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Abstract: Epileptic seizures are usually self. Epileptic seizures are usually self--limited and may ... Epileptic Seizures. 1. Simple partial onset followed by impairment of consciousness. 2. ...
Seizures are symptoms of cerebral dysfunction,
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resulting from paroxysmal hyperexcitable or
hypersynchronous discharges of neurons involving the
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Epilepsy is the condition of recurrent unprovoked
Epileptic seizures are usually self-limited and may be
followed by a period of postictal cerebral depression
manifested clinically as diffuse or localized neurologic
I. Partial (focal, local) seizures
A. Simple partial seizures
1. With motor signs
2 With somatosensory or special sensory symptoms
International 3. With autonomic symptoms or signs
Classification of 4. With psychic symptoms
Epileptic Seizures B. Complex partial seizures
1. Simple partial onset followed by impairment of consciousness
2. With impairment of consciousness at onset
C. Partial seizures evolving to secondarily generalized seizures
1 Simple partial seizures evolving to generalized seizures
2. Complex partial seizures evolving to generalized seizures
3. Simple partial seizures evolving to complex partial seizures evolving
to generalized seizures
II. Generalized seizures (convulsive or nonconvulsive)
A. Absence seizures
1. Typical absences
2. Atypical absences
B. Myoclonic seizures
(Commission on C. Clonic seizures
D. Tonic seizures
o c se u es
Terminology of the
T i l f h
E. Tonic-clonic seizures
League Against F. Atonic seizures (astatic seizures)
Epilepsy 1981) III. Unclassified epileptic seizures
International Classification of Epilepsies, Epileptic Syndromes, and Related Seizure Disorders
1. Localization-related (focal, local, partial)
1.1 Idiopathic (primary) 2.1 Idiopathic (primary)
• Benign neonatal familial convulsions
• Benign childhood epilepsy with centrotemporal spikes
• Benign neonatal convulsions
• Childhood epilepsy with occipital paroxysms
• Benign myoclonic epilepsy in infancy
• Primary reading epilepsy • Childhood absence epilepsy (pyknolepsy)
1.2 Symptomatic (secondary) • Juvenile absence epilepsy
• Juvenile myoclonic epilepsy (impulsive petit mal)
• Temporal lobe epilepsies
• Epilepsies with grand mal seizures (GTCS) on awakening
• Frontal lobe epilepsies
• Other generalized idiopathic epilepsies
• Parietal lobe epilepsies • Epilepsies with seizures precipitated by specific modes of activation
• Occipital lobe epilepsies 2.2 Cryptogenic or symptomatic
• West syndrome (infantile spasms, Blitz-Nick-Salaam Krämpfe)
• Chronic progressive epilepsia partialis continua of
childhood syndromes characterized by seizures with • Lennox-Gastaut syndrome
specific modes of precipitation
• Epilepsy with myoclonic-astatic seizures
1.3 Cryptogenic, defined by:
• Epilepsy with myoclonic absences
• Seizure type
2.3 Symptomatic (secondary)
• Clinical features 2.3.1 Nonspecific etiology
• Etiology • Early myoclonic encephalopathy
• Early infantile epileptic encephalopathy with suppression bursts
• Anatomical localization
• Other symptomatic generalized epilepsies
2.3.2 Specific syndromes
• Epileptic seizures may complicate many disease states.
International Classification of Epilepsies, Epileptic Syndromes, and Related Seizure Disorders
3. Undetermined epilepsies 4. Special syndromes
3.1 With both generalized and focal seizures
4.1 Situation-related seizures (Gelegenheitsanfälle)
• Neonatal seizures
1. Febrile convulsions
• Severe myoclonic epilepsy in infancy
• Epilepsy with continuous spike-waves during slow
wave sleep 2. Isolated seizures or isolated status epilepticus
• Acquired epileptic aphasia (Landau-Kleffner
3. Seizures occurring only when there is an acute or
• Other undetermined epilepsies toxic event due to factors such as alcohol, drugs,
eclampsia, nonketotic hyperglycemia
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3.2 Without unequivocal generalized or focal features
(Commission on Classification and
Terminology of the International League
Against Epilepsy 1989).
