Nursing Management of Seizures and Epilepsy

Ovid: Clinical Practice of Neurological and Neurosurgical Nursing, The

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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 DEFINITIONS References 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 epilepsy and seizure disorder are used interchangeably. Epileptic syndrome: an epileptic disorder characterized by a cluster of signs and symptoms customarily

occurring together.

Epidemiology and Risk Factors Epilepsy 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 specific conditions such as a penetrating brain injury. Third, seizures are episodic, suggesting that triggers precipitate seizure activity.2 P.647 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.

Pathophysiology Seizures 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 excitability may result from energy failure of neurons producing transient depolarization 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 a reas.

Precipitating Factors: Triggers In 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 ca lled reflex epilepsy. Other general triggers include fatigue, sleep deprivation, hypoglycemia, emotional stress, electrical shock, febrile illness, alcohol consumption, certain drugs, drinking too much water, constipation, menstruation, and hyperventilation.

Terminology A 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/IDENTIFICATION Seizures 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 Ta ble 29-3 classifies partial seizures by cerebral lobe involved.

Partial Seizures Three types of partial seizures are recognized: simple, complex , and evolving into secondary generalized seizures . Simple P.648 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, and psychic. 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.

B.

Simp Si mple le pa part rtia iall sei seizu zure ress (co (cons nsci ciou ousn snes esss not not im impa pair ired ed))

1.

Foca Fo call mo moto torr (w (wit ith h an and d wi with thou outt ja jack ckso soni nian an ma marc rch) h)

2.

Somato Soma tose sens nsor oryy or spe speci cial al sen senso sory ry sym sympt ptom omss (e.g (e.g., ., sim simpl ple e hall halluc ucin inat atio ions ns suc such h as tingling, light flashing, buzzing)

3.

With Wi th aut auton onom omic ic sym sympt ptom omss (e.g (e.g., ., as as epig epigas astr tric ic sen sensa sati tion on,, pall pallor or,, flus flushi hing ng))

4.

With Wi th ps psyc ychi hicc sym sympt ptom omss (di (dist stur urba banc nces es of hi high gher er ce cere rebr bral al fu func ncti tion on))

Comp Co mple lex x pa part rtia iall se seiz izur ures es (w (with ith im impa pair irme ment nt of co cons nsci ciou ousn snes ess) s)

1.

Beginn Begi nnin ing g as si simp mple le par parti tial al sei seizu zure ress and and pro progr gres essi sing ng to to impa impair irme ment nt of of consciousness


C.

D.

2.

With no other features

3.

With Wi th fe feat atu ure ress as as in in sim simpl ple e par parti tial al se seiz izu ure ress

4.

With automatism

Wit ith h imp impai airrme men nt of of con conssci ciou ousn snes esss at at ons onset et

1.

With no other features

2.

With Wi th fe feat atu ure ress as as in in sim simpl ple e par parti tial al se seiz izu ure ress

3.

With automatism

Part Pa rtia iall sei seizu zure ress evo evolv lvin ing g to to sec secon onda dari rily ly ge gene nera rali lize zed d sei seizu zure ress

1.

Simpl Sim ple e pa part rtia iall se seiz izur ures es ev evol olvi ving ng to ge gene nera rali lize zed d se seiz izur ures es

2.

Comp Co mple lex x pa part rtia iall sei seizu zure ress ev evol olvi ving ng to ge gene nera rali lize zed d se seiz izur ures es

3.

Simpl Sim ple e part partia iall seiz seizur ures es evo evolv lvin ing g to comp comple lex x part partia iall seiz seizur ures es to to gene genera raliz lized ed seizures

II.. II

Gene Ge nera rali lize zed d se seiz izur ures es (g (gen ener eral aliz ized ed bi bila late tera rall wi with thou outt fo foca call on onse set) t)

A.

Absence seizures

B.

Myoclonic se seizures

C.

Clonic seizures

D.

Tonic seizures

E.

Tonic-clonic seizures

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F.

III.. III

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Atonic seizures

Unclassif Unclas sified ied epi epilep leptic tic sei seizur zures es (in (inclu cludin ding g all all seizu seizures res tha thatt canno cannott be cla classi ssifie fied d due 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 Seizures There 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 a longer 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 tonicclonic 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 a rms extended. If standing, 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. P.649

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.

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.

