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Absence Seizures Last Updated: September 12, 2005 |
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| Synonyms and related keywords: petit mal seizures, generalized seizures, idiopathic generalized epilepsy, symptomatic generalized epilepsy
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AUTHOR INFORMATION
| Section 1 of 11   |
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| Author: Scott Segan, MD, Attending Neurologist, Clinical Assistant Professor, New York College of Osteopathic Medicine, Division of Neurology, St Barnabas Hospital, Bronx, NY |
| Scott Segan, MD, is a member of the following medical societies:
American Academy of Neurology, and
American Epilepsy Society |
| Editor(s): Edward B Bromfield, MD, Associate Professor of Neurology, Faculty Member, Division of Sleep Medicine, Harvard Medical School; Chief, Division of EEG, Epilepsy and Sleep Neurology, Consulting Neurologist, Brigham and Women's Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine;
Jose E Cavazos, MD, PhD, Assistant Professor, Departments of Medicine (Neurology) and Pharmacology, University of Texas Health Science Center at San Antonio;
Selim R Benbadis, MD, Professor of Neurology, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida College of Medicine, Tampa General Hospital;
and Nicholas Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants |
Disclosure
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INTRODUCTION
| Section 2 of 11   |
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Background: Absence seizures are a type of generalized seizures. They were first described Poupart in 1705, and later by Tissot in 1770, who used the term petit access. In 1824, Calmeil used the term absence. In 1935, Gibbs, Davis, and Lennox described the association of impaired consciousness and 3-Hz spike-and-slow-wave complexes on electroencephalograms (EEGs).
Absence seizures occur in both idiopathic and symptomatic generalized epilepsies. Among the idiopathic, or primary, generalized epilepsies (ie, with age-related onset), absence seizures are seen in childhood absence epilepsy (CAE, or pyknolepsy), juvenile absence epilepsy (JAE), and juvenile myoclonic epilepsy (JME, or impulsive petit mal seizures). The seizures in these conditions are called typical absence seizures and usually associated with 3-Hz spike-and-slow-wave complexes on EEG. In CAE, seizures are frequent and brief, lasting just a few seconds (pyknoleptic). Some children can have hundreds of such seizures per day. In other epilepsies, particularly those with an older age of onset, the seizures can last several seconds to minutes and may occur only a few times a day (called nonpyknoleptic or spanioleptic absence seizures). Myoclonic and tonic-clonic seizures may also be present, especially in syndromes with an older age of onset. In these syndromes, the discharge frequency may be faster than 3
Hz.
In the symptomatic generalized epilepsies, absence seizures are often associated with slow spike-wave complexes of 1.5-2.5 Hz; these are also called sharp-and-slow-wave complexes. These seizures are termed atypical absence seizures. Pathophysiology: The etiology of idiopathic epilepsies with age-related onset is genetic. About 15-40% of patients with these epilepsies have a family history of epilepsy; concordance in monozygotic twins is 75%. Family members may have other forms of idiopathic or genetic epilepsy (eg, febrile convulsions, generalized tonic-clonic [GTC] seizures).
Several animal models demonstrate the genetic basis for absence seizures. A strain of Wistar rat, ie, genetic absence epilepsy rats from Strasbourg (GAERS), is a polygenetic model in which all animals have clinical seizures consisting of a behavioral arrest with twitching of facial muscles. This is associated with bilateral synchronous spike-wave discharges. Several single-gene loci in mice, when mutated, result in generalized spike-wave epilepsy. The tottering (chromosome 8), lethargic (chromosome 2), stargazer (chromosome 15), mocha (chromosome 10), and ducky (chromosome 9) loci all have generalized 6-per-second spike-wave EEG paroxysms that are associated with clinical seizures consisting of behavioral arrest. All types respond to ethosuximide (ETX), but the underlying cellular mechanisms for the generation of the discharges are not identical.
Several mutations of genes which encode protein subunits in various ion channels have been found in patients and family members with idiopathic epilepsies. Some forms of JME and absence epilepsy have been shown to result from mutations in Ca++ channels.
