1. Presented by:
Anil k. Pawar
B.Pharm 7th semester
Roll.no - 16338353
Dr.Vitthal. J. chaware
• Convulsion: Sudden attack of involuntary muscular
contractions and relaxations.
• Seizure: Abnormal central nervous system electrical activity or
hyperexcitability of neuron.
• Epilepsy: A group of recurrent disorders of cerebral function
characterized by both seizures and convulsions.
• Epilepsy: Neurological disorder affecting the CNS.
• About 1-2% of whole population have epileptic siezure.
• In about 25% of these patients, the cause can be make out with the help of
EEG or MRI.
• Genetic factors
• Congenital defects
• Severe head trauma
• Low level of oxygen in the blood
• Drug abuse
• Other, repetitive sounds, flashing lights, vedio games,
4. Nerve Cell Communication(normal person)
• Neurons communicate between themselves using small molecules called neurotransmitters.
• These neurotransmitters modulate and regulate the electrical activity of a given neuron,
and tell it when to fire an action potential or when not to.
- Glutamate = excitatory (tells the neuron to fire)
- GABA = inhibitory (control the neuron firing rate)
• The action potential is an electrical signal that travels down the axon, and is created using
sodium ions (Na+), and inhibited by potassium ions (K+).
• Usually these processes work synergistically to produce normal behavior and activity.
• When dysfunctional, abnormal electrical activity occurs and qcan produce seizures.
5. Types of seizure:
• GENERALISED SEIZURE:
• Excessive electrical activity in both cerebral hemispheres.
• Usually originates in the thalamus or brainstem.
• Affects the whole body.
• Loss of consciousness is common.
6. Generalized Seizures
• Myoclonic: Brief shock-like muscle jerks generalized or restricted to part of one extremity.
• Atonic: Sudden loss of muscle tone.
• Tonic Seizures: sudden stiffening of the body, arms, or legs
• Clonic Seizures: rhythmic jerking movements of the arms and legs without a tonic component
• Tonic-clonic (grand mal): in which spam of all body muscle found , prolong sleep and CNS depression.
• Absence siezure (minor): muscle straight and momentary loss of consciousness.
• Mostely found in children
7. Partial (focal) Seizures
• Excessive electrical activity in one cerebral hemisphere. -Affects only
part of the body.
• Simple Partial: Person may experience a range of strange or unusual
sensations and visual disturbances.
• Complex partial: (temporal lobe epilepsy)
• It is localised in the temporal lobe.
• Convulsion occure or attack if bizarre and patient experience confused
behaviour and purposeless movement.
8. Neurochemical basis
The convulsion carried out due to following neurochemical basis:
• K+ stimulated glutamate release
• Increase excitory syaptic transition
• Decrease synaptic transmissions of PABA and AMINO ACID
9. Mechanisms of Action
• 3 main categories of therapeutics:
1.Inhibition of voltage-gated Na+ channels to slow neuron firing.
2.Enhancement of the inhibitory effects of the neurotransmitter
3.Inhibition of calcium channels.
11. • Barbiturates:
- It is first epileptic drug introduced in 1912.
- MOA- enhancement of GABA receptor mediated system- so synaptic inhabition
- DOSE- 30MG (1-2 time day)
- Use: it has broad spectrum activity in generalised tonic- clinic ,partial and
complex partial epilepsy.
- DEOXY- BARBITURATES:
. MOA- act on GABA receptor , Inhabit synaptic transition.
12. • In liver it converted into- Phenobarbitone and phenyl methyl
Pka- half life – 5 to 14 hr. And it is similar to phenobarbitone.
1. phenytoin: it control cycomotor epilepsy
• MOA: it stabilizing influence in neuronal membrane.
- It prevent repetative detonation of normal brain cell during
13. • IMMUNOSTABILINE:
• eg.. Carbamazipine, oxacarbamazipine
• MOA: it reduce post titanic potentiation in synaptic produce inhabiting or
- prolongation of NA+ channel inhabit.
• PKA- orally absorption
• 75% plasma protein binding
• Half life – 20to 40 hr
ADVERSE EFFECT: Neurotoxicity- sedation, dizziness, vertigo, vometing , diarrhea.
MOA: prolongation of NA+ channel inhabitor.
- It is similar to carbamazipine
14. • Succinamide: eg. Ethosuccinamide, methosuccinamide
MOA- it supress the T current type ca+ current without affecting other
Type of ca+ or Na+ current.
- it depress the effect of motor complx area.
- ABSENCE SIEZURE – thalamocortical effect
PKA: - does not bind with plasma protein.
- peak conc.2 to 4 hr
. - liver metabolised and urine excretion
Ad .effects: git intolerance , mood changes, headache, drawasiness.
15. • Aliphatic carboxylic acid: eg. Valporic acid
• MOA: prolongation of NA+ channel inactivation
- weak attenuation of CA+ mediated ‘T’ current.
- inhabit GABA transmission.
PKA: orally absorption and 90% PPB
- Liver metabolisd and kidney excretion
AD- Effect: anorexia , vometing, heart burn, drawasiness, tremor.
Dose: adult- 200mg and child- 15 to 30 mg.
16. • Benzodiazepines: eg.clonazepam, clobazepam, diazepam
• MOA: it facilitates GABA receptor and effect produced on CL-
- Effect on GABA produce sedation.
- Decrease frequency duration and amplitudes signal.
- Pka-: orally absorption and 85% PPB
- Liver metabolised and kidney excretion.
AD- EFFECT: sedation, dullness, irritation, drawasiness
Use: absence siezure
17. • Phenyltriazine eg. Limotrigine
• MOA: prolongation of NA+ channel inactivation and supression of high frequency
has been demonstrated
• Pka-: orally absorb and T ½ = 24 hr
- Valporic acid lower effect of lomotrigine
- SIDE EFFECT: sleepiness, dizziness, diplopia, ataxia, and vometing
- USE: absence and myclonic siezure
18. • GABA ANALOGUE: eg. Gabapentin
• MOA: act on GABA receptor and facilitate CL- opening
• Pka: orally absorbed
• Liver metabolisd and kidney excretion
• SIDE EFFECTS: mild sedation, dizzines
• USEE: generalised tonic- clonic and simple partial, complex partial siezure