manifestation of the underlying mechanism of these disorders. A review of important underlying circuitry will set the stage to discuss the pathological and genetic basis of these disorders, and the chapter will conclude with a review of current and potential therapeutics.

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42

Fox, Susan H., und Marina Picillo. A Rapidly Progressive Movement Disorder. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0028.

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Prion diseases are a rare group of transmissible and untreatable encephalopathies that ultimately result in death after a short and rapidly progressive illness. The clinical features are variable but share a mix of cortical and subcortical features and a tendency for worsening at a speed that is typically faster than the monthly or yearly change seen in degenerative forms of dementia. Movement disorders represent a prominent feature of prion diseases and include cerebellar and extrapyramidal symptoms. Myoclonus is by far the most common involuntary movement in prion diseases. An awareness of the diagnosis is important to avoid the risk of iatrogenic transmission and to allow a discussion about prognosis with family and relatives.

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43

Figorilli, Michela, Monica Puligheddu und Raffaele Ferri. Scoring guidelines for sleep-related movements. Herausgegeben von Sudhansu Chokroverty, Luigi Ferini-Strambi und Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0010.

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This chapter focuses on available and validated scoring guidelines for sleep-related movements, such as periodic limb movements, alternating legs movements, rhythmic movements, sleep bruxism, sleep myoclonus, and REM behavior disorder. Some scoring methods have recently been updated with the use of computerized and automatic techniques; others are based on old criteria derived from visual analysis of events recorded on paper. Further studies are needed to develop and validate automatic scoring methods and to assess their reliability and usefulness for both research purposes and clinical practice. Moreover, scoring methods and related cut-off values have to be validated, not only against controls, but also in specific populations, such as patients with Parkinson disease and REM behavior disorder.

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44

Dionisi-Vici, Carlo, Diego Martinelli, Enrico Bertini und Claude Bachmann. HHH Syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0020.

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Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is an autosomal recessive disorder of the urea cycle characterized by impaired transport of ornithine across the inner mitochondrial membrane. As seen in other urea cycle defects, in the acute phase the disease is characterized by intermittent episodes of hyperammonemia accompanied by vomiting, lethargy, and coma, with or without signs of acute liver failure. The disease course is characterized by a pyramidal tract dysfunction associated with myoclonic seizures and cerebellar symptoms. Most patients reaching adulthood manifest variable degrees of cognitive impairment and abnormal behavior. Long-term treatment consists of a low-protein diet supplemented with citrulline, arginine, or ornithine. Protein restriction may be combined with sodium benzoate. If plasma creatine levels are low, creatine supplementation should be instituted. Acute treatment is similar to other urea cycle defects.

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45

Beal, Jules C., Monika Eisermann, Sunita Misra, Phillip L. Pearl, Perrine Plouin, Eli M. Mizrahi und Solomon L. Moshe. Seizures and Epilepsy in Preterm and Term Neonates, Infants, Children, and Adolescents. Herausgegeben von Donald L. Schomer und Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0018.

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Children are often affected by seizure types and epilepsy syndromes that are specific to their age group and distinct from those seen in adults. At the same time, certain epilepsy syndromes affecting the adult population, such as Lennox–Gastaut syndrome and juvenile myoclonic epilepsy, often begin during childhood, as do seizures related to genetic abnormalities. The use of electroencephalography (EEG) and prolonged EEG monitoring has allowed for further insight and greater specificity in identifying and understanding seizures and epilepsy syndromes in children. This chapter reviews the role of EEG in pediatric seizures and the pediatric epilepsies, including electrographic findings in the ictal state and in the interictal period, as well as the correlation with clinical seizure semiology as it contributes to the diagnosis of epileptic phenomena. The chapter discusses EEG patterns, seizure types, and epilepsy syndromes specific to neonates, infants, children, and adolescents.

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46

Bosworth, Brian P., Brian R. Landzberg und Elisa McEachern. Neurological Manifestations of Gastrointestinal and Hepatic Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0190.

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Digestive diseases may have protean neurological manifestations, and should be considered during neurological evaluation of patients. Neurological manifestations of celiac disease (CD) may involve both central and peripheral nervous system, including syndromes of cerebellar and myoclonic ataxia, encephalopathy and dementia, seizures, CNS vasculitis and progressive multifocal leukoencephalopathy, peripheral neuropathy, and myopathy. Gluten sensitivity has been frequently implicated as a cause of neuropathy, with up to 49% of celiac disease patients experiencing some form of neuropathy and almost 40% meeting the criteria for peripheral neuropathy. Gluten ataxia is one of the most common neurological manifestations of celiac disease. Neurologic manifestations of inflammatory bowel disease (IBD) have long been recognized, with an incidence ranging from less than 1% to 35%. These manifestations may precede or, more commonly, follow a diagnosis of IBD. Hepatic encephalopathy, Wilson’s disease, and acute intermittent porphyria are examples of liver diseases associated with hepatic disorders.

