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1. Seizure
&
Epilepsy
Prof. Nabil Khalil

2. Definitions

3. Seizure
 A sudden wave of synchronous electrical
activity in brain that usually affects how
a person feels or acts for a short time
 Some seizures can hardly be noticed,
while others are totally disabling

4. Epilepsy
 A condition that affects central nervous
system (CNS)
 had at least 2 seizures
 not caused by some known medical
condition like alcohol withdrawal or
extremely low blood sugar
 not indicate anything about the cause of
the seizures, what type they are, or how
severe they are

5. Momentary loss of
consciousness
 Fit
 Faint
 Fake(False)

6. Transient loss of consciousness
Déjà vu
Jamais vu
Aphasia
Olfactory aura
Epigastric sensation
Tongue biting
Post event delirium
Focal neurodeficit
Light-headedness
Sweating
Prolonged standing
Precipitants
eg.micturition
Chest pain
Palpitation
Slow heart rate
Low blood pressure
History and Physical Witness account
Aphasia
Delirium
Head turn
Automatism
Posturing
Convulsion
Postictal
delirium
Myoclonus
or convulsion
after pallor,
sweating
and
collapse
Pallor
Sweating
Slow pulse
Low BP
Syncope Seizure
Convulsive
syncope
Syncope Seizure

7. Character Syncope Epileptic seizure
Position usually upright any
Time daytime day or nighttime
Color pallor normal or cyanotic
Aura dizziness, visual blurring possible specific
aura
Autonomic common uncommon
Duration brief brief or prolonged
Incontinence rare more common

8. Character Syncope Epileptic seizure
Motor activity occasionally brief tonic
seizure or clonic jerks
variable
Automatism none absence,CPS
Disorientation,
posictal
rare can occur with
GTC,CPS

9. Nonepileptic causes for spells
 Physiologic
 Tremor
 Vasovagal syncope
 Cardiac arrhythmias
 Migraine
 Medication adverse effects
 Transient ischemic attacks
 Autonomic dysfunction

10. Nonepileptic causes for spells
 Psychologic
 Anxiety
 Panic attacks
 Mood disorder
 Personality disorder
 Psychosis
 Somatiform illness
 Psychogenic seizures

11. Phase of seizures
 Preictal phase or aura or warning
 Ictal phase : simple or complex partial or
generalized tonic-clonic seizure
 Postictal phase or recovery period : last
from seconds to minutes to hours

12. Precipitants of seizure
 Sleep and lack of sleep
 Drugs and alcohol
 Intercurrent illness : infection, fever
electrolyte imbalance
 Menstruation
 Stress and worry
 Other precipitants-reflex epilepsy

13. Classification of seizure
 Partial (focal, localized) seizures
 Generalized seizures (convulsive or non-
convulsive)
 Unclassified epileptic seizures

14. Partial (focal, localized)seizures
1. Simple partial seizures (preserved consciousness)
2. Complex partial seizures (impaired
consciousness)
3. Partial seizures evolving to secondarily
generalized seizures

15. 1. Simple partial seizures
(preserved consciousness)
With - motor signs
-somatosensory or special
sensory systems
- autonomic symptoms or signs
- psychic symptoms

16. 2. Complex partial seizures (impaired
consciousness)
-Simple partial onset followed by
impairment of conscious
-With impairment of consciousness at
onset

17. 3. Partial seizures evolving to
secondarily generalized seizures
-Simple partial seizures evolving to
generalized seizures
-Complex partial seizures evolving to
generalized seizures
-Simple partial seizures evolving to complex
partial seizures evolving to generalized
seizures

18. Generalized seizures (convulsive
or nonconvulsive)
- Absence seizures
Typical absences
Atypical absences
- Myoclonic seizures
- Clonic seizures
- Tonic seizures
- Tonic-clonic seizures
- Atonic seizures (astatic seizures)

