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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.
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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.
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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.
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1. Specific features that typically define epileptic syndromes do
not include:
a.
b.
c.
d.
Seizure types
Age when seizures begin
Electroencephalogram (EEG) findings
A history of mental illness
2. A factor known to influence an individual’s risk of developing
epilepsy is:
a.
b.
c.
d.
Family History
An electrolyte imbalance
Trauma at birth
A severe psychotic disturbance
3. A ____ % chance of recurring seizures exists after a person
has 2 or more seizures.
a.
b.
c.
d.
35%
50 %
25 %
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.
b.
c.
d.
on the same side of the body
generally in the lower extremities
on the opposite side of the body
resemble a tic disorder
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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
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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
Some types of epilepsy, which are categorized by the type of seizure
Influence
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.
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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
Infectious diseases, such as meningitis, AIDS and viral encephalitis,
Diseases
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
Epilepsy can sometimes be associated with developmental disorders,
Disorders
such as autism and neurofibromatosis.
Brain
Ion Channels - sodium, potassium, and calcium - act as ions in the
Chemistry
brain. They produce electric charges that must fire regularly in order
Factors
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.
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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.
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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.
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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.
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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
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Idiopathic
In idiopathic generalized epilepsy, there is often, but not always, a
Epilepsy
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.
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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
Symptomatic generalized epilepsy (SGE) encompasses a group of
Generalized
challenging epilepsy syndromes. As a group, SGE has 3 main features:
Epilepsy
(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.
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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.
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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
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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
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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.
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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,
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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.
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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.
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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.
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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
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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.
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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
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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
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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.
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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
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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 tonicclonic or absence seizures. The EEG usually shows a pattern of intermittent
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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.
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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
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
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
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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.
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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.
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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.
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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 Coenzyme 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
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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.
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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.
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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.
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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.
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A variety of treatment options are available to patients experiencing epileptic
seizures. Most patients will attempt to manage their symptoms through nonpharmacologic 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.
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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
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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
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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
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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.
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
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
In an animal study, melatonin supplements reduced the
medications
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
A common side effect of antipsychotic medications used to treat
medications
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 longterm benzodiazepine therapy, which is habit-forming.
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Blood Pressure
Melatonin may make blood pressure medications like
Medications
methoxamine and clonidine less effective. In addition,
medications in a class called calcium channel blockers may lower
melatonin levels. Calcium channel blockers include:
Beta-Blockers

Nifedipine

Amlodipine

Verapamil

Diltiazem

Felodipine

Nisoldipine

Bepridil
Use of beta-blockers may lower melatonin levels in the body.
Beta-blockers include:

