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EPILEPSY AND SEIZURES- A DEEP INSIGHT

This presentation provides a deep insight into epilepsy & seizures, covering terminologies, types, etiology, epidemiology, and management strategies. Acknowledgements and references included.

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EPILEPSY AND SEIZURES- A DEEP INSIGHT

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  1. EPILEPSY AND SEIZURES- A DEEP INSIGHT PRESENTED BY:VISHNU.R.NAIR,4TH YEAR PHARM.D,NATIONAL COLLEGE OF PHARMACY,KERALA UNIVERSITY OF HEALTH SCIENCES(KUHS), KERALA STATE.

  2. INDEX/ CONTENTS OF THIS PPT : • GENERAL ACKNOWLEDGEMENT • GENERALIZED TERMINOLOGIES • EPIDEMIOLOGY • TYPES OF EPILEPSIES{INCLUDING CLINICAL MANIFESTATIONS} • ETIOLOGY OF EPILEPSY • PATHOPHYSIOLOGY OF EPILEPSY • RISK FACTORS FOR SEIZURES • DIAGNOSIS OF EPILEPSY • MANAGEMENT STRATEGIES FOR EPILEPSY • BIBLIOGRAPHY/ REFERENCE

  3.  GENERAL ACKNOWLEDGEMENT  : TO THE ALMIGHTY , MY NEAR AND DEAR ONES… AND TO ALL READERS WORLDWIDE!!! THANKFUL TO ALL FOR UR SUPPORT, GUIDANCE AND ENCOURAGEMENT……………… ITS BEEN A REALLY HARD JOB WORKING ON THIS PPT………………… HOPE U LIKE IT!! HAPPY READING!!!   

  4.  GENERALIZED TERMINOLOGIES  : • SEIZURE: “PHENOMENON, characterized by an EXCESSIVE, HYPERSYNCHRONOUS DISCHARGE of CORTICAL NEURONAL ACTIVITY, (measured by EEG), featured by DISTURBANCES in CONSCIOUSNESS, SENSORY MOTOR SYSTEMS, SUBJECTIVE WELL-BEING and OBJECTIVE BEHAVIOUR…………………” 2. EPILEPSY: “CHRONIC SEIZURE DISORDER/ GROUP OF DISORDERS, characterized by SEIZURES, that usually occur UNPREDICTABLY, in the ABSENCE of a SUBSTANTIAL PROVOKING FACTOR…………….” 3. CONVULSION: “VIOLENT, INVOLUNTARY CONTRACTIONS of VOLUNTARY MUSCLES, which may/ may not be present in epilepsy/ seizure disorder………..............”

  5.  EPIDEMIOLOGY OF EPILEPSY  : • Higher risk observed in extremes of age • Prevalence in European countries is 0.5% • Prevalence in developing countries is higher, due to parasitic illnesses like CYSTICERCOSIS • Around 50 million people worldwide have epilepsy • Epilepsy responds to treatment in 70% cases • 75% people in developing countries do not get required anti-epileptic treatment…………………..

  6.  TYPES OF EPILEPSIES (INCLUDING CLINICAL MANIFESTATIONS)  : Based on INTERNATIONAL LEAGUE AGAINST EPILEPSY(ILAE) classification: • PARTIAL SEIZURES (FOCAL SEIZURES) • GENERALIZED SEIZURES ………………………………………

  7. PARTIAL SEIZURES (FOCAL SEIZURES): • Most common seizure type • Localized to a neuronal system, limited to PART OF 1 CEREBRAL HEMISPHERE • Types include: • SIMPLE PARTIAL SEIZURES: • Not associated with loss of consciousness • Associated with: • MOTOR SIGNS (Convulsive jerking, lip smacking) • SENSORY & SOMATOSENSORY SIGNS (Paresthesias, auras) • AUTONOMIC SIGNS (Sweating, flushing) • BEHAVIOURAL MANIFESTATIONS (Dysphasia, structured hallucinations)

  8. B. COMPLEX PARTIAL SEIZURES: - Associated with IMPAIRED CONSCIOUSNESS • Impairment precedes/ follows seizures • Associated with: • Purposeless behavior • Glassy stare • Aimless walking • Hallucinations (visual, auditory) • Aggressive behaviour……………………………….