Applies to all simple partial seizures: may show

abnormal discharges in a very limited region; seizures originating from deep structures may not be noted with scalp electrodes


Autonomic Psychic

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May occur as simple partial seizures. Disturbance in a higher-level function (i.e., distortion of memory), distorted time, feeling of déjà 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

All complex seizures:

generalized 2-4-Hz spike waves

motor, sensory, autonomic, or psychic symptoms as described above.

Partial Seizures Evolving to Secondary Generalized Seizures

One On e cat categ egor oryy

Includ Incl udes es se seiz izur ures es th that at ma mayy evo evolv lve e int into o gen gener eral aliz ized ed 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 tonicclonic seizures

Typical absence seizures: common in children;

Typical absences: 3-

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.

Hz spike-wave complexes with abrupt starts and stops

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


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because of inattention.

Atypical absence seizures—the lapse of consciousness is

usually of longer duration and less abrupt in onset; more obvious motor spike-and-wave pattern, and signs.

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.

Atypical absences: ≤2.5

Hz; slower more irregular

Bilateral, generalized epileptiform discharges, typically polyspikes

Common around time of sleep or awakening; must be differentiated from myoclonic jerks of nonepileptic myoclonus.

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

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

Tonicclonic 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 On e cate catego gory ry

This gro This group up in incl clud udes es al alll seiz seizur ures es th that at can canno nott be cl clas assi sifi fied ed because of inadequate or incomplete data. This self-

paroxysmal fast activity (10 Hz)

epileptiform discharges (spikes, spike-wave complexes)


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explanatory category is a catch-all for seizures that do not conform to any of the other headings.

P.650

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

CEREBRAL HEMISPHERE LOBE

Frontal lobe epilepsy

DESCRIPTION

Many overlapping syndromes with frequent brief attacks (<30 sec) Simple complex seizures Focal motor seizures (from motor strip) Supplemental area motor seizures Tonic and postural signs and symptoms with preserved consciousness; frequent falls Complex partial seizures Complex motor activity, vocalization, and gestural automatism (may be sexual) Common to proceed to secondarily generalized tonic-clonic seizures

Mesial temporal lobe epilepsy

Most common cause is hippocampal sclerosis Mostly complex partial seizures with automatisms and psychic symptoms Often preceded by an aura in 50%-95% of patients; rising epigastric discomfort is the most common aura Seizure may include: Staring Oral or manual automatisms Olfactory and auditory illusions or hallucinations Unilateral dystonic posturing

Parietal lobe epilepsy

Usually simple complex and secondarily generalized seizures >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 epilepsy

Most 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

P.651

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 a lcohol, 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 emergency associated 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 Seizures Seizures 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 poor saturation 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/Identification Physiologic 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 i n 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.

DIAGNOSIS The 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 P.652 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 a bnormal 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 f alse localization. 11 Simultaneous EEG and audio-video recordings of the patient can distinguish seizure from nonseizure activity and assist in classifying seizure type.

Differential Diagnosis Given 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 a ttacks, 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 Electroenceph alograms and Seizures The EEG is a diagnostic test during which the amplified electrical potential of the brain is recorded by placing 14 to 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. P.653

TREATMENT The 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 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, t herapy, 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: Management: Drug Therapy Epilepsy 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 a ny 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 individualized drug program that minimizes side effects and supports compliance. After a diagnosis has been made, the following principles should guide use of drugs 12: 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 about 70% 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 f ree 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 P.654 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 partial seizures, 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


PRIMARY GENERALIZED TONIC-CLONIC

First-line drugs

Valproic acid Lamotrigine

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PARTIAL (I.E., SIMPLE, COMPLEX, AND SECONDARY GENERALIZED SEIZURES)

Carbamazepine Valproic acid Phenytoin

ABSENCE

ATYPICAL ABSENCE, MYOCLONIC, AND ATONIC

Ethosuximide Valproic acid

Valproic acid

Methsuximide Lamotrigine Clonazepam

Lamotrigine Clonazepam Felbamate

Lamotrigine Phenobarbital

Alternative drugs

Primidone Carbamazepine Topiramate Phenobarbital Felbamate

Topiramate Tiagabine Primidone Zonisamide Gabapentin Tiagabine

Data from Holland, K. D. (2001). Epilepsy: Efficacy, pharmacology, and adverse effects of antiepileptic drugs. Neurologic Clinics, 19 (2), (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

0-3

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

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 wi with mi mida daz zolam or or pr propo poffol

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 a llergies, 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 Dosage to 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 be gradually tapered after 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 diary routinely, 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 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 a lter AEDs' protein-binding capacity are malnutrition, older a ge, pregnancy, hypoalbuminemia, burns, liver disease, and chronic renal failure. The following are plasma protein-binding capacities for selected AEDs:


