pediatirc Epilepsy

1. 1
DEBREBIRHAN UNIVERSITY
Asrat weldeyes health science campus
Approach of seizure in childhood
Prepared by: Yohannes Mamo
Shegaw Merkebu
Zelalem Mekonnen
Modulator: Dr.Yemisrach (Pediatrician)
January 2015 E.C

2. Outline
2
 Definition of seizure
 Etiology of seizure
 Classification of seizure
 Approach to children with seizure
 Complication

3. Introduction
3
 A seizure is a transient occurrence of signs and/or
symptoms resulting from abnormal excessive or
synchronous neuronal activity in the brain. this can
cause changes in awareness, behavior, and/or
abnormal movements.

4. 4
 Acute symptomatic/ provoked seizures occur
secondary to an acute problem affecting brain
excitability
 Electrolyte imbalance structural, inflammatory, or
metabolic disorders of the brain
 An unprovoked seizure - without know or fixable
cause. it trigger by stress or sleep deprivation.
 Reflex seizures - seizure precipitated by a
sensory stimulus. including visual (flickering lights,
patterns, reading, music)

5. 5
 Epilepsy is considered when
1. Two or more unprovoked seizures occur in a time
frame of longer than 24 hr.
2. A known epilepsy syndrome.
 Epileptic syndrome is one or more specific seizure
types and has a specific age of onset and a specific
prognosis
 Epileptic encephalopathy is an epilepsy syndrome
in which there is a severe EEG abnormality that is
thought to result in cognitive and other impairments.

6. Epidemiology
6
 4–10% of children experience at least one seizure
(febrile or afebrile) in the first 16 yr of life.
 The cumulative lifetime incidence of epilepsy is 3%,
and more than half of the disorders start in childhood.
 Febrile seizures occur in 2 % to 4 % of the pediatric
population.
 Approximately 30% of patients who have a first
afebrile seizure later develop epilepsy

7. Cause of seizure
7
1. Idiopathic
2. CNS infections
 Meningitis, Encephalitis,
Brain abscess,
Syphilis(tertiary)
3. Metabolic
 Electrolyte imbalance
(calcium, sodium,
magnesium, phosphorus)
 Hypoglycemia
4. Structural
 Head trauma
 Brain tumor
 Stroke
5. Others
 Sepsis
 Drug abuse
 Ingestion of toxins and
accidental

8. 8

9. Mechanism of seizure
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1.Decreased excitability in inhibitory GABAergic
interneurons,
leading to increased excitability (GLUTAMATE) and
epilepsy.
2. Activation of metabotropic and ionotropic glutamate
receptors, as well as the tropomyosin-related kinase
B receptor.

10. Classification of seizures
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 EEG + Clinical
 EEG is an important adjunct in classification of seizures
 Classifying the seizure type
 Provides a clue to the cause of the seizure disorder
 Allows a firm basis for making a prognosis
 Helps in choosing the most appropriate treatment

11. 11

12. 12
1.Focal seizures. initial activation of a system of
nervous limited to one part of hemisphere
2. Generalized seizures, indicate synchronous
involvement of all of both hemispheres
3. Unknown onset if there is not enough clinical
information available to determine if the seizure is
focal or generalized
4. Unclassified are unusual and a determination of
onset cannot be made despite an adequate workup

13. Focal seizure
13
 Accounts 15 % of seizures in children
 limited to only one part of cerebral hemisphere
 Can progress to generalized seizure
 May or may not have change in consciousness

14. 1.Focal seizures without impairment
of consciousness
14
 Can be sensory or motor form
 Lasts not longer than 10 – 20 seconds
 May have jacksonian march from face to arm to
leg, head and eye movements to the contralateral
side or
 postictal (Todd) paralysis that can last minutes or
hours
 EEG: unilateral spikes/sharp waves on temporal

15. 2.Focal seizures with impairment of
consciousness
15
 Usually lasts 1- 2 minute
 Often preceded by an aura (crying, fear
,hallucination)
 But <7 years old children are less likely to report
aura
 Automatisms- confused, repetitive, purposeless
behaviour
 Such as chewing, lip smacking, swallowing, or
“picking” movements of the hands
 limited awareness of his actions and no memory of

16. 3. Generalized seizures that
evolve from focal seizure.
16
 Can be tonic, clonic or tonic-clonic seizure lasts 1-2
min.
 Head movement, tongue biting, urinary and stool
incontinence, vomiting with risk of aspiration,
cyanosis, fracture
 EEG Shows focal or sharp waves lobe where the
seizure originates.