  9. 2. GENERALIZED SEIZURES: • Diffuse seizures • Affect BOTH CEREBRAL HEMISPHERES • Types include: • IDIOPATHIC EPILEPSIES: • Age related onset • Also congenital (genetic origin) B. SYMPTOMATIC EPILEPSIES: • Aftermath of a DOCUMENTED UNDERLYING CNS DISORDER C. CRYPTOGENIC EPILEPSY: • Cause unknown • Presumed to be age- related

  10. Manifestations of generalized seizures include: • ABSENCE SEIZURES: • Also known as ‘PETIT MAL’ seizures • Alterations of consciousness, lasting 10-30 mins. Occurs • Associated with: • Staring, with occasional eye-blinking • Enuresis B. MYOCLONIC SEIZURES: • Also known as ‘BILATERAL MASSIVE EPILEPTIC MYOCLONUS’ • Associated with INCVOLUNTARY, RHYTHMIC JERKING of FACIAL, LIMB/ TRUNK MUSCLES C. CLONIC SEIZURES: - Associated with SUSTAINED MUSCLE CONTRACTIONS, alternating with RELAXATION

  11. D. TONIC SEIZURES: • Associated with SUSTAINED MUSCLE CONTRACTIONS (Stiffening) E. GENERALIZED TONIC-CLONIC SEIZURES (GTCS): • Also known as ‘GRAND MAL’ seizures • Causes sudden loss of consciousness • Individual becomes rigid and falls to the ground • Interrupted respirations • Extended legs • Lasts for 1 min. • Rapid bilateral muscle jerking • Heavy salivation, tongue biting, headache, confusion • In some cases, GRAND MAL seizures occurs repeatedly, with no recovery of consciousness between attacks, leading to state known as ‘STATUS EPILEPTICUS’………………..

  12. F. ATONIC SEIZURES: • Also known as ‘DROP ATTACKS’ • Sudden loss of postural tone  individual falls to the ground • Occurs mainly in children…………………………………..

  13.  ETIOLOGY OF EPILEPSY  : Mainly we will see the causes of: • FOCAL SEIZURES • GENERALIZED SEIZURES…………………………..

  14. CAUSES OF FOCAL SEIZURES: Include: • IDIOPATHIC REASONS: • Benign ROLANDIC epilepsy of childhood (Discovered by Italian Anatomist Luigi Rolando) • Benign OCCIPITAL epilepsy of childhood B. GENETIC REASONS: • Tuberous sclerosis (characterized by tiny benign tumours {angiofibromas} on the face, skin, and abnormalities of kidney, brain and heart) • Autosomal dominant frontal lobe epilepsy • Autosomal dominant partial epilepsy with auditory features (ADPEAF) • Von Hippel-Lindau disease (characterized by hemangioblastomas {benign blood vessel tumours } in brain, spinal cord, retina; kidney cysts & cancer and pheochoromocytomas} • Neurofibromatosis (causes tumours to grow on nerves and inhibits neural growth) • Cerebral migration abnormalities

  15. C. INFANTILE HEMIPLEGIA (acute hemiparesis, that occurs in infancy, caused by vascular accidents, like cerebral infarction or thrombosis) D. DYSEMBRYONIC CAUSES: • Cortical dysgenesis • Sturge-Weber syndrome (mainly affects the skin, featured by ‘port wine stain birthmark’; also known as ‘Encephalotrigeminal angiomatosis’) E. MESIAL TEMPORAL SEIZURES: • Associated with febrile convulsions F. CEREBROVASCULAR DISEASES: • Intracerebral hemorrhage • Cerebral infarction • Arteriovenous malformation • Cavernous hemangioma (occurs on body surface, as red or purplish, blood filled lakes/ channels)

  16. G. PRIMARY AND SECONDARY TUMOURS H. TRAUMA (including neurosurgery) • INFECTIVE CAUSES: • Cerebral abscess (pyogenic) - Toxoplasmosis - Cysticercosis - Tuberculoma • Subdural empyema - Encephalitis - HIV infections J. INFLAMMATORY CAUSES: • Sarcoidosis - Vasculitis………………………..

