EPILEPSY
AND
ANTI-EPILEPTICDRUGS
By:
Nimra Ashraf
&
Syed Usama Shayan
Contents
• Epilepsy???
• Causes???
• Types Of seizures
• Antiepileptic Drugs
INTRODUCTION
• It is the 3rd most common neurological disorder
after cerebrovascular disease and Alzheimer's
disease .
• Epilepsy is not a single entity but the assortment
of different seizure
types and syndrome .
What is EPILEPSY ?
• It is the sudden , excessive and synchronous
discharge of cerebral neurons .
• This abnormal activity result in
loss of conciousness ,
abnormal movement or
odd behaviours .
EPILEPSYCONTD.
• The symptoms that are produced in epilepsy
depends upon the site of origin of abnormal
neuronal firing .
• e.g if motor cortex is involved the patient may
experience abnormal movement and generalized
convulsion . if it
originates from parietal and
occipital lobe so visual , auditory
or olfactory hallucinations occur .
WHATCAUSESEPILEPSY ?
• IN CHILDRENS :
Birth traumas
Infections
Congenital abnormalities
High fever
• IN MIDDLE AGE :
Head injuries
Infection
Alcohol
Drug stimulant
Medication side effects
INELDERLYAGE
• Brain tumor
Strokes
OTHER :
• It can also occur due to chemical imbalance
includes drugs like alcohol, coccaine etc
• Low blood sugar , low oxygen and
low blood Na and Ca can
also cause seizures .
ClassificationofEpilepticSeizures
Generalized:
1.Generalized tonic-clonic seizure
2.Absence seizure
3.Tonic seizures
4.Atonic Seizure
5.Myoclonic seizure
• Partial (focal) Seizures: 80% of Adult
epilepsies
– Simple Partial Seizures
– Complex Partial Seizures
– Simple partial or complex partial
secondarily generalized
Generalizedseizures
1. Generalized tonic-Generalized tonic-clonic
 GTCS/major epilepsy/grand mal
 Commonest of all
 Lasts for 1-2 minutes
 Loss of consciousness followed by tonic phase and then clonic phase
 Usually occurs in both the hemispheres
 Seizures are followed by confusion and exhaustion due to depletion of glucose and
energy stores .
 2 phases: tonic phase followed by clonic phase
 Tonic phase:
 Sustained powerful muscle contraction (involving
all body musculature) which arrests ventilation
 Clonic phase:
 Alternating contraction and relaxation, causing a
jerking movement which could be bilaterally
symmetrical
Absenceseizure:
– Also called minor epilepsy/petit mal
– Generally occurs in 3 to 5 years of age last
untill puberty .
– Momentary loss of consciousness (not
convulsion), patient stares at one
direction
– No convulsions , rapid eye blinking which
last for 3-5 seconds .
– No loss of postural control
 AtonicSeizures :
Unconsciousness with relaxation of all muscles
Patient falls down
Loss of postural tone, with sagging of the head or
falling
 MyoclonicSeizures :
Occur at any age but generally occur at puberty .
Momentary contractions of muscles of limbs or
whole body
No loss of postural control
 Infantilespasm:
An epileptic syndrome
Characterized by brief recurrent
myoclonic jerks (muscle spasm)
of the body with sudden flexion or extension
of the body and limbs
Progressive mental deterioration
Partial(focal)Seizures
• Simple partial seizure (Jacksonian)
– Lasts for 20 – 60 seconds
– Motor, sensory, or psychic symptomatology
– Typically consciousness is preserved
– Seizures are caused by group of hyperactive
neuron exhibiting abnormal electrical activity
and cofined to single locus .
• Complexpartialseizure(temporallobe/psychomotorepilepsy)
• Focus is located in temporal lobe
• Confused behavior and purposeless movements
and emotional changes lasting for 30 seconds to 2
minutes
• Motor dysfunction involve chewing
movement , diarrhea and urination
Classificationon the basisof mechanismof action
• DRUGSFACILATATINGGABAACTIONS: Barbiturates ,
benzodiazepine , gabapentin
• INHIBITORSOF GABATRANSAMINASE: Facilitate GABA
action: valproic acid , vigabatrin
• DRUGSBLOCKINGNa CHANNELS:
Decrease axonal conduction
phenytion , carbamazepine ,valproic
acid , primidone.
