EPILEPSY - · PDF fileacademic textbook on Human Anatomy & Physiology. ABSTRACT Epilepsy is...

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EPILEPSY

Jassin M. Jouria, MD

Dr. Jassin M. Jouria is a medical doctor, professor

of academic medicine, and medical author. He

graduated from Ross University School of Medicine

and has completed his clinical clerkship training in

various teaching hospitals throughout New York,

including King’s County Hospital Center and

Brookdale Medical Center, among others. Dr. Jouria

has passed all USMLE medical board exams, and

has served as a test prep tutor and instructor for

Kaplan. He has developed several medical courses

and curricula for a variety of educational institutions. Dr. Jouria has also served on

multiple levels in the academic field including faculty member and Department Chair.

Dr. Jouria continues to serves as a Subject Matter Expert for several continuing

education organizations covering multiple basic medical sciences. He has also

developed several continuing medical education courses covering various topics in

clinical medicine. Recently, Dr. Jouria has been contracted by the University of

Miami/Jackson Memorial Hospital’s Department of Surgery to develop an e-module

training series for trauma patient management. Dr. Jouria is currently authoring an

academic textbook on Human Anatomy & Physiology.

ABSTRACT

Epilepsy is a seizure disorder of varied etiology and symptomology and its

treatment depends on multiple factors, including age of onset and type of

seizure. Sometimes the seizure is absent or mild enough to go untreated by

medication and resolves over time. Most often, epilepsy is a life long

condition that requires close medical management. Anti-epileptic drug

therapy often requires serum monitoring for dose adjustment and drug

interaction surveillance. Screening for comorbid medical and psychiatric

conditions, especially depression, anxiety, and feelings of social stigma and

isolation is needed. Educating patients and families to increase awareness of

epilepsy and treatment options in their unique circumstance will assist them

to overcome stereotypes and help them obtain a higher quality of life.


Continuing Nursing Education Course Director & Planners

William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,

Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner

Policy Statement

This activity has been planned and implemented in accordance with the

policies of NurseCe4Less.com and the continuing nursing education

requirements of the American Nurses Credentialing Center's Commission on

Accreditation for registered nurses. It is the policy of NurseCe4Less.com to

ensure objectivity, transparency, and best practice in clinical education for

all continuing nursing education (CNE) activities.

Continuing Education Credit Designation

This educational activity is credited for 4 hours. Nurses may only claim credit

commensurate with the credit awarded for completion of this course activity.

Pharmacology content is 1 hour.

Statement of Learning Need

Education about epilepsy for nurses in acute care, outpatient and school

settings for children is needed since nurses are often the main health

professional involved in coordinating care outcomes for patients and

families.

Course Purpose

To provide nurses and health team associates with knowledge about epilepsy

syndromes and treatments in all age groups.


Target Audience

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses and

Medical Assistants may obtain a Certificate of Completion)

Course Author & Director Disclosures

Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA

Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Activity Review Information

Reviewed by Susan DePasquale, MSN, FPMHNP-BC

Release Date: 5/23/2016 Termination Date: 5/23/2017

Please take time to complete a self-assessment of knowledge, on page 4, sample questions before reading the article.

Opportunity to complete a self-assessment of knowledge learned will be provided at the end of the course.


1. Specific features that typically define epileptic syndromes do

not include:

a. Seizure types b. Age when seizures begin

c. Electroencephalogram (EEG) findings d. A history of mental illness

2. A factor known to influence an individual’s risk of developing

epilepsy is:

a. Family History b. An electrolyte imbalance

c. Trauma at birth d. A severe psychotic disturbance

3. A ____ % chance of recurring seizures exists after a person has 2 or more seizures.

a. 35%

b. 50 % c. 25 %

d. 70 %

4. True or False: Febrile seizures (clonic-tonic) can last 1 minute or 30 minutes, and can be repetitive.

a. True

b. False

5. In frontal lobe epilepsy motor areas controlling motor

movement are affected, therefore abnormal movements occur:

a. on the same side of the body b. generally in the lower extremities

c. on the opposite side of the body d. resemble a tic disorder


Introduction

Epilepsy is a complex brain disorder that is characterized by seizures, which

are caused by disturbances in the brain’s electrical functions. The term

epilepsy encompasses a variety of different neurological syndromes, each

ranging in its symptoms, severity, and duration. The characteristic seizures

are present in all types of epilepsy, but they differ in clinical presentation

and symptom severity depending on the type of epilepsy. Epilepsy is most

common in young children and the elderly, but it can affect individuals of all

ages. In many cases, the cause of epilepsy is unknown. In those instances

when a cause is identified, we find that the cause varies between

environmental or genetic factors, or as part of traumatic injury.

Some epileptic syndromes will only last a short time, especially those caused

by trauma; however, some other epileptic syndromes will be lifelong

conditions that cannot be cured. While many individuals will experience a

single, unprovoked seizure at some point in their lives, epilepsy is not

considered as a diagnosis until the patient has had two or more unprovoked

seizures. Once this occurs, the patient will begin the process for assessing

and diagnosing the type of epilepsy.

Overview Of Epilepsy

Epilepsy affects the central nervous system, thereby causing disruptions in

the nerve cell activity in the brain. When this activity is disrupted, seizures

occur. These seizures will cause the patient to experience abnormal

behavior, symptoms, and sensations. In some instances, patients will lose

consciousness. The presentation of seizures will vary. Some patients will

stare blankly for a brief period of time, typically a few seconds. Other

patients may experience twitching and jerking of their bodies. The type of


seizure experienced by the patient depends upon the etiology and the

severity of the condition.

Regardless of the severity of the seizures, most patients will require

treatment, as seizures can pose a significant risk to the patient. Seizures can

occur when the patient is engaging in activities such as driving, operating

machinery, or swimming. When this occurs, the patient is at an increased

risk of experiencing significant injuries.1 Specific symptoms and features

typically define epileptic syndromes. The categories include:

Seizure types

Age when seizures begin

Electroencephalogram (EEG) findings

Brain structure (usually assessed with a brain magnetic resonance

imaging (MRI) scan)

Family history of epilepsy or genetic disorder

Prognosis (future outlook)

Approximately fifty percent of epilepsy cases are caused by unknown

factors. In the remaining cases, the causes are typically genetic,

environmental, or trauma related.2 The following table provides an

explanation of the potential identifiable cause in cases of epilepsy.3

Genetic

Influence

Some types of epilepsy, which are categorized by the type of seizure

the individual experiences, run in families. In these cases, it's likely

that there's a genetic influence.

Researchers have linked some types of epilepsy to specific genes;

though it's estimated that up to 500 genes could be tied to the

condition. For most people, genes are only part of the cause of

epilepsy.


Certain genes may make a person more sensitive to environmental

conditions that trigger seizures. Generalized epilepsy seizure types

appear to be more related to genetic influences than partial seizure

epilepsies.

Head Trauma Head trauma that occurs due to a car accident or other traumatic

injury can cause epilepsy. Head injuries can cause epilepsy in both

adults and children, with the risk highest in severe head trauma. A

first seizure related to the injury can occur years later, but only very

rarely. People with mild head injuries that involve loss of

consciousness for fewer than 30 minutes have only a slight risk that

lasts up to 5 years after the injury.

Brain conditions that result in damage to the brain, such as brain

tumors or strokes, also can cause epilepsy. Stroke is a leading cause

of epilepsy in adults older than age 35.

Infectious

Diseases

Infectious diseases, such as meningitis, AIDS and viral encephalitis,

can cause epilepsy.

Prenatal Injury Before birth, babies are sensitive to brain damage that could be

caused by several factors, such as an infection in the mother, poor

nutrition or oxygen deficiencies. This brain damage can result in

epilepsy or cerebral palsy.

Developmental

Disorders

Epilepsy can sometimes be associated with developmental disorders,

such as autism and neurofibromatosis.

Brain

Chemistry

Factors

Ion Channels - sodium, potassium, and calcium - act as ions in the

brain. They produce electric charges that must fire regularly in order

for a steady current to pass from one nerve cell in the brain to

another. If the ion channels that carry them are genetically damaged,

a chemical imbalance occurs. This can cause nerve signals to misfire,

leading to seizures. Abnormalities in the ion channels are believed to

be responsible for absence and many other generalized seizures.


Neurotransmitters - Abnormalities may occur in neurotransmitters,

the chemicals that act as messengers between nerve cells. Three

neurotransmitters are of particular interest:

Gamma aminobutyric acid (GABA), which helps prevent nerve

cells from over-firing.

Serotonin's role in epilepsy is also being studied. Serotonin is

a brain chemical that is important for wellbeing and associated

behaviors (such as eating, relaxation, and sleep). Imbalances

in serotonin are also associated with depression.

Acetylcholine is a neurotransmitter that is important for

learning and memory.

Risk Factors

Epilepsy and seizure disorders affect nearly 3 million Americans and more

than 45 million people worldwide. While anyone can develop epilepsy, there

are a number of factors (outlined below) that will increase an individual’s

risk of developing epilepsy and seizure disorders.1,4

Age

Epilepsy affects all age groups. The risk is highest in children under the age

of 2 and older adults over age 65. In infants and toddlers, prenatal factors

and birth delivery problems are associated with epilepsy risk. In children age

10 and younger, generalized seizures are more common. In older children,

partial seizures are more common.


Gender

Men are reported to have a slightly higher risk than women of developing

epilepsy. While gender is an area of evolving research, the current general

consensus is that the higher incidence of epilepsy in men is due to their

increased exposure to risk factors associated with acute symptomatic

seizures. This general finding does not preclude the fact that women may

have a higher incidence of idiopathic seizure conditions; however, a detailed

discussion of gender as a factor in epileptic conditions is outside the scope of

this study. The interested learner is encouraged to review the most recent

research on gender related to epilepsy.

Family History

People who have a family history of epilepsy are at increased risk of

developing the condition. While there are numerous factors that may cause

epilepsy, as well as a variety of epileptic syndromes, all types share one

common feature: all forms of epilepsy are characterized by recurrent

seizures. These seizures are caused by uncontrolled electrical discharges in

the nerve cells in the cerebral cortex. Many individuals will experience a

single seizure at some point in their lifetime. This is not considered epilepsy.

Very few initial seizures will recur. In fact, only approximately twenty-five

percent of initial seizures will recur. Once a patient experiences two or more

recurring seizures, he or she has a 70% chance of experiencing recurring

seizures. This will result in a diagnosis of epilepsy.

Epilepsy is generally classified into two main categories based on seizure

type, and these are described in the table below.


PARTIAL SEIZURES

These seizures are more common than generalized seizures and occur in one or

more specific locations in the brain. In some cases, partial seizures can spread

to wide regions of the brain. They are likely to develop from specific injuries, but

in most cases the exact origins are unknown (idiopathic).

Simple Partial

Seizures

A person with a simple partial seizure (sometimes known as

Jacksonian epilepsy) does not lose consciousness, but may

experience confusion, jerking movements, tingling, or odd mental

and emotional events. Such events may include déjà vu, mild

hallucinations, or extreme responses to smell and taste.

After the seizure, the patient usually has temporary weakness in

certain muscles. These seizures typically last about 90 seconds.

Complex Partial

Seizures

Slightly over half of seizures in adults are complex partial type. About

80% of these seizures originate in the temporal lobe, the part of the

brain located close to the ear. Disturbances there can result in loss of

judgment, involuntary or uncontrolled behavior, or even loss of

consciousness. Patients may lose consciousness briefly and appear to

others as motionless with a vacant stare.

Emotions can be exaggerated; some patients even appear to be

drunk. After a few seconds, a patient may begin to perform repetitive

movements, such as chewing or smacking of lips. Episodes usually

last no more than 2 minutes. They may occur infrequently, or as

often as every day.

A throbbing headache may follow a complex partial seizure. In some

cases, simple or complex partial seizures evolve into what are known

as secondarily generalized seizures. The progression may be so rapid

that the initial partial seizure is not even noticed.

GENERALIZED SEIZURES

Generalized seizures are caused by nerve cell disturbances that occur in more

widespread areas of the brain than partial seizures. Therefore, they have a more

serious effect on the patient. They are further subcategorized as tonic-clonic (or

grand mal), absence (petit mal), myoclonic, or atonic seizures.

Tonic-Clonic

(Grand Mal)

Seizures.

The first stage of a grand mal seizure is called the tonic phase, in

which the muscles suddenly contract, causing the patient to fall and

lie stiffly for about 10 - 30 seconds. Some people experience a

premonition or aura before a grand mal seizure; most, however, lose

consciousness without warning.

If the throat or larynx is affected, there may be a high-pitched

musical sound (stridor) when the patient inhales.

Spasms occur for about 30 seconds to 1 minute. Then the seizure

enters the second phase, called the clonic phase. The muscles begin

to alternate between relaxation and rigidity.


After the clonic phase, the patient may lose bowel or urinary control.

The seizure usually lasts a total of 2 - 3 minutes, after which the

patient remains unconscious for a while and then awakens to

confusion and extreme fatigue.

A severe throbbing headache similar to migraine may also follow the

tonic-clonic phases.

Absence (Petit

Mal) Seizures.

Absence (petit mal) seizures are brief losses of consciousness that

occur for 3 - 30 seconds. Physical activity and loss of attention last

for only a moment. Such seizures may pass unnoticed by others.

Young children may simply appear to be staring or walking

distractedly.

Petit mal may be confused with simple or complex partial seizures, or

even with attention deficit disorder. In petit mal seizures, a person

may experience attacks as often as 50 - 100 times a day.

Myoclonic seizures are a series of brief jerky contractions of specific

muscle groups, such as the face or trunk.

Atonic

(Akinetic)

Seizures

A person who has an atonic (akinetic) seizure loses muscle tone.

Sometimes it may affect only one part of the body so that, for

instance, the jaw slackens and the head drops. At other times, the

whole body may lose muscle tone, and the person can suddenly fall.

A brief atonic episode is known as a drop attack.

Simply Tonic or

Clonic Seizures

Seizures can also be simply tonic or clonic. In tonic seizures, the

muscles contract and consciousness is altered for about 10 seconds,

but the seizures do not progress to the clonic or jerking phase.

Clonic seizures, which are very rare, occur primarily in young

children, who experience spasms of the muscles but not tonic rigidity.

Types of Epilepsy

While there are a number of different epilepsy syndromes, there are two

primary types of epilepsy that affect a number of individuals. Each type has

specific features that distinguish it.5


Idiopathic

Epilepsy

In idiopathic generalized epilepsy, there is often, but not always, a

family history of epilepsy. Idiopathic generalized epilepsy tends to

appear during childhood or adolescence, although it may not be

diagnosed until adulthood.

In this type of epilepsy, no nervous system (brain or spinal cord)

abnormalities, other than the seizures, can be identified on either an

EEG or magnetic resonance imaging (MRI) studies. The brain is

structurally normal on a brain (MRI) scan, although special studies

may show a scar or subtle change in the brain that may have been

present since birth.

People with idiopathic generalized epilepsy have normal intelligence

and the results of the neurological exam and MRI are usually normal.

The results of the EEG may show epileptic discharges affecting a

single area or multiple areas in the brain (so called generalized

discharges).

The types of seizures affecting patients with idiopathic generalized

epilepsy may include:

Myoclonic seizures (sudden and very short duration jerking of

the extremities)

Absence seizures (staring spells)

Generalized tonic-clonic seizures (grand mal seizures)

Idiopathic generalized epilepsy is usually treated with medications.

Some people outgrow this condition and stop having seizures, as is

the case with childhood absence epilepsy and a large number of

patients with juvenile myoclonic epilepsy.

Idiopathic partial epilepsy begins in childhood (between ages 5 and 8)

and may be part of a family history. Also known as benign focal

epilepsy of childhood (BFEC), this is considered one of the mildest

types of epilepsy. It is almost always outgrown by puberty and is

never diagnosed in adults.


Seizures tend to occur during sleep and are most often simple partial

motor seizures that involve the face and secondarily generalized

(grand mal) seizures. This type of epilepsy is usually diagnosed with

an EEG.

Symptomatic

Generalized

Epilepsy

Symptomatic generalized epilepsy (SGE) encompasses a group of

challenging epilepsy syndromes. As a group, SGE has 3 main features:

(1) multiple seizure types, especially generalized tonic and atonic

seizures; (2) brain dysfunction other than the seizures, in the

intellectual domain (mental retardation or developmental delay) and in

the motor domain (cerebral palsy); and (3) EEG evidence of diffuse

brain abnormality.

The following are examples of epilepsy syndromes that are included in

the category of SGE:

Early myoclonic encephalopathy

Early infantine epileptic encephalopathy with suppression

bursts or Ohtahara syndrome

West syndrome

Epilepsy with myoclonic atonic seizures

Epilepsy with myoclonic absence

Lennox-Gastaut syndrome

Progressive myoclonic epilepsies

Epilepsy Syndromes

There are a number of different syndromes that fall under the umbrella of

epilepsy. These syndromes are defined based upon the type and severity of

seizures, as well as the area of the brain that is affected.


To further distinguish these syndromes, factors such as age, cause, and

outcome are also included in the defining characteristics. The following

section provides a thorough overview of the various epilepsy syndromes.4,6-8

Temporal Lobe Epilepsy

Temporal Lobe Epilepsy (TLE) means that the seizures arise in the temporal

lobe of the brain. Experiences during temporal lobe seizures vary in intensity

and quality. Sometimes the seizures are so mild that the person barely

notices. In other cases, the person may be consumed with feelings of fear,

pleasure, or unreality. A patient may also report an odd smell, an abdominal

sensation that rises up through the chest into the throat, an old memory or

familiar feeling, or a feeling that is impossible to describe.

