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A selzure dlsorder ls a condlLlon ln whlch Lhe neurons ln Lhe braln funcLlon abnormally resulLlng
ln sudden brlef changes ln how Lhe braln works 1hese changes resulL ln selzures whlch lnvolve
convulslons muscle spasms and loss of consclousness A person needs Lo have Lwo or more selzures Lo
be classlfled as havlng a dlsorder Also known as convulslons epllepLlc selzures and lf recurrenL
epllepsy lL ls a sudden alLeraLlons ln normal braln acLlvlLy LhaL cause dlsLlncL changes ln behavlor and
body funcLlon 1hey are LhoughL Lo resulL from abnormal recurrenL unconLrolled elecLrlc dlscharges of
neurons ln Lhe braln
aLhophyslology ls poorly undersLood buL seems Lo be relaLed Lo meLabollc and elecLrochemlcal
facLors aL Lhe cellular level redlsposlng facLors lnclude head or braln Lrauma Lumors cranlal surgery
meLabollc dlsorders (hypocalcemla hypoglycemla or hyperglycemla hyponaLremla anoxla) cenLral
nervous sysLem lnfecLlon clrculaLlng dlsorders drug LoxlclLy drug wlLhdrawal sLaLes (alcohol
barblLuraLes) and congenlLal neurodegeneraLlve dlsorders
Selzures happen when your braln cells whlch communlcaLe Lhrough elecLrlcal slgnals send ouL
abnormal slgnals Powever even mlld selzures LhaL happen more Lhan once should be LreaLed because
Lhey could cause harm lf Lhey happen whlle you are drlvlng walklng or swlmmlng for example lL
someLlmes do cause braln damage parLlcularly lf Lhey are severe Powever mosL selzures do noL seem
Lo have a deLrlmenLal effecL on Lhe braln Any changes LhaL do occur are usually subLle and lL ls ofLen
unclear wheLher Lhese changes are caused by Lhe selzures Lhemselves or by Lhe underlylng problem LhaL
caused Lhe selzures
Whlle epllepsy cannoL currenLly be cured for some people lL does evenLually go away 1he odds
of becomlng selzurefree are noL as good for adulLs or for chlldren wlLh severe epllepsy syndromes buL
lL ls noneLheless posslble LhaL selzures may decrease or even sLop over Llme

nIS1Ck
Selzure was one of Lhe flrsL braln dlsorders Lo be descrlbed lL was menLloned ln anclenL 8abylon
more Lhan 3000 years ago 1he sLrange behavlor caused by some selzures has conLrlbuLed Lhrough Lhe
ages Lo many supersLlLlons and pre[udlces eople once LhoughL LhaL Lhose wlLh selzures were belng
vlslLed by demons or gods Powever ln 400 8C Lhe early physlclan PlppocraLes suggesLed LhaL selzure
was a dlsorder of Lhe braln and we now know LhaL he was rlghL
Selzure ls a braln dlsorder ln whlch clusLers of nerve cells or neurons ln Lhe braln someLlmes
slgnal abnormally neurons normally generaLe elecLrochemlcal lmpulses LhaL acL on oLher neurons
glands and muscles Lo produce human LhoughLs feellngs and acLlons ln selzure Lhe normal paLLern of
neuronal acLlvlLy becomes dlsLurbed causlng sLrange sensaLlons emoLlons and behavlor or someLlmes
convulslons muscle spasms and loss of consclousness uurlng a selzure neurons may flre as many as
300 Llmes a second much fasLer Lhan normal ln some people Lhls happens only occaslonally for
oLhers lL may happen up Lo hundreds of Llmes a day
lamous people who are known or rumored Lo have had epllepsy lnclude Lhe 8usslan wrlLer
uosLoyevsky Lhe phllosopher SocraLes Lhe mlllLary general napoleon and Lhe lnvenLor of dynamlLe
Alfred nobel who esLabllshed Lhe nobel rlze

kLVALLNCL
More Lhan 2 mllllon people abouL 1 ln 100 have experlenced an unprovoked selzure or been
dlagnosed wlLh epllepsy lor abouL 80 percenL of Lhose dlagnosed wlLh epllepsy selzures can be
conLrolled wlLh modern medlclnes and surglcal Lechnlques Powever abouL 23 Lo 30 percenL of people
wlLh epllepsy wlll conLlnue Lo experlence selzures even wlLh Lhe besL avallable LreaLmenL uocLors call
Lhls slLuaLlon lnLracLable epllepsy Cnly when a person has had Lwo or more selzures ls he or she
consldered Lo have epllepsy

