3. Seizure
A seizure is a paroxysmal event due to
abnormal, excessive, hypersynchronous
discharges from an aggregate of central
nervous system (CNS)neurons (cortical
neurons).
4. Epilepsy
Epilepsy describes a condition in which a
person has recurrent seizures due to a
chronic, underlying process.
Single seizure, or recurrent seizures due to
correctable or avoidable circumstances,
does not necessarily have epilepsy
5. Epilepsy
These are group of disorders of CNS, characterised
by paroxysmal cerebral dysrhythmia, manifesting
as brief episodes (seizures) of loss or disturbance
of consiousness, with or without characteristic
body movements (convulsions)
♦Epilepsy has a focal origin in the brain
6. EPIDEMIOLOGY
• The most common ages of incidence are
under the age of 18 and over the age of 65.
• It has been estimated that about 1% of the
population meets the diagnostic criteria for
epilepsy at any given time, but some
theorize that the prevalence may be much
higher in fact.
7. 5% of the population suffer a single sz at
some time
0.5-1% of the population have recurrent sz
= EPILEPSY
70% = well controlled with drugs
(prolonged remissions); 30% epilepsy at
least partially resistant to drug treatments =
INTRACTABLE EPILEPSY.
13. Seizures are a result of a shift in the
normal balance of excitation and inhibition
within the CNS.
...... i.e. Abnormal discharges of neurons
That may be caused by any pathological
process affecting brain>>>>
14. Types of Epilepsy
A. GENERALISED SEIZURES
i. Generalised tonic-clonic seizures
ii. Absence seizures
iii. Myoclonic seizures
iv. Atonic seizures
v. Infantile seizures (hypsarrhythmia)
15. Types of Epilepsy
B. PARTIAL SEIZURES
i. Simple partial seizures
ii. Complex partial seizures
iii. Secondary generalized seizures
16. Types of Epilepsy
B. UNCLASSIFIED SEIZURES
i. Unclassified seizures
ii. Neonatal seizures
iii. Infantile spasms
17. Partial
Synonymous with focal
Activity is restricted to discrete areas of
cerebral cortex.
Typically associated with structural
abnormalities of the brain.
18.
19. Generalized
Involve difusse regions of the brain
simultaneously in a bilaterally symetric
fashion
May result from cellular, biochemical, or
structural abnormalities that have a more
widespread distribution.
21. Partial Seizures
Discrete regions of the brain.
Consciousness is fully preserved during
the seizure (Simple-partial seizure)
Consciousness is impaired (Complex
partial seizure)
Partial seizure and then spread diffusely
throughout the cortex (partial seizure with
secondary generalization)
22. Simple-Partial Seizure
Motor, sensory, autonomic, or psychic
symptoms.
Without an obvious alteration in
consciousness.
Three additional features
23. Three features
“Jacksonian march” abnormal motor
movements may begin in a very restricted
region, and gradually progress (over
seconds to minutes).
May experience a localized paresis (todd`s
paralysis) minutes to many hours.
Seizure may continue for hours or days.
”epilepsia partials continua”.
24. Simple partial. And Aura
Other forms of simple-partial seizures include
those that cause changes in somatic sensation.
Some patients describe odd internal feelings.
(fear, dejà vu)
When precede a complex-partial or secondarly
generalized seizure, these simple partial seizures
serve as a warning or aura.
25. Complex-Partial Seizures
Focal seizure activity
Patient is unable to respond to visual or
verbal commands during the seizure and
has impaired Consciousness or awareness
of the ictal phase.
Frequently begin with an aura.
26. The start of the ictal phase is often a
sudden behaivoral arrest or motionless
stare.
Usually acompained by automatisms.
The patient is typically confused following
the seizure.(seconds up to an hour).
27.
28. Partial Seizures with Secondary
Generalization
Partial seizures can spread to involve both
cerebral hemispheres and produce a
generalized seizur, usually of the tonic-
clonic variety.
Is often difficult to distinguish from a
primarilly generalized tonic-clonic seizure.
Careful history identifies a preceding aura.
32. Generalized Seizure.
Practically defined as bilateral clinical and
electrographic events without any
detectable focal onset.