19. Unclassified epileptic seizures
- Neonatal seizures
- Recurrent status epilepticus
- Rare or ‘isolated’ seizures

20. Epileptic seizure
Seizure
type (s)
Etiology
All clinical a
laboratory
neuroimagi
Seizure
description
and EEG

21. Seizure
Idiopathic
Generalized
epilepsy likely
Features
of focal
epilepsy
Epilepsy
or PNES
Provoked
seizures
EEG
EEG
MRI/CT
brain
Video
EEG
Treat
cause
+/-AED
PNES=psychogenic non-epileptic seizures AED=antiepileptic drug

22. Laboratory investigation
Mg+2
CBC
FBS, BUN, Creatinine
Electrolyte , Liver function test , Ca+2
Electro-encephalography (EEG)
Video EEG
Neuroimaging : CT Scan, MRI, MR Spect, PET
Special investigation : ammonia, lactate,
pyruvate etc.

23. Electroencephalogram

24. What value is the EEG?
 Add weight to the clinical diagnosis
 Aid classification of epilepsy
 Detection of the structural brain lesion.

25. EEG
 30 minute interictal EEG –useful when
clinical suspicion of epilepsy
 Timing is important
 Within 24 hr of generalized convulsion: 50%
have abnormal EEG
 First 48 hr: 21-34% have epileptiform activity
 Sleep EEG or sleep-deprived EEG might
increase diagnostic yield

26. Normal EEG

27. Primary generalized epilepsy—ictal
EEG

28. Primary generalized epilepsy-
interictal EEG

29. Burst of generalized spike and wave
discharges—typical absence seizure

30. EEG monitoring

31. Video Monitoring
 Helpful in determining nature of seizure
disorder (epilepsy, convulsive syncope, or
psychogenic seizures)

32. Indication for neuroimaging in
patients with seizures
 Partial seizure
 Late onset unprovoked seizure (age > 25)
 Unexplained neurological signs
 Focal slow waves EEG
 poor control or new symptoms / signs

33. Neuroimaging
 In the absence of trauma: CT and MRI
brain for patients presenting with
suspected first unprovoked seizure or with
a focal neurological deficit.
 MRI is preferable for looking for neuronal
migrational disorders, major
malformations, vascular anomalies,
tumors

34. The causes of epilepsy
 Genetic factor
 Congenital abnormalities
 Trauma and the effect of craniotomy
 CNS infection
 Cerebrovascular disease
 Cerebral tumors
 Alzheimer’s disease and other degenerative
disease
 Others

35. Neurocysticercosis

36. Cerebral infarction

37. Intracerebral hemorrhage

38. Brain tumor or metastasis

39. Lt mesial temporal sclerosis

40. Cortical dysplasia

41. 52 year old woman with intractable
seizure
PET scan

42. PET using F-18 FDG-- Decreased FDG
uptake in both temporal lobes, right worse
then left but otherwise relatively symmetric

43. What to do?
 Generalized seizure
 Loosening the patient’s clothing
 Lower the patient gently to the floor, turn them
onto their side and cushion head
 Nothing is put into the mouth
 Remove any items that could cause injury

44. What to do? ---Generalized seizure
 When the seizure is over, allow the patient to
rest or sleep
 If they are able to return to their feet, help
them home
 Obtain medical help if they continue to
experience breathing problems once the
seizure is over, or if the seizure lasts a long
time(over 10 mins), or when another attack
quickly follows the first

45. What to do?
 Partial seizures
 Stay with the patients throughout the seizure
 Protect them from any dangerous object
 Taking care not to restrain them in anyway

46. First aids

47. Treatment

48. Treatment

49. Choose a drug :
considering the
following factors
The seizure type and
prognosis
 Age
The possibility of
pregnancy
 Toxicity
 Drug interaction

50.  The recurrence risk follow a first unprovoked seizure
 50 recurrence occur within 3 months
 Over 10 within 2 years of initial seizures
 twice as likely to have another seizure if you have a
known brain injury or brain abnormality
RISK OF RECURRENT SEIZURE

51. RISK OF RECURRENT SEIZURE
(cont)
 If you do have two seizures, there's about
80% chance that you'll have more

52. Factors predictive of a high rate of
seizure recurrence after the first
unprovoked seizure
 Abnormal neurologic status by NE or
imaging
 EEG abnormalities (especially
epileptiform)
 Partial seizures