In symptomatic generalized epilepsies, absence seizures are due to a wide variety of causes that, at an early stage of neural development, result in diffuse or multifocal brain damage. The causes of secondary generalized epilepsies and the other seizure types that accompany them, and their management, are not discussed in this article.
The pathophysiology of absence seizures is not fully understood. In 1947, Jasper and Droogleever-Fortuyn electrically stimulated nuclei in the thalami of cats at 3 Hz and produced bilaterally synchronous spike-and-wave discharges on EEG. In 1953, bilaterally synchronous spike-and-wave discharges were recorded by using depth electrodes placed in the thalamus of a child with absence seizures.
In 1977, Gloor demonstrated that the bilaterally synchronous 3-Hz spike-wave discharges in the feline penicillin model of absence seizures were generated in the cortex. This led to the corticoreticular theory of primarily generalized seizures.
Abnormal oscillatory rhythms are believed to develop in thalamocortical pathways. This involves GABA-B–mediated inhibition alternating with glutamate-mediated excitation. The cellular mechanism is believed to involve T-type calcium currents. T channels of the GABAergic reticular thalamic nucleus neurons appear to play a major role in the spike-wave discharges of the GABAergic thalamic neurons. GABA-B inhibition appears to be altered in absence seizures, and potentiation of GABA-B inhibition with tiagabine (Gabitril), vigabatrin (Sabril), and possibly gabapentin (Neurontin) results in exacerbation of absence seizures. Enhanced burst firing in selected corticothalamic networks may increase GABAB receptor activation in the thalamus, leading to generalized spike-wave activity. Frequency:
- In the US: The incidence is 1.9-8 cases per 100,000 population.
Mortality/Morbidity:
- No deaths result directly from absence seizures. Accidents from driving or operating dangerous machinery during absence may result in death. In children with absence seizures due to secondary generalized epilepsies, death is related to the underlying disease.
- The morbidity from typical absence seizures is related to the frequency and duration of the seizures, as well as to the patient's activities; effective treatment ameliorates these factors. Educational problems and behavioral problems are sequelae of unrecognized, frequent seizures.
Race: No racial predilection is known.
Sex:
- Absence seizures are generally believed to be more common in females and in males, with some studies showing a 2:1 female-to-male ratio. Other studies have shown no difference between the sexes.
- Absence epilepsy with myoclonus has a male predominance.
Age: The generalized idiopathic epilepsies have age-related onset. Onset of absence seizures in children with symptomatic generalized epilepsies depends on the underlying disorder. While many of these disorders may have their onset at an early (prenatal, perinatal, or postnatal) age, absence seizures do not appear until later in childhood.
An example is the Lennox-Gastaut syndrome. The cause may be a genetic disorder or a perinatal insult, but the absence seizures do not present until age 1-8 years.
- CAE onset is at age 4-8 years, with peak onset at age 6-7 years.
- JAE onset is at age 7-14 years, with peak onset at age 10-12 years. Onset of JAE with myoclonus averages about age 7 years.
- JME has a more varied age of onset (8-26 y), but 79% of patients have an onset at age 12-18 years. Because the absence and myoclonic seizures are brief, they often go unrecognized, and many patients do not present until they experience a tonic-clonic seizure.
History: - Children with idiopathic generalized epilepsies may present with a history of staring spells, but infrequent absence seizures may not be diagnosed until a GTC seizure has occurred.
- Other symptoms, such as behavioral problems, may be the presenting complaint. Although the brief attacks are unrecognized, the lapses of awareness interfere with following up what is happening; as a result, the child becomes frustrated.
- Decline in school performance may be an indication of the onset or breakthrough of absence seizures.
- In symptomatic generalized epilepsies, atypical absence seizures often occur in the setting of developmental delay or mental retardation. (See Table 1 for features of typical and atypical absence seizures.) Other seizure types can be present, such as myoclonic, tonic, atonic, tonic-clonic, and even partial seizures.
- On clinical examination, typical absence seizures appear as brief staring spells.