Types of Seizures in TLE

The most common seizure type in TLE is a complex partial seizure. During

complex partial seizures, people with TLE tend to perform repetitive,

automatic movements (called automatisms), such as lip smacking and

rubbing their hands together. Three-quarters of people with TLE also have

simple partial seizures, and about half have tonic-clonic seizures at some

time. Some people with TLE experience only simple partial seizures.

Temporal lobe seizures usually begin in the deeper portions of the temporal

lobe. This area is part of the limbic system, which controls emotions and

memory. This is why the seizures can include a feeling of déjà vu, fear, or

anxiety, and why some people with TLE may have problems with memory

and depression.


In most cases, the seizures associated with TLE can be fully controlled with

medications used for partial seizures. If drugs are ineffective, brain surgery

is often an option for patients with TLE. Temporal lobectomy is the most

common and successful form of epilepsy surgery. Vagus nerve stimulation

can also be beneficial in cases where temporal lobectomy is not

recommended or has failed.

Frontal Lobe Epilepsy

Frontal lobe epilepsy is the next most common form of epilepsy after

temporal lobe epilepsy (TLE), and involves the frontal lobes of the brain. As

in temporal lobe epilepsy, seizures in frontal lobe epilepsy are partial,

though seizure symptoms differ depending on the frontal lobe area involved.

Since the frontal lobes are responsible for a wide array of functions including

motor function, language, impulse control, memory, judgment, problem

solving, and social behavior, seizure symptoms in the frontal lobes vary

widely. Also, the frontal lobes are large and include many areas that do not

have a precisely known function. Therefore, when a seizure begins in these

areas, there may be no symptoms until it spreads to other or most areas of

the brain, causing a tonic-clonic seizure.

When motor areas controlling motor movement are affected, abnormal

movements occur on the opposite side of the body. Seizures beginning in

frontal lobe motor areas can result in weakness or the inability to use certain

muscles, such as the muscles that allow someone to speak.

Complex partial seizures of frontal lobe origin are usually quite different from

temporal lobe seizures. Frontal lobe seizures tend to be short (less than 1

minute), and occur in clusters and during sleep. They include strange

automatisms such as bicycling movements, screaming, or even sexual


activity, followed by confusion or tiredness. Sometimes a person will remain

fully aware during a frontal lobe seizure, while at the same time having wild

movements of the arms and legs. In fact, a seizure from the frontal lobe

may even involve laughing or crying as the only symptom, though both

laughing (gelastic) and crying (dacrystic) seizures could come from the

temporal lobe as well. The EEG might be the only way to determine which

lobe is involved in these cases.

In many cases, frontal lobe seizures can be well controlled with medications

for partial seizures. If antiepileptic drugs are not effective, surgery to

remove the seizure focus may be an option in selected cases. Those patients

with abnormalities on the brain MRI or CT scans limited to one frontal lobe

are the best candidates, but even those with normal imaging studies may be

successfully treated with surgery. Vagus nerve stimulation can also be

beneficial in cases where brain surgery is not recommended or fails.

Parietal Lobe Epilepsy

Parietal lobe epilepsy is a relatively rare form of epilepsy, comprising about

5% of all epilepsy, in which seizures arise from the parietal lobe of the brain.

Parietal lobe epilepsy can start at any age and occurs in both males and

females equally. It may be a result of head trauma, birth difficulties, stroke,

or tumor, though the cause is unknown in 20% of patients.

The parietal lobe is located just behind the frontal lobe and it plays

important roles in touch perception, the integration of sensory information

and in visual perception of spatial relationships among objects (visuospatial

processing). In the language dominant side of the brain (the left side for

most right-handed individuals), the parietal lobe is also involved with


language, planned movements such as writing, as well as mathematical

skills.

Since the parietal lobe involves the processing and integration of sensory

and visual perception, seizures originating from the parietal lobe can involve

both sensory and visual sensations. Seizure duration varies, from a few

seconds in some patients to a few minutes in others. The following are the

different types of symptoms associated with parietal lobe seizures.

Somatosensory Seizures

Somatosensory seizures are the most common type of seizures in parietal

epilepsies. Patients with these types of seizures describe feeling physical

sensations of numbness and tingling, heat, pressure, electricity and/or pain.

Pain, though a rare symptom in seizures overall, is quite common in parietal

seizures, occurring in up to one quarter of patients. Some patients describe

a typical “Jacksonian march”, in which the sensation marches in a

predictable pattern from the face to the hand up the arm and down the leg.

Rarely, a patient will describe a sensation in the genitalia, occasionally

leading to orgasm.

Somatic Illusions

During a somatic illusion, another common symptom of parietal seizures,

patients may experience a feeling like their posture is distorted, that their

arms or legs are in a weird position or are in motion when they are not, or

that a part of their body is missing or feels like it does not belong. Patients

with parietal seizures may also experience vertigo, a sensation of movement

or spinning of the environment, or of their body within the environment.


Visual Illusions and Hallucinations

Patients with visual illusions report a distortion of visual perception. Objects

seem too close, too far, too large, too small, slanted, moving or otherwise

not right. A patient with hallucinations describes seeing objects that seem

very real, though in fact they do not exist. Rarely, a patient with a parietal

seizure will report difficulty understanding spoken words or language,

difficulty reading or performing simple math.

Treatment with antiepileptic medication is usually effective in controlling

seizures in parietal lobe epilepsy. In severe cases, surgery may be an

option.

Occipital Lobe Epilepsy

In occipital lobe epilepsy, seizures arise from the occipital lobe of the brain,

which sits at the back of the brain, just below the parietal lobe and just

behind the temporal lobe. The occipital lobe is the main center of the visual

system. Occipital lobe epilepsy accounts for about 5-10% of all epilepsy

syndromes. This kind of epilepsy can be either idiopathic (of unknown,

presumed genetic, cause) or symptomatic (associated with a known or

suspected underlying lesion). Benign occipital epilepsies usually begin in

childhood and are discussed elsewhere.

Occipital seizures usually begin with visual hallucinations like flickering or

colored lights, rapid blinking, or other symptoms related to the eyes and

vision. They may occur spontaneously but can often be triggered by

particular visual stimuli, such as seeing flashing lights or a repeating pattern.

Occipital seizures are often mistaken for migraine headache because they

share similar symptoms including visual disturbances, partial blindness,


nausea and vomiting, and headache. The following are the different types of

seizure symptoms associated with occipital lobe seizures:

Visual hallucinations and/or illusions

Blindness or decreased vision

Pallinopsia or image repetition (image replayed again and again) can occur,

and other corresponding symptoms can include:

Sensation of eye movements

Eye pain

Involuntary eye movement to one or other side

Nystagmus or eye jerking to one or other side (rapid involuntary

rhythmic eye movement, with the eyes moving quickly in one direction

(quick phase), and then slowly in the other (slow phase)

Eyelid fluttering

As with any epilepsy syndrome, detailed patient history, neurological

examination, and EEG are very important. In occipital lobe epilepsy, the EEG

may provide information that is very helpful in making the correct diagnosis.

An abnormal response in the EEG to intermittent photic stimulation (rapidly

flashing strobe light) often occurs in occipital lobe epilepsy; however, this

response can occur in other epilepsy syndromes as well.

Treatment with a drug used for partial epilepsy, often carbamazepine, is

usually effective. In intractable cases (those that do not respond to

medication), surgical options may be considered.


Primary Generalized Epilepsy

Primary Generalized Epilepsy (PGE), also called Idiopathic Generalized

Epilepsy (IGE), refers to an epilepsy syndrome of idiopathic or unknown

cause. An idiopathic disease is a primary or intrinsic disorder that cannot be

attributed to a known underlying condition. So, while other types of epilepsy

may be caused by a brain tumor, stroke, or other neurological disorder,

idiopathic epilepsy is a primary brain disorder of unknown cause. In fact,

most idiopathic epilepsy syndromes are presumed to be due to a genetic

cause, but in most cases the specific genetic defect is not known and a

family history of epilepsy may not be present.

There are a number of different PGE syndromes. Each syndrome has its own

characteristic seizure type(s), typical age of onset, and specific EEG

patterns. Some of these syndromes are:

Childhood absence epilepsy

Juvenile myoclonic epilepsy

Juvenile absence epilepsy

Epilepsy with generalized tonic-clonic seizures on awakening

Generalized epilepsies with febrile seizures

Primary generalized epilepsy is a generalized type of epilepsy, which means

there is no single part of the brain where seizures originate. In fact, EEG

results may show epileptic discharges affecting the entire brain. The types of

seizures patients with PGE exhibit may include myoclonic seizures and

absence seizures.


Generalized Tonic-Clonic Seizures in PGE

The seizures in PGE usually respond well to medication. Some of the more

commonly prescribed medications for these syndromes include: valproate,

lamotrigine, topiramate, levetiracetam; and, in childhood absence epilepsy,

ethosuximide.

Nearly all patients with PGE begin having seizures in childhood or

adolescence. Most patients with childhood absence epilepsy (CAE) start

having seizures before age 10, and “outgrow” their seizures within a few

years, meaning that they no longer need medication to control their

seizures. On the other hand, juvenile myoclonic epilepsy (JME) is generally

considered a life-long disease. Once seizures start, usually in adolescence,

most patients need medication treatment for life to prevent seizure

recurrence. Individuals with PGE syndromes usually have normal

development and intelligence.

Idiopathic Partial Epilepsy

Just as there are generalized epilepsies of unidentifiable, presumably

genetic, cause, there are also partial epilepsy syndromes of unknown or

idiopathic cause, or idiopathic partial epilepsies. An idiopathic disease is a

disorder that cannot be attributed to a known underlying condition. So, while

other types of epilepsy may be caused by a brain tumor, stroke, or other

neurological disorder, idiopathic partial epilepsy is a primary brain disorder

of unknown cause. In fact, most idiopathic epilepsy syndromes are

presumed to be due to a genetic cause, but in most cases the specific

genetic defect is not known and a family history of epilepsy may not be

present.


Benign Rolandic Epilepsy

There are a few idiopathic partial epilepsy syndromes. Each individual

syndrome generally has its own characteristic seizure type(s), typical age of

onset, and specific EEG patterns. Some of these syndromes are known as:

benign rolandic epilepsy (also known as benign epilepsy of childhood with

centrotemporal spikes), early onset benign childhood occipital epilepsy, and,

late onset benign childhood occipital epilepsy.

The seizures in idiopathic partial epilepsy typically respond well to

medications used for other partial epilepsy syndromes. However, depending

on the seizure type, time of day, and frequency, some providers and parents

choose not to treat the individual with medication at all. For example, a

patient with benign rolandic epilepsy who experiences rare nocturnal

seizures consisting of only brief face and arm twitching may do well without

any medication treatment.

Though the prognosis of these syndromes varies by syndrome type, it is

usually quite good. Younger patients with these syndromes most often

“outgrow” their seizures by teenage years or young adulthood, and also

have normal intelligence and motor skills.

Symptomatic Generalized Epilepsy

Symptomatic Generalized Epilepsy (SGE) refers to epilepsy syndromes in

which the majority of seizures are generalized, but partial onset seizures can

also occur. The types of generalized seizures that occur in SGE include

myoclonic, tonic, atonic, atypical absence, and generalized tonic-clonic.

Virtually any type of partial onset seizure can also occur, depending on the

underlying brain pathology. Usually (but not always) there is a known

underlying brain disorder or injury, which is often severe. These syndromes


may occur in the setting of certain neurological diseases, such as tuberous

sclerosis (a rare genetic mutation that affects several organ systems), or

may be due to lack of oxygen at birth, trauma, infection, developmental

malformations, chromosomal abnormalities or other causes. SGE syndromes

typically begin in early life.

The following is a list of some symptomatic generalized epilepsy syndromes:

West Syndrome

Lennox-Gastaut Syndrome

Epilepsy with myoclonic-astatic seizures

Epilepsy with myoclonic absences

Early myoclonic encephalopathy

Early infantile epileptic encephalopathy with suppression burst

Progressive myoclonic epilepsies

Antiepileptic medications are the mainstay of treatment in SGE, though

certain syndromes may require additional treatments including

adrenocorticotropic hormone (ACTH) or immunoglobulin. The ketogenic diet

may be helpful in some patients. Additionally, the vagus nerve stimulator

has been studied extensively in patients with SGE. In some patients it has

been very helpful, while others have experienced no benefit. In patients with

atonic (drop) seizures, a surgical procedure called corpus callosotomy may

help reduce the falls that may result from seizures.

There are, however, some SGE syndromes in which other surgical options

may be considered. In tuberous sclerosis, for example, where the epilepsy is

often considered a SGE syndrome, certain tubers may be more epileptogenic

than others. If such a tuber is found to be the cause of the most disabling

seizures, removal of it could reduce the frequency of seizures.


The prognosis of SGE depends largely on the underlying cause of the

seizures. For example, up to 15-30% of patients with West syndrome,

affecting infants, without known cause become seizure free and have normal

or near normal intelligence. However, patients with Lennox-Gastaut

Syndrome or progressive myoclonic epilepsy tend to have seizures

throughout life, and some level of cognitive impairment.

Progressive Myoclonic Epilepsy

Progressive myoclonic epilepsies are rare and frequently result from

hereditary metabolic disorders. They feature a combination of myoclonic and

tonic-clonic seizures. Unsteadiness, muscle rigidity, and mental deterioration

are often also present.

Progressive myoclonic epilepsies are treated with medication, which usually

proves to be successful for a short period of time (months to years).

However, as the disorder progresses, drugs become less effective and

adverse effects may be more severe as more drugs are used at higher

doses. Valproate and zonisamide are most commonly used. Other commonly

prescribed drugs include clonazepam, lamotrigine, topiramate, phenobarbital

and carbamazepine. Types of progressive myoclonic epilepsies include:

Mitchondrial Disorders, involving mutation of genes.

Unverricht-Lundborg Syndrome, a myoclonic disorder.

Reflex Epilepsy

In reflex epilepsies, seizures are triggered by specific stimuli in the

environment. In the most common type of reflex epilepsy, flashing lights

trigger absence, myoclonic or tonic-clonic seizures. This is called

photosensitive epilepsy, which usually begins in childhood and is often


outgrown by adulthood. Other environmental triggers in reflex epilepsy

include sounds such as church bells, a certain type of music or song, or a

person’s voice. For some people, activities such as arithmetic, reading,

writing, and even thinking about specific topics can provoke seizures. These

non-visual stimuli may trigger generalized or partial-onset seizures. Some

patients with reflex epilepsy can have spontaneous seizures that occur

without exposure to their specific trigger.

A two-pronged approach is usually best in treating reflex epilepsy; avoiding

the triggering stimulus as much as possible, and treatment with antiepileptic

drugs. Valproate, carbamazepine and clonazepam have been most

commonly prescribed to control reflex seizures, although lamotrigine,

levetiracetam and other newer antiepileptic medication are promising.

Epilepsy Syndromes In Children

Epilepsy syndromes are defined by a distinctive combination of clinical

features, signs and symptoms, and electrographic patterns, which often

begin in childhood. Medical specialists in the field of neurology generally use

the International League Against Epilepsy (ILAE) classification system to

categorize seizure types and epilepsy syndromes. While the ILAE

classification system is instrumental to diagnose and guide therapeutic

approach, there is ongoing research and evidence that suggests the

observable characteristics and possible biochemical causes of the various

epileptic syndromes may be broader than previously recognized. It is

important for clinicians to realize that the epilepsy classification system will

continue to change and revise clinical descriptions of epilepsy syndromes for

clinicians to diagnosis and plan treatment, beginning during infancy and

childhood. There is also a subsection of pediatric epilepsy focused on

neonatal seizures, which will not be discussed here, nonetheless, it is a


unique and evolving area of epilepsy care. This section will focus on infancy

and childhood seizure disorders, diagnosis and treatment.4-7,18-22

Febrile Seizures

Children aged 6 months to 5 - 6 years may have tonic-clonic seizures when

they have a high fever. These are called febrile seizures and occur in 2% to

5% of children. There is a slight familial (hereditary) tendency toward febrile

seizures. In other words, the chances are slightly increased that a child will

have febrile seizures if their parents, brothers or sisters, or other close

relatives have had them.

The peak age of febrile seizures is about 18 months. The usual situation is a

healthy child with normal development, who has a viral illness with high

fever. As the child's temperature rapidly rises, he or she has a tonic-clonic

seizure. The seizure usually involves muscles on both sides of the body.

Febrile seizures can be as short as one or two minutes, or as long as 30

minutes or more. They also can be repetitive. In most instances,

hospitalization is not necessary, although a prompt medical consultation is

essential after the first seizure.

Most children with recurrent febrile seizures do not require daily antiepileptic

drug therapy. Children who have had more than three febrile seizures or

prolonged febrile seizures, or who have seizures when they have no fever,

are usually treated with antiepileptic drugs including phenobarbital and/or

valproate. Diazepam, if given by mouth or rectum at the time of fever, has

been used effectively to both treat and prevent recurrent febrile seizures.

However, the dose that is effective when given by mouth can cause

irritability, insomnia, or other troublesome side effects that last for days.


The prognosis for febrile seizures is excellent. There is no reason for a child

who has had a single febrile seizure to receive antiepileptic drugs unless the

seizure was unusually long or other medical conditions warrant it.

