Juvenile Myoclonic Epilepsy
What is juvenile myoclonic epilepsy?
Juvenile myoclonic epilepsy (JME) is the most common generalized epilepsy syndrome. It is also called Juvenile Myoclonic Epilepsy of Janz. It usually is first seen in adolescence. Less commonly, it can develop in a child who has had childhood absence epilepsy.
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Seizure Types in JME
Myoclonic seizures are the most common seizure type and occur in everyone with JME.
- Myoclonic jerks or seizures in JME typically happen within 1 to 2 hours of waking up in the morning or after a nap.
- They are described as shock-like and irregular movements of both arms. Sometimes the movements happen only in the fingers, making the person look clumsy or prone to dropping things.
- In about 1 out of 5 people, the myoclonic jerks occur primarily on one side of the body.
- Myoclonic jerks are often triggered by lack of sleep and flashing lights.
- Not all myoclonus or muscle jerks are seizures. Many people have isolated muscle jerks that occur as they are falling asleep. These non-seizure movements are called hypnic jerks.
Myoclonic status epilepticus is rare in JME. This term describes multiple myoclonic seizures that do not readily stop. This occurs when a person first wakes up and is usually triggered by missing a lot of sleep or missing medications.
Generalized tonic-clonic seizures are seen in nearly all people with JME.
- They usually begin a few months after the myoclonic jerks start.
- These also happen in the morning when a cluster of myoclonic jerks may occur before the tonic-clonic seizure.
Absence seizures happen in less than half of people with JME.
- They are often very short (lasting less than 10 seconds) and usually don’t occur every day.
- Absence seizures with JME may not affect a person’s awareness as much as absence seizures in people with childhood or juvenile absence epilepsy.
- Both males and females are affected equally.
What can trigger seizures in people with JME?
One of the most interesting aspects of juvenile myoclonic epilepsy is that there are two very common factors that cause seizures: lack of sleep and stress.
- Lack of sleep and fatigue, primarily after drinking too much alcohol, are the most powerful causes of myoclonic jerks and generalized tonic-clonic seizures in JME.
- Mental and emotional stress are also common triggers, especially excitement or frustration.
- Some people with JME have seizures that are triggered by flickering light, such as strobe lights at dances, TV, video games, or light shining through trees or reflecting off ocean waves or snow. These are called photosensitive seizures.
Learn about managing seizure triggers
Find tips for managing stress
Is JME inherited?
Juvenile myoclonic epilepsy is a genetically determined syndrome. However, most people with JME do not have abnormal results on testing for specific epilepsy genes. About half (50 to 60%) of families with juvenile myoclonic epilepsy report seizures in either a direct relative or a cousin. The inheritance pattern is a complex type, although there are certain subtypes with distinct genetic patterns.
Find information about genetic testing
How is JME diagnosed?
How is JME treated?
- The treatment of juvenile myoclonic epilepsy starts with educating people about lifestyle and avoidance of seziure triggers.
- Valproic acid is the most effective seizure medication to treat juvenile myoclonic epilepsy. However, it is not the appropriate first choice to treat women of childbearing years.
- Lamotrigine is widely used for juvenile myoclonic epilepsy. Infrequently, it may lead to worsening of the myoclonic jerks even though it may help the generalized convulsions and absence seizures.
- Levetiracetam is another possible drug choice. It has been approved for treating myoclonic seizures in juvenile myoclonic epilepsy. However, it has not been well studied for all the seizure types that may be seen.
- Other possible options include topiramate, zonisamide, or clonazepam. Clonazepam given in small doses could be effective for myoclonic jerk.
- Medications that should be avoided include vigabatrin, tiagabine, gabapentin, pregabalin, phenytoin, oxcarbazepine, and carbamazepine, as these can worsen seizures, especially myoclonic jerks and absences in JME. Occasionally, carbamazepine and phenytoin may be useful for generalized convulsions.
- If seizures are not controlled, seek specialized care to determine if seizures are properly diagnosed and to explore all treatment options.
What is the outlook for people with JME?
- Seizures in most people with JME tend to improve after the fourth decade of life.
- Seizures are generally well controlled with medications in up to 90% of people.
- People who have multiple seizure types may require more medications to control them.
