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Books on the topic 'Generalized Epilepsy'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Avoli, Massimo, Pierre Gloor, George Kostopoulos, and Robert Naquet, eds. Generalized Epilepsy. Boston, MA: Birkhäuser Boston, 1990. http://dx.doi.org/10.1007/978-1-4684-6767-3.

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2

Massimo, Avoli, ed. Generalized epilepsy: Neurobiological approaches. Boston: Birkhäuser, 1990.

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3

1951-, Marescaux C., Vergnes M. 1935-, and Bernasconi R. 1929-, eds. Generalized non convulsive epilepsy: Focus on GABA-B receptors. Wien: Springer-Verlag, 1992.

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4

R, Degen, and Dreifuss Fritz E, eds. Benign localized and generalized epilepsies of early childhood. Amsterdam: Elsevier, 1992.

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5

Alain, Malafosse, ed. Idiopathic generalized epilepsies: Clinical, experimental and genetic aspects. London: John Libbey, 1994.

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6

Marescaux, C., M. Vergnes, and R. Bernasconi, eds. Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-9206-1.

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7

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

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8

Moeller, Friederike, Ronit M. Pressler, and 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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9

Avoli. Generalized Epilepsy: Neurobiological Approaches. Springer, 2012.

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10

AVOLI. Generalized Epilepsy: Neurobiological Approaches. Birkhauser Verlag, 2012.

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11

Duncan, J. S., and C. P. Panayiotopoulos. Typical Absences and Related Epileptic Syndromes. Elsevier, 1995.

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12

Malafosse, A. Idiopathic Generalized Epilepsies (Current Problems in Epilepsy). John Libbey Eurotext Limited, 1994.

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13

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Epilepsy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0003.

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This chapter on epilepsy discusses the major classification of epileptic disorders, the management and evidence base for treatment of chronic epilepsy (focal-onset and generalized seizures), the use of antiepileptic drugs in young women, withdrawal of antiepileptic drugs, and the management of status epilepticus.

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14

Marescaux, C., M. Vergnes, and R. Bernasconi. Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors. Springer London, Limited, 2013.

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15

Marescaux, C., M. Vergnes, and R. Bernasconi. Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors. Springer, 2012.

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16

(Editor), C. Marescaux, M. Vergnes (Editor), and R. Bernasconi (Editor), eds. Generalized Non Convulsive Epilepsy: Focus on Gaba-B Receptors ("Journal of Neural Transmission"). Springer-Verlag, Austria, 1992.

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17

Kaplan, Tamara, and Tracey Milligan. Seizures and Epilepsy (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0008.

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The video in this chapter explores seizures and epilepsy, including definitions or focal or generalized seizures and epilepsy, as well as the differences between the two. It discusses risk factors for epilepsy (family history, history of febrile seizures, brain injury) and its diagnosis (by history and EEG), as well as comorbidities of epilepsy (mood and cognitive disorders, accidents, and sudden unexpected death).

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18

Nita, Dragos A., Miguel A. Cortez, Jose Luis Perez Velazquez, and 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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19

Marescaux, C., and M. Vergnes. Generalized Non Convulsive Epilepsy: Focus on Gaba-B Receptors (Journal of Neural Transmission Supplementum). Springer, 1992.

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20

Elwes, Robert. Presurgical evaluation for epilepsy surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0031.

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This chapter describes the preoperative electroclinical assessment of the various epilepsy syndromes and pathologies that are open to surgical treatment. Particular emphasis is placed on medial temporal epilepsy and frontal epilepsy. The assessment of cases considered for hemispherotomy, multiple subpial transection for Landau–Kleffner syndrome, anterior two-thirds callosotomy in symptomatic generalized epilepsy, neural stimulation, and cases with nodular hetertopia are summarized. Throughout the chapter, particular emphasis is placed on the need for multidisciplinary assessment, and the interpretation of the electroencephalogram (EEG) in the context of the clinical features, imaging, and neuropsychology. Evaluation pathways are suggested and the indications for intracranial EEG, the types of electrodes used and the operative complications are discussed in detail. Summaries of the key points in the electroclinical evaluation of temporal and frontal lobe epilepsy are given.

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21

Kessler, Sudha Kilaru. The Ketogenic Diet and Related Therapies in “Novel” Situations. Edited by 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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22

Krishnan, Vaishnav, Bernard S. Chang, and Donald L. Schomer. The Application of EEG to Epilepsy in Adults and the Elderly. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0019.

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Surface or scalp electroencephalography (EEG) has become an indispensable tool for the diagnosis, classification, and care of patients with epilepsy across the age spectrum. This chapter provides an overview of interictal and corresponding ictal scalp EEG patterns observed in adults with certain classical epilepsy syndromes. In patients with one or more new-onset seizures, the value of EEG testing begins with a close examination of the interictal record. The morphology, frequency, and topography of interictal epileptiform discharges (when present) are typically sufficient to broadly distinguish between the propensity to develop “generalized seizures” (those that rapidly engage a distributed epileptogenic network) or “focal seizures” (which have a stereotyped onset within a clearly lateralized focal region or network). Epileptiform discharges may also be seen in patients without epilepsy who are affected by certain acute (e.g., severe metabolic encephalopathies) or chronic neuropsychiatric syndromes (e.g., autism spectrum disorder). An examination of the ictal recording is of crucial importance in patients with medication-refractory focal onset seizures as it serves to guide patient selection and ancillary testing for the possibility of resective surgery for epilepsy. This chapter also highlights the limited anatomical sensitivity of EEG for seizures that lack an associated impairment in consciousness (“simple partial seizures”) or those that remain confined to mesial, deep or inferior cortical regions.