17. Generalized seizures
17
 Discharges from both hemispheres
 There is,
 Always LOC
 No warning
 Symmetrical & Bilateral synchronous discharge
on EEG

18. Generalized tonic-clonic
seizure
18
 The tonic phase appears as full body stiffening
 Typically with the lower extremities extended &
upper extremities either flexed or extended with neck
extension.
 Ictal cry, the sound of forced air expired against a
closed glottis due to contraction of the diaphragm and
chest muscles.
 Tongue biting ,cyanosis ,apnoea ,falling drooling of
saliva, eye roll back associated with the tonic phase

19. Cont..
19
 Generalized tonic-clonic seizures last 1–3 minutes
 The tonic phase is followed by a clonic phase of
rhythmic jerking of the extremities
 Often associated incontinence of urine or stool
 They are always accompanied by loss of
consciousness

20. Cont..
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 Post-ictal period characterized by lethargy, decreased
arousal, confusion aphasia, fatigue, headaches, and
body aches.
 Post-ictal periods can last from minutes up to a few
hours.
 A prolonged post-ictal period or persistent altered
mental status after a seizure should raise concern for
an alternative etiology
 such as a medication effect or non-convulsive status

21. Cont…
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 The EEG pattern during a GTC typically shows
diffuse voltage attenuation with low amplitude fast
generalized poly-spikes or
 beta activity during the tonic phase evolving to
synchronous spike and wave during the clonic
phase

22. Tonic seizure
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 Continuous muscle contraction that can lead to
fixation of limbs and axial musculature in flexion or
extension
 Frequently occur in sleep or when the child is
emerging from sleep.
 They can last up to 1 minute, though most are often
<20 seconds
 The EEG usually shows generalized, low-voltage, fast
polyspikes with diffuse voltage attenuation

23. Clonic seizures
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 Rhythmic, repetitive jerks fast muscle
contractions and slightly longer relaxations
 The extremities are often flexed
 They can be focal or generalized.

24. Atonic seizures
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 Atonic seizures are characterized by a brief loss
of tone & accompanied by impaired
consciousness,
 though these seizures can be so brief that mental
status changes may not be detectable.
 Loss of tone occurs primarily in the trunk, but
more subtle forms can manifest as jaw drops
 Atonic seizures typically last 2–5 seconds
 Atonic seizures often result in a fall if the patient
is standing can lead to signifcant injury

25. Myoclonic seizure
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 Characterized by a brief contraction of a muscle
 The shock-like jerks that occur are very brief
<200 milliseconds
 Appear most often in the upper arms & shoulders
or upper legs
 Commonly no definite impairment in
consciousness
 The EEG during a myoclonic seizure shows a
burst of generalized spike- or polyspike-waves

26. Absence seizures
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 Brief episodes characterized by behavioral
arrest and impaired conscious that externally
present as staring spells.
 The spells are brief, typically lasting only 3–20
seconds
Sudden cessation of motor activity or speech
with a blank facial expression and flickering of
eyelids.
Children noted by their teachers or parents to

27. Typical absence seizures
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 Start and end abruptly, no postictal state &
resume pre seizure activity
 Often associated subtle motor components such
as swallowing or chewing movements, lip
smacking, or repetitive blinking
 Hyperventilation in the office can often induce a
typical absence seizure and is a useful diagnostic
maneuver

