AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Many diseases can cause paroxysmal clinical events. The correct diagnosis of the paroxysmal event is necessary to provide correct treatment. If the event is an epileptic seizure, the seizure type and associated clinical, electroencephalographic (EEG), and neuroimaging findings assist in determining the risk of seizure recurrence and the possible need to begin anticonvulsant therapy. Yet, the correct diagnosis is often missed. In 1998, Scheepers et al found 49 patients with an incorrect diagnosis and 26 patients with an uncertain diagnosis among 214 patients with a diagnosis of epilepsy.

This article focuses on 2 related questions:

• Is the spell truly epileptic?
• If the event is epileptic, is it likely to recur?

In a 1999 report, Davidson describes a similar approach to the patient with a first seizure.

• Is it epilepsy?
• What kind of epilepsy?
• What is the cause?

This article describes the common clinical features of patients with a first seizure, risk factors for seizure recurrence, and a general approach to patient management.

Pathophysiology

The definitions of the following terms come from the International League Against Epilepsy (ILAE) Guidelines (Jallon, 1993; Roger, 1989).

A nonepileptic event is a clinical event presumed to be unrelated to abnormal and excessive neuronal discharge. An example of a nonepileptic event is syncope. Decreased cardiac output causes decreased cerebral perfusion, and this results in loss of consciousness.

An epileptic seizure is a clinical event presumed to result from an abnormal and excessive neuronal discharge. The clinical symptoms are paroxysmal and may include impaired consciousness and motor, sensory, autonomic, or psychic events perceived by the subject or an observer.

Epilepsy occurs when 2 or more epileptic seizures occur unprovoked by any immediately identifiable cause. The seizures must occur more than 24 hours apart. In epidemiologic studies, an episode of status epilepticus is considered a single seizure. Febrile seizures and neonatal seizures are excluded from this category.

Idiopathic epilepsy describes epilepsy syndromes with specific age-related onset, specific clinical and electrographic characteristics, and a presumed genetic mechanism.

Epileptic seizures are classified as cryptogenic or symptomatic. Cryptogenic seizure is a seizure of unknown etiology. This type of seizure is not associated with a prior CNS insult known to increase the risk of developing epilepsy. It does not conform to the criteria for the idiopathic or symptomatic categories. Previous studies use the term idiopathic to describe a seizure of unknown etiology. However, current ILAE guidelines discourage use of the term idiopathic to describe a seizure of unknown etiology.

Symptomatic seizure is a seizure caused by a previously known or suspected disorder of the CNS. This type of seizure is associated with a prior CNS insult known to increase the risk of developing epilepsy.

An acute symptomatic seizure is one that occurs following a recent acute disorder such as a metabolic insult, toxic insult, CNS infection, stroke, brain trauma, cerebral hemorrhage, medication toxicity, alcohol withdrawal, or drug withdrawal. An example of an acute symptomatic seizure is a seizure that occurs within 1 week of a stroke or head injury.

A remote symptomatic seizure is a seizure that occurs more than 1 week following a disorder that is known to increase the risk of developing epilepsy. The seizure may occur a long time after the disorder. These disorders may produce static or progressive brain lesions. An example of a remote symptomatic seizure is a seizure that first occurs 6 months following a traumatic brain injury or stroke.

Seizures are also classified as provoked or unprovoked. A provoked seizure is an acute symptomatic seizure. An unprovoked seizure is a cryptogenic or a remote symptomatic seizure.

Frequency

United States

In 1997, Moore-Sledge reported that the annual incidence of adult-onset seizures in the United States is 84 cases per 100,000 population and that about 6% of the US population experience a nonfebrile seizure sometime during life. She estimates that approximately 50 of each 84 patients develop epilepsy.

International

In European studies, the incidence of first unprovoked seizures ranges from 26-70 cases per 100,000 persons. Beghi et al in a 1997 article attributed the variability to differences in methodology and definitions. The rates were similar in different geographic areas despite technical differences in the studies.

Mortality/Morbidity

The patient who develops recurrent unprovoked seizures has the same mortality and morbidity rates as other patients with epilepsy.

Race

Racial differences have not been studied.