- It is likely that lifelong treatment with a seizure drug will be necessary, even in people with well-controlled JME. Withdrawal could result in a relapse of seizures, even in people who have been seizure free for many years with appropriate drugs.
- In some people with mild forms of the condition, the dose of seizure medication may be reduced slowly over months, particularly in older individuals. If myoclonic seizures come back or persist, medications need to be restarted.
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Treatment of myoclonic seizures
Myoclonic seizures are sudden, brief, shock-like contractions that can vary in distribution and intensity. They may be present in different epilepsy syndromes, including some idiopathic generalized epilepsy, epileptic encephalopathies and progressive myoclonus epilepsies. Despite the fact that there are many studies about the pathophysiology of myoclonic seizures and clear descriptions of the different myoclonic epilepsy syndromes, relatively little has been written on treatment. Valproate and some benzodiazepines are widely used to treat myoclonic seizures. In addition, more treatment options exist today as there is emerging evidence to support the efficacy of some newer antiepileptic drugs. On the other hand, some myoclonic epilepsies remain refractory to drug treatment and some antiepileptic drugs may exacerbate or even induce myoclonus. In the coming years, better understanding of mechanisms of myoclonic seizures and myoclonic epilepsies could result in great improvement of therapy and the quality of life of patients.
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Treatment of myoclonic seizures in patients with juvenile myoclonic epilepsy
Author informationCopyright and License informationDisclaimer
Department of Pediatric Neurology, Lille University Hospital, Lille, France; Pharmacology Laboratory, Lille Medical School, Lille, France
Correspondence: Stéphane Auvin, Pediatric Neurology Department, Hôpital Roger Salengro, Lille Cedex, France, Tel +33 3 20 44 40 57, Fax +33 3 20 44 53 93, Email [email protected]
Copyright © Dove Medical Press Limited. All rights reserved
This article has been cited by other articles in PMC.
Drug treatment of Juvenile myoclonic epilepsy (JME) is mainly based on clinical experience and prospective and retrospective studies, with little evidence from randomized clinical trials. There are no head-to-head comparisons between old and new antiepileptic drugs (AEDs) and no drugs licensed specifically for JME. Valproate is unquestionably the drug of the first choice in men with JME. In women, lamotrigine should be preferred regarding teratogenicity and side effects of valproate. In addition, levetiracetam and topiramate are effective and can be use in combination or as second line treatment. Some AEDs can aggravate JME. In addition of AEDs, non-pharmacological treatments are important in JME. JME usually require lifelong treatment because seizures nearly always return after withdrawal of therapy.
Keywords: myoclonic seizure, myoclonic epilepsy, antiepileptic drugs
Juvenile myoclonic epilepsy (JME) is a common epilepsy syndrome that is classified among the idiopathic generalized epilepsies (IGEs) (ILAE ). It is a collection of seizure patterns that are clinically distinct from those in other forms of IGE, with the major characteristic being adolescence-onset myoclonic seizures. Although the pathogenesis is unknown, recent advances, especially in genetics, suggest several possible mechanisms. JME is both genetically and clinically heterogeneous; some clinical differences may indicate differences in pathogenesis in different groups of patients. The nosology and classification of IGE syndromes are currently under revision (Andermann and Berkovic ; Engel ). JME is characterized by a particular pharmacological sensitivity. Valproate has a specific potency. Others antiepileptic drugs (AEDs) are also efficient, such as lamotrigine, clonazepam, topiramate and levetiracetam, while others may have aggravating effects.
Electroclinical features of juvenile myoclonic epilepsy
JME is a common IGE that is characterized by myoclonic seizures. It is the most common IGE in adults, especially in women. Isolated myoclonic jerks of the arms, especially shortly after awakening, are characteristic. Generalized tonic-clonic seizures often occur, and one-third of individuals have absences. The generalized tonic-clonic seizures are often preceded by a few minutes of generalized myoclonus of increasing frequency and intensity. They occur predominantly after awakening. Seizure occurrence is more likely with sleep deprivation, fatigue and alcohol withdrawal. Onset is usually in adolescence but seizures may begin or be diagnosed only in the early 20s. Eighty percent of patients with JME begin having seizures between ages 12 and The mean age of onset for generalized tonic clonic seizures is years. The most important element in the diagnosis of JME is the clinical history.