• Drug blocking T-type Ca Channels:
Dec. presynaptic Ca influx
Valproic acid
• drudblocking “glutamate ” receptors:
Dec. excitatory affects of glutamic
acid.
Topiramate
DrugblockingGlutamatereceptors
• NMDA (N-myethyl-D-aspartate) receptor sites as
targets
– Ketamine, phencyclidine, dizocilpine block channel
and have anticonvulsant properties but also
dissociative and/or hallucinogenic
properties; open channel blockers.
– Felbamate antagonizes
strychnine-insensitive glycine site
on NMDA complex
GABAInhibitors
• Benzodiazepines (diazapam, clonazapam)
– Increase frequency of GABA-mediated chloride
channel openings
• Barbiturates (phenobarbital, primidone)
– Prolong GABA-mediated chloride
channel openings
– Some blockade of voltage-dependent
sodium channels
Gabapentin
– May modulate amino acid transport into
brain
– May interfere with GABA re-uptake
Tiagabine
– Interferes with GABA re-uptake
Vigabatrin
– elevates GABA levels by irreversibly
inhibiting its main catabolic
enzyme, GABA-transaminase
Na+ChannelsBlockers
Phenytoin,Carbamazepine
– Block voltage-dependent sodium channels at
high firing frequencies—use dependent
Oxcarbazepine
– Blocks voltage-dependent sodium channels at high
firing frequencies
– Also effects K+ channels
Zonisamide
– Blocks voltage-dependent sodium
channels and T-type calcium channels
• Decrease Pre-synaptic Calcium influx resulting in
decrease transmitter release by neurons.
• Ethosuximide: is a specific blocker of T-type currents
and is highly
effective in treating absence
seizures
BlockingT-TypeCa Channels
References
• Lippincott
Epilepsy & Antiepileptic Drugs
Epilepsy & Antiepileptic Drugs
Epilepsy & Antiepileptic Drugs

Epilepsy & Antiepileptic Drugs

  • 2.
  • 3.
    Contents • Epilepsy??? • Causes??? •Types Of seizures • Antiepileptic Drugs
  • 4.
    INTRODUCTION • It isthe 3rd most common neurological disorder after cerebrovascular disease and Alzheimer's disease . • Epilepsy is not a single entity but the assortment of different seizure types and syndrome .
  • 5.
    What is EPILEPSY? • It is the sudden , excessive and synchronous discharge of cerebral neurons . • This abnormal activity result in loss of conciousness , abnormal movement or odd behaviours .
  • 6.
    EPILEPSYCONTD. • The symptomsthat are produced in epilepsy depends upon the site of origin of abnormal neuronal firing . • e.g if motor cortex is involved the patient may experience abnormal movement and generalized convulsion . if it originates from parietal and occipital lobe so visual , auditory or olfactory hallucinations occur .
  • 8.
    WHATCAUSESEPILEPSY ? • INCHILDRENS : Birth traumas Infections Congenital abnormalities High fever • IN MIDDLE AGE : Head injuries Infection Alcohol Drug stimulant Medication side effects
  • 9.
    INELDERLYAGE • Brain tumor Strokes OTHER: • It can also occur due to chemical imbalance includes drugs like alcohol, coccaine etc • Low blood sugar , low oxygen and low blood Na and Ca can also cause seizures .
  • 10.
    ClassificationofEpilepticSeizures Generalized: 1.Generalized tonic-clonic seizure 2.Absenceseizure 3.Tonic seizures 4.Atonic Seizure 5.Myoclonic seizure • Partial (focal) Seizures: 80% of Adult epilepsies – Simple Partial Seizures – Complex Partial Seizures – Simple partial or complex partial secondarily generalized
  • 11.
