Nursing Management of Seizures and Epilepsy

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9/24/12 9:vid: Clinical Practice of Neurological and Neurosurgical Nursing, The

Page 1ttp://ovidsp.tx.ovid.com/sp-3.6.0b/ovidweb.cgi

Authors: Hickey, Joanne V.

Title: Clinical Practice of Neurological and Neurosurgical Nursing, The, 6th Edition

Copyright 2009 Lippincott Williams & Wilkins

> Table of Contents > Section 8 - Nursing Management of Patients With Pain, Seizures, and CNS Infections > Chapter 29 - Seizures and

Epilepsy

Chapter 29

Seizures and Epilepsy

Joanne V. Hickey

This chapter focuses on adults with epilepsy and the nurse's role in assisting patients to self-manage in the

community setting and in assisting hospitalized patients with a seizure disorder. Although seizures and epilepsy are

common in children, the special considerations related to children with these conditions are not addressed in this

chapter. Other resources should be consulted for specific information on childhood and adolescent epilepsy.

Most people with a seizure disorder are managed in the community by a primary care physician or a neurologist.

Patients who are difficult to manage may be referred to an epilepsy center where a neurologist with a practice

focused on seizure disorders and a multidisciplinary team can provide comprehensive management. In many

geographical areas, advanced practice nurses with a focus on seizure management are available to patients and

families or as a consultant to other nurses. Almost all nurses who practice in a hospital environment see patients

who have a seizure secondary to a primary condition, such as metabolic imbalance. Other nurses may see people

with intractable epilepsy who are admitted for surgical intervention. Regardless of the setting in which care is

delivered, nurses play an important role in the management and education of patients and their families.

BACKGROUND AND DEFINITIONSReferences to epilepsy date back to ancient times, and mystical explanations about seizures continued until the

1870s when Jackson theorized that seizures originated from a localized, discharging focus in the brain. The

introduction of the electroencephalogram (EEG) by Berger in 1929 provided the first recordings of epileptic

discharges. This landmark event was followed in the 1930s by the work of Gibbs, who correlated the clinical

indicators of epilepsy with EEG patterns. The development of classification systems for both epilepsies and

seizures has paved the way to a better understanding of the variations in clinical presentation. Research focused

on the clinical and cellular bases for seizures, new drugs, and improved management protocols have all

contributed to better outcomes for patients subject to seizures.

The terminology for seizures and epilepsy is imprecise. The following widely accepted definitions have helped

overcome imprecise terminology, which created confusion about seizures and epilepsy in the past.

Seizure: a single (finite) event of abnormal discharge in the brain that results in an abrupt and temporary

altered state of cerebral function.

Epilepsy: a chronic disorder of abnormal, recurrent, excessive, and self-terminating discharge from neurons.

Periods between seizures can vary widely and can be measured in minutes, hours, days, weeks, months, or

even years. However, there is repetition of seizure activity at some time in the future, regardless of the


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interval. Clinically, epilepsy is characterized by recurring seizures accompanied by a disturbance in some type

of behavior (i.e., motor, sensory, autonomic, consciousness, or mentation).

Seizure disorder: a term adopted by some clinicians when referring to epilepsy. Although this has led to some

confusion, the terms epilepsyand seizure disorderare used interchangeably.

Epileptic syndrome: an epileptic disorder characterized by a cluster of signs and symptoms customarily

occurring together.

Epidemiology and Risk FactorsEpilepsy is one of the most common neurological conditions representing a heterogeneous collection of disorders

that have in common a recurrence of seizures. About 1.25 to 2 million people in the United States have epilepsy.

Approximately 30% of all epilepsies and about 60% of all childhood epilepsies may have a significant genetic

susceptibility. The risk of epilepsy is about 1% from birth through 20 years and 3% for the 70-year and older age

group. The prevalence and cumulative incidence of epilepsy and partial seizures increase in the elderly.1

A few basic concepts guide understanding of seizures in individuals. First, anyone can have a seizure, given the

right circumstances of central nervous system (CNS) imbalance. However, there are differences among people in

their threshold for seizures. Second, there is a high likelihood of a chronic seizure disorder in people with specificconditions such as a penetrating brain injury. Third, seizures are episodic, suggesting that triggers precipitate

seizure activity.2

The major risk factors for developing seizures can be classified according to age group. In young adults, trauma,

alcohol withdrawal, illicit drug use, brain tumor, and other central nervous system conditions are the most

common causes. In the 35-year and older age group, cerebrovascular disease, brain tumor, alcohol withdrawal,

metabolic disorders (e.g., uremia, electrolyte imbalance), Alzheimer's disease, neurodegenerative diseases, and

idiopathic causes rank as the major causes of seizures. The term idiopathic epilepsy is used for the 70% of all

cases for which no specific cause is identified.

PathophysiologySeizures are transient episodes of abrupt and temporary alteration of cerebral function resulting from a

paroxysmal high-frequency or synchronous low-frequency, high-voltage electrical discharge.3 Ropper and Brown

note that seizures require three conditions: (1) a population of pathologically excitable neurons; (2) an increase in

excitatory glutaminergic activity through recurrent connections to spread the discharge; and (3) a reduction in the

activity of the normal inhibitory gamma-aminobutyric acid (GABA) projection.4 Seizures result from an imbalance

between excitation and inhibition within the CNS. Excessive excitation or excessive inhibition may occur in focal

areas of the cerebral cortex (focal seizures) or over the entire cerebral cortex (generalized seizures). A focal or

generalized increase in neuronal excitabilitymay result from energy failure of neurons producing transientdepolarization or lack of local inhibition.

Epilepsy can also result from alterations in membrane potentials that predispose certain hyperactive and

hypersensitive neurons to respond abnormally to changes in the cellular environment. The hypersensitive neurons

have lowered thresholds for firing and can fire excessively, creating an epileptogenic focus from which the seizure

emanates. The epileptogenic focus generates large numbers of autonomous paroxysmal discharges that can be

enhanced or minimized, depending on the neurotransmitter that is active on the postsynaptic membrane. An

epileptogenic focus can induce secondary epileptogenic foci in a synaptically related area and also in opposite


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cerebral hemispheres through connecting pathways between the same anatomic areas.

Precipitating Factors: TriggersIn patients with epilepsy, seizures can be precipitated by various stimuli called triggers. Sometimes the trigger is

very specific for a particular person. Common triggers include particular odors, flashing lights, and certain types of

music. If a specific stimulus can be identified, then the pattern is called reflex epilepsy. Othergeneral triggers

include fatigue, sleep deprivation, hypoglycemia, emotional stress, electrical shock, febrile illness, alcohol

consumption, certain drugs, drinking too much water, constipation, menstruation, and hyperventilation.

TerminologyA few terms describe the general signs and symptoms of seizures:

Aura is a premonitory sensation or warning experienced at the beginning of a seizure, which the patient

remembers. An aura may be a gustatory, visual, auditory, or visceral experience, such as a metallic taste or

flashing lights. If a patient has an aura, it usually is the same experience each time.

Automatisms are more or less coordinated, involuntary motor activities that occur during a state of impaired

consciousness either in the course of or after an epileptic seizure, for which the person is usually amnesic.Several different types of automatism have been recognized. Examples of automatisms are lip smacking,

chewing, fidgeting, and pacing.5 Automatisms are often associated with temporal lobe seizures but can also

occur with complex partial seizures as well as with other types.

Autonomic symptoms are symptoms that occur as a result of stimulation of the autonomic nervous system

(e.g., epigastric sensation, pallor, sweating, flushing, piloerection, pupillary dilation).

Clonus is a term used to describe spasms in which a continuous pattern of rigidity and relaxation is repeated.

In the second phase of a generalized seizure, called the clonic phase, rhythmic movements are followed by

muscle relaxation. In the clonic phase, the process repeats again and again.

Ictus refers to an actual seizure; a seizure may be referred to as an ictal event.

Postictal refers to the period immediately after a seizure has occurred.

Prodromal refers to symptoms, such as a headache or feeling of depression, that precede a seizure by hours.

Tonus is the degree of tone or contraction present in muscle when it is not undergoing shortening.

Todd's paralysis is a temporary, focal weakness or paralysis following a partial or generalized seizure that can

last for up to 24 hours. The deficit can be correlated with an epileptic focus on the motor strip. Temporary

neuronal exhaustion is probably the physiologic basis for the deficit.