The typical abnormality on electroencephalography (EEG) is bilateral multiple spike or polyspike-wave complexes which precede a myoclonic jerk. The EEG discharge includes 520 spikes with a frequency between 12 and 16 Hz. The amplitude of spikes is frequently maximal in anterior areas. An ictal recording is best obtained by polygraphic video-EEG performed a provoked early morning awakening during a full-night sleep recording or at least after noctural sleep deprivation.
JME is one of the epileptic syndrome clearly associated with photosensitivity occurring in about 30% (Janz ; Loiseau and Duche ). Myoclonic seizure can be induced by intermittent luminous stimulation in photosensitive patients, but clinical photosensitivity is less frequent than during EEG recording.
In some cases, focal clinical or EEG features or both in patients with JME can be observed. These features include not only unilateral myoclonic jerks but also version and asymmetrical tonic limb posturing (Aliberti et al ; Lancman et al ; Usui et al ).
Misdiagnosis and delayed diagnosis remain common, as reported in the literature (Grunewald et al ; Atakli et al ). Patients frequently come to medical attention only after a generalized convulsion, and the history of much earlier myoclonic jerks is then often obtained only retrospectively (Grunewald et al ).
The goal of management is to render the individual seizure-free without the side effect of the medication. JME require lifelong treatment because seizures nearly always return after withdrawal of therapy (Delgado-Escueta and Enrile-Bascal ; Baruzzi et al ). JME is difficult to treat in about 15% of patients. The predictors of pharmacoresistance include: (1) the coexistence of all three seizures types (myoclonic jerks, absence seizures and GTCS), (2) the existence of associated psychiatric problems, and (3) focal clinical symptoms and/or focal EEG discharge (Dasheiff and Ritaccio ; Fernando-Dongas et al ; Gelisse et al ).
In JME, lack of sleep and alcohol intake can induce seizures. The sleep-wake rhythm has to be regulated. The circumstances interfering with normal sleep and progressive awakening in the morning should be eliminated. If the patient stays up late at night, he should sleep longer the next morning. Alcoholic drinks will only permitted in small quantities, on social occasions. Patients should be advised not to drink in cases of lack of sleep. If the patient has photosensitivity, they should avoid relevant visual stimuli. Some maneuvers reduce the risk of photosensitive seizures, including monocul complete occlusion, increased distance from a video-display terminal, and the provision of ambient back lighting (Harding and Jeavons ). We suggest these approaches to patients who show photosensitivity on EEG but do not know how successful these environmental alterations are in JME.
Mechanism of action
Valproic acid is a branched-chain fatty acid that markedly differs in structure from all other AEDS in clinical use. Its mechanism of action remains not fully understand. There are evidences that valproic acid increases GABA concentrations, the mechanism by which this occurs remains unknown. A number of mechanisms have been proposed, including inhibition of GABA-T action, activation of GABA synthesis by an increase of GAD activity, and increased release of GABA into the synapse.
Based on clinical experience, valproate was first proposed as a treatment of myoclonic seizure. years ago, the sensitivity of VPA was reported (Delgado-Escueta and Enrile-Bascal ). Although JME is an important syndrome, there have been almost no randomized clinical trials conducted using any medication for its treatment. However, there have been many open case studies conducted with VPA in JME management. The open series that have been published using VPA show a 41%88% seizure-free rate for patients receiving VPA, either as an add-on medication or as monotherapy (Atakli et al ; Kleveland and Engelsen ). Case studies have also shown that a low, once-daily dose ( mg) of VPA can effectively control JME and keep patients seizure free for as long as 2-years (Panagariya et al ; Karlovassitou-Koriari et al ). Newer studies that examined the efficacy of lamotrigine, topiramate and valproate in JME have all shown that valproate has the best efficacy of the three (Prasad et al ; Nicolson et al ; Mohanraj and Brodie ).
Valproate is today one of the most effective AEDs in JME. He should be considered the first line drug at least for man. Taking into an account the teratogenicity (possibly lessened by the concurrent use of folic acid) and some side effects (weight gain), VPA are often considered unacceptable in young women of childbearing age.
Mechanism of action
The benzodiazepines work by primarily enhancing gamma-aminobutyric acid (GABA)ergic inhibition by binding to the benzodiazepine receptor on GABAA receptors (Rudolph et al ).
