This document provides information about Sumit Verma's roll number and then discusses epilepsy. It defines epilepsy as a chronic brain disorder characterized by seizures. It discusses the epidemiology, etiology, pathophysiology, types, diagnosis, treatment and classification of epilepsy. It provides details on common anti-epileptic drugs like carbamazepine and phenytoin, explaining their clinical uses, pharmacokinetics, dosing and side effects.

1. NAME: SUMIT
ROLL NO. 2250981548

2. Sumit Verma
*What is EPILEPSY?
*Epilepsy is a chronic CNS disorder characterized by brief episodes of
seizures.
*Seizure is a sudden time limited involuntary alteration of behavior with
or without loss of consciousness accompanied by an abnormal
electrical discharge.

3. Sumit Verma
*EPIDEMIOLOGY:
*Incidence of epileptic seizures is around 50 cases per 1,00,000 of the
population. Around 50 million people worldwide have epilepsy
*Higher risk observed in extremes of age.
*Prevalence in European countries is 0.5%, prevalence in developing
countries ishigher due to parasitic illnesses like cysticercosis.

4. Sumit Verma
*ETIOLOGY:
*In 20% cases cause can be determined, rest 72% are idiopathic (of
unknown cause).
*1 Inherited/genetic causes: Single gene mutation (<2%), multiple genes +
environmental factors, genetic disorders (down, dravet etc.). >200genes
have the capability of causing epilepsy
*2. Acquired causes: Head trauma, neurosurgery, cerebrovascular disease,
infections (meningitis, influenza toxoplasmosis, mumps, measles,
syphilis), metabolicdisorders (such as hypoglycemia and hypocalcemia),
intracranial neoplasms.
*3. Congenital causes: Inborn error of metabolism.
*4. Withdrawal of drugs: Alcohol, benzodiazepines, barbiturates,
antiepileptics.
*5. Drugs that induce seizures: Some of the antibiotics, antidiabetics,
anesthetics,antimalarials, antispastics, antidepressants, antipsychotics,
mood stabilizers.

5. Sumit Verma
*Pathophysiology of EPLILEPSY:
*Each individual neuron is linked with hundreds of other neuron via
synapses.
*Neurons discharge electrical current and neurotransmitters arereleased at
synaptic levels and permits inter-communication.
* There are two types of Neurotransmitters:
*1. Inhibitory Neurotransmitters: GABA (Gamma amino butyric acid)
acts on ion channels and increases chloride outflow and decreases chances
of action potential.
*2. Excitatory Neurotransmitters: Glutamate and Aspartate allows sodium
and calcium influx which paves way for action potential formation.

6. Sumit Verma
*Seizures occur due to the imbalance between the inhibitory and
excitatory Neurotransmitters.
*A normal neuron discharges repetitively at low baseline
frequencies. If neurons are damaged, injured/ suffer a chemical/
metabolic insult,the changes in discharge pattern develops.
* During epilepsy, regular low frequency discharges are replaced
bybursts of high frequency discharges followed by periods of
inactivity.
*A single Neuron discharging in an abnormal manner is usually not
clinically significant. But when a whole population of neurons
discharge synchronously in an abnormal manner,
epileptic seizure occurs.

7. Sumit Verma
Abnormalities in ion channel (Na, K, Ca or decreased INT
activity/inactivation of INT activity
Increased ENT activity
Rhythmic & repetitive hypersynchronous discharge of neurons
Seizures focus
Seizures
Repetitive seizures
Epilepsy

8. Sumit Verma
*Causes of EPLILEPSY:
*In 28% cases, cause can be determined, in rest 72% cases, cause
isidiopathic.
*Determined causes:
1) Inherited genetic
2) Acquired: Trauma, Metabolic infections, Tumour, Neurosurgery, Drugs, etc.
3) Deficiency of inhibitory neurotransmitter such as the GABA.
4) Increase excitatory neurotransmitter.
5) Concentration of potassium is reversed.
6) Abnormality in the potassium conductance.
7) Defect in the voltage sensitive calcium channel

9. Sumit Verma
*Diagnosis:
*Neurological examination/ Neuropsychological Tests
*Medical history
*Genetic Testing
*Electroencephalogram (EEG)
*CT Scan/ MRI Scan
*fMRI
*Positron Emission Tomography (PET Scan)
*SPECT (Single Photon Emission Computerized Tomography)
*SISCOM (Subtraction Ictal SPECT categorized to MRI)

10. Sumit Verma
*RISK FACTORS:
*1. Sleep deprivation.
*2. Missed doses of anti-epileptic drugs (AEDs) in treated patients
*3. Alcohol withdrawals, recreational drug misuse.
*4. Physical and mental exhaustion.
*5 Flickering lights (includes TV, computer screens; comes under
generalized epilepsy syndrome)
*6. Intercurrent infections.
*7. Metabolic disturbances.
*8. Uncommon reasons like loud noises, very hot baths etc.