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47

Drislane, Frank W., Susan T. Herman und Peter W. Kaplan. Convulsive Status Epilepticus. Herausgegeben von Donald L. Schomer und Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0020.

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Generalized convulsive status epilepticus (GCSE) is a serious neurologic illness causing unresponsiveness, major physiologic disturbances, risk of injury and, if prolonged enough, neuronal damage. Causes are many, and the outcome often depends as much on the etiology as on the epileptic seizure itself. Several anti-seizure medications are used in treatment of GCSE, but some cases continue electrographically when clinical convulsions cease (nonconvulsive SE), and EEG is essential in their diagnosis. About 20% of cases become refractory to initial treatment, and the EEG becomes even more crucial in diagnosis and management. This chapter also covers other forms of SE with significant motor manifestations including: focal motor status (including epilepsia partialis continua); myoclonic status, which includes some relatively benign forms as well as some with a very poor prognosis; and clonic and tonic status. It reviews the many different EEG findings in those forms of status, and the use of EEG in their treatment and management, especially in prolonged cases.

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48

Fletcher, Nicholas. Movement disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0926.

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Almost any neurological disorder can produce a disorder of movement but the ‘movement disorders’ include the akinetic rigid syndromes, hyperkinesias, and some tremors. It can sometimes seem, especially with the use of videotape recordings, that diagnosis of movement disorders is mainly a matter of correct visual recognition. Such an approach is not recommended and can lead to mistakes unless, as in other areas of medicine, the history is considered first and the physical signs second. Obvious examples include the family history in Huntington’s disease, developmental history in dystonic cerebral palsy, and neuroleptic drug treatment in patients with tardive dyskinesia. In addition, a single disorder may give rise to several different types of involuntary movement. For example, Huntington’s disease may give rise to an akinetic rigid state, chorea, myoclonus, tics, or dystonia. Patients with Parkinson’s disease taking levodopa may show different types of movement disorder at different times of the day.In akinetic rigid states the diagnostic issue will be whether the patient has idiopathic Parkinson’s disease or one of the other Parkinsonian syndromes. With involuntary movements, the first step in diagnosis is to classify these as dystonia, tics, tremor, chorea, or myoclonus. It must be remembered that involuntary movements are merely physical signs, not diagnostic entities, and that they do not always occur in a pure form; for example, patients with dystonia may have additional choreiform movements or tremor. If more than one form of abnormal movement seems to be present, the diagnosis should be based on the most obvious one. The next step is to decide on the cause of the movements and at this stage the diagnosis must be based upon an accurate and complete history as noted above.The movement disorders are often associated with abnormalities of the basal ganglia and, to some extent, vice versa. This is not entirely correct. Disturbances of basal ganglia function certainly have profound effects on movement with the development of bradykinesia, rigidity, tremor, or the various forms of dyskinesia. However, it is not correct when considering the pathophysiology of movement disorders to regard the basal ganglia as an isolated movement control centre. In fact, they are an important but poorly understood component of a much wider motor system. It is also important to remember that the basal ganglia are involved in the processing of limbic and other cognitive processes which may also be disturbed by basal ganglia dysfunction.

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49

Schomer, Donald L., und Fernando H. Lopes da Silva, Hrsg. Niedermeyer's Electroencephalography. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.001.0001.

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This book deals with the field of Electroencephalography in the widest possible sense, from the cellular foundations of the electric activities of the brain to a vast number of clinical applications. The basic science sections were up-dated to include advanced computer modeling approaches. The chapters on normal and pathological EEG findings in premature infants, newborns and children were thoroughly revised to keep up with the advances that have taken place recently in studying brain developmental issues. Major advances have taken place in neurophysiological findings in a variety of neurodegenerative disorders, which led to thoroughly revised chapters. Other rapidly changing subjects related to EEG recording/monitoring in ICU's, EMUs, and operating rooms, in patients with epilepsy, head injuries, infectious disorders and those undergoing surgical procedures, led to radically updating a number of chapters and to the addition of a chapter dedicated to invasive recordings for the treatment of patients with movement disorders. A previously missing chapter on the neurophysiology of myoclonus was added. Chapters that deal with automated EEG interpretation techniques and with standardizing EEG reporting using ILAE/IFCN approved terminology, were also added. Many chapters in the on-line version of the book will have the ability to link to a database of over 150 complete EEGs that cover the scope seen in a general EEG Lab. This link will allow the reader to manipulate the EEG display parameters as if they were in their own lab, generate a report and compare it to one generated by a panel of senior EEGers.

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