Objectives Seizure Assessment & Management What is a seizure?

Objectives
Seizure Assessment
& Management
Classification of seizures
 Process of Diagnosing
 Treatments

Maritza Lopez, RN, MSN,CNRN
What is a seizure?

A seizure is an event, characterized by an
excessive and synchronous discharge of
cerebral neurons with associated sensory,
motor, and/or behavioral changes.
What is Epilepsy?
Epilepsy is defined as recurrent,
unprovoked seizures caused
by biochemical, anatomic &
physiological changes.
Etiology
Idiopathic- may arise from an unknown
cause
 Cryptogenic-may arise from an presumed
cause (i.e. genetic) that is unknown or ill
defined
 Symptomatic-arising from a known cerebral
abnormality

 Conditions in the brain that produce
seizures may have been present since birth,
or they may develop later in life due to
injury, infections, structural abnormalities
in the brain, exposure to toxic agents, or for
reasons that are still not well understood.
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Risk factors for provoked seizure
Risk factors for epilepsy
•CNS neoplasms: gliomas/meningiomas
•Vascular: Stroke, AVMs, Cavernous hemangiomas
•Trauma: penetrating head injury, depressed skull fracture,
LOC >24 hours, intracerebral hemorrhage
•Infection: encephalitis, abscess, meningitis,
neurocystercercosis
•Dementia: Alzheimer’s disease
•Prenatal/Perinatal: genetic syndromes, cortical
malformations, hypoxia
•Mental retardation ( occur in 28 % to 38% of children with
epilepsy)
•Cerebral palsy
•Neonatal or febrile seizures?
•Metabolic: Low Na/Mg/Phos/Ca/Gluc, high Na, hepatic
encephalopathy, uremia
•Toxic: drug or drug withdrawal (cocaine/meth v EtOH/BDZ), meds
(ABX, INH, TCA, wellbutrin, clozaril, anesthetics).
•Infectious: meningitis or encephalitis (bact/fungal/TB/viral/parasite), HIV, abscess.
•Endocrine: hyperthyroidism
•Neurodegenerative: advanced AD, VD
•Trauma: penetrating head injury, depressed skull fx, ICH,
LOC>24h
•Tumor: mass or carcinomatous meningitis.
•Vascular: hypertensive encephalopathy, eclampsia, vasculitis, SAH,
ICH, ischemic stroke, SDH, EDH, AVM.
Epidemiology
•Almost 2 million in the U.S. have epilepsy
•500,000 are medically refractory
•Approximately 10% of Americans will experience a
single seizure in their lifetime
•Risk of a recurrent unprovoked seizure (5 years)
–After single unprovoked: ~33%
–After second unprovoked: ~73%
Comorbidities
• Mental Retardation and developmental delay occur in 28 % to
38% of children with epilepsy
• Depression/mood disorders-20%
• SUDEP occurs in greater proportion of patients with epilepsy
compared to the general population
• Memory impairment disorders
• Headaches
Pathophysiology
Epileptogenisis originates from an imbalance
between cerebral excitation and inhibition. In
a sz, brain cells become abnormally linked
together, leading to abnormal electrical firing.
This may occur due to a loss of cells that
inhibit excitatory cells or an overabundance of
excitatory cells.
Excitation
Glutamate-most important CNS excitatory
neurotransmitter involved in epilepsy
 Methyl-D-asparate (MDA) is glutamate
receptor
 Some AEDs work by antagonizing
glutamate receptors
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Inhibition

Aminobutyric acid (GABA)
– Facilitates activity of Cl- (Cl- allows cell
membrane to become more neg charged,
making it difficult for cells to depolarize
– Opens K+ channels (which leads postsynaptic
inhibition) or closes Ca++( acts as a pacemaker
for nl rhythmic brain activity . (AEDs that
inhibit Ca++ work for absence seizures)
– Na+ channels are required for an action
potential to fire. Some AEDs stabilize the
inactive form of Na+
Hypersynchronization
Caused by large number of neuronal cells
firing together
 Inhibition blockade induces polarization,
leading to hyper-synchrony
 Pathological conditions may compromise
inhibition, leading to excitation.

Types of Seizures
(International Classification of
Epileptic Seizures)
Generalized Seizures

Generalized seizures affect both cerebral
hemispheres from the beginning of the
seizure. They produce loss of
consciousness, either briefly or for a longer
period of time, and are sub-categorized into
several major types.
Tonic-Clonic Seizure
Generalized tonic clonic seizures (grand
mal seizures) are the most common and best
known type of generalized seizure. They
begin with stiffening of the limbs (the tonic
phase), followed by jerking of the limbs and
face (the clonic phase).
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Absence Seizures
Absence seizures (also called petit mal
seizures) are lapses of awareness,
sometimes with staring, that begin and
end abruptly, lasting only a few seconds.
There is no warning and no after-effect.

Atonic Seizure
Atonic seizures produce an abrupt loss of
muscle tone
Myolclonic Seizures
Myoclonic seizures are rapid, brief
contractions of bodily muscles, which
usually occur at the same time on both
sides of the body. Occasionally, they
involve one arm or a foot.