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P.655 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 many patients 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 that after 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 i nformation 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 when phenytoin is discontinued. Therefore, serum monitoring is necessary af ter 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 dosage due 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 a dministration 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 that potentiate 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 P.656 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 µ/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 t o 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 be administered 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 rate greater 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 drugs—erythromycin, 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 1 0 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 is still P.657 widely used as an alternative for generalized seizures, except absence and partial seizures. Other drugs a re 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 a bsorbed 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 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 areas 15: 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 t he anteromedial temporal lobe ( mesial temporal lobectomy ) is available. A more limited removal of the underlying hippocampus and amygdala is also available. If scar ti ssue 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 callosotomy has 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 hemispherectomy is 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 P.658 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 a ny 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; a phasia; 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 generator that is implanted in the patient's left upper chest chest 2. A bipolar VNS lead that connects the generator to the left left vagus nerve in the neck 3. Aprogramming wand that uses radiofrequency radiofrequency signals to communicate noninvasively noninvasively with the generator 4. Hand-held magnets used by the patient patient or health care provider to manually turn the stimulator 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 f or intractable seizure management is yet to be established.17

MANAGEMENT OF SEIZURES AND STATUS EPILEPTICUS IN AN ACUTE CARE SETTING Most 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 Seizure in an Acute 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 Documentat Documentation ion Collecting data about the seizure requires well-developed observational observational skills and an a n 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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P.659 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 tonicclonic 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 During a Seizure Seizure in a Community Community Setting Seizures 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 following 9: First aid for generalized tonic-clonic seizures 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 a wake, 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 P.660 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 until consciousness 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 aft er 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 Epilepticus Status 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 pulse oximetry. 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 t reatment 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-BASED CARE Most 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. P.661

CHART 29-1 Components of a Teaching Plan for Persons With Epilepsy or a Seizure Disorder DIET/NUTRITION/BEVERAGES Eat a well-balanced diet; eat on a routine schedule. Avoid excesses of sugar, caffeine, or any other food that may trigger seizures. Discuss alcohol consumption with your doctor; if you choose to drink, limit your consumption to whatever your physician recommends. Seizures may be precipitated by alcohol consumption, and even small amounts may trigger a seizure in some people.

GENERAL HEALTH Any of the following can trigger seizures in some persons and should be avoided: constipation, excessive fatigue, hyperventilation, and stress. Regular exercise is good for general well-being and stress reduction. Avoid overfatigue and hyperventilation. Avoid exercise in hot weather; exercise in a climatecontrolled environment. Regular sleep patterns on a regular schedule are important. Insomnia or awakening tired are indications of insufficient sleep. This may be due to stress, poor sleep hygiene, or a side effect of medication. Determine cause of sleep disturbance and correct it or seek assistance from the health care provider. Showers, rather than tub baths, should be taken. Good oral hygiene and periodic visits to the dentist are important because gingival hyperplasia can occur from some antiepileptic drugs (AEDs) such as phenytoin.

FEVER AND ILLNESS Fever can trigger seizures; the fever and underlying cause must be treated.


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Any prescription or over-the-counter drugs should be reviewed for interaction. If antibiotics are ordered, interactions with t he AEDs should be evaluated.

ENVIRONMENTAL, OCCUPATIONAL, AND RECREATIONAL RISK FACTORS Noisy environments should be avoided; control a noisy environment as much as possible. Avoid bright, flashing lights or fluorescent lights, strobe lights, discos, a flickering television, and flashing bulbs on signs or Christmas trees. Tinted glass on the windshield and eyeglasses will help to control glare. Use a screen filter on the computer screen to control glare. Do not use recreational or street drugs. Work or recreational activities that could cause injury if a seizure occurred should be avoided. Swim with a “buddy”; help should be available if a seizure occurs. Contact sports (e.g., football, boxing) that could lead to unconsciousness should be avoided.

STRESS, ANXIETY, AND DEPRESSION Emotional stress is a trigger to t o seizures; measures need to be taken to uncover the basis for the stress and how this t his can be decreased. Counseling may be helpful. Living with a chronic health problem is stressful and can place a varying degree of limitations on lifestyle. Depression may result. Appropriate psychotherapy through counseling and/or drugs should be provided.

