AUCTORES
Review Article
*Corresponding Author: Giulio Perrotta, Psychologist sp.ing in psychotherapy with a strategic approach, Forensic Criminologist expert in sectarian cults, esoteric and security profiles, Jurist sp.ed SSPL, Essayist
Citation: Perrotta G., (2020 The pharmacological treatment of epileptic seizures in children and adults: introduction, clinical contexts, psychopharmacological profiles and prospects in the neurogenetic field. J. Neuroscience and Neurological Surgery. 6(5); DOI:10.31579/2578-8868/137
Copyright: © 2020 Giulio Perrotta, This is an open-access article distributed under the terms of The Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
Received: 01 September 2020 | Accepted: 12 September 2020 | Published: 17 September 2020
Keywords: epilepsy;neurogenetic field;psychopharmacological
Recalling the concept of "epilepsy", already analyzed in a previous publication, this work focuses on the specific study of the best pharmacological treatments for the morbid condition under examination, paying attention to the clinical and prospective aspects of therapy, also in light of recent discoveries in the neuroinflammatory and neurogenetic field.
“Epilepsy” - from the Greek ἑπιληψία, “to be caught, hit by something” - [1], is a neurological condition characterized by recurrent and sudden (at least two twenty-four hours apart) [2], physical manifestations of sudden loss of consciousness and violent convulsive movements of the muscles (the so-called “epileptic seizures”) [3-4]. We will, therefore, speak of “epilepsy” only when the cause of the seizure will be primary (and not secondary); in all other cases, in the clinical setting, it is preferable to speak of “epileptic seizure” [5-6]. In ancient times, epilepsy was associated with religious experiences and demonic or divine possession. Known as the “sacred disease”, it was widely described in the fifth century BC by Hippocrates of Kos, since epileptic seizures were thought to be a form of attack by demons, or that the visions experienced by patients were messages from the gods; the father of modern medicine himself, however, raised doubts about the divine nature of the phenomenon. However, this belief was more realistic and clinical in the Indian area, where there was already talk of “loss of consciousness”. However, in most ancient cultures (and some modern cultures, in Africa and Asia), people with epilepsy were stigmatized, avoided, or even imprisoned, because they were considered dangerous, contagious, or cursed [7]. [8]
Epilepsy is usually treated through the daily intake of drugs, prescribed after the occurrence of a second seizure treated mainly in the hospital setting. During first aid, it is essential to put people with an active tonic-clonic seizure in the lateral safety position to help prevent inhalation of fluids in the lungs. Putting your fingers in your mouth or inserting a tongue depressor is not recommended as it may cause vomiting or cause the rescuer to be bitten. The interventions should aim to avoid trauma, however, precautions for the spine are generally not necessary. If an attack lasts longer than 5 minutes or there are two attacks within an hour without a return to a normal level of consciousness in between, there is a belief that there is a medical emergency known as a "state of illness epileptic". This situation may need medical attention to keep the airway patency protected. The most commonly used drug for a long-term attack is midazolam per os, while diazepam can also be administered rectally. Intravenous lorazepam is preferred in the hospital. If two doses of benzodiazepines are not effective, other drugs such as phenytoin can be used. Seizures that do not respond to initial treatment typically require hospitalization in an intensive care unit and treatment with major medications such as thiopental sodium or propofol. Anticonvulsant drugs are the main treatment for epilepsy and often have to be taken for life. The choice of the active ingredient is based on the type of seizure, on the presence of epilepsy syndrome, on the other drugs prescribed, on the other health problems, and the age and lifestyle of the person. Initially, a single drug is recommended and if this is not effective, or involves serious side effects, you try to change. Taking two drugs at the same time is only recommended if the single does not provide results. In about half, the first prescription is already effective. If the attacks appear well controlled following a particular treatment, it is generally not necessary to regularly check the drug levels in the blood. In the case of drug-resistant epilepsy, resorting to surgery may be an option for individuals with partial epileptic seizures that do not cease to manifest despite the adoption of other treatments. Before evaluating surgical treatment, however, it is necessary to try at least two or three different drugs. The purpose of surgery is the total control of epileptic seizures. Common procedures include cutting the hippocampus through an anterior temporal lobe resection, removing tumor masses, and removing portions of the neocortex. Some procedures such as callosotomy may be attempted to try to reduce the number of seizures, rather than to cure the condition itself. Following surgery, in many cases, drug therapy can be slowly stopped. Neurostimulation may also be a viable option in those who are not candidates for surgery. Three methods have proven to be effective in those who do not respond to drugs: vagus nerve stimulation, anterior thalamic stimulation, and closed-loop response stimulation. Finally, a ketogenic diet (high-fat content, low carbohydrate content, adequate proteins) seems to decrease the number of attacks by half in about 30-40% of children. [9-18]
