• Approach to epilepsy
• Non-seizure visits
• Post-seizure visits
• Changes in duration, frequency, or type
• Abnormal postictal neurologic exam
• Abnormal postictal labs
• Abnormal neuroimaging
• First or unknown seizure history visits
• Acutely seizing patients
• Treating convulsive SE
• Myoclonic seizures
• Absence seizures
• Nonepileptic psychogenic seizures
• References

Neuroimaging is a useful tool in evaluating some patients with seizures, however. Any change in the patient’s seizure pattern or type warrants an emergent scan, as do prolonged postictal confusion or worsening mental status. An emergent neuroimage should be taken in patients who have epilepsy with recurrent seizures whenever the physician suspects a serious structural lesion.26,27

There is evidence26 supporting a higher frequency of life-threatening lesions in patients with:

• new focal deficits
• persistent altered mental status (with or without intoxication)
• fever
• recent trauma
• persistent headache
• history of cancer
• history of anticoagulation
• suspicion of acquired immunodeficiency syndrome (AIDS)

A patient who has completely recovered from his or her seizure and for whom no clear-cut exacerbating factor has been identified should be scheduled for a scan as part of the disposition from the ED. After obtaining a scan to ensure the absence of a new or developing structural lesion, the physician in the ED may ask the patient to follow up with the primary physician.

If an MRI scan is performed, a seizure protocol should be used. This includes thin coronal cuts through the amygdala, hippocampus, and mesial temporal regions, using T1, T2, and FLAIR pulse sequences.

Neck immobilization

Spinal immobilization in individuals after seizures is rarely necessary. In one retrospective study, 1,656 cases over a 10-year period were reviewed, and no spinal injuries were found.25

Communication

Contacting the patient’s treating physician is vital to good quality and continuity of care. In one study, AED therapy was altered by the ED in nearly 20% of epilepsy patients who were evaluated and discharged from an ED, but documentation that these changes were discussed or communicated to the primary treating physician was lacking in 85% of these patients.5 Also, ask the patient to contact the physician who manages his or her seizures.

Driving

Review issues of compliance with the patient, and inform him or her about the state laws that pertain to driving. In states where the physician is required by law to inform the Department of Motor Vehicles of acute seizures (e.g., California, Delaware, New Jersey, Pennsylvania), this should be done by form from the ED.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

If the period is short or an appropriate alternative medication specific to the patient’s seizure type and history cannot be chosen immediately, another alternative is to administer periodic low-dose benzodiazepines, such as lorazepam, chlorazepate, or clonazepam, as bridge therapy to suppress seizures for a relatively short time. If necessary, this approach can be used for several weeks, although initial sedation from benzodiazepines can be problematic or even contraindicated—for example, when the neurologic exam must be followed closely in the case of head injury or stroke. Although diazepam is a reasonable choice of medication for the acute suppression of seizures, it is not desirable as bridge therapy. Its antiepileptic half-life is usually about 30 minutes after IV administration, owing to redistribution out of the brain, whereas its sedative half-life may be much longer. The antiepileptic half-life of lorazepam, in comparison, may be more than 4 to 6 hours.1

Raising the seizure threshold

Factors that could potentially lower the seizure threshold should be minimized. Certain types of medications must be administered with care, with doses closely in line with the manufacturer’s recommendations, if possible. These medications include:

• butyrophenones (e.g., haloperidol)
• phenothiazines (e.g., chlorpromazine)
• antihistamines
• xanthines (e.g., aminophylline)
• meperidine (particularly in the setting of renal dysfunction)
• tricyclic antidepressants

Electrolytes such as sodium, calcium, and magnesium should be monitored closely and abnormalities treated aggressively. Clinically significant hyperammonemia and hypoglycemia or hyperglycemia should be treated.

Exploring drug interactions

The ED staff should pay attention to factors that may alter AED absorption, metabolism, distribution, or excretion. Giving antacids, histamine 2 blockers, or sucralfate (Carafate), for example, may affect levels of AEDs that require an acidic pH for absorption (e.g., phenytoin). Antibiotics (e.g., erythromycins, quinolones) and antifungal agents can raise the level of AEDs, resulting in dramatic toxicity, often delayed several days after the patient is given a prescription in the ED.

Potential drug interactions between current AEDs and with newly prescribed medications should be quickly researched. A few minutes proactively spent in this manner may prevent a second ED visit several days later.

