A new method of treating epilepsy has been found: all the secrets. Russian scientists have figured out how to cure temporal lobe epilepsy The most effective drugs for epilepsy
Epilepsy is a rare disease, but those who suffer from it need medical help. As of 2016, not a single method has yet been found to eliminate seizures in patients. They can happen at the most unexpected time and in any place, so doctors must be prepared for such cases.
To find effective ways to combat the consequences of epilepsy, scientists from China and the USA have joined forces. They conducted one large study, the purpose of which was to identify effective methods for blocking seizures in representatives of different ages.
The experiment involved animals and rodents. Thanks to him, it was possible to find out that the first signs of the disease in humans appear during puberty. It falls on the ages of 12−16 years (girls) and 13−18 years (boys).
It turned out that at puberty the child develops GABA receptors, which help suppress the activity of the nervous system. One consequence of this is that neurons in the “olfactory” part of the brain (the hippocampus) go to sleep. Against the background of such changes, the epileptic seizure passes. 
A study conducted by Chinese and American scientists showed that rodents with GABA receptors have a 30-40% lower chance of developing epilepsy than other mice from the control group.
It should be noted that the most well-known GABA receptor is “α4βδ”, and it has already been proven that it can eliminate seizures in patients. In the near future, doctors hope to use it to develop effective methods for the prevention and treatment of people suffering from epilepsy.
It should also be noted that people with this disease are still labeled as “asocial individuals” who do not fit into normal society. Now, of course, everything is much simpler than in the 70s. 
At that time in Great Britain there was a law prohibiting the marriage of a healthy person and a sick person. According to the European Convention on Human Rights, this is a gross violation of them.
Let us recall that epilepsy is a neurological disease, which is characterized by convulsive attacks with the discharge of white foam from the mouth. In Russia it is often called “falling disease.” It occurs not only in humans, but also in mice, cats, and dogs.
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" />In a few years, people with drug-resistant epilepsy will be able to take a new drug to suppress seizures only when needed, much like people with headaches take painkillers today.
Worldwide, approximately 50 million people suffer from epilepsy.
Of these, only 70% respond well to antiepileptic drugs (AEDs).
After 2-5 years of successful treatment, drugs can be discontinued in 70% of children and 60% of adults without subsequent exacerbations. However, millions of patients who do not respond to drug therapy must, in some cases, undergo surgical treatment.
Researchers from University College London in the UK are confident that a new anticonvulsant drug that can be taken "as needed" will be a real lifesaver for the 30% of patients who do not respond to standard medications.
The new treatment, which has so far only been tested in rodents, makes nerve cells more sensitive to certain substances in the brain that are normally inactive.
The lead author of the study, the developer of the new therapy, Professor Dimitri Kullmann from the Institute of Neuroscience at University College London, explains how his drug works: “First, we inject a modified virus into the area of the brain where seizure activity begins. The virus instructs brain cells to produce a protein that is activated by the substance CNO (clozapine-N-oxide). This substance can be taken in tablet form. The activated protein suppresses the excessive excitability of the cells responsible for seizures, but only in the presence of CNO."
Today, severe epileptic seizures are treated with drugs that suppress the excitability of all brain cells, and this leads to serious side effects. If the dose required by the patient is very high, then patients have to be hospitalized.
“If we could transfer our new method into clinical practice, which we hope to do over the next decade, we could treat such patients with CNO tablets on an as-needed basis, after having given one single injection of the virus for the entire time,” says Professor Kullmann .
Many people with drug-resistant epilepsy experience episodes of petit mal seizures. The professor envisages taking the new drug in these situations, as well as in cases where the patient feels an approaching severe attack.
Factors that increase the risk of seizure activity in this group of patients include illness, lack of sleep, certain periods of the menstrual cycle, etc. In these situations, taking CNO is also advisable to prevent the worst-case scenario.
A team of scientists is working on alternative methods of delivering the drug. One of them will be an injection that will quickly and effectively stop an attack that has already begun. Work is also underway on an automatic drug delivery system, in which CNO will be administered according to the same principle as in insulin pumps for diabetics.
“Fully reversible” treatment without permanent side effects
Professor Kullmann claims that the “new method is completely reversible”, so any side effects that may occur while taking the drug will go away once it is stopped.The professor also answered questions about possible side effects associated with the introduction of a modified virus into the body of patients.
