2. SEIZURE
DISORDERS
BY- SAMPURNA DAS

3. WHAT IS SEIZURES
Seizures are discrete, time-limited alterations
in brain function - including changes in
motor activity, autonomic function,
consciousness, or sensation -that result
from an abnormal and excessive electrical
discharge of a group of neurons within the
brain.

4. CAUSES
• Genetic influence
• Head trauma
• Brain conditions
• Infectious diseases
• Prenatal injury
• Developmental disorders

5. RISK FACTORS
• Age
• Family history
• Stroke
• Other vascular diseases
• Dementia
• Seizures in childhood.

6. PATHOPHYSIOLOGY
Seizure producing stimuli(trauma,high
fever,brain injury)
a small group of abnormal neurons undergo
prolonged depolarizations associated with
the rapid firing of repeated action potentials.
These abnormally discharging epileptic
neurons recruit adjacent neurons or
neurons with which they are connected into
the process

7. PATHOPHYSIOLOGY (CONT.)
the electrical discharges of a large number of
cells become abnormally linked together
creating a storm of electrical activity in the
brain
Seizures may spread to involve adjacent
areas of the brain or through established
anatomic pathways to other distant areas

9. GENERALIZED
SEIZURES
• 1. Generalized Tonic-Clonic
(Grand Mal)
• 2. Absence (Petit Mal)
• 3 Atypical Absence
• 4. Atonic seizures
• 5. Myoclonic Seizure
• 6. Tonic seizures

10. PARTIAL SEIZURES
SIMPLE PARTIAL
• a. Motor seizures
• d. Sensory seizures
• e. Autonomic seizures
• f. Psychic seizures
COMPLEX PARTIAL
• . Impairment of
consciousness
• b. Associated with
initial aura
• c. Simple to complex
automatisms

11. OTHERS
• Partial Seizures Secondarily Generalized
• Selected Epileptic Syndromes
A. Infantile Spasms
B. Febrile Seizure
C. Lennox-Gastaut Syndrome
D. Benign Rolandic epilepsy
E. Juvenile myoclonic epilepsy

12. PHASES OF CONVULSION
(1)PRODROMAL PHASE WITH SIGNS OR
ACTIVITY WHICH PRECEDE A SEIZURE;
(2)AURAL PHASE, WITH A SENSORY
WARNING;
(3)ICTAL PHASE WITH FULL SEIZURE;
(4) POSTICTAL PHASE WHICH IS THE
PERIOD OF RECOVERY AFTER THE
SEIZURE.

13. GENERALIZED TONIC-CLONIC SEIZURE
• Loss of consciousness is quickly followed by a
sudden fall to ground.
• In the tonic phase, muscles become rigid and
the simultaneous contractions of diaphragm
and chest muscles may produce the
characteristic "epileptic cry".
• The patient's eyes roll up or turn to the side and
the tongue may be bitten.
• The rigidity is replaced shortly by series of
synchronous clonic movements of head, face,
legs and arms.

14. GENERALIZED TONIC-CLONIC SEIZURE
• Autonomic changes also observed
included: increased blood
pressure,increased heart rate, and bladder
pressure; pupillary mydriasis;
hypersecretion of skin and salivary glands;
cyanosis of skin.
• Average duration 2 to 5 minutes.
• Postictally, patients lethargic/sleepy lasting
several minutes to hours.
• Incontinence seen in early postictal phase

16. ABSENCE SEIZURE
• Onset between 4 and 14 years and
often resolve by age 18.
• Brief episodes of staring with
impairment of awareness and
responsive that begin without warning
and end suddenly, leaving patient
alert and attentive.
• In simple absence seizures, patient
only stares.

