Anticonvulsant or Antiepileptic Drugs
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1 Anticonvulsant or Antiepileptic Drugs Munir Gharaibeh, MD, PhD, MHPE School of Medicine, The University of Jordan February, 2019 Note Done by : Raneen Hamdan Corrected by :Haneen Khriesat
2 Anticonvulsant or Antiepileptic Drugs or antiseizure Epilepsy: a disease characterized by recurrent attacks of convulsions and seizures. (describes.convulsion (Fit): the attack itself what happens to the patient) Seizure: an abnormal electrical activity, not necessarily to result in a convulsion.
3 -Epilepsy, convulsions and seizures can be used interchangeably as synonyms, but they are actually (scientifically) different. - One incidence (fit) of the disease is called convulsion. - A patient may have a convulsion once in his life, but he might not develop a disease (epilepsy) because epilepsy is defined as recurrent attacks of convulsions and seizures.
4 Neuronal Mechanisms involved in Seizures Suppression of Inhibition---Onset (brain has inhibitory and excitatory mechanisms and inhibition of inhibition leads to over activity of excitatory mechanisms) Post-tetanic Potentiation---Spread and Maintenance (of abnormal electrical activity) Reinstitution of Inhibition---Termination (the inhibitory mechanisms in the brain will take over again after being disinhibited) 4
5 Pathophysiological Conditions Enhancing convulsions LowPO2(hypoxia) HighpH(alkalosis) Increased IntracranialPressure LowCa++(hypocalcemia) LowGlucose(hypoglycemia) Overhydration Fatigue EmotionalState 5
6 Causes of Convulsions Poisons(chemical and non chemical) Trauma(to the head) Infection(causes fever, which is one of the causes of convulsion especially in children before age of 1 = infants) Space Occupying Lesions(like a tumor, hemorrhage or thrombosis) Fever Drugs Idiopathic, Epilepsies (in most cases) 6
7 classifications vary between different sources and books. / localized *Complex partial seizures might be confused with psychological and psychiatric problems 7
8 Classification of Epilepsies Grand Mal or Major Epilepsy or Tonic-Clonic Epilepsy: characterized by: 1-Aura(the patient feels that he will get an attack and that there is something wrong with him and he might suffer from visual or auditory hallucinations; just like schizophrenic patients) *aura happens in migraine patients 2-Cry-Loss of consciousness(spasm of the vocal cords, followed by a rush of air through these spastic vocal cords causing crying or loud voice followed by loss of consciousness which might continue all through the attack as well as afterward) 3-Tonic Phase: Rigid violent muscle contraction with limbs fixed. 4-Clonic Phase: Repetitive muscle jerks (shaking) 5-Post-ictal depression and incontinence(the patient goes into deep sleep lasts for hours or very long period of time relative to the attack itself, this is accompanied with loss of reflexes and urination) 8
9 *Different phases of tonic-clonic type of epilepsy February 19 Munir Gharaibeh, MD, PhD, MHPE 8
10 Classification of Epilepsies Petit Mal or Minor Epilepsy or Absence States: A Condition characterized by absence state; you might see the patient with a brief loss of consciousness that happens many times a day, one episode may last for less than a minute or a few minutes. it happens in children and may retard the learning process,usually these attacks are noticed and reported when the child goes to school by his teacher. It was proved that these absent states are triggered by TV or mobile light. Psychomotor Epilepsy:(characterized by) Clouded dreamy feeling Aggressiveness Automatic movements *Could be confused with conditions like schizophrenia or psychotic conditions. 10
11 Classification of Epilepsies Status Epilepticus (recurrent attacks during the day despite the usual treatment, so the patient is taking his regular treatment but the attacks come recurrently) Parietal Lobe Epilepsy Infantile Myospasm (benign attacks of epileptic convulsions characterized by sudden movements or spasms of the upper and lower limbs which usually occurs in infants less than 1 year of age, sometimes they are called Salaam attacks, the baby will extend his hands as if he is greeting people ) etc.. 11
12 12
13 Regarding the table : *The electrical activity of the brain is recorded or detected by electroencephalogram (EEG ). *In absence seizures (petit) the recorded waves are small waves or spikes and they are presented all the time, in other conditions you might find abnormal EEG during the attacks but not in between.