- Patients have no warning or postictal phase, and if engaged in gross motor activity, such as walking, may stop and stand motionless or may continue to walk.
- Children are not responsive during the seizure and have no memory of what happened during the attack; they are generally unaware that a seizure has occurred.
Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures*
| Type of Clinical Seizure |
EEG Findings |
Typical absence
Impairment of consciousness only
Mild clonic components
Atonic components
Tonic component
Automatisms
Autonomic components |
Usually regular and symmetrical 3 Hz, possible 2- to 4-Hz spike-and-slow-wave complexes, and possible multiple spike-and-slow-wave complexes |
Atypical absence
Changes in tone more pronounced
than those of typical absence seizure
Nonabrupt onset and/or cessation abrupt |
EEG more heterogeneous than in typical absence; may include irregular spike-and-slow-wave complexes, fast activity, or other paroxysmal activity; abnormalities bilateral but often irregular and asymmetric |
Source.—Adapted from Dreifuss, 1977.
*May be seen alone or in combination.
- Absence seizures may be confused with complex partial seizures, especially in cases of prolonged seizures with automatisms (see Table 2). The occurrence of automatisms is dependent on duration of the seizure; the longer the seizure, the more likely automatisms are to occur (see Image 1).
- Atypical absence seizures, which occur in patients with symptomatic generalized epilepsies, are usually longer than typical absences and often have more gradual onset and resolution.
Physical: - Physical and neurologic findings are normal in children with idiopathic generalized epilepsies.
- Having the child hyperventilate for 3-5 minutes can often provoke absence seizures.
- This procedure can easily be performed in the clinic or office, and the result is diagnostic.
- In symptomatic generalized epilepsies, physical and/or neurologic findings may be abnormal, reflecting the underlying disorder.
- Physical examination may reveal stigmata of a genetic disease, such as a neurocutaneous disorder (eg, tuberous sclerosis) or an inborn error of metabolism.
- Neurologic examination may show signs of developmental delay or more specific signs, such as spastic paresis in cerebral palsy.
Causes: After noncompliance with treatment, lack of sleep is the most frequent cause of seizure exacerbations. Drugs that lower the seizure threshold (eg, alcohol, cocaine, high-dose penicillin, isoniazid [INH] overdose, neuroleptics) are most likely to cause seizures in patients with epilepsy. Withdrawal of alcohol, benzodiazepines (BZP), and other sedatives is also a common cause.
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DIFFERENTIALS
| Section 4 of 11 |
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Complex Partial Seizures
Confusional States and Acute Memory Disorders
Febrile Seizures
First Seizure: Pediatric Perspective
Migraine Variants
[Psychogenic Seizures]
Reflex Epilepsy
Shuddering Attacks
Status Epilepticus
Other Problems to be Considered:
Breath-holding spells
Nonconvulsive generalized status epilepticus |
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Imaging Studies:
- Because neuroimaging findings are normal in idiopathic epilepsies, neuroimaging is not indicated if the typical clinical pattern is present.
- Neuroimaging often is ordered by primary care providers and the emergency department (ED), especially if a child presents with a GTC seizure. A normal result helps support the diagnosis of idiopathic epilepsy.
- For cryptogenic and symptomatic generalized epilepsies, neuroimaging can help in diagnosing the underlying abnormality.
- If imaging is performed, MRI is preferred to CT scanning. MRI is more sensitive for certain anatomic abnormalities, such as heterotopias, lissencephaly, and other developmental malformations.
Other Tests:
- The only diagnostic test for absence seizures is the EEG.
- Findings in typical absence seizures
- Background activity is normal.
- In syndromes with frequent absence seizures, such as CAE, a routine awake recording is often pathognomonic.
- Bursts of frontally predominant, generalized 3-Hz spike-and-wave complexes are seen during the seizures.
- In syndromes with less frequent absence seizures (JAE or JME), an awake recording may be normal; a sleep or sleep-deprived recording may be needed.
- Typical absence seizures have generalized 3-Hz spike-and-wave complexes (see Image 2).