28. Atypical absence seizures
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 Marked by a loss of awareness
 The onset and offset of impaired to
consciousness is more gradual.
 Due to incomplete impairment in consciousness
,the patient may continue performing an activity
with less attention, coordination
 There can be a gradual loss of truncal tone
resulting in slumping but not falls.
 The spells are not provoked by hyperventilation

29. Febrile Seizure
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 seizure that occur at 38oc or higher, that are not
the result of CNS infection or any metabolic
imbalance, and in the absence of prior afebrile
seizures w/c occurs b/n 6-60 months
 Pick age of onset 12 -18 months
 Recur in approximately 30% in 1st episode, in
50% after 2nd or more episodes, & 50% of infants
onset of febrile seizure younger than 1 yrs.

30. 30
Simple febrile seizure
 Primary generalized, usually tonic-clonic seizure
 Attack associated with fever
 Lasting for a maximum of 15 min
 Not recurrent with in 24hrs
 do not have an increased risk of mortality

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Complex febrile seizure
 Focal seizure persisting for more than 15 minute
 Repeated convulsions occur within 24 hr
 Approximately 2-fold long-term increase in mortality
rates

32. Febrile infection–related (or
refractory) epilepsy (FIRES)
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 Predominantly in older >5 yr.
 Male children and associated with an
encephalitis-like illness but without an identifiable
infectious agent

33. Risk factors for recurrence of febrile seizure
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major
 Age <1 yr
 Duration of fever <24
hr
 Fever 38 – 39⁰c
 Having no risk factors
carries a recurrence risk
of approximately 12%; 1
risk factor, 25–50%; 2
risk factors, 50–59%; 3
or more risk factors, 73–
minor
 Family history of febrile
seizure
 Family history of
epilepsy
 Complex febrile seizure
 Daycare
 Male gender
 Lower serum sodium at
time of presentation

34. Risk Factors for Occurrence of
Subsequent Epilepsy After a Febrile
Seizure
34

35. Indication for LP in febrile
seizure
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Indication
 Children <06 month of age
 Children 06-12 month of age
I. Immunization status unknown
II. Immunizations deficient in HIB & S.
pneumonia
 Children at any age
I. Signs & symptoms of meningitis /ill
appearing
II. Child has received antibiotics prior to

36. Mgt of febrile seizure
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 Counseling & anti pyretic
 Anti epileptic
 Only acute treatment of seizure is necessary if seizure
lasts >5minutes.
 Diazepam, 0.3 mg/kg orally TID for the duration of the
illness, usually 2–3 days
 Otherwise long term antiepileptic treatment is not
recommended.

37. Neonatal seizure
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 Neonates are at particular risk for the
development of seizures because:
 Metabolic, toxic , structural and; infectious
diseases are more likely than at any other period
of life.
 Generalized tonic-clonic convulsions tend not to
occur in the 1st month of life
 Because arborisation & myelination are

38. Neonatal seizure types
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1. Focal Seizures
 Rythmic twiching of muscle groups
 Often associated with localized structural lesion,
infections & subarachnoid hemorrhage
2. Tonic Seizures
 Characterized by rigid posturing of the extremities
& trunk

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3. Myoclonic Seizures
 Brief focal or generalized jerks of extremities
4. Subtle seizures
 More common in full-term infants.
 Not associated with EEG seizures
 Have poor response to conventional
anticonvulsants
 Consist of chewing motion, excessive salivation
,apnea, pedaling movements

40. Correlation of Timing and aetiology
of Neonatal Seizure
40

41. Investigation
41
Depend on history and physical examination
 Blood glucose
 Serum electrolytes
 CBC
 Blood culture
 CSF analysis
 Cranial USG and CT
 Metabolic profile in cases of inborn error of
metabolism

42. Treatment
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 Stabilize vital signs, ABC of life
 Correct transient metabolic disturbances
 Hypoglycemia- 2ml/kg 10% dextrose IV over
1 min, followed by a continuous
 Hypocalcaemia – IV 5% calcium gluconate 2
ml/kg under careful cardiac monitoring,repeat
every 6 hrs over the first 24 hrs.
 Hypomagnesemia – 50% magnesium sulfate
IM at 0.2 ml/kg