18. Atypical Absence:
• Onset between 1 to 7 years of age
• similar to typical absence except that loss of
responsiveness during seizure is often less
complete and more gradual in onset and
cessation; Also clonic, tonic and atonic
components (i.e., increase or decreases in
muscle tone) are more pronounced than in
typical absence
• EEG findings: slow spike and wave (< 2.5 Hz)
discharge and/or incompletely generalized
spike-waves

19. ATONIC SEIZURE
• In the more common complex absence
seizures, staring is accompanied by
simple automatic movements such as
blinking of eyes, drooping of head, or
chewing.
• Duration - short (10-45 secs), patients
usually unaware of occurrence.
• Abrupt recovery without after effects

20. Myoclonic Seizure
• Sudden, brief shock-like jerk of a
muscle or group of muscles, often
occurs in healthy people as they
fall asleep.
• Epileptic myoclonus usually
causes synchronous and bilateral
jerks of the neck, shoulders, upper
arms, body, and upper legs.

21. Tonic seizures
• Characterized by sudden bilateral
stiffening of the body, arms, or legs.
Tonic seizures usually last less than 20
seconds and are more common during
sleep.
• Primarily seen in younger children;
commonly associated with metabolic
disorder or underlying neurological
deficit
• Duration 10-60 seconds; brief, if any,
postictal symptoms

22. SIMPLE PARTIAL SEIZURES
• a. No loss of consciousness;
• b. Motor seizures :
• c. Sensory seizures:
• d. Autonomic seizures:
• e. Psychic seizures:

23. Complex partial seizures (temporal lobe,
psychomotor epilepsy)

24. • A. IMPAIRMENT OF CONSCIOUSNESS
OBSERVED:
• Patients may appear to be conscious, closer
examination shows that they are unaware of
their environment
• fail to respond or respond inappropriately to
questions
• are unable to remember the seizure episode.

25. • B. ASSOCIATED WITHINITIAL AURA(I.E., SIMPLEPARTIAL
SEIZURE)IN >50% OF PATIENTS
• The aura is a simple partial seizure which may
then progress to a complex partial (and/or
generalized tonic-clonic) seizure. Most common
forms of aura: fear, rising epigastric sensation,
unilateral "funny feeling" or "numbness", or
visual disturbances; focal twitching of face or
fingers.

26. C. SIMPLE TO COMPLEX AUTOMATISMS (REPETITIVE MOTOR ACTIVITY
THAT IS PURPOSELESS, UNDIRECTED, AND INAPPROPRIATE)
• They are frequently observed during complex
partial seizures. Examples include repetitive
chewing or swallowing, lip smacking, fumbling
movements of fingers or hands, picking at clothing,
mumbling, moving about aimlessly, purposeless
behavior, and clumsy perseverance of a preceding
motor act.
• Average duration 1 to 3 minutes
• Postictal phase - confusion, lethargy, altered
behaviour, amnesic for event

27. 3. PARTIAL SEIZURES
SECONDARILY
GENERALIZED –

28. • partial seizure may progress through several
stages reflecting spread of discharge to different
brain areas. For example, seizure may begin as
simple partial (i.e., aura), progress to complex
partial and subsequently become secondarily
generalized (tonic-clonic).

29. 4. Selected Epileptic
Syndromes-

30. A. Infantile Spasms
• Consist of sudden flexion of the head with
abduction and extension of arms, accompanied by
flexion of knees and often a little grunt or cry.
Spasms may also be extension rather than flexion..
• Onset -between 4 to 7 months of age
• Characterized by spasms, developmental
retardation.
• Spasms may be flexor (jackknife), extensor or
mixed flexor-extensor.
• spasms usually disappear by age 3 or 4, but child
left profoundly handicapped, retarded, and often
with Lennox-Gaustaut syndrome

31. • B. Febrile Seizures
• Convulsions that occur with fever (> 38oC)
in children between 6 months and 6 years of
age, not secondary to an infection of brain
or meninges.
• Prevalence: 2 to 5% of all children will have
a febrile seizure before 6 y/o; Peak
incidence at 2 years of age.
• Intellectual dysfunction and neurologic
sequelae may occur following febrile status
epilepticus.