What Causes It?
A selzure dlsorder can be caused by a varleLy of facLors AnyLhlng LhaL dlsLurbs Lhe normal
paLLern of neuron acLlvlLy from lllness Lo braln damage Lo abnormal braln developmenL can cause a
selzure 1he condlLlon may develop as Lhe resulL of abnormallLy ln braln wlrlng an lmbalance of nerve
slgnallng chemlcals called neuroLransmlLLers or some comblnaLlon of Lhese facLors Selzure dlsorders
are noL conLaglous and are noL caused by menLal lllness or menLal reLardaLlon
D|agnos|ng a Se|zure D|sorder
Lxperlenclng a slngle selzure does noL necessarlly mean LhaL a person has a selzure dlsorder Cnly when
a person has had Lwo or more selzures ls he or she consldered Lo have a dlsorder 8raln scans and
elecLroencephalograms (LLCs) are common LesLs used Lo make a dlagnosls

kCGNCSIS
Whlle a selzure dlsorder cannoL currenLly be cured for some people lL does evenLually go away Cne
sLudy found LhaL chlldren wlLh ldlopaLhlc epllepsy or a selzure dlsorder wlLh an unknown cause had a
68 Lo 92 percenL chance of becomlng selzurefree by 20 years afLer Lhelr dlagnosls 1he odds of
becomlng selzurefree are noL as good for adulLs or for chlldren wlLh severe selzure dlsorders buL lL ls
noneLheless posslble for selzures Lo decrease or even sLop over Llme 1hls ls more llkely lf Lhe dlsorder
has been wellconLrolled by medlcaLlon or lf Lhe person has had surgery
MosL selzures do noL cause braln damage however lL ls noL uncommon for people wlLh a
dlsorder especlally chlldren Lo develop behavloral and emoLlonal problems someLlmes Lhe
consequence of embarrassmenL and frusLraLlon or bullylng Leaslng or avoldance ln school and oLher
soclal seLLlngs
lor many people wlLh a selzure dlsorder Lhe rlsk of selzures resLrlcLs Lhelr lndependence (some
sLaLes refuse drlvers llcenses Lo people wlLh a dlsorder) and recreaLlonal acLlvlLles eople wlLh a selzure
dlsorder are aL speclal rlsk for Lwo llfeLhreaLenlng condlLlons sLaLus epllepLlcus and sudden
unexplalned deaLh
MosL women wlLh a selzure dlsorder can become pregnanL buL Lhey should dlscuss Lhelr
condlLlon and Lhe medlcaLlons Lhey are Laklng wlLh Lhelr docLors Women wlLh Lhe condlLlon have a 90
percenL or beLLer chance of havlng a normal healLhy baby