14 Provocative Procedures *experimental procedures have been done on animals, you can provoke epileptic attacks by giving drugs like: Pentylene tetrazole "Metrazole"(which was used as a CNS stimulant to stimulate respiration in respiratory depressed patients/patients with hypoventilation but it's no longer used ) Hyperventilation(might result in respiratory alkalosis which can provoke or enhance convulsion attacks ) Photic stimulation - Flicker Fusion (important in absence state ) 14
15 Principles of Epilepsy Treatment * Seizures are self-limiting ( we don t treat the seizure we treat the disease (epilepsy) so you have to leave the seizure and let it go by itself, but you have to protect the patient during the attack {protect him from falling down + breaking his body/head/limbs + biting his tongue}and you have to ensure a patent airways) * Use one drug at a time( Monotherapy): Lower incidence of adverse reactions. Avoidance of drug interactions. Improved patient compliance. Lower medication cost. * Start with a small dose.(start with a small dose, then you can increase it with time or keep it as it is ) * Monitor serum level. 15
16 16
17 17
18 Notes on the table : -SRF=sustained high frequency repetitive firing -GABA ( and its agonists ) activity in the brain is inhibitory - Calcium currents :1- T, IN THE BRAIN 2-M 3-N Notes on the picture : - Sodium channels present in 3 phases : 1- closed but capable of opening 2- open/activated 3- closed and not capable of opening (inactivated) - So activity refers to opening of channels and allowing sodium current to enter as a result of the arrival of the action potential to a certain point in the membrane of neurons
19 Barbiturates the long acting barbiturates are utilized in the treatment and prevention of epileptic attacks, especially when we talk about: Phenobarbital Mephobarbital Methabarbital Primidone 19
20 Barbiturates Oldest but still used. ( since 1930s ) Relatively safe, but sedating.(cause excessive sedation, so children under the influence of this drug will not be able to learn in school normally compared to their peers ) Effective in Grand mal and partial seizures. Might worsen patients with other types. Bind to GABA receptor, to prolong opening of Cl- channels. Also, at high doses, block Na+ and Ca++ channels (L and N type). Also block Glutamate receptors. 20
21 Barbiturates Adverse Effects: Sedation Allergies Anemia Drug Interactions (they are highly bound to plasma proteins so they can displace other drugs from their binding sites on proteins and cause drug interactions) Enzyme Induction Withdrawal!!(they can induce the metabolism of other drugs as well as their own, so this cause lowering of barbiturate blood levels and we will need to increase the dose to achieve the desired effect. Withdrawing the drug will lead to the recurrence of the epileptic attacks ) Additive to CNS depressants.(like alcohol and benzodiazepine) 21
22 Phenytoin(1938) (Diphenyl Hydantoin DPH- the old name) Generalized tonic - clonic seizures Partial seizures with complex symptomatology Antipsychotic Antiarrhythmic Many others Revolutionary *good for digitalis induced cardiac arrhythmia *used in healing skin ulcers as cream also in diabetic patients * Almost all types of epilepsy can be treated with phenytoin 22
23 Phenytoin Mechanism of Action: Acts on several physiologic systems. Major action is sodium channel blockade, arising from preferential binding to and prolongation of the inactivated state of the Na + channel. Also, inhibits Ca++ influx, membrane potential, as well as, the concentrations of amino acids, NE, ACh, and GABA. Blocks sustained high-frequency repetitive firing of action potentials(srf). *all will lead to suppression of epileptic activity in the brain 23
24 Pharmacokinetics: Slow absorption(from GIT) 90% bound to proteins. Metabolized: Phenytoin Zero order in high doses used in epilepsy, so, no SSL achieved.(ssl=steady state level>>it doesn t follow first order kinetics in which you can achieve a steady state level if you give a definitive dose every half life, but here if you give the drug at half life, it will keep going up in zero order meaning that it depends on the timing first order depends on half life) but Interactions: Protein binding. (high binding capability so it can replace other drugs for their binding site) Enzyme induction.(induce metabolism of 24 other drugs)
25 Phenytoin Adverse Effects: (not serious and tolerable by the patient; because it is very effective drug in the suppression of epileptic attacks ) Skin rashes, fever Blood: megaloblastic anemia, agranulocytosis,lymphadenopathy. Gingival hyperplasia (50%) Hirsutism "Hydantoin Facies"(patients receiving the drug will have peculiar faces ) Peripheral neuropathy Cerebellar degeneration(causes ataxia and dizziness) Teratogenic Folate Deficiency(might cause congenital abnormalities) 25
26 Hypertrophy of gums might need excision and it will not be reduced by reducing the dose or after stopping the drug(irreversible ) Hirsutism Cause skin allergic reaction and hirsutism 26
