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The Diagnosis Of Epilepsy
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Typical absence attacks start almost exclusively in childhood and early adolescence, but can continue into adulthood. The individual has motor arrest, and stares; there may be fluttering of the eyelids and swallowing. The attacks usually last only a few seconds and often pass unrecognized. Absence seizures are associated with a characteristic electroencephalographic pattern with anterior predominant 3-per-second generalized spike-and-wave discharges. They may be precipitated by hyperventilation, which is a useful diagnostic manoeuvre, and by missing sleep. Atypical absences are usually associated with more severe epilepsy syndromes, such as the Lennox–Gastaut syndrome. The electroencephalogram (EEG) of atypical absences is less homogenous and more irregular. The onset and cessation of the seizure is not as abrupt as with typical absence seizures, and additional features are usually pronounced. The presence of photosensitivity depends upon the epilepsy syndrome, ranging from 20 to 40 per cent of individuals with absence seizures.
Structure–activity relations for antiepileptic drugs through omega polynomials and topological indices
Published in Molecular Physics, 2022
Medha Itagi Huilgol, V. Sriram, Krishnan Balasubramanian
Epilepsy is one of the leading neurological diseases that has affected more than 50 million people worldwide, and it continues to pose significant challenges for drug discovery and administration. Epilepsy is often a chronic neurological disease that is somewhat less understood in terms of the underlying causes and mechanisms. It is characterised by abrupt seizures that are not related either to high fever such as febrile seizures in young children or other explicable seizures caused by substance withdrawal. A number of other types of sudden seizures are classified as epilepsy, and these seizures could vary from several seizure types and epilepsy syndromes such as Lennox-Gastaut syndrome (LGS). Many of these seizures could be life shortening or life threatening. It is undeniable that epilepsy can impact the quality of life without proper therapeutic intervention. Consequently, understanding epilepsy, antiepileptic drug discovery and administration for this neurological disease have been the focus of several studies over the years [1–7]. Therapeutic administration requires understanding the underlying causes and the types of seizures such as focal seizures, generalised seizures (tonic, atonic, myoclonic, clonic, etc.,) and neonatal seizures. Diagnostic tools such as EEG, brain study and high contrast brain MRI are some of the primary tools that facilitate the diagnosis for early therapeutic intervention. Therapeutic intervention of epilepsy often involves the administration of multiple drugs that include a primary first-line agents and adjunctive therapeutic agents. At present, there are a few proposed mechanisms for the drug action for treating epilepsy [1–7]. Some of the antiepileptic drugs (AED) act as GABAA potentiators, that is, drugs that strengthen the nerve impulses pertinent to the gamma aminobutyric acid (GABA)A receptor. It is well known that for mammals GABA is the dominant inhibitory neurotransmitter and its primary receptor is the GABAA receptor, which is characterised by a ligand-gated Cl- that is opened upon GABA release. Hence many AEDs such as valproate, vigabatrin, toprimate, phenobarbitals, and all–zepams, etc., target the GABAA receptors. The other prominent mechanism of AED action is through blocking of Na+ or Ca2+ channels. Finally, the glutamate (the other amino acid involved in neurotransmitter mediation) inhibitors are yet another group of AEDs, for example, valproate, toprimate, parempanel, etc. Typically, AEDs contain suitable electronic features or functional groups that enact the desired mechanisms for the intended targets which could be GABAA or Na+/Ca2+ channel blockade or Glutamate inhibitors. A common needed feature for almost all AEDs is their propensity to cross the blood–brain–barrier in order for them to reach the target and act as potent neurological drugs. Typically drugs that simultaneously cause multiple actions such as GABAA potentiation, glutamate inhibition, sodium and calcium ion blockades are employed as the primary line of drugs in combination with adjunctive therapeutic AEDs which are more selective in the mechanism of action.