Arise from both cerebral hemispheres
simultaneously
34. Absence Seizures (Petit Mal)
Sudden brief lapses of consciousness
without loss of postural control.
Typically last for only seconds,
consiousness returns as suddenly as it was
lost.
No postictal confusion
35. Absence seizures are usually accompained
by subtle, bilateral motor signs (rapid
blinking of the eyelids, chewing
movements, or small clonic movements of
the hands.
36. Can occur hundreds of times per day.
Always begin in childhood (ages 4 to 8) or
early adolescence.
Hyperventilation tends to provoke.
37. Typical Absence seizure are not associated
with other neurologic problems and
respond well to treatment with specific
anticonvulsants.
60 – 70 % will have a spontaneous
remission during adolescence.
38. Atypical Absence Seizures:
– Lapse of consciousness is usually of longer
duration.
– Less abrupt in onset and cessation
– Accompained by more obvious motor signs.
39.
40. Generalized Tonic – Clonic
Seizures (Grand Mal)
The most common seizure type resulting
from metabolic derangements.
41. The initial phase of the seizure is usually
tonic contraction of muscles throughout
the body.
After 10 to 20 s. The tonic phase of the
seizure typically evolves into the clonic
phase, produced by the superimposition of
periods of muscle relaxion on the tonic
muscle contraction.
42. Aura
A sensation perceived by a patient that
precedes a condition affecting the brain.
An aura occurs before a seizure.
It may consist of flashing lights, a gleam
of light, blurred vision, an odor ,
numbness, weakness, or difficulty in
speaking.
43. Phases of grand-mal seizures
Tonic phase:
• Contraction of muscle start
• Rigidity of arm
• Duration 15 sec
• Person loss consciousness and fall down
• Saliva merge from the mouth
• Tongue biting
• Sweating increase
44. Clonic phase
Arm and leg jerk rapidly
After 30 sec or few minutes jerking slow
down and end
Consciousness return slowly
Eye rolled
Show painful expressions
Than person falls, unresponsive sleep for
15 minutes
Than after awaking then sleep again for
hours
45.
46. The periods of relaxation progressively
increase until the end of the ictal phase.
Usually last no more than 1 min.
47. Postictal phase is characterized by:
– Unresponsiveness
– Muscular flacciditidy
– Excessive salivation
– Bleadder or bowel incontinence
48. Patients gradually regain consciousness
over minutes to hours
Tipically a period of postictal confusion.
Headache, fatigue, and muscle ache.
49.
50. Atonic Seizure
Sudden loss of postural muscle tone lasting
1 to 2 s.
Consciousness is briefly impaired
Usually no postictal confusion
51. Very brief seizure may cause only a quick
head drop or nodding movement.
Longer seizure will cause the patient to
collapse. (extremelly dangerous)
52.
53.
54. Myoclonic Seizure.
Sudden and brief muscle contraction that
may involve one part of the body or the
entire body.
Pathologic myoclonus is most commonly
seen in association with metabolic
disorders, degenerative CNS diseases, or
anoxic brain injury.
59. Neonatal Seizure
Less than 1 month of age.
Brief episodes of apnea, eye deviation, eye
blinking, or repetitive movements of the
arms and legs.
60. Infantile Spasms
Infants under 12 months.
Abrupt movements of the head, trunk, or
limbs.
The classic spasm is a sudden flexion of
the neck and abdomen with extension of
the limbs.
61. SEIZURE SYNDROMES
• There are many different epilepsy syndromes,
each presenting with its own unique combination
of seizure type, typical age of onset, EEG
findings, treatment, and prognosis.
• Infantile spasms (West syndrome) is associated
with brain development abnormalities, tuberous
sclerosis, and perinatal insults to the brain. It
affects infants, which by definition is between 30
days to 1 year of life.
62. • Generalized 3 Hz spike and wave
discharges in EEG Childhood absence
epilepsy affects children between the ages
of 4 and 12 years of age. These patients
have recurrent absence seizures that can
occur hundreds of times a day.
• Benign focal epilepsy of childhood
(Benign Rolandic epilepsy) begins in
children between the ages of 4 and 13
years.
