Epilepsy is a chronic disease and seizure control is the mainstay of epilepsy treatment. With the in-depth understanding of the pharmacokinetics of antiepileptic drugs, the implementation of antiepileptic drug blood concentration monitoring, the introduction of new antiepileptic drugs, and the progress of non-pharmacological treatment (such as surgery, vagus nerve stimulation, r a knife, etc.), the treatment of epilepsy has made great progress, but in clinical practice, there are still many misconceptions worth noting, which are listed below.
1. Treatment without clinical diagnosis of epilepsy
Many non-epileptic seizure disorders such as migraine (including those with non-specific abnormal EEG) and pseudo-seizures are misdiagnosed as epilepsy and given anti-epileptic treatment (including drugs and even r-knife).
① Misdiagnosis as epilepsy leads to great mental stress for the patient and family members due to deep-rooted social prejudice and public discrimination;
(ii) Unwarranted risk of adverse effects caused by antiepileptic drugs, some of which are fatal, such as exfoliative dermatitis, necrotizing hepatitis, and suppression of the hematopoietic system;
(③) Adding an unnecessary financial burden.
Therefore, detailed history is the key to diagnosis, including patients, relatives and seizure witnesses. The past history and family history are also very important. The EEG examination has a great reference value for diagnosis, especially when the seizure is recorded, but such opportunities are rare. The epileptiform discharges recorded between seizures, such as spike (sharp) waves and spike (sharp) and slow complex waves, have the most reference value, while non-specific abnormalities (such as slow waves) must be combined with typical medical history. It is important to point out that epilepsy is a clinical diagnosis, and even if there are abnormalities in the EEG without clinical seizures, it cannot be diagnosed as epilepsy and given antiepileptic treatment.
2. Failure to select drugs according to seizure type
There are many types of seizures, and the determination of seizure type involves both drug selection and etiological examination. For example, complex partial seizures are often characterized by transient impairment of consciousness, especially when there is a focal lesion in the amygdala, and immobility gaze seizures, which are characterized by sudden cessation of active movements, wide-open eyes, staring forward, unresponsive to the surroundings, complete cessation of limb and trunk activities or increased muscle tone. This kind of seizure is often mistaken for anhedonia and given as ethosuximide, which aggravates the condition. On the contrary, it is not uncommon to mistakenly treat a transient partial seizure with carbamazepine or phenytoin because of a failure to recognize it correctly. Another example is myoclonic seizures in adolescents with myoclonus often appearing on one side and therefore mistakenly treated as clonic seizures of focal origin, resulting in treatment with carbamazepine, phenytoin sodium or the new selective GABAergic drugs – gabapentin, tiagabine and aminoglutethimide. Some partial seizures in frontal lobe epilepsy have been misdiagnosed as non-epileptic psychotic seizures, which delays treatment. Bilateral frontal spikes are common and are mistaken for bilaterally synchronized full-blown seizures from time to time.
Recommendations.
①A detailed medical history is essential to determine the type of seizure;
(2) Video EEG can be used to determine the type of seizures if seizures are frequent; video EEG is also very useful in confirming the diagnosis of epilepsy;
③In the case of difficult to determine partial seizures or akathisia seizures, myoclonic seizures, then broad-spectrum sodium valproate, clobazam (oxyisoclopramide) lamotrigine or topiramate can be used first
3. Failure to ensure maximum tolerated dose in poorly controlled seizures
Failure to apply the maximum tolerated dose in poorly controlled seizures is a very common error in epilepsy drug therapy due to experience alone. The standard first-line antiepileptic drugs plus valproic acid, carbamazepine, and newer drugs such as oxcarbazepine, topiramate, and gabapentin are all dose-response related, and if the patient is not given the so-called “conventional dose” on an individualized basis, the patient will be in a “subtherapeutic state” The patient will be in a “subtherapeutic state” resulting in poor control.
Recommendations.