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 Phenobarbital – Loading 20mg/kg, additional dose of
10mg/kg can be given if seizure not controlled, then
maintenance of 5mg/kg/day divided twice daily OR
 Phenytoin 20mg/kg loading, and maintenance of 4 –
6mg/kg/day
 For immediate cessation of seizure,Diazepam 0.1 to
0.3 mg/kg slowly IV until seizures stop
Prognosis
 Underlying etiology is the main determinant of
outcome

44. Status Epilepticus
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 Is a continuous convulsion lasting longer than 05
min, or
 The occurrence of serial convulsions between which
there is not return of consciousness

45. Type of status epilepticus
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 Convulsive status epilepticus the most common in
older child
 Non convulsive status
 Febrile status epilepticus-
 Most common in preschool child
 Is a continuous convulsion lasting longer than 30 min
 Neonatal status epilepticus

46. Managment of status epilepticus
46
General measures:
 Check airway, breathing and circulation
 Give oxygen (facemask)
 Insert nasogastric tube
 Open iv line & draw blood for CBC, electrolytes,
glucose & creatinine
 If hypoglycemia - give glucose (5 ml/kg of 10 %
dextrose)

47. Cont…
47
 Emergent antiseizure treatment should start with
a benzodiazepine.
 If the patient has IV/IO access
 Lorazepam IV 0.1 mg/kg/dose (max 4 mg) or
Diazepam IV 0.15–0.2 mg/kg/dose (max 10 mg)
 If the patient does not have IV access
 Diazepam PR
 2–5 years: 0.5 mg/kg
 6–11 years: 0.3 mg/kg
 ≥ 12 years: 0.2 mg/kg (max 20 mg)

48. Cont.…
48
 If the seizure persists after 5 minutes following
the first treatment, a second benzodiazepine
dose (lorazepam or diazepam) should be
administered
 If the seizure persists 2nd line treatment loading
dose of phenobarbital 20mg/kg/dose IV infusion
for 20 minute , or valproate 40 mg/kg/dose IV
infusion for 5 minute
 If seizure doesn't stop with in 30 minutes repeat
loading dose of the second-line treatment

49. Cont..
49
 For persistent seizure activity following repeat 2nd
line, treatment transitions to the initiation of
continuous infusion of anesthetic agents &
secured airway
 Midzaolam initial loading dose of 0.1–0.2 mg/kg
and a continuous infusion rate of 0.1–0.2
mg/kg/hr or
 Pentobarbital with a loading dose of 2–5 mg/kg
followed by a continuous infusion at a rate of 0.5–
1 mg/kg/hr

50. Approach to a children with
Seizure
50
Evaluation of the First Seizure
 The initial evaluation of an infant or a child
during or shortly after a suspected seizure
should include:
 Assessment of the adequacy of the airway,
ventilation, and circulation (ABC).
 Positioning
 Measure vital signs and glucose
concentration.

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History
 Ensure whether seizure really occurred
 Previous seizure
 Seizure characteristics
 Associated symptoms or signs, (hypoglycemia,
meningitis, cardiac arrhythmia, or acute pulmonary
embolism)
 History of trauma
 A past and current psychosocial history, including
potential stressors

52. 52
Evaluate for acute & provocative causes:
 Withdrawal (sedatives & alcohol)
 Hypertension (Hypertensive encephalopathy)

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 Past Hx of meningitis
 Past Hx of seizure & use of antiepileptic drugs
 Family Hx of seizures
 Any evidence of active CNS infection

54. Physical Examination
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 G/A- cardiorespiratory distress
 V/S-Increase PR, BP, RR-irregular, hypoxia, respiratory
acidosis, fever
 Anthropometry: Growth & HC percentiles
 HEENT
 Bulged anterior fontanel
 Upward deviation of the eye, Pupils- size, papiledema,
retinal hemorrhages
 Otorrhea, CSF rhinorrhea, drooling, tongue laceration