• Juvenile myoclonic epilepsy (JME) begins
in patients aged 8 to 20 years.
63. • Temporal lobe epilepsy is the most
common epilepsy of adults. In most
cases, the epileptogenic region is
found in the temporal structures (e.g.,
the hippocampus, amygdala, and
parahippocampal gyrus). Seizures
begin in late childhood and
adolescence.
• Frontal lobe epilepsy
• Lennox-Gastaut syndrome
66. Approach:
– History (from patient and witness)
– Physical examination
– Investigations
– Treatment
– Follow up
67. Three basic questions
1. Is it a seizure?
– If so, what kind?
2. What caused it?
3. What should be done?
68. History
Event
– Localization
– Temporal relationship
– Factors
– Nature
– Associated features
Past medical history
Developmental history
Drug and immunization history
Family history
Social history
69. Physical Examination
General
– esp. syndromal or non-syndromal
dysmorphic features, neurocutaneous
features
Neurological
Other system as indicated
– E.g. Febrile convulsion, infantile spasm
72. Investigations
I. Exclusion of differentials:
– Bedside: urinalysis
– Haematological: CBP
– Biochemical: U&Es, Calcium, glucose, ABGs
– Radiological: CXR, CT head
– Toxicological: screen
– Microbiological: LP
(Always used with justification)
73. II. Confirmation of epilepsy:
– Dynamic investigations : result changes
with attacks
• E.g. EEG
– Static investigations : result same
between and during attacks
• E.g. Brain scan
74. Electroencephalography
(EEG)
EEG indicated whenever epilepsy
suspected
Uses of EEG in epilepsy
– Diagnostic: support diagnosis, classify
seizure, localize focus, quantify
– Prognostic: adjust anti-epileptic treatment
75. Electroencephalography
(EEG)
Hemispheric or lobar asymmetries
– Periodic (regular, recurring)
– Background activity:
• Slow or fast
• Focal or generalized
– Paroxysmal activity:
• Epileptiform features – spikes, sharp waves
• Interictal or ictal
• Spontaneous or triggered
79. Antiepileptic Drug
A drug which decreases the frequency
and/or severity of seizures in people with
epilepsy
Treats the symptom of seizures, not
the underlying epileptic condition
Goal—maximize quality of life by
minimizing seizures and adverse drug
effects
80. Ideal Agent: If Exists
Ideal drug for treating SE
– Rapid entry into CNS
– Rapid onset of action
– Long duration of action
– Safety
– Absence of sedation
– Useful as maintenance AED
83. Carbamazapine
First line drug for partial seizures
Inhibits Na+ channels—use dependent
Half-life: 6-12 hours
Adverse effects: CNS sedation. Agranulocytosis
and aplastic anemia in elderly patients, very rare
& serious adverse. A mild, transient leukopenia
in about 10% disappears in first 4 months of
treatment ,impired balnnce ,rash , diplopia
Start100mg12h then increase to 200mgd upto
max1000mg/12h
84. Phenobarbital
Partial seizures, effective in neonates
Second-line drug in adults due to more severe CNS
sedation
Allosteric modulator of GABAA receptor (increase
open time)
Absorption: rapid
Half-life: 53-118 hours (long)
Adverse effects:
but may produce excitement in some patients. Skin
rashes
Tolerance and physical dependence possible.
85. Benzodiazapines (Diazapam and
clonazapam)
Status epilepticus (IV)
Allosteric modulator of GABAA receptors—
increases frequency
Absorption: Rapid onset. Diazapam—rectal
formulation for treatment of SE
Half-life: 20-40 hours (long)
Adverse effects: CNS sedative, tolerance,
dependence. Paradoxical hyperexcitability in
children
87. Ethosuximide
Absence seizures
Blocks T-type Ca++ currents in thalamus
Half-life: long—40 hours
Adverse effects: gastric distress—pain,
nausea, vomiting. Less CNS effects that
other AEDs, transient fatigue, dizziness,
headache
Drug interactions: administration with
valproate results in inhibition of its
metabolism
88. Phenytoin
Inhibits Na+ channels—use dependent
Prodrug fosphenytoin for IM or IV
administration. Highly bound to plasma proteins.