- They can range from 2.5-6 Hz, with the faster frequencies seen in syndromes with older age of onset.
- Bursts of generalized polyspikes and waves (multiple spike-and-slow-wave complexes) may also be seen, especially during sleep and in syndromes with older age of onset.
- The onset and ending of these seizures are abrupt; no postictal EEG slowing is noted.
- Hyperventilation often provokes these seizures and should be a routine part of all EEGs in children.
- EEG-video monitoring demonstrates that clinical seizure manifestations may lag behind the start of ictal EEG activity; bursts lasting less than 3 seconds are usually clinically silent. During the absence seizure, rhythmic eye blinks and mild clonic jerks may be present. As a seizure progresses, automatisms may be seen.
- Findings in atypical absence seizures
- Seizures are characterized by slow spike-and-wave paroxysms, classically 2.5 Hz (see Image 3). The onset may be difficult to discern, and postictal EEG slowing may be noted.
- Background activity is often abnormal, reflecting the diffuse or multifocal underlying encephalopathy of symptomatic generalized epilepsy.
- Generalized polyspike-and-wave complexes also may be present, and focal features may be observed.
- The clinical correlation of generalized spike-and-wave complexes with clinical seizures is not as clear-cut as in typical absence seizures. Generalized slow spikes and waves may be present as an interictal pattern, as in Lennox-Gastaut syndrome.
- EEG-video monitoring can show a more varied alteration of consciousness than in typical absence seizures. If the patient has underlying mental retardation, discerning changes in mental status also may be more difficult in atypical absence.
- Changes in postural tone, most noticeably head nods, are common.
- Ambulatory EEG monitoring over 24 hours may be useful to quantitate the number of seizures per day and their most likely times of occurrence.
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TREATMENT
| Section 6 of 11 |
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Medical Care: Treatment involves antiepileptic drugs (AEDs). Once the proper diagnosis (ie, of the specific epilepsy syndrome) is made, the likelihood of other coexistent seizure types, such as myoclonic or tonic-clonic, should be considered and an appropriate medication selected. - ETX (Zarontin) is effective only against absence seizures.
- Valproic acid (VPA; Depakene, Depacon) and divalproex sodium (Depakote) is considered a broad-spectrum AED because it is effective against absence, myoclonic, and tonic-clonic (as well as partial) seizures.
- Newer broad-spectrum medications, not yet approved by the US Food and Drug Administration (FDA) for treatment of absence seizures, include lamotrigine (LTG, Lamictal), topiramate (TPM, Topamax), zonisamide (ZNS, Zonegran), and levetiracetam (LEV, Keppra).
- Symptomatic generalized epilepsies are often refractory to first-line AEDs. LTG is approved by the FDA as adjunctive therapy for the generalized seizures of Lennox-Gastaut syndrome in adult and pediatric patients (at least aged 2 y). Clonazepam (Klonopin, felbamate (Felbatol), TPM, and the ketogenic or medium-chain triglyceride diet have been attempted to reduce seizure frequency. However, these adjunctive therapies have limited efficacy.
- Treatment with tiagabine (Gabitril), vigabatrin (Sabril), and possibly gabapentin (Neurontin) has been associated with the exacerbation of absence seizures. The use of carbamazepine (Tegretol) has also been associated with the exacerbation of absence seizures in some patients.
Consultations: All patients with suspected absence seizures should be examined by a neurologist who has expertise in diagnosing epileptic syndromes. Patients with refractory seizures, especially those with symptomatic epilepsies, may need to be referred to an epileptologist for prolonged EEG-video monitoring and medication adjustments. Diet: Patients with medically intractable seizures may be tried on a ketogenic or medium-chain triglyceride diet. The results are often only temporary, and these diets are difficult to maintain. Children in whom such diets are being considered should be referred to a center with specialized dietary services. Activity: Physical activity should not be restricted any more than necessary. Activities in which a seizure might pose a threat, such as swimming or rock climbing, may be allowed with appropriate supervision. A child with epilepsy should not be unnecessarily handicapped. Patients with uncontrolled absence seizures should not be allowed to drive. The situation may be unclear when the patient's clinical seizures are controlled but the EEG still shows some spike-wave activity.
