This gives an overall idea and knowledge about epilepsy and epileptogenesis. This does not serve as a complete medical tool,but as a learning material for, health and allied health students. Epilepsy is a fascinating disease and cannot be understood in a single ppt, this just gives out and outline on the definition, diagnostic tools, incidence, types, and a intro on treatment protocols medical and surgical It is a great source of comprehensive knowledge on the topic and information on the treatment

2. DEFINITION OF
EPILEPSY
Epilepsy Is A Brief
Recurrent Disorder Of
Cerebral Function That Is
Usually Associated With
Disturbance Of
Conciousness And
Accompanied By A Sudden,
Excessive, Electrical
Discharge Of Cerebral
Neurons
- MEDECINE (K GRORGE MATHEW)

3. BRIEF ON FUNCIONAL
ASPECTS OF BRAIN
1. NEUROANATOMY.
2. SYNAPSE.
3. NEUROTRANSMITTERS.
4. DEVELOPMENT

4. NEURO-ANATOMY
• NEURONS ARE THE STRUCTURAL AND FUNCTIONAL UNIT
OF NERVOUS SYSTEM.
• NERVOUS SYSTEM COMPRAISES OF CENTRAL AND
PERIPHERAL NERVOUS SYSTEM.
• CENTRAL NERVOUS SYSTEM COMPRAISES OF BRAIN AND
SPINAL CORD.
• PHERIPHERAL NERVOUS SYSTEM COMPRAISES OF ALL
PHERIPHERAL NERVES.
• BRAIN WEIGHS 2% OF THE BODY WEIGHT AND UTILIZES
25% OF THE CARDIAC OUTPUT.
-TEXTBOOK OF CLINICAL NEUROANATOMY - SNELL

5. SYNAPSE
• SYNAPSE IS THE JUNCTION BETWEEN TWO
NEURONS THROUGH WHICH THE NERVE
IMPULSE PASSES FROM ONE NEURON TO
ANOTHER NEURON – IT IS NOT AN
ANATOMICAL CONTINUATION AND ONLY A
PHYSIOLOGICAL CONTINUITY.
• FUNCIONALLY IT IS CLASSIFIED AS
• ELECTRICAL SYNAPSE.
• CHEMICAL SYNAPSE.
-TEXTBOOK OF MEDICAL PHYSIOLOGY – SEMBULINGAM

6. NEUROTRANSMITTERS
• NEUROTRANSMITTER IS A CHEMICAL SUBSTANCE
THAT ACTS AS A MEDIATOR FOR THE
TRANSMISSION OF NERVE IMPUSE FROM ONE
NEURON TO ANOTHER NEURON THROUGH A
SYNAPSE.
• FUNCTIONALLY CLASSIFIED INTO
• EXCITATORY NEUROTRANSMITTER.
• INHIBITORY NEUROTRANSMITTER.
-TEXTBOOK OF MEDICAL PHYSIOLOGY – SEMBULINGAM

7. DEVELOPMENT
• DEVELOPMENTALLY THE NERVOUS SYSTEM IS NEURO-
ECTODERMAL IN ORGIN
• IT ORGINATES AS A MIGRATION OF ECTODERMAL CELLS ON THE
2ND WEEK OF PREGNENCY WHICH FORMS THE NEURAL PLATE
WHICH DEEPENS TO FORM THE NEURAL CLEFT FORMING THE
NEURAL TUBE.
• IT FUSES CAUDALLY FIRST AND CEPHALIC END CLOSES AFTER.
• THE NEURAL TUBE DIFFERENTIATES INTO VARIOUS PARTS OF
THE BRAIN AND SPINAL CORD.
INSIGHTS ON EEG AND F-MRI
-LARSEN’S BOOK OF HUMAN EMBRYOLOGY

8. ELECTRO-ENCEPHALOGRAM(EEG)
ELECTROENCEPHALOGRAPHY (EEG) IS A METHOD TO
RECORD AN ELECTROGRAM OF THE SPONTANEOUS
ELECTRICAL ACTIVITY OF THE BRAIN. THE
BIOSIGNALS DETECTED BY EEG HAVE BEEN SHOWN TO
REPRESENT THE POSTSYNAPTIC POTENTIALS OF PYRAMIDAL
NEURONS IN THE NEOCORTEX AND ALLOCORTEX.
HANS BERGER INVENTED THE HUMAN
ELECTROENCEPHALOGRAM

9. FUNCTIONAL MRI (BOLD)
FUNCTIONAL MAGNETIC RESONANCE
IMAGING OR FUNCTIONAL MRI (FMRI) MEASURES BRAIN ACTIVITY BY
DETECTING CHANGES ASSOCIATED WITH BLOOD FLOW.THIS TECHNIQUE
RELIES ON THE FACT THAT CEREBRAL BLOOD FLOW AND NEURONAL
ACTIVATION ARE COUPLED. WHEN AN AREA OF THE BRAIN IS IN USE,
BLOOD FLOW TO THAT REGION ALSO INCREASES.[3]
THE PRIMARY FORM OF FMRI USES THE BLOOD-OXYGEN LEVEL
DEPENDENT (BOLD) CONTRAST.

