2. Definition
• Epilepsy : The occurrence of transient (short-
term) paroxysms (sudden attack) of excessive
or uncontrolled discharges of neurons in the
cerebral cortex, which may be caused by a
number of different etiologies, leading to
epileptic seizures.
• The term seizure needs to be carefully
distinguished from convulsions and epilepsy.
3. What is the differences between
Seizure and Epilepsy
• Epilepsy is a disorder characterized by
recurring seizures (also known as “seizure
disorder”)
• A seizure is a brief, temporary disturbance in
the electrical activity of the brain
“A seizure is a symptom of epilepsy”
4. Historical Background
Epilepsy derived from a Greek term:
Epilambane -to posses, to take hold of, to
grab or to seize.
Vedic period of 4500-1500BC : Ancient Indian
Medicine refined and developed the basic
concept of epilepsy
Charaka Samhita- The Ayurvedic literature
400 BC: Describe epilepsy as ‘Apasmara’
means loss of consciousness.
5. Cont…
Hippocrates 400 BC: ‘This is not a sacred
disease rather disorder of brain’ . He described
some physical treatment of epilepsy and
stated it is an incurable chronic illness.
Ibn Sina 370 AH: describe epilepsy as a brain
disease
6. Timeline
• 1909: Formation International league against
epilepsy (ILAE).
• 1912: Use Phenobarbitone as AED.
• 1938: Use Phenytoin as AED.
• 1950-1970: Developed many AED.
• 1981: ILAE classified epilepsy.
• 1997: ILAE, IBE and WHO jointly established
Global campaign against epilepsy.
7. The Brain Is the Source of Epilepsy
• All brain functions -- including feeling, seeing,
thinking, and moving muscles -- depend on
electrical signals passed between nerve cells
in the brain
• A seizure occurs when too many nerve cells in
the brain “fire” too quickly causing
an “electrical storm”
8. Epidemiology
The most common ages of incidence are under the
age of 18 and over the age of 65.
About 1% of the population meets the diagnostic
criteria for epilepsy at any given time.
Prevalence:
Developed countries- 0.5% (0.4% - 1%)
Developing countries- five times higher
Incidence:
After infancy annual incidence- 20-70/100000 in
developed countries.
Developing countries- Incidence is double.
(100/100000)
9. Causes
• In 28% cases cause can be determined. Rests
(72%) are Idiopathic.
Determined causes:
• Inherited genetic
• Acquired : trauma, Neuro surgery, Inflammatory,
Metabolic, Infections, Tumor, Toxic disorders,
drugs, etc.
• Congenital: inborn error of metabolism.
• Withdrawal of drugs : Alcohol,Benzodiazepine,
Barbiturates, Other Anti-Epileptics
13. Groups at higher risk
The risk is higher in people with certain medical
conditions:
• Mental retardation
• Cerebral palsy (movement disorder)
• Alzheimer’s disease (neuro-degeneration)
• Stroke (poor blood flow to brain
• Autism (troubles with
social interaction)
15. Symptoms
• Confused memory
• Occasional “fainting spells”
• Episodes of blank staring (looking somewhere
without any reason) in children
• Sudden falls for no apparent reason
• Episodes of blinking or chewing at
inappropriate times
• A convulsion, with or without fever
• Swift jerking movements in babies
16. First Aids
Stay calm and track time
Do not restrain the person, but help them avoid
hazards
– Protect head, remove glasses, loosen tight neckwear
– Move anything hard or sharp out of the way
– Turn person on one side, position mouth to ground
Check for epilepsy or seizure disorder ID
Understand that verbal instructions may not be obeyed
Stay until person is fully aware and help reorient them
Call ambulance if seizure lasts more than 5 minutes or
if it is unknown whether the person has had prior
seizures
17. NOT TO DO
Put anything in the person’s mouth
Try to hold down or restrain the person
Attempt to give oral anti-seizure medication
Keep the person on their back face up
throughout convulsion
19. Classification Of Seizures
I. Partial seizures
A. Simple partial
seizures
B. Complex Partial
Seizures
C. Partial Seizures
evolving to
secondary
generalized seizures
II. Generalized seizures
A. Absence seizures
B. Myoclonic seizures
C. Clonic seizures
D. Tonic seizures
E. Tonic-Clonic seizures
F. Atonic seizures
III. Unclassified epileptic
seizures
a. Febrile epilepsy
b. Infantile spasm
20. Partial seizures
A. Simple seizures (without impairment of
consciousness)
• With motor symptoms
• With special sensory or somatosensory symptoms
• With psychic symptoms
Signs &symptoms:
Motor – convulsive jerking, chewing motions, lip smacking
Sensory & somatosensory – paresthesias, auras
Automatic – sweating, flushing, pupil dilation
Behavioral – hallucinations, dysphasia, impaired
consciousness (rare)
21. B.Complex seizures (with impairment of
consciousness)
1.Simple partial onset followed by impairment
of consciousness
2.Impaired consciousness at onset
• Impairment of consciousness
• Purposeless behaviour is common
• Affected person may wander about aimlessly
• Aggressive behaviour (violence)
• Automatism (eg: picking at clothes)
• Visual, auditory, or olfactory hallucinations
22. Generalised Seizures
Generalized Tonic-clonic (grand mal)
Convulsive seizures
No Aura but have prodormal phase- general
malaise
a.)Tonic phase: These are characterized by rigid
violent muscular contraction with stiff and fixed
extended
b.)Clonic phase: These are characterized by
repetitive muscle jerks.