In clinical practice, a few simple general rules should be followed to best approach this particular neurological condition:
Generally, broad-spectrum anticonvulsants (which are effective in focal onset crises and various types of generalized onset crises) include lamotrigine, levetiracetam, topiramate, valproate, and zonisamide. For generalized partial and tonic-clonic seizures, more recent anticonvulsants (e.g., clobazam, clonazepam, ezogabine, felbamate, lacosamide, lamotrigine, levetiracetam, oxcarbazepine, pregabalin, tiagabine, topiramate, zonisamide) are no more effective than established drugs. However, newer medications tend to have fewer adverse effects and are better tolerated. Epileptic spasms (previously, childhood), atonic seizures, and myoclonic seizures are difficult to treat. Valproate or vigabatrin is usually preferred, followed by clonazepam. In epileptic spasms, the use of corticosteroids, for 8-10 weeks, is often effective. The optimal dosage remains controversial; the 20-60 intramuscular hormone adrenocorticotropic hormone can also be used once/day. A ketogenic diet (a diet very rich in fat that induces ketosis) can help, although it is difficult to maintain. For juvenile myoclonic epilepsy, treatment is generally recommended throughout life. Carbamazepine, oxcarbazepine, or gabapentin can however aggravate seizures. Lamotrigine can be used as second-line monotherapy or additional therapy for juvenile myoclonic epilepsy; however, it may aggravate myoclonic seizures in some patients with juvenile myoclonic epilepsy. For febrile seizures, medication is not recommended unless the children have a subsequent seizure in the absence of febrile disease. Many doctors pre-emptively prescribe phenobarbital or other anticonvulsants to children with complicated febrile seizures to prevent the development of non-febrile seizures, but this treatment does not seem effective and, in the long term, phenobarbital reduces learning ability. For seizures due to alcohol withdrawal, drugs are not recommended; on the contrary, treatment of withdrawal syndrome tends to prevent seizures. Treatment usually includes a benzodiazepine.
The different negative effects of anticonvulsants can then influence the choice of drugs for each patient. For example, anticonvulsants that cause weight gain (e.g. valproate) may not be the best option for an overweight patient, and topiramate or zonisamide may not be suitable for patients with a history of kidney stones. Some adverse effects of anticonvulsants can be minimized by gradually increasing the dosage. Overall, recent anticonvulsants have advantages such as better tolerability, better sedation, and fewer drug interactions. All anticonvulsants can cause an allergic scarlatiniform or measles-like rash. Some types of seizures can be aggravated by certain anticonvulsants. For example, pregabalin and lamotrigine may worsen myoclonic seizures; carbamazepine may worsen absence, myoclonic, and atonic seizures. Anti-convulsants are also associated with an increased risk of teratogenicity (in gestation). Fetal antiepileptic syndrome (cleft lips, cleft palate, cardiac abnormalities, microencephaly, growth retardation, developmental delay, abnormal facies, digital or limb hypoplasia) occurs in 4% of children of epileptic mothers taking anticonvulsants during pregnancy; however, since uncontrolled generalized seizures during pregnancy can lead to fetal harm and death, prolonged pharmacological treatment is generally advisable. Women should be made aware of the risk of anticonvulsants to the fetus, and this should be taken into account: alcohol is more toxic to fetal development than any antiepileptic drug. Taking folic acid supplements before conception helps to reduce the risk of neural tube defects and should be recommended to all women who are of childbearing age and taking anticonvulsants. Many anticonvulsants decrease serum folate and B12 levels, so oral vitamin supplements can prevent this effect. However, the risk of teratogenicity is lower with monotherapy and varies depending on the drug; none is completely safe during pregnancy. The risk with carbamazepine, phenytoin, valproate, and benzodiazepines is relatively high; there is evidence that they have caused congenital malformations (spina bifida, fetal hydantoin syndrome, cleft lip palate, neural tube abnormalities); in particular, the risk of neural tube defects is somewhat higher with valproate than with other commonly used anticonvulsants, while the risk with some of the new drugs (e.g. lamotrigine) seems to be lower.