SEIZURE CLASSIFICATION AND OBSERVATIONS/IDENTIFICATIONSeizures and epilepsy have been classified for clinical and research purposes using several different forms. Most of

these are complex and cumbersome to use. In 1981, the International League Against Epilepsy (ILAE) published a

modified version of the International Classification of Epileptic Seizures that continues to be a useful classification

system (Table 29-1).6

The following section briefly discusses partial and generalized seizures. Tonic-clonic seizures, as examples of

generalized seizures, are described in greater detail because they are so common. Table 29-2 describes the major


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subtypes of partial and generalized seizures, and Table 29-3 classifies partial seizures by cerebral lobe involved.

Partial SeizuresThree types of partial seizures are recognized: simple, complex, and evolving into secondary generalized seizures.

Simple

and complex seizures are distinguished on the sole basis of consciousness. When consciousness is not impaired, the

seizure is classified as a simple partial seizure; if consciousness is impaired, the seizure is classified as a complex

partial seizure. The four subcategories of simple partial seizures are named for the areas of their presenting

symptoms: motor, sensory, autonomic, andpsychic. Complex partial seizures include both complex

symptomatology and impaired consciousness. Another term for complex symptomatology is automatisms. These

seizures consist of involuntary, but coordinated, motor activity that is purposeless and repetitive. The final

category is a partial seizure evolving into a generalized seizure. These seizures are further categorized based on

the type of partial seizure that preceded the generalized seizure (i.e., simple partial seizure only, complex partial

seizure only, or simple partial seizure evolving into complex partial seizure).7 On EEG, partial seizures are noted as

focal epileptiform discharges with spikes or sharp waves.

TABLE 29-1 CLASSIFICATION OF SEIZURES

I. Partial (focal, local) seizures

A. Simple partial seizures (consciousness not impaired)

1. Focal motor (with and without jacksonian march)

2. Somatosensory or special sensory symptoms (e.g., simple hallucinations such

as tingling, light flashing, buzzing)

3. With autonomic symptoms (e.g., as epigastric sensation, pallor, flushing)

4. With psychic symptoms (disturbances of higher cerebral function)

B. Complex partial seizures (with impairment of consciousness)

1. Beginning as simple partial seizures and progressing to impairment of

consciousness


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2. With no other features

3. With features as in simple partial seizures

4. With automatism

C. With impairment of consciousness at onset

1. With no other features

2. With features as in simple partial seizures

3. With automatism

D. Partial seizures evolving to secondarily generalized seizures

1. Simple partial seizures evolving to generalized seizures

2. Complex partial seizures evolving to generalized seizures

3. Simple partial seizures evolving to complex partial seizures to generalized

seizures

II. Generalized seizures (generalized bilateral without focal onset)

A. Absence seizures

B. Myoclonic seizures

C. Clonic seizures

D. Tonic seizures

E. Tonic-clonic seizures


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F. Atonic seizures

III. Unclassified epileptic seizures (including all seizures that cannot be classified due to

inadequate or incomplete data and some that defy classification)

From Commission on Classification and Terminology of the International League Against Epilepsy.(1981). Proposal for revised clinical and electroencephalographic classification of epileptic seizures.

Epilepsia, 22, 489-501.

Generalized SeizuresThere are six categories of generalized seizures: absence, myoclonic, clonic, tonic, tonic-clonic, and atonic. Each

seizure type has characteristic clinical and EEG findings that are outlined in Table 29-2. The absence seizure is

subdivided into typical and atypical absence seizures according to the presence of different EEG patterns and

clinical presentation. Clinically, atypical absence seizures have a less abrupt onset and termination and are of alonger duration. The most common type of generalized seizure is the tonic-clonic seizure, formerly called the

grand mal seizure.

Description of Generalized Tonic-Clonic Seizures

A tonic-clonic seizure progresses through distinct phases including the prodromal, tonic, clonic, and postictal

phases. The prodromal phase of irritability and tension may precede the seizure by several hours or days. Some

individuals experience an aura, whereas in others the seizure begins without warning. Characteristically, the tonic-

clonic seizure begins with a sudden loss of consciousness. Neuronal hyperexcitation spreads to the subcortex,

thalamus, and upper brainstem, and consciousness is suddenly lost. In the tonic phase, there is a major tonic

contraction (increased tonus) of the voluntary muscles so that the body stiffens with legs and arms extended. Ifstanding, the person falls to the ground. The jaw snaps shut and the tongue may be bitten in the process. A shrill

cry may be heard because of the forcible exhalation of air through the closed vocal cords as the thoracic muscles

initially contract. The bladder and, less often, the bowel may empty. The pupils dilate and are unresponsive to

light. Apnea occurs and lasts for only a few seconds, but the patient may appear pale and dusty. The tonic phase

lasts less than 1 minute (average of 15 seconds).

The clonic phase begins with a gradual transition from the tonicity of the tonic phase. Inhibitory neurons of the

cortex, anterior thalamus, and basal ganglion nuclei become active, intermittently interrupting the tonic seizure

discharge with clonic activity. The clonic phase is characterized by violent, rhythmic, muscular contractions

accompanied by hyperventilation. The face is contorted, the eyes roll, and there is excessive salivation with

frothing from the mouth. Profuse sweating and a tachycardia are common.

In the postictal phase, the clonic jerking gradually subsides in frequency and amplitude over a period of about 30

seconds, although it may be longer. The involved cells cease firing. The extremities are limp, breathing is quiet,

and the pupils, which may be equal or unequal, begin to respond to the light reflex. With awakening, most

patients are confused, disoriented, and amnesic for the event. Headache, generalized muscle aching, and fatigue

are common. If undisturbed, the patient often falls into a deep sleep for several hours. There may also be

temporary paresis, aphasia, or hemianopsia. Following a seizure (i.e., generalized or partial), focal weakness,

called Todd's paralysis, may occur and last up to 24 hours. If it occurs, the focal deficit is important in localization


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of a focal epileptogenic site.

Because the seizure frequently occurs without warning, it is possible for injury to be sustained from falls or other

accidents related to the seizure. Head injury, fracture of the limbs or vertebral column, and burns are examples of

serious injuries that may be sustained. Tonic-clonic seizures may occur at any time of the day or night, whether

the patient is awake or asleep. The frequency of recurrence can vary from hours to weeks, months, or years.

TABLE 29-2 MAJOR SUBTYPES OF PARTIAL AND GENERALIZED SEIZURES

TYPE DESCRIPTION EEG FINDINGS

Partial Seizures

Simple partial

seizures

Motor

Symptoms depend on the motor region activated

May remain focal or may spread to other areas on

the motor strip, a process called march; seizures

called jacksonian seizures. For example, the seizure

may begin in the fingers of one side, and march to

the hand, wrist, forearm, and arm on the same side

of the body. The particular sequence of involvement

is helpful in locating the epileptic foci on the motor

strip in the hemisphere opposite the convulsive

movement.

Focal motor attack may cause head to turn to side

opposite epileptic foci.Todd's paralysis may result; last minutes to hours.

Continuous focal motor seizure is called epilepsia

partialis continua.

Applies to all

simple partialseizures: may show

abnormal discharges

in a very limited

region; seizures

originating from

deep structures

may not be noted

with scalp

electrodes

Sensory Arise from cortical sensory strip.

Usually feels like pins and needles or numbness;

sometimes, spatial disorientation.

May march to other areas or may become a complex

partial or generalized tonic-clonic seizure.

Special sensory symptoms may include visual

seizures such as flashing lights or visual

hallucinations, auditory seizures with various

sounds, gustatory sensations such as metallic taste

or primary tastes (salty, sweet, sour, or bitter), or

vertigo and floating sensations.


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Autonomic

Psychic

May occur as simple partial seizures.

Disturbance in a higher-level function (i.e.,

distortion of memory), distorted time, feeling of

dj vu, illusions, depersonalization, or

hallucinations.

Usually occur with impairment of consciousness and

become complex partial seizures.

Complex Partial Seizures

One category Only symptoms may be impaired consciousness or it

may progress to include automatisms; note

automatisms may occur in partial or generalized

seizures.

Simple partial seizure followed by impairment of

consciousness resulting in a complex seizure with

motor, sensory, autonomic, or psychic symptoms as

described above.

All complex

seizures:

generalized 2-4-Hz

spike waves

Partial Seizures Evolving to Secondary Generalized Seizures

One category Includes seizures that may evolve into generalized

seizures: simple partial, complex partial, or simple

partial evolving into complex and then to generalized

seizures.