Sex

Most authors report a small-to-moderate preponderance of men in their studies of first seizures in adults (van Donselaar, 1992; Musicco, 1997; Hopkins, 1988; King, 1998).

• In 1986, Annegers et al found a slight overall preponderance of women. Their etiologic categories were neurologic deficit from birth, remote symptomatic, and no known prior etiology. They identified a preponderance of men in the group with neurologic deficit from birth, no sex preponderance in the group with remote symptomatic seizures, and a slight preponderance of women in the group with no known prior etiology. These authors did not determine if these sexual differences were statistically significant.
• Among patients who had an initial generalized tonic-clonic seizure, Bora et al found that only 45.5% were men (Bora, 1995). Patients with partial seizures and structural lesions proven on CT scan were excluded from this study.

Age

• In a study of consecutive patients aged 2 years or older, the age distribution for a first unprovoked seizure was the following (Musicco, 1993):
  • Younger than 16 years - 28%
  • Aged 16-60 years - 66%
  • Older than 60 years - 6%
• Among adults, young adults are affected most often.
  • In a study of patients aged 15 years and older, the mean age of first unprovoked seizure was 38 years (van Donselaar, 1992).
  • In a study of patients 16 years and older, the most frequently affected group was aged 20-29 years (Hopkins, 1988).

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

The following information should be obtained in the history:

• Patient's age should be recorded.
• If a family history of seizures is noted, the clinical epilepsy syndrome of the affected family member should be determined.
• Ask about a history of any previous provoked seizure.
• Determine if the first seizure was status epilepticus.
• Ask the time of day of the seizure occurrence.
• Identify any symptoms that may indicate a nonepileptic event, such as convulsive syncope, syncope, transient ischemic attack, transient global amnesia, migraine, sleep disorder, movement disorder, vertigo, or nonepileptic psychogenic seizure (pseudoseizure).
• • Because of the frequency with which nonepileptic seizures occur, the first step should be to rule out nonepileptic events. Leppik estimates that about 9% of the population will have a seizure of some sort in their lifetime, and he estimates that about two thirds of these are nonepileptic seizures while the remainder are epileptic seizures.
  • Kostopoulos and coworkers (2003) studied 350 patients from the Maastricht and surroundings in a population-based prospective study. The patients were all older than 14 years and had been diagnosed with a suspected first seizure. Kostopoulos and coworkers divided the patients into 3 groups: 49.7% with unprovoked (presumed epileptic) seizures, 22.3% with nonepileptic seizures of organic origin, and 18% with nonepileptic seizures of psychogenic origin. Discriminative features for epileptic seizures were postictal confusion longer than 1 minute, epileptiform EEG, and abnormal neuroimaging. For nonepileptic seizures, a history of hypertension and provoking factors, such as exercise or warmth, was present. For psychogenic seizures, a history of febrile seizures; treatment by a psychiatrist or psychologist; and presentiment of the seizure, such as choking and palpitations, was present.
• Seek a possible etiology (see Causes).

Physical

• The neurologic examination should be directed at finding clinical evidence of a focal brain lesion.
• A general physical examination should be performed to exclude a nonneurologic cause of the seizure (Moore-Sledge, 1997).

Causes

• Epileptic seizure
• • Prenatal, perinatal, or postnatal complications of pregnancy and delivery
  • Febrile seizure: Distinguish a complex febrile seizure from a simple febrile seizure.
  • Cerebrovascular disease such as cerebral infarction, cerebral hemorrhage, and venous thrombosis
  • Head trauma: Head trauma is more significant when it occurs with loss of consciousness lasting longer than 30 minutes, posttraumatic amnesia lasting longer than 30 minutes, focal neurologic findings, or neuroimaging findings suggesting a structural brain injury.
  • CNS infections such as meningitis or encephalitis
  • Neurodegenerative diseases
  • Autoimmune disease
  • Brain neoplasm
  • Genetic diseases
  • Drug intoxication, drug withdrawal, or alcohol withdrawal
  • Metabolic medical disorders such as uremia, hypoglycemia, hyponatremia, and hypocalcemia
• Nonepileptic events
• • Transient ischemic attack
  • Migraine
  • Sleep disorders
  • Transient global amnesia
  • Movement disorder
  • Paroxysmal vertigo
  • Convulsive syncope: Decreased cardiac output causes reduced cerebral perfusion with loss of consciousness and convulsive motor activity. In 1998, Scheepers et al found that cardiovascular disease was the most common diagnosis among patients whose conditions were initially misdiagnosed as epilepsy. Using a comprehensive battery of cardiovascular tests in a population of patients diagnosed with epilepsy, in 2000 Zaidi et al found alternative cardiovascular diagnoses in 41%.
  • Psychiatric disorders such as conversion disorder (psychogenic seizures, pseudoepileptic seizures, pseudoseizures)
  • Malingering