Recurrence rates or the chances of having another seizure vary from 50% (if

the seizure occurred before age one year) to 25% (if the seizure occurred

after that age). In addition, 25% to 50% of recurrent febrile seizures are not

preceded by a fever. In some cases, the seizure is the first sign of an illness

(usually viral) and the fever comes later.

The vast majority of children with febrile seizures do not have seizures

without fever after age five. Risk factors for later epilepsy include:

Abnormal development before the febrile seizure.

Complex febrile seizures (seizures lasting longer than 15 minutes,

more than one seizure in 24 hours, or body movements during the

seizure restricted to one side).

A history of seizures without fever in a parent or a brother or sister.

If none of these risk factors is present, the chances of later epilepsy are the

same or nearly the same as in the general population. If one risk factor is

present, the chances of later epilepsy are 2.5%; and, if two or more risk

factors are present, the chances of later epilepsy range from 5% to over

10%. Rarely, febrile seizures that last more than 30 minutes may cause scar

tissue in the temporal lobe and chronic epilepsy that can be effectively

treated with medication or a temporal lobectomy.

Benign Rolandic Epilepsy

Benign rolandic (sylvian) epilepsy (BRE, also called BECTS (benign epilepsy

of childhood with centrotemporal spikes), is a common childhood seizure


syndrome, with seizures beginning between 2 and 13 years of age. A

hereditary factor is often present. The seizures most commonly observed in

BRE are partial motor seizures (twitching) or a sensory seizure (numbness or

tingling sensation) involving the face or tongue and which may cause

garbled speech. In addition, tonic-clonic seizures may occur, especially

during sleep. Although the seizures are often infrequent, or may occur in

infrequent clusters, some patients need medication. These include children,

in addition to the typical seizure disorder, that have daytime seizures, a

learning disorder, a mild mental handicap, or multiple seizures at night,

which leave the child lethargic in the morning.

The EEG shows a characteristic pattern of abnormal spikes over the central

and temporal regions of the brain, especially during sleep. Despite the

abundant abnormal spike activity, the child may have only one or a few

seizures. This illustrates that the amount or frequency of abnormal spike

activity in the EEG is not necessarily related to the severity of the epileptic

disorder. Siblings or close relatives may have the same EEG pattern during

childhood without ever having seizures.

The seizures are usually easily controlled with low to moderate doses of

carbamazepine, oxcarbazepine, or gabapentin (or, outside the United States,

clobazam). Medication is usually continued until age 15, when the seizures

spontaneously stop in almost all patients.

Juvenile Myoclonic Epilepsy

Juvenile myoclonic epilepsy (JME) accounts for about 7% of the cases of

epilepsy, making it one of the most common epilepsy syndromes. The

syndrome is defined by myoclonic seizures (jerks) with or without tonic-

clonic or absence seizures. The EEG usually shows a pattern of intermittent


spike-and-wave or polyspike-and-wave, even in between seizures. CT and

MRI scans of the brain are normal and typically are not needed.

Seizures usually begin shortly before or after puberty, or sometimes in early

adulthood. They usually occur in the early morning, within a couple hours of

awakening. Persons with JME often have photosensitive myoclonic seizures

in addition to spontaneous seizures. The intellectual functions of persons

with JME are the same as those in the general population.

Juvenile myoclonic epilepsy often has a genetic basis. In some families,

genes associated with an increased risk of JME are located on chromosomes

6, 8, or 15. The chance that a child born to a parent with JME will also have

JME is about 15%. In most cases, the seizures are well controlled with

medication, but the disorder is lifelong. Valproate is the treatment of choice.

Other options include lamotrigine, levetiracetam, or topiramate.

Carbamazepine may actually worsen the myoclonic jerks.

Infantile Spasms

Infantile spasms (West's syndrome), a very uncommon form of epilepsy,

begins between 3 and 12 months of age. The seizures, or spasms, consist of

a sudden jerk followed by stiffening. With some spells, the arms are flung

out as the body bends forward (also called jackknife seizures). Other spells

have more subtle movements limited to the neck or other body parts. A

brain disorder or brain injury, such as birth trauma with oxygen deprivation,

precedes the seizures in 60% of these infants, but in the other 40% no

cause can be determined, and development is normal prior to the onset of

seizures.


Several antiepileptic drugs and hormonal therapy can be used to treat

infantile spasms. Some experts recommend a trial of an antiepileptic drug

(i.e., vigabatrin, valproate, topiramate) before hormonal therapy, but others

use hormonal therapy as the first treatment. In countries where it is

available, vigabatrin is often used as the initial therapy because it is

relatively safe (especially for short-term use) and effective. Vigabatrin is

especially effective in children with infantile spasms due to tuberous

sclerosis (a disorder associated with abnormalities involving the brain, skin,

heart, and other parts of the body).

If vigabatrin does not control the seizures in 3 or 4 days, adrenocorticotropic

hormone (ACTH) is usually used next. ACTH is a hormone made by the

pituitary gland. It stimulates the adrenal glands to make and release

additional cortisol, which acts much like prednisone. ACTH has been proven

to be slightly more effective than prednisone, but it must be given as an

injection, once a day for the first several weeks, then every other day.

Steroid hormones such as prednisone, on the other hand, can be given by

mouth. ACTH stops seizures in more than half of children with infantile

spasms.

In the United States, ACTH is often used as the first therapy and is typically

given for 1 month. The dosage is highest during the first 2 weeks and then

usually lowered gradually. The adverse effects of ACTH depend on the dose

used, the duration of therapy, and the baby’s sensitivity to the drug.

Although rare allergic reactions may occur, all other adverse effects occur

because ACTH stimulates the infant’s body to produce cortisol, a steroid

hormone. Excessive cortisol can cause the following:

Irritability

Increased appetite


High blood pressure

Kidney problems

Redistribution of body fat to make the face and trunk fatter and the

arms and legs thinner

Increased risk of infection or gastrointestinal bleeding

Metabolic changes that alter the concentrations of glucose (sugar),

sodium, and potassium in the blood

For most babies with infantile spasms, the adverse effects of ACTH can be

safely managed. Often the baby will be given another anti-epileptic drug

after the spasms have stopped and the ACTH therapy has been completed.

The future course of the disorder and of the child's development is related to

the cause of the seizures, the child's intellectual and neurological

development before the seizures began (the better the condition at that

time, the better the outlook), and whether they are controlled quickly. The

sooner therapy is begun, the better the results. When the spasms stop,

some children will later develop other types of seizure. Untreated children

often have frequent spasms for many years, and later develop partial and

generalized seizures. Approximately one-fifth of the cases of West’s

syndrome will evolve into Lennox-Gastaut syndrome.

Lennox-Gastaut Syndrome

Lennox-Gastaut syndrome is serious but uncommon. Three things define it:

Difficult-to-control generalized seizures

Mental handicap

Slow spike-and-wave pattern on the EEG


The seizures usually begin between 1 and 6 years of age, but can begin

later. The syndrome involves some combination of tonic, atonic, atypical

absence, myoclonic, and tonic-clonic seizures that are usually resistant to

medications. Useful medications for controlling the seizures of patients with

Lennox-Gastaut syndrome include valproate, carbamazepine, clobazam (not

available in the U.S.), lamotrigine, and topiramate. Felbamate is also an

effective drug and can often improve behavior and quality of life, but it

carries a risk of life-threatening blood or liver disorders and must be used

carefully.

In children or adults with frequent, poorly controlled seizures, it is often wise

to avoid high doses of antiepileptic drugs because they may intensify the

behavioral, social, and intellectual problems, especially when two or more

drugs are used together. It may be better to tolerate slightly more frequent

seizures in order to have a more alert and attentive family member.

In those patients whose seizures are not controlled with medication, there

are other options. These include the vagus nerve stimulator, the ketogenic

diet or corpus callosotomy (a palliative surgical procedure). Vagus nerve

stimulation or corpus callosotomy can be helpful treatments for some

patients. However, experts typically recommend vagus nerve stimulation

before consideration of corpus callosotomy because of lower risks.

Most children with Lennox-Gastaut syndrome have intellectual impairment

ranging from mild to severe. Behavioral problems are also common and

probably relate to a combination of the brain dysfunction, seizures, and

antiepileptic drugs. The course of the seizures varies greatly. Some children

will later have fairly good seizure control. Others will continue to have

multiple types of poorly controlled seizures throughout life.


The intellectual and behavioral development of children whose seizures come

under fair to good control may be almost normal, but the development of

those who have frequent seizures and are given high doses of more than

one drug may be severely delayed. This syndrome usually persists into

adulthood and affected persons often need to live in a residential foster care

or group home when their parents are no longer able to care for them.

Childhood Absence Epilepsy

Absence seizures are generalized seizures that occur in school-aged children

usually between the ages of 5 and 9. Sometimes childhood absence epilepsy

(CAE) can be inherited, but it can also occur as a sporadic event. Typical

absence seizures consist of sudden cessation of movement, staring, and

sometimes blinking. Sometimes, there may be a mild loss of body tone,

causing the child to lean forwards or backwards slightly. Unlike other types

of seizures, absence seizures occur without an aura or warning. When

diagnosing CAE, typical absence seizures need to be differentiated from

atypical absence seizures, which can occur at an earlier age. An EEG of a

child with CAE will show a typical pattern known as 3-Hz generalized spike

and wave complexes.

Many children with CAE have normal neurological examinations and

intellectual abilities. However, some children may have developmental and

intellectual impairments and may have other types of seizures including, but

not limited to, tonic clonic seizures. The medications that are usually used to

treat CAE include ethosuximide and valproic acid, but other medications can

also be used successfully. Usually children are treated for a minimum of 2

years.


The prognosis for CAE is excellent. Remission can be achieved in

approximately 80% of patients. Close attention must be paid to seizure

control to avoid academic or social difficulties.

Benign Occipital Epilepsy

In this epilepsy syndrome, seizures usually begin between the ages of 5 and

7, and originate in the occipital lobe. Seizure symptoms often include the

following:

visual hallucinations

loss of vision, or forced deviation of the eyes

vomiting

The hallucinations can take any form, but tend to be of brightly colored

shapes of all sizes. Children may then complain of intense headache and

may have extended periods of nausea and/or vomiting. Benign occipital

epilepsy (BOE) can sometimes be mistaken for migraines due to the visual

changes and headaches associated with this type of epilepsy. In addition to

hallucinations and visual disturbances children may also experience jerking

movements on one side of their body.

The EEG of a child with BOE shows spikes in the occipital region of the head

during sleep, or when the eyes are closed during wakefulness. An MRI scan

of the brain will be normal. By definition, BOE is not caused by a structural

lesion or abnormality. Since the seizures are of partial origin, medications

such as carbamazepine and oxcarbazepine are good treatment options.

Children with BOE are usually neurologically normal and complete seizure

control can be attained in 60% of patients.


Mitochondrial Disorders

Mitochondria are the energy factories of the cell. Abnormalities in

mitochondrial DNA or genes produce metabolic disorders that affect different

parts of the body, including muscle and brain. Mitochondrial disorders can be

inherited or sporadic. When inherited, the abnormal genes always come

from the mother, since all mitochondria are of maternal origin. Two

mitochondrial disorders can be associated with epileptic seizures: one is

MELAS (mitochondrial encephalopathy lactic acidosis) where there is too

much lactic acid in the blood, and the other is a stroke-like episode. MELAS

can lead to stroke-like episodes in younger persons (usually before the age

of 40), seizures, dementia, headaches, vomiting, unsteadiness, and ill

effects from exercise. Persons with MELAS can have both generalized

(including myoclonic and tonic-clonic) and partial seizures.

The other mitochondrial disorder with epileptic seizures is MERRF, which

stands for myoclonic epilepsy with ragged red muscle fibers. MERRF is one of

the progressive myoclonic epilepsies. It can also be associated with hearing

loss, unsteadiness, dementia, and ill effects from exercise. In addition to

myoclonic seizures, patients with MERRF often have generalized tonic-clonic

seizures. There are other mitochondrial disorders that do not fit clearly into

the MELAS or MERRF syndromes but which can cause epilepsy and additional

neurological problems.

There is no specific cure yet for mitochondrial disorders. Treatment is geared

towards controlling symptoms and slowing the progression of the disease. A

medical provider may prescribe a combination of supplements such as Co-

enzyme Q-10 or L-Carnitine in addition to other supplements. For patients

who have isolated deafness, evaluation for a cochlear implant may be

possible. For patients with seizures, standard antiepileptic medications are


used, such as those mentioned below in the section on anti-epileptic

medications.

Landau-Kleffner Syndrome

The Landau-Kleffner syndrome (acquired epileptic aphasia) is another rare

disorder. Acquired aphasia means the loss of language abilities that had

been present. In the typical case, a child between 3 and 7 years of age

experiences progressive language problems, with or without seizures. The

language disorder may start suddenly or slowly. It usually affects auditory

comprehension (understanding spoken language) the most, but it may affect

both understanding speech and speaking ability, or it may affect speaking

only. Seizures are usually rare and often occur during sleep. Simple partial

motor seizures are most common, but tonic-clonic seizures can also occur.

Seizure control is rarely a problem.

The EEG is often the key to the diagnosis. A normal EEG, especially one

done when the child is awake, does not rule out this disorder. Sleep

activates the abnormal spike activity, and therefore sleep recordings are

extremely important.

The boundaries of the Landau-Kleffner syndrome are imprecise. Some

children may first have a delay in language development followed by a loss

of speech abilities. Landau-Kleffner syndrome (or a variant of it) may also

occur in some children in whom language function never develops, or in

others whose language skills move backward but who very seldom have

spike-wave discharges on the EEG. The exact relationship between the EEG

findings and the language disorder is imprecise, although in some cases the

epilepsy activity may contribute to the language problems.


Standard antiepileptic drugs may help the seizures but are ineffective in

treating the language disorder. Steroids are effective in some children,

improving both the EEG abnormalities and the language problems. A form of

epilepsy surgery, multiple subpial transections, may improve both the EEG

abnormalities and the language disorder in a small number of children, but

results to confirm this finding are still coming in from various epilepsy

centers. In some cases, intravenous immunoglobulin (IVIG) has proven to

be helpful.

Rasmussen Syndrome

Rasmussen syndrome usually begins between 14 months and 14 years of

age and is associated with slowly progressive neurologic deterioration and

seizures. Seizures are often the first problem to appear. Simple partial motor

seizures are the most common type, but in one-fifth of these children, the

first seizure is an episode of partial or tonic-clonic status epilepticus.

Although Rasmussen syndrome is rarely fatal, its effects are devastating.

Progressive weakness on one side (hemiparesis) and mental handicap are

common, and language disorder (aphasia) often occurs if the disorder affects

the side of the brain that controls most language functions, which is usually

the left side.

Mild weakness of an arm or leg is the most common initial symptom besides

seizures. The weakness and other neurologic problems often begin 1 to 3

years after the seizures start. CT and MRI scans of the brain show evidence

of a slow loss (atrophy) of brain substance. Recent studies suggest that the

cause of Rasmussen’s syndrome is an autoimmune disorder (antibodies are

produced against the body’s own tissues) directed against receptors on the

brain cells. The process may be triggered by a viral infection.


Treatment of this disease with antiepileptic drugs has been disappointing.

Steroids may be effective, but additional studies are needed. Immunologic

therapies (gamma globulin, plasmapheresis, prednisone) may be helpful in

some cases. In children with severe weakness and loss of touch sensation

and vision on the side of the body opposite to the involved hemisphere of

the brain, a surgical procedure called a functional hemispherectomy may be

successful.

Hypothalamic Hamartoma & Epilepsy

Small tumors in the base of the brain that affect the hypothalamus can

cause a syndrome consisting of abnormally early puberty, partial seizures

with laughing as a frequent feature, and increased irritability and aggression

between the seizures. The partial seizures may be simple or complex and

there may be secondary generalized tonic-clonic seizures.

Affected individuals are often short and have mild abnormalities in their

physical features (dysmorphisms). A high-quality MRI brain scan is

necessary for diagnosis. If the tumor extends beyond the hypothalamus and

below the brain, treatment with surgery may be an option. Antiepileptic

drugs can also be beneficial, as well as drugs aimed at hormonal and

behavioral problems, if needed.

Treatment Of Epilepsy

Treatment is typically required to control the seizures associated with

epilepsy. However, some patients may not require treatment. The initiation

and continuation of treatment will depend on a number of factors, including

the severity of the condition, the extent and duration of seizures, the

presence of other physical conditions, and the patient’s individual needs.


Therefore, it is important for providers to work with each patient to

determine what type of treatment will best meet the needs of the patient.

In addition, regular monitoring is crucial once treatment is initiated, as the

patient may require adjustments depending on how he or she responds to

the therapy. This is especially crucial when treating the patient

pharmacologically.9 Some patients will require lifelong treatment to manage

their seizures, while others will only require short term, intermittent

treatment to manage symptoms. In many instances, patients will only

experience seizures during specific periods during their lifetime. In fact, a

number of cases of epilepsy will include seizures that present in childhood

and diminish over time.10 In these instances, treatment will only be required

during the time that the patient is experiencing seizures. The following

guidelines are typically used when determining if treatment is required:8

Usually, Anti-Epileptic Drug (AED) treatment will not begin until after an individual has

had a second seizure. This is because a single seizure is not a reliable indicator that an

individual has epilepsy. In some cases, treatment will begin after a first seizure if:

An electroencephalogram (EEG) test shows brain activity associated with epilepsy.