  17. 2. CAUSES OF GENERALIZED SEIZURES : Includes: • GENETICS: • Inborn metabolism errors - Storage diseases - Phacomatoses (Tuberous sclerosis) B. CEREBRAL BIRTH INJURY C. HYDROCEPHALUS D. CEREBRAL ANOXIA E. ALCOHOL WITHDRAWAL F. TOXINS: • Organophosphates (SARIN) • Heavy metals (LEAD, TIN)

  18. G. DRUGS: • ANTIBIOTICS (Penicillin, metronidazole, Isoniazid) • ANTIMALARIALS (Chloroquine, mefloquine) • CYCLOSPORINE • ANTI-ARRRHYTHMICS (Lidocaine, disopyramide) • PSYCHOTROPICS (Phenothiazines, TCAs, Lithium) • AMPHETAMINE WITHDRAWAL H. METABOLIC DISEASE : • Hypocalcemia • Hyponatremia • Hypomagnesemia • Hypoglycemia • Renal failure • Liver failure

  19. INFECTIVE CAUSES: • Post- infective encephalopathy • Meningitis J. INFLAMMATORY CAUSES: • Multiple sclerosis • SLE K. DIFFUSE DEGENERATIVE DISEASES: • Alzheimer’s disease • CREUTZFELDT- JAKOB DISEASE (Degenerative, invariably fatal brain disorder, associated with failing memory ,behaviour changes, weakness of extremities, mental deterioration and coma)……………………………..

  20.  PATHOPHYSIOLOGY OF EPILEPSY  : • Neurons are inter-connected in a complex network • Each individual neuron  linked via synapses with hundreds of others • Neurons  discharge electrical current  neurotransmitters are released at synaptic levels  permits inter- communication • Neurotransmitters are of 2 types: • INHIBITORY NEUROTRANSMITTER (GABA): • GABA (Gamma amino butyric acid )  acts on ion channels  increases chloride inflow  decreases chances of action potential formation b. EXCITATORY NEUROTRANSMITTER ( ASPARTATE, GLUTAMATE): • Above agents  allow sodium and calcium influx  paves way for action potential formation 5. In this manner, information is conveyed, transmitted and processed throughout the CNS 6. Imbalance between above excitation and inhibition  seizures occur

  21. 7. A normal neuron discharges repetitively at LOW BASELINE FREQUENCIES 8. If neurons are damaged, injured/ suffer a chemical/ metabolic insult  changes in discharge pattern develops 9. During epilepsy  regular low frequency discharges are replaced by BURSTS of HIGH FREQUENCY DISCHARGES  followed by periods of INACTIVITY 10. A single neuron discharging in an abnormal manner is usually not clinically significant 11. When a WHOLE POPULATION of NEURONS DISCHARGE SYNCHRONOUSLY in an ABNORMAL MANNER  EPILEPTIC SEIZURE IS PRECIPITATED 12. This abnormal discharge may remain LOCALIZED/ it may SPREAD TO ADJACENT AREAS, RECRUITING MORE NEURONS as it EXPANDS…………………………….

  22.  RISK FACTORS FOR EPILEPSIES  : • Sleep deprivation • Missed doses of anti-epileptic drugs(AEDs) in treated patients • Alcohol withdrawals • Recreational drug misuse • Physical and mental exhaustion • Flickering lights (includes TV, computer screens; comes under generalized epilepsy syndrome) • Intercurrent infections • Metabolic disturbances • UNCOMMON REASONS: • Loud noises • Very hot baths…………………………………

  23.  DIAGNOSIS OF EPILEPSIES  : Based on the following criteriae: • TO CHECK THE LOCATION OF EPILEPTIC ORIGIN: • Standard EEG • Sleep EEG • EEG, with special electrodes 2. TO CHECK FOR STRUCTURAL LESIONS: • CT SCAN - MRI SCAN 3. FOR METABOLIC DISORDER DIAGNOSIS: • Urea and electrolytes - LFTs • Blood glucose levels - Serum calcium and magnesium levels

  24. 4. FOR INFLAMMATORY/ INFECTIVE DISORDER DIAGNOSIS: • CBC - ESR - CRP TEST - CHEST XRAY • SEROLOGY FOR SYPHILIS, HIV, COLLAGEN DISEASE • CSF EXAMINATION 5. FOR CONFIRMING ATTACKS TO BE OF EPILEPTIC ORIGIN: • Ambulatory EEG - Video telemetry 6. BRAIN IMAGING: Indicated for: • Epilepsy starting after 16 yrs. of age • Seizures, with clinical focal features • EEG, showing a focal seizure source • Difficult/ deteriorating seizure control…………………………..