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

See Causes.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Metabolic screening for uremia, hypoglycemia, drug intoxications, and electrolyte disorders should be conducted for patients with first seizure who present to the emergency department (Tardy, 1995).
• Other laboratory investigations may be indicated for specific clinical situations.

Imaging Studies

• Neuroimaging should be performed because discovery of an epileptogenic lesion can have an impact on the diagnosis, prognosis, and treatment of new-onset seizures.
• MRI improves diagnostic accuracy. Using clinical and EEG data alone, In 1998 King et al were able to identify 23% of patients as having primary generalized epilepsy, 54% as having partial epilepsy, and 23% as having unclassified seizures. Using clinical, EEG, and MRI data, they were able to determine that 23% of patients had primary generalized epilepsy, 58% had partial epilepsy, and 19% had unclassified seizures.
• CT scanning might miss surgically remedial brain lesions that would otherwise be detected by MRI. King et al found that CT scanning detected only 12 of the 28 brain lesions that were detected by MRI; 7 of the missed lesions were brain tumors.
• Neuroimaging is unlikely to detect brain lesions in patients with clinical and EEG features of idiopathic generalized epilepsy or benign rolandic epilepsy. King et al found that MRI did not detect any brain lesions in 49 patients with clinical and EEG features of idiopathic generalized epilepsy or in 11 patients with benign rolandic epilepsy.
• In 1998, Chadwick and Smith concluded that plausible arguments may be made for obtaining routine early CT scanning and reserving MRI for patients with epilepsy whose seizures are not controlled by antiepileptic drugs.