A magnetic resonance imaging (MRI) scan shows damage to the brain.

The patient has a condition that has damaged the brain, such as a stroke.

For some people, surgery may be an option. However, this is only the case if removing

the area of the brain where epileptic activity starts would not cause damage or disability.

If successful, there is a chance the epilepsy will be cured.

If surgery is not an option, an alternative may be to implant a small device under the skin

of the chest. The device sends electrical messages to the brain. This is called vagus nerve

stimulation.


A variety of treatment options are available to patients experiencing epileptic

seizures. Most patients will attempt to manage their symptoms through non-

pharmacologic therapies. If these treatments are not successful, the patient

will begin pharmacologic treatment.11

Ketogenic Diet

Some patients will attempt to manage the symptoms of epilepsy through a

change in diet. The ketogenic diet is a high fat, low carbohydrate diet that

has been shown to reduce symptoms of epilepsy, especially in children.12

While the diet is effective, it is also very difficult to manage and can be quite

limiting for the patient. The success of the ketogenic diet relies on strict

adherence to carbohydrate restriction. Therefore, patients cannot allow any

flexibility in their daily eating patterns.

When excess amounts of carbohydrates are consumed, the patient will

“reset” ketone metabolism for up to two weeks, which will minimize the

efficacy of the diet in managing seizure activity. Many patients find the diet

too restrictive and are unable to fully adhere to it. In fact, less than ten

percent of patients are able to commit to the diet for more than a year.12

Ketogenic, and in some instances, modified Atkins diets have been shown to

reduce epileptic seizures by approximately fifty percent. The most significant

results occur in patients who reduce daily carbohydrate levels to ten grams

or less per day. However, some patients will still experience a reduction in

seizures while allowing for a higher number of carbohydrates each day. In

these patients, twenty to thirty grams of carbohydrates appears to be an

appropriate number.13 The diet is especially successful in children, but does

appear to be helpful in adults experiencing epileptic seizures.


In most cases, patients will require a period of adjustment to determine if

the diet will reduce symptoms. Often, medical providers will require patients

to adhere to the diet for three months before making a determination

regarding its effectiveness.13 In the early stages of the diet, the patient will

continue medication. However, once the patient has had time to adjust to

the diet, medication will be tapered. The eventual goal is complete

discontinuation, but, in some instances, the patient will still require low

doses of medication.14

While the ketogenic diet is quite effective, there are some potential side

effects.15 Reported side effects include dehydration, constipation, and,

sometimes, complications from kidney stones or gall stones. Adult women

on the diet may have menstrual irregularities. Pancreatitis (inflammation

of the pancreas), decreased bone density and certain eye problems have

also been reported. Again, this is why the medical team closely follows

children or adults who are on the diet.

The diet lacks several important vitamins, which have to be added

through supplements. Sometimes high levels of fat build up in the blood,

especially if a child has an inborn defect in ability to process fat. This

possibility can lead to serious effects, which is another reason for careful

monitoring.

The ketogenic diet is very effective, but it is not the right treatment for all

patients. If a patient will be unable to adhere to the strict guidelines required

of the diet, it is not considered an appropriate method of treatment.

Therefore, the treating provider must work with the patient to determine of

if he or she is a viable candidate for diet therapy. If it is determined that the


patient is not suited for this type of treatment, other methods must be

considered.

Electroencephalography Biofeedback

Electroencephalography (EEG) biofeedback has been used to treat many

forms of epilepsy since the early 1970’s. It is especially helpful in treating

petit mal, grand mal, and complex partial seizures.16 In earlier years, the

technique was used infrequently, as it was quite expensive. In addition,

training for the procedure required a long-term commitment and was not

easily accessible.17 However, recent advances in technology and

methodology have made the procedure more affordable, while also reducing

the cost and length of training. Therefore, EEG biofeedback is utilized more

frequently as a treatment for epilepsy.

Although access to the procedure has increased the number of individuals

who revive biofeedback treatment, there are still discrepancies in the

outcomes experienced. Some patients will respond to treatment quickly,

requiring only a few sessions to experience a reduction in seizures. Other

patients may require a more extensive treatment period, often requiring 80

– 100 treatment sessions before experiencing any reduction in seizures.

Therefore, the procedure is still not a viable option for some patients. In

addition, many patients will require complementary treatment with other

therapies in conjunction with biofeedback.

In most instances, biofeedback is used as part of a comprehensive treatment

program that includes other therapies such as dietary management, lifestyle

changes, and pharmacologic intervention. This multi-faceted approach to

treatment typically produces the greatest results in patients who have more


severe cases of epilepsy. In patients with less severe cases, a single

treatment such as biofeedback is often adequate for reducing seizures.17

Biofeedback can help regulate behavioral disturbances in patients with

epilepsy, even when it does not eliminate seizures. In addition, it can help

reduce the dose of medication the patient requires to achieve seizure

elimination. The neurons in the brain are divided into bands, some slow,

some moderate and some fast, measured by cycles per second.17 The varied

bands of brain activity are outlined below.

Delta (.05-3 hertz)

Produced in deep, dreamless sleep

Theta (4-7 hertz)

Drowsiness, inattention, deep meditation. A person with epilepsy will

often produce bursts of theta.

Alpha (8-12 hertz)

General relaxation and meditation

SMR (sensorimotor rhythm) (12-15 hertz)

Relaxed concentration (often used for seizure control)

Beta (15-18 hertz)

Focused attention

Gamma (24 hertz and above)

Intense concentration or anxiety

EEGs of people with epilepsy appear as follows:

Spike-and-slow-wave

3-second spike-and-wave (Absence or Petit Mal)

During Tonic Clonic seizure


Melatonin

Melatonin is a hormone secreted by the pineal gland in the brain. It helps

regulate other hormones and maintains the body's circadian rhythm. It also

plays an important role in epilepsy treatment and management. Many

individuals with epilepsy have lower than normal melatonin levels. In fact,

seizure activity may be linked to the body’s need to increase melatonin

levels, as the individual experiences a significant increase of melatonin when

a seizure occurs.18 Therefore, some recent clinical studies have attempted to

link melatonin supplementation with reduced seizure activity. In some

studies, there was a direct link between melatonin supplementation and a

decrease in seizure activity, especially in children.19,21 However, other trials

have been inconclusive.

Since melatonin supplementation is relatively new, there is no standard

dosage amount that is recommended. Some individuals may only require low

doses, while others will benefit from a larger dose. The medical provider will

need to experiment with dosage amounts to identify the appropriate amount

for each patient.20

Melatonin can cause side effects in individuals. Therefore, the patient should

be closely monitored to ensure the side effects do not become problematic.

The most common side effects include:21

Some people may have vivid dreams or nightmares when they take

melatonin. Taking too much melatonin may disrupt circadian rhythms

(“body clock”).

Melatonin can cause drowsiness if taken during the day. If an

individual is drowsy the morning after taking melatonin, a lower dose

may be necessary.


Additional side effects include stomach cramps, dizziness, headache,

irritability, decreased libido, breast enlargement in men (called

gynecomastia), and decreased sperm count.

Pregnant or nursing women should not take melatonin because it could

interfere with fertility.

Some studies show that melatonin supplements worsened symptoms

of depression. For this reason, people with depression should consult

their medical provider before using melatonin supplements.

Melatonin may interact with various medications. The following table

provides an overview of the drugs that have the highest risk of interacting

with melatonin:

Antidepressant

medications

In an animal study, melatonin supplements reduced the

antidepressant effects of desipramine and fluoxetine. More

research is needed to know if the same thing would happen in

people. In addition, fluoxetine (a member of a class of drugs

called selective serotonin reuptake inhibitors, or SSRIs) can

cause low levels of melatonin in people.

Antipsychotic

medications

A common side effect of antipsychotic medications used to treat

schizophrenia is a condition called tardive dyskinesia, which

causes involuntary movements. In a study of 22 people with

schizophrenia and tardive dyskinesia caused by antipsychotic

medications, those who took melatonin supplements had fewer

symptoms compared to those who did not take the supplements.

Benzodiazepines The combination of melatonin and triazolam improved sleep

quality in one study. In addition, a few reports have suggested

that melatonin supplements may help people stop using long-

term benzodiazepine therapy, which is habit-forming.


Blood Pressure

Medications

Melatonin may make blood pressure medications like

methoxamine and clonidine less effective. In addition,

medications in a class called calcium channel blockers may lower

melatonin levels. Calcium channel blockers include:

Nifedipine

Amlodipine

Verapamil

Diltiazem

Felodipine

Nisoldipine

Bepridil

Beta-Blockers Use of beta-blockers may lower melatonin levels in the body.

Beta-blockers include:

Acebutolol

Atenolol

Bisoprolol

Carteolol

Metoprolol

Nadolol

Propranolol

Anticoagulant

Medications

Melatonin may increase the risk of bleeding from anticoagulant

medications such as warfarin.

Interleukin-2 In one study of 80 cancer patients, use of melatonin along with

interleukin-2 led to more tumor regression and better survival

rates than treatment with interleukin-2 alone.

Nonsteroidal Anti-

Inflammatory Drugs

(NSAIDs)

NSAIDs such as ibuprofen may lower levels of melatonin in the

blood.


Steroids and

Immunosuppressant

Medications

Melatonin may cause these medications to lose their

effectiveness. Do not take melatonin with corticosteroids or

other medications used to suppress the immune system.

Tamoxifen Preliminary research suggests that the combination of tamoxifen

(a chemotherapy drug) and melatonin may benefit some people

with breast and other cancers. More research is needed to

confirm these results.

Other Caffeine, tobacco, and alcohol can all lower levels of melatonin in

the body.

Vitamins

Many epileptic patients will benefit from supplementation with vitamins. In

many instances, epileptic seizures and other symptoms increase if the

patient is deficient in a specific vitamin.23 In other instances, patients may

benefit from an increase in nutritional supplementation as it will improve

basic body composition and increase the patient’s ability to withstand the

negative effects of epilepsy. The following section provides a thorough

overview of the vitamins most beneficial in epilepsy treatment:24-30

Folic Acid

Supplementation with folic acid on a daily basis is important for both women

as well as men. The vitamin named folic acid (also known as folate) is an

important part of the production of blood cells, of the function of some

nerves and to help prevent heart disease. Low levels (deficiency) of folic acid

can be the cause of intrauterine growth delay, inherited malformations,


miscarriages and neural tube defects in women, and heart disease in both

men and women.

For patients who have epilepsy, this is especially important since some

seizure medicines can cause low levels of folic acid by changing the way it is

absorbed in the body. Patients who take more than one seizure medicine

may be advised to take higher doses of folic acid. Babies born to women

who did not get enough folic acid early in their pregnancies are more likely

to have birth defects, especially a type called neural tube defects, which

affect the brain and spinal cord. The most well known such defect is spina

bifida, in which the spinal column is not completely closed. By the time a

woman knows for sure that she is pregnant, it may be too late to prevent

these defects.

Folic acid should be added to a person’s daily diet, either as food or as a

supplement, starting in the teenage years for women, and young adulthood

for men with epilepsy. Some providers recommend up to 4 mg per day for

patients who have been taking daily anti-seizure medications for many

years.

Epileptologists are now concerned that folic acid may be too low in persons

with epilepsy taking some antiepileptic drugs. Low serum and red blood cell

levels of folic acid in women of childbearing potential increase the risk of

fetal birth defects. For men and women, low levels of folic acid are

associated with elevated homocysteine and an increased risk for

cardiovascular disease. A convincing argument now develops that routine

folic acid supplementation is important for women and men receiving

antiepileptic drugs.


Folic acid (vitamin B9) is a water-soluble B vitamin that is essential for DNA

repair, cell division, and normal cellular growth. Low folic acid levels during

pregnancy in women with epilepsy have been associated with fetal

malformation, and older enzyme-inducing antiepileptic drugs are known to

reduce serum folate levels. As mentioned earlier, profound deficiency of folic

acid during pregnancy has been associated with neural tube defects such as

spina bifida. Deficiency in adults has been associated with megaloblastic

anemia and peripheral neuropathy. In both men and women, low serum

levels of folate can increase homocysteine levels, which are correlated with

elevated cardiovascular risk.

Certain antiepileptic drugs, but not all agents, can potentially decrease folate

levels, either via hepatic enzyme induction and/or decreased absorption.

Addressing the question of which patients on AEDs need folic acid

supplementation is challenging because it depends on whether the patient is

pregnant or has a history of epilepsy. For example, the risk of having a

pregnancy complicated by a major congenital malformation (i.e., neural tube

defect) is doubled in epileptic women taking AEDs compared with those

women with a history of epilepsy not taking these agents. In fact, that risk is

tripled with AED polypharmacy, especially when valproic acid is included.

Additionally, many AEDs are used for conditions other than epilepsy, such as

chronic pain and mood disorders, but the effect of AEDs on folate has not

been adequately assessed in this population.

There are some general guidelines about folic acid supplementation.

Consensus statements recommend 0.4-0.8 mg of folic acid per day in all

women planning a pregnancy. Ideally, this should be started at least 1

month prior to pregnancy if possible. These guidelines recommend higher

daily folic acid doses (4 mg/day) in women with a history of neural tube


defects. In addition, enzyme-inducing anticonvulsants, such as phenytoin,

carbamazepine, primidone, and phenobarbital, are known to decrease folate

levels, and valproic acid may interfere with folate metabolism. Other AEDs,

such as oxcarbazepine, lamotrigine, and zonisamide, do not appear to alter

folate levels.

Unfortunately, the effectiveness of folic acid supplementation for the

prevention of AED-induced teratogenicity and the appropriate dose of folic

acid for specific AEDs has not been determined. Not all studies designed to

determine effects of fetal AED exposure consistently demonstrate a

protective effect against congenital malformations with folic acid

supplementation. However, this may be due in part to inadequate dosage.

Because many pregnancies are unplanned, most authorities recommend that

folic acid supplementation be given routinely to all women of childbearing

potential at 0.4 mg/day. Women who have already had a child with a neural

tube defect are encouraged to consult with their clinician regarding

appropriate dosage, and those on AEDs should receive 0.4 - 4 mg/day.

Current data are inconclusive to support high-dose folic acid use in women

without epilepsy on AEDs for other indications, though supplemental folic

acid should not be regarded as harmful. For men and women on AEDs that

reduce folate levels, such as phenytoin, carbamazepine, primidone, and

phenobarbital, it seems prudent to monitor homocysteine and folate levels

and monitor for the development of megaloblastic anemia.

Guidelines have been developed for folate supplementation for women of

childbearing years to enhance patient education and awareness of the

potential vitamin deficiencies that can occur when taking antiepilepsy

medications (AED's). Guidelines on folate supplementation help to promote


the general health of women, and minimize potential birth defects associated

with folate deficiency.

Folate (or folic acid) deficiency and medications used to treat epilepsy are

associated with an increased risk of birth defects. Specifically, they are

associated with spina bifida and anencephaly, two of the most common and

severe neurologic birth defects. Clinical studies have shown that

supplementing a woman's diet with folate can reduce this risk by 50-75%.

In order to reduce the risk of neural tube defects, the Center for Disease

Control and Prevention (CDC) recommends that all women who are capable

of becoming pregnant should take 0.4 mg of folate each day. Neural tube

defects occur early in the pregnancy, often before a woman is aware that

she is pregnant. In addition, about one-half of pregnancies in the United

States are unplanned. Therefore, supplementation with folate should

continue throughout a woman's reproductive years. A woman who has a

family history of neural tube defects or has a previous child born with neural

tube defects should receive folate supplementation of 4.0 mg per day.

Guidelines for folate supplementation are as follows:

All women should supplement their diet by taking 1 prenatal

multivitamin each day. Prenatal multivitamins are available over-the-

counter (OTC) or by prescription. OTC prenatal multivitamins contain

0.8 mg of folate while prescription prenatal multivitamins contain 1.0

mg of folate. Generic multivitamins are generally the least expensive,

followed in order of expense by brand name over-the-counter

vitamins, and finally prescription tablets.

A woman who is planning on becoming pregnant or who is pregnant,

and has a family history of neural tube defects, or has had a previous


child born with neural tube defects, or is on either Tegretol or

Depakote, should receive 3.0 mg of folate in addition to a prenatal

multivitamin.

All other women who are planning to become pregnant or are pregnant and

taking an antiepilepsy medication other than Tegretol or Depakote should

receive 1.0 mg of folate in addition to a prenatal multivitamin.

Calcium

Calcium is an important element in the body, and so important that an

individual has more calcium in his or her body than any other mineral.

Calcium is a necessary part of bone formation, development and repair. The

majority of calcium in the body is stored within bones, while the rest is in

the blood and the body’s other fluids. Abnormal calcium levels may result in

major health problems. Both hypocalcemia (low calcium levels), and

hypercalcemia (high calcium levels) can cause seizures. The main sources of

calcium are dairy products, such as milk, yogurt and ice cream. Green leafy

vegetables, such as broccoli and kale, canned sardines and shellfish are also

good sources of calcium.

Initially, low calcium levels may not give any warning signs. However, as the

level decreases, a person may feel confused and have hallucinations,

memory loss and depression. Because of calcium’s importance in muscle

movement and the function of the nervous system, hypocalcemia can cause

muscle aches, spasms, stiffening of the muscles, and tingling sensations in

the face, mouth, lips, fingers and toes.