  25.  MANAGEMENT OF EPILEPSY  : • Includes: • GOALS OF THERAPY • GENERAL GUIDELINES FOR ANTICONVULSANT THERAPY • PHARMACOTHERAPY • GUIDELINES FOR CHOICE OF ANTI-EPILEPTIC DRUGS(AEDs) • NON-PHARMACOTHERAPY/ PATIENT- COUNSELLING TIPS+ HOME REMEDIES FOR EPILEPSY

  26.  1. GOALS OF THERAPY  : • To control and reduce SEIZURE FREQUENCY • To focus on MINIMUM POSSIBLE DOSAGE OF AEDs • To minimize ADRs associated with therapy • To ensure PATIENT MEDICATION COMPLIANCE • To ensure that person lives a normal life as far as possible • To balance COMPLETE SUPPRESSION of SEIZURES against ADR TOLERABILITY • To reduce MORBIDITY and MORTALITY • To improve QUALITY OF LIFE(QOL)………………………………..

  27.  2. GENERAL GUIDELINES FOR ANTICONVULSANT THERAPY :  • Start with 1 FIRST LINE DRUG • Start with a low dose  gradually increase dose until effective control of seizures is achieved/ ADRs develop • Optimize compliance (use minimum no. of doses/ day) • If 1st line drug fails (seizures continue/ ADRs develop)  start 2nd (1st line drug) , followed (if possible) , by gradual withdrawal of the drug presently being used • If 2nd line drug fails (due to above reasons)  start 2nd line drug, in combination with preferred 1st line drug at maximum tolerated doses (keep in mind possible interactions) • If above combination fails (due to above reasons)  replace 2nd line drug with alternative 2nd line drug

  28. 7. If above combination fails (due to above reasons)  check compliance & reconsider diagnosis, based on the following criteriae: • If the events are seizures/ not • Presence absence of occult lesions • Treatment compliance/ alcohol/ drugs confounding responses 8. Consider alternative, non-drug treatments, like: • Epilepsy surgery • Vagal nerve stimulation 9. Use minimum number of drugs in combination at any one time………………………….

  29.  3. PHARMACOTHERAPY :  • BARBITURATES : Include: • PHENOBARBITONE (LUMINAL): • Drug has 3 actions: • Drug  depresses sensory, motor cortex and cerebellum • Drug  acts on GABA(A) receptors  increases synaptic inhibition  increases seizure threshold and decreases spread of seizure activity from a seizure focus • Drug  inhibits CALCIUM channels  decreases excitatory transmitter release • ADR : • Sedation c. Headache • Respiratory depression (when given i.v)

  30. DRUG INTERACTION: • Phenobarbital + oral contraceptives  decreased efficacy of latter • USES: • Febrile convulsions (8 mg/kg/day; child) • GTC c. Neonatal seizures d. Status Epilepticus (SE) B. DEOXYBARBITURATES : Includes: • PRIMIDONE (MYSOLINE): • MOA: Drug  enters body  metabolized by liver to PHENOBARBITONE  Shows remaining effects • ADR: • STEVEN-JOHNSON SYNDROME (SJS) • Hypotension • Hepatitis

  31. DRUG INTERACTION: • BZDs + Drug  increased sedation • USES: • GTCS (250-500 mg BD) • Partial epilepsy C. HYDANTOINS : Includes: • PHENYTOIN (BARBITOIN): • Drug has 3 actions: • Drug  promotes sodium efflux/ decreased sodium influx from membranes in motor cortex neurons • Drug  stabilizes neuronal membranes • Drug  slows conduction velocity

  32. ADR: • Gingival hyperplasia • Hirsutism • Megaloblastic anemia • Diabetes mellitus • FETAL HYDANTOIN SYNDROME (Drug  used in pregnancy  causes hare lips, microcephaly in neonates etc) • DRUG INTERACTIONS: • Drug + Pyridoxine(in high dose)  decreased levels of phenytoin • USES: • Tonic clonic seizures • SE (10-15 mg/kg i.v/ infusion)

  33. B. FOSPHENYTOIN (FOSPHEN): • MOA: Drug  converted to PHENYTOIN after injection  shows actions of PHENYTOIN • ADR: • Hypersensitivity b. SJS c. Hepatotoxicity • DRUG INTERACTIONS: • Drug + CBZ(Carbamazepine)  decreased CBZ efficacy • USES: • Seizures, associated with NEUROSURGERY/ HEAD INJURY • SE (20 mg/kg i.v)………….