Other Tests

• EEG should be performed within 24 hours of the seizure because it is significantly more sensitive when obtained during that period (King, 1998). If the routine EEG findings are normal, a sleep-deprived EEG should be performed.
• Standard EEG detects epileptiform discharges in 29% of patients. Standard EEG combined with sleep-deprived EEG shows epileptiform discharges in 48% of patients (van Donselaar, 1992).
• EEG significantly improves diagnostic accuracy in patients with a first seizure. Using clinical data alone, King et al were able to determine that 8% of patients had primary generalized epilepsy, 39% had partial epilepsy, and 53% had unclassified seizures. Using clinical and EEG data, they were able to determine that 23% of patients had primary generalized epilepsy, 53% had partial epilepsy, and 23% had unclassified seizures (King, 1998).
• In 2000, Simpson et al described a case in which the placement of an insertable loop recorder, an important new tool in the diagnostic evaluation of patients with syncope, led to an unexpected diagnosis of a seizure. Whenever cardiovascular causes are considered as the cause of a patient's spells but cannot be proven with conventional investigations, the use of the insertable loop recorder should be considered.
• Schreiner and Pohlman-Eden studied the value of an EEG taken within 48 hours of the first seizure in an adult. They found that 38.0% of patients without seizure recurrence had normal EEGs, while only 10.2% of patients with seizure recurrence had normal EEGs. Focal epileptiform activities were found significantly more frequently (26.5% vs 13.0%) in patients with seizure recurrence than in patients without seizure recurrence.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Many patients who have a single seizure do not require anticonvulsant therapy. The physician and patient should decide jointly whether to institute anticonvulsant therapy after a single seizure. This decision is based on a discussion of the risk of seizure recurrence, the effectiveness of anticonvulsant treatment, and the adverse medical and socioeconomic effects of anticonvulsant treatment.
• Among medically untreated patients in one study, the cumulative 2-year risk of seizure recurrence was 51% (Musicco, 1993). Hauser et al, in a 1990 review of previous studies, found that variability in the reported risks of seizure recurrence may have been due to the following:
• • Variations in patient populations: Some studies reflect the risk in referral populations; other studies reflect the risk in a more general patient population.
  • Variations in the specificity and sensitivity of case definitions
  • Misclassification of cases: Hauser et al found that 74% of the patient cohort required exclusion because of a previous unprovoked seizure.
  • Variations in time of ascertainment
  • Biases from retrospective study design
  • Confounding effect of anticonvulsant treatment: Many of the previous studies included patients who received anticonvulsant therapy after their first seizure.
• Risk factors for recurrent seizures include the following:
• • Age younger than 16 years: Musicco et al found that children younger than 16 years had almost double the risk of recurrent seizures as adolescents and adults aged 16-60 years (Musicco, 1993).
  • Remote symptomatic seizure (Annegers, 1986; Hauser, 1990; Berg, 1991): In the case of seizures after a first stroke, Labovitz et al found that lesion location and stroke subtype are strong predictors of early seizure risk, and early seizures are a predictor of recurrent seizures (Labovitz, 2001).
  • Seizures occurring between midnight and 8:59 am (Hopkins, 1988; Martinovic, 1997; Bora, 1995)
  • Prior provoked seizures (Hauser, 1990)
  • Remote symptomatic seizure in a patient whose sibling is affected with epilepsy (Hauser, 1990)
  • Status epilepticus or multiple seizures within 24 hours as the initial remote symptomatic seizure (Hauser, 1990)
  • Partial seizures (Annegers, 1986; Berg, 1991)
  • Todd paralysis in patients with a remote symptomatic seizure (Hauser, 1990)
  • History of neurologic deficit from birth such as cerebral palsy or mental retardation (Annegers, 1986)
  • Abnormal examination findings in patients without a remote symptomatic seizure (Annegers, 1986; Camfield, 1985)
  • CT scan that shows a brain tumor (Hopkins, 1988)
  • EEG that shows epileptiform discharges
    • In patients with a first seizure and no known etiology, van Donselaar obtained a routine EEG in all cases and a second sleep-deprived EEG if the first EEG did not show epileptiform discharges. His pooled results showed the following 2-year cumulative risks of seizure recurrence: in patients with epileptiform discharges, 83%; in patients with nonepileptiform abnormalities, 41%; and in patients with normal EEGs, 12% (van Donselaar, 1992).
    • In 1997, Beghi et al found that epileptiform discharges were associated with a 1.5- to 3-fold increase in the risk of seizure recurrence.
    • In 1993, Musicco et al found that epileptiform discharges were associated with a 1.7-fold increased seizure recurrence risk.
    • Berg and Shinnar found that epileptiform discharges were associated with a 2-fold increased seizure recurrence risk (Berg, 1991).
    • In 1990, Hauser et al found that generalized spike and wave increased the risk of recurrent seizure in patients with no known etiology.
    • In 1997, Beghi et al found that an abnormal EEG finding and the presence of an underlying etiology (remote symptomatic) are the most consistent predictors of recurrence.
• Immediate anticonvulsant treatment reduces the likelihood of a second seizure by half (Musicco, 1993). According to a 1993 report, Chandra found that valproate treatment reduced seizure recurrence rates from 63% to 4.3%.
• Immediate anticonvulsant therapy does not affect the long-term prognosis for achieving 1- or 2-year seizure-free remission and exposes many patients who would never have a recurrent seizure to anticonvulsant side effects (Musicco, 1997).
• The general consensus is that anticonvulsant treatment is needed after 2 seizures. The decision to provide anticonvulsant treatment after one seizure should be individualized.
• • Two situations that are often encountered in clinical practice and should be distinguished are a first seizure and new-onset epilepsy with more than one unprovoked seizure. Berg and Shinnar emphasized the need to distinguish between these two entities in clinical studies (Berg, 1991).
  • Seizure recurrence risk is substantially higher after 2 or more unprovoked seizures than after just one (Hauser, 1990).