11. Sumit Verma
Types of
epilepsy
Generalized
seizures
Localized (partial
or focal)
Simple partial
seizure
jacksoninan)
Complex partial
(psychomotor)
seizure
Tonic –
clonic
seizur
e
(gran
mal
seizur
e)
Absenc
e
seizure
(petit
mal
seizure
)
Atonic
seizur
e
Myoclo
nic
seizure

12. Sumit Verma
*Types of EPLILEPSY:
*Generalized seizures
*1. Tonic-clonic seizures(Major epilepsy, Grand mal)
• Lasts 1-2 min
• Usual sequences is aura-cry-unconsciousness-tonic spasm of all body
muscles-clonic jerking followed by prolong sleep
• Stiffening of arms and legs followed byrhythmic jerking.

13. Sumit Verma
2. Absence seizures (Minor epilepsy, Petit mal)
• Lasts about 1-2 min
• Momentary loss of consciousness
• Stare in one direction
• Little jerking
• Often subside prior to puberty.

14. Sumit Verma
3. Atonic seizures (Akinetic epilepsy)
• Unconsciousness with relaxation of all muscles.
• Due to excessive inhibitory discharge
• Patient may fall, after 10 seconds to a minute, they recover and regain
consciousness and can stand and walk again.

15. Sumit Verma
4. Myoclonic seizures
• Shock like momentary contraction ofmuscles of limb or the whole body
• Juvenile myoclonic epilepsy (JME) is the most common form
of this condition.

16. Sumit Verma
*Simple partial seizure(Cortical focal epilepsy)
• Lasts 1/1-2 min
• Convulsion are confined to a group of muscles or localized sensory disturbance
depending on the area of cortex involved in seizure
• Without loss of consciousness
*Complex partial seizure(Temporal lobe epilepsy, Psychomotor
epilepsy)
• Attack of bizarre and confused behavior and purposeless movement
• Emotional changes lasting 1-2 min along with impairment ofconsciousness.
• The seizure focus is located in the temporal lobe.

17. Sumit Verma
*TYPES OF TREATMENT:
*Medication
*Surgery
*Non-pharmacologic treatment
• 1. Ketogenic diet
• 2. Vagus nerve stimulation (VNS)
• 3. Lifestyle modifications

18. Sumit Verma
*CLASSIFICATION:
*1. Barbiturate: Phenobarbitone
*2. Deoxybarbiturate: Primidone
*3. Hydantoin: Phenytoin, Fosphenytoin
*4. Iminostilbene: Carbamazepine, Oxcarbazepine
*5. Succinimide: Ethosuximide
*6. Aliphatic carboxylic acid: Valproic acid (sodium valproate)
*7. Benzodiazepines: Clonazepam, Diazepam, Lorazepam, Clobazam
*8. Phenyltriazine: Lamotrigine
*9. Cyclic GABA analogue: Gabapentin
*10. Newer drugs: Vigabatrin, Topiramate, Tiagabine,
Zonisamide,Levetiracetam

19. Sumit Verma
• Group 1- Blockade of voltage-dependent Na+ or Ca channels
(generalised and partial seizures)
• Group 2- Enhance inhibitory events mediated by GABA
(absence,generalised, partial seizures)
• Group 3- Blocks T-type calcium channels (absence seizures).
• Group X- Reduce events mediated by excitatory amino acid glutamate

20. Sumit Verma
*Carbamazepine
*Clinical uses:
*Primary generalized tonic clonic seizures.
*Partial seizures with or without secondarily generalization.
*Bipolar disorders.
*Chronic pain syndromes: Trigeminal neuralgia.
*Pharmacokinetics:
*Initial half-life is 20-40 hrs but decreases to 20-40 hr on
chronicmedication.
*Active metabolite: 10-11 epoxy carbamazepine.

21. Sumit Verma
*Dose:
*Available only in oral form.
*Effective in children, in whom a dosage of 15-25 mg/kg/d is appropriate.
*In adults, daily doses of 1 g or even 2 g are tolerated.
*Neurotoxic side effects:
*Blurred or double vision
*Lethargy, headache.
*Worsening of myoclonic, Atonic & absence seizures.

22. Sumit Verma
*Systemic side effects:
*Nausea, vomiting, diarrhea
*Hyponatremia & fluid retention.
*Rash, pruritus
*Rare side effects:
*Blood dyscrasias: Agranulocytosis, aplastic anemia.
*Dermatitis/rash
*Stevens-Johnson syndrome.
*Serum sickness, pancreatitis
*Hepatic failure

23. Sumit Verma
*Phenytoin
*Clinical uses:
*Partial & generalized tonic clonic seizures.
*2nd line agent for patients with mixed seizures (myoclonic/tonic-clonic).
*Status epilepticus.
*Neurotoxic Side effects:
*Dose related: Diplopia & Ataxia.
*Peripheral neuropathy.
*Behavior changes.

24. Sumit Verma
*Systemic side effects:
*Skin rash
*Lymphadenopathy (abnormally enlarged lymph nodes)
*Gingival hyperplasia
*Pulmonary fibrosis
*Hirsutism
*Teratogenic (Fetal Hydantoin syndrome includes cleft lip and palate.
congenital heart disease)
*Megaloplastic anemia (folate deficiency).
*NOTE- phenytoin is also an anti-arrthymetic drug treatment with
phenytoin should not be stopped abruptly.

25. Sumit Verma