  34. D. IMINOSTILBENES : Includes: • CARBAMAZEPINE (CARBATOL): • Drug shows 2 actions: • Drug  stabilizes inactivated state of sodium channels  makes neurons less excitable • Drug  decreases activity of NUCLEUS VENTRALIS of thalamus / synaptic transmission associated with neuronal discharge • ADR: a. SJS b. Arrhythmia c. CHF • DRUG INTERACTIONS: • Drug + warfarin  decreased anticoagulant effect • USES : • Trigeminal neuralgia c. Epilepsy (200-400 mg TDS) • Bipolar disorder

  35. B. OXCARBAZEPINE (CARBOX): • Drug shows 5 actions: • Drug  blocks sodium channels  stabilizes neuronal membranes • Drug  inhibits repetitive firing • Drug  reduces synaptic impulse propagation • Drug  increases potassium conductance • Drug  modulates activity of high voltage activated calcium channels • ADR: • SJS b. Hepatitis c. Pancreatitis • DRUG INTERACTION: • Furosemide + drug  increased risk of HYPONATREMIA • USES : a. Partial seizures , with/ without secondary generalization (in adults: 0.6-2.4 g/day, in divided doses)……………………

  36. E. SUCCINIMIDES: Includes: • ETHOSUXIMIDE (ZARONTIN): • Drug shows 2 actions: • Drug  depresses nerve transmission in motor cortex • Drug  increases convulsive stimuli threshold in CNS • ADR: • GI disturbances b. Dizziness • DRUG INTERACTION: • Drug + sodium oxybate  pharmacodynamic synergism  increased toxicity of each other  additive CNS depression • USE: a. Absence seizures : 500 mg P/O QID…………………….

  37. F. ALIPHATIC CARBOXYLIC ACIDS: Includes: • VALPROIC ACID (VALPROL): • Drug shows 3 actions: • Drug  increases GABA levels in brain • Drug  increases / mimics action of GABA at postsynaptic receptor sites • Drug  inhibits sodium and calcium channels • ADR: • SJS b. Pancreatitis c. Thrombocytopenia • DRUG INTERACTION: • Drug + Chlorpromazine  severe HEPATOTOXICITY • USES: • Complex partial seizures (For adults: max. 60 mg/kg/day) • Simple and complex absence seizures…………………..

  38. II. DIVALPROEX (DIVAA): • MOA : Same as that of SODIUM VALPROATE • ADR: • Increased bleeding time • Encephalopathy • Dementia • DRUG INTERACTION : • Drug + cholestyramine  decreased levels of divalproex • USES : • Complex partial seizures (max.: 60 mg/kg/day) • Mania • Migraine prophylaxis • Simple and complex absence seizures………………………………

  39. G. BENZODIAZEPINES : Includes: • CLONAZEPAM (CLONA): • Long acting BZD • Drug shows 3 actions: • Drug  increases presynaptic GABA inhibition • Drug  decreases monosynaptic and polysynaptic reflexes • Drug  facilitates GABA neurotransmission and other inhibitory neurotransmitters  suppresses muscle contractions • ADR: • Blood disorders b. Increased LFTs c. Respiratory depression • DRUG INTERACTION: • Amiodarone + drug  increased drug toxicity

  40. USES: • Panic disorder • Seizure disorders (For adult: up to 1.5 g , in 3 divided doses) • SE II. CLOBAZAM (CLOBA): • 1,5- BENZODIAZEPINE (Contrary to others) • MOA: Drug  binds to GABA(A) receptor  potentiates GABA- ergic neurotransmission • ADR: • Hypotension b. Respiratory depression c. Jaundice - DRUG INTERACTION: • CBZ + Clobazam  decreased drug levels • Alcohol + Clobazam  increased drug levels

  41. III. DIAZEPAM (DIZEP): • Drug shows 2 actions: • Drug  modulates postsynaptic effects of GABA(A) transmission  results in an increase in presynaptic inhibition • Drug  acts on part of limbic system, thalamus and hypothalamus  induces CALMING EFFECT • ADR: • Respiratory depression • Hypotension • Jaundice • DRUG INTERACTION: • Hormonal contraceptives + Drug  increased drug effects  increased incidence of BREATH-THROUGH BLEEDING

  42. USES: • STATUS EPILEPTICUS (Adult: 5-10 mg every 5-10 mins. ; maximum 30 mg.) • Anxiety • Conscious sedation for procedures • Ethanol withdrawal • Insomnia associated with anxiety • Muscle spasm with tetanus • Night terrors • Sedation • Skeletal muscle relaxation • Sleep walking………………………………..