Generalized Seizures

Absence

seizures

Note: may

be seen

along with

tonic-clonic

seizures

Typical absence seizures: common in children;

characterized by brief interruption in consciousness

without loss of postural control. Typically, there is an

interruption of activity with a momentary lapse of

consciousness lasting 3 to 30 sec. If talking, the speech

stops or slows; if eating, the hand and mouth stop, and

if patient is called, there is no response.

During an attack, the eyes may appear vacant,

stare, or roll upward; the eyelids may twitch.

Seizures occur a few times to hundreds of times per

day; person may not be aware of them.

People who have several attacks daily most often

experience difficulty in learning or employment

Typical absences: 3-

Hz spike-wave

complexes with

abrupt starts and

stops


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because of inattention.

Atypical absence seizuresthe lapse of consciousness is

usually of longer duration and less abrupt in onset;

more obvious motor spike-and-wave pattern, and signs.

Atypical absences:

2.5 Hz; slower

more irregular

Myoclonic

seizures

Sporadic jerks that are sudden, brief; contractions

that are usually symmetric.

When confined to one area, it may be the face and

trunk; one or more extremities; an individual

muscle; or a muscle group.

Myoclonic jerks are rapidly repetitive or relatively

isolated.

Common around time of sleep or awakening; must

be differentiated from myoclonic jerks of

nonepileptic myoclonus.

Bilateral,

generalized

epileptiform

discharges, typically

polyspikes

Clonic

seizures

Repetitive rhythmic clonic movements that are

bilateral and symmetric.

Associated with

symmetric

spikewave

complexes

Tonic

seizures

Stiffening of the musculature, mostly of the body,

but may also involve the arms.

Low-voltage

paroxysmal fast

activity (10 Hz)

Atonic

seizures

Abrupt loss of postural muscle tone; last 1-2 sec.

Consciousness is briefly impaired, but usually there

is not postictal confusion.

Common in children.

Generalized

epileptiform

discharges (spikes,

spike-wave

complexes)

Tonic-

clonic

seizures

Most common of the generalized seizures (see p.

648 for detailed description).

Fast high-voltage

spikes seen in all

leads

Unclassified Epileptic Seizures

One category This group includes all seizures that cannot be classified

because of inadequate or incomplete data. This self-


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explanatory category is a catch-all for seizures that do

not conform to any of the other headings.

TABLE 29-3 SEIZURE ACTIVITY OF PARTIAL SEIZURES (SIMPLE, COMPLEX, AND SECONDARYGENERALIZED) BY LOBE

CEREBRAL HEMISPHERE

LOBE DESCRIPTION

Frontal lobe

epilepsyMany overlapping syndromes with frequent brief attacks (75% have somatosensory auras

May have a distorted body image, visual or auditory hallucinations

Usually proceeds to impaired consciousness and contralateral motor

activity

Occipital lobe

epilepsyMost have visual auras

Elemental visual hallucinations (e.g., flashing lights, colored lights) or

sometimes blindness, scotoma, or hemianopsia


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Eye blinking, nystagmus, head deviation, tonic and clonic eye movement

common

Visual phenomena usually contralateral to side of the seizure

Often progress to complex partial seizures or secondarily generalized

seizure depending on pathways stimulated

Status Epilepticus

Although there are many definitions for status epilepticus, it is generally defined as either continuous seizures

lasting at least 5 minutes or two or more discrete seizures between which there is incomplete recovery of

consciousness.8 The most common cause of status epilepticus is an abrupt discontinuation of antiepileptic drugs

(AEDs). Other causes include withdrawal from alcohol, sedatives, or fever.

Clinically, status epilepticus can present with obvious tonic, clonic, or tonic-clonic movements; with subtle

twitching of the hand or face; or with absence of movement. Absence of observable movement is most commonly

seen in hospitalized patients. In this case, the detection of ongoing seizures requires electroencephalography.

With tonic-clonic seizure, the most common type of status epilepticus, the patient is unconscious. Convulsive

seizures can be easily observed clinically, but partial seizures are less obvious and more difficult to identify.

Subclinical seizures are seizures that do not present with overt clinical signs and symptoms but are apparent on

continuous EEG tracing. Suspicion of subclinical seizure should be considered in patients who seem to be improving

generally but have not regained consciousness. Continuous EEG monitoring can assist in the recognition of this

serious problem. Therefore, an EEG or continuous EEG monitoring is required for any patient with significant

alterations in consciousness or when unconsciousness is sustained.

Status epilepticus constitutes a medical emergencyassociated with significant morbidity and mortality (20%). If not

treated aggressively, cardiorespiratory dysfunction, hyperthermia, and metabolic imbalances can develop, leading

to cerebral ischemia and neuronal death. Treatment of status epilepticus is discussed later in this chapter.

Epileptic Versus Nonepileptic SeizuresSeizures may also be classified as either epileptic or nonepileptic. Epileptic seizures include partial and

generalized seizures discussed earlier. Nonepileptic seizures or nonepileptic events account for about 20% of

referrals to epilepsy centers. Clinically, the signs and symptoms can look like seizures, but there is no

epileptogenic origin. Nonepileptic seizures include physiologic events, psychogenic events, and malingering.9

Cardiac, respiratory, metabolic derangement, and drug toxicity can disturb consciousness as a result of decreased

oxygen tension to the brain. Perfusion problems as a result of transient ischemic attacks, stroke, or Stokes-Adams

syndrome account for underlying cardiac or cerebrovascular problems. Decreased oxygen tension from poorsaturation can result from pneumonia, pulmonary emboli, shunting, or coma. Metabolic causes such as

hypoglycemia and electrolyte imbalance can cause nonepileptic events. Toxicity resulting from use of street drugs

or prescription drugs, including AEDs; alcohol toxicity; and environmental exposures to toxic substances such as

lead can also result in nonepileptic seizures.

Differentiation between nonepileptic psychogenic seizures and epileptic seizures can be made only through

analysis of simultaneous EEG tracings and audio-video monitoring during a seizure.10 The audio-video portion


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records the behaviors of the peri-ictal events, and the EEG demonstrates the presence or absence of abnormal

tracings associated with epileptic seizures. The behavior is triggered by psychogenic internal or external factors.

The basis for psychogenic nonepileptic events is secondary gains for the individual such as sympathy or relief from

unwanted responsibilities.

Observations/IdentificationPhysiologic causes of nonepileptic seizures must be ruled out with a basic diagnostic work-up of a thorough history,

physical examination, and laboratory screening.

With nonepileptic psychogenic seizures, the onset is often dramatic, bizarre, gradual, and in the presence of

witnesses. By comparison, epileptic seizures are sudden, paroxysmal, and orderly. Emotional upset usually

precipitates nonepileptic seizures, and such an episode lasts longer than a true seizure. The dramatic, violent

flinging of the extremities, wiry movements, and inconsistent pattern of development are a sharp contrast to the

tonic-clonic, orderly, repetitive movements of true seizures. If a scream is heard during a true seizure, it is at the

onset of the event. With nonepileptic seizures, screams are usually heard throughout the course of the episode.

Observing the features, development, and finale of seizure activity can be most helpful in differentiating between

epileptic and nonepileptic seizures.

DIAGNOSISThe first step in the evaluation of a patient with possible epilepsy is to determine whether the patient did or did

not have a seizure. The diagnostic process requires a past medical history and a careful history of the clinical

presentation and events related to the alleged seizure. The history is followed by a general physical and

neurological examination and diagnostic testing. A prenatal history and achievement of developmental milestones

are very important in infants, children, and adolescents. In adults, a history of trauma, drug use, and toxic

environmental exposure are critical. Detailed descriptive information about the seizures is collected, including

onset and surrounding events such as fever or withdrawal from alcohol, prodromal or aura experiences,

precipitating factors, frequency, loss of consciousness, subjective and objective characteristics of the event,

postictal behavior, and any injuries associated with seizures. In addition to the usual baseline blood chemistries, a

toxicology screen (e.g., drug levels, barbiturates, street drugs, and lead) may be helpful for some, based on

history. Other diagnostic tests that may be ordered include:

Computed tomography (CT) scan

Magnetic resonance imaging (MRI) (two to three times more sensitive than CT scan in identifying potential

epileptogenic lesions)

EEG

Video-EEG monitoring with either noninvasive scalp electrodes or deep invasive electrodes

Possibly a positron emission tomography (PET) scan (limited availability due to high expense)

Single proton emission computerized tomography (SPECT) scan (helpful for seizure localization and not

diagnosis)

Most patients do not require all diagnostic tests listed, whereas others may require additional studies. The

objective of the studies is to identify systemic or CNS processes that are manifested, in part, by seizure activity.