WOMEN'S HEALTH There may be an increase in seizures around the time of menses. This should be discussed with your health care provider; some adjustment may be made in your medications. If the occurrence of seizures increases around the menses, control other triggers for seizures. AEDs decrease the effectiveness of oral contraceptives; intrauterine devices or other contraceptive devices may be preferred. The seizure pattern often changes during pregnancy; discuss this with your health care provider. Some AEDs can cause birth defects. If pregnancy is planned, it should be discussed with the gynecologist and health care provider following the epilepsy.

LEGISLATION TO PROTECT PERSONS WITH EPILEPSY AND SEIZURE DISORDER The following laws protect persons with epilepsy or seizure disorders from discrimination: Americans With Disabilities Act Rehabilitation Act Individuals With Disabilities Education Act Driver's licenses are controlled by individual states; information on the laws governing driving can be obtained from the Division of Motor Vehicles.

OTHER


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Issues related to marriage, child-bearing, and parenting need to be discussed. Risk factors and questions related to children with epilepsy need a frank discussion. The role of the nurse in managing patients with epilepsy will continue to be important, and in many settings this role will be expanded. In the community, nursing management is initially directed at assisting with the assessment and diagnostic work-up. The components of these activities are discussed in earlier sections. However, the nurse's major role is to provide patient education and patient monitoring. The next section focuses on this aspect of management. The major patient problem and nursing diagnosis for a newly diagnosed patient with epilepsy is Knowledge Deficit. An individualized teaching plan is developed (Chart 29-1) to educate the patient and family. P.662

Patient Teaching: General Points Patient teaching requires a comprehensive teaching plan to help the patient adjust to the health problem. Family teaching cannot be excluded because the family needs help to adjust to a chronic condition that is, by its very nature, frightening. The family must be instructed in what to do when a seizure occurs, including first aid. The teaching plan is based on a systematic assessment of patient needs. Physical, social, psychological, and vocational dimensions must be considered along with a drug teaching plan. Each teaching plan is individual, that is, tailored to the needs of the patient and the problems that arise over time. Major points of information that should be presented to the patient are outlined in Chart 29-1. The plan should expand on these points to include the implications that apply to the patient's i ndividual lifestyle.19 The plan must be revised periodically to update its relevance. Because nonadherence is a common problem, adherence must be evaluated at each encounter with the health care professional. It is important to reinforce information each time the patient is seen. Patients may express concerns about how they will cope with certain aspects of their lives. One common concern of most adults is whether they should reveal their condition when applying for a job. Many report discrimination by employers when they reveal their condition. Those who choose to conceal this information often feel guilty and live in fear that they will experience a seizure on the job or that their seizure disorder will become known to the employer. If a seizure did occur on the job, it could endanger the patient and others, depending on the kind of work that is done. Information that is deliberately concealed is cause for immediate dismissal in most places of employment. It is the patient's decision to determine whether to disclose the epileptic condition.

Patient Teaching Related to Drug Therapy It is imperative to provide detailed information to the patient and/or a responsible family member about epilepsy and drug therapy. Side effects and signs of toxicity should be discussed. The patient must understand that the drug must be taken as ordered every day. The most common cause of seizures in patients who have previously been controlled is failure to take the AEDs. The patient should be asked to maintain a drug chart of time, amount taken, and side effects, along with a record of the frequency and characteristics of any seizures. Because seizures represent a chronic condition (i.e., they are usually not completely arrested), the person must understand the nature of the problem, the precipitating factors, and the adaptations in lifestyle that are required. The following is an outline of the major points of a drug teaching plan: The drug must be taken as ordered to maintain a therapeutic blood level, even if there is no seizure activity. AEDs may be necessary for a few years or longer; for some patients, they may be necessary for a lifetime.


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There are criteria for when and how a trial of drug discontinuation should be managed; discuss this with the health care provider. Discontinuation of drugs without the knowledge of the health care provider is the most common cause of seizure activity (e.g., status epilepticus); this should not be done. 20 Know the signs of toxicity of the drugs prescribed. Symptoms of toxicity should be reported promptly to the physician. Keep drug and seizure charts and bring them with you for your appointment. Because there are serious side effects from some drugs, be sure to have blood work done as ordered (e.g., CBC for anemia and blood dyscrasias). Because phenytoin is absorbed slowly from the gastrointestinal tract, daily drug schedules can be adjusted for convenience. Missed doses can be “made up” safely. Some individuals may be able to take extended-release phenytoin with once-daily dosing; discuss this with your health care provider. A Medic Alert bracelet or a card should be carried to indicate a chronic condition. The patient is encouraged to carry a card that indicates that he or she is being treated by a particular physician. If the patient is found unconscious or injured, the physician can be notified. Keep follow-up appointments with a health care provider for periodic monitoring and re-evaluation.

