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classass"tb-sticker-stickerb-ISBN9785970438831-0027-000equivalents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.uivalents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.valents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.lents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.nts (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.s (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.(loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.s or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy. impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.airment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.rment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy. consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.onsciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.ehavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.avioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.ioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.al and autonomic disorders, other) that occur periodically in different forms of epilepsy. and autonomic disorders, other) that occur periodically in different forms of epilepsy.nd autonomic disorders, other) that occur periodically in different forms of epilepsy. that occur periodically in different forms of epilepsy.hat occur periodically in different forms of epilepsy.t occur periodically in different forms of epilepsy.occur periodically in different forms of epilepsy.cur periodically in different forms of epilepsy.r periodically in different forms of epilepsy.iodically in different forms of epilepsy.dically in different forms of epilepsy.cally in different forms of epilepsy."txttThe mechanism of action of such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.pan class="">The mechanism of action of such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.n class="">The mechanism of action of such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.f such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.ch drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.ly inhibitory effect on the spread of the pathological impulses. inhibitory effect on the spread of the pathological impulses.nhibitory effect on the spread of the pathological impulses.ibitory effect on the spread of the pathological impulses.itory effect on the spread of the pathological impulses.ory effect on the spread of the pathological impulses.y effect on the spread of the pathological impulses.fect on the spread of the pathological impulses.ct on the spread of the pathological impulses. on the spread of the pathological impulses.the spread of the pathological impulses.e spread of the pathological impulses.ad of the pathological impulses. of the pathological impulses.f the pathological impulses.cal impulses.l impulses.impulses.ulses.ses.s.="txtt">an class="">It is likely that the primary reactions, underlying the mechanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. class="">It is likely that the primary reactions, underlying the mechanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.lass="">It is likely that the primary reactions, underlying the mechanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.hanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.nism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.sm of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.tion of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.on of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.leptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.e level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.vel of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.l of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.euronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.nal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.l membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.nes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.here is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.re is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.at some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ome antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ntiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.iepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.annels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.nels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ls (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.toin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.in, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action., carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.enzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.zodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.epines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.es, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.e). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.. It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.kade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.de of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.f T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.pe calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.alcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.um channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.els is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.s is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.echanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.hanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.nisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.eading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.zure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.re activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ctivity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ivity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.hosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.suximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.m. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.rugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.hat suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.t suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ing effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.terest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.rest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.st. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.rs of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action. of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.f different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.erent subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.ent subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.s that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. 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    h3 class="title-contents">Table of contents
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    class="table-of-contents">lass="table-of-contents">ss="table-of-contents">table-of-contents">ble-of-contents">e-of-contents">of-contents">tents">nts">ivasss=TCont aTCont-bkt1ont aTCont-bkt1t aTCont-bkt1kt11"divv docc" nt-ISBN9785970438831-0000-ISBN9785970438831-0000SBN9785970438831-0000970438831-00000438831-000038831-0000-00000000reffhttps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.htmltps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.htmls://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.html://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.html/prior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.htmlrior.studentlibrary.ru/en/doc/ISBN9785970438831-0000.htmlor.studentlibrary.ru/en/doc/ISBN9785970438831-0000.htmldentlibrary.ru/en/doc/ISBN9785970438831-0000.htmlntlibrary.ru/en/doc/ISBN9785970438831-0000.htmlrary.ru/en/doc/ISBN9785970438831-0000.htmlry.ru/en/doc/ISBN9785970438831-0000.html.ru/en/doc/ISBN9785970438831-0000.htmldoc/ISBN9785970438831-0000.htmlc/ISBN9785970438831-0000.htmlISBN9785970438831-0000.html785970438831-0000.html5970438831-0000.html70438831-0000.html00.html.htmltml classasssst-row-doc-arow-doc-aoc-a-aEFACEACEEivssTCont-row-docont-row-doct-row-docrow-docc"d="t-ISBN9785970438831-0001ISBN9785970438831-0001BN9785970438831-00015970438831-000170438831-0001438831-00011-0001000101 hrefefttps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0001.htmlps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0001.htmlprior.studentlibrary.ru/en/doc/ISBN9785970438831-0001.htmlior.studentlibrary.ru/en/doc/ISBN9785970438831-0001.htmlr.studentlibrary.ru/en/doc/ISBN9785970438831-0001.htmlntlibrary.ru/en/doc/ISBN9785970438831-0001.htmllibrary.ru/en/doc/ISBN9785970438831-0001.htmlbrary.ru/en/doc/ISBN9785970438831-0001.html.ru/en/doc/ISBN9785970438831-0001.htmlu/en/doc/ISBN9785970438831-0001.htmlen/doc/ISBN9785970438831-0001.htmlc/ISBN9785970438831-0001.htmlISBN9785970438831-0001.htmlBN9785970438831-0001.html970438831-0001.html0438831-0001.html38831-0001.html8831-0001.html31-0001.html-0001.html001.htmlmlclassasssTCont-row-doc-aont-row-doc-at-row-doc-a-doc-aoc-a-a>I. INTRODUCTION. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT INTRODUCTION. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTDUCTION. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTCTION. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTION. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTON. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT. 1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT1. SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT SUBJECT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTCT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT AND AIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTAIMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTMS OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT OF PHARMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTRMACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTACOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTOLOGY. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT. ITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTITS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTS POSITION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTTION AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTON AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT AMONG OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT OTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTTHER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTER MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT MEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTEDICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTICAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTAL DISCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTCIPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTPLINES. MAIN STAGES OF PHARMACOLOGY DEVELOPMENTS. MAIN STAGES OF PHARMACOLOGY DEVELOPMENT MAIN STAGES OF PHARMACOLOGY DEVELOPMENTAIN