!1tC!t>CCG.
The clinical neurophysiologic hallmark of partial-onset seizures is the focal interictal epileptiform
spike or sharp wave. The cellular neurophysiologic correlate of an interictal epileptiform discharge in
single cortical neurons is the paroxysmal depolarization shift (PDS). The PDS is characterized by a
prolonged calcium-dependent depolarization that results in multiple sodium-mediated action potentials
during the depolarization phase, and it is followed by a prominent after hyperpolarization, which is a
hyperpolarized membrane potential beyond the baseline resting potential. Calcium-dependent potassium
channels mostly mediate the after-hyperpolarization phase. When multiple neurons fire PDSs in a
synchronous manner, the extracellular field recording shows an interictal spike. f the number of
discharging neurons is more than several million, they can usually be recorded with scalp electrographic
(EEG) electrodes. Calculations show that the interictal spikes need to spread to about 6 cm
2
of cerebral
cortex before they can be detected with scalp electrodes. Several factors may be associated with the
transition from an interictal spike to an epileptic seizure. When any of the mechanisms that underlie an
acute seizure become a permanent alteration, patients are assumed to then develop a propensity for
recurrent seizures.The mechanisms discussed below may coexist in different combinations to cause
partial-onset seizures. f the mechanisms leading to a net increased excitability become permanent
alterations, patients may have pharmacologically intractable partial-onset epilepsy. Currently available
medications were developed in acute models of convulsions. n clinical use, they are most effective at
blocking propagation of a seizure. Further understanding of the mechanisms that permanently increase
net excitability may lead to development of true antiepileptic drugs that alter the natural history of
epilepsy. Mechanisms leading to decreased inhibition and those leading to increased excitation are
discussed in this section. Mechanisms leading to decreased inhibition include the following:
Defective gamma-aminobutyric acid (GABA)A inhibition, Defective GABA-B inhibition,
Defective activation of GABA neurons and Defective intracellular buffering of calcium
The clinical neurophysiologic hallmark of partial-onset seizures is the focal interictal epileptiform spike or sharp wave.
The cellular neurophysiologic correlate of an interictal epileptiform discharge in single cortical neurons is the
paroxysmal depolarization shift (PDS). The PDS is characterized by a prolonged calcium-dependent depolarization
that results in multiple sodium-mediated action potentials during the depolarization phase, and it is followed by a
prominent after hyperpolarization, which is a hyperpolarized membrane potential beyond the baseline resting
potential. Calcium-dependent potassium channels mostly mediate the after-hyperpolarization phase. When multiple
neurons fire PDSs in a synchronous manner, the extracellular field recording shows an interictal spike. f the number
of discharging neurons is more than several million, they can usually be recorded with scalp electrographic (EEG)
electrodes. Calculations show that the interictal spikes need to spread to about 6 cm
2
of cerebral cortex before they
can be detected with scalp electrodes. Several factors may be associated with the transition from an interictal spike to
an epileptic seizure. When any of the mechanisms that underlie an acute seizure become a permanent alteration,
patients are assumed to then develop a propensity for recurrent seizures (ie, epilepsy). The mechanisms discussed
below may coexist in different combinations to cause partial-onset seizures. f the mechanisms leading to a net
increased excitability become permanent alterations, patients may have pharmacologically intractable partial-onset
epilepsy. Currently available medications were developed in acute models of convulsions. n clinical use, they are
most effective at blocking propagation of a seizure. Further understanding of the mechanisms that permanently
increase net excitability may lead to development of true antiepileptic drugs that alter the natural history of epilepsy.
Mechanisms leading to decreased inhibition and those leading to increased excitation are discussed in this section.
Mechanisms leading to decreased inhibition include the following:
O Defective gamma-aminobutyric acid (GABA)A inhibition,Defective GABA-B inhibition, Defective activation of
GABA neurons, Defective intracellular buffering of calcium
1he Lerm selzure dlsorder refers Lo a condlLlon LhaL occurs when clusLers of nerve cells or neurons ln Lhe braln someLlmes
slgnal abnormallly When Lhese braln cells are noL worklng properly a persons consclousness movemenL or acLlons may be
alLered for a shorL Llme 1hese physlcal changes are called epllepLlc selzures AffecLlng lacLor Lhen gray maLLer whlch conLalns
Lhe nerve cell bodles wlll lncrease flrlng 1here wlll be alLeraLlons ln enzymes and neuroLransmlLLer subsLances wlLhln Lhe braln
AfLer LhaL epllepLlc neurons wlll recrulL ad[acenL neurons Lo flre abnormal acLlvlLy ulsLrubance ln Lhe exclLaLory and lnhlblLory
synapses lmplnglng on Lhe epllepLlc neuron Defective GABA-A inhibition = GABA is the main inhibiting
neurotransmitter in the brain, and it binds to 2 major classes of receptors: GABA-A and GABA-B. GABA-A receptors
are coupled to chloride channels, and they are one of the main targets modulated by the anticonvulsant agents that
are currently available. The reversal potential of chloride is about -70 mV. The contribution of chloride channels
during resting potential in neurons is minimal, because at the typical resting potential, which is near -70 mV, no
significant electromotive force exists for net chloride flux. However, chloride currents become more important at more
depolarized membrane potentials. These channels make it difficult to achieve the threshold membrane potential
necessary for an action potential. Their influence in the neuronal membrane potential increases, as the neurons
become more depolarized by summation of the excitatory postsynaptic potentials (EPSPs).
Properties of the chloride channels associated with the GABA-A receptor are often clinically modulated by using
benzodiazepines (eg, diazepam, lorazepam, clonazepam), barbiturates (eg, phenobarbital, pentobarbital), or the
anticonvulsive drug topiramate. Benzodiazepines increase the frequency of openings of chloride channels, whereas
barbiturates increase the duration of openings of these channels. Topiramate increases the frequency of channel
openings but binds to a site different from the benzodiazepine-receptor site. Either benzodiazepines or barbiturates,
but not both, appear to modulate individual chloride channels. Whether combining topiramate with either class of
agents increases the chloride currents is unknown. Alterations in the normal state of the chloride channels described
above increase membrane permeability and conductance of chloride ions. n the end, the behavior of all individual
chloride channels sum to form a large chloride-mediated hyperpolarizing current that counterbalances the
depolarizing currents created by summation of excitatory postsynaptic responses (EPSPs) induced by activation of
the excitatory input.
The EPSPs are the main form of communication between neurons, and the release of the excitatory amino acid
glutamate from the presynaptic element mediates EPSPs. Three main receptors mediate the effect of glutamate
release in the postsynaptic neuron: -methyl-D-aspartic acid (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole
propionic acid (AMPA)/kainate, and metabotropic, which are coupled by means of different mechanisms to several
depolarizing channels. nhibitory postsynaptic potentials (PSPs), mediated mainly by the release of GABA in the
synaptic cleft with postsynaptic activation of GABA-A receptors, temper these effects. All channels in the nervous
system (and essentially any living organism) appear to be subject to modulation by several mechanisms, such as
phosphorylation and possibly a change in the tridimensional conformation of a protein in the channel. The chloride
channel has several phosphorylation sites, one of which topiramate appears to modulate. Phosphorylation of this
channel induces a change in normal electrophysiologic behavior, with an increased frequency of channel openings
but for only certain chloride channels. Each channel has a multimeric structure with several subunits of different
types. Chloride channels are no exception; they have a pentameric structure. The subunits are molecularly related
but different proteins.
The heterogeneity of electrophysiologic responses of different GABA-A receptors is due to different combinations of
the subunits. n mammals, at least 6 alpha subunits and 3 beta and gamma subunits exist for the GABA-A receptor
complex. A complete GABA-A receptor complex (which in this case is the chloride channel itself) is formed from 1
gamma, 2 alpha, and 2 beta subunits. The number of possible combinations of the known subunits is almost 1000;
therefore, more than 1000 receptor types theoretically exist.
n practice, only about 20 of these combinations have been found in the normal mammalian brain. Some epilepsies
may be due to mutations or lack of expression of the different GABA-A receptor complex subunits, the molecules that
govern their assembly, or the molecules that modulate their electrical properties. For example, hippocampal
pyramidal neurons might not be able to assemble alpha 5 beta 3 gamma 3 receptors because of deletion of
chromosome 15 (ie, Angelman syndrome).
Changes in the distribution of subunits of the GABA-A receptor complex have been demonstrated in several animal
models of partial-onset epilepsy, such as the electrical-kindling, chemical-kindling, and pilocarpine models. n the last
model, decreased concentrations of mRNA for the alpha 5 subunit of the surviving interneurons were observed in the
CA1 region of the rat hippocampus.
[4]