Definitions of Key Terms
Epileptic seizure type: An ictal event believed to represent a unique
pathophysiological mechanism and anatomical substrate. This is a diagnostic
entity with etiological, therapeutic, and prognostic implications. (new concept)
Epilepsy syndrome: A complex of signs and symptoms that define a unique
epilepsy condition with different etiologies. This must involve more than just
the seizure type; thus, frontal lobe seizures per se, for instance, do not
constitute a syndrome. (changed concept)
Epilepsy disease: A pathological condition with a single specific, well-defined
etiology. Th progressive myoclonus epilepsy is a syndrome, but
i l Thus, i l il i d b
Unverricht-Lundborg is a disease. (new concept)
Epileptic encephalopathy: A condition in which the epileptiform
abnormalities themselves are believed to contribute to the progressive
disturbance in cerebral function. (new concept)
Benign epilepsy syndrome: A syndrome characterized by epileptic seizures
that are easily treated, or require no treatment, and remit without sequelae.
( f ed ep )
Reflex epilepsy syndrome: A syndrome in which all epileptic seizures are
precipitated by sensory stimuli. Reflex seizures that occur in focal and
generalized epilepsy syndromes that are also associated with spontaneous
seizures are listed as seizure types. Isolated reflex seizures can also occur in
situations that do not necessarily require a diagnosis of epilepsy. Seizures
precipitated by other special circumstances, such as fever or alcohol
withdrawal, are not reflex seizures. (changed concept)
Definitions of Key Terms Continued
Focal seizures and syndromes: Replaces the terms partial seizures and
localization l t d
l li ti -related syndromes. ( h d terms)
d (changed t )
Simple and complex partial epileptic seizures: These terms are no longer
recommended, nor will they be replaced. Ictal impairment of consciousness
will be described when appropriate for individual seizures but will not be used
to classify specific seizure types. (new concept)
Idiopathic epilepsy syndrome: A syndrome that is only epilepsy, with no
underlying structural brain lesion or other neurologic signs or symptoms.
These are presumed to be g
p genetic and are usually age-dependent. (unchanged
y age- p
g ( g
Symptomatic epilepsy syndrome: A syndrome in which the epileptic seizures
are the result of one or more identifiable structural lesions of the brain.
Probably symptomatic epilepsy syndrome: Synonymous with, but preferred
to, the term cryptogenic; used to define syndromes that are believed to be
symptomatic but with no identified etiology. (new term)
How can seizures manifest?
Weakness (Todd’s palsy)
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Jerks and twitches
Drop attacks or loss of tone (Atonic)
Staring spells/lapses and automatisms
Fluctuations in consciousness
Bizarre complex behavior or movements
Always look for a cause
Be sure to take a good history
Cerebrovascular disease such as cerebral infarction, cerebral
hemorrhage, and venous thrombosis
CNS infections such as meningitis or encephalitis
Substance intoxication or withdrawal
Metabolic medical disorders such as uremia, hypoglycemia,
hyponatremia, and hypocalcemia
Clues for un-witnessed seizures
Feel worn out?
F l ?
Gaps in memory?
After particular trigger? (substance, exertion,
↓ sleep, missed meds, new medication, infection)
p, , , )
Examples of common AED
Phenytion (Dilantin) Gabapentin (Neurontin)
Carbamazepine Lamotrigine (Lamictal)
( g ) Topiramate (Topamax)
Valproic acid (Depakine) Levetiracetam (Keppra)
29 year old female with recurrent episodes of
LOC for 10 years. They are preceded by a
peculiar smell followed by loss of contact and
staring. The right hand and arm develop
dystonic posturing, while the left hand
performed semi-automatic repetitive
f d semi-
i i ii
movements. Towards the end of the event, there
is extreme right head deviation.