Communicating about changes

Communication and follow-up should be underlying themes in caring for individuals with epilepsy who are treated in the ED. Just as important as changing the regimen is ensuring that these changes are communicated effectively to the patient (or the patient’s family or caregivers) and to the physician who treats the patient after the ED discharge. If appropriate follow-up is arranged and changes are communicated rapidly and effectively, many difficulties can be avoided and exacerbations often are prevented.

For example, patients in the ED may be given medications that rapidly elevate AED levels. If these changes are communicated, toxicity can be avoided by monitoring levels and adjusting AED doses appropriately. If these changes are not communicated, patients may later present to the ED for acute toxicity or, as in status epilepticus, be taken off their medications owing to acute toxicity.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Almost one-third of people with epilepsy do not gain complete seizure control by standard therapy.2 These individuals frequently present to the ED after typical seizures. The ED physician must determine whether the patient has merely had a typical seizure, which may require no acute therapy, or whether the seizure was atypical or due to some other condition that might require immediate evaluation and treatment.

As with many other aspects of neurology, the key to appropriate diagnosis and treatment is the history. Unfortunately, history is often lacking in this setting, as individuals with epilepsy are often confused after seizures, reliable historians are often hard to contact in the ED, and patients are usually brought in by ambulance, leaving witnesses behind.

The simplest scenario is the one in which the patient is brought to the ED after a seizure and returns to his or her normal interictal baseline by the time of assessment by the ED physician. If the patient is completely normal, recounts a typical aura before seizure onset, has a normal examination and no fever, and has appropriate medical care in place, then the visit may only require sending serum for electrolytes, complete blood count (CBC), and AED levels and calling the patient’s physician to arrange appropriate follow- up. It is preferable in such circumstances to discharge the patient into the care of family, friends, or other caretakers who can observe the patient and initiate a return to the ED at the first sign of any recurrence, illness, or unusual change in behavior.

Such clear-cut cases are relatively rare, however, because most individuals with seizures usually become cognizant of their seizures and the events that surround them only by hearing accounts from witnesses or by surmising that they have occurred after they awaken in the ED with sore muscles, a lacerated tongue, or urine incontinence. This complicates their ED care and decisions about whether to release them or admit them to the hospital.

Issues that complicate the care of epilepsy patients in the ED after seizures usually pertain to one of the following deviations from their typical seizures:

• Change in seizure duration, frequency, or type (e.g., prolonged seizures, clustering, or change from complex partial to generalized convulsive seizures)
• Abnormal postictal examination (e.g., focal weakness; altered awareness; fever; or visual, sensory, language, or behavioral abnormalities)
• Abnormal laboratory findings (e.g., leukocytosis; low sodium, magnesium, or calcium; “abnormal” AED levels; cerebrospinal fluid [CSF] pleocytosis)
• Abnormal neuroimaging

When deviations from the previously mentioned perfect scenario occur, always err on the side of caution. Admit the patient if there is any significant concern or unexplained findings. This approach may result in admitting individuals to the hospital who could probably go home, but it means that serious conditions are unlikely to remain untreated.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Abnormal postictal labs
Abnormal postictal neurologic exam

If no abnormalities are found, then a plan for altering the patient’s AED regimen should be made in conjunction with the patient’s neurologist, if the contact can be made. Alternatively, immediate outpatient follow-up should be arranged with the patient’s treating physician, or a new physician should be found if the patient is not under continued care.

If there are no contraindications, consideration should be given to prescribing treatment with an oral benzodiazepine as needed for clusters. Choices may include:

• lorazepam (usually 1 mg up to 3 times a day)
• clonazepam (0.5–1.0 mg by mouth up to 2 times a day)
• clorazepate (up to one-half of a 3.75-mg tablet by mouth up to 2 times a day)

Alternatively, diazepam gel for rectal administration (Diastat) can help individuals who are unable to recover sufficiently or otherwise cooperate to take an oral medication between seizures during a cluster. The patient or caretakers should be instructed not to use these medications regularly but only as needed, as their efficacy wears off over a period of weeks to a few months, and it is sometimes difficult to taper off these medications without withdrawal seizures. Only a few doses should be provided, and the patient should be encouraged to obtain refills from his or her treating physician, if needed.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

A transient deficit that results from seizure activity is usually called a postictal state. Postictal phenomena might include transient blindness after an occipital seizure and loss of memory after a complex partial seizure that originates in one or both temporal lobes. Generalized convulsive seizures may be followed by minutes to hours of sleep, confusion, or unresponsiveness. A postictal state that is characterized by a motor weakness in the distribution of muscles controlled by seizing neurons is called Todd’s paralysis.3

In the emergency department (ED), it is critical to determine whether a postictal neurologic deficit is due to a postictal state, which resolves spontaneously, or to another process that may require immediate treatment. This task is complicated by the fact that fever, headache, disorientation, and focal weakness may be normal sequelae of seizures.