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MEDICATION
| Section 7 of 11 |
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Most AEDs are relatively toxic. Patients often take them every day, usually several times a day, for many years. Therefore, the decision to start such a medication is difficult. Once a patient has more than one unprovoked seizure, the decision to start medication is straightforward; EEG studies can help to confirm this decision.
Most AEDs are not effective against absence seizures. Also, many patients have both absence and generalized convulsive (myoclonic and GTC) seizures. Only 2 first-line AEDs are currently used for absence seizures.
Drug Category: Antiepileptics -- If the patient has only absence seizures, then ETX (Zarontin) is an appropriate medication. This may be the case for patients with CAE. ETX also may be used in conjunction with an anticonvulsive AED, such as phenytoin (PHT, Dilantin) for patients at risk of tonic-clonic seizures in whom VPA is contraindicated. Drug Name
| ETX (Zarontin) -- Succinimide AED effective only against absence seizures. No effect on GTC, myoclonic, atonic, or partial seizures. Mechanism of action based on reducing current in T-type calcium channels on thalamic neurons. Spike-and-wave pattern during petit mal seizures thought to be initiated in thalamocortical relays by activation of these channels. Available in large 250-my capsules, which may be difficult for some children to swallow, and as syrup (250 mg/5 mL). |
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| Adult Dose | 250 mg PO bid; increase by 250-mg increments q4-7d until seizures controlled or maximum daily dose reached; not to exceed 1.5 g/d |
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| Pediatric Dose | <6 years: 15 mg/kg/d PO divided bid initially; initial dose not to exceed 250 mg; may increase to effect q4-14d
>6 years: Administer as in adults
Maintenance dose: 15-40 mg/kg/d PO divided bid| Contraindications | Documented hypersensitivity; blood dyscrasias; renal or hepatic disease |
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| Interactions | Generally minimal; enzyme-inducing drugs (eg, PHT, carbamazepine, phenobarbital) may lower levels by 15-25%; valproic acid may elevate levels; has weak enzyme-inhibiting effect, usually insignificant with respect to metabolism of other drugs |
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| Pregnancy |
C - Safety for use during pregnancy has not been established.
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| Precautions | Blood dyscrasias may occur and may be fatal (monitor CBC); caution in hepatic or renal disease; abrupt withdrawal may precipitate absence status |
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Drug Name
| Valproic acid (Depakene, Depacon, Depakote, Depakote ER) -- DOC for patients who have absence and GTC and/or myoclonic seizures; aliphatic compound, carboxylic acid. Discovery was serendipitous; used as solvent potential AEDs, and all test compounds seemed to work. Mechanism of action not known but believed related to ability to increase brain GABA. May inhibit rapid opening of sodium channels and block T-type calcium channels.
VPA (Depakene) available as syrup (250 mg/5 mL), 250- or 500-mg capsules, and IV preparation (100 mg/5 mL; Depacon). Divalproex sodium (Depakote) available as 250- or 500-mg tab and 125-mg capsule (Depakote Sprinkles), which can be opened and mixed with food.
Syrup rapidly absorbed through stomach and produces gastric irritation. Rapidly produces high serum levels and may cause peak-dose toxicity. Must be given in 3-4 divided doses. Other oral preparations absorbed more slowly from GI tract and better tolerated. Because of slower absorption, some patients who have achieved control may be treated with bid dosing.
Highly protein bound; protein binding is level dependent. At 40 mg/mL, 90% bound, but at 130 mg/mL, 80% bound. Therefore, as total level increases from 40 to 130 mg/mL, free level increases from 4 to 26 mg/mL. Therapeutic range originally 50-100 mg/mL; patients with hard-to-control seizures may require higher level.
