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EPILEPSY DEPARTMENT OF GENERAL MEDICINE MADURAI MEDICAL COLLEGE DEFINITION CLASSIFICATION ETIOLOGY MECHANISM OF SEIZURES STAGES IN EVOLUTION GTCS SYMPTOMS OF INDIVIDUAL SEIZURE TYPES INVESTIGATION MANAGEMENT SPECIAL CONSIDERATION REFRACTORY / INTRACTABLE SEIZURE IN PREGNANCY AND WOMEN STATUS EPILEPTICUS PSEUDO SEIZURES WHEN TO STOP ANTIEPILEPTICS A seizure is a paroxysmal event due to abnormal excessive or synchronous neuronal activity in the brain. Epilepsy is condition in which a person has recurrent seizures due to chronic underlying process. Convulsion. An intense paroxysm of involuntary repetitive muscular contractions. Seizure (is a generic term) Convulsive seizure or motor seizure. Non convulsive seizure sensory seizure. Psychic seizure. Autonomic seizure. All seizures are not convulsions. Not all convulsions are seizure. CLASSIFICATION OF SEIZURES ILAE CLASSIFICATION (1981) II. Generalized seizures (Convulsive and nonconvulsive) I. Partial (Focal)seizures A. Simple partial seizures B. Complex Partial Seizures C. Partial Seizures evolving to secondary generalized seizures (tonic-clonic, tonic or clonic) A. Absence seizures i) Typical ii) Atypical B. Myoclonic seizures C. Clonic seizures D. Tonic seizures E. Tonic-Clonic seizures F. Atonic seizures (Combinations may occur: myoclonic and atonic or myoclonic and tonic) III. Unclassified epileptic seizures Anatomical site Cortex Temporal Frontal Parietal Occipital Generalised (diencephalon) Multifocal Pathological cause Genetic Developmental Tumours Trauma Vascular Infections Inflammation Metabolic Drugs, alcohol and toxins Degenerative Causes of partial seizures Idiopathic Benign Rolandic epilepsy of childhood • Benign occipital epilepsy of childhood • Focal structural lesions Genetic Tuberous sclerosis von Hippel–Lindau disease Neurofibromatosis Cerebral migration abnormalities infantile hemiplegia Dysembryonic Cortical dysgenesis Sturge–Weber syndrome Mesial temporal sclerosis(associated with febrile convulsions Cerebrovascular disease Intracerebral haemorrhage Cerebral infarction Arteriovenous malformation Cavernous haemangioma Tumours(primary and secondary) Trauma(including neurosurgery) Infective Cerebral abscess (pyogenic) Toxoplasmosis Cysticercosis Tuberculoma Subdural empyema Encephalitis Human immunodeficiency virus (HIV) Inflammatory Sarcoidosis • Vasculitis • Causes of partial seizures Genetic Inborn errors of metabolism Storage diseases Phakomatoses (e.g. tuberous sclerosis,) Cerebral birth injury Hydrocephalus Cerebral anoxia Drugs Antibiotics: penicillin, isoniazid, metronidazole • Antimalarials: chloroquine, mefloquine Ciclosporin • Cardiac anti-arrhythmics: lidocaine, disopyramide • Psychotropic agents: phenothiazines, tricyclic antidepressants, lithium Amphetamines (withdrawal) Alcohol (especially withdrawal) Toxins Heavy metals (lead, tin) • Organophosphates (sarin) • Metabolic disease Hypocalcaemia • Hypoglycaemia • Hyponatraemia • Renal failure • Hypomagnesaemia • Liver failure Infective Meningitis Post-infectious encephalopathy Inflammatory Multiple sclerosis (uncommon) SLE Diffuse degenerative diseases Alzheimer’s disease (uncommonly) Creutzfeldt–Jakob disease (rarely) s The Causes of Seizures and Epilepsy Seizures are a result of a shift in the normal balance of excitation and inhibition within the CNS The normal brain is capable of having a seizure under the appropriate circumstances, and there are differences between individuals in differences between individuals in the susceptibility or threshold for seizures. seizures may be induced by high fevers in children who are otherwise normal and who never develop other neurologic problems, including epilepsy. Normal development also plays an important role, since the brain appears to have different seizure thresholds at different maturational stages There are a variety of conditions that have an extremely high likelihood of resulting in a chronic seizure disorder. severe, penetrating head trauma long-lasting pathologic change in the CNS that