vaibhav presentation on the epilepsy 29-12-2001.pptx
1. A SEMINAR ON “EPILEPSY AND ITS
MANAGEMENT”
NAGARGOJE VAIBHAV ADINATH
B.PHARM
4th YEAR STUDENT
GUIDE: Jangam sir
M pharm.
ARIHANT COLLEGE OF PHARMACY,KEDGAON,
AHMEDNAGAR, 2022-23. 1
2. CONTENT
INTRODUCTION
CAUSES OF EPILEPSY
PATHOPHYSIOLOGY OF EPILEPSY
TYPES OF EPILEPSY
SYMPTOMS OF EPILEPSY
DIAGNOSIS
MANAGEMENT OF EPILEPSY
MECHANISM OF ACTION OF ANTIEPILEPTIC
DRUGS
CONCLUSION
REFERENCE
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3. INTRODUCTION
Epilepsy is a group of disorders of the CNS characterized by paroxysmal cerebral
dysrhythmia, manifesting as brief episodes (seizures) of loss or disturbance of consciousness,
with or without characteristic body movements (convulsions), sensory or psychiatric
phenomena.
Epilepsy is a chronic noncommunicable disease of the brain that affects people of all ages.
It is a ‘disease of lightening’, it was correctly described by JH Jackson.
Epilepsy involves the decrease in the inhibitory neurotransmitter like GABA and increase
in the excitatory neurotransmitter.
So the treatment of the disease depend on the decease in the excitatory neurotransmitter
and increase in the inhibitory neurotransmitter in the brain.
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5. CAUSES OF EPILEPSY
Emotional stress
Sleep deprivation
Alcohol
Febrile illness
Menstrual cycle in epileptic women can influence patterns of seizure
recurrence.
Head injury (a clear cause of seizures) will develop epilepsy
Stroke.
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6. PATHOPHYSIOLOGY OF THE
EPILEPSY
In the epilepsy the excitatory neurotransmitters increases and the inhibit
neurotransmitters likes GABA decrease which results in seizure.Based on
the types of contraction and relaxation seizures are classified accordingly
Certain neurotransmitters (e.g. glutamate, Aspartate, acetyl choline,
norepinephrine) enhance the excitability of neuronal Activity, whereas ã-
amino butyric acid (GABA) and dopamine Inhibit neuronal activity and
propagation
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7. TYPES OF EPILEPSY
I. Generalised seizures
1. Generalised tonic-clonic seizures (GTCS, major epilepsy, grand mal):
lasts 1–2 min.
2. Absence seizures (minor epilepsy, petit mal): prevalent in children, lasts
about 1/2 min.
3. Atonic seizures (Akinetic epilepsy): Brief loss of consciousness with
relaxation of all muscles due to excessive inhibitory discharges.
4. Myoclonic seizures Shock-like momentary contraction of muscles of a
limb or the whole body.
5. Infantile spasms (Hypsarrhythmia) Seen in infants.
II.Partial seizure
1.Simple partial seizure [SPS]
2.Complex
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9. DIAGNOSIS
A. EEG {Electroencephalogram}- find out the abnormal electrical activity in the
brain.
B. Brain Scan
CT--------Computed Tomography
PET-------Positron Emission Tomography-A positron emission tomography (PET)
scan may be used to locate the part of the brain that is causing seizures. PET (positron emission
tomography) shows the brain's use of oxygen or sugar (glucose).
MRI------Magnetic Resonance Imaging .
SPECT---Single Photon Emission Computed Tomography.--- Single-photon
emission computed tomography (SPECT) is a nuclear radiology study that measures the
blood flow in the brain
C. Blood Test-Blood sample will be collected to check for signs of infection, genetic
conditions etc.
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10. MANAGEMENT OF THE EPILEPSY
The patients should be educated about the disease, duration
of Treatment.
Precipitating factors should be avoided, e.g., alcohol, sleep
Deprivation, emotional stress.
Natural variation should be anticipated, e.g., fits may occur
Particularly or exclusively around periods in women.
Antiepileptic drug should be given only if seizure type and
Frequency require it, i.e., more than one fit every 6-12
months.
