Download Seizures

Seizure Disorder
Jeffrey T. Reisert, DO
University of New England
Physician Assistant Program
27 AUG 2009
Contact Information
Jeffrey T. Reisert, DO
Jeffrey.T.Reisert@Hitchcock.org
Tenney Mountain Internal Medicine
251 Mayhew Turnpike
Plymouth, NH 03264
(603) 536-6355
(603) 536-6356 (fax)
Objectives
Define different patterns of seizures
 Recognize symptoms of seizure
 Be able to differentiate types of common
seizures/patterns in children and adults
 Recognize treatments of acute seizure,
status epilepticus, and prevention of
seizures

Illustrative Case
You are covering the ED when a 40 year
old male presents by ambulance,
reportedly for “Loss of consciousness”
 You interview a sleepy patient and
interview their friend.
 The patient works as a carpenter for a
home construction firm. His history is
benign.

What questions do you have?
Important facts
The patient was at the job site and stated
he didn’t feel well. His co-worker informs
you he collapsed after saying he didn’t
feel well.
 He was noted to have “eyes that rolled
back in his head” and drewling.
 Then he tensed up and began shaking for
“a long time.”

What is your differential diagnosis?
Seizure
 Cardiac event
 Alcohol withdrawal?

Definition of Seizure Disorder
Harrison’s Principles of Internal Medicine defines
a seizure as a paroxysmal event due to
abnormal CNS discharge with resultant
manifestations depending on area involved.
 5-10% of population in lifetime have a seizure
 More prevalent in early childhood and later in
adulthood
 Epilepsy defines a patient with recurrent
seizures (not a single seizure).

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About 0.3-0.5% of population
Types of seizures
International League Against Epilepsy
(ILAE)-1981
 International classification of epileptic
seizures
 Table 348.1

Two basic types of seizures

Partial
 Deranged
area of cerebral cortex often due to
a structural anomaly-Consciousness is
preserved
 Further divided in to simple partial and
complex partial-Consciousness is impaired
 Third where partial seizures secondarily
generalized

Generalized-Next slide
Generalized
Diffuse region of brain firing
simultaneously
 Often due a widespread problem

 Cellular
disorder (i.e.: mental retardation)
 Biochemical disruption (i.e.: low sodium)
 Structural issue (i.e.: brain tumor)
Simple Partial Seizures
May be motor, sensory, autonomic,
psychic but without loss of consciousness
(LOC)
 Example: May get a hand tremor on
opposite side of abnormal brain activity
 Often clonic with repetitive
flexion/extension
 EEG: Abnormal impulses in focal area of
brain

Variations of simple partial seizures

Jacksonian March
 Motor
activity begins distally, like fingers, and
spreads to whole extremity
 EEG: spike waves

Todd’s paralysis
 Local

paresis lasting minutes to hours
Epilepsia partialis continua
 Continues
hours to days
Additional symptoms in simple partial
seizures
Changes in somatic sensations
(paresthesias)
 Change in vision (flashing lights,
hallucinations)
 Changes in equilibrium (falling, vertigo)
 Autonomic changes (flushing, sweating)
 Odd feelings (déjà vu)

Complex Partial Seizures

Focal activity progresses to loss of contact with
environment (ictal stage)


Stare
Amnesia – may forget what happened
Often begins with an aura stereotypical for the
patient……Feel funny.
 Followed by ictal stage

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Involuntary behaviors
Chewing, picking
Post ictal confusion
Lasts seconds to hours
EEG between spells (inter ictal) usually normal (or may
show brief discharge of spikes (sharp waves)
Partial seizures with secondary
generalization
Electrical discharge spread and both
hemispheres become involved
 Results in tonic-clonic seizure
 Common when partial seizures in frontal
lobe
 Look like generalized seizures

Generalized seizures
Arise in both cerebral hemispheres
simultaneously
 Look like focal seizure that secondarily
generalized though not associated with a
specific focal onset event
 Includes absence seizures and tonic-clonic
seizures

Absence Seizures (Petit mal)
Brief LOC without postural control.
 Usually last a few seconds
 No post ictal confusion
 May have other subtle findings

 Eye
blinking
 Chewing
 Clonic movement of hands
Absence seizures cont.
Onset typically in childhood, 4-8 y/o or
early adolescence
 Makes up 15-20% of childhood seizures
 May occur all day long…..Daydreaming
appearance

Absence seizures cont.