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

In a 1995 report, Heller et al found that phenytoin, carbamazepine, valproate, and phenobarbital were equally effective in treating newly diagnosed epilepsy and that phenobarbital had more adverse effects. Mattson and coworkers found similar results (Mattson, 1985; Mattson, 1992).

Drug Category: Anticonvulsants

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity.

Drug Name	Carbamazepine (Tegretol)
Description	Indicated for complex partial seizures and trigeminal neuralgia. May block posttetanic potentiation by reducing summation of temporal stimulation. Following therapeutic response, may reduce dose to minimum effective level or discontinue treatment at least once every 3 mo.
Adult Dose	100 mg PO bid on day 1; increase by 200 mg/d with 100-mg increments q12h prn; not to exceed 1200 mg/d
Pediatric Dose	<6 years: 10-20 mg/kg/d PO bid/tid (qid with susp); increase weekly to achieve optimal clinical response tid/qid; not to exceed 100 mg/d 6-12 years: 100 mg bid (50 mg qid susp) 12 years: Administer as in adults; not to exceed 1000 mg/d in children 12-15 y or 1200 mg/d in children >15 y
Contraindications	Documented hypersensitivity; history of bone marrow depression; MAOI use within last 14 d
Interactions	Danazol use within last 30 d may increase serum levels significantly (avoid whenever possible); cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; may decrease primidone and phenobarbital levels (their coadministration may increase carbamazepine levels)
Pregnancy	D - Unsafe in pregnancy
Precautions	Do not use to relieve minor aches or pains; caution with increased intraocular pressure; obtain CBCs and serum iron baseline levels prior to treatment, during first 2 mo, and yearly or every other year thereafter; can cause drowsiness, dizziness, and blurred vision; caution while driving or performing other tasks requiring alertness

Drug Name	Valproic acid (Depakote)
Description	Chemically unrelated to other drugs used to treat seizure disorders. Although mechanism of action not established, activity may be related to increased brain levels of GABA or enhanced GABA action. Also may potentiate postsynaptic GABA responses, affect potassium channels, or have a direct membrane-stabilizing effect. For conversion to monotherapy, concomitant antiepilepsy drug dosage can usually be reduced by approximately 25% every 2 wk. This reduction may start at initiation of therapy or be delayed by 1-2 wk if concern exists that seizures may occur with reduction. Monitor patients closely during this period for increased seizure frequency. As adjunctive therapy, divalproex sodium may be added to the patient's regimen at 10-15 mg/kg/d. May increase by 5-10 mg/kg/wk to achieve optimal clinical response. Ordinarily, optimal clinical response achieved at daily doses <60 mg/kg.
Adult Dose	10-15 mg/kg/d PO qd or divided bid/tid; increase by 5-10 mg/kg/wk until seizures are controlled or adverse effects prevent further increases; not to exceed 60 mg/kg/d If daily dose >250 mg, administer in divided doses
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; hepatic disease or dysfunction
Interactions	Cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce levels; in children, salicylates decrease protein binding and metabolism; may result in variable changes of carbamazepine concentrations with possible loss of seizure control; may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels, while either may decrease valproate levels; may displace warfarin from protein-binding sites (monitor coagulation test results); may increase zidovudine levels in HIV-seropositive patients
Pregnancy	D - Unsafe in pregnancy
Precautions	Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough plasma concentrations >110 mcg/mL in females and 135 mcg/mL in males; at periodic intervals and prior to surgery, determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or hemostasis or a coagulation disorder occurs; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; pancreatitis can be observed; may cause drowsiness