①Some drugs such as carbamazepine, phenobarbital, etc. can be monitored therapeutically and the dose can be adjusted to achieve effective blood levels;
②The dose can be gradually increased until the initial clinical adverse effects appear;
③Some patients reduce the dose on their own for fear of adverse reactions at high doses, so it is important to understand whether there are compliance problems;
④If there is no satisfactory response with the maximum tolerated dose, then reduce the dose to avoid chronic toxicity and switch to the second antiepileptic drug.
4. Add a second drug before negating the efficacy of the first drug
Some people add another low-dose drug soon after the first antiepileptic drug to obtain high efficiency. In fact, first-line antiepileptic drugs are effective at effective doses or blood concentrations. Currently, monotherapy remains an important principle, and polypharmacy is used only in more refractory epileptic patients who have failed monotherapy.
Recommendations.
① Gradually switch to a second effective antiepileptic drug after the first drug is definitely ineffective;
(2) The first drug is effective, but the control is not satisfactory;
(3) The two drugs used together should be chemically different, preferably with two different antiepileptic mechanisms, and the interaction between the two drugs should be minimal;
(4) If the second drug responds well, the first drug should be withdrawn.
5. Failure to diagnose epilepsy syndrome
Epilepsy syndromes can provide additional information such as age of onset, etiology, seizure type, contributing factors, severity, circadian pattern, chronicity, prognosis, and treatment options. Many epilepsy syndromes are age-related, and the age of seizure onset can provide clues to the correct diagnosis of the epilepsy syndrome, and the diagnosis of the syndrome can in turn guide appropriate drug therapy. This type of epilepsy also does not require imaging such as MRI. It is best to use sodium valproate instead of sodium phenytoin, carbamazepine, aminocaproic acid, tiagabine and gabapentin, because these drugs are not only ineffective but also aggravate the seizures.
Recommendations.
① Familiarize yourself with the classification of epilepsy and epilepsy syndromes;
②Supplement with EEG, especially video EEG;
③Avoid the precipitating factors as much as possible.
6. Use of too high a dose of antiepileptic drugs
In the treatment of newly diagnosed epileptic patients, some people are given high doses of excessive treatment at the beginning in order to accelerate seizure control, or in chronic epileptic patients who have partial response to antiepileptic drugs, further higher doses are given. Theoretically, every early stage epilepsy should be treated with a gradual increase of low doses at the beginning of treatment. In general, simple tonic-clonic seizures require a lower amount of antiepileptic drugs than partial seizures.
Recommendations.
①Epilepsy treatment should be started with small doses and gradually increased. Some antiepileptic drugs can be monitored by blood levels to adjust the dose;
(2) If any patient is treated with the maximum tolerated dose without significant improvement, the dose should be slowly reduced so that side effects are reduced without affecting the level of seizure control;
If the maximum tolerated dose of antiepileptic drugs is needed to control seizures, surgical treatment should be considered.
7. Inappropriate application of new antiepileptic drugs
Many new antiepileptic drugs have been developed internationally, nine of which have been approved by the FDA, including felbamate, lamotrigine, gabapentin, topiramate, aminoglutethimide, levan tiracetam (levetiracetam), tiagabine, oxcarbazepine and zonisaguan, which raises the question of how to apply them rationally. For example, the selective GABAergic compounds gabapentin, tiagabine, and aminoglutethimide cannot be used to treat akathisia or myoclonic seizures, but can exacerbate them, and tiagabine can even cause non-convulsive status epilepticus in some patients. The different side effect profiles limit the use of certain antiepileptic drugs in certain patients, such as topiramate in patients with renal calculi; fexofenprox is not suitable for patients with acute liver disease or acute blood disorders because it can cause aplastic anemia or acute liver failure; when sodium valproate and lamotrigine are used together, the latter is slow to be dosed because sodium valproate significantly inhibits the metabolism of lamotrigine; similarly, the standard antiepileptic drugs should be reduced by 25% in the former when felbamate is added, because felbamate has a dose-dependent inhibition of valproate, phenytoin, and carbamazepine epoxide metabolism.