Acebutolol

Atenolol

Bisoprolol

Carteolol

Metoprolol

Nadolol

Propranolol
Anticoagulant
Melatonin may increase the risk of bleeding from anticoagulant
Medications
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-
NSAIDs such as ibuprofen may lower levels of melatonin in the
Inflammatory Drugs
blood.
(NSAIDs)
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Steroids and
Melatonin may cause these medications to lose their
Immunosuppressant
effectiveness. Do not take melatonin with corticosteroids or
Medications
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,
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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.
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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
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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
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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-thecounter (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
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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
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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.
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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
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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 antiepileptic 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
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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 calciumcontaining 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
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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.
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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.
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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
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Procedure
Description and Benefits/Risks
Vagus Nerve
VNS is a palliative technique that involves surgical implantation
Stimulation
of a stimulating device. VNS is FDA approved to treat medically
(VNS)
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 longterm 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.
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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 metaanalysis 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
Multiple subpial transection was pioneered as an alternative to
Transection
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.
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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.
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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.
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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
The most common surgical procedure performed for epilepsy is
Resection
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.
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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.
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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.
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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
The largest part of the brain, the cerebrum, can be divided down
Hemispherectomy
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.
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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.
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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.
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Corpus
The corpus callosum is a band of nerve fibers located deep in the
Callosotomy
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.
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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
dura and bone are fixed back into place, and the scalp is closed
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.
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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
Extra-temporal seizure surgery constitutes about a quarter of the
Cortical Resection
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.
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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.
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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
dura and bone are fixed back into place, and the scalp is closed
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.
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Implantable
The NeuroPace RNS System, a device that is implanted into the
neurostimulator
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 drugresistant 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 nonpharmacologic 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 antiepileptic medication:34,52-65
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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
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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.
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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.
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
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
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
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
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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
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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.
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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
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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.
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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
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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,
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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
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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
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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 overattention 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. Selfesteem 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
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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
Attention deficit disorder with or without hyperactivity is considered a
Deficit
common behavioral problem in children with epilepsy. It is estimated
Disorder
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.
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Measures such as rating scales and reports from teachers and parents
can be helpful in making the diagnosis.
Anxiety
Anxiety disorders associated with epilepsy may take the form of
Disorders
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.
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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
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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.
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
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.
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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
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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.
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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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1. Specific features that typically define epileptic syndromes do
not include:
a.
b.
c.
d.
Seizure types
Age when seizures begin
Electroencephalogram (EEG) findings
A history of mental illness
2. A factor that influences an individual’s risk of developing
epilepsy is:
a.
b.
a.
b.
Family History
An electrolyte imbalance
Trauma at birth
A severe psychotic disturbance
3. A ____ chance of recurring seizures exists after a person has 2
or more seizures.
a.
b.
c.
d.
35%
50%
25%
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.
b.
c.
d.
on the same side of the body.
generally in the lower extremities.
the opposite side of the body.
resemble a tic disorder.
6. A somatosensory seizure most commonly occurs in
a.
b.
c.
d.
parietal epilepsy.
frontal lobe epilepsy.
temporal lobe epilepsy.
None of the above
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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.
b.
c.
d.
Onset of menopause.
Between 3 and 12 months of age.
In women during the later stages of pregnancy and childbirth.
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.
b.
c.
d.
high in fat and low in carbohydrate.
high in protein and low fat.
consisting of high carbohydrate and dairy shakes.
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.
b.
c.
d.
Vivid dreams or nightmares.
GI disturbances, dizziness and headaches.
Decreased libido, gynecomastia and decreased sperm count.
All of the above
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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.
b.
c.
d.
complications of fetal development such as spina bifida.
megaloblastic anemia and peripheral neuropathy in adults.
increased cardiovascular disease in women only.
Answers a., and b.
13. People taking anti-seizure medications should:
a.
b.
c.
d.
Add vitamin D and calcium to their daily diet.
Not worry about vitamin D deficiency.
Immediately start on vitamin D 50,000 iu twice daily.
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.
b.
c.
d.
high dosing of vitamin D.
surgery.
smoking cessation.
genetic testing.
15. Lamotrigine (Lamictal) is an approved adjunctive therapy for:
a.
b.
c.
d.
Partial seizures.
Generalized seizures associated with Lennox-Gestaut syndrome.
Children aged 2 years and older and in adults.
All of the above
16. True or False: Levetiracetam (Keppra) has properties similar
to Phenytoin and Carbamezapine.
a. True
b. False
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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.
b.
c.
d.
15%
25%
50%
80%
18. Children with epilepsy are particularly prone to behavioral
and emotional problems that typically fall into two categories:
a.
b.
c.
d.
Internal and external factors.
Depression and anxiety.
Body dysmorphic disorder and feels of stigmatization.
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.
b.
c.
d.
symptomatic
partial
*idiopathic
parietal
21. Occipital seizures are often mistaken for ________________
because they share similar symptoms.
a.
b.
c.
d.
vertigo
tuberous sclerosis
tonic-clonic seizures
*migraine headaches
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22. Epilepsy is not considered as a diagnosis until the patient has
had
a.
b.
c.
d.
*two or more unprovoked seizures.
a seizure as an adult.
two or more seizures lasting over a minute.
a documented seizure.
23. Slightly over half of seizures in adults are
a.
b.
c.
d.
caused by benign rolandic epilepsy.
*complex partial seizures.
caused by early myoclonic encephalopathy.
febrile seizures.
24. In patients with atonic (drop) seizures, a surgical procedure
called ____________________ may help reduce the falls that
may result from seizures.
a.
b.
c.
d.
lesionectomy
multiple subpial transections
*corpus callosotomy
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.
b.
c.
d.
caused by migraine headaches.
*of unknown cause.
and is always a life-long disease.
and is untreatable.
26. True or False: Most idiopathic epilepsy syndromes are
presumed to be due to a genetic cause.
a. *True
b. False
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27. _____________ is/are a type of progressive myoclonic
epilepsy that involves a genetic mutation.
a.
b.
c.
d.
Unverricht-Lundborg Syndrome
*Mitchondrial disorders
Benign rolandic epilepsy
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.
b.
c.
d.
hospitalization.
multiple subpial transections.
*trying to avoid the triggering stimulus.
immunologic therapies.
30. With febrile seizures, the following is/are true:
a.
b.
c.
d.
*The peak age is 18 months.
In most instances, hospitalization is necessary.
Seizures are absent with high fever.
All of the above
31. Medication to treat benign rolandic (sylvian) epilepsy is
usually continued
a.
b.
c.
d.
for the patient’s lifetime.
for the first 18 months.
into the patient’s adulthood.
*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
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33. Remission in childhood absence epilepsy (CAE) cases can be
achieved in approximately ____ of patients.
a.
b.
c.
d.
25%
10%
50%
*80%
34. _______________ is defined as the loss of language abilities
that had been present.
a.
b.
c.
d.
Acquired atrophy
Dysmorphism
*Acquired aphasia
Pallinopsia
35. Which of the following treatments may be effective to treat
acquired aphasia?
a.
b.
c.
d.
*Multiple subpial transections
Antiepileptic drugs
Immunologic therapies
Vagus nerve stimulation
36. Electroencephalography (EEG) biofeedback is especially
helpful in treating
a.
b.
c.
d.
febrile seizures.
*partial seizures.
benign rolandic epilepsy.
acquired aphasia.
37. Routine _________ supplementation is important for women
and men receiving antiepileptic drugs.
a.
b.
c.
d.
melatonin
calcium
*folic acid
valproic acid
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38. One of the most common side effects caused by valproate
products (which are anticonvulsants) is
a.
b.
c.
d.
hair thinning.
dizziness.
*weight gain.
difficulty concentrating.
39. Carbamazepine is used for many types of epilepsy. In addition
to controlling seizures, it may help
a.
b.
c.
d.
treat nausea.
treat insomnia.
treat acquired aphasia.
*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
11.
d
21.
d
31.
d
2.
a
12.
d
22.
a
32.
b
3.
d
13.
a
23.
b
33.
d
4.
a
14.
b
24.
c
34.
c
5.
c
15.
d
25.
b
35.
a
6.
a
16.
b
26.
a
36.
b
7.
a
17.
d
27.
b
37.
c
8.
b
18.
a
28.
a
38.
c
9.
a
19.
a
29.
c
39.
d
10.
b
20.
c
30.
a
40.
a
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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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