Clonazepam can also be effective in the treatment of JME. Obeid and Panayiotopoulos () treated 17 patients who had JME with Clonazepam. All of the patients had myoclonic seizures before treatment, and 14 of the 17 had GTC seizures before treatment. After Clonazepam treatment, myoclonic seizures were controlled in 15 (88%) of 17 patients, and the remaining two patients had a 75% reduction in seizure frequency. However, Clonazepam did not produce effective results for reducing GTC seizures. Six (43%) of the 14 patients with GTC seizures were controlled. In addition, two patients sustained injuries during GTC seizures because Clonazepam eliminated their myoclonic seizures, which had served as a warning, and they went directly into a GTC seizure. The authors concluded that Clonazepam, while effective in treating myoclonic seizures, probably should not be used to control GTC seizures.
Mechanism of action
Lamotrigine is a phenyltriazine derivative. Lamotrigine acts through inhibition of voltage-activated sodium channels and possibly calcium channels, so that it prevents the release of glutamate (Lees and Leach ).
Lamotrigine is effective in controlling generalized tonic clonic seizure and absence while there are some reports of myoclonic seizures exacerbation (Biraben et al ; Carrazana and Wheeler ).
Many studies performed over recent years have demonstrated clinical utility for the treatment of JME. An Open-label study to evaluate lamotrigine as an alternative to valproate (63 patients switched from valproate to lamotrigine) demonstrated an improvement in 67% of patients. No aggravation of clinical symptoms was also reported (Morris et al ). Buchanan conducted a study of 12 patients with JME who were treated with LTG monotherapy (Buchanan ). Five (41%) of these 12 patients became seizure free while receiving LTG monotherapy, and the authors concluded that LTG might be effective in the management of JME. In a retrospective study, valproate monotherapy (n = 36) and lamotrigine monotherapy (n = 14) were compared, as well valproate (n = 22), lamotrigine (n = 21) and topiramate polytherapy (n = 15) were compared. The results suggested that lamotrigine were an effective option as monotherapy and polytherapy (Prasad et al ). Furthermore, the efficacy of lamotrigine in JME was evaluated in bitherapy. The polytherapy is especially interesting in case of drug resistance. The combination of lamotrigine with valproate appears to be synergistic in many type of epilepsy. But the same combination is lead to an increased risk to develop an important skin rash (Gerike et al ; Pisani et al ).
Mechanism of action
Levetiracetam is a pyrrolidone derivative, is the S-enantiomer of the ethyl analogue of piracetam. While the exact mechanism of action of levetiracetam is not known, it appears to act via a specific binding site within the brain (but does not directly affect GABA or glutamate), does not alter sodium channel properties, produces a limited reduction in high-voltage-activated calcium currents, and possibly modulates intracellular calcium transients (Herdon et al ; Zona et al ). Molecular studies involving transgenic mice suggest that levetiracetam binds to a synaptic vesicle protein (SVA2) that is involved in vesicle neurotransmitter exocytosis, and that the binding affinity to SVA2 is directly proportional to seizure protection (Lynch et al ).
Levetiracetam is probably the best new AED in the treatment of JME and may replace valproate for the treatment of the disorder because of high and sustained efficacy, fast action, and an excellent safety profile. More than 60% of patients with intractable JME became seizure-free with levetiracetam monotherapy or polytherapy (Czapinski and Czapinska ; Resor and Resor ). Resor and colleagues assessed levetiracetam monotherapy in 24 patients with JME and GTCS (Resor and Resor ). Sixteen patients (%) became free of GTCS; three of them had a single convulsive seizure after either stopping levetiracetam for 24 h or reducing the dose to mg/day but subsequently have remained free of convulsive seizures. Myoclonic seizures were effectively controlled in 22 of 24 patients. Moreover, Sharpe and colleagues performed a retrospective review on the medical record of 30 patients with JME, whose age was between 5 and years, treated with levetiracetam with dosage range from 12 to 50 mg/kg/j (Sharpe et al ). The length of follow-up was months. 24 patients (80%) became seizure free with levetiracetam monotherapy and 2 additional patients had an improvement of seizure control. Andermann and colleagues evaluated levetiracetam in patients ( with JME and 9 with juvenile absence epilepsy). The study was a double-bind multicenter placebo controlled trial conducted in patients without control on one AED. The responder rate was % with levetiracetam versus % with placebo (Andermann et al ). Specchio et al conducted a multicenter, prospective open-label study in patients with JME (Specchio et al ). 10 patients were newly diagnosed and 38 were resistant and/or intolerant to previous AED. 5 patients dropped out. 18 patients (%) were without myoclonia and 35 (73%) had no generalized tonic seizure.