Low calcium levels can also cause several types of seizures, including the

following: tonic-clonic seizures, categorized by whole body shaking and loss


of consciousness; focal muscle seizures, during which a set of muscles

contract against a person’s will; and absence seizures, during which a

person appears to be staring off into space. Certain anti-seizure medications

can contribute to lowering calcium levels, especially when taken daily for a

long time period. This happens when the medication makes the liver work

harder than usual, and it causes the elimination of the calcium deposits from

the bone, leading to what is known as brittle bones, bone loss or

osteoporosis.

From a physiological perspective, it is logical that calcium supplementation

may be indicated when myoclonic seizures are encountered; when calcium

ion concentration falls below about one half of normal, tetanic contraction of

muscles throughout the body are likely to result because of spontaneous

nerve impulses in the peripheral nerves. Since calcitonin and the parathyroid

hormone affect serum calcium concentrations, it is possible that problems in

the production of either can lead to limited tetanic contractions.

Significant changes in important body chemicals such as calcium and

magnesium can cause seizures; so can a lack of certain vitamins. These

chemical changes may provoke a disturbance in the brain, or a single

seizure, by influencing the thresholds for firing. Calcium is a very important

mineral for the normal functioning of brain cells, and low levels of calcium

(hypocalcemia) can cause seizures. Hypocalcemia can be a consequence of

severe kidney disease when too much calcium escapes from the kidney into

the urine. It may also, but rarely, be caused by a hormonal problem that has

the same effects. A deficiency of magnesium, a mineral that interacts with

calcium, may cause low blood calcium and, thus, seizures. With a ketogenic

diet, a calcium supplement must be taken every day to be nutritionally

complete.


There is growing evidence that elevated extracellular calcium levels and

homeostatic calcium control mechanisms may be factors in developing

acquired epilepsy (epilepsy that occurred after an injury). It is important to

evaluate the possible functional consequences of altered CA 2+ dynamics in

epileptogenesis. The ability of the neuron to restore CA 2+ loads to resting

[CA 2+] is regulated by CA 2+ homeostatic mechanisms. Increased or

prolonged entry of extracellular CA 2+ could contribute to the altered CA 2+

homeostatic mechanisms in epilepsy. It is important to note that cellular

calcium levels tend to be inversely correlated with extracellular calcium

levels. Thus, it does not seem unreasonable to conclude that those without

injury could have seizures caused by calcium problems.

Those that were on long-term anticonvulsant medications had higher levels

of calcium than non-medicated controls. This might suggest that one of the

reasons that some of these medications are continued long-term is that, for

some people, they somehow increase the retention of calcium, which may

account for some of their anticonvulsant effects.

Some forms of juvenile myoclonic epilepsy can result from mutations of a Ca

2+ channel. This line of evidence suggests the involvement of channels

expressed in the brain in the pathogenesis of certain types of epilepsy. Ca

2+ influx into excitable cells is a prerequisite for neurotransmitter release

and regulated exocytosis. Within the group of ten-cloned voltage-gated Ca

2+ channels, the Ca(v) 2.3-containing E-type Ca 2+ channels are involved in

various physiological processes, such as neurotransmitter release and

exocytosis together with other voltage-gated Ca 2+ channels of the Ca(v)1,

Ca(v)2 and Ca(v)3 subfamily. The interaction of Ca(v) 2.3 with the EF-hand

motif containing protein EFHC1 is involved in the etiology and pathogenesis

of juvenile myoclonic epilepsy. However, E-type Ca 2+ channels also exhibit


several subunit-specific features, most of which still remain poorly

understood. While they are not fully understood, it seems apparent that

calcium control mechanisms play some role in myoclonic seizures.

Mutations in the calcium-sensing receptor gene (CaSR) may result in

disorders of calcium homeostasis manifesting as familial benign hypocalciuric

hypercalcemia (FBHH), neonatal severe hyperparathyroidism (NSHPT) or

autosomal dominant hypocalcemia with hypercalciuria (ADHH). The ADHH

condition may result in asymptomatic hypocalcemia and a minority

experience seizures in infancy, which can recur into adulthood.

Even in generalized seizures, epileptics are generally mildly hypocalcemic,

especially in the period before the seizure. Stress, which releases

epinephrine and corticotropin, results in high serum citrate concentration,

which probably contributes to decreased serum [Ca2+] just before a seizure.

Long-term treatment of epileptic children with various anticonvulsant

medications was found to raise the TSH and diminished T3 and T4.

Calcitonin levels were lowered as well. Long-term use of certain

anticonvulsant medications tended to impair at least a portion of thyroid

function.

Myoclonic seizures tend to be resistant to drug therapies. Since many anti-

epileptic medications impair thyroid function and/or somehow result in

increased calcium levels, perhaps a partial reason for their occasional

success with myoclonic seizures is the partial suppression of the thyroid

hormone calcitonin, which results in an increase of serum calcium levels.

There are scattered reports that the anticonvulsant medications

phenobarbital, carbamazepine, valproate, lamotrigine, gabapentin, and

vigabatrin can cause or induce myoclonic seizures in epileptics who had not


been experiencing those types of seizures. It is possible this occurs because

some anticonvulsant medications can reduce vitamin D levels. Other

researchers have thus suggested supplemental vitamin D when taking

certain anticonvulsant medications.

Myoclonic seizures can have an appearance of a limited tetanic contraction

associated with insufficient calcium levels. It is important to note that

others, while not specifically discussing myoclonic seizures, have also

suggested that somehow increasing calcium levels should be looked at for

the treatment of epileptics. Hence, it may be wise to consider nutritional

interventions that affect calcium levels as a first-line treatment. Currently,

this is rarely the case. Even though some antiepileptic drugs could also

worsen some types of seizures, it is known that other therapies can be

efficient in refractory epilepsies; steroids, vague nerve stimulation, ketogenic

diet and surgery, nutritional therapies (especially outside the ketogenic diet)

seem to be often overlooked. It should be noted that it is theoretically

possible that, for some types of seizures, calcium could be contraindicated.

Yet, it is not unheard of that nutrition, including calcium supplementation,

should be considered as a first-line treatment for intractable forms of

epilepsy, as others have sometimes advocated it (though this investigator

appears to be the first advocating supplemental calcium, vitamin D, etc., as

first-line nutrients, as well as first to advise nutrients specifically for

myoclonic seizures). One of the reasons that nutrition should be considered

as a front-line therapy is that it is low risk. Consumption of calcium-

containing foods and/or calcium-containing supplements is so safe that,

although calcium can react with some medications, over dosage has not

been reported with calcium supplements. Forms other than calcium

carbonate are preferred, as calcium carbonate may cause gastrointestinal


side reactions such as constipation, bloating, gas and flatulence. Prolonged

use of large doses of calcium carbonate — greater than 12 grams daily

(about 5 grams of elemental calcium) — may lead to milk-alkali syndrome,

nephrocalcinosis and renal insufficiency.

There is no specific quantitative recommendation for each possible

substance that could affect calcium levels, as the amount needed appears to

vary by individual (as well as size in the case of children). But irrespective of

the quantities, it does appear reasonable to conclude that calcium control

mechanisms can play a causal role in myoclonic seizures and that calcium

and other nutrients should be considered as possible front-line therapies for

these hard to treat myoclonic seizures.

Vitamin D

Vitamin D is a necessary part in the process of proper breakdown and use of

calcium. Because of this, vitamin D deficiency caused or worsened by daily

use of anti-seizure medications for a long time can make the bones very soft

and brittle, causing them to break more easily. Adding vitamin D to the daily

diet can prevent this. In addition, patients taking anti-seizure medications

should increase their calcium intake every day. Exposure to sunlight is a

natural way to speed up the body’s ability to produce vitamin D.

Nearly half of people with epilepsy are also vitamin D deficient, but despite

this well-known association, only a single study has been published on the

effect of vitamin D for seizure control in the last 40 years. That study

revealed that treating epileptic patients with vitamin D2 – the far inferior

type of synthetic vitamin D – reduced the number of seizures, and in 1974

researchers concluded that the results may support prophylactic vitamin D

treatment for individuals with epilepsy.


Now, nearly four decades later researchers continue to reveal that the

normalization of serum vitamin 25(OH)D [vitamin D] level provides an

anticonvulsant effect or protection against seizure activity. The findings are

even more important given that people with epilepsy face an even greater

risk of vitamin D deficiency than the general population (and even the

general population is vastly vitamin D deficient). The reasons are two-fold,

with the first being that having frequent seizures may interfere with a

person’s ability to get outdoors and stay active.

If an individual spends most of his or her time inside, regular sun exposure

will be missed, which is key for the natural production of vitamin D. Even

exposing the skin to sunlight through a windowpane will prevent the entry of

the UVB rays, which are the specific wavelength that produces vitamin D in

the skin. It is crucial for epilepsy patients to get outside and experience

direct skin contact with the sunlight instead of sunning in a sunroom, for

instance. Second, anti-epileptic drugs that are often given to epilepsy

patients can interfere with vitamin D metabolism, leading to deficiency. If

these drugs are taken, it is especially crucial that vitamin D levels are

actively monitored to avoid this side effect.

Vitamin D has a significant impact on epileptic seizures because epilepsy is a

disorder of the central nervous system, particularly of the brain. Vitamin D is

a vitamin that is also a neuroregulatory steroidal hormone that influences

nearly 3,000 different genes in the body. Vitamin D receptors can be found

in the brain, spinal cord, and central nervous system, and may enhance the

amount of important chemicals in the brain needed to protect brain cells.


Surgical Options

A number of individuals with epilepsy may benefit from surgical intervention.

There are a variety of surgical procedures that can help with various aspects

of the disorder. While medication is effective at controlling most seizure

activity, approximately thirty percent of individuals will not respond to

pharmacologic treatment and will require more advanced therapy.31 These

individuals often benefit from surgery.

There are three primary forms of surgery that are used to treat individuals

with epilepsy:32

Surgery to remove the area of the brain producing seizures

Surgery to interrupt the nerve pathways through which seizure

impulses spread within the brain

Surgery to implant a device used to treat epilepsy

Surgery is an invasive procedure and should only be considered if the

section of the brain where the seizures originate can be clearly identified. In

addition, the physician must ensure that surgery will not negatively affect

any areas that are responsible for critical functions.33,34 A thorough

assessment is required before determining if surgery is a viable option.

There are a number of different surgical procedures that can be used to treat

epilepsy. The specific type of surgery performed on a patient will be

determined based upon the type of seizures the patient is experiencing and

the area of the brain where seizure activity originates.31 The following

section provides an overview of the risks and benefits of various surgical

procedures.7,35-51


Procedure Description and Benefits/Risks

Vagus Nerve

Stimulation

(VNS)

VNS is a palliative technique that involves surgical implantation

of a stimulating device. VNS is FDA approved to treat medically

refractory focal-onset epilepsy in patients older than 12 years.

Some studies demonstrate its efficacy in focal-onset seizures and

in a small number of patients with primary generalized epilepsy.

Randomized studies showed modest efficacy at 3 months, but

post marketing experience showed delayed improvement in

another group of patients.

In August 2013, the American Academy of Neurology issued an

update to its 1999 guidelines on the use of VNS for epilepsy.

VNS is currently indicated for patients older than 12 years with

medically intractable partial seizures who are not candidates for

potentially curative surgical resections, as well as for the

adjunctive long-term treatment of chronic or recurrent

depression in patients older than 18 years with a major

depressive episode not adequately relieved by 4 or more

antidepressant treatments. Recent reports also indicate long-

term efficacy and successful VNS use in pediatric epilepsy and

other seizure types and syndromes.

Key recommendations of the updated guidelines include the

following:

VNS may be considered for (1) the adjunctive treatment

of partial or generalized epilepsy in children, (2) seizures

associated with Lennox-Gastaut syndrome, and (3)

improving mood in adults with epilepsy

VNS may have improved efficacy over time

Children should be carefully monitored for site infection

after VNS implantation

According to the manufacturer's registry, efficacy of the

stimulating device at 18 months is 40-50%, where efficacy is

defined as a seizure reduction of 50% or more.


Many patients report improvement in seizure intensity and

general mood. However, seizure-free rates for pharmacologically

intractable focal-onset epilepsy are less than 10%. A meta-

analysis of VNS clinical studies reported an average reduction in

seizures of at least 50% in approximately 50% of patients at last

follow-up. Although VNS was not initially FDA approved for

children or patients with generalized epilepsy, the authors also

found that these groups benefitted significantly from VNS.

Positive predictors of a favorable outcome with VNS therapy

include posttraumatic epilepsy and tuberous sclerosis. Few

patients achieve complete seizure freedom with VNS, and about

a quarter of patients receive no benefit in their seizure

frequency. Some patients have clinical improvement in terms of

milder and shorter seizures.

Multiple Subpial

Transection

Multiple subpial transection was pioneered as an alternative to

removal of brain tissue. It is used to control partial seizures

originating in areas that cannot be safely removed. For example,

if the seizure focus involves the dominant temporal-lobe

language area (Wernicke’s area), which is critical for

comprehension, the removal of this area to control seizures

would cause a devastating complication: the inability to

understand spoken or written language. Similarly, if the primary

motor area is part of the seizure focus, its removal would cause

permanent weakness on the opposite side of the body.

The operation involves a series of shallow cuts (transections) into

the cerebral cortex. The transections are made only as deep as

the gray matter, approximately a quarter of an inch deep.

Because of the complex way in which the brain is organized,

these cuts are thought to interrupt some fibers that connect

neighboring parts of the brain, but they do not appear to cause

long-lasting impairment in the critical functions served by these

areas.


Examination of brain tissue after multiple subpial transections

reveals that some nerve cells are destroyed.

Sometimes, brain seizures begin in a vital area of the brain - for

example, in areas that control movement, feeling, language, or

memory. When this is the case, a relatively new epilepsy

treatment called multiple subpial transection (MST) may be an

option. MST stops the seizure impulses by cutting nerve fibers in

the outer layers of the brain (gray matter), sparing the vital

functions concentrated in the deeper layers of brain tissue (white

matter). Most people with epilepsy can control their seizures with

medication. However, about 20% of people with epilepsy do not

improve with drugs. In some cases, surgery to remove the part

of the brain causing the seizures may be recommended.

MST may be an option for people who do not respond to

medication and whose seizures begin in areas of the brain that

cannot be safely removed. In addition, there must be a

reasonable chance that the person will benefit from surgery. MST

may be done alone or with the removal of a section of brain

tissue (resection). MST also may be used as a treatment for

children with Landau-Kleffner syndrome (LKS), a rare childhood

brain disorder which causes seizures and affects the parts of the

brain that control speech and comprehension.

Candidates for MST undergo an extensive pre-surgery evaluation

- including seizure monitoring, electroencephalography (EEG),

magnetic resonance imaging (MRI), and positron emission

tomography (PET). These tests help to pinpoint the area in the

brain where the seizures occur and determine if surgery is

feasible.

Another test to assess electrical activity in the brain is EEG-video

monitoring, in which video cameras are used to record seizures

as they occur, while the EEG monitors the brain's activity.


In some cases, invasive monitoring - in which electrodes are

placed inside the skull over a specific area of the brain - is also

used to further identify the tissue responsible for seizures.

MST requires exposing an area of the brain using a procedure

called a craniotomy. ("Crani" refers to the skull and "otomy"

means "to cut into.") After the patient is put to sleep with

anesthesia, the surgeon makes an incision (cut) in the scalp,

removes a piece of bone and pulls back a section of the dura, the

tough membrane that covers the brain. This creates a "window"

in which the surgeon inserts his or her surgical instruments. The

surgeon utilizes information gathered during pre-surgical brain

imaging to help identify the area of abnormal brain tissue and

avoid areas of the brain responsible for vital functions.

Using a surgical microscope to produce a magnified view of the

brain, the surgeon makes a series of parallel, shallow cuts

(transections) in gray matter, just below the pia mater (subpial),

the delicate membrane that surrounds the brain (it lies beneath

the dura). The cuts are made over the entire area identified as

the source of the seizures. After the transactions are made, the

dura and bone are fixed back into place, and the scalp is closed

using stitches or staples. There may be bleeding at the site of

the transection, but the procedure is generally well tolerated.

Major complications appear to be rare. Transections in language

areas may cause mild impairments in the language function

served by that area.

The risks and benefits of multiple subpial transections need to be

better defined. Multiple subpial transections can help reduce or

eliminate seizures arising from vital functional cortical areas.

Transections have been used successfully in Landau-Kleffner

syndrome, a disorder in which language problems appear in a

child whose language was previously developing normally.


One concern is that the epileptic activity may recur after a period

of 2 to 20 months. It is uncertain whether this procedure can

achieve long-term seizure control

Temporal Lobe

Resection

The most common surgical procedure performed for epilepsy is

the removal of a portion of the temporal lobe, or temporal

lobectomy. These brain structures play an important role in the

generation or propagation of the majority of temporal lobe

seizures. In most cases, a modest portion of the brain measuring

approximately 2 inches long is removed. The temporal lobes are

important in memory, emotion and language comprehension.

However, extensive preoperative assessments (MRI, Wada tests,

PET scans) ensure that removal of the area causing seizures will

not disrupt any of these critical functions.

The largest part of the brain, the cerebrum, is divided into four

paired sections - the frontal, parietal, occipital, and temporal

lobes. Each lobe controls a specific group of activities. The

temporal lobe, located on either side of the brain just above the

ear, plays an important role in hearing, language, and memory.

The most common type of epilepsy in teens and adults originates

in the temporal lobe, the seizure focus.