Although controlled trials have shown that new antiepileptic drugs (e.g., lamotrigine, gabapentin, oxcarbazepine, and aminoglutethimide) are effective for partial-onset seizures, most experts oppose their use as first-line agents, one reason being that they are too expensive, and advocate their use when patients cannot tolerate first-line agents such as valproate and carbamazepine. However, some new drugs have their advantages, such as lennoxGastaut syndrome and West syndrome, which are refractory epilepsies, and the new antiepileptic drugs topiramate, lamotrigine and felbamate have a better control effect; also, gabapentin and lamotrigine have no drowsiness effect, which is beneficial to the application of elderly patients, and they rarely interact with each other. They are also welcomed by patients with medical conditions or using other drugs for contraception.
Recommendations.
①New antiepileptic drugs should be considered in any patient whose seizures cannot be controlled with standard antiepileptic drugs or who develops severe side effects, especially topiramate and aminoglutethimide are more effective in the control of refractory seizures;
②Indications should be mastered;
③ Pay attention to new adverse reactions.
8. Premature withdrawal of antiepileptic drugs
After the seizures are controlled, premature withdrawal of drugs may lead to recurrent seizures, and sudden withdrawal may also promote persistent status epilepticus. According to Chadwick [1], in 1031 patients who had been in remission for more than 2 years, the recurrence rate was 43% in the withdrawal group and only 10% in the continued medication group. Of course, prolonged drug withdrawal for fear of relapse
fear of relapse is not a good strategy.
Recommendations.
(1) Consider the time to stop medication according to the risk factors for possible relapse (e.g. frequent seizures, long duration of disease, still abnormal EEG, previous polypharmacy, etc.);
②Electroencephalography (EEG) should be performed for many years after the clinical seizures have disappeared to understand the presence of seizure-like waves, ideally 24h dynamic EEG;
③When withdrawing medication, it should be done slowly, not less than 1 year for generalized tonic clonic seizures and not less than 6 months for disoriented seizures;
④If there is a relapse, the original treatment plan should be resumed immediately.
9. Failure to obtain the cooperation of patients and families
The data from home and abroad show that poor compliance is an important factor in the failure of epilepsy drug therapy. Patients often reduce the dosage, increase the dosage, reduce the number of doses or stop the medication arbitrarily for various reasons, and some are deceived by socially inaccurate advertisements and abuse the so-called pure Chinese medicine, which results in either failure to control or toxic side effects. Therefore, the cooperation of patients and families is an important part of successful treatment.
Recommendations.
①Strengthen the propaganda of scientific knowledge about epilepsy and strive for active cooperation of patients;
② Follow up patients in regular outpatient clinics to understand the patient’s seizures and treatment cooperation and correct unreasonable medication practices in a timely manner.
10. Indiscriminate surgical treatment
The treatment of epilepsy is non-pharmacological, such as surgery, stereotactic radiosurgery (r-knife), vagus nerve stimulation. The main target of these treatments should be refractory epilepsy where drug therapy is ineffective. The fundamental prerequisite for surgery and r-knife treatment is accurate diagnosis and lesion localization, so a combination of clinical manifestations, structural imaging (e.g., MRI, CT), and functional examinations (e.g., conventional EEG, dynamic EEG, magnetic resonance spectroscopy, single-photon emission computed tomography, positron emission computed tomography, and magnetoencephalography) are needed to identify the epileptic lesion so as to achieve better This is the only way to achieve better results. In some medical units, for economic reasons, surgical treatment is indiscriminately administered to patients who can be controlled by drugs, whose localization is not clear, and whose diagnosis is not even determined. The surgical treatment is ultimately destructive, so it is self-evident that it leads to serious adverse consequences.
Recommendations.
① Strictly grasp the indications for surgical treatment – refractory epilepsy;
②Integrate clinical manifestations, structural and functional examinations for localization, and accurately identify the lesion site.