10. TERMS APPLIED
1. PRODROME – MOOD OR BEHAVIOURAL
CHANGES THAT MAY PRECEDE THE ATTACK
2. AURA – SYMPTOM IMMEDIATELY BEFORE
SIEZURE
3. ICTUS – THE ATTACK ITSELF
4. POSTICTAL – STATE AFTER THE ATTACK WHEN
THE PATIENT MAY BE
CONFUSED,DISORIENTED AND
DEMONSTRATE AUTONOMIC BEHAVIOUR

11. HISTORICAL PRESPECTIVE
Epilepsy's spiritually based pathophysiology remained largely
unchallenged until around the 5th century BC, when the School of
Hippocrates in Greece hypothesized that the brain might be the root cause of
epilepsy. Hippocrates believed that the Sacred Disease
(epilepsy), was no more divine than other diseases, but was named "sacred"
due to its unique and inexplicable characteristic appearance. He also
hypothesized that epilepsy could be cured like other diseases, though once
it becomes chronic, it was no longer curable. Hippocrates was also one of
the first to introduce the concept of post-traumatic epilepsy; through his
observations of head trauma, he observed convulsions which were always
contralateral to the head wound.
Hallmarks in the history of epilepsy: epilepsy in antiquity. Magiorkinis E,
Sidiropoulou K, Diamantis A. Epilepsy Behav. 2010;17:103–108

12. PATHOLOGY
• Epilepsy is the excessive discharge of cerebral neurons which either
be precipitated by the depolarization shift fron cellular influx of Na+,K+
ions due to the action of excitatory neurotransmitter glutamate.
• Epilepsy genitically has an complex inherent pathology which is still
not understood.
• Abnormalities in genomes forming the ionic channel sub-units said to
precipitate epileptic episodes.

13. In a mechanistic context, epileptogenesis is the process by
which a brain network that was previously normal is
functionally altered toward increased seizure susceptibility,
thus having an enhanced probability to generate spontaneous
recurrent seizures (SRSs) (Dudek and Staley 2012; Goldstein
and Coulter 2013). Traditionally, epileptogenesis has been
considered in the context of the “latent period,” a pragmatic or
operational term referring to the time period between the
epileptogenic insult and the appearance of the first clinical
seizur
EPILEPTOGENISIS:

14. INCIDENCE
• Epilepsy presents most commonly in childhood
and adolescence or in those over 65, but may
occur for the first time at any age.
• 5% of the population suffer a single seizure at
some time.
0%
10%
20%
30%
40%
50%
60%
70%
80%
WELL CONTROLLED WITH DRUGS PARTIALLY RESISTANT TO DRUGS

15. • Idiopathic – thought to be primarily genetic with
generalised seizures,sometimes grouped as more
specific syndromes
• Symptomatic – partial onset seizures associated
with a structural lesion, such as tumour, cortical
dysplasia, infection, head injury or trauma – about 30–
40% of cases. The combinationof the site of seizure onset
and the underlyingpathologyleads to the diagnosis:for
example ‘post traumatic frontal lobe epilepsy’or
‘temporallobe epilepsy due to mesial temporal sclerosis’
or ‘symptomaticoccipital lobe epilepsy secondary to an
arteriovenous malformation’.
• Cryptogenic – partial onset seizuresfor which no
cause has been found. Account for about 50% of patients.
IDIOPATHIC SYMPTOMATIC CRYPTOGENIC

16. TONIC PHASE:
• EYES OPEN
• ELBOWS FLEXED
• ARMS PRONATED
• LEGS EXTENDED
• TEETH CLENCHED
• PUPILS DILATED
• BREATH HELD
• BOWEL AND BLADDER
CONTROL MAY BE LOST
CLONIC PHASE:
• TREMOR GIVES WAY TO
VIOLENT GENERALIZED
SHAKING
• EYES ROLL BACKWARD
ANDFORWARD
• TONGUE MAY BE BITTEN
• TACHYCARDIA DEVELOPS
• BREATHING RECOMMENCES
AT THE END OF PHASE

17. CLASSIFICATION OF seizures
Attacks which begin focally from a single location within one
hemisphere are distinguished from those of a generalised nature which
probably commence in deeper midline structures and project to both
hemispheres simultaneously
1. PARTIAL SIEZURE
2. GENERALIZED SIEZURE
3. UNCLASSIFIED SIEZURE

18. PARTIAL SEIZURES:
Orginates from specific parts of the brain.
Based on their cortical orgin seizures are classified into:
1) Frontal lobe seizures.
2) Parietal lobe seizures.
3) Temporal lobe seizures.
4) Occipital lobe seizures.
FRONTAL LOBE SEIZURES:
JACKSONIAN motor seizures defines as the
spreading of invoulantary movements form one muscle group to another,The
seizures are clonic in nature.
Jacksonian march usually leads to short term
muscle weakness – TODD’s Paralysis.
The patient often progresses to loss of
consciousness, head and eyes move away from thefocii