  43. IV. LORAZEPAM (LOPEZ): • Short onset of effect • Long half-life • Drug shows 2 actions: • Drug  increases action of GABA • Drug  depresses all levels of CNS, including lumbar and reticular formation • ADR: • Respiratory depression b. Hypotension c. Jaundice • DRUG INTERACTIONS: • Loxapine + drug  increased respiratory depression • Zidovudine + drug  increased headache

  44. USES: • Antiemetic (adjuvant therapy) • Acute anxiety • Insomnia associated with anxiety • Panic disorder • Pre-operative medication • Sedation • SE (For adult: 4 mg; repeat once after 10 mins, if necessary)………………………..

  45. H. PHENYLTRIAZINES: Includes: LAMOTRIGINE (LAMORIN): • Drug shows 2 actions: • Drug  inhibits release of excitatory amino acids (glutamate) • Drug  inhibits voltage sensitive sodium channels  stabilizes neuronal membranes • ADR: • SJS b. DIC c. Lymphadenopathy • DRUG INTERACTION: • Drug + Phenytoin/Phenobarbital  decreases levels of drug • USES: • Bipolar disorder • GTC( For adult: 25 mg/day for initial 14 days  then increase dose to 50 mg/day for next 14 days  then increase dose to 50-100 mg/day for next 7-14 days)……………………..

  46. CYCLIC GABA ANALOGUES: Includes: • GABAPENTIN (GABAPENTIN): • Structurally related to GABA, but has no effect on GABA binding, uptake/ degradation • MOA: Drug  modulates voltage sensitive calcium channels  decreases entry of calcium into presynaptic neurons  decreases glutamate release  decreases neuronal excitability • ADR : • SJS b. ARF c. Hepatitis • DRUG INTERACTION: • Drug + phenytoin/antacids decreased levels of latter

  47. USES: • Diabetic neuropathy • Focal seizures, with/ without secondary generalization (For child: 12-18 yrs 300 mg TID/ 0.9-3.6g/day ,in 3 divided doses) • Restless legs syndrome • Post- therpetic neuralgia / neuropathic pain……………… B. PREGABALIN (PREGALIN): • Drug shows 2 actions: • Drug  binds to a subunit of voltage gated calcium channels in CNS  remaining same as GABAPENTIN • Does not affect sodium channels • ADR: a. Primary AV block b. CHF c. SJS

  48. DRUG INTERACTIONS: • Drug + Lorazepam/ alcohol  increased efficacy of latter • USES: • Partial seizures, with/ without secondary generalization (50-300 mg/day, in 2-3 divided doses, for adults; maximum: 600 mg/day) • Anxiety • Peripheral and central neuropathic pain • Fibromyalgia……………………………..

  49. J. NEWER DRUGS: Include: I .TOPIRAMATE II.ZONISAMIDE III. LEVETIRACETAM IV. VIGABATRIN V. TIAGABINE VI. LACOSAMIDE VII. FELBAMATE VIII. RUFINAMIDE IX. STIRIPENTOL X. ESLICARBAZEPINE ACETATE XI. PERAMPANEL…………………………………..

  50. TOPIRAMATE (TOPIRATE): • CLASS: SULFAMATE SUBSTITUTED DERIVATIVE • Drug shows 2 actions: • Drug  inhibits neuronal voltage dependent sodium channels • Drug  enhances activity of GABA • ADR: • SJS b. Thrombocytopenia c. Toxic epidermal necrolysis(TEN) • DRUG INTERACTION: a. Zonisamide+ drug  increased risk of renal calculi • USES: • Epilepsy (200-1000 mg/day) • Migraine prophylaxis • Partial seizures……………………………….

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