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Противоэпилептически е means
The groupПротивоэпилептически е Vehicles-retroviral drugs, as well as the ability to prevent the development of seizures in patients with epilepsy.
Historically, the first for the treatment of epilepsy were used bromides (1853). During the 19th century, in spite of the low efficiency, even in high doses, bromides were the main means of treatment of the disease. In 1912 was synthesized phenobarbital and a first high противоэпилептическо е tool. However, the side effects of phenobarbital as a sedative pills and the lead researchers continue to search. Synthesis and the analogs of phenobarbital, the protivosudorojna activity, but without the undesirable characteristics led to the emergence of fenitoina (1938) benzobarbitala, primidona and trimetadiona. Then, for the treatment of epilepsy were ethosuximide, carbamazepine, lamotridgin, gabapentin, etc.
As the arsenal and the experience of противоэпилептически х formed the requirements they must meet. These include high activity and high duration, good absorption of blood sufficient latitude of action and little toxicity. Furthermore, the drugs should not be able to accumulate in the body, causing addiction, Drug dependence and the development of heavy undesirable effects in the long-term (years) admission.
Epilepsy, a chronic disease characterized by recurrent occasional episodes of uncontrolled neuronal excitation brain. Depending on the cause of fetal neuronal initiation and localization center opening in the brain, epileptic seizures can have many forms, manifesting itself in the form of motor, cognitive, and vegetative (viszeralnah) phenomena. Initiate epileptic fit kletki- "peismekkera" different from the rest of neuronal membrane instability building peace. The pharmacological effects is stabilisicia building peace and thus reducing neuronal excitability epileptogennogo hearth.
The exact mechanism of action противоэпилептически х funds remains unknown and continues intensively studied. It is clear, however, that reduced neuronal excitability epileptogennogo home can lead different mechanisms. Conceptually, they are either semi aguiruth neuronal or inhibiting activation of nerve cells. In recent years found that most suits neuronal disposal history, or glutamatergicakimi are. There are three types of glutamatnah receptors, the most important of which is a subtype NMDA (selective synthetic agonist-N-metil-d-aspartat). NMDA receptors are receptor ion channels and in initiating glutamatom increase entrance ions Na ^ + and Ca ^ 2 + in the cell, causing sea neirona activity. Phenytoin, and lamotridgin phenobarbital inhibit glutamate release from the tip incident neuronal warn thereby neuronal activation epileptic focus.
Valproeva acid and some other противоэпилептически е means on contemporary perceptions are antagonists neuronal receptor and prevent interaction with glutamate Nmda-retseptorami.
Transmitter inhibiting neuronal is GABA. Increased Gamkergicaka transmission (increasing inhibiting neuronal) is another way to stabilize the building peace neuronal epileptogennogo hearth. Benzodiazepines and phenobarbital interact with Gamk_a-retseptorian complex. There have been a change allostericakie Gamk_a-retseptora enhance its sensitivity to GABA and more input chlorine ions in the neuron, that, as a result, prevents the development of depolarization. Progabid (not registered in the Russian Federation) is a direct Gamk-mimetikom and is the same one described above effect immediately launch Gamk_a-retseptora. Противоэпилептическо е tiagabina effect is a consequence of the blockade reverse takeover GABA from the synaptic junctions. Stabilizing the brake mediator in the synaptic junctions potenzirovaniem by its interaction with the neuronal Gamk_a-retseptorami epileptic focus and the increased inhibition of their anxiety. Vigabatrin-inhibitor Gamk-transaminaza-locks catabolised GABA and increases its content in okonchaniah inhibiting nerve cells.
Recently, the opportunity to increase the level of GABA in Gamkergicescom neirone not at the expense of its braking metabolism, but because of the reclamation predecessor GABA-glutamate. Ability to enhance education GABA has gabapentin. Mechanism of противоэпилептическо го action is the ability to open channels for potassium ions.
Apart from the brake modulation and aguiruth mediator systems противоэпилептически й effect can be the result of direct effects on ion channels neurons. Carbamazepine, and valproata phenytoin change inachtiwatia potencialzawisimah sodium and calcium channels, thereby reducing the spread of the electrical capacity. Ethosuximide blocks calzieve T-tipa channels.