32. • C. Lennox-Gastaut Syndrome:
• This syndrome is characterized by the triad
of intractable seizures, mental and
developmental retardation, and slow spike
and wave pattern on the EEG.
• begin between ages 1 and 6 years
• respond poorly to antiepileptic drugs.
• Behavioral problems are common
• Probably result from the underlying
neurologic injury, effects of frequent
seizures and head injuries, and high-dose
combinations of antiepileptic drugs.

33. • D. Benign Rolandic epilepsy:
• This syndrome frequently begins in children
with a family history of epilepsy.
• Characteristic sign is a partial motor or
somatosensory seizure involving the face.
• Tonic-clonic seizures may also occur,
especially during sleep.
• The seizures are infrequent (some patients
require no medications), are easily
controlled with antiepileptic drug therapy,
and stop spontaneously by age 15.

34. • E. Juvenile myoclonic epilepsy:
• These myoclonic seizures, with or without tonic-
clonic or absence seizures, usually begin
shortly before or after puberty but may first
occur in early adulthood.
• Mental developemnt is normal.

35. COMPLICATION:
• Physical Injuries from Epilepsy
• Status Epilepticus
• Sudden Unexplained Death in
Epilepsy
• Eclampsia
• Social Challenges
• Anxiety

36. WHAT IS STATUS EPILEPTICUS?
Status epilepticus (acute prolonged seizure
activity) is a series of generalised that
occur without full recovery of
consciousness between attack.The term
has been broadened to include clinical or
electrical seizure lasting at least 30
minutes,even without impairment of
consciousness.

38. TREATMENT
• DIAZEPAM
• PHENYTOIN
• PHENOBARBITOL
• GENERAL ANAESTHESIA

39. FIRST AID

41. DIAGNOSTIC STUDIES

42. • 1. HISTORY
• 2. PHYSICAL EXAMINATION
• 3. NEUROLOGICAL EXAMINATION
• 4.BLOOD TESTS
• 5.ELECTROENCEPHALOGRAM

43. 6.CT SCAN
7.MAGNETIC RESONANCE IMAGING
8.FUNCTIONAL MRI (FMRI)
9.POSITRON EMISSION TOMOGRAPHY
10.SINGLE-PHOTON EMISSION
COMPUTERIZED TOMOGRAPHY
11.NEUROPSYCHOLOGICAL TESTS

44. MEDICAL MANAGEMENT

45. ANTI-EPILEPTIC DRUG (AED)
• 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
• Currently no “anti-epileptogenic” drugs
available

46. Choosing
the right AED
 Seizure type
 Epilepsy syndrome
 Pharmacokinetic profile
 Interactions/other medical conditions
 Efficacy
 Expected adverse effects
 Cost

47. Classification of AEDs
Classical
• Phenytoin
• Phenobarbital
• Primidone
• Carbamazepine
• Ethosuximide
• Valproate (valproic
acid)
• Trimethadione (not
currently in use)
Newer
• Lamotrigine
• Felbamate
• Topiramate
• Gabapentin/Prega
balin
• Tiagabine
• Vigabatrin
• Oxycarbazepine
• Levetiracetam
• Fosphenytoin

48. Targets for AEDs
• Increase inhibitory neurotransmitter system—
GABA
• Decrease excitatory neurotransmitter
system—glutamate
• Block voltage-gated inward positive
currents—Na+ or Ca++
• Increase outward positive current—K+
• Many AEDs pleiotropic—act via multiple
mechanisms

49. A = activation gate
I = inactivation gate
McNamara JO. Goodman & Gilman’s. 9th ed. 1996:461-486.
AEDs:
Mechanisms of Action
Na+
Na+
Carbamazepine
Phenytoin
Lamotrigine
ValproateNa+ Na+
I I
Voltage-gated sodium channel
Open Inactivated
X

50. AEDs:
Mechanisms of Action
• Calcium channel blockade

51. AEDs:
Mechanisms of Action
• GABA

52. Side effect issues
• Sedation - especially with barbiturates
• Cosmetic - phenytoin
• Weight gain – valproic acid, gabapentin
• Weight loss - topiramate
• Reproductive function – valproic acid
• Cognitive - topiramate
• Behavioral – felbamate, leviteracetam
• Allergic - many