transforms a presumably normal neural network into This process is known as epileptogenesis, epileptogenic factors. stroke, infections, and abnormalities of CNS development. Seizures are episodic. completely normal for months or even years between seizures. important provocative or precipitating factors that induce seizures in patients with epilepsy. Precipitants psychological physical stress sleep deprivation hormonal changes associated with the menstrual cycle. exposure to toxic substances and certain medications. These observations emphasize the concept that the many causes of seizures and epilepsy result from a dynamic interplay between endogenous factors, epileptogenic factors, and precipitating factors. Mechanisms of Seizure Initiation and Propagation seizure initiation phase The initiation phase is characterized by two concurrent events in an aggregate of neurons: (1) high-frequency bursts of action potentials and (2) hypersynchronization. The bursting activity is caused by a relatively long-lasting depolarization of the neuronal membrane due to influx of extracellular calcium (Ca2+), which leads to the opening of voltage-dependent sodium (Na+) channels, influx of Na+, and generation of repetitive action potentials. This is followed by a hyperpolarizing afterpotential mediated by ℽ -aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the cell type. seizure propagation phase. Normally, the spread of bursting activity is prevented by intact hyperpolarization and a region of inhibitory neurons. With sufficient activation there is a recruitment of surrounding neurons via a number of synaptic and (1) an increase in extracellular K+, which blunts hyperpolarization and depolarizes neighboring neurons; (2) accumulation of Ca2+ in presynaptic terminals, leading to enhanced neurotransmitter release; and (3) depolarization-induced activation of the N-methyl-D-aspartate (NMDA) subtype of the excitatory amino acid receptor, neuronal activation; (4) ephaptic interactions related to changes in tissue osmolarity and cell swelling. The recruitment of a sufficient number of neurons leads to the propagation of seizure activity into contiguous areas via areas via long commissural pathways such as the corpus callosum Mechanisms intrinsic to the neuron include changes in the conductance of ion channels, response characteristics of membrane receptors, cytoplasmic buffering, second-messenger systems, and protein expression as determined by gene transcription, translation, and posttranslational modification. Mechanisms extrinsic to the neuron include changes in the amount or type of neurotransmitters present at the synapse, modulation of receptors by extracellular ions and other molecules, and temporal and spatial properties of synaptic and non synaptic input. Nonneural cells such as astrocytes and oligodendrocytes, have an important role in many of these mechanisms as well. The basic mechanisms of other precipitating factors of seizures such as sleep deprivation, fever, alcohol withdrawal, hypoxia, and infection, are not as well understood but presumably involve analogous perturbations in neuronal excitability Mechanisms of Action of Antiepileptic Drugs Antiepileptic drugs appear to act primarily by blocking the initiation or spread of seizures. inhibition of Na+-dependent action potentials in a frequency-dependent manner (e.g., phenytoin, carbamazepine, lamotrigine, topiramate, zonisamide, lacosamide, rufinamide inhibition of voltage-gated Ca2+ channels (phenytoin, gabapentin, pregabalin), attenuation of glutamate activity (lamotrigine, topiramate, felbamate), potentiation of GABA receptor function (benzodiazepines and barbiturates), increase in the availability of GABA (valproic acid, gabapentin, tiagabine), and modulation of release of synaptic vesicles (levetiracetam). The two most effective drugs for absence seizures, ethosuximide and valproic acid, probably act by inhibiting T-type Ca2+ channels in thalamic neurons. SIMPLE PARTIAL SEIZURES SIMPLEX PARTIAL SEIZURES No loss of consciousness Symptoms depend on area of brain involved: Motor Sensory Autonomic Psychosensory It can be the introductory phase of a complex partial or generalised tonic- clonic seizure (‘aura’) COMPLEX PARTIAL SEIZURES COMPLEX PARTIAL SEIZURES Origin is most often in the temporal lobe A common seizure type in adulthood Can be introduced by a simplex partial psychosensory seizure: olfactory hallucination déjà vu, jamais vu feeling of alienation Loss of consciousness: stare, ‘going blank’ Automatisms: oral automatisms fiddling with the hands Additional 1. features of partial motor seizures. JACKSONIAN SEIZURE Motor seizure begins in a restricted region such as the fingers and gradually progresses over seconds to minutes to include a larger portion of the extremity. 2. TODDS PARALYSIS. Patients may experience paresis of the involved limb for minutes to many hours following the seizure. 3. EPILEPSIA PARTIALIS CONTINUA. Rarely the seizure may continue for hours to days when it is called epilepsia partialis continua. Often refractory to treatment. 4. VERSIVE SEIZURES A frontal epileptic focus may involve the frontal eye field causing forced deviation of the eyes and sometimes turning of the head to the opposite side. Such seizures often become generalised to a tonic clonic seizure. Somatosensory seizures. Special sensory seizures. PARTIAL SENSORY SEIZURES Focus in the contralateral post rolandic convolution. Sensory seizures described as Numbness Tingling Pins and needles feeling Sensation of crawling (formication) Electric sensation, Sensation of movement of the part. Pain and thermal sensations occur occasionally. SOMATOSENSORY SEIZURES Visual seizures. Rare. Occur as sensation of darkness or flashes of light which may be stationary or moving. May appear colourless or coloured. There may be twinkling or pulsating lights. Visual hallucinations may occur with involvement of occipito-temporal or antero-medial temporal areas. SPECIAL SENSORY SEIZURES Auditory hallucinations. Rare. There may be sensation of buzzing or roaring in the ears or sensation of human voice repeating unrecognisable words. Vertiginous sensations. occur with supero posterior temporal region or parieto temporal region involvement. Olfactory hallucinations. assoc with lesions of inferior and medial parts of temporal lobe usually in the region of parahippocampal convolution or uncus and hence the term uncinate seizures. patient perceives a foul smell Gustatory hallucinations. in temporal lobe disease. salivation and sensation of thirst is present. Vague and often indefinable visceral sensations arising in the thorax, epigastrium and abdomen may occur with temporal lobe focus. COMPLEX PARTIAL SEIZURES OR PSYCHOMOTOR SEIZURES OR TEMPORAL LOBE SEIZURES. These patients have Aura- in the form of a simple focal seizure or a hallucination or illusion suggestive of a temporal lobe origin. have a period of altered behavior, altered consciousness and amnesia to the event. Psychic experiences which occur in complex partial seizures. 1. Sensory illusions and distortions Micropsia and macropsia- objects and persons in the environment appear to shrink or recede into distance or may enlarge 2. Hallucinations. visual and auditory common. Olfactory and gustatory rare. 3. Dyscognitive states. Dejavu- feelings of increased familiarity. Jamais vu- feelings of strangeness or unfamiliarity. Feeling of depersonalisation. Sudden interruption in memory. Fragments of old memories and scenes appear in patients mind and recur with striking clarity. 4. Emotional experiences. Less commonly observed. sadness,loneliness,anger,happiness,sexual excitement. Fear and anxiety-most common affective experiences. Sense of rage and intense anger. 