He said: “The modified virus has been rendered harmless so it is unable to produce new viruses and spread. The injection is a short surgical procedure in which a small hole is drilled into the patient's skull, a needle is inserted through the lining of the brain, and medication is delivered directly to the problem area. "This operation is much simpler and safer than what patients with drug-resistant epilepsy usually face - they sometimes have to remove several cubic centimeters of brain tissue."
Another advantage of CNO is that this substance has a short lifespan (only a few hours), and only affects areas of the brain tissue treated with the virus. This avoids problems in other areas of the brain that are common with other antiepileptic drugs, and also prevents permanent damage from more invasive treatment.
“Short-acting drugs are rarely used for epilepsy. However, because they affect the entire brain and have a limited role, they are used only as second-line drugs for acute treatment of seizures in a hospital setting. Limitations of short-acting drugs include potentially dangerous respiratory depression. Our approach avoids such complications,” concluded Professor Kullmann.
The definition of epilepsy was proposed in 2005 year by a group of experts from the International League Against Epilepsy (ILAE) led by Stanford University professor Robert Fisher.
This definition of epilepsy involves the development of at least one epileptic seizure .
IN 2014 needed to formulate practical clinical definition of epilepsy to eliminate discrepancies. A wider group of experts was assembled under the leadership of the same Robert Fisher.
The April 2014 issue of Epilepsy magazine published:
Epilepsy is a brain disease corresponding to any of the following conditions:
- 1. At least two unprovoked (or reflex) epileptic seizures with an interval of more than 24 hours.
- 2. One unprovoked (or reflex) epileptic seizure and the probability of repeated seizures, corresponding to the overall risk of relapse after two unprovoked epileptic seizures of more than 60%.
- 3. An established diagnosis of a specific epileptic syndrome.
Additionally, the term “resolution from epilepsy” has been proposed.
Epilepsy Resolution Includes :
- Reaching a certain age in patients with age-dependent syndrome. For example, the absence of seizures in adults with benign epilepsy of childhood with centrotemporal spikes.
- Or the absence of epileptic seizures for 10 years in patients who have not received antiepileptic therapy for more than 5 years.
We are approaching the new classification of epilepsies 2017.
New classification of epilepsies 2017 presented by Dr Ingrid E. Scheffer (Australia), who chairs the ILAE Classification of Epilepsy Task Force, at the International Congress on Epilepsy in Barcelona, 2-6 September 2017. Previously used, although we will be referring to it for a long time.
To ensure that specialists and patients use clear language, when words mean what they say, a new classification of epileptic seizures and forms of epilepsy was proposed.
New classification of epilepsy 2017 - multi-level system. Several levels of classification are due to the large variability of available methods for examining patients.
The starting point is type of attack.
Key changes in the classification of epilepsies 2017:
1. The classification contains three diagnostic levels:
First level:type of attack (indicates the onset of an attack) - focal, generalized, unknown (with unknown onset, unknown).
Second level: type of epilepsy – focal, generalized, combined (generalized and focal) and unknown.
Third level: epileptic syndrome.
The classification did not affect epileptic syndromes; they remained the same as in 1989.
2. The etiological diagnosis should be considered at each stage of diagnosis, which may lead to significant changes in therapy.
Epilepsy is divided into six etiological categories :
structural, genetic, infectious, metabolic, immune and with an unknown etiological factor.
Fourth level – comorbid conditions .
The ILAE 2017 operational classification of seizure type is not hierarchical. This means that levels may be skipped.
How to use the new classification of epilepsies 2017
We must make sure that these are indeed epileptic paroxysms.
The classification does not consider the differential diagnosis between epileptic and.
To establish a diagnosis in a patient, the seizures he or she is having must first be classified. The classification of seizures was developed primarily for neurologists, who must differentiate the type of seizures.
Second level classification - determination of the form of epilepsy; the third level is a specific epileptic syndrome.
Separately, it should be taken into account comorbidity, which refers to intellectual and mental disorders. Particular attention is paid to the assessment of cognitive and behavioral disorders in epileptic encephalopathies and developmental encephalopathies.
First, we determine what kind of attacks they are: focal or generalized.
- has origin from networks of neurons limited to one hemisphere. These networks can be local or widespread. A focal seizure may originate from subcortical structures.
When widespread, the attack becomes bilateral tonic-clonic . The previously used term "" is obsolete and is not recommended for use.