Temporal Lobe Resection

A temporal lobe resection is a surgery performed on the brain to

control seizures. In this procedure, brain tissue in the temporal

lobe is resected, or cut away, to remove the seizure focus. The

anterior (front) and mesial (deep middle) portions of the

temporal lobe are the areas most often involved.

Temporal lobe resection may be an option for people with

epilepsy whose seizures are disabling and/or not controlled by

medication, or when the side effects of medication are severe

and significantly affect the person's quality of life.


In addition, it must be possible to remove the brain tissue that

contains the seizure focus without causing damage to areas of

the brain responsible for vital functions, such as movement,

sensation, language, and memory.

Candidates for temporal lobe resection undergo an extensive

pre-surgery evaluation - including seizure monitoring,

electroencephalography (EEG), magnetic resonance imaging

(MRI), and positron emission tomography (PET). These tests help

to pinpoint the seizure focus within the temporal lobe and to

determine if surgery is possible.

A temporal lobe resection requires exposing an area of the brain

using a procedure called a craniotomy. After the patient is put to

sleep with anesthesia, the surgeon makes an incision in the

scalp, removes a piece of bone and pulls back a section of the

dura, the tough membrane that covers the brain. This creates a

"window" in which the surgeon inserts special instruments for

removing the brain tissue. Surgical microscopes also are used to

give the surgeon a magnified view of the area of the brain

involved. The surgeon utilizes information gathered during the

pre-operative evaluation - as well as during surgery - to define,

or map out, the route to the correct area of the temporal lobe.

In some cases, a portion of the surgery is performed while the

patient is in a ''twilight state'' - awake but under sedation - so

that the patient can help the surgeon find and avoid areas of the

brain responsible for vital functions. While the patient is awake,

the doctor uses special probes to stimulate different areas of the

brain. At the same time, the patient is asked to count, identify

pictures, or perform other tasks. The surgeon can then

determine the area of the brain associated with each task. After

the brain tissue is removed, the dura and bone are fixed back

into place, and the scalp is closed using stitches or staples.


Permanent complications associated with temporal lobe resection

surgery are very low. Mortality is less than 0.1% and permanent

unexpected morbidity less than 1%. In dominant hemisphere

resections, temporary language difficulties are seen in 10% of

the cases although these usually resolve. An upper

quadrantanopsia (partial upper peripheral vision loss) is expected

in large temporal resections, but seen in less than 25% of the

patients. Memory impairment rarely occurs from temporal

lobectomies because of extensive preoperative testing of

language and memory functions.

The success rate for seizure control in temporal lobectomy

varies:

60%-70% of patients are free of seizures that impair

consciousness or cause abnormal movements, but some

still experience auras

20%-25% of patients have some seizures but are

significantly improved (greater than 85% reduction of

complex partial and tonic-clonic seizures)

10%-15% of patients have no worthwhile improvement

Therefore, over 85% of patients enjoy a marked improvement in

seizure control. Most of them need less medication after surgery.

Approximately 25% of those who are seizure-free eventually can

discontinue antiepileptic drugs.

Lesionectomy

Twenty-five percent of patients with epilepsy will have lesions

identified by MRI as the cause of recurrent seizures.

Abnormalities such as low-grade astrocytomas, cortical

dysplasias, cavernous angiomas, and areas of focal atrophy are

the common causes of refractory seizures. Since surgical

removal of these lesions can result in complete seizure control in

many patients, the patient is considered an excellent candidate

for epilepsy surgery depending on the location of the lesion and

its relationship to eloquent cortex.


If the seizures have been present for many years then invasive

monitoring is often recommended to further identify the

involvement of the adjacent cortical rim around the lesion. When

lesions are within the non-dominant temporal lobe, removal of

the lesion along with a temporal lobectomy yields excellent

results in over 80% of cases.

A lesionectomy is the surgical removal of lesions. MRI identifies

small lesions as the cause of recurrent seizures in up to 25% of

patients. Common types of lesions include low-grade

astrocytomas, cortical dysplasias, cavernous angiomas, and

areas of focal atrophy.

Functional

Hemispherectomy

The largest part of the brain, the cerebrum, can be divided down

the middle lengthwise into two halves, called hemispheres. A

deep groove splits the left and right hemispheres, which

communicate through a thick band of nerve fibers called the

corpus callosum. Each hemisphere is further divided into four

paired sections, called lobes - the frontal, parietal, occipital, and

temporal lobes.

The two different sides or hemispheres are responsible for

different types of activities. The left side of the brain controls the

right side of the body and vice versa. For most people, the ability

to speak and understand the spoken word is a function of the left

side of the brain.

A functional hemispherectomy is a procedure in which portions of

one hemisphere - which are causing the seizures - are removed,

and the corpus callosum, which connects the two sides of the

brain, is cut. This disconnects communication between the two

hemispheres, preventing the spread of electrical seizures from

one side of the brain to the other. As a result, the person

usually has a marked reduction in physical seizures.


This procedure generally is used only for people with epilepsy

who do not experience improvement in their condition after

taking many different medications and who have severe,

uncontrollable seizures. This type of epilepsy is more likely to be

seen in young children who have an underlying disease, such as

Rasmussen's encephalitis or Sturge-Weber syndrome, which has

damaged the hemisphere.

Candidates for functional hemispherectomy undergo an extensive

pre-surgery evaluation - including seizure monitoring,

electroencephalography (EEG), and magnetic resonance imaging

(MRI). These tests help the doctor identify the damaged parts of

the brain and confirm that it is the source of the seizures. An

intracarotid amobarbital test, also called a WADA test, is done to

determine which hemisphere is dominant for critical functions

such as speech and memory. During this test, each hemisphere

is alternately injected with a medication to put it to sleep. While

one side is asleep, the awake side is tested for memory, speech,

and ability to understand speech.

A functional hemispherectomy requires exposing the brain using

a procedure called a craniotomy. Surgical microscopes are

utilized to give the surgeon a magnified view of the brain

structures. During the procedure, the surgeon removes portions

of the affected hemisphere, often taking all of the temporal lobe

but leaving the frontal and parietal lobes. The surgeon also

gently separates the hemispheres to access and cut the corpus

callosum. After the tissue is removed, the dura and bone are

fixed back into place, and the scalp is closed using stitches or

staples.

The patient generally stays in an intensive care unit for 24 to 48

hours and then stays in a regular hospital room for three to four

days.


Most people who have a functional hemispherectomy will be able

to return to their normal activities, including work or school in six

to eight weeks after surgery. Most patients will need to continue

taking anti-seizure medication, although some may eventually be

able to stop taking medication or have their dosages reduced.

About 85% of people who have a functional hemispherectomy

will experience significant improvement in their seizures, and

about 60% will become seizure-free. In many cases, especially in

children, the remaining side of the brain takes over the tasks

that were controlled by the section that was removed. This often

improves a child's functioning and quality of life, as well as

reduces or eliminates the seizures.

The following symptoms may occur after a functional

hemispherectomy, although they generally go away over time

and with therapy:

Scalp numbness.

Nausea.

Muscle weakness on the affected side of the body.

Puffy eyes.

Feeling tired or depressed.

Difficulty speaking, remembering, or finding words.

Headaches.

The risks associated with a functional hemispherectomy include

the following:

Risks associated with surgery, including infection,

bleeding, and an allergic reaction to anesthesia.

Loss of movement or sensation on the opposite side of

the body.

Swelling in the brain.

Delayed development.

Loss of peripheral (side) vision.

Failure to control seizures.


Corpus

Callosotomy

The corpus callosum is a band of nerve fibers located deep in the

brain that connects the two halves (hemispheres) of the brain. It

helps the hemispheres share information, but it also contributes

to the spread of seizure impulses from one side of the brain to

the other. A corpus callosotomy is an operation that severs

(cuts) the corpus callosum, interrupting the spread of seizures

from hemisphere to hemisphere. Seizures generally do not

completely stop after this procedure (they continue on the side

of the brain in which they originate). However, the seizures

usually become less severe, as they cannot spread to the

opposite side of the brain.

A corpus callosotomy, sometimes called split-brain surgery, may

be performed in people with the most extreme and

uncontrollable forms of epilepsy, when frequent seizures affect

both sides of the brain. People considered for corpus callosotomy

are typically those who do not respond to treatment with

antiseizure medications. Candidates for corpus callosotomy

undergo an extensive pre-surgery evaluation - including seizure

monitoring, electroencephalography (EEG), magnetic resonance

imaging (MRI), and positron emission tomography (PET). These

tests help the doctor pinpoint where the seizures begin and how

they spread in the brain. It also helps the doctor determine if a

corpus callosotomy is an appropriate treatment.

A corpus callosotomy requires exposing the brain using a

procedure called a craniotomy. After the patient is put to sleep

with anesthesia, the surgeon makes an incision in the scalp,

removes a piece of bone and pulls back a section of the dura, the

tough membrane that covers the brain. The surgeon inserts

special instruments for disconnecting the corpus callosum, gently

separates the hemispheres to access the corpus callosum.

Surgical microscopes are used to give the surgeon a magnified

view of brain structures.


In some cases, a corpus callosotomy is done in two stages. In

the first operation, the front two-thirds of the structure is cut,

but the back section is preserved. This allows the hemispheres to

continue sharing visual information. If this does not control the

serious seizures, the remainder of the corpus callosum can be

cut in a second operation. After the corpus callosum is cut, the


using stitches or staples.

The patient generally stays in the hospital for two to four days.

Most people having a corpus callosotomy will be able to return to

their normal activities, including work or school, in six to eight

weeks after surgery. The hair over the incision will grow back

and hide the surgical scar. The person will continue taking

antiseizure drugs.

Complications of corpus callosotomy are greater than with frontal

or temporal lobe surgery. Behavioral, language, and other

problems may affect function and the quality of life, but serious

problems are temporary or uncommon. The potential risks of

callosotomy must be weighed against its possible benefits, such

as a reduction in the frequency of seizures that cause injury and

other problems.

The persons most susceptible to behavioral problems after

callosotomy are those in whom language and motor dominance

are controlled by different hemispheres. In left-handed persons,

for example, the left side of the brain controls language, but the

right side of the brain controls movement. Some of the problems

resulting from callosotomy are caused by injury to the frontal

lobes during the operation. Since the corpus callosum is buried

deep between the frontal lobes, the middle portions of these

lobes must be separated, which poses some risk. Surgical

advances may help to minimize this risk.


Seizure frequency is reduced by an average of 70% to 80% after

partial callosotomy and 80% to 90% after complete callosotomy.

Partial seizures are often unchanged, but they may be improved

or worsened. In many cases, especially after partial callosotomy,

seizures are less frequent but persist.

Extratemporal

Cortical Resection

Extra-temporal seizure surgery constitutes about a quarter of the

surgical procedures for epilepsy and includes resection of the

frontal lobes, parietal lobes or occipital lobes. These resections

are guided by localization from invasive subdural electrodes and,

if necessary, detailed cortical functional mapping. Extra-temporal

resections are individualized to the seizure onset focus, the type

of seizure or syndrome, and the functional mapping, which

defines a safe resection boundary. Motor and sensory cortex and

language cortex localization is performed and greatly minimizes

neurological deficits from surgery.

The largest part of the brain, the cerebrum, is divided into four

paired sections, called lobes - the frontal, parietal, occipital, and

temporal lobes. Each lobe controls a specific group of activities.

The temporal lobe is the most common ''seizure focus,'' the area

where most seizures start, in teens and adults.

However, epileptic seizures can be ''extratemporal,'' or outside of

the temporal lobe, originating in the frontal, parietal or occipital

lobes, or even more than one lobe. If this is the case,

extratemporal cortical resection surgery may be warranted in

some cases. An extratemporal cortical resection is an operation

to resect, or cut away, brain tissue that contains a seizure focus.

Extratemporal means the tissue is located in an area of the brain

other than the temporal lobe. The frontal lobe is the most

common extratemporal site for seizures. In some cases, tissue

may be removed from more than one area/lobe of the brain.


Extratemporal cortical resection may be an option for people with

epilepsy whose seizures are disabling and/or not controlled by

medications, or when the side effects of the medication are

severe and significantly affect the person's quality of life. In

addition, it must be possible to remove the brain tissue that

contains the seizure focus without causing damage to areas of

the brain responsible for vital functions, such as movement,

sensation, language, and memory. Candidates for extratemporal

cortical resection undergo an extensive pre-surgery evaluation

including video electroencephalographic (EEG) seizure

monitoring, magnetic resonance imaging (MRI), and positron

emission tomography (PET). Other tests include

neuropsychological memory testing, the Wada test (to determine

which side of the brain controls language function), Single

Photon Emission Computed Tomography (SPECT), and magnetic

resonance spectroscopy. These tests help to pinpoint the seizure

focus and determine if surgery is possible.

An extratemporal cortical resection requires exposing an area of

the brain using a procedure called a craniotomy. After the patient

is put to sleep (general anesthesia), the surgeon makes an

incision in the scalp, removes a piece of bone and pulls back a

section of the dura, the tough membrane that covers the brain.

The surgeon inserts special instruments to remove brain tissue.

Surgical microscopes are used to give the surgeon a magnified

view of the area of the brain involved. The surgeon utilizes the

information gathered during the pre-operative evaluation - as

well as during surgery - to define, or map out, the route to the

correct area of the brain. In some cases, a portion of the surgery

is performed while the patient is awake, using medication to

keep the person relaxed and pain-free. This is done so that the

patient can help the surgeon find and avoid areas in the brain

responsible for vital functions such as brain regions of language

and motor control.


While the patient is awake, the doctor uses special probes to

stimulate various areas of the brain. At the same time, the

patient may be asked to count, identify pictures, or perform

other tasks. The surgeon can then identify the area of the brain

associated with each task. After the brain tissue is removed, the


using stitches or staples.

The risk of a major complication, such as a stroke, is about 1%

in these types of surgery. The risk of behavioral changes is

higher than with temporal lobectomy although these are often

difficult to measure and define. Personality, motivation, ability to

plan and to follow up on a multistep process, ability to organize

actions over time, social graces, and demeanor are among the

behaviors that the frontal lobes help to serve. In parietal and

occipital lobectomies, there may be a risk of losing touch

sensation or vision.

Results of surgical management for extratemporal epilepsy vary

depending upon seizure types, invasive mapping, and epilepsy

syndrome. Overall:

50%-60% of patients are free of seizures that impair

consciousness or cause abnormal movements.

20%-40% of patients are markedly improved (more than

90% reduction of complex partial and tonic-clonic

seizures)

20%-30% of patients have no worthwhile improvement.

Although extratemporal surgical cure rates are not as

high as temporal surgery rates, patients with well-defined

epileptic zones limited to smaller areas of the brain which

can be resected do better than in cases of widespread

seizure areas. It is in the area of extratemporal seizures

that improved success rates occur as these more difficult

problems are managed with the latest techniques,

imaging modalities and greater understanding.


Implantable

neurostimulator

The NeuroPace RNS System, a device that is implanted into the

cranium, senses and records electrocorticographic patterns and

delivers short trains of current pulses to interrupt ictal discharges

in the brain. The Neurological Devices panel of the FDA

concluded that this device was safe and effective in patients with

partial-onset epilepsy in whom other antiepileptic treatment

approaches have failed and that the benefits outweigh the risks.

In November 2013, the FDA approved the NeuroPace RNS

System for the reduction of seizures in patients with drug-

resistant epilepsy. Approval was based on a clinical trial involving

191 subjects with drug-resistant epilepsy. The neurostimulator

was implanted in all of these patients but activated in only half of

them. After 3 months, the average number of seizures per

month in patients with the activated device fell by a median of

34%, compared with an approximately 19% median reduction in

patients with an unactivated device.

Anti-Epileptic Medication

Anti-epileptic medication is often a necessary component of treatment.

Many patients will require pharmacologic therapy to control seizures. In

most instances, medication will be used in conjunction with other non-

pharmacologic therapies to provide a comprehensive approach to

treatment.8 Utilizing numerous options together provides the best means of

seizure control, especially in patients who experience severe or frequent

seizures.

The following section provides an overview of the various types of anti-

epileptic medication:34,52-65


Valproate Sodium

Valproate sodium, valproic acid, and divalproex sodium are anticonvulsants

that are chemically very similar to each other. (In this section, they are

referred to together as valproate). Valproate products are the most widely

prescribed anti-epileptic drugs worldwide. They are the first choice for

patients with generalized seizures and are used to prevent nearly all other

major seizures as well.

Side Effects: These drugs have a number of side effects that vary depending

on dosage and duration. Most side effects occur early in therapy and then

subside. The most common side effects are upset stomach and weight gain.

Less common side effects include dizziness, hair thinning and loss, and

difficulty concentrating.

Serious side effects include a higher risk for serious birth defects than other

AEDs especially if taken during the first trimester of pregnancy. In particular,

these drugs are associated with facial cleft deformities (cleft lip or palate)

and cognitive impairment.

Liver damage or failure is a rare but extremely dangerous side effect that

usually affects children under 2 years of age who have birth defects and are

taking more than one antiseizure drug. Pancreatitis (inflammation of the

pancreas) and kidney problems are also rare but serious side effects.

Carbamazepine

Carbamazepine is used for many types of epilepsy. It is taken alone or in

combination with other drugs. In addition to controlling seizures, it may help


relieve depression and improve alertness. A chewable form is available for

children.