Special Populations: Women and the Elderly Two patient populations that have unique needs when discussing epilepsy and seizure disorders are women and the elderly.

Women Some of the special needs of women are included in the teaching plan in Chart 29-1. Women who have a seizure disorder need anticipatory guidance about contraception and the implications of child-bearing. The effectiveness of oral contraceptives is decreased by AEDs, which induce liver enzymes and increase the rate of metabolism. A sign of ineffectiveness of the oral contraceptive is breakthrough bleeding; an oral contraceptive with a higher estrogen content needs to be taken or other forms of birth control used. Women taking AEDs who wish to become pregnant should discuss their particular situation with the physician. Myths need to be dispelled and real risks, including risk of teratogenic effects of many AEDs on a fetus, need to be examined. There is evidence that there is a doubling of the rate of malformations i n babies born to mothers taking AEDs. Further, the risk may be dose related. 21 Acombination of AEDs, especially carbamazepine, phenytoin, and valproate, causes a much higher risk of neural tube defects. The question arises as to what should be done about AEDs if a woman wants to become pregnant. There is no simple answer. The variables include the particular drugs and dosages involved and the severity of the seizure disorder. For some women, discontinuation of the AEDs may be an option. This is a decision that should be made after careful discussion with the physician. After a woman is pregnant, it does no good to discontinue the AEDs. P.663 During pregnancy, many women notice a change in their seizure pattern, which is unpredictable. The increased risk of complications during pregnancy, delivery, and the postpartum period requires that the neurologist or


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primary care physician and the obstetrician collaborate closely. If breast-feeding is planned, consideration of the effect of the AED in breast milk on the infant needs to be addressed. For details of management, other sources should be consulted.

The Elderly Ahigh incidence of new onset of epilepsy is found in persons 65 years old and older. The risk factors associated with the increased incidence in this group include stroke, head trauma, dementia, infection, alcoholism, and aging.22 Of these, stroke associated with paresis and cortical involvement is the leading risk factor for the development of epilepsy in the elderly. Although generalized tonic-clonic seizures are easily recognizable, simple and complex seizures may pose a more difficult problem because of the subtle symptoms and other competing diagnoses. The differential diagnosis includes transient ischemic attacks, syncope, drop attacks, transient global amnesia, psychiatric disorders, and sleep disorders. To make a diagnosis of a seizure disorder, nurses and physicians first need to recognize it as a possibility when evaluating older patients. 23 With seizure disorder in the differential diagnosis, the health care provider is alerted to collect a detailed history from the person and family member and conduct a complete physical and neurological examination. In addition, MRI and an EEG may be useful. It is noteworthy that a normal EEG does not necessarily exclude the diagnosis of epilepsy. An EEG with stresses such as sleep deprivation increases the possibility of observing epileptiform abnormalities. Focal or diffuse slowing on EEG is not necessarily an indicator of epilepsy in older persons. An EEG finding known as periodic lateralized epileptiform discharges (PLEDs) is of particular interest; these are abnormal interictal EEG wave patterns characterized by paroxysmal, sharp wave complexes suggestive of an underlying focal seizure disorder. Management consists of treating the underlying problem and choosing the right AED for the seizure type. In choosing an AED for an elderly person, several points should be considered24: The pharmacokinetics (absorption, distribution, metabolism, and excretion) are altered in the elderly owing to hematologic, renal, and hepatic function changes. Before ordering any AEDs, CBC, clotting factors, albumin, liver function studies, and creatinine values should be evaluated to determine whether the AED would have an unusual effect given any abnormal values. Many older people are taking several drugs for chronic health problems such as cardiac and respiratory problems. Consider drug interactions when choosing an AED. Consider the effect of the drug on cognitive function and balance and how it will affect daily living and patient safety. Consider cost. If the drug is too expensive for the patient, compliance will not be maintained. Begin with AED monotherapy, starting at a low dose, and titrate slowly to monitor seizure control or toxicity. Monitor the patient for side effects such as folate deficiency with phenytoin. Free AED concentrations should be measured in any patient with renal or hepatic dysfunction who has signs of toxicity when within the therapeutic range.

Long-Term Management of Persons With Epilepsy Long-term management and periodic re-evaluation are necessary with any chronic condition. Because all drugs have side effects and toxicity, patients must be monitored for any signs of toxicity. When adverse reactions occur, medications need to be adjusted or discontinued. Periodic re-evaluation provides the opportunity for assessment of emotional, psychological, social, and vocational problems that are apt to develop as the patient adjusts to living


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with a seizure disorder.