It occurs at a certain point with the rapid involvement of the neural networks of both hemispheres. May include cortical and subcortical structures, but not necessarily the entire cortex.
The border between focal and generalized seizures is quite blurred.
Expanded classification of seizures 2017
Classification of seizure type 2017
| Initial manifestations are focal | Initial manifestations are generalized | Initial manifestations are unknown | |
| With consciousness preserved | With impaired consciousness | Motor:
tonic-clonic |
Motor:
tonic-clonic |
| Motor symptoms at the onset of the attack: | clonic | epileptic spasms | |
| Automatism | myoclonic | ||
| Atonic | myoclonic-tonic-clonic | Non-motor: | |
| Clonic | myoclonic-atonic | conduct disorder | |
| Epileptic spasms | atonic | ||
| Hyperkinetic | epileptic spasms | ||
| Myoclonic | Non-motor (absence): | Unclassifiable | |
| Tonic | typical | ||
| Non-motor symptoms at the onset of the attack: | atypical | ||
| Autonomous | myoclonic | ||
| conduct disorder | eyelid myoclonia | ||
| cognitive impairment | |||
| emotional disturbances | |||
| sensory disturbances | |||
| ABOUTt focal to bilateral tonic-clonic | |||
- From the classification of seizure types, it is clear that tonic, clonic, myoclonic and other seizures can be either focal or generalized.
- Instead of “focal attack with secondary generalization” it is proposed to use the term “ seizures with focal onset and transition to bilateral tonic-clonic seizures «.
- For focal seizures, determination of level of consciousness is not necessary.
- Retained consciousness means that a person is aware of himself and his environment during an attack, even if he is motionless.
- The classification is in English; when translating into many languages, difficulties arose in the correctness of the translation and a number of questions arose.
So instead of the word “ consciousness" in Russian " consciousness" the term is used " aware“, translated as “awareness, activity, attentiveness, knowledge about oneself and the world around us.” Therefore, if strictly translated from English, we get “conscious seizures with a focal onset” and “seizures with a focal onset and impairment of awareness (awareness) «.
Since in Russian it is impossible to discern the difference between the words consciousness and aware, they can be translated as “ focal seizures in clear consciousness " And " focal seizures with impaired awareness «.
These terms replace the older terms simple and complex partial seizures.
- Stopping activities (or behavior) sounds like " behavior arrest«.
Summary table of old and new seizure terms:
| New term (select from, specify) | |
| Frontal, temporal, parietal partial | Focal |
| Secondarily generalized | Focal with evolution into bilateral tonic-clonic |
| Complex partial, dialeptic, limbic, psychomotor, mental, dyscognitive | Focal with disturbance/change in consciousness, or focal with impaired awareness |
| Aura, simple partial | Focal in consciousness, or conscious focal |
| Atonic, astatic | Focal or generalized atonic |
| Dacristic, gelastic | Focal (conscious or with impaired awareness) emotional (dacristic, gelastic) |
| Olfactory, visual, gustatory | Focal (conscious or impaired awareness) sensory (olfactory, visual or gustatory) |
| Jacksonian, Rolandic, sylviary | Focal conscious motor |
| Akinetic | Focal with cessation of activity, generalized absence |
| Freezing, freezing, stopping, freezing, pause | Focal (conscious or impaired awareness) with cessation of activity |
| Drop attack | (Focal or generalized) atonic, (focal or generalized) tonic |
| Infantile spasms | (Focal, generalized or unknown origin) epileptic spasms |
New seizure abbreviations can be found in the publication on the ILAE Classification of Epilepsies 2017 website.
Glossary of terms
:
Focal YBR FAS- focal conscious seizure, previously called a simple partial seizure.
FBTCS- focal seizure with evolution into bilateral Tonino-clonic seizure.
After determining the type of seizures, we move on to the second stage of classification of epilepsies: type of epilepsy.
- Added a new type of epilepsy: combined (generalized and focal). This category is for cases in which there are features of both generalized and focal forms of epilepsy (for example, Dravet syndrome).
- Multifocal epilepsy is classified as focal.
- The etiology of epilepsies is also not always only structural or genetic (for example, tuberous sclerosis, cytomegalovirus encephalitis).
- Instead of the term " symptomatic » epilepsy we use an established etiological factor (structural, or infectious, or genetic, or infectious, or metabolic, or immune), otherwise with a combination of etiological factors (structural, infectious, etc.).