For many patients, an extensive search for an underlying etiology will yield negative results. The diagnosis of


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epilepsy is made after ruling out other possible causes (discussed later). The clinical presentation and EEG findings

help classify the particular type of epilepsy. Accurate diagnosis of seizure type is important because selection of

appropriate drug therapy is seizure specific in many cases. The EEG is a vital diagnostic procedure because it

identifies patterns of abnormal electrical activity that can be correlated with particular types of seizure patterns.

An EEG can also aid in lateralization and localization of an epileptogenic trigger focus. However, in about 50% to

60% of patients with confirmed epilepsy, the interictal EEG can be normal.

Several special techniques are useful in augmenting the data from an EEG. Asleep study, in which there is

continuous EEG monitoring, is helpful because sleep activates anterior temporal spike discharges and bitemporal

discharges in 80% to 90% of persons with complex partial seizures. The increased interictal epileptiform

abnormalities are noted most in non-rapid eye movement (non-REM) sleep. Sleep deprivation also increases the

frequency of interictal abnormalities. Extra scalp electrodes, nasopharyngeal electrodes, and sphenoid electrodes

help to increase the detection of mesial temporal discharges. The ability to detect and localize abnormal ictal

discharges in complex partial seizures is greatly enhanced with the use of invasive procedures such as depth,

subdural, and cortical electrodes. Surface electrodes often provide false localization.11 Simultaneous EEG and

audio-video recordings of the patient can distinguish seizure from nonseizure activity and assist in classifying

seizure type.

Differential DiagnosisGiven the long list of possible causes of seizure activity, diagnosis can become very difficult. Differentiation

between epileptic and nonepileptic seizures (discussed earlier) must be made. Brain tumor, cerebral aneurysm,

cerebral arteriovenous malformation, transient ischemic attacks, stroke, migraine headaches, syncope, sleep

disorders, myoclonus, cardiac sources, drug and alcohol abuse, drug toxicity, metabolic disorders, breath holding,

and psychogenic problems such as anxiety attacks, hysterical responses, and psychosis are some of the possibilities

that must be excluded. Nevertheless, accurate classification of seizure type is important to specific treatment

choices.

Electroencephalograms and SeizuresThe EEG is a diagnostic test during which the amplified electrical potential of the brain is recorded by placing 14to 21 electrodes on the patient's scalp. Electrodes may also be placed on the cortical surface using an invasive

procedure. The tracings reflect the combined electrical activity of several neurons, rather than only one. The basic

resting electrical pattern of the brain is altered by opening the eyes, focusing attention on a problem,

hyperventilation, photic stimulation, drugs, or sleep. Therefore, recordings are taken at rest, after

hyperventilation, during stimulation with a strobe light, and during sleep. The patient must be quiet, relaxed,

cooperative, able to follow directions, and seated comfortably in a chair with the eyes closed, although not

asleep. The testing room must be shielded from extraneous electrical interference and noise. Often, preparation

for the EEG includes keeping the patient awake all night before the recordings. The stress of sleep deprivation is

more apt to result in the recording of abnormal EEG tracings.

Even though the EEG is important in diagnosing seizures, these data must be considered in conjunction with other

information, including the history, physical examination, and other laboratory studies. Between seizures, normal

EEGs are often recorded in patients with epilepsy. In addition, EEGs that are considered to be borderline by one

interpreter may be read as normal by another, indicating subjectivity in interpretation.

The tracings for the EEG are made with special ink on electromagnetic paper. The recorded tracings signify the

electrical potential difference from the scalp to the ear electrodes and from the scalp to the scalp electrodes. The

average EEG consists of 150 to 300 or more pages of recordings, with each page accounting for 10 seconds of


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tracings. In the normal adult, the most characteristic, normal tracings noted at rest are as follows:

Alpha waves: 8 to 12 Hz (Hz = cycles per minute)

Beta waves: 18 to 30 Hz, a faster wave, seen in the anterior areas of the brain

Both alpha and beta waves are bilaterally symmetric. Each has its own characteristic shape and amplitude.

Changes occur in the normal EEG pattern with various activities. For example, when the eyes are opened, there is

an immediate decrease in the amplitude of the brain waves; in the early stages of sleep, the waves slow (lower

voltage); and in the later stages of sleep, sleep spindles, occurring at a rate of 14 to 16 Hz, develop with

subsequent higher voltage and slower waves.

Patients with seizure disorders have abnormal recordings on their EEGs. The most common abnormal findings

include:

Delta waves: less than 4 Hz with high amplitude; often associated with destruction of brain tissue, such as occurs

with infarction, tumor, or abscess (localized over abnormal area)

Theta waves: 4 to 7 Hz (not always abnormal)

Spikes or sharp waves: high-voltage, faster waves; asymmetry of frequency and amplitude from one side to the

other

On an abnormal EEG, slow and fast waves may be combined in paroxysmal runs, thereby interrupting the normal

pattern. These paroxysmal waves are highly suggestive of epilepsy. Recordings taken between seizures in the

epileptic patient often include isolated spikes without evidence of a clinical seizure.

TREATMENTThe approach to a patient with a seizure disorder is multidimensional and comprehensive. It includes:

Treatment of any underlying condition

Avoidance of precipitating factors

Suppression of recurrent seizures by prophylactic therapy with AEDs or surgery

Comprehensive management of physiologic and social issues related to having seizures

An individual plan of care must be developed for each patient. If there is an underlying problem responsible for

seizures, it must be addressed. For example, if the diagnostic work-up revealed a brain tumor as the cause of

seizures, the primary problem, the brain tumor, must be treated. Seizures related to the brain tumor can be

managed with AEDs. If the diagnosis is epilepsy, identification of the specific type of epilepsy is imperative in

developing an effective treatment plan.

After epilepsy has been diagnosed, the patient needs to be made aware of precipitating factors and taught to

avoid these situations or conditions. About 75% of patients with epilepsy can be managed satisfactorily with AEDs.

Surgery is considered for a small group of patients for whom an epileptogenic focus can be identified or in whom

seizures are intractable even with drug therapy. In addition to drug therapy, the management plan must address

the behavioral, social, and economic consequences of having epilepsy. For successful adaptation to this chronic

problem, it is critical that patients receive education in self-management. Patient counseling and support are also

essential components of the management plan.


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Medical Management: Drug TherapyEpilepsy treatment seeks to enable the patient to live as free of the medical and psychosocial complications of

seizures as is possible. Pharmacologic therapeutics play a large role in helping to achieve this goal. As with any

drug therapy, there is concern about side effects, toxicity, ease of administration, efficacy, and effect on

different age groups. Management of epilepsy is complicated by the range of age of patients, the number of

categories of drugs, and the psychosocial impacts involved.

Effective drug treatment for epilepsy has two goals: to control or reduce the frequency of seizures, and to

minimize side effects. AEDs do not cure epilepsy but provide a chemical means of controlling seizures. As with any

drug, side effects, such as sedation, may interfere with activities of daily living. Therefore, effective medical

management includes the development of an individualizeddrug program that minimizes side effects and supports

compliance.

After a diagnosis has been made, the following principles should guide use of drugs12:

Assess the patient (diagnosis of seizure type and classification, patient characteristics such as age and presence

of comorbidity, and insurance drug coverage).

Select the primary drug that is the most effective for the seizure type; monotherapy is preferred, and about70% of patients with epilepsy can be maintained on one drug.

Begin with monotherapy and titrate dosage to achieve appropriate blood concentrations and control.

Consider the pharmacokinetics of AEDs and free AED concentrations.

Provide patient education.

Provide follow-up to assess control, tolerance, and side effects.

Consider the length of time the patient has been taking AEDs.

Selecting the Primary Drug Most Effective for the Seizure Type

The classifications of epileptic seizures and epilepsies/epileptic syndromes has made easier the selection of the

drug of choice for a given seizure problem. Seizure types and drugs of choice plus alternative drug options are

outlined in Table 29-4. Table 29-5 outlines the management of status epilepticus.

Some AEDs have a narrow spectrum of action and are effective for only a selected seizure type, whereas other

drugs are broad spectrum and effective against many different types of seizures. Drugs also have different

mechanisms of action. Some types of seizures can be exacerbated by AEDs designed to treat another seizure type.