EEG
 Generalized
symmetrical discharge
 Spike and wave
 Start stop with inter-ictal normal EEG
 Worsen with hyperventilation maneuver
May be associated with T-C seizures
 60-70% of cases remiss in childhood

Atypical absence seizures
Similar to absence but symptoms last
longer
 More motor features
 May have a brain abnormality such as
mental retardation/developmental delay
 Harder to tx than ordinary absence
seizures

Generalized Tonic-Clonic Seizures
10% of patients with epilepsy
 Are the most common type when seizures
are due to metabolic derangement
 Episodes are of sudden onset

 May
have prodrome but less so than aura in
focal seizures that secondarily generalize
T-C Seizures-Characteristics

Tonic phase

Increased muscle tone
Often a moan or cry
 Change in respiration

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Secretions pool
Cyanosis
Jaw clenches, bite tongue
Sympathetic symptoms
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Increased BP, HR
Pupil dilation
T-C Seizure Features cont.
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Clonic activity
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Post-ictal state
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Muscles relax and contract
Usually lasts about a minute
Unresponsive
Flaccid
Salivation or airway obstruction
Bowel or bladder incontinence
Seizures may last minutes to hours before awakening
Post seizure



Headache
Fatigue
Muscle aches
T-C Seizures-EEG

Tonic phase
 Increased
low voltage fast activity
 High amplitude polyspike discharges

Clonic phase
 Spike

and wave activity develops
Post ictal
 Slowing
then recovery
T-C Seizures-Variations

Atonic seizures
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1-2 seconds lose motor tone
Brief loss of consciousness (LOC)
No post-ictal confusion
Risk after head injury
Also associated with other epileptic syndromes
Myoclonic seizures
Brief contraction or jerk
 Like when you fall asleep and you twitch
 Seen in brain injuries

Other Generalized Seizure categories
Juvenile myoclonic epilepsy
 Lennox Gastaut syndrome
 Mesial temporal lobe epilepsy

Juvenile Myoclonic epilepsy
Adolescence
 Bilateral jerk with maintained
consciousness
 Worse with awakening, sleep deprivation
 Benign

 Good
response to meds
 May spontaneously remit

Associated with other epileptic syndromes
Lennox Gastaut syndrome
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Seen in children
Multiple seizure types
EEG slowing and spike waves
Usually impaired cognitive function
Associated with central nervous system (CNS)
disease
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Developmental delay
Trauma
Infection
Neural injuries
Often difficult to control
Mesial temporal lobe epilepsy
Difficult to control
 Partial epilepsy with characteristic features
 MRI shows hippocampal sclerosis

Seizures-Etiology
Harrison’s: Shift in balance of excitation
and inhibition in CNS
 Mechanisms

 Change
in seizure threshold (i.e.: Fevers in
children)
 Genetic role
 Traumatic brain injury
 Other events (strokes, infection)
 Precipitating factors
Seizure causes cont.

Precipitating factors
 Stress
 Sleep
deprivation
 Menses
 Medications
 Etc.

May take years to develop after event
What happens?

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A burst of electrical activity
Influx of extracellular calcium
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Influx of sodium
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Excitatory molecules such as NMDA (N-methyl-D-aspartate) may
further calcium influx
Under influence of GABA (Gamma-aminobutyric acid) or
potassium channels
Spike discharge
Inhibitory neurons overwhelmed by calcium and
potassium
Propagation of action potentials
Channel problems may be source of genetic epilepsy
Seizures, age basis
Table 348-4
 Neonates

 Birth
injury, hypoxemia
 Congenital abnormalities
 Drugs (maternal)

Early Childhood
 Febrile
seizures
Febrile Seizures
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3-5% of children
Most occur from 3mo to 5ys
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Infection types
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Otitis media
Respiratory infection
Gastroenteritis
Presentation
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Most 18-24 mo
Early on in febrile illness T-C activity
Recurrence about 1/3 of pts
Can be a simple febrile seizure (one event) or complex
febrile seizure (repeated activity)
Not epilepsy
Age cont.
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Childhood
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Adolescence
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Usually when epilepsy becomes apparent
Think trauma
The worse the trauma the worse the seizures
Adulthood
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Cerebrovascular disease (50% of new onset seizures in adults)
Trauma
CNS tumors
Degenerative diseases
Medical (Hypo/hyperglycemia, renal failure, liver disease, and
drugs
Diagnosis seizure disorder
History is key (observer/bystander)
 EEG
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ASAP to measure brain activity
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Awakeness/activity
Burst of action potentials
Baseline alpha wave (8-13 Hz) with eyes closed
Faster beta activity (>13 Hz) increase with
activity/eye opening. Amount varies.
Slower theta activity (4-7 Hz) and delta (<4 Hz)
EEG Cont.