Defective GABA-B inhibition
The GABA-B receptor is coupled to potassium channels, forming a current that has a relatively long duration of action
compared with the chloride current evoked by activation of the GABA-A receptor. Because of the long duration of
action, alterations in the GABA-B receptor are thought to possibly play a major role in the transition between the
interictal abnormality and a partial-onset seizure. The molecular structure of the GABA-B receptor complex consists
of 2 subunits with 7 transmembrane domains each.
G proteins, a second messenger system, mediate coupling to the potassium channel, explaining the latency and long
duration of the response. n many cases, GABA-B receptors are located in the presynaptic element of an excitatory
projection. Therefore, release of GABA from the interneuron terminal inhibits the postsynaptic neuron by means of 2
mechanisms: (1) direct induction of an PSP, which a GABA-A chloride current typically mediates, and (2) indirect
inhibition of the release of excitatory neurotransmitter in the presynaptic afferent projection, typically with a GABA-B
potassium current. Once again, alterations or mutations in the different subunits or in the molecules that regulate their
function might affect the seizure threshold or the propensity for recurrent seizures.
Defective activation of GABA neurons GABA neurons are activated by means of feedforward and feedback
projections by excitatory neurons. These 2 types of inhibition in a neuronal network are defined on the basis of the
time of activation of the GABAergic neuron relative to that of the principal neuron output of the network, such as the
hippocampal pyramidal CA1 cell. n feedforward inhibition, GABAergic cells receive a collateral projection from the
main afferent projection that activates the CA1 neurons, namely, the Schaffer collateral axons from the CA3
pyramidal neurons. This feedforward projection activates the soma of GABAergic neurons before or simultaneously
with activation of the apical dendrites of the CA1 pyramidal neurons.
Activation of the GABAergic neurons results in an PSP that inhibits the soma or axon hillock of the CA1 pyramidal
neurons almost simultaneously with the passive propagation of the excitatory potential (ie, EPSP) from the apical
dendrites to the axon hillock. The feedforward projection thus primes the inhibitory system in a manner that allows it
to inhibit the pyramidal cell's depolarization and firing of an action potential. Feedback inhibition is another system
that allows GABAergic cells to control repetitive firing in principal neurons, such as pyramidal cells, and to inhibit the
surrounding pyramidal cells. Recurrent collaterals from the pyramidal neurons activate the GABAergic neurons after
the pyramidal neurons fire an action potential. n the last few years, experimental evidence has indicated that some
other kind of interneuron might be a gate between the principal neurons and the GABAergic neurons. n the dentate
gyrus, the mossy cells of the hilar polymorphic region appear to gate inhibitory tone and activate GABAergic neurons.
The mossy cells receive both feedback and feedforward activation, which they convey to the GABAergic neurons.
However, in certain circumstances they appear highly vulnerable to seizure-related neuronal loss.
After some of the mossy cells are lost, activation of GABAergic neurons is impaired.
[5]
Synaptic reorganization is a
form of brain plasticity induced by neuronal loss. Formation of new circuits that include excitatory and inhibitory cells
has been demonstrated in several animal models and in humans with intractable temporal-lobe epilepsy. nsufficient
sprouting that attempts to restore inhibition might alter the balance between excitatory and inhibitory tone in the
neural network.
Defective intraceIIuIar buffering of caIcium = Recurrent seizures induced by a variety of methods result in a
pattern of interneuron loss in the hilar polymorphic region in rodents, with striking loss of the neurons that lack
calcium-binding proteins parvalbumin and calbindin. n rat hippocampal sections, these interneurons demonstrate a
progressive inability to maintain a hyperpolarized resting membrane potential; eventually, they die. An experiment in
which researchers used microelectrodes containing the calcium chelator BAPTA demonstrated reversal of the
deterioration in the membrane potential as the calcium chelator was allowed to diffuse in the interneuron
[6]
; the result
showed the critical role of adequate concentrations of calcium-binding proteins. A postulated contributor is medical
intractability in some patients, which may contribute to the abnormally low concentrations or even dysfunction of
these proteins. The end result is the premature loss of interneurons, which alters inhibitory control over the local
neuronal network in favor of net excitation. This effect may explain, for example, why 2 patients who have a similar
event (eg, simple febrile convulsion) have remarkably dissimilar outcomes: One may have completely normal
development, and the other may have intractable partial-onset epilepsy after a few years.
Mechanisms leading to increased excitation include the following:
O ncreased activation of NMDA receptors
O ncreased synchrony between neurons due to ephaptic interactions
O ncreased synchrony and/or activation due to recurrent excitatory collaterals
ncreased activation of NMDA receptors
Glutamate is the major excitatory neurotransmitter in the brain. The release of glutamate causes an EPSP in the
postsynaptic neuron by activating the glutaminergic receptors AMPA/kainate and NMDA and the metabotropic
receptor. Fast neurotransmission is achieved with the first 2 types. The metabotropic receptor alters cellular
excitability by means of a second-messenger system with late onset but prolonged duration. The major functional
difference between the 2 fast receptors is that the AMPA/kainate receptor opens channels that primarily allow the
passage of monovalent cations (ie, sodium and potassium), whereas the NMDA type is coupled to channels that also
allow passage of divalent cations (ie, calcium).
Calcium is a catalyst for many intracellular reactions that lead to changes in phosphorylation and gene expression.
Thus, it is in itself a second-messenger system. NMDA receptors are generally assumed to be associated with
learning and memory. The activation of NMDA receptors is increased in several animal models of epilepsy, such as
kindling, kainic acid status, pilocarpine, and other models. Some patients with epilepsy may have an inherited
predisposition for fast or long-lasting activation of NMDA channels that alters their seizure threshold. Other possible
alterations include the ability of intracellular proteins to buffer calcium, increasing the vulnerability of neurons to any
kind of injury that otherwise would not result in neuronal death.
ncreased synchrony between neurons due to ephaptic interactions
Electrical fields created by synchronous activation of pyramidal neurons in laminar structures, such as the
hippocampus, may increase further the excitability of neighboring neurons by nonsynaptic (ie, ephaptic) interactions.
Other possible nonsynaptic interactions include electrotonic interactions due to gap junctions or changes in
extracellular ionic concentrations of potassium and calcium.
ncreased synchrony and/or activation due to recurrent excitatory coIIateraIs
Neuropathologic studies of patients with intractable partial-onset epilepsy have revealed frequent
abnormalities in the limbic system, particularly in the hippocampal formation. A common lesion is hippocampal
sclerosis, which consists of a pattern of gliosis and neuronal loss primarily affecting the hilar polymorphic region and
the CA1 pyramidal region. These changes are associated with relative sparing of the CA2 pyramidal region and an
intermediate lesion in the CA3 pyramidal region with dentate granule cells. Prominent hippocampal sclerosis is found
in about two thirds of patients with intractable temporal-lobe epilepsy. Animal models of status epilepticus reproduced
this pattern of injury; however, animals with more than 100 brief convulsions induced by kindling seizures had a
similar pattern.
[7]