For example, carbamazepine, useful for partial seizures, can exacerbate absence seizures. Phenytoin,

phenobarbital, and carbamazepine, which are effective in controlling generalized tonic-clonic seizures and partialseizures, are ineffective for absence seizures and may actually precipitate an increase in their incidence. In

addition, with a broad-spectrum drug that can be used for various seizure types, the therapeutic range may differ

for different seizure types. For example, blood concentrations for complex partial seizures may need to be higher

than the concentration for tonic-clonic generalized seizures.

TABLE 29-4 ANTIEPILEPTIC DRUGS AND RELATED SEIZURE TYPES


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PRIMARY GENERALIZED

TONIC-CLONIC

PARTIAL (I.E., SIMPLE,

COMPLEX, AND

SECONDARY GENERALIZED

SEIZURES) ABSENCE

ATYPICAL ABSENCE,

MYOCLONIC, AND

ATONIC

First-line

drugs

Valproic acid

Lamotrigine

Carbamazepine

Valproic acidPhenytoin

Lamotrigine

Phenobarbital

Ethosuximide

Valproic acid

Valproic

acid

Alternative

drugsPrimidone

Carbamazepine

Topiramate

Phenobarbital

Felbamate

Topiramate

Tiagabine

Primidone

Zonisamide

Gabapentin

Tiagabine

Methsuximide

Lamotrigine

Clonazepam

Lamotrigine

Clonazepam

Felbamate

Data from Holland, K. D. (2001). Epilepsy: Efficacy, pharmacology, and adverse effects of antiepileptic

drugs. Neurologic Clinics, 19(2), 313-345; Ropper, A. H., & Brown, R. H. (2005).Adams and Victor's

principles of neurology(8th ed., pp. 292-293). New York: McGraw-Hill; and Lowenstein, D. H. (2005).

Seizures and epilepsy. In D. L. Kasper, E. Braunwald, A. S. Fauci, S. L. Hauser, D. L. Longo, & J. L.

Jameson (Eds.). Harrison's principles of internal medicine (16th ed., p. 2367). New York: McGraw-Hill.

TABLE 29-5 MANAGEMENT OF STATUS EPILEPTICUS

TIME LINE IN

MIN

DRUG THERAPY (PROGRESSION ALONG THIS ALGORITHM ASSUMES THAT THE PREVIOUS DRUG ADMINISTERED DID NOT

TERMINATE THE SEIZURES)

0-3 1. Lorazepam (Ativan): 0.1 mg/kg IV at 2 mg/min

Note: additional emergency therapy may not be needed if the seizures terminate

Seizures continue

4-23 2. Phenytoin (Dilantin): 20 mg/kg (about 1 g) in normal saline at a rate of 50

mg/min


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OR

Fosphenytoin (20 mg/kg PE (PE = phenytoin equivalent) intravenously at 150

mg/min)

Seizures continue

22-33 3. Phenytoin: (additional) 5-10 mg/kg

OR

Fosphenytoin 5-10 mg/kg PE

Seizures continue

Proceed immediately to step (6) anesthesia with midazolam or propofol if:

Patient develops status epilepticus while in the ICU

Patient has severe systemic problems (e.g., extreme hyperthermia)

Patient has seizures that have continued for more than 60-90 min

37-58 4. Phenobarbital: 20 mg/kg IV at 50-75 mg/min

Seizures continue

58-68 5. Phenobarbital: additional 5-10 mg/kg

Seizures continue

6. Anesthesia with midazolam or propofol

Lowenstein, D. H., & Alldredge, B. K. (1998). Status epilepticus. New England Journal of Medicine,

338(14), 970-976.

In addition to a particular seizure type, patient characteristics influence drug selection. The plan of care must be


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individualized to consider age, comorbidity, liver and kidney function, previous drug history for allergies, tolerance

of side effects, cost, other drug therapy and potential interactions, and child-bearing potential.

Principles of Drug Therapy: Begin With Monotherapy and Titrate the Dosageto Achieve Appropriate Blood Concentrations

The following are principles recommended for seizure management:

Begin with a single drug, called monotherapy, which is the drug of choice for the particular seizure type.

Increase the drug gradually over 3 to 4 weeks until seizure control is achieved, intolerable side effects occur,

toxicity develops, or the maximum therapeutic range has been reached.

Recognize that many AEDs are CNS depressants and that drowsiness, lethargy, and tiredness are common in the

beginning of therapy; however, these symptoms will usually subside in 7 to 10 days.

Because of pharmacokinetics (cited later) and variations in requirements for specific seizure types with the

same drug, expect to make individual adjustments in dosage.

Some patients may need more or less than the recommended average therapeutic range for a particular drug.

Titrate a single drug until maximum benefit is achieved or intolerance or serious side effects occur. If a

therapeutic blood concentration has been achieved and seizure control has not been achieved, a second drug

may be added. A second drug may be used in combination with the first or replace the first. With replacement,

the first drug should begradually taperedafter the second drug has been titrated to the desired dosage. This

practice is necessary because the sudden withdrawal of a drug can cause status epilepticus, even though a new

drug has been introduced in its place.

If the patient is seizure free, check drug concentration in blood after 5 to 8 half-lives or a period of 3 to 4

weeks.

The drug's half-life is important because drugs of long duration (phenytoin, phenobarbital) may be taken once

daily in some circumstances.

Have the patient keep a daily drug diaryroutinely, but especially when a new drug is introduced. The diary

should include dosage and side effects. The diary is helpful in evaluating the effectiveness of the drug therapy.

Refractory Epilepsy. About one third of patients with epilepsy do not respond well to treatment with

monotherapy. It then becomes necessary to try a combination of drugs to control seizures. Although there are no

guidelines for combining drugs, in most instances a combination of two first-line drugs (i.e., carbamazepine,

phenytoin, valproic acid, lamotrigine) is tried. If this is not effective, adding one of the newer drugs (i.e.,

gabapentin or topiramate) is suggested. When seizures cannot be controlled by drug therapy, the condition is

called refractory epilepsy and surgery becomes a consideration.

Considering Pharmacokinetics and Free Antiepileptic Drug Concentrations

The pharmacokinetics of AEDs are important to keep in mind. Many AEDs are highly bound to plasma protein. It is

the unbound, or free, concentration that represents the active drug capable of penetrating the blood-brain

barrier and interacting with receptor sites. For this reason, patients on high-protein tube feeding will require a

higher drug dosage to maintain adequate drug blood levels. Conditions known to alter AEDs' protein-binding

capacity are malnutrition, older age, pregnancy, hypoalbuminemia, burns, liver disease, and chronic renal failure.

The following are plasma protein-binding capacities for selected AEDs:


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Phenytoin and valproic acid (high protein binding)

Carbamazepine (variable binding)

Phenobarbital and primidone (minimal binding)

Ethosuximide (not bound)

Although therapeutic ranges are cited for each drug, patients vary with regard to pharmacokinetics. Therefore,

dosage requirements for individual patients vary. For determining dosage, use the gold standard that the patient

should become seizure free. The onset of serious side effects or intolerance is a reason to discontinue a drug.

Clinical judgment must be used and patient response and blood levels must be monitored to determine the ideal

dose and blood concentration for a patient.

Patient Education

Patient education is the cornerstone of drug therapy and promotes a partnership that supports compliance.

Patients who understand the purpose of drug therapy and the drugs that they are taking are more compliant.

Patient education must be an ongoing process with reinforcement and updates at each appointment. Because manypatients are on long-term or life-long therapy, education must also anticipate and prepare patients for

developmental changes and changes in normal life routine. If they are to provide comprehensive patient

management, health care providers who treat patients with seizures must develop and implement an

individualized teaching plan that includes how to initiate and provide ongoing patient education.

Considering Length of Time on Antiepileptic Drug Therapy

Whether AED therapy must be life-long depends on many factors. About 60% of adults who have their seizures

completely controlled with AEDs can eventually discontinue therapy. The following conditions are recommended:

seizures are controlled for 1 to 5 years; seizures are of a single type (partial or generalized); there is a normal

neurological examination; and the patient has a normal EEG.2 The American Academy of Neurology has noted thatafter at least a 2-year seizure-free period, health care providers can explore discontinuation of AEDs by gradually

tapering them over 2 to 3 months.13,14 Many individual considerations, such as psychological issues and patient

comfort, should be included in the decision. The risk of recurrent seizures is greatest during the first 3 months

after discontinuation of AEDs. State laws vary on loss of driving privileges for persons with seizures. In general,

most states allow patients to drive after a seizure-free period (on or off medications) of between 3 months and 2

years.2

Nursing management associated with a few commonly ordered drugs is discussed below. These drugs include

phenytoin, fosphenytoin, carbamazepine, valproic acid, and phenobarbital. More information on drug therapy can

be found in Chapter 12.