Thus, the modern arsenal противоэпилептически х of the various mechanisms of action, the doctor possibility of an epilepsy drug. Selection противоэпилептическо го means determined mainly of stroke (Generalized or stiffness, loss or no loss of consciousness, etc.). There has also been a collaborator age, the frequency of attacks, the presence of neurological symptoms of intelligence and other factors. Particular attention is given the length of therapy, on the toxicity of drugs and the likelihood of side effects.
General principles of pharmacotherapy of epilepsy include :
1. Selecting appropriate for the particular type of stroke and traumatic epilepsy drug.
2. Aciclovir, as a primary treatment. Benefits alone are high clinical effectiveness (adequate control seizures made in 70-80% of patients), the opportunity to assess the suitability of the chosen drug for the treatment of a patient and find the most effective dose and its associated regime destination. In addition, monotherapy with fewer adverse events, with a direct link of the undesirable effects of the appointment of a specific drug meant to address them by reducing the dose or the drug. Obviously, the monotherapy exclude undesirable interactions противоэпилептически х funds. For example, carbamazepine, phenytoin, phenobarbital, etc. inducyruut mikrosomaiona liver enzymes and intensify biotransformatia, incl. and own.
Some противоэпилептически е means (difenin, valproata, carbamazepine) almost entirely associated with blood plasma proteins. Substances with a high degree of bonding with the squirrels, including et al. противоэпилептически е equipment may drive them out of the blood supply and raise free concentration in the blood. The combination противоэпилептически х between each other and with products from other pharmaceutical groups should be accompanied by the emergence of clinically significant interactions.
3. The effective dose. Treatment started with the standard average age doses (it is assigned immediately in full, but is achieved in the next few days). After reaching equilibrium concentration in the plasma (by the preparation appointed reception 3-4), and in the absence of side effects is dose increase prior to symptom intoxication (sedation, drowsiness, ataxy, eye, diplopia, vomiting, etc.). Then several dose reduction with a view to eliminating the symptoms of intoxication and determine the level of drug in the blood, the self-therapeutic dose.
The important advantage over conventional drugs are drugs, with a slow release of the active substance (retardnye, "" hrono "forms). The prolonged preparations were relegated once a day in the same dose as a normal product to reduce peak concentrations in the blood, reducing the risk of side effects and stabilize effectiveness.
4. Appointment politerapii with inefficiency consistent different monotherapies противоэпилептически ми drugs. Combine противоэпилептически е preparations with a different mechanism of action (farmakodinamika), and in accordance with the range of actions. The combination therapy drugs include some of the best value in the appointment of the monotherapies. Avoid the combination of a sedative effect and oppressive cognitive functions. Be sure to take into account the interaction between drugs comprising the combination therapy.
Phased abolition противоэпилептическо й therapy (typically within 3-6 months) by reducing doses of drugs. Sudden removal of therapy may be accompanied by the development of stroke until epileptic status. In deciding whether to lift the treatment of the primary criteria is the absence of stroke. Depending on the form of the disease bespristupny the disease for the drug should be two years or more. In many cases, patients are противоэпилептически е Preparations for life.
Virtually all противоэпилептически е means a sedative effect, in violation of the ability to focus and slow down the speed of emotional reactions. At the same time, each of the products in this group has its own range of side effects. Appointment of phenobarbital fenitoina and can be accompanied by osteomalaciei and megaloblasticescoy anaemia fenitoina - giperplaziei gums (the 20% of patients). Valproeva acid can cause tremor, violations of the blood, the increase in body mass index, forming hair, etc. By carbamazepina effects are eye, ataxy, diplopia, violations of the stomach and intestine, and skin rashes, antidiureticescoe effect.
Valproata, carbamazepine, etc. противоэпилептически е Preparations are risk teratogenicity (the expectant mother should be informed). In the case of a significant risk of adverse effects on stroke fruit treatment can be continued as far as possible, in the least to provide a safe and effective prevention of stroke doses.
Противоэпилептически ми properties of some funds from other pharmaceutical groups, including acetazolamide, digoxin, allopurinol, ACTG, prednisolone, bemitil, levodopa, alfa-tokoferol et al.