Seizures are paroxysmal manifestations of the electrical properties of the cerebral cortex. A seizure results
when a sudden imbalance occurs between the excitatory and inhibitory forces within the network of cortical neurons
in favor of a sudden-onset net excitation. f the affected cortical network is in the visual cortex, the clinical
manifestations are visual phenomena. Other affected areas of primary cortex give rise to sensory, gustatory, or motor
manifestations. The pathophysiology of partial-onset seizures differs from the mechanisms underlying generalized-
onset seizures. Overall, cellular excitability is increased, but the mechanisms of synchronization appear to
substantially differ and are therefore discussed separately.



|CDC |GC|C1.
CfLen a person who has had a new or severe selzure wlll be seen ln an emergency room raLher
Lhan a docLors offlce 1he healLh care provlder wlll Lry Lo dlagnose Lhe Lype of selzure based on Lhe
sympLoms CLher medlcal condlLlons LhaL can cause a selzure or slmllar sympLoms wlll be ruled ouL
ulsorders LhaL may cause slmllar sympLoms lnclude falnLlng 1lA or sLroke rage or panlc aLLacks
mlgralne headaches sleep dlsLurbances and condlLlons LhaL cause loss of consclousness

Ant|ep||ept|c Med|cat|ons
1reaLmenL for paLlenLs wlLh epllepsy Lyplcally beglns wlLh anLlepllepLlc drug (ALu) Lherapy 1he
goal of LreaLmenL ls compleLe selzure conLrol wlLh no slde effecLs 1here are many facLors Lo conslder ln
chooslng whlch medlcaLlon(s) are prescrlbed Lo paLlenLs 1he mosL lmporLanL ls Lhe selzure Lype CLher
facLors lnclude buL are noL llmlLed Lo age sex longLerm goals healLh hlsLory drug lnLeracLlons
poLenLlal slde effecLs and psychologlcal hlsLory rescrlblng medlcaLlon ls based on research and cllnlcal
pracLlce 1he uS lood and urug AdmlnlsLraLlon (luA) has approved cerLaln ALus Lo be used for cerLaln
selzure Lypes 1he followlng are examples of luA approved ALus for selzure Lypes
- Carbamazeplne lelbamaLe CabapenLln LamoLrlglne LeveLlraceLam Cxcarbazeplne
henobarblLal henyLoln regaballn 1lagablne 1oplramaLe valprolc acld dlvalproex sodlum
Zonlsamlde