19. TEMPORAL LOBE SEIZURES:
Visceral disturbance: Gustatory (taste) and olfactory (smell)
hallucinations, lip smacking, epigastric fullness, choking sensation, nausea, pallor,
pupillary changes (dilatation), tachycardia.
Memory disturbance: Déjà vu (‘something has happened
before’), jamais vu (‘feeling of unfamiliarity’), depersonalisation, derealisation, flashbacks,
formed visual or auditory hallucinations.
Motor disturbance: Fumbling movement, rubbing, chewing,
semipurposeful limb movements.
Affective disturbance: Displeasure, pleasure, depression,
elation, fear

20. OCCIPITAL LOBE SEIZURES:
These are uncommon. Typically there is an elementary
visual hallucination – a line or flash – prior to a tonic-clonic seizure.
PARIETAL LOBE SEIZURES:
These arise in the sensory cortex (parietal lobe), the
patient describing paraesthesia or tingling in an extremity or on the face
sometimes associated with a sensation of distortion of body image. A ‘march’
similar to the Jacksonian motor seizure may occur. Motor symptoms occur
concurrently – the limb appears weak without involuntary movement.

21. GENERAL SEIZURES
Generalised seizure attacks arise from subcortical structures and
involve both hemispheres. Consciousness may be impaired and
motor manifestations are bilateral.
Classified into
1)Abscenc seizure
2)Myoclonic seizure
3)Clonic seizure
4)Tonic seizure
5)Tonic/clonic seizure
6)Atonic seizure

22. 1)ABSENCE SEIZURES
The patient (usually a child) stares vacantly, eyes may
blink. The absence may occur many times a day with a duration of
5–15 seconds and may be induced by hyperventilation.
2)MYOCLONIC SEIZURES
Sudden, brief, generalised muscle contractions. They often
occur in the morning and are occasionally associated with tonic/clonic
seizures. The commonest disorder is benign juvenile myoclonic
epilepsy (JME) with onset after puberty. Myoclonus on the edge of
sleep is normal. Myoclonus also occurs in degenerative and metabolic
disease

23. Sudden sustained muscular contraction associated with
immediate loss of consciousness. Tonic episodes occur as frequently as
tonic/clonic episodes in children and should alert the physician to a
possible anoxic aetiology. In adults, tonic attacks are rare.
3)TONIC SEIZURES
4)TONIC/CLONIC SEIZURES
Primary tonic/clonic seizures occur without warning or
aura. The epileptic cry at onset results from tonic contraction of
respiratory muscles with partial closure of vocal cords. The tonic
phase is associated with rapid neuronal discharge. The clonic phase
begins as neuronal discharge slows.

24. 5)ATONIC SEIZURES
These are rare and almost always occur in patients with
other types of seizure. They are characterised by a loss of muscle tone
and a sudden fall. Consciousness may only be lost briefly. The EEG shows
polyspike activity or low voltage fast activity.
OTHER CAUSES:
1. Trauma
2. Drugs and alcohol
3. CNS infection
4. Intracranial hemmorrhage
5. Tumors
6. Vascular disease
7. Hypoglycemia

25. A succession of tonic/clonic convulsions, one after the other
with a gap between each, is referred to as serial epilepsy. When
consciousness does not return between attacks the condition is then
termed status epilepticus. This state may be life-threatening with the
development of pyrexia, deepening coma and circulatory
collapseStatus epilepticus may occur with frontal lobe lesions,
following head injury, on reducing drug therapy (especially
phenobarbitone), with alcohol or other sedation withdrawal, drug
intoxications (tricyclic antidepressants), infections, metabolic
disturbances (hyponatraemia) or pregnancy.
STATUS EPILEPTICUS

26. INVESTIGATION:
1. EEG – EEG MONITERING DURING SEIZURES IN
GOAL OF FINDING THE FOCII OF ORGIN
2. MRI STUDIES TO FIND OTHER POSSIBLE CAUSES
3. CT IN TRAUMATIC CASES TO RULE OUT
HEMMORRHAGE
MANAGEMENT:
DRUG THERAPY
1)SODIUM VALPORATE
2)LAMOTRIGINE
3)PHENYTOIN
4)CARBAMAZEPINE

27. SURGICAL TECHNIQUES:

28. VAGAL NERVE STIMULATION:
Involves periodic stimulation
of the left vagus nerve by an implanted stimulator.
Considered in patients with intractable epilepsy not
suited to the resective procedures. VNS appears to
reduce neuronal excitability, but the exact
mechanism remains obscure. About 30% of patients
show a 50% seizure reduction within two years.

29. “NEURONS THAT FIRE TOGETHER
WIRE TOGETHER”
PRESENTATION BY
P.ARUNAGIRI B.P.T(3RD YEAR)