Attribute abnormal postictal neurologic findings to a postictal state as a diagnosis of exclusion. This rule should be violated only when:

• there is a clear history of identical postictal deficits after typical seizures
• no other significant abnormalities are found on physical and laboratory examination
• the patient can be discharged into the care of reliable individuals and will rapidly return to the ED if symptoms do not resolve typically or new symptoms emerge

Other causes of postictal neurologic deficits must be investigated, especially when any postictal state lasts for more than 24 hours. If there is any question about the nature of the patient’s deficits, the patient should be admitted to the hospital, and an appropriate neuroimaging study, preferably a magnetic resonance imaging (MRI) scan with and without contrast, should be performed.

In the ED, investigate any fever in the postictal period as a new fever and assume that it is unrelated to the seizure until no other source is found. Send blood for CBC, electrolytes, and blood cultures from two independent sites.

Perform lumbar puncture whenever a central nervous system infection is suspected. It should be performed on most patients who present with a new-onset seizure, but may not be needed if the patient returns rapidly to normal baseline and the fever rapidly abates, as long as someone reliable can observe the patient. Lumbar puncture is strongly recommended, however. In competent hands, it is a relatively painless and low-morbidity procedure, and the consequences of missing a meningitis or encephalitis can be devastating.

If there is a postictal fever and the patient refuses lumbar puncture, the patient should be admitted for observation for at least 24 hours. Further studies should include urinalysis; urine culture, when appropriate; a thorough lung examination; and a chest x-ray, if indicated.

Patients who are febrile postictally and immunocompromised (e.g., patients on chemotherapy, chronic alcoholics, or individuals with HIV infection or chronic renal failure) or cognitively impaired (particularly those who cannot communicate well) should undergo aggressive, thorough evaluations, including lumbar puncture, unless there is a contraindication.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

CSF abnormalities should be noted. CSF pleocytosis can occur after an acute seizure. Although significant numbers of white blood cells (over 20) have been reported in the CSF after seizures,4 cell counts of more than 10 are quite unusual after acute seizures. Broad-spectrum antibiotic therapy and hospital admission for presumed CNS infection should be initiated for white blood cell counts of more than 6 to 8 in the setting of an acute seizure, for any number of polymorphonuclear white blood cells in the CSF, or for fewer cells with abnormal CSF protein or glucose. The threshold for therapy is lower for immunocompromised individuals. Treatment is continued only until CSF cultures are negative at 24 hours.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

The use of neuroimaging in patients with seizures is discussed on the page Approach to epilepsy in the emergency department.

In the setting of a known seizure disorder, abnormal neuroimaging results rarely require acute intervention. Exceptions include finding an acute hemorrhage, suggestive of a possible rupture of an aneurysm or arteriovenous malformation, or finding acute hydrocephalus or imminent brain stem herniation due to mass effect.

In most cases, emergency physicians do not have access to old brain images, and it is rare that intervention needs to be undertaken in the emergency department, unless the patient becomes unstable. If the patient’s treating physician cannot be reached, patients with worrisome lesions can be admitted overnight for observation and for formulation of a treatment plan by the next day.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

A first generalized seizure accounts for nearly 1% of all visits to the emergency department (ED).5 A patient who presents with a first seizure actually may have had seizures in the past that had not generalized or were not noticed, however.

The vast majority of new-onset seizures seen in the ED are due to factors that lower the seizure threshold, not epilepsy. This necessitates a thorough and immediate workup for the cause of the seizure. In one retrospective study6 of a 3-year period during which 247 patients were admitted for a first generalized seizure, the principal etiologies were:

• unknown—23.9%
• alcohol abuse—19.8%
• stroke—13.4%
• tumor—10.4%
• intoxication—9.3%

The evaluation of a patient after a first known seizure should proceed as described for patients with known epilepsy, except that few tests are routinely omitted. (See Abnormal postictal labs)

Another test that is important to consider in these patients is the evaluation of the patient for pregnancy7 to determine limits on testing, such as computed tomography scanning. Pregnancy also may suggest the need to evaluate for hemorrhage or ischemia related to arteriovenous malformations, cavernous angiomata, or venous thrombosis, all of which are more likely to present in pregnancy.