D|agnost|c 1ests
L|ectroencepha|ogram (LLG) baslc nonlnvaslve LesL capLurlng elecLrlcal changes wlLhln Lhe
braln by uslng scalp elecLrodes 1hese elecLrodes are placed ln varlous monLages uslng a dlfferenL
number of conLacLs 1hese LesLs can be ordered for as llLLle as a half hour up Lo 23 hours wlLh or
wlLhouL a vldeo camera for added cllnlcal lnformaLlon lor monlLorlng greaLer Lhan 23 hours Lhe
physlclan would conslder admlsslon lnLo Lhe LMu Care of Lhe paLlenL ln Lhe LMu ls dlscussed below
Magnet|c resonance |mag|ng (MkI) nonlnvaslve LesL used Lo look for sLrucLural changes wlLhln
Lhe braln 1here are dlfferenL Lypes of M8ls LhaL can be used Cne Lype ls Lhe LhlncuL M8l allowlng for
Lhe coronal and 12 cuLs Lo beLLer vlsuallze Lhe meslal sLrucLures of Lhe braln ln looklng for hlppocampal
changes 1here are aL leasL Lhree dlfferenL magneLs LhaL can be used for Lhe M8l 1wo of Lhe magneL
Lypes normally used for Lhe M8l are Lhe 13 1esla and 2 1esla A paLlenL who has a vagal nerve
sLlmulaLor (vnS) can have Lhe devlce Lurned off prlor Lo Lhese Lwo magneL M8ls wlLhouL damage up Lo
a 13 1esla magneL 1he devlce needs Lo be Lurned back on afLer Lhe M8l 1he 3 1esla magneL M8l ls
used Lo vlsuallze corLlcal dysplasla
1he MkS ls a nonlnvaslve LesL LhaL looks aL chemlcal changes wlLhln Lhe braln especlally around
Lhe hlppocampus 1hls LesL can be performed aL Lhe same Llme as Lhe M8l (whlch can add
approxlmaLely 1330 mlnuLes more dependlng on Lhe faclllLy) CurrenLly a number of lnsurance
companles vlew Lhe M8S as experlmenLal for Lhe dlagnosls of epllepsy leavlng Lhe paLlenL Lo cover Lhe
expense of Lhe LesL
Magnetoencepha|ography (MLG) 1he MLC ls nonlnvaslve neurolmaglng LhaL deLecLs analyzes
and noLes Lhe lnLerrupLlons ln Lhe magneLlc fleld by elecLrlcal acLlvlLy ln Lhe braln capLured aL hundreds
of polnLs around Lhe head ln snapshoLs 1hls ls a relaLlvely new lmaglng Lechnlque for Lhe epllepsy
paLlenL LhaL looks aL neuronal acLlvlLy wlLhln Lhe braln ln a quanLlLaLlve way Lomographlc lmages of Lhe
elecLrlcal currenL denslLy ln Lhe braln can be exLracLed from each snapshoL of Lhe MLC slgnal allowlng
ldenLlflcaLlon of superflclal and deep daLa ln Lhe form of Lomographlc lmages 1he MLC musL have
splkes from Lhe scalp LLC ln order for Lhe LesLlng Lo occur 1he LesL allows for Lhe varlablllLy ln a slngle
area Lo be seen ln Lhe conLexL of acLlvlLy ln oLher areas and background rhyLhmlc acLlvlLy (loannldes
2006)
1he Wada test or lnLracaroLld amobarblLal procedure ls an lnvaslve LesL used Lo locallze Lhe
language and memory ueveloped by ur !uhn Wada lL has been Lhe gold sLandard for laLerallzaLlon of
language domlnance before epllepsy surgery (Aboukhalll 2007) lnformed consenL needs Lo be
obLalned prlor Lo Lhe Wada LesL Scalp elecLrodes are placed Lo monlLor Lhe braln waves durlng Lhe LesL
An anglographlc caLheLer ls lnserLed vla Lhe groln by Lhe neuroradlologlsL When Lhls caLheLer reaches
Lhe caroLld arLerles locaLlon ls checked wlLhln Lhe braln 1hen amobarblLal ls ln[ecLed ln Lhe caroLld
arLerles one aL a Llme for hemlspherlc anesLhesla LesLlng of sponLaneous speech counLlng
comprehenslon namlng repeLlLlon readlng and memory Cnce boLh sldes have been LesLed Lhe
caLheLer ls removed and a pressure dresslng ls applled Lo Lhe caLheLer slLe 1he nurse should carefully
monlLor Lhe paLlenL for compllcaLlons for approxlmaLely 6 hours afLer Lhe anglogram (Level 3 1renerry
Lorlng 2003) Cnce Lhe paLlenL ls cleared Lo leave by Lhe physlclan Lhe paLlenL ls able Lo leave wlLh a
less bulky pressure dresslng 1he resulLs of Lhe Wada LesL are analyzed and placed wlLh Lhe resulLs of all
Lhe oLher LesLs Lo deLermlne wheLher proceedlng Lo a resecLlon would be beneflclal for Lhe paLlenL
8ecause of Lhe rlsks of Lhls lnvaslve procedure alLernaLlves Lo Lhe Wada LesL are belng consldered and
developed lncludlng fM8l CwaLer L1 and Lranscranlal uoppler