Mechanism of action
Topiramate is a sulphamate-substituted monosaccharide that exhibits some inhibition of carbonic anhydrase. Its AED activity is independent of this effect. Topiramate has multiple modes of action, including modulation of voltage-dependent sodium channels, potentiation of GABAergic inhibition at a novel site on the GABAA receptor, and possible action at non-Nmethyl- D-aspartate (NMDA) receptors (Hanaya et al ; White et al ; Zona et al ).
Several studies have shown the usefulness of topiramate in patients with JME. There is one randomized-controlled study on the efficacy of topiramate in patients with generalized tonic clonic seizure including patients with JME (Biton et al ). A reduction of more than 50% of generalized tonic clonic seizure were reported in 8/11 patients treated by topiramate compare to 2/11 in placebo-treated patients. A reduction in myoclonic and absence seizures was also reported but did not achieve statistical significance. Topiramate efficacy and tolerability were evaluated in 22 patients with JME (Sousa Pda et al ). 16 patients completed the first year of the follow-up, while 4 left the study because of poor seizure control and 2 because of low compliance. Myoclonic seizures were controlled in 11 patients and persisted in 5 patients. Generalized tonic clonic seizures were completely controlled in 10 patients, 4 patients had more than 50% reduction of seizures and 2 had reduction less than 50%. In a randomized open-label treatment, 28 patients with a recent diagnosed JME received topiramate or valproate (Levisohn et al ). 12 of 19 patients treated by topiramte completed the study, while 7 of 9 patients treated by valproate completed the study. Generalized tonic clonic, myoclonic and absence seizures were totally controlled in 10/12, 9/14 and 2/2 topiramate-treated patients, respectively, and 3/4, 7/9 and 1/2 valproate-treated patients. In a retrospective cohort, topiramate monotherapy and polytherapy were considered as an alternative to VPA (Prasad et al ).
Mechanism of action
Zonisamide by blocking the voltage-sensitive sodium channels prevents repetitive neuronal firing. It also reduces voltage-dependent T-type calcium channels, facilitates dopaminergic and serotoninerigic neurotransmission, weakly inhibits carbonic anhydrase and may protect neurones from free-radical damage, thereby stabilizing neuronal membranes (Suzuki et al ; Kito et al ).
Few studies focused on the effects of zonisamide are available. A retrospective study analyzing 15 patients (monotherapy in 13 patients and added to valproate in 2 patients) reported a good control of seizures. 69%, 62%, and 38% were free for generalized tonic clonic, myoclonic and absence seizures, respectively. Side effects were reported in 20% of patients (Kothare et al ). In a neurophysiological study of a patient, zonisamide permits almost complete disappearance of generalized spike and wave discharges (Szaflarski ). These data suggest the possible useful of this AED in JME.
AED aggravating JME
It is now well known that AEDs can aggravate epilepsy. Phenytoin and carbamazepine have shown to aggravate the myoclonic and absence seizures of JME and therefore should be avoided (Genton et al ; Gelisse et al ; Thomas et al ). Genton et al () conducted a study with CBZ and PHT to determine the risk of seizure aggravation in 40 patients with JME. In the CBZ group, 19 (68%) of 28 patients had a seizure aggravation, usually affecting the myoclonic seizure, and only six (21%) of 28 patients improved. In the PHT group, six (38%) of 16 patients had a seizure aggravation, and only two (12%) of 16 patients improved. Aggravation mostly was in the form of increased myoclonic jerks. The authors concluded that among commonly prescribed AEDs, CBZ appears to have the strongest aggravating potential in patients with JME, whereas the aggravating effect of PHT is less prominent.
There have been isolated series of reports indicating that lamotrigine can exacerbate or aggravate myoclonic seizures. Biraben et al reported four patients with JME receiving LTG therapy that experienced myoclonus seizure aggravation (Biraben et al ). Carrazana et al also found two patients with JME (2/24) developed dramatic exacerbation of myoclonus and two other (2/24) had mild transient increases in morning myoclonus with lamotrigine (Carrazana and Wheeler ).