Depakote ER is extended-release product intended for once-a-day oral administration. When converting from Depakote to Depakote ER, dose 8-20% higher than total daily dose of Depakote is needed. IV Depacon may be given as maintenance therapy; amount mixed with at least 50 mL of compatible diluent and infused at rate not >20 mg/kg/min over at least 60 min; research ongoing concerning IV loading at more rapid rates.| Adult Dose | 10-15 mg/kg/d PO initially; increase by 5-10 mg/kg/d weekly until seizures controlled or adverse effects develop; not to exceed 60 mg/kg/d divided tid/qid |
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| Pediatric Dose | 15 mg/kg/d PO initial dose, increasing by 5-10 mg/kg/d weekly until seizures controlled or adverse effects develop; maximum recommended dosage 60 mg/kg/d divided tid/qid; for select patients with complete control, bid dosing may be tried |
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| Contraindications | Documented hypersensitivity; hepatic disease or dysfunction; because of teratogenicity, first trimester of pregnancy and in women of childbearing age who are not on adequate birth control, unless it is clearly the most effective drug for a woman planning pregnancy and aware of risks |
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| Interactions | Cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin, phenytoin, phenobarbital, and carbamazepine may significantly reduce levels; in children, salicylates decrease protein binding and metabolism; carbamazepine may result in variable changes of carbamazepine concentrations with possible toxicity or loss of seizure control; may increase diazepam and ETX toxicity (monitor closely); may increase phenobarbital and phenytoin levels; may displace warfarin from protein-binding sites (monitor coagulation tests) and can displace phenytoin, resulting in transient increase in free levels; may increase zidovudine levels in HIV-seropositive patients |
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| Pregnancy |
D - Unsafe in pregnancy
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| Precautions | Hepatic dysfunction may occur (more common in children taking multiple AEDs) during first 6 mo of therapy, and may be fatal; assess liver function test (LFT) results before therapy and at frequent intervals during first 6 mo; clinical symptoms (loss of seizure control, malaise, weakness, lethargy, facial edema, anorexia, vomiting) may precede LFT abnormalities; hyperammonemia reported and may be occur despite normal LFTs; may cause lethargy or coma; when asymptomatic elevations of ammonia are present, more frequent monitoring indicated; carnitine supplementation may be beneficial in addition to platelet dysfunction, thrombocytopenia may occur and associated with high doses; pancreatitis may occur, even after several years of therapy; perform appropriate tests in patients with malabsorption, abdominal pain, or other GI symptoms; spina bifida in 1-2% of children born to women taking VPA during first 12 wk of pregnancy; women planning to become pregnant should take folic acid 1-5 mg/d, and consider crossing
over to ETX before conception; for women with have GTC seizures, ETX and anticonvulsant AED can be used |
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FOLLOW-UP
| Section 8 of 11 |
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Further Outpatient Care:
- Children with absence seizures should be monitored closely during titration or crossover of AEDs. The dose of the medication should be increased weekly until seizures are controlled or adverse effects develop.
- The aim in therapy is to control seizures completely with the minimum required amount of medication to minimize adverse effects.
- The therapeutic effect of VPA for absence seizures may lag several weeks behind reaching a therapeutic level.
- LFT, amylase and/or lipase, and CBC results should be monitored during drug treatment to watch for adverse reactions.
- Drug levels should be monitored to ensure compliance and to watch for toxic levels in patients who are too young or too developmentally disabled to articulate subjective adverse effects.
Complications:
- Absence status epilepticus may occur spontaneously, after the administration of a drug that lowers the seizure threshold, or (in rare cases) after the administration of a BZP.
- On clinical evaluation, the patient appears to be in a dreamy state with partial responsiveness and automatisms; at times the presentation may be more subtle, with only mild encephalopathy. The diagnosis is made by EEG confirmation of generalized 3-Hz spike-and-wave complexes, although the discharges may be slower and less regular than with isolated seizures.
- Treatment has been IV BZP. In some patients, this may be replaced by or supplemented with IV VPA (Depacon) because IV BZPs have been reported to produce tonic status in patients with symptomatic generalized epilepsy.