Surg|ca| Management
Surglcal opLlons wlll depend on Lhe resulLs of medlcaLlon conLrol and LesL resulLs llrsL
lnLracLablllLy musL be esLabllshed lf a selzure focus has been ldenLlfled and Lhe resulLs of LesLlng are
concordanLand Lhere ls a low poLenLlal for posLoperaLlve deflclLsa lobecLomy would be consldered
1he Lemporal lobecLomy ls Lhe mosL common resecLlon 1he resulLs of Lhe Wada LesL and addlLlonal
lnformaLlon from depLh elecLrodes and neuropsychologlcal LesLlng would provlde lnformaLlon wheLher
an amygdalohlppocampecLomy or hlppocampecLomy mlghL be lncluded wlLh Lhe Lemporal lobecLomy ln
order Lo spare memory LxLraLemporal resecLlon may occur wlLh or wlLhouL lnvaslve monlLorlng local
resecLlons for leslonecLomy can be consldered ln Lhe presence of benlgn Lumors cavernomas or
arLerlovenous malformaLlons lf Lhe epllepsy ls nonleslonal and Lhe LLC ls suggesLlve of laLerallzaLlon Lo
one lobe or hemlsphere lnvaslve monlLorlng ls ofLen used Lo beLLer locallze Lhe selzure focus ln
chlldren wlLh caLasLrophlc epllepsy ln Lhe seLLlng of malformaLlons of corLlcal developmenL
hemlmegalencephaly SLurgeWeber syndrome 8asmussen encephallLls or perlnaLal sLroke a
hemlspherecLomy mlghL be Lhe mosL prudenL course of acLlon and afford Lhe chlld Lhe besL opporLunlLy
for reduclng selzure burden
1he reducLlon of ALus afLer resecLlve epllepsy surgery ls consldered on an lndlvldual basls
1here ls currenLly no sLandard meLhod Lo deLermlne selzure efflcacy once ALus have been dlsconLlnued
posLoperaLlvely 1here are a number of research arLlcles currenLly avallable Lo glve guldance concernlng
Lhls lssue (eg 8erg eL al 2006 klm eL al 2003 SchmldL 8aumgarLner Loscher 2004)
A corpus callosecLomy ls a procedure LhaL dlsconnecLs Lhe hemlspheres by secLlonlng Lhe corpus
callosum Lo prevenL selzures from spreadlng from one hemlsphere Lo Lhe oLher lL ls noL rouLlnely
performed 1hls procedure can reduce Lhe rlsk of selzurerelaLed ln[ury Lo paLlenLs wlLh aLonlc selzures
or drop aLLacks or who repeaLedly ln[ure Lhemselves serlously 1hls surglcal opLlon ls noL used unless
medlcally necessary because of poLenLlal recovery deflclLs

1he vagus nerve SLlmulaLor (vnS) 1he vnS ls anoLher surglcal opLlon for epllepsy paLlenLs who are noL
candldaLes for lobecLomy 1he vnS ls placed LranscuLaneously ln Lhe C8 1he generaLor ls Lyplcally
lmplanLed ln Lhe lefL upper chesL under Lhe clavlcle whlle Lhe leads are wrapped around Lhe lefL vagus
nerve 1he devlce works by sendlng mlld elecLrlcal lmpulses Lo Lhe vagus nerve whlch ln Lurn sends
slgnals Lo Lhe braln 1he lnLenslLy and duraLlon of lmpulses ls deLermlned by Lhe pracLlLloner and ls
ofLen programmed durlng an ouLpaLlenL vlslL uurlng sLlmulaLlon paLlenLs may experlence hoarseness a
deeper Lone of volce or a buzzlng sensaLlon AlLhough noL recommended Lhe paLlenL can suspend Lhe
sLlmulus by Laplng Lhe magneL over Lhe generaLor Lo decrease Lhe buzzlng feellng durlng sleep
(Cyberonlcs vagus nerve 1herapy 2003)

Lxper|menta| 1reatments 1here ls ongolng research Lo help lmprove Lhe llves of epllepsy paLlenLs
numerous poLenLlal medlcaLlons are ln varlous phases of sLudy boLh precllnlcal and cllnlcal

Surg|ca| Cpt|ons
An lmplanLaLlon devlce called Lhe neuroace (8esponslve neurosLlmulaLor) ls also belng
lnvesLlgaLed 1he neuroace ls deslgned Lo deLecL abnormal elecLrlcal acLlvlLy ln Lhe braln and respond
by dellverlng elecLrlcal sLlmulaLlon Lo normallzed braln acLlvlLy before Lhe paLlenL experlences selzure
sympLoms (wwwneuroacecom) 1hese ongolng research efforLs reflecL Lhe common goal of
healLhcare professlonals and lndusLry Lo glve epllepsy paLlenLs hope for a beLLer quallLy of llfe

Nonsurg|ca| Cpt|ons
nonsurglcal opLlons lnclude dlfferenL dleLs ln addlLlon Lo Lhe dally ALus 1he keLogenlc dleL has
been uLlllzed ln Lhe pedlaLrlc populaLlon wlLh some success (8uelow eL al 2004 Lpllepsy loundaLlon of
Amerlca LlA 2003) resenLly some lnvesLlgaLors and lnsLlLuLlons are evaluaLlng lLs effecLs on adulLs
wlLh epllepsy 1he Lheory behlnd Lhls dleL ls based on produclng keLoacldosls whlch has anLlselzure
properLles CLher dleLs such as Lhe ALklns uleL whlch also puL Lhe body lnLo keLosls are currenLly belng
researched for Lhelr effecLlveness