Had a single febrile seizure 9 months of age.
A 21 year old male presents with recurrent
nocturnal events (never happened when awake)
of sustained extension of his left arm and flexion
of the right. They last not more then 30 seconds.
Although he is amnestic to the event he has no
A 38-year-old man had experienced several
episodes of graying of vision and feeling of
faintness subsequent to weight lifting. He was
observed to fall to the floor and to have jerking
movements of all limbs. He rapidly awoke with
no confusion but was sweating and nauseous.
Distinctive Features of Syncope and Generalized Tonic-Clonic Seizures
Syncope Generalized tonic-clonic Seizure
Duration Usually less than 30 seconds 1 to 2 minutes
Percentage of 50% None
Falls Flaccid or stiff Stiff
Convulsion 80% mostly brief, arrhythmic, multifocal Always 2 to 3 minutes, rhythmic,
Pattern or generalized generalized
Eyes Open, transient upward or lateral Open, often sustained deviation
Hallucinations Late in the attack May precede generalized seizure in focal
Color of the face Pale Cyanotic
Hypersalivation frothing Absent Common
Incontinence Common Common
Tongue bite Rare Common
Postictal confusion Less than 30 seconds 2 to 30 minutes
Creatine kinase Normal Often elevated
A 25-year-old woman developed episodes of
loss of consciousness at 15 years of age. The
initial episodes were a sudden loss of
consciousness with collapse and without
associated movements. A cardiac evaluation
identified baseline low blood
id ifi d b li l bl d pressure and an d
abnormal tilt table test.
Treatment with midodrine and nadolol was
T i h id d i d d l l
begun. This treatment was effective.
The episodes returned during the patient s first
year of college but were different at their onset,
which now was a shaking of the right shoulder
that spread across the entire right side. Around
this time, the patient identified the development
of a persisting right hemiparesis that i
f i i i h h i i h impairs i
ambulation to the extent that a cane is necessary.
EEG and CT were normal and Dil i was
d l d Dilantin
started with good response.
The episodes then returned and have increased
in frequency despite continued treatment with
Dilantin Their current manifestation does not
include asymmetric shaking, but intermittent
truncal contractions that sometimes are
associated with oral injury or urinary
incontinence The duration of the episodes vary
from 2 to 30 minutes and resolve with headache
Neurologic examination identified an
inconsistent and variable right-sided weakness,
and MRI of the brain was normal.
Video EEG monitoring was normal during
interictal and ictal periods.
Neuropsych assessment also suggested a
Studies show that experienced epileptologists are wrong in distinguishing between psychogenic and
epileptic seizures from videotapes 20% to 30% of the time (King et al 1982).
Clinical discrimination between Epileptic and non-epileptic events
Non- p p
Non-Epileptic Epileptic events
Onset Gradual Rapid
Audience Common Unusual
Pelvic Thrusting/ Common Uncommon
Opisthotonus (Consider Frontal)
Tongue biting Uncommon (tip) Lateral aspect
Eyes Closed (Resisting Deviated/
Autonomic Uncommon Common
Plantars Normal Babinski +
According to Hx & P/E, consider:
CBC and differential
Urea & creatinine
Important Electrolytes (↓ Na, ↓ Ca, and ↓ G)
I El l N C d
Other Labs: Na, K, Mg, and LFTs
Specific tests for suspected diseases.
Toxic screen/Drug levels
Urine, CXR, EKG
Neuroimaging (CT, MRI)
Prolactin and CK levels helpful?
AAN PRL Recommendations
Elevated serum PRL, when measured in appropriate
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clinical setting at 10 to 20 minutes after a suspected
event, should be considered a useful adjunct to
differentiate GTC or CPS from psychogenic NES
among adults and older children.
Serum PRL, when measured more than 6 hours after a
suspected event, should be representative of the
baseline PRL level.