55. 55
 LGS: Lymphadenopathy
 Chest: Lung findings
 CVS- Abnormal heart rhythm symptoms of heart failure
 Abdomen- organomegaly /metabolic or storage diseases
 GUS- Incontinence
 Intg & Mss- Injuries, shagreen patch , multiple cafeau-lait
spots

56. 56
CNS
 level of conscious: using modified GCS or Blantyre coma score
 Posture: decorticate or decelerbrate
 Focal neurological deficit: slow-growing glioma, as the cause
of the seizure disorder
 Meningeal signs

57. Investigation
57
 CBC, ESR
 Serum glucose
 Serum electrolytes (Na ,
Ca)
 Blood culture
 Serum level of
anticonvulsant
 Toxicology screening
(urine and serum )
 Blood film
 LP
 EEG: - help predict the
risk of seizure
recurrence and to
assess for focal
abnormalities.
 CT or MRI: -for
structural underlying

58. Principle of Management
58
 Assess airway ,breathing ,circulation(ABC of life)
 Give oxygen
 Don’t put anything in the mouth
 Avoid sharp material around the pt.
 Establish diagnosis
 Arresting seizure by treating underling conditions
 Principles of pharmacologic therapy

59. When to Initiate Ant seizure Drug
59
 Should be started in any patient with recurrent
seizures of unknown aetiology
 A known cause that cannot be reversed.
 Initiate therapy in a patient with a single seizure
is controversial.

60. Cont..
60
 Establish diagnosis
 correctly determine seizure type , epileptic
syndrome , etiology and precipitating factors.
 Principles of pharmacologic therapy
 use a single drug till maximum dose or side
effect
 Add additional drug with different site of

61. Type of seizure and drug of
choice
61
Seizure type Drug of choice
Focal seizure
Carbamazepine, phenytoin
phenobarbitone
Absence seizure Ethosuximide,
Valproite, clonazepam
Tonic-clonic seizure
Phenytoin ,phenobarbitone
Myoclonic
Valproate, Clonazepam
Infantile spasm Predinsolone

62. Management of acutely
convulsing child
62
 Assess ABC of life
 Give oxygen
 Correct hypoglycemia
 Arrest the seizure with:
 Diazepam 0.2-0.5 mg/kg iv/rectal or
 Lorazepam 0.05-0.1mg/kg iv
 Position the child –recovery position

63. 63

64. Cont…
64
 If seizure persists –load with phenytoin or
phenobarbital
 Initial screening history and physical examination
 Obtain laboratory studies

65. Epilepsy surgery
65
 Seizures must be medically intractable (a patient
has failed 3 drugs)
 Seizures must be debilitating
 properly defined epileptogenic zone

66. Causes of intractable epilepsy
66
 Improper diagnosis of seizure type
 Improper dose
 Genetic syndromes and brain malformations

67. When to stop anticonvulsant
67
 Two seizure free years are required for a patient with
no risk factors.
 Drugs should be withdrawn slowly , weaning
process may take 2-3 months
 Normal EEG finding
 Risk factors for recurrence:
 Age > 12 yrs at onset
 Neurologic dysfunction
 History of prior neonatal seizures

68. Complications
68
 Cerebral palsy
 Hypoxischemic
encephalopathy
 Hydrocephalus
 Status epilepticus
 Learning disability,
cognitive impairment
 Developmental delay
 Injury
 Aspiration of secretions
or vomited stomach
contents
 Skull or vertebral
fractures, shoulder
dislocation
 Cardio respiratory arrest

69. Prognosis
69
 There is a high incidence of early death (24 -30 %)
associated
with neonatal seizures, and a high incidence of neurologic
impairment, developmental delay, and post neonatal
epilepsy
among survivors.

70. Reference
70
1. Nelson textbook of Pediatrics, 21th edition
2. UpToDate 21.6
3. Handbook of Pediatric Epilepsy2nd edition

71. 71
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