5. EPILEPSY
ī It is known as âDisease of lighteningâ.
ī They are group of disorders of the CNS.
Characterized by:
ī Paroxysmal cerebral dysrhythmia (a diffusely
abnormal electroencephalogram often seen with
epilepsy).
ī Loss / disturbance of consciousness,
ī With or without characteristic body movements.
ī Autonomic hyperactivity.
6.
7. īMost of the epilepsies are primary (Idiopathic)
Idiopathic - cause is not known
īSome may be secondary
occurs due to:
Trauma/surgery on head
Intracranial tumor
Tuberculoma
(non-neoplastic mass (a tumor-like mass that is not a cancer)
caused by ifection with mycobacterium tuberculosis)
Cysticercosis
It is a tissue infection by the pork tapeworm
8.
9. GENERALISED SEIZURES
GENERALISED TONIC â CLONIC SEIZURES (GTCS):
īAlso known as major epilepsy, grand mal
īCommonest,
īLasts 1-2min
īThe usual sequence is
AURA â CRY â UNCONSCIOUSNESS
â TONIC Spasm of all body muscles
â CLONIC Jerking
prolonged sleep and depression of all CNS
functions
10.
11. ABSENCE SEIZURES
ī Also known as Minor Epilepsy, Petit Mal
ī Prevalent in children,
ī Lasts about ÂŊ minute.
ī Momentary loss of consciousness, patient
apparently freezes and stares in one direction,
no muscular component or little bilateral
jerking.
ī EEG shows characteristic 3 cycles per second
spike and wave pattern
(Electroencephalography - EEG measures voltage
fluctuations resulting from ionic current flows
within the neurons of the brain
12.
13. ATONIC SEIZURES:
ī¸Also known as Akinetic Epilepsy
ī¸Unconsciousness with relaxation of all muscles
ī¸Patient may fall
MYOCLONIC SEIZURES:
ī¸Shock-like momentary contraction of muscles
of a limb or the whole body
15. INFANTILE SPASMS:
īAlso known as Hypsarrhythmia
īSeen in infants.
īProbably not a form of epilepsy.
īIntermittent muscle spasm and progressive
mental deterioration.
16. PARTIAL SEIZURES
SIMPLE PARTIAL SEIZURES (SPS)
īĨIt is also known as cortical focal epilepsy
īĨLasts ÂŊ -1 min,
īĨOften Secondary
īĨConvulsions are confined to a group of
muscles or localized sensory disturbance
depending on the area of cortex involved in
the seizure, without loss of consciousness.
17. COMPLEX PARTIAL SEIZURES (CPS)
īAlso known as Temporal lobe epilepsy,
Psychomotor
īSeizure attack , Confused behavior, Purposeless
movements, Emotional changes
īLasting 1-2 min along with impairment of
consciousness,
īAn Aura often proceeds. (a warning sensation
experienced before an attack of epilepsy)
īThe seizure focus is located in the temporal lobe.
īThe partial seizure occurs first and evolves into
generalized tonic-clonic seizures with loss of
consciousness.
20. MECHANISM OF ACTION
There are THREE major mechanisms
1st TYPE:
DRUGS:
ī¨PHENYTOIN,
ī¨CBZ,
ī¨SOD.VALPORATE,
ī¨LAMOTRIGINE
21. MECHANISM ;1
PROLONGATION OF INACTIVATED Na+
CHANNELS
ī¯
DECREASE THE ENTRY OF Na+ IONS IN TO THE
NEURON
ī¯
PROLONGS THE DEPOLARIZATION
ī¯
DECREASE THE EPILEPTIC EPISODES
ī¯
ANTI EPILEPTIC ACTIVITY
25. MECHANISM ;2
FALICITATE THE BINDING OF GABA TO GABA-A
RECEPTOR
ī¯
INCREASE THE ENTRY OF Cl- IN TO THE NEURON
ī¯
HYPERPOLARIZATION
ī¯
PROLONGED DEPOLARIZATION
ī¯
CALMNESS & ANTI EPILEPTIC ACTIVITY
29. BARBITURATES:
Eg: PHENOBARBITONE
īĒMost older anticonvulsant
īĒPhenyl substitution present in the structure
responsible for its Activity against Tonic-Clonic
seizure [Grand mal epilepsy]
īĒIt is the first efficacious anti epileptic drug
[1912]
īĒIt act by depressing the CNS
īĒIt is the cheapest and least toxic anti epileptics.