A toxicology screen is indicated if there is a suspicion of drug abuse. Testing for human immunodeficiency virus (HIV) and syphilis should be considered, if suggested by the patient’s history.

If the patient is not actively seizing at the time of evaluation, obtain a clear history of the event, preferably in person and from a witness, so as to be able to distinguish the event from syncope, fainting, hyperventilation, psychogenic nonepileptic seizures, and other types of events that can mimic epileptic seizures. (See Nonepileptic seizures)

If the cause of the event cannot be clearly determined by the history, as is often the case, initial screening can help to determine whether the event was an acute symptomatic seizure or an idiopathic event. The focus of the initial evaluation is to look for acute medical conditions that could have precipitated the event. These include:

• a focal brain lesion
• infection
• inflammatory process
• toxic exposure
• trauma
• systemic/metabolic disorder

If such a condition is found, rapid admission to the hospital, evaluation, and treatment are indicated.

If the patient provides a good history, it is common in those who present with idiopathic seizures to find that multiple prior events have gone unreported.8 These events might be as subtle as brief episodes of morning myoclonus after sleep deprivation, occasional auras of déjà vu, a rising abdominal sensation, or unusual smells or tastes. The patient should be screened for epilepsy risk factors, such as:

• head trauma resulting in loss of consciousness or amnesia
• premature birth
• history of febrile seizures (especially prolonged or focal ones)
• family history of seizures
• cognitive dysfunction
• other causes of an abnormal neurologic examination

Laboratory studies, including lumbar puncture if indicated, and a seizure-protocol MRI scan should be performed. If the patient rapidly returns to normal and the neurologic examination, screening blood work, and screening neuroimaging (e.g., CT scan) are normal, it is reasonable to discharge the patient from the emergency room without prescribing medication, provided that the patient can be seen promptly by a neurologist to complete the evaluation. In this setting, the patient should be told that, statistically, antiepileptic drugs reduce the risk of seizure recurrence by approximately 50% over 2 years, but nearly all patients experience at least some minor side effects.9–11 (See Approach to epilepsy)

If therapy with an antiepileptic drug is initiated, it should be chosen to treat the patient’s seizure type, or, if there is uncertainty, a broad-spectrum agent should be chosen. Such agents include:

• levetiracetam
• lamotrigine
• zonisamide
• topiramate
• valproic acid

If there is no clear family history of epilepsy and the patient presented with a generalized convulsive seizure, most ED physicians are still inclined to start therapy with phenytoin. This is an acceptable choice, since physicians are usually wise to use medications with which they feel comfortable. In many of these patients, this medication is eventually discontinued or replaced with another agent that may have fewer long-term side effects.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Status epilepticus is often defined as continuous seizure activity or periodic seizures that last 30 minutes or more without recovery to baseline consciousness between seizures. If a patient has been seizing for 30 minutes, however, valuable time for treatment has been lost. It should therefore be considered a retrospective diagnosis. Every emergency department should have a published protocol or critical pathway for treating status epilepticus in adults and children,2 and this protocol should be initiated for every acutely seizing patient. The protocol is then aborted when seizing stops and the patient’s condition comes under control.

Nonconvulsive status epilepticus (NCSE), in which there may be few or no outward signs that the patient is seizing, differs from the acute, life-threatening emergency of convulsive status13 with regard to the urgency and aggressiveness of treatment. It is more commonly a concern in the intensive care unit.

The clinical outcome in status epilepticus is determined by its cause.12 Patients with easily treatable toxic, metabolic, or other nonstructural causes of status epilepticus usually experience a good clinical outcome. Those with devastating structural, infectious, or other catastrophic causes usually have a poor prognosis for meaningful recovery.