27 Phenytoin Overdose:(these are signs of cerebellar degeneration) Nystagmus, Ataxia, Vertigo, Diplopia Loss of consciousness. 27
28 Partial seizures Generalized tonic - clonic Carbamazepine Like phenytoin and barbiturates, it is not useful for petit mal Initially marketed for Trigeminal Neuralgia.(a type of headache might be confused with migraine headache which affects the trigeminal nerve) Bipolar mood disorders, it is a tricyclic compound.(very important in the treatment of depression and mood disturbances) Peripheral Neuropathy (in diabetic patients) Migraine etc 28
29 Carbamazepine Mechanism of Action: Like phenytoin, blocks Na+ channels. 29
30 Carbamazepine Slow and erratic absorption (absorbed from GIT) T½ hr.(wide range, vary between patients) Induces liver enzymes = Autoinduction.(induce the metabolism of its own) Interactions. Blood monitoring is necessary. 30
31 Carbamazepine Adverse Effects: Vertigo, Ataxia, Diplopia appear early. Drowsiness, nausea, headache, dizziness. Tolerance develops to the above effects. Skin rashes, fever, hepatosplenomegaly, lymphadenopathy. Blood dyscrasias: leukopenia, aplastic anemia, and agranulocytosis. 31
32 Oxacarbazepine. *it's a derivative of carbamazepine Less capacity to induce enzymes. T½1-2hr. May be safer than carbamazepine 32
33 Vigabatrin GABA-Transaminase irreversible inhibitor, which breaks down GABA in the brain. (increasing the level of GABA in the brain ) Renal elimination. ( won't affect liver enzymes activity) Partial seizure Not for absence or myoclonic Well tolerated: drowsiness, dizziness, weight gain, visual field defects. 33
34 Lamotrigine Inhibits Na+ and Ca++ channels, also decreases release of glutamate. (glutamate is an excitatory neurotransmitter in the brain so if you decrease glutamate and inhibit sodium and calcium channels this will enhance the inhibitory activity of the brain) Partial and generalized seizures Completely absorbed Glucoronidated, so will not induce or inhibit enzymes(glucoronation (conjugation with glucuronic acid ) in liver, so it is not metabolized by microsomal liver enzymes and not fully metabolized by oxidizing liver enzymes) Side Effects: Similar to carbamazepine. 34 Skin rashes Cerebellovestibular symptoms.
35 Gabapentin and Pregabalin GABA analogs, but work indirectly to increase GABA levels in the brain. Partial Seizures. Good PK Properties.(PK= pharmacokinetics) Effective when combined with others. Safe: somnolence, dizziness, ataxia. 35
36 Benzodiazepines GABA mechanism, and Na+ channel inhibition in doses used in status epilepticus. *classified as sedative hypnotic agents and have antiepileptic activity * They intensify chloride entrance through GABA receptors {GABA receptor permits cl- as inhibitory ion inside the cell while barbiturate prolong entrance of cl-} 36
37 Benzodiazepines Diazepam Status epilepticus){10mg IV} Lorazepam Longer acting(one injection compared to multiple injections of diazepam ) Clonazepam Petit mal, but causes Nitrazepam sedation and drooling Infantile Spasms Infantile spasm might not need treatment, they usually disappear after the first year of life, but if the attacks are very frequent and parents required treatment, then this is the drug of choice. 37
38 Valproic Acid(old new drug-was used as an organic solvent in laboratory) Increases GABA levels by enhancing synthesis and inhibiting transaminase. (which breakdown GABA) Also, blocks NMDA receptors(glutamate receptor), Na+ channels and T-Ca++ channels. 90% bound to plasma proteins. 38
39 Valproic Acid (1969) Petit mal and myoclonic epilepsy Mixed seizures. Bipolar disorder and migraine prophylaxis. 39
40 Valproic Acid Toxicity: Hepatotoxic Neural tube defects(in pregnant women) Thrombocytopenia. Alopecia GI. Inhibits metabolism of many drugs. 40
41 Ethosuximide (1960s) Blocks transient Ca++ currents. Petit mal, still first choice. Safe. 41
42 Acetazolamide Diuretic, works by inhibiting Carbonic Anhydrase Enzyme, so decreases intracellular ph, causing mild acidosis. *carbonic anhydrase enzyme responsible for the conversion of H2CO3 into HCO3 and H+ *it is a weak diuretic and it is used in the treatment of glaucoma *alkalosis is one of the conditions that enhance convulsions so by reducing PH we can indirectly control seizures. Helpful in all types of seizures. Used as an adjunct to others in refractory seizures. Tolerance develops. Special role for seizures at the time of menses( alone or in combination with other drugs ) 42
43 43
44 Regarding the table : *Blood levels are very important in control and follow up of epileptic patients, we have to make sure the drug level is within the acceptable range ( above the range side effects appear and below the range appearance of epileptic attacks) *you have to distinguish between most serious and most frequent adverse effects *the numbers in the boxes are the only ones mentioned by the doctor
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