Drug Name	Phenobarbital (Luminal, Barbita)
Description	Exhibits anticonvulsant activity in anesthetic doses and can be administered PO; in status epilepticus, achieving therapeutic levels as quickly as possible is important. IV dose may require approximately 15 min to attain peak levels in brain. If injected continuously until convulsions stop, brain concentration may continue to rise and can exceed that required to control seizures. Use the minimal amount required and wait for anticonvulsant effect to develop before administering second dose. If IM route is chosen, administer into areas with little risk of encountering nerve trunk or major artery, such as large muscles (eg, gluteus maximus, vastus lateralis). Permanent neurologic deficit may result from injecting into or near peripheral nerves. Restrict IV use to conditions in which other routes not possible, either because patient is unconscious or because prompt action is required.
Adult Dose	60-100 PO mg/d
Pediatric Dose	3-6 mg/kg/d PO
Contraindications	Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis
Interactions	Alcohol may produce additive CNS effects and death; chloramphenicol and MAOIs may increase effects; may decrease chloramphenicol effects; MAOIs may enhance sedative effects; rifampin may decrease effects; valproic acid appears to decrease metabolism and increase toxicity; can decrease effects of anticoagulants—patients stabilized on anticoagulants may require dosage adjustments if phenobarbital is added to or withdrawn from their regimen; may decrease serum carbamazepine levels; may decrease effects of contraceptives by inducing microsomal enzymes—in women, may cause menstrual irregularities and pregnancy; may decrease corticosteroid effects by inducing hepatic microsomal enzymes; may increase digitoxin metabolism; may decrease antimicrobial effects of metronidazole; decreases theophylline levels, possibly resulting in decreased effects; may decrease bioavailability of verapamil
Pregnancy	D - Unsafe in pregnancy
Precautions	In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; exercise caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia because adverse reactions can occur; exercise caution in patients with myasthenia gravis and myxedema

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Many patients who have a seizure recover spontaneously and fully with normal consciousness after a short time interval. Patients with incomplete recovery or a prolonged postictal state may require inpatient hospitalization (Moore-Sledge, 1997).
• Inpatient management may be necessary if the clinical course is complicated by other medical problems requiring inpatient management.
• A short hospitalization may be necessary for patients who are at risk of recurrent seizures and have no adequate supervision at home. Patients admitted from an emergency department had a 16.8% risk of an early recurrent seizure during their brief hospitalization (Tardy, 1995). This risk of early recurrent seizures was higher than reported in other studies (Hauser, 1990; Musicco, 1993; Annegers, 1986).

Patient Education

• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education article Epilepsy.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Patients who have had a single epileptic seizure are at increased risk of having a second seizure. They should be informed that they are at increased risk of injury to themselves or others if another seizure occurs. Risk of injury is especially important if patients are driving, operating dangerous machinery, or performing other activities that could put themselves or others at risk. These same concerns also apply to nonepileptic conditions such as syncope that might recur and put the patient or others at risk of injury. The patient should be advised to contact the state agency that regulates driving privileges. This discussion with the patient should be documented in the medical record. Driving regulations vary from state to state. The restrictions sometimes apply to any alteration or loss of consciousness from any etiology.
• Counseling patients about driving after a first seizure revolves around 2 issues: the diagnosis and the chance of recurrence.
• Patients with a first epileptic seizure and with risk factors such as remote symptomatic etiology or EEG with epileptiform discharges are at higher risk for a second seizure. Restrictions of hazardous activity should be more emphatic for these patients.

Special Concerns

• The diagnosis of epilepsy refers to recurrent seizures and cannot be made on the basis of a single episode, even if anticonvulsant treatment is administered. This is especially important because of the serious medical, social, economic, and legal consequences surrounding the diagnosis of epilepsy.
• The annual cost of misdiagnosis of nonepileptic spells as epileptic seizures is estimated to be between $650 million and $4 billion (Nowack, 1997).

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Annegers JF, Shirts SB, Hauser WA, Kurland LT. Risk of recurrence after an initial unprovoked seizure. Epilepsia. Jan-Feb 1986;27(1):43-50. [Medline].
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• Berg AT, Shinnar S. The risk of seizure recurrence following a first unprovoked seizure: a quantitative review. Neurology. Jul 1991;41(7):965-72. [Medline].
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• Mattson RH, Cramer JA, Collins JF. A comparison of valproate with carbamazepine for the treatment of complex partial seizures and secondarily generalized tonic-clonic seizures in adults. The Department of Veterans Affairs Epilepsy Cooperative Study No. 264 Group. N Engl J Med. Sep 10 1992;327(11):765-71. [Medline].
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Article Last Updated: Aug 29, 2006