īĒMECHANISM OF ACTION: 2nd TYPE
30. Pharmacokinetics:
ī§Slowly absorbed orally
ī§t ÂŊ is long 80 -120 hrs in plasma
ī§Metabolized in liver
ī§Excreted unchanged by kidney
ī§Single daily dose used for maintenance
ADR:
ī§Sedation
ī§Behavioral abnormalities
ī§Diminution of intelligence
ī§Impairment of learning and memory
ī§Rashes
ī§Anemia
32. HYDANTOIN:
Eg : Phenytoin
âĸ It is a diphenyl hydantoin
âĸ It was Synthesized as barbiturate analogue
âĸ Its anti convulsant activity was tested in
1938, since then this is the major anti
epileptic drug.
âĸ It is not a CNS depressant
âĸ Little sedation produced at therapeutic dose
âĸ It abolishes the tonic phase of maximal
electro shock seizures
âĸ It limits the spread of seizure activity
33. Mechanism of action:
īAt therapeutic dose: 1st type
īHigher toxic doses: 2nd &3rd types
Pharmacokinetics:
īOral route âslowly absorbed due to poor
solubility
īWidely distributed in body
ī80-90% drug bound to plasma proteins
īMetabolized in liver by hydroxylation and GA
conjugation
īExcreted in urine
34. ADR:
īĄGum hypertrophy,
īĄHirsutism, (excessive hairiness on women)
īĄRashes,
īĄMagloblastic anaemia
īĄOsteomalacia
USE:
īĄGTCS-Grand mal epilepsy
īĄSimple and complex partial seizure
īĄTrigemial neuralgia
īĄIneffective in absence seizure
36. IMINOSTILBENE
Eg:
CARBAMAZEPINE
OXCARBAZEPINE
CARBAMAZEPINE
īŦChemically related To Imipramine
īŦFirst introduced in 1960s for trigeminal neuralgia (A
chronic pain condition affecting the trigeminal nerve in
the face)
īŦDue to good anticonvulsant activity currently used as
first line anti-epileptic drug
īŦIts pharmacological activity resembles Phenytoin
īŦIt modifies maximal electro shock seizures as well as
raise threshold to PTZ and electro shock convulsion
īŦAlso has anti-diuretic activity
37. MECHANISM OF ACTION:
1st type
PHARMACOKINETICS:
īOral absorption is slow because of poor water
soluability
ī75% bound to plasma proteins
īMetabolized in lever by oxidation and
hydroxylation
īt1/2 20-40 hours
38. ADR:
īĒDose related neurotoxicity
īĒSedation
īĒVertigo
īĒAtaxia (is a neurological sign consisting of lack of
voluntary coordination of muscle movements)
īĒVomiting
īĒDiarrhea
īĒRashes
Uses
īĒMost effective drug for CPS
īĒFirst choice drug with Phenytoin for GTCS and
Simple partial seizure
39. SUCCINAMIDES
Eg: Ethosoximide
ī§ Most predominantly antagonizes the PTZ induced
clonic seizure
ī§ It raise the seizure threshold ( the balance between
excitatory and inhibitory forces in the brain which
affect how susceptible a person is to seizures)
ī§ Clinically effective only in absence seizures
MECHANISM OF ACTION: 3rd type
PHARMACOKINETICS:
ī§ Rather slowly but completely absorbed on oral
administration
ī§ Not protein bound
ī§ Metabolized in liver by hydroxylation &GA
conjugation
ī§ Excreted in urine
41. ALIPHATIC CARBOXYLIC ACID
VALPORIC ACID
īĻAlso known as sodium valporate
īĻIt is a branched chain aliphatic carboxylic acid
īĻHas broad spectrum anti-convulsant activity
īĻEffective in partial seizures >CS
īĻAt therapeutic doses it produce little sedation
MECHANISM OF ACTION:
īĻIt acts through all the three types
42. Pharmacokinetics:
īĄOral absorption is good
īĄ90% bound to plasma protein
īĄCompletely metabolized in liver by oxidation
&GA conjugation
īĄExcreted in urine
ADR
īĄAnorexia
īĄVomiting
īĄDrowsiness
īĄAlopecia
USES
īĄDrug of choice for Absence seizure
īĄAlternative/Adjuvant drug for GTC, SPS, CPS.