Partial Seizures
 In partial seizures the electrical
disturbance is limited to a specific area of
one cerebral hemisphere.
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Complex Partial Seizures
Simple Partial Seizures

People who have simple partial seizures
do not lose consciousness during the
seizure. However, some people, although
fully aware of what's going on, find they
can't speak or move until the seizure is
over. Often times aura’s are sps.
CPS may be preceded by SPS
 Automatisms such as lip smacking,
blinking, or picking at clothes often
accompany CPS
 Motor phenomena such as wandering,
running, or arm jerking often accompany
frontal seizures.
 A partial seizure may evolve to a
secondarily generalized seizure

Epilepsy Syndromes

Idiopathic epilepsy w/ age-related onset
 Localization-related/symptomatic epilepsies
 Generalized/idiopathic epilepsies
 Generalized cryptogenic or symptomatic
epilepsies.
 Generalized/either idiopathic or
symptomatic epilepsies

Is Seizure Classification
Important?
Differential diagnosis
Syncope
 Panic attacks
 TIA
 Narcolepsy
 Myoclonus
 Multifocal chorea
 Migraines

Complex partial seizures affect a larger
area of the brain than simple partial
seizures. Per AANN, CPS have an onset
of synchronous cortical discharges
resulting in symptomatology r/t brain
region affected.

Yes. Accurate classification provides the
key of seizure management from the initial
diagnostic evaluation to decision-making
about further evaluations and treatment.
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Epilepsy Center Tests

Assessment
History, neuro exam, med hx
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MRI
PET- positron Emissin Tomography
MEG- Magnetoencephalography
MSI-magnet source imaging
Ictal SPECT-single photon emission computed
tomography
EEG-routine/sleep/sleep deprived
NeuroPsych test
Wada
•Epileptic & behavioral events are
synchronized with EEG data to establish
the diagnosis and identify the treatment
options.
Why VET
Diagnosing
 Classifying seizures
 Matching medications
 Localizing and lateralizing focus

Seizure Safety precautions
Padded side rails
 Side rails up
 IV
 O2
 Suction
 Standing orders, ie. Ativan , when to notify
HO

Seizure Assessment
Keep patient safe. ABC’s
 Position patient flat and on their side for
grand mal seizures
 Remove all restrictive clothing or wires or
glasses.
 Take blankets off.
 Stay away from view of camera.
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Tonic-Clonic
Make sure patient is safe
 Do not have to really have do language or
motor.
 Describe facial twitching, eye deviation,
head deviation
 Then do post ictal assesment every 5
minutes until baseline.

Simple partial
Describe out loud what they feel during and
after
CPS
Safety
 How do you feel, describe
 Orientation,
 Ask them if they recognize object or repeat
what you said.
 Lip smacking, facial twitching, eye
deviation, hand automatisms, is there
dystonic posturing in hands, head deviation