53. Counseling before treatment
1. Aims of treatment
2. Prognosis and duration of the
expected treatment
3. Importance of compliance
4. Side effects

54. Starting antiepileptic
treatment
Prospective risks Usual clinical
Factors that may modify
of epilepsy practice usual practice
Single seizure No treatment
Progressive cerebral disorder
Clearly epileptic EEG
2 or more seizure
widely separated
precipitating,
Monotherapy Seizures
in time (> 1 year)
Identified
factors
eg, drugs,
alcohol,reflex stimuli)

55. Antiepileptic Drug Development
1840 1860 1880 1900 1960 1980 2000
5
10
15
20
Bromide
0
Phenobarbital
Phenytoin Primidone
Ethosuximide
Zonisamide
SodiumV
alproate
Lamotrigine
Vigabatrin
Carbamazepine
Benzodiazepines
Tiagabine
T
opiramate
Felbamate
Levetiracetam
More
1920 1940
Calendar year
Antiepileptic drugs
Pregabalin
Oxcarbazepine
Fosphenytoin
Gabapentin

56. First-line choice of AEDs according to seizure
type
Seizure type First line
Absence (typical and VPA, LTG
atypical)
Myoclonic VPA
Tonic-clonic VPA, CBZ, PHT, PB
Atonic VPA
Simple and complex partial,
with or without secondary
generalization
CBZ, PHT,
PB,OXC,LTG,TPM, GBP
Unclassifiable VPA

57. Advantages of Monotherapy
 Better seizure control
 Reduced side effects
 Absence of drug interactions
 Reduced teratogenic effects
 Better compliance
 Reduced cost of medication
 Improved quality of life

58. Expected outcomes of AED
therapy
Well
controlled
65%
Unsatisfactorily
controlled
35%
Well
controlled
10%
Unsatisfactorily
controlled
25%
Well
controlled
5%
Unsatisfactorily
controlled
20%
Monotherapy
Add-on therapy
Multiple drug
therapy

59. Managing newly diagnosed
epilepsy
Newly diagnosed epilepsy
Seizure free
First drug
Second drug
Refractory
Surgical assessment
Rational duotherapy
Seizure free
47%
13%

60. Adverse effect of AED
 Dose related
 Idiosyncratic / allergic
 Chronic toxicity
 Teratogenicity

61. Older AEDs
Drugs Side effects
CBZ
Tegretol
Diplopia, headache, dizziness, N/V, rash, mild leukopenia, mild
hyponatremia
PHT Ataxia,nystagmus, dysarthria, somnolence,gingival hyperplasia,
hirsutism, acne, facial coarsening, folate, deficiency, osteopenia,
peripheral neuropathy, cerebellar atropy
VPA Dose-related tremor, weight gain,loss of hair, menstrual
irregularities, PCOS, stupor and encephalopathy(rare),
hepatotoxicity
PB
Somnilleta
Sedation and behavioral problem(depression, agitation,
hyperactivity)
CZP
clonezipzm
revotril
Sedation, ataxia, behavioral changes(depression)

62. AED interactions
 CBZ : autoinduction, VPA, PHT, -PB
 PHT :
 PB :
 VPA :
CBZ, VPA, PB
CBZ, VPA, PHT
CBZ, PB, PHT

63. AEDs
 Drug interaction with AED and other drugs: via
effect on hepatic CYP450 enzyme system
 PB, primidone, PHT, CBZ induce CYP enz. :
Accelerate breakdown of many prescribed
lipid-soluble drugs metabolized by the same
system: OCP, cytotoxic, antiarrythmic, warfarin
 VPA is a weak CYP enz. Inhibitor:
Slow clearance of other AEDs such as PHT,
LTG.
 Newer AEDs : less likely to interfere with
hepatic metabolism.
 GBP, LEV,PGB,VGB do not undergo hepatic
metabolism

64. Newer AEDs
 Adjunctive treatment of refractory epilepsy
 Some of these AEDs: LTG, GBP, OXC,
TPM have also demonstrated efficacy as
monotherapy

