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

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

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

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
description
and EEG
Seizure
type (s)
All clinical a
laboratory d
neuroimagi
Etiology

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
CBC
FBS, BUN, Creatinine
Electrolyte , Liver function test , Ca+2 Mg+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
minute interictal EEG –useful when
clinical suspicion of epilepsy
 Timing is important
 30


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 epilepsyinterictal 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. RISK OF RECURRENT SEIZURE

The recurrence risk follow a first unprovoked seizure

50

Over 10

twice as likely to have another seizure if you have a
recurrence occur within 3 months
within 2 years of initial seizures
known brain injury or brain abnormality

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,
(eg, drugs,
alcohol,reflex stimuli)
Monotherapy
Seizures
in time (> 1 year)
Identified
factors

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

56. First-line choice of AEDs according to seizure
type
Seizure type
First line
Absence (typical and
atypical)
Myoclonic
VPA, LTG
Tonic-clonic
Atonic
Simple and complex partial,
with or without secondary
generalization
Unclassifiable
VPA
VPA, CBZ, PHT, PB
VPA
CBZ, PHT,
PB,OXC,LTG,TPM, GBP
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
Monotherapy
Well
controlled
65%
Unsatisfactorily
controlled
35%
Well
Add-on therapy controlled
10%
Multiple drug
therapy
Unsatisfactorily
controlled
25%
Well
controlled
5%
Unsatisfactorily
controlled
20%

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

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 : CBZ, VPA, PB
 PB :
CBZ, VPA, PHT
 VPA :
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
 Some
treatment of refractory epilepsy
of these AEDs: LTG, GBP, OXC,
TPM have also demonstrated efficacy as
monotherapy

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

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

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

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

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




Remote symptomatic




Past stroke
CNS infection
Cerebral palsy
Progressive encephalopathy



Electrolyte disturbance
Encephalitis
Head trauma
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
 congenital
outcome
anomalies 4-8%
(2-3 times > normal population)

79. The most common malformation
 Congenital
 orofacial
 neural
heart disease
cleft
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
 Review
the family regarding risks
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
 Check
vitamin K predelivery
antiepileptic drug levels prior to
delivery and increase doses if needed

86. After Delivery

Check levels

Examine infant

87. Thank you