53. Carbamazepine,
Oxcarbazepine, Phenytoin
Topiramate, Valproate
Ethosuximide
Levetiracetam
Pregabalin
Valproate
Barbiturates
Benzodiazepines, Gabapentin
Levetiracetam,Topiramate
Valproate,Vigabatrin
Na+ Ca2+
GABA

54. GENERALIZED
TONIC-CLONIC
SEIZURES
PARTIAL
SEIZURES
ABSENCE
SEIZURES
MYOCLONIC
& ATYPICAL
SYNDROMES
STATUS
EPILEPTICUS
Drugs of
Choice
Valproic Acid
Carbamazepine
Phenytoin
Carbamazepine
Lamotrigine
Phenytoin
Ethosuximide
Valproic
Valproic Acid
Clonazepam
Diazepam
Lorazepam
Alternative
Agents
Phenobarbital Felbamate
Phenobarbital
Topiramate
Valproic Acid
Clonazepam Levetiracetam
Topiramate
Zonisamide
Phenytoin
Phenobarbital
Adjunctive
Drugs
Lamotrigine
Topiramate
Gabapentin
Pregabalin
Lamotrigine
Levetiracetam
Zonisamide
Lamotrigine
Felbamate

55. Other Clinical Uses
Valproic acid –mania
Carbamazepine, Lamotrigine –
bipolar disorder
Carbamazepine –trigeminal
neuralgia
Gabapentin –pain of neuropathic
origin
Topiramate –migraine
Pregabalin –neuropathic pain

56. MAIN INDICATIONS OF ANTIEPILEPTIC DRUGS

57. TOXICITY
• Teratogenicity
• Overdosage Toxicity
• Life-Threatening Toxicity

58. Teratogenicity
Valproic acid –neural tube defects
Carbamazepine –craniofacial
anomalies, spina bifida
Phenytoin –fetal hydantoin syndrome

59. Overdosage Toxicity
• Respiratory depression
Management: supportive
 Airway management
 Mechanical ventilation

60. Life-Threatening Toxicity
Valproic acid –fatal hepatoxicity
Lamotrigine –Stevens-Johnson
syndrome
Zonisamide –severe skin reactions
Felbamate –aplastic anemia, acute
hepatic failure

62. KETOGENIC / LOW CARBOHYDATE
DIET
 VAGAL NERVE STIMULATION (VNS)

63. SURGICAL MANAGEMENT

64. • Temporal lobe resection
• Lesionectomy
• Functional Hemispherectomy
• Corpus Callosotomy
• Extratemporal Cortical Resection

66. DO WITH PRECAUTION------
•DRIVING
•ASCENDING HEIGHTS
•WORKING WITH FIRE OR COOKING
•USING POWER TOOLS
•DANGEROUS ITEMS
•TAKING UNSUPERVISED BATHS

68. ASSESSMENT:
• HISTORY, INCLUDING PRENATAL,
BIRTH, AND DEVELOPMENTAL
HISTORY, FAMILY HISTORY, AGE AT
SEIZURE ONSET, HISTORY OF ALL
ILLNESS AND TRAUMAS.
•DETERMINE WHETHER THE PATIENT
HAS AN AURA BEFORE AN EPILEPTIC
SEIZURE, WHICH MAY INDICATE THE
ORIGIN OF SEIZURE.

69. •OBSERVE AND ASSESS
NEUROLOGICAL CONDITION.
•ASSESS VITALS AND NEUROLOGICAL
SIGNS CONTINUOUSLY.
•ASSESS EFFECT OF EPILEPSY ON
LIFESTYLE.

70. NURSING DIAGNOSIS
1. Risk for trauma
2. Risk for suffocation
3. Risk for Ineffective Airway Clearance
4. Risk for Ineffective Breathing Pattern
5. Low Self-Esteem related to Stigma
associated with condition perception of being
out of control
6. Knowledge Deficit related to lack of exposure, unfamiliarity
with resources Information misinterpretation lack of recall;
cognitive limitation