Serum PRL assay is not of utility to distinguish seizure
The utility of serum PRL assay has not been established
in the evaluation of SE, repetitive seizures, or neonatal
The 1st Seizure
History-Majority will have a previous
unrecognized epileptic event. (eg: aura)
Provoked or unprovoked
Basic and specific Investigations
Recurrence Risk of 1st Seizure
Everyone has an 8-10% lifetime risk of a single seizure,
and 3% chance of epilepsy.
A first seizure caused by an acute disturbance of brain
function (provoked) is unlikely to recur (3-10%).
A first unprovoked seizure has a recurrence risk of 30-
50% over the next two years and 70-80% after a second
60-70% of recurrences are within six months of the
Investigating the 1st Seizure
EEG does not give the diagnosis.
When performed within 24-48 hours of a first
seizure EEG shows substantial abnormalities in
about 70% of cases and if negative, sleep
deprived EEG will detect epileptiform
discharges in an additional 13-31% of cases
(King 1998), (Schreiner 2003).
CT & MRI
Likely to Recur?
Patients with epileptiform discharges 83%
Patients with non-epileptiform abnormalities
Patients with normal EEGs, 12%
(van Donselaar, 1992).
Management of 1st Seizure
The significance of two definite unprovoked seizures
within 24 hours is uncertain.
Starting treatment after first seizure can reduce
recurrence but does not affect long term remission.
Lifestyle changes (avoid stress, adequate sleep) and
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specific precautions (driving, swimming, operating
Consider AED further if EEG and/or imaging is
A 50-year-old patient (70 kg) presents to the emergency
room with a 30-min history of continuous generalized
Upon admission, the patient is comatose, shows
twitching of the right face and arm, has a blood glucose
of 4.5mmol/L, and has stable vital signs. He has no
history of seizures.
Further history of the present illness and past medical
history are not available.
First-line therapy. What AED would you give
and at what dose?
Second-line therapy The patient is still seizing
10 min after receiving the 1st agent. He has now
been intubated, and vital signs are stable. What
would be your next anticonvulsant medication
and what would be the dose?
Third-line therapy. Twenty minutes after
receiving the first-line anticonvulsant
medication the patient is still seizing. Vital signs
are stable. He is now in your ICU. What would
be your next anticonvulsant medication and
what would be the dose?
Fourth-line therapy. After receiving maximum
doses of the above medications, the patient
remains in convulsive status epilepticus. What
would be your next anticonvulsant medication
and what would be the dose?
Recommended Treatment Protocol by Epilepsy Foundation
Dodson, W. E., Delorenzo, R. J., Pedley, T. A., Shinnar, S., et al. 1993
Diagnose status epilepticus by observing continued seizure activity or If status persists, administer phenytoin, 15-20 mg/kg IV, no
0-5 one additional seizure. faster than 50 mg/min in adults and 1 mg/kg/min IV in
children; monitor ECG and blood pressure during the
Give oxygen by nasal cannula or mask; position patient's head for 10- infusion; phenytoin is incompatible with glucose-
optimal airway patency; consider any abnormalities as necessary; 30 containing solutions; the IV line should be purged with
initiate ECG monitoring. normal saline before the phenytoin infusion. Alternatively,
fosphenytoin, 20 mg/kg phenytoin equivalents at 150
Obtain and record vital signs at onset and periodically thereafter; mg/min in adults or 3 mg/kg/min in children, can be used.
control any abnormalities as necessary; initiate ECG monitoring. If status does not stop after 20 mg/kg of phenytoin or
fosphenytoin, give additional doses of 5-10 mg/kg of
40 phenytoin or fosphenytoin to a maximal dose of 30 mg/kg.
Establish IV access; draw venous blood samples for glucose level,
serum chemistries, hematology studies, toxicology screens, and If status persists, give phenobarbital, 20 mg/kg IV at 50-
determinations of antiepileptic drug levels.
levels 100 mg/min; when phenobarbital is given after a
benzodiazepine, the risk of apnea or hypopnea is great, and
Assess oxygenation with oximetry or periodic arterial blood gas 60 assisted ventilation usually is required. If seizures
determinations. continue, give an additional 5-10 mg/kg of phenobarbital.