The most common cause of status epilepticus in individuals with epilepsy is acute medication withdrawal related to noncompliance.14

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Although status epilepticus is defined as seizure activity that lasts for more than 30 minutes or that continues intermittently during this period without recovery of alertness, in practice, a treatment regimen should begin when a seizure lasts for more than a few minutes. The approach discussed here closely follows the recommendations of the Epilepsy Foundation’s Working Group on Status Epilepticus, with a few exceptions.12,45,46 (See Table: Protocol for Treatment of SE)

The initial priority is given to the airway, breathing, and circulation. Oxygen is given by nasal cannula, and the patient is often placed on his or her side to minimize the chance of aspiration. Objects should not be placed in the patient’s mouth. Within the first 5 minutes of a seizure, two reliable IV lines should be established. Venous blood is sent for electrolytes, glucose, and hematology studies and determination of AED levels. If there is any question of hypoglycemia, give 100 mg thiamine followed by 50 mL of 50% glucose by direct push into the IV line.

The pharmacologic approach to status epilepticus begins with treatment with a benzodiazepine, followed by phenytoin and then, if needed, barbiturates for refractory seizures. Lorazepam is preferred because of its longer duration of action, but diazepam is also an acceptable initial treatment. The initial dose can be 2 mg IV of lorazepam, repeated every 5 minutes up to a total dose of 0.1 mg/kg. If the status is stopped, phenytoin loading can then be used to prevent recurrent status.

Phenytoin often controls those seizures not effectively terminated by benzodiazepines. For most adults, the loading dose of 20 mg/kg is sufficient to produce blood levels of 10–15 mg/liter. If the initial dose of phenytoin is not effective, a second dose of 10 mg/kg can be given, which increases the blood level to approximately 25 mg/liter. Phenytoin must be given at a rate no faster than 50 mg per minute in adults, and cardiac monitoring should be used to watch for arrhythmias and hypotension.

Fosphenytoin, a phenytoin prodrug, is preferred when available, as it does not require a glycol diluent that renders phenytoin incompatible with glucose-containing solutions. This compound carries a much lower incidence of thrombophlebitis, can be given at a faster IV rate than phenytoin, and can be loaded intramuscularly when IV access is not available.

Seizures that are refractory to benzodiazepines and adequate doses of phenytoin can be treated with barbiturates. Adequate doses of barbiturates may lead to hypotension and respiratory depression, however, so dopamine should be present at the bedside when therapy with barbiturates is begun, and assisted ventilation should be readily accessible. Phenobarbital is given with an initial loading dose of 20 mg/kg at a rate of no more than 50 mg per minute.

EEG testing is required if the patient does not stop seizing. Continuous EEG is necessary to guide the degree of cerebral electrical suppression. Anesthetic doses of pentobarbital are initiated if the patient remains in status epilepticus (See Table: Pentobarbital-induced anesthesia in refractory generalized tonic-clonic status epilepticus). All patients are intubated before this step, if this has not been done before this time. (Separation of the effects of pentobarbital from the cardiorespiratory complications of refractory generalized tonic-clonic status epilepticus may be difficult.) A loading dose of pentobarbital is 10 mg/kg, which is followed by a continuous infusion at a rate of 0.5 to 4.0 mg/kg per hour. This infusion is titrated to maintain the EEG in a 3-to-1 burst-suppression pattern. (More recent evidence may suggest that titrating therapy to complete suppression of the EEG background may be more effective than titrating to burst suppression.47) When 12 to 24 hours have passed since suppression of epileptiform discharges, the amount of sedation can be lightened with EEG guidance. If seizures recur, a small bolus of pentobarbital is given to return the EEG to burst suppression or complete suppression, and the infusion is continued for another 48 to 60 hours. If seizures recur after this period, the prognosis for meaningful recovery is often poor, although many centers have pursued prolonged drug-induced coma, some for up to 50 days. Surviving patients have significant neurologic impairment.48

Many relatively small studies have tested medications other than pentobarbital for the treatment of refractory status epilepticus, including IV midazolam and propofol infusions.49 In general, these therapies may be useful in certain circumstances (particularly with children53), but their absolute indications have yet to be determined.

Bilateral motor activity with preserved consciousness is rare in epilepsy, with the exception of epileptic myoclonus and supplementary motor seizures. Motor signs may become subtle during prolonged seizures, as the neurons subserving motor function become fatigued and refractory to activation. Animal data suggest that 30 minutes of sustained seizure activity results in irreversible neuronal injury.44

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

In patients with a history of myoclonic epilepsy, seizures consist of focal or generalized, rapid, uncontrolled muscle movements that are usually synchronous. Consciousness may or may not be impaired. When these patients present with uncontrolled seizures, the prognosis for full recovery is generally good with proper treatment.15 Usually, they are exquisitely sensitive to treatment with IV benzodiazepines, although the addition of IV valproate preparations is sometimes required.