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23

O’Neal, M. Angela. A Young Woman with Jerking Movements. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0002.

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The case raises some of the important points to consider when choosing an antiepileptic drug, AED, for women with epilepsy, WWE. The most important factor is to define the epilepsy type, as many AEDs are not efficacious for primary generalized epilepsy. Knowing the interaction of an AED with contraceptives is also vital in order to prevent an unplanned pregnancy. Folate supplementation is recommended to decrease the risk of neural tube defects. It should be initiated at the same time as the prescription for an AED. For women in the reproductive years, the least teratogenic AED that is effective for their epilepsy should be chosen.

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24

Idiopathic Generalised Epilepsies. Springer, 2012.

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25

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

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26

Mills, Kerry R., ed. Oxford Textbook of Clinical Neurophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.001.0001.

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The Oxford Textbook of Clinical Neurophysiology provides a comprehensive account from world experts of the modern practice of the specialty. It deals with the full range of techniques giving the underpinning basic science and clinical use. The importance of clinical skills, as well as technical expertise are emphasized. Section I reviews the physiology of nerve, muscle, and cortex, and the digital techniques used to study them. Section II discusses the techniques for nerve conduction, electromyography (EMG), electroencephalography (EEG), magnetoencephalography, evoked potentials, and transcranial magnetic stimulation, including axonal excitability measurement, reflex studies, sleep studies pelvic floor neurophysiology and intracranial EEG. Section III reviews focal and generalized neuropathy, nerve, root, and plexus lesions, neuromuscular junction disorders, muscle disease, paediatric conditions, neurodegenerations, such as amyotrophic lateral sclerosis and EMG-guided botulinum toxin therapy. Section IV reviews generalized and focal epilepsy, status epilepticus, coma, presurgical evaluation for epilepsy, syncope, paediatric conditions, sleep disorders and intraoperative monitoring. This title incudes video content and is written for trainees and trainers in clinical neurophysiology.

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27

Haldeman, Clayton L., and John S. Kuo. Dysembryoplastic Neuroepithelial Tumors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190696696.003.0005.

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Dysembryoplastic neuroepithelial tumors (DNETs) are World Health Organization grade I tumors and have a low potential for malignant transformation. However, DNETs often affect a patient’s quality of life and can cause medically intractable seizures. The estimated prevalence of DNET is 0.6% to .0.8%; however, they are found in approximately 20% of patients undergoing surgery for epilepsy. Greater than 90% of patients with DNET have onset of epilepsy prior to the age of 20. The most common presentations of DNET are complex partial seizures and simple partial seizures. Generalized tonic–clonic seizures are present in about 50% of patients. Patients are often seizure-free after surgical resection.

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28

Weiner, Howard, and Peter B. Crino. Familial tumour syndromes: tuberous sclerosis complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0017.

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Tuberous sclerosis complex (TSC) is a multisystem, genetic disorder that results from mutations in TSC1 or TSC2 genes. Neurological and neuropsychiatric disabilities include epilepsy, intellectual disability, autism, attention deficit disorder, and generalized anxiety. Cortical dysplasias (also known as tubers) are developmental abnormalities of the cerebral cortex that are believed to be responsible for seizures, cognitive disability, and autism. Subependymal giant cell astrocytomas (SEGAs) are intraventricular tumours that can cause hydrocephalus, increased intracranial pressure, and death. TSC results from hyperactivation of the mammalian target of rapamycin (mTOR) pathway in neurons in the brain. This chapter reviews the clinical presentations of TSC as well as diagnostic approaches for epilepsy and SEGAs. It discusses the genetics and cellular pathogenesis of TSC as well as reviewing the link to mTOR signalling. This chapter also presents evidence for different treatment modalities for seizures and SEGAs. It is written for qualified specialist physicians and caregivers.

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29

Bäumer, Dirk. Seizures. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0042.

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Seizures are transient neurological events caused by abnormal excessive or synchronous neuronal activity in the brain. This can arise from a localized brain region, causing focal seizures, or simultaneously from both hemispheres, leading to generalized seizures. Epilepsy is the tendency to develop recurrent seizures and is usually diagnosed after two or more unprovoked seizures. This chapter covers simple partial seizures (sometimes called aura), complex partial seizures, and focal (or partial) seizures, their differential diagnosis, context, approach to diagnosis, key diagnostic tests, therapy, and prognosis, as well as dealing with uncertainty in a diagnosis.

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30

Drislane, Frank W., Susan T. Herman, and Peter W. Kaplan. Convulsive Status Epilepticus. Edited by Donald L. Schomer and 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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