STAGES OF PHARMACOLOGY DEVELOPMENTGES OF PHARMACOLOGY DEVELOPMENTS OF PHARMACOLOGY DEVELOPMENTOF PHARMACOLOGY DEVELOPMENTARMACOLOGY DEVELOPMENTMACOLOGY DEVELOPMENTCOLOGY DEVELOPMENT DEVELOPMENTEVELOPMENTELOPMENTNTv classTCont-row-doc-row-docow-doc-doc" idTCont-ISBN9785970438831-0002ont-ISBN9785970438831-0002-ISBN9785970438831-0002SBN9785970438831-0002N9785970438831-0002785970438831-00025970438831-0002438831-00028831-000231-00022"ttps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0002.html//prior.studentlibrary.ru/en/doc/ISBN9785970438831-0002.htmlprior.studentlibrary.ru/en/doc/ISBN9785970438831-0002.htmlior.studentlibrary.ru/en/doc/ISBN9785970438831-0002.htmlntlibrary.ru/en/doc/ISBN9785970438831-0002.htmllibrary.ru/en/doc/ISBN9785970438831-0002.htmlbrary.ru/en/doc/ISBN9785970438831-0002.htmlru/en/doc/ISBN9785970438831-0002.html/en/doc/ISBN9785970438831-0002.htmln/doc/ISBN9785970438831-0002.htmlBN9785970438831-0002.html9785970438831-0002.html85970438831-0002.html970438831-0002.html0438831-0002.html31-0002.html-0002.html02.html.htmlassCont-row-doc-a CREATION OF NEW DRUGSTION OF NEW DRUGS OF NEW DRUGS NEW DRUGSW DRUGSDRUGSUGSv>t-ISBN9785970438831-0003BN9785970438831-00039785970438831-000385970438831-00038831-000331-0003-0003tlibrary.ru/en/doc/ISBN9785970438831-0003.html438831-0003.htmlt-row-doc-aONS OF PHARMACOLOGY. PRINCIPLES OF CLASSIFICATION OF DRUGS PHARMACOLOGY. PRINCIPLES OF CLASSIFICATION OF DRUGSHARMACOLOGY. PRINCIPLES OF CLASSIFICATION OF DRUGSRMACOLOGY. PRINCIPLES OF CLASSIFICATION OF DRUGSGY. PRINCIPLES OF CLASSIFICATION OF DRUGS. PRINCIPLES OF CLASSIFICATION OF DRUGSPRINCIPLES OF CLASSIFICATION OF DRUGSINCIPLES OF CLASSIFICATION OF DRUGSLES OF CLASSIFICATION OF DRUGSS OF CLASSIFICATION OF DRUGSOF CLASSIFICATION OF DRUGS CLASSIFICATION OF DRUGSLASSIFICATION OF DRUGSFICATION OF DRUGSCATION OF DRUGSTCont-ISBN9785970438831-0005ont-ISBN9785970438831-0005ISBN9785970438831-0005BN9785970438831-00059785970438831-0005970438831-00050438831-00051-0005000505efhttps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0005.htmltps://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0005.htmls://prior.studentlibrary.ru/en/doc/ISBN9785970438831-0005.html/doc/ISBN9785970438831-0005.htmloc/ISBN9785970438831-0005.html/ISBN9785970438831-0005.htmlSBN9785970438831-0005.htmlN9785970438831-0005.html785970438831-0005.html0438831-0005.html38831-0005.html831-0005.htmlTION ROUTES. ABSORPTIONON ROUTES. ABSORPTION ROUTES. ABSORPTIONS. ABSORPTION ABSORPTIONBSORPTIONICAL BARRIERS. STORAGEAL BARRIERS. STORAGE BARRIERS. STORAGEARRIERS. STORAGERIERS. STORAGEERS. STORAGES. 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LOCAL AND SYSTEMIC EFFECTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTION LOCAL AND SYSTEMIC EFFECTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTION AND SYSTEMIC EFFECTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONND SYSTEMIC EFFECTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTION SYSTEMIC EFFECTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONTS OF THE DRUGS. DIRECT AND REFLEX EFFECTS. LOCALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. 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DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONALIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONIZATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONATION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTION AND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONND MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTION MECHANISM OF ACTION. DRUG «TARGETS». REVERSIBLE AND IRREVERSIBLE ACTIONS. SELECTIVE ACTIONREVERSIBLE ACTIONS. SELECTIVE ACTIONVERSIBLE ACTIONS. SELECTIVE ACTIONRSIBLE ACTIONS. SELECTIVE ACTION ACTIONS. SELECTIVE ACTIONCTIONS. SELECTIVE ACTIONIONS. SELECTIVE ACTIONCTIONIONNior.studentlibrary.ru/en/doc/ISBN9785970438831-0010.htmlr.studentlibrary.ru/en/doc/ISBN9785970438831-0010.htmlstudentlibrary.ru/en/doc/ISBN9785970438831-0010.htmludentlibrary.ru/en/doc/ISBN9785970438831-0010.htmlentlibrary.ru/en/doc/ISBN9785970438831-0010.htmltlibrary.ru/en/doc/ISBN9785970438831-0010.htmlibrary.ru/en/doc/ISBN9785970438831-0010.htmlry.ru/en/doc/ISBN9785970438831-0010.html.ru/en/doc/ISBN9785970438831-0010.htmlu/en/doc/ISBN9785970438831-0010.html/doc/ISBN9785970438831-0010.htmloc/ISBN9785970438831-0010.htmlN9785970438831-0010.html785970438831-0010.html5970438831-0010.html.htmltmlllass6. 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    Antiepileptic drugs are administered to prevent or decrease (in intensity and frequency) seizures or their equivalents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.

    The mechanism of action of such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.

    It is likely that the primary reactions, underlying the mechanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.

    Inhibition of synaptic transmission by antiepileptic drugs can be related both to inhibition of neuronal excitation and to intensification of inhibitory effects (for example, from inhibitory neurons' stimulation).

    There are several convulsive and non-convulsive forms of epilepsy, each one of which is characterized by a special clinical presentation and certain changes in the EEG (the latter has especially high diagnostic significance). There are grand mal1

    1 From French grand - big, mal - disease; generalized tonic-clonic seizures with loss of consciousness, which last for several minutes and then are followed by general inhibition of the CNS. Long-lasting seizure or several seizures closely in a row are defined as «status epilepticus».