Phenytoin

Phenytoin (Dilantin), introduced in 1938, is a synthetic drug that is classified as a hydantoin. It is used for the

treatment of simple partial, complex partial, and generalized tonic-clonic seizures. It is not effective for absence,

myoclonic, or atonic seizures. Phenytoin blocks posttetanic potentiation (PTP) by influencing synaptic transmission

through voltage-sensitive sodium channels. Phenytoin is primarily absorbed through the duodenum. There is no

first-pass metabolism. Oral absorption is affected by the particle size of the particular brand's formulation so that


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there can be variations among brands. The brand of phenytoin that a patient is receiving should not be switched

without careful monitoring. Phenytoin enters the brain quickly and is then redistributed to other body tissues,

including breast milk. It crosses the placenta and reaches a state of equilibrium with the mother and fetus.

Phenytoin is bound to serum and tissue protein. In the serum, the drug binds primarily to albumin in a predictable,

linear fashion provided that the albumin level is normal (see the exceptions in the previous section). Phenytoin is

metabolized in the liver and excreted in the urine. At an often unpredictable concentration level, metabolism of

phenytoin ceases because of saturation. Any change in dosage at this point will result in significant changes in

serum concentrations. In addition, serum concentration does not decline at a predictable linear rate whenphenytoin is discontinued. Therefore, serum monitoring is necessary after any dosage change. Because the half-life

of phenytoin is 10 to 34 hours (average 22 hours), it may be given once daily.

Administration of phenytoin may be oral or intravenous (IV). Because the pH of phenytoin is about 12,

intramuscular (IM) injection should be avoided to prevent tissue irritation. Oral phenytoin comes in three dosage

forms. The tablets and suspension contain phenytoin acid, whereas the capsules contain phenytoin sodium.

Phenytoin sodium is 92% phenytoin. The parenteral form is phenytoin sodium. If they contain equivalent amounts

of phenytoin acid, tablets, capsules, and suspension have the same bioavailability. Phenytoin capsules are

designated as immediate release or extended release. Only the extended release should be used for once-daily

dosing. The suspension form comes in two strengths; either can settle and thus deliver doses of unequal

concentration. To maintain an even blood level, patients on enteral feeding will probably need increased dosagedue to the high protein binding of phenytoin. After enteral feeding has been discontinued, the dosage must be

decreased. Monitoring phenytoin blood levels provides a guide for adjusting the drug dosage.

If phenytoin is administered IV, it must be administered slowly, at a rate no faster than 50 mg/min in a solution of

normal saline. Maintaining the proper rate is very important because rapid administration depresses the

myocardium and can cause cardiac arrhythmias and cardiac arrest. If given in solution such as 5% dextrose in

water, the drug will precipitate into crystals in the solution. If given by IV push, it must be given slowly (no more

than 50 mg/min); the effect of rapid administration of phenytoin on the myocardium is dangerous arrhythmias.

Patients receiving IV phenytoin should also be observed for the development of phlebitis at the IV site.

Various drugs in common use can interact with phenytoin:

Drugs thatpotentiate the action of phenytoin include aspirin, cimetidine, chloramphenicol, felbamate,

methsuximide, fluconazole, isoniazid, disulfiram (Antabuse), propoxyphene, sulfonamides, and warfarin.

Drugs that decrease the action of phenytoin include antacids, barbiturates, antihistamines, calcium, calcium

gluconate, chronic alcohol, carbamazepine, folic acid, valproic acid, and vigabatrin.

Phenytoin decreases the action of amiodarone, carbamazepine, corticosteroids, cyclosporine, digitalis,

dopamine, estrogen, furosemide, haloperidol, oral contraceptives, phenothiazines, quinidine, and

sulfonylureas.

There are many potential side effects from phenytoin. Lethargy, fatigue, incoordination, visual blurring, higher

cortical dysfunction, and drowsiness are related to CNS depressant effects. When serum concentrations exceed 20

/mL, patients may experience nystagmus, ataxia, and slurred speech. Amorbilliform rash may occur in some

patients 7 to 14 days after beginning the drug. The appearance of such a rash indicates that the drug should be

discontinued. Alupuslike syndrome has also been reported and is reversible when phenytoin is withdrawn.

Effects seen with long-term, chronic use include gingival hyperplasia (about 50% of patients), decreased cognitive

ability, osteomalacia, hirsutism, hypothyroidism, peripheral neuropathy, megaloblastic anemia, blood dyscrasias,


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and low serum folate concentrations. Periodic complete blood cell counts (CBCs) are important to monitor the

development of anemia or dyscrasias. The low folic acid levels respond to folic acid therapy. There is an increased

incidence of malformations in children born of women who are taking AEDs.

Fosphenytoin

Fosphenytoin (Cerebyx) is a water-soluble drug that is rapidly and completely converted to phenytoin after IV or IM

administration and has a conversion half-life of 8 to 15 minutes. However, protein binding for fosphenytoin is

exceedingly high and nonlinear. Therefore, fosphenytoin displaces phenytoin from albumin, thus increasing the

unbound phenytoin concentration. This increase in unbound concentration (pharmacologically active form of

phenytoin) offsets the delay in phenytoin formation from the prodrug (i.e., phenytoin), making it bioequivalent to

phenytoin at 50 mg/min.

Fosphenytoin is administered IM or IV. Compared with phenytoin, fosphenytoin is rapidly and completely absorbed

following IM administration, reaching a peak level in 3 hours. Fosphenytoin is administered in units called

phenytoin equivalents (PE, which is the amount of phenytoin to be used) rather than fosphenytoin itself.

Fosphenytoin is compatible with standard IV solutions (5% dextrose and water or normal saline [NS]) and can be

infused for adults at a rate of 100 to 150 mg PE/kg/min.22 The most common side effects are nystagmus, ataxia,

and sedation. Although fosphenytoin is more expensive than phenytoin, fosphenytoin is safer and can beadministered more quickly. IV fosphenytoin is replacing phenytoin in the treatment of status epilepticus.22 As with

phenytoin, continuous electrocardiograms (ECGs), blood pressure, and respiratory status must be monitored when

providing a loading dose of fosphenytoin.

Carbamazepine

Carbamazepine (Tegretol, Tegretol-XR) is a relative safe drug used as a first-line agent for the treatment of simple

partial, complex partial, and generalized tonic-clonic seizures. Carbamazepine can exacerbate absence and

myoclonic seizures. The mechanism of action is depression of transmission via the nucleus ventralis anterior

thalamus, which acts to decrease the spread of seizure discharge. In addition, it has some depressive effect on

posttetanic potentiation, but to a lesser degree than with phenytoin. Carbamazepine has an absorption rategreater than 75%; the dosage peak is reached in 6 to 24 hours. It has a high affinity for lipids that bind to body fat;

it also binds to albumin. Carbamazepine is metabolized by the liver.

Carbamazepine is available only in oral form. It is given in divided doses two to four times daily. Dosage should be

adjusted gradually. Because the suspension form of the drug may adhere to the nasogastric tube if not diluted, it is

recommended that the suspension form be diluted in an equal amount of diluent before administration with an

enteral tube. Some drugs, such as phenytoin and phenobarbital, may interact with carbamazepine by enzyme

induction, thus decreasing the concentration of carbamazepine. Other drugserythromycin, cimetidine, and

isoniazid interact by enzyme induction; these drugs increase the concentration of carbamazepine.

Carbamazepine interacts with other drugs by inducing their metabolism; these drugs include valproic acid,

theophylline, warfarin, and ethosuximide. The major dose-dependent side effects are diplopia, nystagmus, ataxia,unsteadiness, dizziness, and headache. Cognitive deficits are minimal, although present. Carbamazepine has been

associated with neural tube defects.

Valproic Acid

Valproic acid, which is marketed as both valproic acid (Valproate, Depakene) and divalproex sodium (Depakote), is

approved for management of myoclonic, tonic, atonic, absence, and generalized tonic-clonic seizures, and

especially for patients with more than one type of generalized seizure. The drug has low toxicity and is well


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tolerated. Its mechanism of action is unclear. Valproic acid is completely absorbed orally when taken on an empty

stomach. Its peak concentration is achieved at between 1 and 3 hours. Food delays the time of absorption but does

not interfere with the amount absorbed. Valproic acid distributes widely; it is about 90% bound to albumin. The

liver is the site of metabolism. At least 10 metabolites of valproic acid have been identified.