REFERENCES 1. Browne, T. R., & Holmes, G. L. (2000). Handbook of epilepsy (2nd ed., pp. 1-18). Philadelphia: Lippincott Williams & Wilkins.

2. 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., pp. 2357-2372). New York: McGraw-Hill.

3. Ropper, A. H., & Brown, R. H. (2005). Adams and Victor's principles of neurology (8th ed., pp. 271-301). New York: McGraw-Hill.

4. Ropper, A. H., & Brown, R. H. (2005). Adams and Victor's principles of neurology (8th ed., p. 281). New York: McGraw-Hill.

5. Kotagel, P. (1997). Complex partial seizures with automatisms. In F. Wylie (Ed.). The treatment of epilepsy: Principles and practice (2nd ed., pp. 385-400). Baltimore: Williams & Wilkins.

6. Commission of Classification and Terminology of the International League Against Epilepsy. (1981). Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia, 22, 489-501.

7. Benbadis, S. R. (2001). Epilepsy. Neurologic Clinics, 19 (2), (2), 251-270

8. Lowenstein, D. H., & Alldredge, B. K. (1998). Status epilepticus. New England Journal of Medicine, 338(14), 970-976.

9. Gumnit, R. J. (1995). The epilepsy handbook: The practical management of seizures (2nd ed., pp. 124127). New York: Raven.

10. Schachter, S. C. (2001). Epilepsy. Neurologic Clinics, 19 (1), (1), 57-78.

11. Trescher, W. H., & Lesser, R. P. (20 04). The epilepsies. In W. G. Bradley, R. B. Daroff, G. M. Fenichel, & J. Jankovic (Eds.). Neurology in clinical practice (4th ed., pp. 1953-1992). Philadelphia: ButterworthHeinemann.

12. Graves, N. M., & Garnett, W. R. (1999). Epilepsy. In J. T. DiPiro, R. L. Talbert, G. C. Yee, G. R. Matzke,


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B. G. Wells, & L. M. Posey (Eds.). Pharmacotherapy: A pathophysiologic approach (4th ed., pp. 952-975). Stamford, CT: Appleton & Lange.

13. Quality Standards Committee of AAN. (1996). Practice parameter: A guideline for discontinuing antiepileptic drugs in seizure-free patients-summary statement. Neurology, 47 , 600-602.

14. French, J. A., & Pedley, T. A. (2008). Initial management of epilepsy. New England Journal of Medicine, (2), 166-176. 359 (2),

15. Engel, J. (1996). Surgery for seizures. New England Journal of Medicine, 334 (10), 647-652.

16. Wiebe, S., Blume, W. T., Girvin, J. P., & Eliasziw, M. (2001). Arandomized controlled trial of surgery for temporal-lobe epilepsy. New England Journal of Medicine, 345 (5), 311-318. P.664 17. Wyllie, E. (Ed.). (1997). The treatment of epilepsy: Principles and p ractice (2nd ed.). Baltimore: Williams & Wilkins.

18. Lowenstein, D. H., & Alldredge, B. K. (1998). Status epilepticus. New England Journal of Medicine, 338(14), 970-976.

19. Shafer, R. O. (1994). Nursing support of epilepsy self-management. Clinical Nursing Practice in Epilepsy, 2(1), 5-6.

20. O'Dell, C., & Shinnar, S. (2001 ). Epilepsy: Initiation and discontinuation of antiepileptic drugs. Neurologic Clinics, 19 (2), (2), 289-311.

21. Foldvary, N. (2001). Epilepsy: treatment issues for women with epilepsy. Neurologic Clinics, 19 (2), (2), 491515.

22. Collins, N. S., Shapiro, R. A., & Ramsay, R. E. (2006). Elders with epilepsy. Medical Clinics of North America, 90 (5), (5), 945-966.

23. Nadkarni, S., LaJoie, J., & Devinsky, O. (2005). Current treatments of epilepsy. Neurology, 64(12 Suppl), S2-11.

24. Palsalos, P. N., & Perucca, E. (2003). Clinically important drug interactions in epilepsy: Interactions between antiepileptic drugs and other drugs. Lancet Neurology, 2(8), 473-481.


RESOURCES Websites http://www.efa.org/

http://www.epilepsyfoundation.org/gene

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Nursing Management of Seizures and Epilepsy

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