Side Effects: Different side effects may develop or resolve at different points

during treatment. Initial side effects may include the following: Double

vision, headache, sleepiness, dizziness, and stomach upset. These usually

subside after a week and can be greatly reduced by starting with a small

dose and building up gradually.

Some people experience visual disturbances, ringing in the ears, agitation,

or odd movements when drug levels are at their peak. The extended-release

form of carbamazepine (Carbatrol) may help reduce these symptoms.

Serious side effects are less common but can include: skin reactions,

including toxic epidermal necrolysis and Stevens-Johnson syndrome, so

severe the drug has to be discontinued develop in about 6% of patients.

These skin reactions cause skin lesions, blisters, fever, itching, and other

symptoms. People of Asian ancestry have a 10 times greater risk for skin

reactions than other ethnicities.

A decrease in white blood cells occurs in about 10% of those taking the

drug. This is generally not serious unless infection accompanies it. Other

blood conditions can arise that are also potentially serious. Patients should

be sure to inform their doctors if they have any sign of irregular heartbeats,

sore throat, fever, easy bruising, or unusual bleeding.

Long-term therapy can cause bone density loss (osteoporosis) in women,

who should take preventive calcium and vitamin D supplements to improve

bone mass.


Children are at higher risk for behavioral problems.

(Note: Grapefruit, Seville oranges, and tangelos can increase

carbamazepine's blood levels and risk of adverse effects).

Phenytoin

Phenytoin (Dilantin, generic) is effective for adults who have the following

seizures or conditions:

Grand mal seizures

Partial seizures

Status epilepticus

Can be effective for people with head injuries who are at high risk for

seizures. This drug is not useful for the following seizures:

Petit mal seizures

Myoclonic seizures

Atonic seizures

Side effects are sometimes difficult to control. Some people may develop a

toxic response to normal doses, while others may require higher doses to

achieve benefits. As with any drug, side effects generally depend on dosage

and duration.

Side effects may include the following:

Excess body hair, eruptions and coarsening of the skin, and weight

loss

Gum disease

Staggering, lethargy, nausea, depression, eye-muscle problems,

anemia, and an increase in seizures can occur as a result of excessive

doses.


Liver damage may develop in rare cases.

Bone density loss from long-term therapy. Patients should take

preventive calcium and vitamin D supplements and exercise regularly

to improve bone mass.

Severe and even rare life-threatening skin reactions (Stevens-Johnson

syndrome, toxic epidermal necrosis)

A possible increased risk for birth defects (cleft palate, poor thinking skills)

Barbiturates (Phenobarbital and Primidone)

Phenobarbital, also called phenobaritone, is a barbiturate anticonvulsant.

Primidone is converted in the body to phenobarbital, and has the same

benefits and adverse effects.

Barbiturates may be used to prevent grand mal (tonic-clonic) seizures or

partial seizures. They are no longer typically used as first-line drugs,

although they may be the initial drugs prescribed for newborns and young

children.

Side Effects: Phenobarbital has fewer toxic effects on other parts of the body

than most anti-epileptic drugs, and drug dependence is rare, given the low

doses used for treating epilepsy. Nevertheless, many patients experience

difficulty with side effects.

Patients sometimes describe their state as "zombie-like." The most common

and troublesome side effects are:

Drowsiness

Memory problems

Problems with tasks requiring sustained performance


Problems with motor skills

Hyperactivity in some patients, particularly in children and the elderly

Depression in some adults

When taken during pregnancy, phenobarbital, like phenytoin and valproate,

may lead to impaired cognitive function in the child. There has been some

evidence that phenobarbitol may cause heart problems in the fetus.

Ethosuximide and Similar Drugs

Ethosuximide is used for petit mal (absence) seizures in children and adults

when the patient has experienced no other type of seizures. Methsuximide, a

drug similar to ethosuximide, may be suitable as an add-on treatment for

intractable epilepsy in children.

Side Effects: This drug can cause stomach problems, dizziness, loss of

coordination, and lethargy. In rare cases, it may cause severe and even fatal

blood abnormalities. Periodic blood counts are recommended for patients

taking this drug.

Clonazepam

Clonazepam is recommended for myoclonic and atonic seizures that cannot

be controlled by other drugs and for Lennox-Gastaut epilepsy syndrome.

Although clonazepam can prevent generalized or partial seizures, patients

generally develop tolerance to the drug, which causes seizures to recur.

Side Effects: People who have had liver disease or acute angle glaucoma

should not take clonazepam, and people with lung problems should use the

drug with caution. Clonazepam can be addictive, and abrupt withdrawal may

trigger status epilepticus. Side effects include drowsiness, imbalance and

staggering, irritability, aggression, hyperactivity in children, weight gain, eye


muscle problems, slurred speech, tremors, skin problems, and stomach

problems.

Lamotrigine

Lamotrigine is approved as add-on (adjunctive) therapy for partial seizures,

and generalized seizures associated with Lennox-Gastaut syndrome, in

children aged 2 years and older and in adults. Lamotrigine is also approved

as add-on therapy for treatment of primary generalized tonic-clonic (PGTC)

seizures, also known as “grand mal” seizures, in children aged 2 years and

older and adults.

Lamotrigine can be used as a single drug treatment (monotherapy) for

adults with partial seizures. Birth control pills lower blood levels of

lamotrigine.

Side Effects: Common side effects include dizziness, headache, blurred or

double vision, lack of coordination, sleepiness, nausea, vomiting, insomnia,

and rash. Although most cases of rash are mild, in rare cases the rash can

become very severe.

The risk of rash increases if the drug is started at too high a dose or if the

patient is also taking valproate. (Serious rash is more common in young

children who take the drug than it is in adults.) Rash is most likely to

develop within the first 8 weeks of treatment. The medical provider should

be immediately notified for development of a rash, even if it is mild.

Lamotrigine may cause aseptic meningitis. Symptoms of meningitis may

include headache, fever, stiff neck, nausea, vomiting, rash, and sensitivity to


light. Patients who take lamotrigine should immediately contact their doctors

if they experience any of these symptoms.

Gabapentin

Gabapentin is an add-on drug for controlling complex partial seizures and

generalized partial seizures in both adults and children.

Side Effects: Side effects include sleepiness, headache, fatigue, and

dizziness. Some weight gain may occur. Children may experience

hyperactivity or aggressive behavior. Long-term adverse effects are still

unknown.

Pregabalin

Pregabalin is similar to gabapentin. It is approved as add-on therapy to treat

partial-onset seizures in adults with epilepsy.

Side Effects: Dizziness, sleepiness, dry mouth, swelling in hands and feet,

blurred vision, weight gain, and trouble concentrating may occur.

Topiramate

Topiramate is similar to phenytoin and carbamazepine and is used to treat a

wide variety of seizures in adults and children. It is approved as add-on

therapy for patients 2 years and older with generalized tonic-clonic seizures,

partial-onset seizures, or seizures associated with Lennox-Gastaut

syndrome. It is also approved as single drug therapy.

Side Effects: Most side effects are mild to moderate and can be reduced or

prevented by beginning at low doses and increasing dosage gradually.


Common side effects may include numbness and tingling, fatigue,

abnormalities of taste, difficulty concentrating, and weight loss. Serious side

effects may include glaucoma and other eye problems.

A medical provider should be notified right away for blurred vision or eye

pain. If used during pregnancy, topiramate can increase the risk for cleft lip

or palate birth defects.

Oxcarbazepine

Oxcarbazepine is similar to phenytoin and carbamazepine but generally has

fewer side effects. It is approved as single or add-on therapy for partial

seizures in adults and for children ages 4 years and older.

Side Effects: Serious side effects, while rare, include Stevens-Johnson

syndrome and toxic epidermal necrolysis.

These skin reactions cause a severe rash that can be life threatening. Rash

and fever may also be a sign of multi-organ hypersensitivity, another serious

side effect associated with this drug. Oxcarbazepine can reduce sodium

levels (hyponatremia). Serum sodium levels should be monitored. This drug

can reduce the effectiveness of birth control pills. Women who take

oxcarbazepine may need to use a different type of contraceptive.

Zonisamide

Zonisamide is approved as add-on therapy for adults with partial seizures.

Side Effects: Zonisamide increases the risk for kidney stones. It may reduce

sweating and cause a sudden rise in body temperature, especially in hot


weather. Other side effects tend to decrease over time and may include

dizziness, forgetfulness, headache, weight loss, and nausea.

Levetiracetam

Levetiracetam is approved both in oral and intravenous forms as add-on

therapy for treating many types of seizures in both children and adults.

Side Effects: These tend to occur mostly in the first month. They include

sleepiness, dizziness, and fatigue.

More serious side effects may include muscle weakness and coordination

difficulties, behavioral changes, and increased risk of infections.

Tiagabine

Tiagabine has properties similar to phenytoin and carbamazepine.

Side Effects: Tiagabine may cause significant side effects including dizziness,

fatigue, agitation, and tremor. The FDA has warned that tiagabine may

cause seizures in patients without epilepsy. Tiagabine is only approved for

use with other anti-epilepsy medicines to treat partial seizures in adults and

children 12 years and older.

Ezogabine

Ezogabine, a potassium channel opener, was approved in 2011 for treatment

of partial seizures in adults. Ezogabine is used as an add-on (adjunctive)

medication.


Its most serious side effect is urinary retention. Patients should be

monitored for symptoms such as difficulty initiating urination, weak urine

stream, or painful urination. Other side effects may include coordination

problems, memory problems, fatigue, dizziness, and double vision.

Perampanel

Perampanel was approved in 2012 as add-on treatment for partial onset

seizures in patients age 12 years and older. It is the first in a new class of

AEDs for uncontrolled partial epilepsy. Perampanel targets the AMPA

glutamate receptor, which is involved in seizure activity. Perampanel is

taken as a once-daily tablet.

Common side effects may include dizziness, drowsiness, and fatigue.

Peramanel also has a boxed warning to alert about potential risks of serious

mood changes and mental disturbances including irritability, aggression,

anxiety, and violent thoughts or behaviors.

Less Commonly Used AEDs

Felbamate is an effective antiseizure drug. However, due to reports of

deaths from liver failure and from a serious blood condition known as

aplastic anemia, felbamate is recommended only under certain

circumstances. They include severe epilepsy, such as Lennox-Gastaut

syndrome, or as monotherapy for partial seizures in adults when other drugs

fail.

Vigabatrin has serious side effects, such as vision disturbances, and is

generally prescribed only in specific cases. It is sometimes given in low

doses for patients with Lennox-Gastaut syndrome. Vigabatrin is also


prescribed as a low-dose oral solution to treat infantile spasms in children

ages 1 month to 2 years.

Emotional Impact And Support

Individuals with epilepsy are more prone to behavioral and emotional

problems than their peers. In fact, mental health and behavioral problems

occur at a rate of approximately thirty to fifty percent in those with epilepsy,

while only affecting 8.5 percent of individuals who do not have epilepsy.66

Children with epilepsy are especially prone to behavioral and emotional

problems as a result of the condition. These problems typically fall into two

categories: internal and external factors.

Internal factors are a direct result of complications in the affected area of

the brain. They are typically caused by structural or functional problems and

are biologically based. External factors are not biologically based and occur

as a result of the social response to the individual’s epilepsy. External factors

include feelings of anxiety and depression. In most instances, patients will

experience a combination of internal and external factors. The following

section provides an overview of the main factors involved in the

development of emotional and behavioral problems.

For the person with epilepsy, a range of factors can combine to produce a

heightened sense of anxiety, depression, low self-esteem, and feelings of

isolation. While most people with the condition learn how to deal with these

feelings, some may respond to such pressures by reacting in an overly

aggressive, asocial, irritable, or introverted manner.

It is often the possibility of having a seizure, rather than the seizure itself,


which may be handicapping to the person with epilepsy. Afraid of having a

seizure in public and the very real possibility of injury, the person with

epilepsy may seclude her- or himself. As a result a person may become very

isolated. As well, the person with seizures may be anxious about other

people's reactions to a seizure. Many people who witness a seizure may

react by being afraid and embarrassed by the situation. Since the individual

who has seizures has no control over other people's reactions during a

seizure, he or she may prefer to stay alone and in isolation.

One of the greatest concerns for the person who has recurring seizures is

the perceived loss of control, which goes along with having seizures.

Contemporary western culture has glorified the image of the controlled and

independent adult. The unpredictability of having a seizure, as well as the

very obvious loss of control during seizures clearly does not reflect this

image. By thus "failing" to meet the basic standards of our culture, a

person's sense of self-worth may well be affected. This sense of not being in

control may also extend to include other aspects of a person's life.

Being stigmatized for having epilepsy is also an important aspect. Popular

misconceptions about epilepsy are still widespread. Again, other people's

negative responses may considerably add to the stress of the person with

epilepsy and may lead them to choose isolation over social interaction.

Sometimes, if the condition is well controlled, and a person has only a few

seizures, he or she may not feel compelled to deal with the condition. Then,

the denial of the condition can compound feelings of anxiety. In a sense, the

person does not get "used" to having seizures, and each seizure becomes

yet another traumatic experience. A person's own attitudes towards having

seizures can also very much influence their emotional state. By not

accepting the reality of having seizures, some persons may go through some


length to hide it from the people around them. The anxieties of possibly

being found out may reinforce the desire to socially isolate themselves.

Another important factor for the person with epilepsy that can greatly

increase stress and thereby emotional strain is economic hardship. High

rates of unemployment and underemployment - more than 50% for persons

with seizures - severely restricts the income of many people with epilepsy.

Thus they may have difficulty sustaining a household, not to mention the

added expenses of anticonvulsant medication.

Most persons who take anticonvulsant medication to control their seizures do

not experience serious and intolerable side effects from it. In some cases,

however, the side effects from taking medication may affect an individual's

behavior and/or emotional state. Such changes may include an impairment

of drive, mood, sociability, alertness, or concentration. People who

experience side effects in response to taking one single drug will generally

find that these effects will disappear over the first few months. However,

side effects may become a problem when the person is taking more than

one kind of anticonvulsant medication to control different types of seizures.

It may be that the side effects of one medication are compounded by the

side effects of another. If these effects are not well tolerated, changes in

behavior and mood can occur. However, it has been found that, if the

amount of medication an individual receives is reduced, these changes are

reversed. While it is important to be aware of the possible effects of

medication, it should be recognized that they do not usually present a

serious problem to adults with epilepsy as long as they are administered in

the appropriate dosage.

The place in the brain where seizures originate may also have an effect on a


person's emotions and on her or his behavior. Seizures with temporal lobe

involvement, complex partial seizures (formerly known as psychomotor or

temporal lobe epilepsy) are most commonly associated with behavioral

changes. Such changes can include rapid fluctuations in mood, or over-

attention to detail.67-69

The type of seizure will often impact the severity, and type, of emotional and

behavioral problems experienced by patients. The seizure type can impact

the basic functions of the brain, thereby causing internal factors that will

affect the emotional and behavioral health of the patient. In addition, the

severity and type of the seizure can lead to the development of external

factors such as depression and anxiety. When a patient feels impacted by

potential seizures, he or she is more apt to develop anxiety. In addition, the

limitations caused by epilepsy can cause patients to experience depression

and anger.66

Patients will also experience stress, anxiety, and depression as a result of

treatment from others. Many patients will feel stigmatized and will allow

these feelings to affect how they perceive their situation. For some, the

impact will cause high levels of stress and depression.70 This is especially

common in patients who are already prone to mental health issues. Self-

esteem issues are quite prevalent in patients who feel stigmatized, as well

as in those who are concerned with the attention they will receive when a

seizure occurs. Patients who are prone to frequent seizures in public places

will see an increase in self-esteem issues as a result.68

Some patients will experience emotional and behavioral issues as a result of

the anti-epilepsy medication they take to control their seizures. Since

anticonvulsants primary function involves the inhibition of electrical activity


in the brain, they can also impact behavioral and cognitive function. This can

lead to the development of emotional and behavioral issues in some

patients, especially children. Some emotional and behavioral problems are

more common in those with epilepsy. The following table provides an

overview of the most common behavioral and emotional conditions in

individuals with epilepsy:66,71-73

Depression

Depression is the mood disorder most commonly associated with

epilepsy. However, it can often go unrecognized and untreated in

people with the disorder, especially in children. Epilepsy-related

depression can occur before, during, or after seizures, but is most

often associated with periods between seizures.

The symptoms of depression vary widely from one individual to

another. Those most often seen in children with epilepsy are sleep

disturbances, fatigue or listlessness, lack of enthusiasm, and frequent

emotional outbursts. Other behavioral issues, such as anxiety,

agitation, frustration, or impulsive behaviors, often accompany

depression.

Although the cause of depression in people with epilepsy is unknown,

it is thought to result from both internal and external factors.

Attention

Deficit

Disorder

Attention deficit disorder with or without hyperactivity is considered a

common behavioral problem in children with epilepsy. It is estimated

that nearly 8 percent of children with epilepsy have problems with

attention. In general, attention deficit/hyperactivity disorder (ADHD) is

a neurobehavioral disorder that causes individuals to be easily

distracted, frustrated, fidgety, impulsive, and forgetful. The disorder

makes learning and social interactions difficult, regardless of an

individual's cognitive abilities. While ADHD is a clinical diagnosis made

on the basis of observation and medical history, mental health experts

and scientists agree that there are identifiable characteristics of the

disorder.


Measures such as rating scales and reports from teachers and parents

can be helpful in making the diagnosis.