Lxpected Cutcomes
1he goal of managemenL of all people wlLh epllepsy ls Lo aLLaln selzurefree sLaLus wlLh no or
mlnlmal slde effecLs of Lherapy ln addlLlon Lhe paLlenL wlll remaln free from ln[ury and be empowered
Lo meeL lndlvldually deflned goals 1hrough hollsLlc approaches Lo paLlenL care nurses asslsL paLlenLs
and famllles Lo achleve and malnLaln a hlgh level of funcLlon and hlgh quallLy of llfe WlLh proper
knowledge nurses lnvolved ln Lhe managemenL of paLlenLs wlLh epllepsy can provlde valuable
asslsLance Lo lmprove Lhe quallLy care provlded Lo paLlenLs wlLh Lhls condlLlon


tC1t 1CCtG.
To prevent injury, educate patients who have lapses of consciousness during wakefulness and in
whom seizures are suspected about seizure precautions. Most accidents occur when patients have
impaired consciousness. This is one of the reasons for restrictions on driving, swimming, taking
unsupervised baths, working at significant heights, and the use of fire and power tools in people who
have epileptic seizures and other spells of sudden-onset seizures.
The restrictions differ for each patient because of the individual features of the seizures; the
degree of seizure control; and, in the United States, state laws. Other countries have more permissive or
more restrictive laws regarding driving.
Selzure lans should Lell oLhers whaL Lo do ln case you have a selzure Whlle Lhere are general
sLeps for all selzure Lypes you may have speclflc Lhlngs you wanL oLhers Lo do when you have a selzure
8evlew Lhls secLlon wlLh your docLor or nurse Lo make sure you are all ln agreemenL on Lhe besL way for
oLhers Lo help you durlng a selzure Cn your Selzure lan flll ln Lhe followlng
- llrsL ald sLeps Check off each box LhaL applles Lo you and your selzures lf you have more Lhan
one Lype of selzure check off all Lhe sLeps LhaL should be done regardless of selzure Lype
- uslng Lhe onllne Lpllepsy ulary Some of Lhe flrsL ald sLeps wlll already be checked ?ou may
uncheck Lhem lf you and your docLor declde Lhey donL perLaln Lo you and check oLher sLeps LhaL may
apply
- CLher care needed lf Lhere are speclflc Lhlngs LhaL should be done for your selzures wrlLe Lhem
down here lor example lf you Lend Lo wander or run durlng a selzure wrlLe down lf lL's okay Lo leL you
walk ln an enclosed place or Lo be sure and shuL a door Lo prevenL you from runnlng

nome Care
As a nurse you are responslble for glvlng and assurlng Lhe a paLlenL wlLh epllepsy Lo always
wear a medlcal alerL Lag A person havlng a generallzed selzure may be ln[ured breaLhe food fluld or
vomlL lnLo Lhe lungs or noL geL enough oxygen uurlng a generallzed selzure lL ls lmporLanL Lo proLecL
Lhe person from ln[ury 1urn Lhe person on Lhe slde so LhaL any vomlL leaves Lhe body and does noL
enLer Lhe lungs AfLer a generallzed selzure mosL people go lnLo a deep sleep uo noL prevenL Lhe
person from sleeplng 1he person wlll probably be dlsorlenLed or posslbly aglLaLed for awhlle afLer
awakenlng
LMLkGLNC IIkS1 AID
- uo noL aLLempL Lo force a hard ob[ecL (such as a spoon or a Longue depressor) beLween Lhe
LeeLh ?ou can cause more damage Lhan you can prevenL
- uo noL Lry Lo hold Lhe person down durlng Lhe selzure
- 1urn Lhe person Lo Lhe slde lf vomlLlng occurs keep Lhe person on hls or her slde whlle sleeplng
afLer Lhe selzure ls over
- lf Lhe person havlng a selzure Lurns blue or sLops breaLhlng Lry Lo poslLlon Lhelr head Lo prevenL
Lhelr Longue from blocklng Lhelr alrways 8reaLhlng usually sLarLs on lLs own once Lhe selzure ls over
- C8 or mouLhLomouLh breaLhlng ls rarely needed afLer selzures and cannoL be performed
durlng Lhe selzure
lf a person has repeaLed or prolonged selzures wlLhouL regalnlng consclousness or reLurnlng Lo normal
behavlor Lhe body may develop a severe lack of oxygen 1hls ls an emergency slLuaLlon Seek lmmedlaLe
medlcal help
Al1L8 1PL SLlZu8L
1reaL any ln[urles from bumps or falls 8ecord deLalls of Lhe selzure Lo reporL Lo Lhe persons prlmary
healLh care provlder ?ou should noLe Lhe followlng deLalls
- Pow long lL lasLed
- WhaL body parLs were affecLed
- 1ype of movemenLs or oLher sympLoms
- osslble causes
- Pow Lhe person behaved afLer Lhe selzure

revent|on
lnsLrucLlons for Laklng any prescrlbed medlcaLlons should be sLrlcLly followed lamlly members
should observe and record any selzure lnformaLlon Lo make sure Lhe person geLs proper LreaLmenL
Cood healLh hablLs may help Lo conLrol selzures 8ecause sleep deprlvaLlon sLress and a poor dleL can
conLrlbuLe Lo lncreased selzures good sleep hablLs sLress reducLlon proper exerclse and sound
nuLrlLlon may help
1here ls no speclflc way Lo prevenL all selzures use helmeLs when approprlaLe Lo prevenL head
ln[ury 1hls wlll lessen Lhe llkellhood of a braln ln[ury and subsequenL selzures Avold recreaLlonal drugs
eople wlLh epllepsy should Lake medlcaLlon as dlrecLed and avold excesslve amounLs of alcohol
eople wlLh unconLrolled selzures should noL drlve Lach sLaLe has a dlfferenL law LhaL deLermlnes whlch
people wlLh a hlsLory of selzures are allowed Lo drlve eople wlLh unconLrolled selzures also should
avold acLlvlLles where loss of awareness would cause greaL danger such as cllmblng Lo hlgh places
blklng and swlmmlng alone