• Duration: few minutes
• Post ictal period: drowsiness, confusion,
headache, deep sleep
23.
24. C.) Typical Absence Seizures (Petit mal):
• There is no aura associated with this disorder and
attack appears without warning.
• There is usually no loss of consciousness.
• Absence seizures are characterized by subtle
bilateral motor symptoms such as rapid blinking
of eyelids, chewing movements.
• Attacks last only a few seconds (<10 sec) and
often pass un- recognized.
• About 100-200 attacks may occur/day.
• Attacks precipitate by fatigue, drowsiness,
relaxation , photic stimulation or hyperventilation
25. D.) Myoclonic seizures: Bilateral epileptic
myoclonus
- sudden and brief skeletal muscle contraction
(entire or part of the body)
- sudden jerking movements appearing during
sleep.
E.) Atonic seizures (Akinetic seizures):
- sudden loss of postural tone.
- The head may sag to one side or the patient
may fall all of a sudden.
- The consciousness may be impaired
26. Unclassified Seizures
• Febrile seizures : wherein young children
frequently develop seizures with illness
accompanied by hyperpyrexia.
• Infantile spasm : with progressive mental
retardation. These are generalized tonic-clonic
convulsions of short duration . These have not
yet been classified because of insufficient data
or atypical pattern of the seizures
27. Classification Based On Epilepsy Syndrome
• Idiopathic in which no cause could be identified
except for genetic linkage.
Examples : Juvenile myoclonic epilepsy
syndrome.
• Symptomatic in which the seizures are associated
with some identifiable underlying disorders.
Examples : Lennox-Gastaut epilepsy syndrome
(impaired cognitive functions)
• Cryptogenic in which the epilepsy appears to be
symptomatic but the exact cause is unknown.
Examples : west’s syndrome (infantile spasm).
28. Diagnosis
Thorough History taking :
From patients
From reliable valid informants
From observer (who observed seizures)
Physical Examination:
Specially neurological system
Higher Psychic function
Laboratory Investigation:
Serum Electrolytes, Serum Prolactin, Blood sugar, Complete
blood count, Function tests (liver, thyroid, renal), CSF study
Imaging:
EEG, Video EEG telemetry, CT Scan of Brain, MRI of
Brain.
Polysomnography (a type of sleep study)
30. S.NO DRUG
DOSE
(in mg)
MECHANISM OF ACTION
1
Phenytoin 100
Blocks Na+ channels inhibits the
generation of repetitive action
potential.
Reduces the influx of Ca2+
decrease the glutamate synthesis.
2 Phenobarbitol 30, 60
Binds to the GABA Receptors and
enhances the GABA mediated
inhibitory effects by increasing the
duration of Cl- channel opening.
3 Carbamazepine 100,200
It also blocks the use-dependent Na+
channels and inhibits high-frequency
repetitive firing of neurons in brain
31. S.NO DRUG
DOSE
(in mg)
MECHANISM OF ACTION
4 Ethosuximide
500
inhibits T-type Ca2+ channels
generates thalamic cortical
pacemaker current.
5 Valproic acid 200 , 300
Blocks Na+ channels increase
the GABA activity by activating
glutamic acid decarboxylase and
inhibiting GABA transaminase.
6 Benzodiazepines 5 , 10, 20
Enhances the frequency of
GABA-mediated Cl- channels
opening.
34. In-vitro methods
• Hippocampal slices.
• Electrial recording from isolated brain cells.
• GABA uptake in rat cerebral cortex.
• TBPS binding assay
35. Withdrawal Of Anti-epileptic Drugs
• After complete control of seizures for 2-4 years,
withdrawal of Anti Epileptic drugs may be
considered. But in case of special professional
group (car driver, machine man etc) withdraw the
AED after keen follow-up.
• AED should be tapered during the stopping of
medications.
• Slow reduction by increments over at least 6
months.
• If the patient is taking two AEDs one drug should
be slowly withdrawn before the second is tapered
36. AED SIDE EFFECTS
Nausea
Rashes
vomitting
Altered sleep cycles
Behavioural changes
Blurred vision
Diarrhoea
Ataxia
Stevens – johnson
syndrome
Aplastic anaemia
Hepatic failure
Weight gain
Menstrual irregularity
Hair loss
Osteomalacia (long term use)
Neuropathy (long term use)
Dermatitis e.t.c…..
Even causesDeath.