An analysis of the individual-specific anticonvulsant drugs currently on the market gives the following overview, taking into account that the dosage for adults is based on a weight of 70 kg (unless otherwise specified):
Recently, a British study described the presence of an "epileptic network" of 320 genes, called "M30", which is associated with epilepsy. It is thought that the genes in the network are involved in the way brain cells communicate with each other. The results of the study suggest that when this network malfunctions it causes epilepsy: “The relationship between monogenic and polygenic forms of epilepsy is poorly understood and the extent to which the genetic and acquired epilepsies share common pathways is unclear. Here, we use an integrated systems-level analysis of brain gene expression data to identify molecular networks disrupted in epilepsy. (…) We identified a co-expression network of 320 genes (M30), which is significantly enriched for non-synonymous de novo mutations ascertained from patients with monogenic epilepsy and for common variants associated with polygenic epilepsy. The genes in the M30 network are expressed widely in the human brain under tight developmental control and encode physically interacting proteins involved in synaptic processes. The most highly connected proteins within the M30 network were preferentially disrupted by deleterious de novo mutations for monogenic epilepsy, in line with the centrality-lethality hypothesis. Analysis of M30 expression revealed consistent downregulation in the epileptic brain in heterogeneous forms of epilepsy including human temporal lobe epilepsy, a mouse model of acquired temporal lobe epilepsy, and a mouse model of monogenic Dravet (SCN1A) disease. These results suggest functional disruption of M30 via gene mutation or altered expression as a convergent mechanism regulating susceptibility to epilepsy broadly. Using the large collection of drug-induced gene expression data from Connectivity Map, several drugs were predicted to preferentially restore the downregulation of M30 in epilepsy toward health, most notably valproic acid, whose effect on M30 expression was replicated in neurons. (…) Taken together, our results suggest targeting the expression of M30 as a potential new therapeutic strategy in epilepsy”. [19]
In the same line, the neurogenetic one, a more recent Italian research has stated that the epileptic crisis is due to a disorder in the passage of ions through the channels of neurons altered by a genetic mutation: “The mutation of genes causes a structural and functional alteration of the neuronal channels and therefore the flow of ions entering and leaving the nerve cells is no longer balanced: the imbalance in electrical regulation determines a hyperexcitability of brain cells and therefore the appearance of an epileptic crisis. It has thus been discovered that neonatal family seizures are linked to a pathology of the potassium channels determined by two different genes located on chromosomes 20 and 8, while epilepsy with nocturnal frontal seizures is due to a disease of the chlorine channels caused by several genes on chromosomes 20 and 15. Also, some generalized epilepsies, which can be accompanied by febrile seizures, are caused by diseases of the sodium channels, due to a gene located on chromosome 2”. [20-22]
Recently, another Italian study has focused attention on the neuroinflammatory condition that favors epileptic symptoms: "It has been shown that neuroinflammation plays an important role in the genesis and progression of epilepsy; it is also accompanied by a high degree of localized oxidative stress, which can promote the onset of the epileptic attack. (...) Anti-neuroinflammatory therapy can have different effects depending on whether it is epilepsy caused by brain damage such as head trauma or stroke or central nervous system infections, where there is an important neuroinflammatory component before epileptic episodes or epilepsy with genetic and metabolic causes. In any case, it has been demonstrated that the ultra-micro compound Pealut (palmitoylethanolamide co-ultra micronized with Luteolin) can intervene on the neuroinflammatory process modulating the action of non-neuronal cells and the effect of oxidative stress thanks to the antioxidant action of luteolin". (...) In the case of drug-resistant epilepsies, i.e. epilepsies in which the neuroinflammatory component may be the cause itself, the molecule may delay the onset of the epileptic episode; in all other cases, Pealut is a pharmacological support to the antiepileptic drug, which often cannot be ignored, facilitating its action no longer hindered by neuroinflammatory cells. The antiepileptic drug will, therefore, work on the activity of the neuron and the supportive drug will reduce the neuroinflammatory process obtaining an improvement in treatment". [23]
Epilepsy often has negative effects on social and psychological well-being. These effects may include social isolation, stigmatization or a real state of disability, poor academic performance, and on average lower occupations, but also learning difficulties, attention disturbances, and socialization problems. All aspects that deserve to be adequately addressed with the help of a psychotherapist, supported by the clinical staff. Progress in research is giving encouraging signals and new, less and less invasive, targeted therapies are passing the test of scientific reliability. It is assumed, in the recent future, that attention will be increasingly focused on the well-being of patients and their definitive recovery. The best pharmacological therapy is therefore one which, in addition to taking into account clinical and anamnestic aspects, also takes into account the patient's general well-being and quality of life.
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