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 a great deal of mental stress for the patient and family members due to deep-rooted social prejudice and public discrimination.
(2) Unwarranted risk of adverse reactions due to antiepileptic drugs, some of which, such as exfoliative dermatitis, necrotizing hepatitis, and suppression of the hematopoietic system, are lethal.
(3) An unnecessary financial burden is added.
Most of the epilepsy consultations are in the interictal period, and physicians rarely witness seizures, and most of the physical examinations have no abnormal findings. 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 such as spike (sharp) waves and spike (sharp) slow complex waves recorded between seizures have the most reference value. It is important to note 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, which often appear on one side and are therefore mistakenly treated with carbamazepine, phenytoin sodium, or the newer selective GABAergic drugs, gabapentin, tiagabine, and aminoglutethimide, as clonic seizures of focal origin. 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: (1) detailed history taking is essential to determine the type of seizure; (2) video EEG can be used to determine the type of seizure if seizures are more frequent; video EEG is also extremely useful in confirming the diagnosis of epilepsy; (3) broad-spectrum sodium valproate, clobazam (oxymorphone) lamotrigine, or tolclozapine can be used first if it is difficult to determine partial seizures or atonic seizures or myoclonic seizures Pyridoxine
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” with poor control.
(1) Some drugs such as carbamazepine and phenobarbital can be monitored therapeutically and the dose can be adjusted to achieve effective blood levels; (2) the dose can be increased gradually until the initial clinical adverse effects occur; (3) some patients reduce the dose on their own for fear of adverse effects at high doses, so it is important to understand whether there are compliance problems; (4) if there is no satisfactory response with the maximum tolerated dose, the dose should be reduced to avoid chronic toxicity. (4) If there is no satisfactory response with the maximum tolerated dose, reduce the dose to avoid chronic toxicity and switch to a 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, but in fact, first-line antiepileptic drugs are effective at effective doses or blood concentrations. Current monotherapy remains an important principle, and polypharmacy is used only in more refractory epileptic patients who have failed monotherapy.
It is recommended that: (1) the first drug is definitely ineffective and then gradually replaced by a second effective antiepileptic drug; (2) the second drug can be added if 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, with less interaction between the two drugs; (4) the first drug should be withdrawn if the second drug responds well after addition. (4) If the second drug responds well, the first drug should be withdrawn.
(5) Failure to diagnose an 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.
It is recommended to (1) be familiar with the classification of epilepsy and epileptic syndromes; (2) supplement with EEG, especially video EEG; (3) try to avoid precipitating factors.
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 overtreatment at the beginning in order to accelerate seizure control, or chronic epileptic patients who have partial response to antiepileptic drugs are given further increased doses. 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.
It is recommended that: (1) epilepsy treatment should be started with small doses and gradually increased, and some antiepileptic drugs can be monitored by blood concentration to adjust the dose; (2) any patient with maximum tolerated dose without significant improvement should be slowly reduced, so as to reduce side effects without affecting the level of seizure control; (3) if antiepileptic drugs beyond the maximum tolerated dose are 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, 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 for the treatment of akathisia or myoclonic seizures and can exacerbate them. The different side effect profiles limit the use of certain antiepileptic drugs in certain patients, such as topiramate in patients with kidney stones; 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 valproate and lamotrigine are used together, the latter is slow to increase because 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 lennox Gastaut syndrome and West syndrome, which are refractory epilepsies, and the new antiepileptic drugs topiramate, lamotrigine and felbamate have better control effects; also, gabapentin and lamotrigine have no drowsiness effect, which is beneficial for elderly patients, and they rarely interact with each other. They are also popular among patients with medical conditions or using other drugs for contraception.
Recommendations: (1) Any patient whose seizures cannot be controlled with standard antiepileptic drugs or who develops serious side effects should consider new antiepileptic drugs, especially topiramate and aminoglutethimide are more effective in the control of refractory seizures; (2) the indications should be mastered; (3) attention should be paid to new adverse effects.
8. Premature withdrawal of antiepileptic drugs
After 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 relapse rate was 43% in the withdrawal group and only 10% in the continued medication group. Of course, not stopping medication for a long time for fear of relapse is not a good policy.
It is recommended that (1) the time to stop medication should be considered according to the risk factors of possible relapse (such as frequent seizures, long duration of illness, EEG still abnormal, and multi-drug treatment); (2) EEG should be performed to understand whether there are seizure-like waves after the clinical seizures have disappeared for many years. (3) Withdrawal should be slow, less than 1 year for generalized tonic-clonic seizures and less than 6 months for disoriented seizures, and longer for those with high doses of the original medication.
9. Failure to obtain the cooperation of patients and families
Domestic and international data 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 due to 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 family members is an important part of successful treatment.
It is recommended to (1) strengthen the propagation of scientific knowledge about epilepsy and seek the active cooperation of patients; (2) follow up patients in regular outpatient clinics to understand the situation of seizures and treatment cooperation of patients and correct the unreasonable medication practices in time.
10. Indiscriminate surgical treatment
The treatment of epilepsy is non-pharmacological, including surgery, stereotactic radiosurgery (r-knife), and vagus nerve stimulation. The main target of these treatments should be refractory epilepsy for which drug therapy is ineffective. The fundamental prerequisite for surgical and r-knife treatment is an accurate diagnosis and localization of the lesion, 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) is required to identify the epileptic lesion so that better The results can be better. Currently, some medical units, for economic reasons, indiscriminately administer surgical treatment to patients who can be controlled by drugs, whose localization is not clear, and whose diagnosis is not even determined. Surgical treatment is ultimately destructive, so it is self-evident that it leads to serious adverse consequences.
It is recommended to (1) strictly grasp the indications for surgical treatment – refractory epilepsy; (2) integrate clinical manifestations, structural and functional examinations for localization, and accurately identify the lesion site.