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11. CHEMICAL CLASS EXAMPLE OF DRUG
Barbiturate Phenobarbitone
Deoxybarbiturate Primidone
Hydantoin Phenytoin, fosphenytoin
Iminostillbene Carbamazepine
Succinimide Ethosuximide
Aliphatic carboxylic
acid
Valproic acid
Benzodiazepines Clonazepam, Diazepam lorazepam,
Clobazam
Cyclic GABA
analogue
Gabapentin
Phenyltriazine Lamotrigine
Newer drugs Tiagabine
Zonisamide
Vigabatrin
Lacosamide
CLASSIFICATION OF ANTIEPILEPTIC DRUGS
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12. MECHANISM OF ACTION OF ANTIEPILEPTIC
DRUGS
(I) Reducing electrical excitability of cell membranes, particularly (by
blocking) the voltage dependent sodium channels which are responsible
for the inward current that generates an action potential.
(II) Enhancing GABA mediated synaptic inhibition, by inhibiting GABA
transaminase or by drugs with direct GABA agonist properties; the
result is increased membranes permeability to chloride ion, which
reduces cell excitability.
(III) Inhibiting T-type calcium channels (important in controlling absence
Seizure).
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14. CONCLUTION
The selection of an anticonvulsant agent is based primarily on Its efficacy
for specific types of seizures and epilepsy. Although Seizure control is
generally good in most patients, a significant Proportion of patients with
epilepsy suffer from intractable or drug resistant epilepsy, despite early
treatment and an optimum daily Dosage of an adequate anticonvulsant
agent. There is thus a need for new drugs with a greater benefit as related
to side effects and Tolerability, even at the expense of efficacy, when
compared to the Existing antiepileptic agents
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15. REFERENCE
1.Rang HP, Dale MM, Ritter JM, Moore PK. Pharmacology. New Delhi: Churchill Livingstone Reed
Elsevier India (P) Ltd, 5th ed. 2006:550-60.
2.. Kd Tripathi pharmacology. New Delhi: Jaypee Brothers Medical publishers (P) Ltd, 8th ed. 2019:438
3.Carl E S. Epilepsy: a review of selected clinical syndromes and Advances in basic science. Journal of
Cerebral Blood Flow & Metabolism 2006; 26:983-04.
4.Epilepsy: aetiogy (Sic), epidemiology and prognosis, World Health Organization. 2001; Archieved form
the original on 2007-05-18. A v a I l a b l e a t
http://web.archieve.org/web/20070518073641/http://www.who.int/mediacentre/facsheets/
fs165/en/Retrieved 2007-06-14.
5.Chadwick D, Taylor J, Johnson T. 1996. Outcomes after seizure recurrence in people with well-
controlled epilepsy and the factors that influence it. The MRC Antiepileptic Drug Withdrawal Group.
Epilepsia 37: 1043–1050. [PubMed] [Google Scholar]
6.Cornejo BJ, Mesches MH, Coultrap S, Browning MD, Benke TA. 2007. A single episode of neonatal
seizures permanently alters glutamatergic synapses. Ann Neurol 61: 411–426. [PubMed] [Google Scholar]
7.Duchowny M, Cross JH, Arzimanoglou A. 2012. Pediatric epilepsy. McGraw-Hill, New York. [Google
Scholar]
15
16. 8.Dudek FE, Sutula TP. 2007. Epileptogenesis in the dentate gyrus: A critical perspective. Prog
Brain Res 163: 755–773. [PubMed] [Google Scholar]
9.Engel J Jr. 2013. Seizures and epilepsy. Oxford University Press, Oxford. [Google Scholar]
10.World Health Organization. Improving Access to Epilepsy Care. Available at:
https://www.who.int/mental_health/neurology/epilepsy/en/. Accessed December 20, 2018. 25
11. E S. Epilepsy: a review of selected clinical syndromes and advances in basic science. Journal of
Cerebral Blood Flow & Metabolism 2006; 26:983-04.
12.Epilepsy: aetiogy (Sic), epidemiology and prognosis, World Health organization. 2001;
Archived form the original on 2007-05-18. A v a I l a b l e a t:
http://web.archieve.org/web/20070518073641/http://www.who.int/mediacentre/facsheets/
fs165/en/Retrieved 2007-06-14.3.
13.Commission on Epidemiology and prognosis. International League Against Epilepsy. Guidelines
for epidemiologic studies on epilepsy. Epilepsia 1993; 34(4):592-96.
14.Blume W, Luders H, Mizrahi E, Tassinary C, Van Emde Boas W, Enjel J. Glossary of
descriptive terminology for ictal semiology; report of the ILAE taskforce on classification and
terminology.
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