During seizure, test…
Remember word
What are you feeling/impaired awareness
 Language- Demonstration of Ictal speech.
Are they amnestic? Comprehension(show
elbow), Repetition (the train came to station
a half hour late)& Naming(point to watch)
 Motor response-tone?
 Memory-what is the word you asked him to
remember.
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Post ictal
NES
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Orientation- Language (comprehension, naming &
repetition)
Motor response (upper and lower)-Todd’s
paralysis
Psychogenic non-epileptic seizures seem to
be caused by stressful psychological
experiences or emotional trauma. It is one
way that the body indicates excessive stress.
Repeat assessment until pt is at baseline.
NOTIFY FELLOW/HO if sz lasts longer than 5 min.
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Treatments
Medications
 Surgery
 Vagus Nerve Stimulation
 Ketogenic Diet
 Complementary Treatment
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“Older” Drugs
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Phenobarbital
1912
Phenytoin (Dilantin)
1938
Primidone (Mysoline)
1952
Ethosuximide (Zarontin)
1960
Carbamazepine
1974
(Tegretol, Tegretol XR, Carbatrol)
Valproate/Valproic Acid
1978
(Depakote, Depakene, Depakote ER)
Antiepileptic Drugs - Spectrum of Activity
“Newer” Drugs
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Felbamate (Felbatol)
Gabapentin (Neurontin)
Lamotrigine (Lamictal)
Topiramate (Topamax)
Tiagabine (Gabatril)
Levetiracetam (Keppra)
Oxcarbazepine (Trileptal)
Zonisamide (Zonegran)
1993
1994
1995
1996
1998
1999
2000
2000
Partial Seizures
PHT, CBZ, PBR, GBP
TGB, OXC, PGB
They all can cause drowsiness, cognition
problems, dizziness
 Phenytoin-gingival hyperplasia
 VPA- hair loss
 Lamotrigine- rash, insomnia
 Topomax and Zonisamide- kidney stones
 Keppra- Behavioral issues
 Felbatol- aplastic anemia
ACTH
ESM
VPA, LTG, TPM, FBM, ZNS, LEV
PHT=phenytoin; CBZ=carbamazepine; PBR=phenobarbital; GBP=gabapentin; TGB=tiagabine;
OXC=oxcarbazepine; LEV=levetiracetam; VPA=valproate; LTG=lamotrigine; TPM=topiramate; FBM=felbamate;
ZNS=zonisamide; ACTH=adrenocorticotropic hormone; ESM=ethosuximide; PGB=pregabalin
Side effects
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Generalized Seizures
Absence
Simple
Tonic-clonic Tonic
Infantile
Complex
Myoclonic spasms
Secondarily generalized
Atonic
Medications
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Pharmacokinetic properties-study of conc of drugs
and metabolites in body
Bioavailability- how much drug reaches circ
Elimination- how drugs are metabolized &
excreted
Concentration: amt necessary to cause effect
Absorption-transfer of drug from site to tissue
Distrubion- rate of penetration of drug to tissue
Monotherapy vs polytherapy
Herbs
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Medications- Protein binding
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Determines amount of drug in plasma r/t amount
in tissue
Affected by age, pregnancy, amt of albumin in
blood and concomitant meds.
Enzyme system: Cytochrome P-140 (major drug
metabolizing enzyme in body). Enzymes usually
in gut and liver. Other drugs may cause inhibition
or induction causing side effects or drug/drug
interaction.
Laboratory monitoring (more in older drugs b/c
newer drugs have less protein binding
Pregnancy
All women of child bearing age should take
Folic acid to prevent birth defects (many are
folic antagonists)
 Infants of mothers exposed to AED in utero
are 2x likely for birth defects
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Ketogenic Diet
The ketogenic diet, which is very high in
fats and low in carbohydrates, was first
developed almost 80 years ago. It makes the
body burn fat for energy instead of glucose
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Invasive Monitoring
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Depth electrodes: fine wires placed into the
brain tissue.
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Subdural strips: strands of electrodes placed
on the surface of brain via burr holes in the
skull. Usually 4-8 are placed in a given
time, covering different pt of brains
Invasive Monitoring
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Subdural Grid: a rectangular sheet of
electrodes placed on the surface of the
brain. The grid records seizure activity, and
can also be used to map speech and motor
areas to help guide the surgeon in the
resection.
•Neuropsychological testing includes a battery of tests used
to assess language, memory and intelligence. It is useful as a
tool to aid in the identification of the sz focus as well as to
track cognitive and behavioral functioning over time.
•Wada tests (sodium amytal) determines the dominant
hemisphere for language an memory
•Functional brain mapping
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Surgery
Surgery
Temporal lobectomy -70-80% of being sz
free.
 Extratemporal neocortical resection
 Corpus Callosotomy-palliative
 Functional hemispherectomy
 Multipal Subpial Transection (MST)-offers
reduction in seizures
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Status Epilepticus
Vagus Nerve Stimulator

Vagus nerve stimulation (VNS) is a type
of treatment in which short bursts of
electrical energy are directed into the
brain via the vagus nerve.
(50-60 thousand per year)
>30 min
 > 2 seizures consecutively w/o mental
clearing between seizures.
 Usually because of sub-therapeautic levels
 Meningitis, encephalitis, eclampsia, drug
w/drawal, hypoglycemia, hypoxia, trauma
or stroke
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S.E.
Convulsive
 NCSE
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– Simple partial
– Complex partial
– Absence status
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Pathophysiology-changes occur due to a
massive release of epi and norepi during the
seizure.
Compensatory mechinisms
 BP & CO
 Cerebral Metabolic rate
 glycemia
Late Changes
 CV –BP falls, decrease O2 to brain
 Respiratory-Hypoxia
 Metabolic-glucose rises, making pancreas
work harder
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Either continuous seizures lasting at least
five minutes, or two or more discrete
seizures between which there is
incomplete recovery of consciousness
– Tonic-clonic seizures rarely last > 2
minutes
– Complex partial seizures rarely > 10
minutes
Convulsive SE is a life-threatening
medical emergency!
Non-convulsive SE often requires
aggressive management but the level of
urgency is dependent on several clinical
factors
Subtle signs of Nonconvulsive SE
Persistent coma
Forced gaze deviation or
nystagmus
 Rhythmic twitching of one region
(e.g. face, digit)
 Repetitive/stereotyped language
 Echolalia
 Persistent confusion + seizure risk
factors
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Management of Status Epilepticus
Time
(min)
Agent
Dose (IV)
0-20
Lorazepam
0.1 mg/kg
Rate
2 mg boluses q5 min
20-30
Fosphenytoin
20 mg/kg
150 mg/min
30-35
Fosphenytoin
5-10 mg/kg
150 mg/min
Consider intubation, skipping ahead to Midazolam
35-55
Phenobarbital
20 mg/kg
50-75 mg/min
55-65
Phenobarbital
5-10 mg/kg
50-75 mg/min
Midazolam OR
Propofol
0.2 mg/kg
load
1-2 mg/kg
load
0.1 -0.4 mg/kg/hr
2-10 mg/kg/hr
Pentobarbital
20 mg/kg
load
50-100 mg/min
Valproic acid
40 mg/kg
Give over 10 mins
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