If status persists, give anesthetic doses of drugs such as
If hypoglycemia is established or a blood glucose determination is midazolam (loading dose of 0.2 mg/kg by slow
unavailable, administer glucose; in adults, give 100 mg of thiamine intravenous bolus, then 0.75-10.00 µg/kg/min), propofol
6-10 first, followed by 50 mL of 50% glucose by direct push into the IV (loading dose of 12 mg/kg IV, followed by 2-10 mg/kg/hr),
line; in children, the dose of glucose is 2 mL/kg of 25% glucose. > or pentobarbital (5-15 mg/kg IV bolus over 1 hour,
60- followed by 0.5-3.0 mg/kg/hr); ventilatory assistance and
70 vasopressors are virtually always necessary. Continuous
p y y y
Administer either lorazepam, 0.1 mg/kg IV at 2 mg/min, or diazepam, EEG monitoring is indicated throughout therapy, with the
0.2 mg/kg IV at 5 mg/min. If diazepam is given, it can be repeated if primary endpoint being suppression of EEG spikes or a
5-20 seizures do not stop after 5 minutes; if diazepam is used to stop the burst-suppression pattern with short intervals between
status, phenytoin should be administered next to prevent recurrent bursts.
Definition of Status Epilepticus
How much time should pass before determining
status epilepticus ?
When is SE considered to be refractory?
After 60 i f i i ? L ? M ?
Af 60min of seizing? Less? More?
After failure of 1st, 2nd, 3rd, or 4th line of therapy?
Subtle Status Epilepticus: When GCSE, clinical
and electroencephalographical features become
P l treated Status Epilepticus: When clinical
dS E il i Wh li i l
seizures stop but electrographic seizures
150 000 new cases/year in the U.S. (DeLorenzo et al, 1995)
50% have an epilepsy disorder. (DeLorenzo et al, 1996)
7-22% associated with mortality. (Chin et al, 2004)
i d ih li
Higher incidence in the extremes of age, elderly
have worse outcome.
M=F equal incidence
Importance of Status Control
Memory deficits and learning disabilities.
Predisposes neurons to further injury from
seizures in the future. (Koh et al, 1999)
Status epilepticus can cause cerebral injury,
as seizure activity itself is sufficient to
damage the central nervous system. (Lownstein et al,
Longer SE duration the more difficult to
control. (Kapur et al, 1997)
A 64-year-old woman presented with the new
onset of loss of consciousness followed by brief
jerking of extremities. After having dinner, she
had stood for a long time and then suddenly
dropped to the floor with pallor and sweating.
She was able to answer questions within a minute,
and had no confusion. She was incontinent of
Past history: Some complaints of dizziness and
lightheadedness when she stood up for a long
i Hypertensive on an alpha-receptor bl k
l h blocker.
Precipitants of Syncope: Clues for Etiological Diagnosis
Standing up Orthostatic hypotension due to autonomic failure,
dehydration, or drugs or as an idiopathic disorder in
Carbohydrate meals Postprandial hypotension of the elderly
Prolonged standing, micturition, pain, invasive Vasovagal (neurally mediated) syncope with reflex
medical procedures, swallowing, unpleasant sights vasodilatation/bradycardia/asystole
and smells, psychological shock
Heat, alcohol, antihypertensive drugs Vasodilatation
Coughing, blowing a trumpet, screaming, weight- Valsalva-maneuver resulting in decreased cardiac output
Lying supine in advanced pregnancy Venous obstruction
Hyperventilation (”stuffy air”) Hypocapnic cerebral vasoconstriction
Exertion Cardiac or pulmonary obstruction, eg, valve stenosis,
myxoma, pulmonary hypertension
Changing body position Atrial myxoma
Rock concert Combination of dehydration, prolonged orthostasis,
hyperventilation, and Valsalva (pressing crowd, screaming)
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