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FACULTY OF LIFE SCIENCE DEPARTMENT OF BIOCHEMISTRY
UNIVERSITY OF BENIN FACULTY OF LIFE SCIENCE DEPARTMENT OF BIOCHEMISTRY BCH417(UNDERGRADUATE SEMINAR) TOPIC : EPILEPSY (MECHANICAL, CHEMICAL AND GENETIC CAUSES) PRESENTED BY OKORIE MICHAEL IFEANYI LSC 13th DECEMBER,2012
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INTRODUCTION Epilepsy occurs when permanent changes in the brain tissues causes the brain to be too excitable, leading to an unexpected and reoccurring seizures. The term seizure refers to a transient alteration of behaviour due to abnormal, synchronized, and repetitive burst firing of neuronal populations in the central nervous system (CNS). Epilepsy can develop in any person at any age, 1% of persons will develop epilepsy during their life time. Out of 60,000 persons 500 will have epilepsy . The duration, severity and interval of seizure differ from individual to individual depending on the extent to which the brain is damaged.
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Cases of Epilepsy In Children Birth traumas
New cases of epilepsy are common among children especially during their first year. The rate gradually decline until about 10years of age, after age 60 the rate increases again Figure 1.1 In Children Birth traumas Infections such as meningitis, brain abscess, encephalitis Congenital abnormalities High fever
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Cases of Epilepsy Middle Age Head injuries Infections
Stimulant drugs (cocaine) Medication side effect ( Tramadol, Antidepressant, amphetamines) Alcohol Elderly Tumor Stroke figure1.2 showing the development of brain tumor
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TYPES OF EPILEPSY Temporal lobe Frontal lobe
There are several types of epilepsy depending on the part of the brain that is damaged. Temporal lobe Frontal lobe Generalised epilepsy (tonic clonic seizures) Absence seizure (common in children) Complex partial seizure Simple partial seizures Side view of the human brain figure1.3
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CAUSES OF EPILEPSY Brain injuries and tumors
Any thing that injures the brain can lead to abnormality in brain wiring and imbalances in neuronal signaling. Chemical Imbalances Abnormally high level of excitatory neurotransmitter. Examples are acetylcholine, glutamate. Abnormally low level of inhibitory neurotransmitter. Examples are Gamma-aminobutyric acid(GABA), Serotonin. Genetic Factors Genetic defect in the code for a protein called cystatinB which regulates enzymes that help to breakdown other proteins (myoclonic epilepsy). Defect in gene that help to breakdown carbohydrate (lafora’s disease). Mutations in several genes that code for protein subunits of voltage-gated and ligand-gated ion channels. Examples are defective sodium channels, mutations in some non-ion channel genes . Changes in the non-neuronal brain cells called glia. These cells regulates concentrations of chemicals in the brain that can affect neuronal signalling. Regardless of what initiates the seizure, neurons that are normally firing simultaneously in the normal pattern begin to fire together like an electric storm that eventually gains momentum and spread to other parts of the brain. Figure1.4 showing neuronal firing in the brain
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CLINICAL BIOCHEMISTRY OF EPILEPSY
In generalised epilepsy serum glucose and cholesterol concentrations tend to be low especially just before the seizure Electrolyte balance is disturbed and epileptics tend towards alkalosis Serum sodium ion is unaffected, but potassium ion is normally low between attacks and increases after. Chloride ion is high before seizure. Epileptics are usually mildly hypocalcemic especially in periods before the seizure, this is due to a high serum citrate resulting in hypo-ionic calcemia A. Stress which releases epinephrine and corticotropin results in high serum citrate. Apparently the dynamic system that controls glucose and lipid metabolism, and thus electrolyte balance through the hormones epinephrine, corticotropin, insulin, glucagon, calcitonin, and parathromone is abnormal in the epileptic.
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MECHANISM OF TEMPORAL LOBE EPILEPSY
Figure1.5 Mossy cells are damaged following intense synaptic activation, probably through excitotoxic mechanisms by activation of N-methyl-D-asparate (NMDA) subtype of glutamate receptors, resulting in excessive rise of intracellular calcium
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MECHANISM OF ACTION IN COMMONLY USED ANTIEPILEPTIC DRUGS
barbiturates: (Mysoline), phenobarbital Enhances GABAergic inhibition by blocking the special attachment place for the inhibitory neurotransmitter Carbamazepine: (Tegretol, Carbatrol) Blocks ion channels, reduces the amount of sodium that enters the neuron (general seizures) Ethosuximide: (Zarontin) blocks certain types of calcium ion channel in neurons (absence seizures) lamotrigine: (Lamictal) inhibits voltage-dependent sodium channels, resulting in decreased release of the excitatory neurotransmitter glutamate and aspartate valproate (Depakote, Depakene, valproic acid reduces h-frequency neuronal firing and sodium-dependent action potentials enhances GABA effect Folbamate: folbatal Last resort medicine because it damages the liver or bone marrow, seem to be safer in children with severe seizures.
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WHO IS REALLY AT RISK? Parents with epilepsy wonder whether their children will have epilepsy. In most cases they won't, but they do have a higher risk than others. If the mother has a generalized type of epilepsy, then the child's chance of having epilepsy may be as high as 5‐20%. But if a parent has epilepsy due to a brain injury, the child's chance of having epilepsy is only about 5%.
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CONCLUSION Today, the aetiology of seizures in most cases remains idiopathic, fortunately doctors do not have to know the cause to treat the seizure. It is sad to know that no known cure has been found for epilepsy but to a great extent this disease can be managed. Due to the increasing case of epileptic seizures world wide, scientist are seeking a better way to cure the disease with less side effect. Recently, scientist have thought that it would be very important to test if embryonic stem cell transplant might be effective to repair damages caused by epilepsy.
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