Valproic acid is available in capsule, syrup, and sprinkle forms. The tablet form contains divalproex sodium,

which must be metabolized in the gut to valproic acid; it is enterically coated to reduce gastrointestinal

symptoms. Valproic acid is altered by salicylates, which increase its free concentration. The addition of

phenobarbital or phenytoin decreases the concentration of valproic acid.

Mild transient drowsiness and minimal cognitive effects are seen with valproic acid. Hepatic dysfunction, including

liver failure, and pancreatitis have been reported. The more common adverse effects include nausea and vomiting,

which can be controlled by using enterically coated Depakote or by taking the drug with food. Weight gain,

transient hair loss, tremor, and dose-related thrombocytopenia are common. Menstrual disturbances and

hyperandrogenism may occur in women. Neural tube defects and congenital abnormalities have been reported in

the infants of mothers on the drug.

Phenobarbital

Phenobarbital (Luminal) was introduced in 1912. One of the first drugs available for the control of seizures, it isstill

widely used as an alternative for generalized seizures, except absence and partial seizures. Other drugs are

replacing phenobarbital for treatment of status epilepticus. The drug of choice for seizures in infants, its adverse

cognitive and sedative-hypnotic effects make it less than ideal for children and adults. Phenobarbital is a CNS

depressant; it elevates the seizure threshold by decreasing postsynaptic excitation, possibly by stimulating

postsynaptic GABA inhibitor responses. Phenobarbital is rapidly and completely absorbed by all routes (oral, IM,

rectal). The biphasic distribution includes initial penetration of highly perfused organs, including the brain,

followed by even distribution to all body tissues, including fat. By the IV route, peak cerebral concentration is

achieved in 3 to 20 minutes. Drugs affecting liver enzymes may alter phenobarbital's metabolism. The elimination

pattern of phenobarbital is linear. About 20% to 40% of a dose is excreted through the kidneys unchanged. Urinary

pH affects tubular absorption of phenobarbital, and the amount of excreted drug can be increased by

administering diuretics and urinary alkalizing drugs. The binding of phenobarbital to protein is 50%.

The routes of administration are oral and parenteral. In an emergency, phenobarbital can be given IV as a loading

dose. The half-life of phenobarbital is so long that it can be given as a single daily dose. Because it takes about 3

to 4 weeks to reach steady state, changing doses rapidly is not recommended. Phenobarbital decreases the

efficacy of oral contraceptives. The chief side effects are sedation, drowsiness, and fatigue. In addition,

impairment of higher cortical function and depression of cognitive performance (e.g., learning) are found with the

use of phenobarbital.

Summary of Drug Therapy

Any patient receiving long-term drug therapy should be monitored carefully for the development of side effects or

toxicity. Most drugs are metabolized by the liver and excreted by the kidneys. Periodic drug blood levels should be

monitored. If anemia or blood dyscrasias are common side effects, a CBC should be done routinely. Folic acid

deficiency has also been reported with some AEDs; therefore, folic acid levels should be monitored.

Surgical Management


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About 20% of patients with epilepsy do not respond well to drug therapy. Those patients who have been given a

trial (e.g., 1 year or more) on AEDs and continue to have refractory seizures that impact on their quality of life

should be considered for surgical evaluation. Selection criteria are important. Patients who have not responded to

medical management of seizure, who have a unilateral focus that will not cause a major neurological deficit if

excised, and who have had a significant alteration in their quality of life are good candidates for surgery. Surgery

should be preceded by an extensive diagnostic work-up that includes electrophysiology, neuropsychology, and

imaging studies. All three should suggest an epileptogenic focus. The purpose of surgery is to locate and excise as

much of the epileptogenic area as possible without causing neurological deficits.

The presurgical work-up is comprehensive and directed at identifying the functional and structural basis of the

seizure disorder. The work-up includes the following areas15:

In-patient video-EEG monitoring to identify the anatomic location of the seizure site and to correlate behavior

patterns with abnormal EEG patterns

Routine scalp or scalp-sphenoidal recording for localization of lesion

MRI high resolution with thin slices to localize lesion

Possible SPECT or PET scans

Neuropsychological testing

Possible amobarbital test (Wada's test) to assess language and memory location

Other tests as necessary

Surgical Procedures

The most common surgical procedure for the treatment of seizures is a cortical excision (lobectomy). A large

number of patients with partial complex seizures with a localized focus have that focus in the temporal lobe. With

refractory temporal lobe epilepsy, resection of the anteromedial temporal lobe (mesial temporal lobectomy) is

available. A more limited removal of the underlying hippocampus and amygdala is also available. If scar tissue or

other focal epileptogenic area exists, the identified lesion (lesionectomy) can be removed. When the cortical

region cannot be removed, multiple subpial transection designed to disrupt intracortical connections is sometimes

effective in controlling seizures.

A corpus callosotomyhas been helpful for persons with tonic and atonic seizures. Outcomes vary depending on the

type of surgical procedure. For example, outcomes of temporal lobe resections break down as follows:

approximately 68% seizure free, 24% improved, and 8% no improvement at all.15 Outcomes from surgery are

superior to prolonged medical therapy for temporal lobe epilepsy.16 Data on corpus callosotomy surgeries indicate

that about 8% became seizure free, 61% had worthwhile improvement, and 31% had no improvement. The best

results are reported from centers where large numbers of surgeries for epilepsy are performed.

A hemispherectomyis reserved for selected catastrophic infant and early childhood epilepsies. Currently, the

practice is to perform a modified radical hemispherectomy leaving the frontal and occipital poles in place although

disconnected. The response has been good in that about 67% were seizure free, another 21% had a worthwhile

response, and 11% had no improvement.16

Local anesthesia is used for adolescents and adults unless they have behavioral problems and need to be sedated.

In that case, a light general anesthetic is given. Often, the patient must be able to follow commands and answer


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questions during the EEG and cortical stimulation portion of the lengthy surgical procedure. After surgical exposure

of the brain surface and depth, electrodes are applied so that an EEG can be taken to identify the epileptogenic

focus. Cortical stimulation is used to identify sensory, motor, and speech areas. After the tissue to be excised has

been identified, cortical resection is undertaken. Following excision, the electrodes are reattached to determine

the presence of any other epileptogenic activity that would require further resection. If

the EEG pattern is satisfactory, the patient is anesthetized so that the incision can be closed. Postoperatively, the

patient is managed in the same way as any craniotomy patient (see Chapter 14).

Postoperatively and at discharge, the patient continues on an AED, often carbamazepine. EEG recordings are

obtained to determine the presence of seizure activity. The decision to discontinue drug therapy after 2 to 4 years

is based on an evaluation of the specific patient.

Complications of Surgery

The mortality from a temporal resection is lower than 1%. The complications of surgery include infection;

hydrocephalus; cerebral edema, ischemia, or hematoma; hemiparesis or hemiplegia; aphasia; alexia; or visual field

deficits. Higher-level functions of cognition, memory, attention, concentration, or language may be affected. In

addition, psychosocial impairment such as family interpersonal dynamics, self-esteem, adverse response to

treatment failure, and vocational/education disruption are possible.

Vagus Nerve Stimulation

In 1997, vagus nerve stimulation (VNS) was approved for use in the United States as an adjunctive therapy for

adults and adolescents over 12 years of age who have partial-onset seizures that are refractory to AEDs. It consists

of:

1. Aprogrammable signal generator that is implanted in the patient's left upper chest

2. A bipolar VNS lead that connects the generator to the left vagus nerve in the neck

3. Aprogramming wand that uses radiofrequency signals to communicate noninvasively with the generator

4. Hand-held magnets used by the patient or health care provider to manually turn the stimulator on or off

The mechanism of action is uncertain. The surgical procedure takes approximately 1 hour and can be done under

general or regional anesthesia. The procedure is well tolerated except for hoarseness in some cases. Minimal

surgical complications have been reported. Several trials report a decrease in frequency of seizures by 25% or more

in patients previously resistant to all AEDs. The role of VNS for intractable seizure management is yet to be

established.17

MANAGEMENT OF SEIZURES AND STATUS EPILEPTICUS IN AN ACUTE CARESETTINGMost nurses who practice in an acute care setting manage patients who have seizures, regardless of whether they

are assigned to a neuroscience unit or to other types of units. Seizures may also occur in community-based settings

where such patients are managed. Nurses need to know how to manage seizures and status epilepticus. The

following is designed to provide that information.