- Instead of the term " probably symptomatic " epilepsy or " cryptogenic"We use the term epilepsy of unknown etiological factor.
- Instead of the term " idiopathic"recommended term" genetic «.
Idiopathic - the term denotes some predisposition to the development of epilepsy. The cause of genetic forms of epilepsy is the development of a de-novo mutation. For most genetic forms of epilepsy, mutations are unknown (JME, DAE), so molecular genetic testing is not required to establish a diagnosis.
TO genetic generalized epilepsies (GGE) include: (DAE), (JME), JAE, epilepsy with isolated GSP.
In GGE, the mutation is usually unknown.
Molecular - genetic testing is not required.
The diagnosis is made based on the clinical picture and research into familial forms of the disease.
- The term " benign ". These forms are fraught with serious complications. For example, with DAE, psycho-social problems are noted, and with Rolandic epilepsy, learning difficulties are noted. Therefore, instead of benign, it is recommended to use the term self-limiting, or “ self-limiting ", or "responsive to pharmacotherapy", or pharmacoresponsive forms, which should be used in appropriate cases. “Self-limited” refers to the probable spontaneous resolution of the syndrome.
- In addition, the use of the terms “malignant” and “catastrophic” is no longer recommended.
- Terms " dyscognitive", "simple partial", "complex partial", "psychic" and " secondary generalized » are no longer used.
- It is necessary to dwell separately on epileptic encephalopathies or developmental encephalopathies , in which epileptic activity itself serves as a severe damaging factor, which causes serious mental and behavioral disorders. The condition may worsen over time.
The new classification emphasizes that developmental encephalopathy, or encephalopathy of the developing brain, or simply an abnormality of brain development, can co-occur with epileptic encephalopathies.
Developmental delay in such children often precedes seizures.
In addition to epilepsy, they are often comorbid with other severe disorders, such as cerebral palsy or ASD ().
For many childhood encephalopathies, the prognosis remains unfavorable even after the cessation of attacks, often even after the disappearance of epileptic activity on the EEG.
Unlike developmental encephalopathies that begin in the womb or after birth, epileptic encephalopathies can begin at any age . Their course largely depends on the correctness of antiepileptic therapy.
Recently, people have been talking not about developmental disorders or epileptic encephalopathy, but about the genetic pathology underlying a particular case.
The old term “symptomatic generalized epilepsy” refers to both encephalopathy associated with developmental disorders and seizures, epileptic encephalopathies, and nonprogressive encephalopathies accompanied by generalized epileptic seizures.
- Information about epileptic syndromes is constantly updated. There are currently no recognized or unrecognized ILAE syndromes. The syndromes remained the same.
Epileptic syndrome
Epileptic syndrome is a set of characteristics, including seizure type, EEG and neuroimaging data; often has an age-dependent nature, provoking factors, chronological dependence and (sometimes) prognosis.
There may be a characteristic comorbidity- intellectual and mental disorders.
The syndrome may have associated etiological, prognostic and therapeutic implications.
It often does not correspond to the etiology of epilepsy, but determines the tactics of treatment and monitoring of the patient.
ICD will be released in 2018 and will take into account the new classification of epilepsies.
There is active discussion and adoption of the new classification of epilepsies in 2017 at conferences of neurologists and epileptologists. Thus, in October 2017, the annual VIII Russian Congress on Pediatric Epileptology was held in Moscow within the framework of the XVI Russian Congress “Innovations in Pediatrics and Pediatric Surgery”.
Current issues were presented and discussed, the most important of which was the new classification of epilepsies in 2017. I was able to take part in the Russian Congress and listen to scientific reports from respected colleagues. This memorable photograph shows E.D. Belousova, V.I. Guzev, O.K. Volkov and E.E. Ermolenko. at the symposium Genetic epilepsies.
So we switched to a new classification of epilepsies 2017, the terminology, capabilities and approach to diagnosis, determining optimal antiepileptic therapy have changed, which improves the quality of care for people with epilepsy.
32nd International Congress on Epilepsy in Barcelona 2017
Author of the article: doctor, neurologist –
Relevance of the topic of new treatment for epilepsy
- More than 75% of patients with epilepsy in the world do not receive adequate anticonvulsant therapy
- Achieving remission is possible in 60–70% of cases
- Resistance is the lack of effect from the use of first-line drugs (carbamazepines, valproates) at maximum tolerated doses in mono- or duotherapy, or a combination of one of them with new generation AEDs (lamotrigine, topiramate, levetiracetam and others).