Half-life: 22-36 hours
Adverse effects: CNS sedation (drowsiness,
ataxia, confusion, insomnia, nystagmus, etc.),
gum hyperplasia, hirsutism
Interactions: carbamazapine, phenobarbital will
decrease plasma levels; alcohol, diazapam,
methylphenidate will increase. Valproate can
displace from plasma proteins. Stimulates
cytochrome P-450, so can increase metabolism of
some drugs.
90. Oxcarbazepine
Approved for add-on therapy, monotherapy in
partial seizures that are refractory to other AEDs
Activity-dependent blockade of Na+ channels,
may also augment K+ channels
Half-life: 1-2 hours, but converted to 10-
hydroxycarbazepine 8-12 hours
Adverse effects: similar to carbamazepine (CNS
sedative) but may be less toxic.
91. Lamotrigine
Add-on therapy, monotherapy for refractory partial
seizures. Also effective in Lennox Gastaut Syndrome and
newly diagnosed epilepsy. Effective against generalized
seizures.
Use-dependent inhibition of Na+ channels, glutamate
release, may inhibit Ca++ channels
Half-life—24 hours
Adverse effects: less CNS sedative effects than classic
AEDs, dermatitis potentially life-threatening in 1-2% of
pediatric patients.
Drug interactions: levels increased by valproate,
decreased by carbamazepine,, phenytoin
92. Gabapentin
Add-on therapy for partial seizures,
May interfere with GABA uptake
Adverse effects: less CNS sedative effects than
classic AEDs
93. Levetiracetam
Add-on therapy for partial seizures
Binds to synaptic vesicle protein SV2A,
may regulate neurotransmitter release
Half-life: 6-8 hours (short)
Adverse effects: CNS depresssion
94. Avoid• DRIVING
• ASCENDING HEIGHTS
• WORKING WITH FIRE OR COOKING
• USING POWER TOOLS OR
• DANGEROUS ITEMS
• TAKING UNSUPERVISED BATHS
• SWIMMING
95. EFFECTS OF AEDs ON
PREGNANCY
Teratogenicity(folic a 5mg) avoid valorate
Breast feeding(except valorate-
carbamazep)
Contraception non enzyme inducing AEDs
no effect
96. When star AEDs in pt with first
SZ
• Presented with stutus epilepticus
• Abnormal EEG
• Abnormal nerological examination
• Strong family Hx of epielpsy
97. When we decrease the dose of
AEDs
Normal CNS examination
Normal EEG
Normal IQ
2years free of SZ
99. DIET & OTHER
TREATMENT
• Ketogenic diets may occasionally be effective in
controlling some types of epilepsy.
• The mechanism behind the effect is not fully understood,
shifting of pH towards a metabolic acidosis and alteration
of brain metabolism may be involved.
• Ketogenic diets are high in fat and extremely low in
carbohydrates, with intake of fluids often limited.
• Ketogenic diets are sometimes prescribed in severe cases
where drugs have proven ineffective.
100. Ketogenic Diet
Traditionally started gradually in the hospital after a 24-
48 hour fast
– Families educated daily
Ratio (fat: carbs and protein)
– 4:1 more strict
– 3:1 for infants, adolescents
Calories 60-100%
Fluids 85-100%
Solid foods and/or formula
Requires dietician support
Strong family committment
101. • Ketogenic diet is not good for the heart or
kidneys and medical problems resulting
from the diet have been reported.
• The diet is extremely unpalatable and few
patients are able to tolerate it for any
length of time.
• Since a single potato chip is adequate to
break the ketosis, staying on the diet
requires either great willpower or perfect
control of a person's dietary intake.
• People fed via gastrostomy or young
children who receive all their food in the
presence of a caregiver are better
candidates.
102. Brain Stimulation for Epilepsy
Vagal Nerve Stimulation
Transcranial Magnetic stimulation
Intracranial stimulation
– Surface electrodes (‘responsive’)
– Deep Brain Stimulation
• Hippocampus
• Thalamus
• Cerebellum
103. • Surgical treatment can be an option for
epilepsy when an underlying brain
abnormality, such as a benign tumor or an
area of scar tissue (e.g. hippocampal
sclerosis) can be identified.