Prognosis:
- The prognosis for the primary generalized epilepsies depends on the particular epileptic syndrome. Because seizures, particularly GTC seizures, may occur well after patients appear to achieve good control, a long seizure-free period of perhaps 4 years should be achieved before discontinuation of therapy is considered.
- The remission rate for CAE is about 80%.
- GTC seizures may develop in about 40% of children with CAE.
- Persistence of seizures is more likely in those with GTC seizures.
- Early onset of absence seizures, quick response to therapy, and normal EEG background are good prognostic signs.
- The remission rate for JAE is less favorable than that for CAE. JAE carries a greater risk of GTC seizures (as high as 80% in some studies) than CAE.
- JME carries a high risk of GTC seizures.
- Despite excellent control with relatively small doses of an AED, the relapse rate is >90%, possibly as high as 97%.
- Patients with JME generally need to be treated for life, though occasional patients achieve control with careful attention to lifestyle issues (eg, adequate sleep, abstinence from alcohol).
Patient Education:
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MISCELLANEOUS
| Section 9 of 11 |
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Medical/Legal Pitfalls:
- The 2 main pitfalls in treatment of absence seizures both involve incorrect diagnosis.
- On occasion, a patient without epilepsy is identified as having epilepsy.
- Staring spells, daydreaming, migraine equivalents, and panic and/or anxiety attacks all may be confused with nonconvulsive seizures.
- Certain epileptic syndromes are often undiagnosed or misdiagnosed.
- Patients who present with a GTC seizure are often given an AED without efficacy against absence or myoclonic seizures. Their GTC seizures may be controlled, but they may have unrecognized absence or myoclonic seizures.
- Patients with absence seizures may be identified as having complex partial seizures, and vice versa. This leads to incorrect treatment and an inaccurate understanding of the prognosis.
- Careful history taking and EEG studies can help avoid these pitfalls.
Special Concerns:
- Patients who are old enough to drive should be warned about driving and operating heavy machinery. Physicians should be familiar with state laws concerning driving with epilepsy; inform patients concerning these legal matters.
- Women of childbearing age who are not using adequate birth control should not be treated with VPA, if equally effective alternatives are available for them.
- If a woman taking VPA wishes to become pregnant, treatment may be crossed over to ETX, and she may be given folic acid 1-5 mg/day before conception. After the first trimester, treatment may be switched back to VPA.
- Women with GTC seizures need an additional AED along with ETX.
- Most clinicians believe that women treated with VPA or any hepatic enzyme-inducing AED should be treated with vitamin K before delivery.
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PICTURES
| Section 10 of 11 |
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BIBLIOGRAPHY
| Section 11 of 11 |
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Gibbs FA, Davis H, Lennox WG: The EEG in epilepsy and in conditions of impaired consciousness. Arch Neurol Psychiat 1935; 34: 1134-48.
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Gloor P, Quesney LF, Zumstein H: Pathophysiology of generalized penicillin epilepsy in the cat: the role of cortical and subcortical structures. II. Topical application of penicillin to the cerebral cortex and to subcortical structures. Electroencephalogr Clin Neurophysiol 1977 Jul; 43(1): 79-94[Medline].
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Hirose S, Mitsudome A, Okada M: Genetics of idiopathic epilepsies. Epilepsia 2005; 46 Suppl 1: 38-43[Medline].
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Jasper HH, Droogleever-Fortuyn J: Experimental studies on the functional anatomy of petit mal epilepsy. Assoc Res Nerv Ment Dis 1947; 26: 272-98.
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Loiseau P: Childhood absence epilepsy. In: Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby 1985: 106-20.
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Stefan H, Snead OC: Absence seizures. In: Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven 1997: 579-90.
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Tassinari CA, Bureau M: Epilepsy with myoclonic absences. In: Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985; 121-9.
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Temkin O: The Falling Sickness. Baltimore, MD: Johns Hopkins Press 1971; 250.
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Wolf P: Juvenile absence epilepsy. In: Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London; England: John Libby; 1985; 242-6.
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