Different situations are assessed (montages)
Awake/asleep
 Eyes open/closed or with photo stimulation
 Hyperventilation
 Sleep deprivation
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Key findings
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Abnormal activity that starts/stops abruptly OR
Abnormal activity during T-C seizure
Inter-ictal may see spikes or sharp waves in 40% of
cases (worse prognosis) – harder to treat
Evaluation and Workup
EEG
 Imaging

 Most
get
 MRI best

Blood tests
 Usually
normal (not helpful)
 May see elevated prolactin level in first 30
mins.
Differential diagnosis

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Table 348-6
Syncope

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Tired, sweaty, tunnel vision
May have 10 sec of convulsive activity
(Seizures may have aura, cyanosis, LOC, >30 sec. activity, postictal disorientation, muscle soreness, or sleepiness)
Psychogenic seizures
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Non-epileptiform behaviors that resemble seizures
Seen with stress/conversion reaction
Head turning, shaking, twitching, no LOC, pelvic thrust that
waxes and wanes
? Video EEG
Overview of treatment

Basic life support

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Vital signs, CPR
Treat cause if identified
Infection, tumor, drugs
 Cerebrospinal fluid tap?
 Imaging (MRI preferred)
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Meds if more than one episode or high risk
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Assess for likelihood of recurrence
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31-71% risk of second seizure in one year
Are meds needed long term?
2 year trial on meds?
Safety
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Work
Driving
Seizure meds, overview
Right drug for certain type of seizure
 One drug?
 Add slowly
 Older meds first line

 Phenytoin
(Dilantin®), valproic acid
(Depakote®), carbamazepine (Tegretol®)
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Newer meds second
Medications-Mechanism of Action
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Block activity of ion channels or neurotransmitters
Inhibit Na+ dependent action potentials
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Inhibit Ca++ channels
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Benzodiazepines, phenobarbital
Increase GABA availability
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Lamotrigine
Increase GABA function
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Phenytoin
Decrease glutamate release
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Phenytoin, carbamazepine, lamotrigine (Lamictal®), topiramate
(Topamax®), zonisamide (Zonegran®)
Valproic acid, gabapentin (Neurontin®), tiagabine (Gabitril®)
Inhibit Ca++ channels in thalamus (absence seizures)

Ethosuximide, valproic acid
Treatment by seizure type
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Partial seizures
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Carbamazepine (3-4 x per day, low WBC, bone
marrow aplasia, hepatotox)
Phenytoin (1-2 x per day, levels, tox, hirsuitism,
coarse facial features, gingival hyperplasia, affect on
bone metabolism)
Lamotrigine (Rash)
Valproic acid (GI tox, bone marrow suppression,
hepatotox)
Generalized seizures

Valproic acid, lamotrigine, carbamazepine, phenytoin
Medications-Monitoring
Adverse drug reactions
 Effectiveness
 Levels
 Liver function tests
 Blood counts
 Drugs in combo?
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Stopping drugs

Consider if
 Low
risk
 One seizure then seizure free
 Normal exam (no developmental delay, head
injury, etc.)
 Normal EEG
 Do slowly
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Driving implications?
Status epilepticus
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Continuous seizure
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Some say if more than 15-30 mins
Others if > 15 seconds
May range from T-C seizure to more subtle (finger or
eye movement)
May need EEG to verify
Medical emergency
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Cardiovascular implications
Hyperthermia
Metabolic derangements
CNS injury
Status epilepticus-Causes
Metabolic problems
 Drug toxicity
 CNS infection or tumor
 Head injury
 Refractory epilepsy
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Status epilepticus-Treatment
Metabolic work up
 Benzodiazepine (Lorazepam, diazepam
(Valium®), others
 Phenytoin – can burn arm
 Phenobarbital
 Anesthesia
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Surgical treatment of seizures
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Use is primarily in refractory epilepsy
Procedures
Temporal lobectomy
Focal lesion removal (or more such as
hemispherectomy)
 Corpus callosotomy
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Requires
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EEG, Video EEG
Neuroimaging
SPECT or PET scans (functional)
Electrical mapping
Vagal nerve stimulator
Place a bipolar electrode in L vagus nerve
 Generator delivers a pulse
 May take a while to work
 MOA: May simply increase seizure
threshold
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Other issues
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Developmental delay/mental retardation
Parenting
Stigma
2-3x greater death rate
Work? Driving?
Menstrual cycles may increase risk
Pregnancy
Seizures may worsen or improve in half of pts
 May alter drug levels
 Tx may cause birth defects
 May affect contraception
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Case wrap up
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History
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Exam
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Post ictal grogginess
Wet pants
Work up?
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No prior event
Incontinence
Sudden onset
Prodrome
Tonic clonic activity
Imaging
EEG
Check glucose, chemistries, drug level?
Meds or observe?
Treatment

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Dilantin or similar
No driving/ladders
Questions?
References
Harrison’s
 Up-To-Date
 Netter