Postanoxic myoclonus

About 17% of patients who experience hypoxic or ischemic injury that results in coma develop focal, multifocal, or generalized periodic myoclonic movements, often manifested by eye blinking, chewing movements, or multifocal twitching.16 When this type of seizure activity is seen after a global ischemic event, the prognosis for a meaningful recovery is poor. Most experts believe that, with rare exception, this clinical presentation probably represents an agonal neurologic event in an irreparably injured brain rather than an electrical dysfunction in salvageable tissue.

Postanoxic myoclonus is notoriously difficult to control and may be continuous, giving rise to myoclonic status epilepticus. Sometimes paralytic agents are used to eliminate myoclonic movements, but this is not recommended. If the likelihood of survival is poor, it may be done purely for cosmetic reasons, to make the patient’s death easier for the family. In this case, nothing is done to treat the agonal discharges of the dying brain, and electrical status epilepticus persists. Benzodiazepines and other antiepileptic drugs have been used to treat postanoxic myoclonus, but the results are generally poor.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Occasionally, absence seizures develop in elderly patients with no prior history of seizures.17,18 Patients with this condition appear confused, are variably responsive, and may express automatisms. This state may persist for weeks or months before it is detected.19 It is easy to miss in the emergency department unless one is aware of its presentation. It is usually diagnosed in elderly individuals who are confused, sometimes with a low-grade fever and no other obvious cause of altered sensorium. Diagnosis of this type of absence seizure requires urgent, bedside electroencephalogram (EEG).

Absence seizures in seniors usually respond to low-dose IV benzodiazepines.20,21

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535. With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

Nonepileptic psychogenic seizures (NESs) are episodes of clinical seizurelike activity that do not result from abnormal electrochemical activity in the brain. NESs are potentially life-threatening, owing to iatrogenic morbidity from futile attempts to control the seizurelike activity. About 20% or more of patients with NESs also have epileptic seizures.22,23

Patients with NESs may have a history of psychiatric disease, an unusual medical history, or an atypical response to AEDs. Clinically, they may present with unresponsiveness and minor movements, although sometimes they may present with generalized convulsive movements. Features that sometimes identify NESs include:

• side-to-side head movements
• asynchronous motor movements
• pelvic thrusting
• forced eye closure and guarding the face when presumed to be unresponsive
• alerting to stimuli during convulsive movements

Diagnosis and treatment of this condition are usually beyond the ED setting. Its presentation often results in hospital admission.24

See more information on nonepileptic seizures.

Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535. With permission from Elsevier (www.elsevier.com).

Reviewed and revised May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.

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2. Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342:314–319.

3. Todd RB. Clinical Lectures on Paralysis, Disease of the Brain and Other Affections of the Nervous System. Philadelphia: Lindsay & Blakiston, 1855.

4. Edwards R, Schmidley JW, Simon RP. How often does a CSF pleocytosis follow generalized convulsions? Ann Neurol 1983;13:460–462.

5. Krumholz A, Grufferman S, Orr ST, et al. Seizures and seizure care in an emergency department. Epilepsia 1989;30:175–181.

6. Tardy B, Lafond P, Convers P, et al. Adult first generalized seizure: etiology, biological tests, EEG, CT scan, in an ED. Am J Emerg Med 1995;13:1–5.

7. Dalessio D. Seizure disorders and pregnancy. N Engl J Med 1984;312:559–563.

8. Hauser WA, Annegers JF, Kurland LT. Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota: 1935–1984. Epilepsia 1993;34:453–468.

9. Beghi E. Randomized clinical trial of the efficacy and safety of the treatment of the first unprovoked epileptic seizure. First Seizure Trial Group. Neuroepidemiology 1992;11:50.

10. Beghi E, Ciccone A. Recurrence after a first unprovoked seizure. Is it still a controversial issue? First Seizure Trial Group (first). Seizure 1993;2:5–10.

11. Randomized clinical trial on the efficacy of antiepileptic drugs in reducing the risk of relapse after a first unprovoked tonic-clonic seizure. First Seizure Trial Group (FIRST Group). Neurology 1993;43:478–483.

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Adapted from: Kolb SJ and Litt B. Management of epilepsy and comorbid disorders in the emergency room and intensive care unit. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;515–535.
With permission from Elsevier (www.elsevier.com).

Reviewed May 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.