• The abnormality must be removable by a
neurosurgeon.
• Surgery is usually only offered to patients
when their epilepsy has not been
controlled by adequate attempts with
multiple medications.
104. • The most common form of resective surgical
treatment for epilepsy is to remove the front part
of either the right or left temporal lobe.
• Palliative surgery for epilepsy is intended to
reduce the frequency or severity of seizures.
• Hemispherectomy is a drastic operation in
which most or all of one half of the cerebral
cortex is removed.
• It is reserved for people suffering from the most
catastrophic epilepsies, such as those due to
Rasmussen syndrome.
105. Prolonged seizure activity lasting greater
than 30 minutes
Or, recurrent seizures without the interval
of recovery (consciousness) lasting greater
than 30 minutes
106. Remember
Most seizures are brief, lasting less than 5
minutes
If a seizure is lasting greater than 10
minutes, are likely to be prolonged
108. Treatment
Step 1
ABCDE
– Maintain Airway- patient at risk for aspiration
– Breathing- place O2, be ready for intubation
– Circulation- obtain IV access
– : check glucose levels if can not check give
50ml of D50 thiamine after take sample for
RBG &
– Electrolytes: check electrolytes (Na, Ca, Mg,
PO4), and anticonvulsent levels, toxiclogy
screen ,RFT,LFT,RBG,
110. Diazepam
Highly lipid soluble
– Rapid CNS entry- stops seizures in 1-3 minutes
Rapid redistribution in fatty tissues
– Brain concentrations fall quickly
– Duration of action is 15-30 minutes
– T1/2= 30 hr
Dose: <3yrs, 0.5mg/kg, >3yrs, 0.3mg/kg
Side Effects: sedation, decreased respiration and
blood pressure
111. Lorazepam
Less lipid soluble than diazepam
– Slower CNS, stops seizures in 6-10 min
Not as rapidly redistributed to fat stores
– Longer duration of action 12-24 hr
– T1/2 =14 hr
Dose: 0.05—0.1mg/kg NO rep within 2min
Side Effects: decreased LOC, respiration and BP
T :10min
112. Treatment
Step 3
T : 15min
Phenytoin/Fosphenytoin
Phenytoin
• IV dosing 20 mg/kg load
• Stops seizures in 10-30 minutes
• Duration of action 24 hrs, T ½=24hr
• Max infusion rate of 1mg/kg/min, max- 50 mg/min
• Side Effects: arrhythmias, hypotension, wide QT
interval, phelibitis
• pH=11-12, may only give IV or po
113. Treatment
Step 4
T : 20min
Phenobarbital
– Lipid solubility < phenytoin
– Duration of action>48 hrs, T1/2= 100 hours
– Dose 20 mg/kg
– Inert cath + I V fluid
– Side Effects: sedation, decreased respiration
and BP
– Be ready to intubate!!
115. Refractory Status Epilepticus
Status epilepticus that fails to respond to 2
AED.
Nearly 40% of status epilepticus are
refractory!
Intubation, IV access
Continuous EEG monitoring
Medication Coma
– Pentobarbital |_Propofol
– Midazolam _Very high dose phenobarb
116. Malignant/super- refractory status
epilepticus
Status epilepticus that does not respond to
a course of anesthetic drug.
20% of refractory status epilepticus
patients.
Needs combination therapy (AED &
Anesthetic drugs) /immune therapy.
117. Consider the Etiology
LP: necessary for any febrile seizure
under the age of 18 months
– Must strongly consider in comatose patient –
please check imaging first
– Remember SE can cause pleocytosis (usually
< 20 cells)
– Do not delay antimicrobial therapy if CNS
infection is suspected
– Consider acyclovir
118. SUMMARY
ABCDE
Lorazepam (0.1mg/kg) or Diazepam
– Give 5 minute interval then may repeat
Fosphenytoin: 20mg/kg, may give additional
10mg/kg after initial load
Phenobarb: 20mg/kg- be ready for intubation
If neurology not involved, call us
General anasethesia (eg, propofol)