Managing the Patient During a Seizure in an Acute Care Setting


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When a patient has a seizure, the nurse's role is to protect the patient from injury, care for him or her after the

seizure, and document the details of the event. In the hospital environment, persons who are at risk for having a

seizure are placed on seizure precautions. This means that (1) the side rails of the bed are up and padded if the

patient is at risk for falls, (2) a suction set-up and plastic oral airway are available at the bedside, and (3) the bed

is kept in low position.

Management of the patient during a seizure is directed toward preventing injury and observing for complications.

The following points should be observed:

Before and During a Seizure

If the patient is seated when a major seizure occurs, ease him or her to the floor, if possible.

Provide for privacy by pulling the bed curtains or screen or closing the door.

If the patient experiences an aura, have him or her lie down to prevent injury that might occur from falling to

the floor.

Remove patient's eyeglasses and loosen any constricting clothing.

Do not try to force anything into the mouth.

Guide the movements to prevent injuries; do not try to restrain the patient.

Stay with the patient throughout the seizure to ensure safety.

After a Seizure

Position the patient on the side to facilitate drainage of secretions.

Provide for adequate ventilation by maintaining a patent airway; suctioning may be necessary to prevent

aspiration.

Allow the patient to sleep after the seizure.

On awakening, orient the patient (he or she will probably be amnesic about the event).

Nursing Assessment and DocumentationCollecting data about the seizure requires well-developed observational skills and an understanding of what to look

for and how to document observations. It may be helpful to verbalize the observations as events occur. Verbal

reinforcement provides for better recall.

The following are several points to consider when organizing information about a seizure:

Was the seizure witnessed or not witnessed?

Were there any warning signs or was there an aura?

Where did the seizure begin and how did it proceed?

What type of movement was noted and what parts of the body were involved?

Were there any changes in the size of the pupils or was there conjugate gaze deviation?


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What was the duration of the entire attack and of each phase?

Was the patient unconscious throughout the seizure?

Was there urinary or bowel incontinence?

What was the person's behavior after the seizure?

Was there any weakness or paralysis of the extremities after the seizure?

Were there any injuries noted?

Did the patient sleep after the seizure? How long?

Figure 29-1 A sample of a seizure activity chart.

The observations can be recorded in narrative form in the nurse's notes or on a separate seizure activity sheet,


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which becomes a part of the patient's permanent record. A sample of a seizure activity sheet for generalized tonic-

clonic seizures is found in Figure 29-1. Observations are the same for a seizure that was witnessed in a community

setting.

Managing a Person During a Seizure in a Community SettingSeizures may occur in community settings such as ambulatory clinics, work and recreational environments, and the

home. The same first aid principles taught to the person and family should be followed by the bystander nurse who

comes upon the individual having a seizure. The first aid management of both generalized tonic-clonic seizures and

complex partial seizures includes the following9:

First aid forgeneralized tonic-clonic seizures that occur in a community setting is similar to the management of

this type of seizure in an acute care setting. The seizure may begin abruptly and the person may fall to the ground,

become stiff, and demonstrate clonic movements. The following is recommended:

If the patient is seated, help him or her to lie down.

Remove eyeglasses and loosen any constricting clothing.

Do not try to force anything into the mouth.

Guide the movements to prevent injuries; do not try to restrain the person.

Stay with the patient throughout the seizure.

After the seizure has stopped, one should position the patient on the side to facilitate drainage of secretions; have

someone stay with the patient until he or she is fully awake; and once the patient is awake, orient him or her as

necessary.

First aid for a patient with complex partial seizures is more subtle. The patient may not seem quite right, engaging

in

such behaviors as lip smacking or making chewing motions, walking aimlessly, or not responding to questions

(symptoms of automatism). Before and during a seizure one should do the following:

Remove harmful objects from the patient's environment or try to coax the patient away from anything that

could be harmful.

Demonstrate a calm manner that does not agitate the patient.

Do not try to restrain the patient.

If alone, do not try to approach an angry or agitated patient.

After the seizure has seized, one should not leave the patient alone, should stay with the patient untilconsciousness is fully regained, and should reorient him or her.

With any type of seizure activity, a decision may need to be made to call for emergency medical assistance if:

The person does not begin breathing after the seizure (cardiopulmonary resuscitation should be activated).

A generalized tonic-clonic seizure lasts for more than 2 minutes.

The person has one seizure right after another without regaining consciousness.


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The individual is injured.

Status EpilepticusStatus epilepticus is defined as either continuous seizures lasting at least 5 minutes or two or more discrete

seizures between which there is incomplete recovery of consciousness.18 The most common type of status

epilepticus is tonic-clonic status epilepticus. In over 50% of cases, status epilepticus is the patient's first seizure.

Although there are many types of status epilepticus, the following discussion focuses on the management of

convulsive status epilepticus because this form is most common and constitutes a medical emergency.

The initial management of a patient with status epilepticus includes the standard ABCs of life support (supporting

respirations, maintaining blood pressure, and supporting circulation), administering an AED, finding and treating

any underlying cause, and preventing or treating medical complications.

ABCs of Life Support. The ABCs of life support are similar to any other life-threatening situation. Position the

patient to avoid aspiration or inadequate oxygenation. A soft, plastic oral airway may be inserted if it is possible to

do so without forcing the teeth apart. The airway will need to be suctioned to remain patent. Oxygen is

administered at 100% through a nasal cannula. In most instances, patients will breathe on their own as long as the

airway is kept patent. Suction the airway to maintain patency. Monitor respiratory function with ongoing pulseoximetry. IV access should be secured, and vital signs and neurological signs should be monitored frequently.

Extreme cerebral hypoxia can result in severe, irreversible neurological deficits. Monitor arterial blood gases

because many patients will have a profound metabolic acidosis that corrects itself after seizures are controlled.18

Support of adequate oxygenation and cerebral perfusion is critical to preventing these serious problems. Monitor

glucose by fingerstick. Hyperglycemia followed by hypoglycemia is common and needs to be treated. Give 50 mL of

50% glucose for hypoglycemia. Hyperthermia occurs often with status epilepticus. If it occurs, it must be treated

aggressively with passive cooling to prevent further ischemia to the brain.

Administering Antiepileptic Drugs. The goal of drug therapy is prompt termination of clinical and electrical

seizure activity. The best drug treatment protocol for status epilepticus remains under discussion. Table 29-5

outlines a recommended protocol that proceeds along a time-line and assumes that the previous drug

administration did not terminate the seizure.18 If the patient is not already in the intensive care unit, he or she

must be moved to that area where intubation, ventilatory support, continuous ECG monitoring, and invasive

monitoring can be provided.

Treating the Underlying Cause. The health care provider must try to identify any underlying cause of seizures

(e.g., precipitous withdrawal of AEDs, brain tumor) and treat the primary problem. Various possible causative

factors are discussed earlier in the chapter.

Preventing or Treating Medical Complications. Adverse physiologic consequences of status epilepticus include

hypoxia, hypoglycemia, hypotension, and hyperthermia. Severe metabolic acidosis can occur as a result of loss of

base reserve. This change may prevent seizure control with anticonvulsants by increasing the amount of potassium

in the extracellular space. It may also contribute to cerebral damage. Blood gases should be monitored. Other

medical complications that may develop include cardiac arrhythmias, myocardial infarction, and aspiration

pneumonia.

Nursing Management of Status Epilepticus

The nurse works as part of a collaborative team in addressing the medical emergency. Goals and responsibilities


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include:

Maintaining a patent airway to ensure adequate ventilation

Suctioning as necessary to prevent obstruction of the airway and possible aspiration

Providing oxygen by nasal cannula as ordered

Protecting the IV site to allow for continuous access for medication

Protecting the patient from injury

Providing information to the family

NURSING MANAGEMENT OF PATIENTS WITH EPILEPSY: COMMUNITY-BASEDCAREMost people with epilepsy are managed by their primary care physicians or by a neurologist in the community. In a

managed care environment, more patients with epilepsy, who were previously managed by a neurologist, come

under the care of the primary care physician. Those with complicated or intractable epilepsy will probably still be

managed by a neurologist or in an epilepsy center.

CHART 29-1 Components of a Teaching Plan for Persons With Epilepsy or a

Seizure Diso

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Nursing Management of Seizures and Epilepsy

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