What approaches to overcome pharmacoresistance?
- Surgery
- Vagus nerve stimulation
- Hormone therapy
- Immunoglobulins
- New AEDs with a new, previously unused mechanism of action
We present 1 clinical case of a drug-resistant form of epilepsy
Patient M., age over 20 years.
Seizures: gelastic (epileptic seizures of laughter), serial (6 – 12/day), almost daily; motor-tonic; versive 1-3/week; VGSP 1-4/year.
Ill since age 10. The diagnosis was made: Tuberous sclerosis.
He was observed by a pediatric epileptologist, geneticist, and psychiatrist.
In treatment I received:
Combinations of AEDs: Depakine + Topamax; depakine + phenobarbital; Depakine + Topamax +
The frequency of attacks remained: VGSP 1 - 2/year, focal attacks from 1-3/week, to series of 6-15/day. There has been an increase in attacks over the past year.
Hospitalization to the neurological department for treatment correction. On the day of admission, a series of gelastic attacks (twice stopped with IV benzodiazepines).
In therapy I received: 175 mg/day, Topamax 150 mg/day, Keppra 1000 mg/day.
The introduction of a new generation of AEDs has begun: Titration of perampanel 2 mg/day with weekly intervals up to 8 mg/day.
At a dose of 4 mg/day, gradual withdrawal of Keppra was started.
Discharged after 21 days. The attacks did not recur
After 1.5 months at a second consultation
No seizures. AEDs taken: Depakine - Chronosphere 1750 mg/day, perampanel 6 mg/day (dysphoria appears at a dose of 8 mg/day), Topamax 100 mg/day. Topamax is being gradually withdrawn.
2 clinical case
Patient D., age over 30 years.
Seizures:
1. dizziness, version of the head to the left, sometimes – tonic tension in the right hand;
2. freezing, staring, automotor;
3. rare VGSP.
The duration of focal attacks is from 30 seconds. up to 1.5 min. Frequency is from 1-2/day to 1-3/month.
Ill since age 12. He connects his illness with a previous head injury and concussion. Hippocampal sclerosis on the left was discovered for the first time 20 years after the onset of attacks using high-field MRI. This congenital pathology was not previously detected on MRI.
About 10 years ago, she suffered from status epilepticus of focal and secondary generalized convulsive seizures during pregnancy. There were hospitalizations for emergency reasons with an increase in attacks.
Treatment: Carbamazepine, Valproate.
Polytherapy: valproate + carbamazepine; valproate + lamotrigine; valproate + topiramate + keppra; topiramate + lamotrigine + valproate.
The introduction of a new generation of AEDs has begun: titration of perampanel to 8 mg/day. Then gradual withdrawal of topiramate, gradual withdrawal of lamotrigine.
Termination of focal attacks at a dose of perampanel 6 mg/day.
There were no epileptic seizures for 2 months.
She received AEDs: perampanel 8 mg/day + valproate 1500 mg/day.
At the patient’s insistence, resection of the left hippocampus and part of the temporal lobe was performed. Intraoperatively, focal cortical dysplasia (FCD) of the left temporal lobe was detected. The postoperative period was complicated by hemorrhage in the surgical area.
A month after surgical treatment, there was a recurrence of focal and secondary generalized attacks. Emergency hospitalization to the neurological department, where the emergency situation was stopped within one day. She was discharged with the same doses of AEDs.
When repeated MRI— FCD was detected in both frontal lobes, postoperative changes in the left temporal lobe.
No seizures for 3 months.
3 clinical case
Patient L., age after 40 years
Seizures: staring, freezing, smacking, wrist automatisms, dystonic positioning of the left hand, there may be ambulatory automatisms, VGSP. The frequency of focal attacks is from 1-2/week to serial 5–8/day; VGSP 1 – 3 /month.
It is observed from 1.5 years of age (febrile complex seizures), from 3 years of age – focal and VGSP.
Therapy: Phenobarbital, Benzonal + diphenine; valproate + finlepsin; valproate + topiramate + lamotrigine; lamotrigine + topiramate + levetiracetam.
