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Epilepsy and exanthema
Published in Dinesh Kumar Jain, Homeopathy, 2022
Epilepsy is a group of disorders characterized by chronic recurrent paroxysmal changes in neurological function caused by abnormal electrical activity of the brain. Causes of seizures are intracranial birth injury, acute infection, metabolic disturbances, genetic disorders, febrile convulsion, alcoholism, brain tumor, and cardiovascular disease (Dichter, 1983, pp. 2018–2027). “Epileptic attacks usually recur at intervals throughout life but in some cases they disappear spontaneously either for years or permanently. Occasionally isolated fits may not be repeated” (Warner, 1964, p. 1141).
Management of the Sick Child
Published in Miriam Orcutt, Clare Shortall, Sarah Walpole, Aula Abbara, Sylvia Garry, Rita Issa, Alimuddin Zumla, Ibrahim Abubakar, Handbook of Refugee Health, 2021
Common causes of seizures include the following:Febrile seizures (benign but a diagnosis of exclusion, must find source of fever)Meningitis (neck stiffness and photophobia)Cerebral malaria (consider if positive malaria test)EncephalitisMetabolic abnormalities such as hypoglycaemiaIntracranial bleeding (ask about thunderclap headache)Drugs, intoxication or poisoning (history may be concealed)Parasites such as neurocysticercosis
Neurological disorders
Published in Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize, Developmental and Adapted Physical Education, 2019
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize
A seizure or convulsive disorder is a neurological condition initiated by abnormal discharges in the brain (NINDS, 2015). There are no specific causes for seizures; seizures are symptoms of a period when consciousness is impaired, which may or may not be accompanied by convulsive movements. Recently, terminology concerning epilepsy, which comes from the Greek word for seizure, has expanded to include convulsive and/or seizure disorders. Seizures may be misunderstood by educators and/or other children, causing a social stigma, depression, or a connotation of disease (de Souza & Salgado, 2006).
Oral glutamine supplementation increases seizure severity in a rodent model of mesial temporal lobe epilepsy
Published in Nutritional Neuroscience, 2022
Roni Dhaher, Eric C. Chen, Edgar Perez, Amedeo Rapuano, Mani Ratnesh S. Sandhu, Shaun E. Gruenbaum, Ketaki Deshpande, Feng Dai, Hitten P. Zaveri, Tore Eid
The activity of GS is also reduced in patients with mesial temporal lobe epilepsy (MTLE) [6], neocortical epilepsies [7], and glioblastoma-associated epilepsy [8]. However, the reduction is limited to discrete brain regions, such as the hippocampus in the case of MTLE. We have demonstrated that chemical inhibition or genetic deletion of GS in the hippocampus and neocortex of rodents causes epileptic seizures and neuropathological changes similar to human MTLE [9,10]. This suggests that the focal loss of brain GS in human epilepsy is implicated in the causation of the disease. Thus, we now ask whether supplementation with glutamine can be used to treat MTLE. To this end, we used long-term video-intracranial EEG monitoring to quantify the effects of oral glutamine supplementation on the frequency and behavioral severity of epileptic seizures using a well-established rat model of GS-deficient MTLE [9,11]. Our working hypothesis is that glutamine supplementation will reduce the frequency and severity of recurrent seizures.
Vaccination deferral among children with seizures in Zhejiang: influence, recommendation, safety and implications
Published in Expert Review of Vaccines, 2021
Chai Ji, Mingyan Li, Yan Zeng, Yan Liu, Xia Wang, Dan Yao, Junxia Guo, Yuyang Xu
A total of 1867 children with a history of seizure visited VCC during the study period. Among them, 1539 children who provided complete medical records vaccination records and followed up for more than 6 months were enrolled in this study, while the rest of children who did not meet any of the conditions were excluded. The clinical diagnose was confirmed by neurologist or pediatrician. Based on different causes of seizures, children were divided into four groups: (1) Febrile seizure (FS) group: the children were clinically diagnosed as epileptic seizure with temperature above 38°C or caregivers reported fever within 24 hours, excluding those with intracranial infection, metabolic disturbance, or no history of afebrile seizure; (2) Epilepsy (EP) group: children with epilepsy diagnosed by a neurologist, with or without treatment; (3) Unclassified Seizure (US) group: children had unexplained convulsion symptoms unrelated to fever; (4) other Symptomatic seizure (SS) group: children with epileptic seizures with definite etiology, such as neonatal hypoglycemia, intracranial hemorrhage, hypoxia-ischemic encephalopathy, encephalitis, traumatic brain injury, and so on.
EEG Pattern in Neonatal Maple Syrup Urine Disease: Description and Clinical Significance
Published in The Neurodiagnostic Journal, 2021
Rajesh P. Poothrikovil, Khalid Al Thihli, Amna Al Futaisi
Maple syrup urine disease (MSUD) is a rare autosomal recessive disorder characterized by deficiency of branched-chain keto acid dehydrogenase complex, which is required to metabolize the three branched chain amino acids (BCAAs) leucine, isoleucine and valine. This deficiency leads to an abnormal accumulation of BCAAs and their toxic byproducts, namely alpha-ketoacids, typically detectable in the blood and urine. MSUD is thus one of the main organic acidurias, a group of disorders characterized by the excretion of non-amino organic acids in urine (Clague and Thomas 2002). During the neonatal period, this metabolic dysfunction results in progressive encephalopathy with symptoms of lethargy, vomiting, posturing and abnormal movements in neonates; the classic form of the disease. If untreated, progressive brain damage causes coma, seizures and death usually within a few weeks (Seashore 2009). The major clinical features of MSUD are delayed psychomotor development, feeding difficulties and a characteristic odor of maple syrup which can be detected in the urine (Papetti et al. 2013). Currently, there are five types of MSUD: classic, intermediate, intermittent, thiamine responsive and dihydrolipoamide dehydrogenase deficient (Seashore 2009). These classifications are based on the severity of the disease, age of onset, response to thiamine therapy and the affected gene locus. All forms are inherited as autosomal recessive traits. Imaging in classic MSUD patients may show brain edema affecting the myelinated white matter, thalami and globi pallidi (Poretti et al. 2013)