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Classification of Seizures and Epilepsy
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
The subtypes of temporal lobe and frontal lobe epilepsies are really anatomic specifications of seizures, not epileptic syndromes. And while temporal lobe epilepsy is surely a welcome addition as the most common syndrome encountered in adults and is additionally supported by a wealth of clinical data, the other various anatomic subtypes, especially of the frontal lobe epilepsies, can hardly be justified by the available information and, in any event, depend almost entirely for recognition upon availability of intracranial epidural or depth electrodes. A simple distinction between “temporal lobe epilepsy” and “extratemporal symptomatic epilepsy” might have been wiser, more practical, and easier to support with information now available. Finally, the appendix listing “Symptomatic generalized epilepsies of specific etiologics” is illogical and out of date. Why separate out different forms of neuronal ceriod lipofuchsinosis but not do the same for the various variants of the gangliosidoses or sialodoses? The mitochondrial disorders, now one of the best understood groups causing progressive myoclonus epilepsy, are not mentioned. And some authors, including me, do not believe Ramsay-Hunt syndrome can any longer be defended as a specific disease (17).
Disorders of the nervous system
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
Overall seizure threshold and hence an individual’s tendency to have epilepsy, seems to be genetically determined. Everyone can have seizures given certain conditions, such as a high fever or after heavy drinking. Seizures in an infant can be outgrown as the brain develops. Epilepsy is generally classified into two types. Primary (idiopathic) epilepsy is where an inherited low convulsive threshold exists and there is no other obvious lesion. Secondary (symptomatic) epilepsy is when an identified lesion interferes with brain tissue (Lawal, 2005). Box 8.1 lists systemic causes of seizures.
General Synonyms
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
As etiologic modifiers, contrasted to GS: Congenital (= Primary = Idiopathic = Essential = Developmental = Familial = Hereditary [Inherited]). 1a. acquired epilepsies (Adams & Victor,1981, p. 212)1b. secondary epilepsies (A&V, p. 244)1c. symptomatic epilepsy (Walt, p. 114; A&V, p. 233)2a. secondary parkinsonism (Rowl, p. 526)2b.symptomatic parkinsonism (ibid.)
Accurate Neurosurgery for the Establishment of the Electric Kindling Model of Epilepsy in Mice
Published in Journal of Investigative Surgery, 2022
Verónica Custodio, Jorge Acosta, Carmen Rubio, Leonardo Hernández, Javier Brito, Elisa Taddei
The necessary knowledge to understand the basic mechanisms underlying the epileptogenesis and the generations of seizures cannot be comprehensively understood exclusively with clinical trials in humans. The main strategy to understand the physiopathology of the epilepsy has been the use of experimental models [4, 5]. Most of the experimental models currently available can replicate the natural history of the focal symptomatic epilepsy using an epileptogenic agent usually followed by a period of latency and the subsequent spontaneous seizures [6]. Experimental models have mainly produced knowledge on the pathophysiology of epilepsy. However, some of the experimental models involves the focal application of a cytotoxic agent and the most widely used are kainic acid or pilocarpine. These models are characterized by provoking continuous seizures that are difficult to control and usually produce a high rate of mortality on the experimental subjects [5,6]. The expression of spontaneous seizures in these models is therefore difficult to predict and there is evidence of extensive neural damage such as; mossy fibers sprouting, cellular loss, a decrease in efficiency of the blood-brain barrier and gliosis in hippocampal and limbic regions [1, 7].
An association between the rs1799853 and rs1057910 polymorphisms of CYP2C9, the rs4244285 polymorphism of CYP2C19 and the prevalence rates of drug-resistant epilepsy in children
Published in International Journal of Neuroscience, 2021
Marianna Makowska, Beata Smolarz, Magdalena Bryś, Ewa Forma, Hanna Romanowicz
Whole blood samples (1 ml), used as an input material for molecular studies, were collected from the children with drug-resistant (n = 106) and drug-responsive (n = 80) epilepsy, as well as from non-epileptic children (n = 97), hospitalised at the Department of Neurology, Polish Mother’s Memorial Hospital, Research Institute, during the years 2010–2016. The children with drug-resistant epilepsy included 52 boys and 54 girls and the group with symptomatic epilepsy included 37 boys and 43 girls, while the group of non-epileptic children comprised 54 boys and 43 girls. All the study groups were age-matched. All the patients were subjected to pharmacotherapy (Table 1). The administered medicinal agents included: carbamazepine (CBZ), topiramat (TPM), oxcarbazepine (OXC), gabapentin (GBP), lamotrigine (LTG) and levetiracetam (LEV)—all in various doses and configurations, depending on the health status of a given patient. A formal consent was obtained from the Bioethical Committee of the Institute-Polish Mother’s Memorial Hospital in Lodz (the decision of 15 December 2010) Genetic studies were performed at the Laboratory of Molecular Biology, Department of Clinical Pathomorphology, Institute-Polish Mother’s Memorial Hospital in Lodz and at the Department of Cytobiochemistry, University of Lodz.
Caring for Children with Non-Accidental Head Injuries: A Case for a Child-Centered Approach
Published in Comprehensive Child and Adolescent Nursing, 2020
Kristy-Anne Gibbs, Annette Dickinson, Shayne Rasmussen
The long-term outcome for survivors of NAHI is poor. Barlow, Thompson, Johnson, and Minns (2004) confirmed the high morbidity rate of survivors with NAHI. Sixty-eight percent of survivors had significant morbidity, with 36% of those acquiring severe neurological disabilities requiring long-term nursing support in the community. The disabilities seen were extensions of the pathologies seen in the acute phase of injury and included delayed psychomotor development and motor deficits (central hypotonia, spastic hemiplegia/quadriplegia, ataxia, dystonia, and cranial nerve abnormalities), sensory deficits (speech, hearing, and visual deficits), and epilepsy. Twenty percent had remote symptomatic epilepsy secondary to the head injury, and 60% of those had intractable (uncontrolled) epilepsy. The significance here is that developmental delays and difficulties with speech and language, as well as motor and cognitive skills and behavioral abnormalities, are further exaggerated by uncontrolled epileptic seizures (Barlow et al., 2004). Cognitive deficits make up the majority of impairments in the long term and include speech and language difficulties, intellectual disability and behavioral problems (Chevignard & Lind, 2014; Lind et al., 2016). Adaptive behavior is especially impaired (e.g. the ability to perform daily living activities, communicate, and socialize) and, combined with other deficits, can have a profound impact on the child’s future prospects (Chevignard & Lind, 2014).