65. Effects of phenytoin levels
Level (mg/ml) Effect
0-10
10-20
20-30
30-40
> 40
Subtherapeutic
Therapeutic
Mild toxicity; nystagmus, mild ataxia
Moderate toxicity ; ataxia prominent
Severe toxicity; ataxia, conscious -
ness, encephalopathy

66. Potential Causes of Treatment
Resistant Epilepsy
 Diagnostic errors:
 Non-epileptic events
 Wrong diagnosis of seizure types epileptic
syndrome
 Missing of underlying causes lesions
 Patient’s errors:
 Non-compliance
 Inappropriate life style, inappropriate metabolism

67. Potential Causes of Treatment
Resistant Epilepsy
 Treatment errors:
 Wrong choice of drugs
 Less optimal doses of drugs
 Inadequate dosing schedules
 Antiepileptic drug toxicity
 Disease itself:
 Treatment resistant epilepsy
 metabolic disorder

68. Absolute
requirement
- years free of all
seizures
Stopping antiepileptic
treatment

69. Factors in favour
 Childhood epilepsy
Primary generalized
epilepsy
Absence of cerebral
disorder
Short duration of
epilepsy
 Normal EEG

70. Adverse prognostic
factors
 Symptomatic etiology, identifiable brain pathology
 Partial-onset seizures or Atonic seizures
 Late-onset or first-year epilepsy
 Specific epilepsy syndrome (particularly JME)
 Abnormal EEGs
 Multiple seizure types in the same patient
 Additional mental or motor handicap
 Long duration or severe epilepsy prior to treatment
 Poor initial response to treatment

71. Features common to the surgically
privileged seizure disorders
 Presence of a well-circumscribed structural
lesion on the MRI (lesional epilepsy)
 Presence of well-localized interictal epileptiform
discharged on the EEG
 Clinical features of habitual seizures indicating
focal onset
 Absence of discordance between above feature
 Focus localized by above features is surgically
accessible and involves little or no eloquent
cortex
 Absence of other potentially epileptogenic
abnormalities

72. Status epilepticus
A condition in which epileptic activity
persists for 30 minutes or more

73. Common etiologies for status
epilepticus in children and adolescents
 Idiopathic
 Acute symptomatic
 Electrolyte disturbance
 Encephalitis
 Head trauma
 Remote symptomatic
 Past stroke
 CNS infection
 Cerebral palsy
 Progressive encephalopathy
 Tuberous sclerosis
 Other neurodegeneration
 Febrile

74. Status epilepticus management

77. Epilepsy and
pregnancy
 Seizure control
Obstetric
complication
 Neonatal outcome

78. Neonatal outcome
 Risk of seizure
(3 times > normal population)
 developmental outcome
 congenital anomalies 4-8%
(2-3 times > normal population)

79. The most common malformation
 Congenital heart disease
 orofacial cleft
 neural tube defect
 intestinal atresia
 urogenital defects
Neural tube defect

80. Fetal antiepileptic drug
syndrome (minor anomalies)
 Facial dysmorphism
 Distal digital hypoplasia
 Developmental delay
 Mental deficiency

81. Factors affecting neonatal outcome
 AED
 genetics
 folic acid
 socioeconomic
 maternal health

82. Recommendations for managing Women
With Epilepsy
Before Conception
 Educate the family regarding risks
 Review classification of epilepsy
 Determine most appropriate medicine for
seizure control

83.  Determine need for continued medication
-may discontinue if seizure-free for 2 or more
years
-do not discontinue medication if epilepsy
syndrome
suggests continued need for treatment
 Reduce medicines to monotherapy, lowest dose
possible
 Start folic acid 1 mg/day
 Eliminate other risk factors –
smoking, drugs, alcohol

84. After conception
 Do not change antiepileptic medication
 Refer for prenatal care
 Prescribe vitamins, including folic acid
 Check ‘free’ drug levels every trimester and change
doses as needed
 Evaluate for neural tube defects at 12 to 16 weeks
(ultrasound, alpha-fetoprotein, amniocentesis)

85.  Consider vitamin K predelivery
 Check antiepileptic drug levels prior to
delivery and increase doses if needed

86. After Delivery
 Check levels
 Examine infant

87. Thank you