Over the course of 3 years, gradual abolition of barbiturates and diphenine. Phenobarbital 50 mg/day was maintained. The following are observed: VGSP 1 – 2 / year; focal - with the same frequency, but the duration decreased by 2 times.
Then there was an increase in attacks throughout the year. In a neurological hospital, therapy: topiramate 300 mg/day, levetiracetam 2500 mg/day, lamotrigine 250 mg/day, phenobarbital 50 mg/day. The frequency of focal attacks is 2 – 6/day; VGSP 1 in 1 – 2 months.
Change in therapy: Titrate perampanel 2 mg/week to 6 mg/day. Gradual withdrawal of levetiracetam (for financial reasons). There is a decrease in focal seizures by 75%.
She was discharged from the hospital on therapy: topiramate 300 mg/day, lamotrigine 250 mg/day, perampanel 6 mg/day, phenobarbital 50 mg/day. Severe aggression was observed with perampanel at a dose of 8 mg/day.
Therapy after 4 months: perampanel 6 mg/day, lamotrigine 250 mg/day, phenobarbital 50 mg/day.
: hippocampal sclerosis on the left + FCD in the left temporal lobe.
Perampanel (Ficompa)
2-(2-oxo-1-phenyl-pyridin-2-yl-1,2-dihydropyridin-3-yl) benzonitrile hydrate (4:3)
The first representative of selective non-competitive antagonists of inotropic, sensitive to a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), glutamate receptors of postsynaptic neurons.
Mechanisms of action of antiepileptic drugs
Rogawski MA, Löscher W. Nat Rev Neurosci 2004; 5:553–564; Rogawski MA. Epilepsy Currents 2011; 11:56–63.
Competitive antagonists can be displaced by high doses of glutamate
1. Glutamate cannot bind to the receptor and activate it. But at high concentrations of glutamate, glutamate displaces the antagonist, binds to the receptor and activates it, opening the channel and allowing an inward Na+ current.
In the presence of a competitive antagonist
In the presence of perampanel, glutamate binds but cannot activate the receptor. The noncompetitive antagonist is not displaced by glutamate. The action of the antagonist on the receptor is maintained, and the channel remains closed.
Rang HP, et al. From: Pharmacology.1995.
Perampanel (Faycompa) is a non-competitive AMPA receptor antagonist
In the presence of perampanel1
1Hanada T, et al. Epilepsia 2011;52:1331–1340; 2Kenakin T. Molecular Interventions 2004;4:222–229.
Pharmacological properties of Faikompa (perampanel)1
Possibility of single dosing
- Bioavailability when taken orally is almost 100%
- Peak PC after 2.5 hours
- PC leveling 14 days.
- Half-life 105 hours
No clinically significant effect on drug metabolism - can be combined with any other AEDs
When combined with inducers, dose adjustment is necessary
- Linear pharmacokinetics – no need for PC control
- Plasma protein binding 95% - any displacement by other drugs that bind to plasma proteins is quickly balanced.
- Unique mechanism of action - the ability to combine with any other AEDs
- Neither an inducer nor an inhibitor of P450
- CYP3A4 inductors increase the clearance of Fycompa
- Equilibrium PC Faycompa is achieved faster
Drug interactions Fycompa (perampanel)
Indications for use
As an adjuvant drug for the treatment of partial seizures in patients with epilepsy aged 12 years and older in the presence or absence of secondary generalized seizures.
Side effect (adverse events)
FREQUENT(greater than or equal to 1/100; less than 1/10):
- Decreased or increased appetite
- Aggression, anger, anxiety, confusion
- Dizziness, drowsiness, ataxia, dysarthria, imbalance, irritability
- Diplopia, blurred vision
- Central vertigo
- Nausea
- Backache
- General disorders: fatigue, gait disturbances
- Weight gain
- Falls
Safety: Commonly reported adverse events noted in at least 5% of patients and identified using SMQs related to hostility/aggression
Perampanel titration scheme (Ficomps)
- Initial dose 2 mg/day (evening)
- Titration of 2 mg/week when taking enzyme-inducing AEDs
- Titration of 2 mg/2 weeks when taking non-enzyme-inducing AEDs
Half-life 105 hours
Clinically significant improvement in seizure control was observed at a dose of 4 mg/day and increased as the dose was increased to 8 mg/day.