Anxiety

Disorders

Anxiety disorders associated with epilepsy may take the form of

chronic, generalized worrying; acute, overwhelming panic attacks; or

obsessive-compulsive tendencies. The disorders often arise in

response to the unpredictability and lack of control associated with

seizures. For some people with epilepsy, anxiety may cause them to

overestimate the threat posed by future seizures, or underestimate

their ability to cope. Such thoughts can cause physical symptoms that

accentuate the feeling of a lack of control.

Aggression

Impulse-control problems are common among children with epilepsy.

One of the most common forms of impulsivity is aggression. Although

the cause of aggression in people with epilepsy varies, the

unpredictability of seizures and the individual's lack of control over

them may contribute to frustration and irritability. In addition, children

who are more severely affected and lack good communication skills

may act out their frustration with aggressive or even violent

outbursts.

In general, aggressive behaviors tend to become less frequent and

decrease in severity as a person grows older. However, aggressive

tendencies may then be replaced by depression and anxiety.

Autism

Autism is a spectrum disorder, or combination of symptoms,

characterized by deficits in verbal and nonverbal communication skills,

severe social dysfunction, and repetitive behaviors. Such behavioral

problems are sometimes seen in children with Lennox-Gastaut

syndrome, tuberous sclerosis complex, Angelman syndrome, and

other genetic disorders. Despite decades of research attempting to

link autism to a wide variety of potential causes, there still is no

consensus, and effective medical treatments have yet to be found.

However, there are behavioral and educational interventions that have

been developed specifically for individuals with autism.


Individuals with epilepsy will often require support in coping with the

emotional and behavioral problems associated with their condition. At the

most basic level, patients can benefit from having a support team that will

help manage the various aspects of the illness.74 Patients who have such a

network will be more involved in the care and will feel less stigmatized by

their peers. In addition, providing access to knowledge will enable patients

to make informed decisions and feel empowered and confident.

Beyond the basic level of support, patients will often require a combination

of medication and cognitive and behavioral interventions. This

comprehensive approach will combine pharmacological support with therapy

and peer support. Patients who receive this level of treatment often report

reduced feelings of stress, anxiety, and depression.66 In most instances, the

patient will be prescribed antianxiety medication and/or antidepressants. If

the patient is experiencing other forms of emotional or behavioral distress,

additional medications may be prescribed.

To ensure the patient receives appropriate medical care, he or she should

receive a thorough assessment to determine the specific type of emotional

and behavioral problems that are present. Patients who receive

comprehensive care to manage emotional and behavioral problems will often

benefit from the care of a team of specialists. The specific type of provider

will be determined based upon the individual patient’s needs, and various

specialists supporting care are listed below:75

Neurologist

A neurologist and a pediatric neurologist are physicians who care for

people affected by disorders of the nervous system. An epileptologist


is a neurologist or a pediatric neurologist who specializes in the

treatment of epilepsy.

Psychiatrist

A psychiatrist is a medical doctor who specializes in the diagnosis and

treatment of mental and behavioral disorders. A psychiatrist who

treats people with epilepsy is familiar with the cognitive and behavioral

issues that are common to the disorder and know what treatment

options are most effective for these issues, including medication

options.

Psychologist

A psychologist is a licensed professional who specializes in the

diagnosis and treatment of mental and emotional problems, and may

be involved in evaluation, testing, counseling, and/or psychotherapy.

Social Worker

A social worker is a licensed professional who provides support to

families and children with medical or psychological issues.

Stigma

Many individuals experience problems as a result of the stigma attached to

epilepsy. Stigma causes social avoidance of all age groups and challenges in

an employment setting. There are various levels of stigma associated with

epilepsy:76-78

Internalized stigma is felt within the person with the condition and

reflects their feelings, thoughts, beliefs and fears about being

different.


Interpersonal stigma occurs in interactions with others both within and

external to the family system; and in these interactions the person

with the illness is treated differently and negatively because of the

health condition.

Institutionalized stigma reflects indirect expressions of different

treatment of persons with an illness as a group in the larger society,

i.e., discrimination of persons with epilepsy by policies of an insurance

company.

Most of the stigma associated with epilepsy is caused by a long history of

misinformation and misrepresentations of the impact of the illness. Fear of

sudden seizures and the physical impact they can have on an individual

often causes anxiety in those who have contact with them. Poor portrayal of

the illness in the media further enhances the stigma associated with it.79

These misperceptions have existed for centuries. As a result, people with

epilepsy have experienced prejudice and discrimination. They have felt

stigmatized and ostracized because of their medical condition and, as a

result, have limited their social engagement and involvement in the

workforce. In addition, the stigma associated with epilepsy can often lead to

increased feelings of depression and anxiety in the patient.

Due to the level of stigma associated with epilepsy, many individuals have

been hesitant to disclose their status due to feelings of shame and fear. This

can have detrimental effect on the individuals as they struggle to obtain care

and treatment without bringing attention to their medical disorder. In fact,

some patients may feel so stigmatized that they refuse to admit that they

are afflicted with epilepsy. These individuals often refrain from receiving,

medical treatment in favor of maintaining anonymity.


To combat the stigma associated with epilepsy, a number of education and

awareness programs have been developed. In addition, to education and

awareness programs, support networks can help patients cope with the

repercussions of the stigma.80 Public campaigns to reduce stigma has been

ongoing since the 1970s, but their long-term impact on attitudes is

unknown. Advocacy campaigns for other health conditions provide a variety

of lessons and best practices for the epilepsy community; some efforts have

effectively used carefully selected spokespeople and have achieved

important policy changes. Actions needed to improve public awareness and

knowledge include informing journalists as well as writers and producers in

the entertainment industry; engaging people with epilepsy and their families

in public awareness efforts; coordinating public awareness efforts and

developing shared messaging; and ensuring that all campaigns include

rigorous formative research, considerations for health literacy and audience

demographics, and mechanisms for evaluation and sustainability.

In recent years, the education and awareness campaigns aimed at reducing

the stigma associated with epilepsy have been somewhat successful. Recent

studies have shown that there has been a reduction in negative attitudes

toward the illness, especially in the social sphere. However, some negative

attitudes still exist. They are most prevalent in the employment sector,

where individuals still experience discrimination based upon misinformation

and misrepresentations. Many individuals with epilepsy still experience

barriers to employment. The following dation fact sheet provides an

overview of the employment barriers individuals may experience as a result

of their epilepsy:81


According to a 2008 Needs Assessment Survey, 38% of adult respondents were

unemployed (as compared to the overall rate of 9.6% at the time). Furthermore, the

mean annual personal income of full-time, year-round workers with epilepsy was

$39,690, as compared to the U.S. average of $52,703 (American Community Survey,

2007). Unemployment and underemployment among adults with epilepsy have a

significant impact on financial security and quality of life.

Perhaps the greatest barrier to employment for people with epilepsy is the inability to

reliably get to and from work because of driving restrictions and a lack of other

transportation options. Unless a person has been seizure-free for six months, he or she is

not allowed to drive and, therefore, must rely upon family members, co-workers, or

public transportation to get to work. Unfortunately, in most areas of the state, public

transportation is only an option if you work in the community in which you live, and you

live in a community that has good public transportation. In addition, it’s not always

feasible to get a ride from friends, family members, or co-workers.

The symptoms of epilepsy (i.e., seizures, medication side effects, memory problems,

depression, etc.) can also be major barriers to employment. Seizures can limit one’s

ability to safely perform certain job duties and disrupt one’s work schedule, especially if

the individual has a prolonged recovery period after seizures. Drowsiness, poor

coordination, and cognitive problems can make it difficult to perform at the level

expected by employers and can also pose safety risks. If you develop epilepsy as a

working adult, it can be difficult to adjust to new restrictions and limitations. In some

cases, you may need to consider switching the field in which you work, and this may

require additional education or training.

Despite these challenges, though, most people with epilepsy can work effectively and are

not at significantly higher risk of injury on the job. In most cases, simple

accommodations can help people with epilepsy get around these barriers to employment;

however, this is dependent on having an employer that understands epilepsy and

employment rights. Unfortunately, many employers have fears about epilepsy that are

largely unfounded. These fears can ultimately result in discrimination in the form of

dismissal from employment or failure to get hired in the first place. Therefore, it is

important for an individual to know when to disclose epilepsy to an employer, how to

anticipate and address employer concerns, and what your rights are.


Summary

Epilepsy is a complex brain disorder that is characterized by seizures, which

are caused by disturbances in the brain’s electrical functions. The term

epilepsy encompasses a variety of different syndromes, each ranging in its

symptoms, severity, and duration. The characteristic seizures are present in

all types of epilepsy, but they differ in presentation and severity depending

on the type of epilepsy. Epilepsy is most common in young children and the

elderly, but it can affect individuals of all ages. Often, the cause of epilepsy

is unknown. When a cause is identified, it varies between environmental or

genetic factors, or as part of traumatic injury. Some epileptic syndromes will

only last a short time, especially those caused by trauma; however, some

other epileptic syndromes will be lifelong conditions that cannot be cured.

Epilepsy can be a frustrating and scary condition, but recent advances in

medication and surgical options have made it easier to control. Even though

the cause of this disorder is still not understood, great strides have been

made in the effort to improve care of the epileptic patient. Understanding

current trends in epilepsy care will assist medical providers and nurses to

provide best practice care to patients and ensure that they have the best

quality of life possible.

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requirement.


1. Specific features that typically define epileptic syndromes do

not include:

a. Seizure types b. Age when seizures begin

c. Electroencephalogram (EEG) findings d. A history of mental illness

2. A factor that influences an individual’s risk of developing

epilepsy is:

a. Family History b. An electrolyte imbalance

a. Trauma at birth b. A severe psychotic disturbance

3. A ____ chance of recurring seizures exists after a person has 2 or more seizures.

a. 35%

b. 50% c. 25%

d. 70%

4. True or False: Febrile seizures (clonic-tonic) can last 1 minute or 30 minutes, and can be repetitive.

a. True

b. False

5. In frontal lobe epilepsy motor areas controlling motor

movement are affected, therefore abnormal movements occur:

a. on the same side of the body. b. generally in the lower extremities.

c. the opposite side of the body. d. resemble a tic disorder.

6. A somatosensory seizure most commonly occurs in

a. parietal epilepsy.

b. frontal lobe epilepsy. c. temporal lobe epilepsy.

d. None of the above


7. True or False: Occipital seizures usually begin with visual

hallucinations like flickering or colored lights, rapid blinking, or other symptoms related to the eyes and vision.

a. True

b. False

8. West's syndrome “jackknife seizures” is an uncommon form of epilepsy involving sudden jerking followed by stiffening with

the arms flung out as the body bends forward that start at:

a. Onset of menopause. b. Between 3 and 12 months of age.

c. In women during the later stages of pregnancy and childbirth. d. In infants immediately after being born.

9. Some patients attempt to manage the symptoms of epilepsy through the ketogenic diet, which is a diet:

a. high in fat and low in carbohydrate.

b. high in protein and low fat. c. consisting of high carbohydrate and dairy shakes.

d. that eliminates all acidic foods.

10. True or False: Benign rolandic (sylvian) epilepsy seizures, beginning between 1 and 2 years of age, stem from a genetic

defect and are commonly observed as clonic-tonic.

a. True b. False

11. Melatonin side effects to monitor for include:

a. Vivid dreams or nightmares. b. GI disturbances, dizziness and headaches.

c. Decreased libido, gynecomastia and decreased sperm count. d. All of the above


12. Folic acid (vitamin B9) is a water-soluble B vitamin that is

essential for DNA repair, cell division, and normal cellular growth. Low folic acid levels have been associated with

a. complications of fetal development such as spina bifida.

b. megaloblastic anemia and peripheral neuropathy in adults. c. increased cardiovascular disease in women only.

d. Answers a., and b.

13. People taking anti-seizure medications should:

a. Add vitamin D and calcium to their daily diet. b. Not worry about vitamin D deficiency.

c. Immediately start on vitamin D 50,000 iu twice daily. d. Avoid sunlight because it can cause a drug reaction.

14. Approximately 30% of individuals will not respond to pharmacologic treatment and often benefit from

a. high dosing of vitamin D.

b. surgery. c. smoking cessation.

d. genetic testing.

15. Lamotrigine (Lamictal) is an approved adjunctive therapy for:

a. Partial seizures. b. Generalized seizures associated with Lennox-Gestaut syndrome.

c. Children aged 2 years and older and in adults. d. All of the above

16. True or False: Levetiracetam (Keppra) has properties similar

to Phenytoin and Carbamezapine.

a. True b. False


17. Lesions within the non-dominant temporal lobe removed by

surgery (lesionectomy) along with a temporal lobectomy yield excellent results in over _____ of cases.

a. 15%

b. 25% c. 50%

d. 80%

18. Children with epilepsy are particularly prone to behavioral and emotional problems that typically fall into two categories:

a. Internal and external factors.

b. Depression and anxiety. c. Body dysmorphic disorder and feels of stigmatization.

d. Early childhood and late childhood.

19. True of False: Individuals with epilepsy will often require

support in coping with the emotional and behavioral problems associated with their condition.

a. True

b. False

20. With __________ generalized epilepsy, no brain or spinal cord abnormalities, other than the seizures, can be identified

on an EEG (electroencephalogram) or MRI magnetic resonance imaging study.

a. symptomatic

b. partial

c. *idiopathic d. parietal

21. Occipital seizures are often mistaken for ________________

because they share similar symptoms.

a. vertigo b. tuberous sclerosis

c. tonic-clonic seizures d. *migraine headaches


22. Epilepsy is not considered as a diagnosis until the patient has

had

a. *two or more unprovoked seizures. b. a seizure as an adult.

c. two or more seizures lasting over a minute. d. a documented seizure.

23. Slightly over half of seizures in adults are

a. caused by benign rolandic epilepsy.

b. *complex partial seizures. c. caused by early myoclonic encephalopathy.

d. febrile seizures.

24. In patients with atonic (drop) seizures, a surgical procedure

called ____________________ may help reduce the falls that may result from seizures.

a. lesionectomy

b. multiple subpial transections c. *corpus callosotomy

d. a functional hemispherectomy

25. Certain types of epilepsy may be caused by a brain tumor, stroke, or other neurological disorder; however, idiopathic

epilepsy is a primary brain disorder

a. caused by migraine headaches. b. *of unknown cause.

c. and is always a life-long disease.

d. and is untreatable.

26. True or False: Most idiopathic epilepsy syndromes are presumed to be due to a genetic cause.

a. *True

b. False


27. _____________ is/are a type of progressive myoclonic

epilepsy that involves a genetic mutation.

a. Unverricht-Lundborg Syndrome b. *Mitchondrial disorders

c. Benign rolandic epilepsy d. Reflex epilepsies

28. True or False: Many individuals with epilepsy continue to

experience barriers to employment.

a. *True b. False

29. A two-pronged approach used to treat reflex epilepsy

includes

a. hospitalization.

b. multiple subpial transections. c. *trying to avoid the triggering stimulus.

d. immunologic therapies.

30. With febrile seizures, the following is/are true:

a. *The peak age is 18 months. b. In most instances, hospitalization is necessary.

c. Seizures are absent with high fever. d. All of the above

31. Medication to treat benign rolandic (sylvian) epilepsy is

usually continued

a. for the patient’s lifetime.

b. for the first 18 months. c. into the patient’s adulthood.

d. *until the patient reaches age 15.

32. True or False: In patients with frequent, poorly controlled seizures, it is often wise to use high doses of antiepileptic

drugs to reduce behavioral, social, and intellectual problems.

a. True b. *False


33. Remission in childhood absence epilepsy (CAE) cases can be

achieved in approximately ____ of patients.

a. 25% b. 10%

c. 50% d. *80%

34. _______________ is defined as the loss of language abilities

that had been present.

a. Acquired atrophy b. Dysmorphism

c. *Acquired aphasia d. Pallinopsia

35. Which of the following treatments may be effective to treat acquired aphasia?

a. *Multiple subpial transections

b. Antiepileptic drugs c. Immunologic therapies

d. Vagus nerve stimulation

36. Electroencephalography (EEG) biofeedback is especially helpful in treating

a. febrile seizures.

b. *partial seizures. c. benign rolandic epilepsy.

d. acquired aphasia.

37. Routine _________ supplementation is important for women

and men receiving antiepileptic drugs.

a. melatonin b. calcium

c. *folic acid d. valproic acid


38. One of the most common side effects caused by valproate

products (which are anticonvulsants) is

a. hair thinning. b. dizziness.

c. *weight gain. d. difficulty concentrating.

39. Carbamazepine is used for many types of epilepsy. In addition

to controlling seizures, it may help

a. treat nausea. b. treat insomnia.

c. treat acquired aphasia. d. *relieve depression and improve alertness.

40. True or False: Many individuals with epilepsy have lower than normal melatonin levels.

a. *True

b. False

Correct Answers:

1. d

2. a

3. d

4. a

5. c

6. a

7. a

8. b

9. a

10. b

11. d

12. d

13. a

14. b

15. d

16. b

17. d

18. a

19. a

20. c

21. d

22. a

23. b

24. c

25. b

26. a

27. b

28. a

29. c

30. a

31. d

32. b

33. d

34. c

35. a

36. b

37. c

38. c

39. d

40. a


References Section

The reference section of in-text citations include published works intended as

helpful material for further reading. Unpublished works and personal

communications are not included in this section, although may appear within

the study text.

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http://umm.edu/health/medical/reports/articles/epilepsy

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epilepsy#sthash.GXR004kE.IwfwMlfd.dpbs

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