Antiepileptic drug selection
When presented with a patient with epilepsy, physicians should prescribe the medication that will effectively control the seizures yet not endanger the patient with adverse events or seizure aggravation. Although JME is an important syndrome, there have been no randomized clinical trials conducted using any medication for its treatment. Drug treatment of JME is mainly based on clinical experience and prospective and retrospective studies. There are no head-to-head comparisons between old and new AEDs and no drugs licensed specifically for JME.
The and expert consensus surveys on adult epilepsies (Karceski et al , ) ranked valproate as the treatment of choice for idiopathic generalized epilepsy when the patients sex was not specified. However, in the survey adult epilepsy, when it was specified that the patient was a woman, the experts rated lamotrigine as treatment of choice. In the expert opinion about pediatric epilepsy treatment, valproate and lamotrigine was the for year-old male with JME, while lamotrigine was the only choice for year-old female with JME (Wheless et al ).
Valproate is unquestionably the drug of the first choice in men with JME. In women, where considerations of teratogenicity, weight gain, and polycystic ovary syndrome are relevant, other options include levetiracetam, lamotrigine, topiramate and perhaps zonisamide. In patients with symptoms refractory to treatment with one drug, valproate with small doses of lamotrigine is often an effective combination. When valproate is undesirable, combining levetiracetam with lamotrigine may be effective.
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What is a myoclonic seizure?
Myoclonic (MY-o-KLON-ik) seizures are brief, shock-like jerks of a muscle or a group of muscles. "Myo" means muscle and "clonus" (KLOH-nus) means rapidly alternating contraction and relaxation—jerking or twitching—of a muscle. Usually they don't last more than a second or two. There can be just one, but sometimes many will occur within a short time.
Even people without epilepsy can experience myoclonus in hiccups or in a sudden jerk that may wake you up as you're just falling asleep. These things are normal.
In epilepsy, myoclonic seizures usually cause abnormal movements on both sides of the body at the same time. They occur in a variety of epilepsy syndromes that have different characteristics:
- Juvenile myoclonic epilepsy: The seizures usually involve the neck, shoulders, and upper arms. In many patients the seizures most often occur soon after waking up. They usually begin around puberty or sometimes in early adulthood in people with a normal range of intelligence. In most cases, these seizures can be well controlled with medication but it must be continued throughout life.
- Lennox-Gastaut syndrome: This is an uncommon syndrome that usually includes other types of seizures as well. It begins in early childhood. The myoclonic seizures usually involve the neck, shoulders, upper arms, and often the face. They may be quite strong and are difficult to control.
- Progressive myoclonic epilepsy: The rare syndromes in this category feature a combination of myoclonic seizures and tonic-clonic seizures. Treatment is usually not successful for very long, as the patient deteriorates over time.
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Who is at risk for myoclonic seizures?
The epileptic syndromes that most commonly include myoclonic seizures usually begin in childhood, but the seizures can occur at any age. Other characteristics depend on the specific syndrome.
What happens after a myoclonic seizure?
When a myoclonic seizure ends, the person usually continues doing whatever they were doing before and during the seizure. They are awake and able to think clearly. No first aid is needed because of this seizure.
If someone is having a myoclonic seizure, how often will they happen?
There can be just one, but sometimes many will occur within a short time.
How can I tell if someone is having a myoclonic seizure?
These seizures can be easily overlooked because they are so brief and appear as extra normal movements. These seizures can be mistaken for tics, tremors or clumsiness.
How are myoclonic seizures diagnosed?
The seizures themselves are easy to identify. The syndromes usually can be diagnosed on the basis of the medical history and often an EEG test.
How are myoclonic seizures treated?
There are several medicines that can help prevent myoclonic seizures. Myoclonic seizures often respond well to the appropriate medicine.
What should I do if I think my child, loved one or myself may have myoclonic seizures?
If you think that you or your loved one are having myoclonic seizures, talk to your child’s doctor or your own and share your concerns right away. Because myoclonic seizures are often associated with certain syndromes, seeing a doctor quickly to make a diagnosis and begin treatment is essential.
Find an epilepsy specialist.
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