Dose more than 8 mg/day – no significant increase in effectiveness was observed
Contraindications
- Hypersensitivity
- Pregnancy and lactation
- Severe renal or liver failure, patients on hemodialysis
- Children under 12 years of age (no data on efficacy or safety)
- Galactose intolerance, lactase deficiency or glucose-galactose malabsorption.
So, using clinical examples, we were convinced of the effectiveness of the newest drug for the treatment of epilepsy Perampanel (Ficompy) . Reviews about the drug help you choose the right treatment tactics; select an administration regimen and therapeutic dose; avoid side effects and take into account contraindications; start taking modern medications earlier; achieve control over epileptic seizures, despite the ineffectiveness of previously used various drugs in high doses and their combinations.
Watch the video new treatments for epilepsy
MOSCOW, December 26 - RIA Novosti. Biologists from Russia monitored how the functioning of memory center cells in rats changes after the onset of an epileptic seizure and created a substance that dulls their severity, according to an article published in the journal Epilepsy Research.
Scientists have created the first potential cure for epilepsyAmerican doctors have created a small protein molecule that suppresses neurons in the temporal lobe of the brain that are responsible for causing epileptic seizures, without killing them, which will allow doctors in the near future to save patients from the most common form of epilepsy.“The use of our drug or its analogues may contribute to the development of a new approach for the treatment of temporal lobe epilepsy. The development of new strategies for the treatment of pharmacologically resistant forms of epilepsy can help reduce the damage caused to brain cells during seizures, and opens up new possibilities for the treatment of this disease,” said Valentina Kichigin from the Institute of Theoretical and Experimental Biophysics of the Russian Academy of Sciences in Pushchino, whose words are quoted by the press service of the institution.
According to statistics from the World Health Organization, today there are approximately 50 million people living in the world suffering from various forms of epilepsy. Approximately 40% of these cases are not treatable, and approximately half of epileptics cannot take medications without experiencing side effects.
Epileptic seizures and all the symptoms associated with them arise as a result of the fact that nerve cells suddenly begin to synchronize their impulses, simultaneously “turning on” and “turning off.” Scientists do not yet know why this happens, and without revealing the reasons for this behavior, a full fight against epilepsy is impossible. Recently, scientists from ITEB RAS discovered that epileptic seizures can occur due to the fact that nerve cells mistakenly believe that there are almost no nutrients left inside them.
Kichigina and her colleagues at the institute studied the roots of one of the most severe forms of epilepsy, the foci of which are located inside the hippocampus, the brain's memory center, located in the temporal lobe of the brain. In some cases, doctors have to remove some of its cells if the seizures cannot be stopped, which deprives the patient of the ability to remember new information.
Russian scientists tried to uncover the roots of this epilepsy and find a way to treat it in less radical ways, observing what happened to the neurons of the hippocampus of rats during an artificial epileptic seizure caused by a powerful neurotoxin - kainic acid.
These observations showed that injection of the toxin into the hippocampus led to massive death of so-called pyramidal cells, the main signal processors in the cerebral cortex and memory center, and damage to the surviving cells, especially those parts responsible for the synthesis of new protein molecules and metabolism.
The nature of this damage has led scientists to believe that most of it can be suppressed using one of the neurons' built-in repair systems, which are controlled by so-called cannabinoid receptors. They are special outgrowths on the surface of nerve cells that respond to analogues of the active substances of marijuana that are produced by the brain.
The problem, as the researchers note, is that the concentration of such molecules in the brain is kept at a minimum level by a special enzyme called FAAH, which destroys most of the cannabinoid molecules before they have time to connect with neurons. Guided by this idea, Russian biophysicists injected a special substance, URB597, into the brains of rats, which blocks the action of this protein, about a day after the seizure.
As this experiment showed, URB597 significantly improved the hippocampus and well-being of rats in which the neurotoxin caused relatively mild seizures in which they did not have convulsions. In such cases, the number of dead neurons was reduced by approximately half, and the surviving cells were not damaged.
With the development of more severe seizures and convulsions, the effect of URB597 was noticeably weaker - hippocampal neurons died almost as en masse as in rats from the control group, and not all traces of damage disappeared from the surviving cells.
However, scientists believe that URB597 and other substances that promote the activation of the cannabinoid "self-repair" system of neurons may protect the brains of epileptics from damage and could save thousands of people from having to undergo surgery that would forever send them into endless Groundhog Day.