    Generalizedseizures 1. Generalized tonic-Generalizedtonic-clonic  GTCS/major epilepsy/grand mal  Commonest of all  Lasts for 1-2 minutes  Loss of consciousness followed by tonic phase and then clonic phase  Usually occurs in both the hemispheres  Seizures are followed by confusion and exhaustion due to depletion of glucose and energy stores .  2 phases: tonic phase followed by clonic phase  Tonic phase:  Sustained powerful muscle contraction (involving all body musculature) which arrests ventilation  Clonic phase:  Alternating contraction and relaxation, causing a jerking movement which could be bilaterally symmetrical
  • 12.
    Absenceseizure: – Also calledminor epilepsy/petit mal – Generally occurs in 3 to 5 years of age last untill puberty . – Momentary loss of consciousness (not convulsion), patient stares at one direction – No convulsions , rapid eye blinking which last for 3-5 seconds . – No loss of postural control
  • 13.
     AtonicSeizures : Unconsciousnesswith relaxation of all muscles Patient falls down Loss of postural tone, with sagging of the head or falling  MyoclonicSeizures : Occur at any age but generally occur at puberty . Momentary contractions of muscles of limbs or whole body No loss of postural control  Infantilespasm: An epileptic syndrome Characterized by brief recurrent myoclonic jerks (muscle spasm) of the body with sudden flexion or extension of the body and limbs Progressive mental deterioration
  • 14.
    Partial(focal)Seizures • Simple partialseizure (Jacksonian) – Lasts for 20 – 60 seconds – Motor, sensory, or psychic symptomatology – Typically consciousness is preserved – Seizures are caused by group of hyperactive neuron exhibiting abnormal electrical activity and cofined to single locus .
  • 15.
    • Complexpartialseizure(temporallobe/psychomotorepilepsy) • Focusis located in temporal lobe • Confused behavior and purposeless movements and emotional changes lasting for 30 seconds to 2 minutes • Motor dysfunction involve chewing movement , diarrhea and urination
  • 18.
    Classificationon the basisofmechanismof action • DRUGSFACILATATINGGABAACTIONS: Barbiturates , benzodiazepine , gabapentin • INHIBITORSOF GABATRANSAMINASE: Facilitate GABA action: valproic acid , vigabatrin • DRUGSBLOCKINGNa CHANNELS: Decrease axonal conduction phenytion , carbamazepine ,valproic acid , primidone.
  • 19.
    • Drug blockingT-type Ca Channels: Dec. presynaptic Ca influx Valproic acid • drudblocking “glutamate ” receptors: Dec. excitatory affects of glutamic acid. Topiramate
  • 20.
    DrugblockingGlutamatereceptors • NMDA (N-myethyl-D-aspartate)receptor sites as targets – Ketamine, phencyclidine, dizocilpine block channel and have anticonvulsant properties but also dissociative and/or hallucinogenic properties; open channel blockers. – Felbamate antagonizes strychnine-insensitive glycine site on NMDA complex
  • 21.
    GABAInhibitors • Benzodiazepines (diazapam,clonazapam) – Increase frequency of GABA-mediated chloride channel openings • Barbiturates (phenobarbital, primidone) – Prolong GABA-mediated chloride channel openings – Some blockade of voltage-dependent sodium channels
  • 22.
    Gabapentin – May modulateamino acid transport into brain – May interfere with GABA re-uptake Tiagabine – Interferes with GABA re-uptake Vigabatrin – elevates GABA levels by irreversibly inhibiting its main catabolic enzyme, GABA-transaminase
  • 23.
    Na+ChannelsBlockers Phenytoin,Carbamazepine – Block voltage-dependentsodium channels at high firing frequencies—use dependent Oxcarbazepine – Blocks voltage-dependent sodium channels at high firing frequencies – Also effects K+ channels Zonisamide – Blocks voltage-dependent sodium channels and T-type calcium channels
  • 24.
    • Decrease Pre-synapticCalcium influx resulting in decrease transmitter release by neurons. • Ethosuximide: is a specific blocker of T-type currents and is highly effective in treating absence seizures BlockingT-TypeCa Channels
  • 25.