3. Dyscognitive states. Dejavu- feelings of increased familiarity. Jamais vu- feelings of strangeness or unfamiliarity. Feeling of depersonalisation. Sudden interruption in memory. Fragments of old memories and scenes appear in patients mind and recur with striking clarity. AUTOMATISMS - occur in the form of Lipsmacking Chewing Swallowing Fumbling of hands Shuffling of feet Inappropriate acts. OTHER AUTOMATISMS. Gelastic epilepsy — laughter may be the most striking feature of an automatism. Volvular epilepsy—patient may walk repititively in small circles. Epilepsia procursiva—runs repititively. Poriomania—wanders aimlessly as an ictal or postictal phenomenon. During the episode, patient is not in contact with his surroundings. Patient is typically confused following the seizure. May take seconds to an hour for full recovery of consciousness. Postictally patient may show anterograde amnesia or aphasia (if dominant hemisphere) Interictal EEG is often normal or may show brief epileptiform spikes or sharo waves. Since CP seizures can arise from the medial temporal lobe or inferior lobe which are distant from the scalp, EEG during seizure may be non localising but detected using sphenoidal or surgically placed intracranial electrodes CP seizures can occur at any age. Usually seen in adolescence and adults. H/o febrile seizures in childhood is often present. 2/3rds of CP seizure pts have GTC seizures. Cp seizure pts may show - features of Depressive illness Psychotic symptoms Paranoid delusional state and Abnormalities of behaviour and Personality during interictal period. TONIC-CLONIC SEIZURES GENERALISED TONIC-CLONIC SEIZURE (GRAND MAL) The most common seizure Acute symptomatic seizures are generalised tonic-clonic seizures Course: Cry, loss of consciousness, fall Tonic phase- generalised muscle contraction, apnoea Clonic phase- rhythmic contraction of muscles, tongue bite, foaming, enuresis Terminal sleep and gradual regaining of consciousness (transient confusion) ABSENCE SEIZURES ABSENCE Cognitive dysfunction with a sudden onset and end, lasting 5- 10 seconds Stare, expressionless face; arrest of ongoing activity; generally no motor phenomena EEG: generalised 3 Hz spike and wave activity Occurs in genetic (idiopathic) epilepsies, mostly in children Absence seizures may be accompanied by rapid blinking movements, chewing, or clonic movements of the hands. Begin in childhood (4-8 yrs age) or early adolescence. Main seizure type in 15-20% of children with epilepsy. May occur 100 times a day (pykno epilepsy) May manifest as unexplained day dreaming or poor performance. EEG-typically reveals characteristic generalised 3 -Hz/sec spike and wave discharges. Respond well to treatment. About 60—70% usually have a spontaneous remission during adolesence. May be associated with GTC seizures. ATYPICAL ABSENCE SEIZURES LOC may be longer. Focal motor signs may be present. EEG not characteristic and may show generalised slow spike and wave pattern with a frequency of about 2.5Hz/sec. Often associated with diffuse structural abnormalities of the brain and patients may have neurologic dysfunction like mental retardation. Less responsive to treatment. ATONIC SEIZURE ATONIC SEIZURES Sudden loss of muscle tone lasting 1—2 secs Brief impairment of consciousness. No post ictal confusion. EEG reveals brief generalised spike and wave discharges followed immediately by diffuse slow waves that correlate with loss of muscle tone. Usually seen in association with known epileptic syndromes. MYCLONIC SEIZURES MYOCLONIC SEIZURE Sudden, quick, arrhythmic muscle contraction, twitch of a limb; no loss of consciousness EEG: generalised polyspike and wave activity Occurs in genetic (idiopathic) epilepsies Not only an epileptic phenomenon- it can be the sign of diffuse encephalopathies CLINICAL PRESENTATIONS Myoclonic seizures Abrupt , very brief, involuntery flexion movements. Involve whole body or part of the body Occur most commonly at morning, shortly after walking. May occur in healthy people (physiological) Atonic Seizures Brief loss of muscle tone. Heavy fall , with or without loss of consciousness. Versive seizures A frontal epileptic foci may involve the frontal eye field. Force deviation of the eyes and turning head to the opposite side. Status Epilepticus Series of recurrent Tonic-Clonic seizures occurs without regaining consciousness over 30 min. Catamenial epilepsy: Epileptic women experienced that their seizures worsen during menstruation; due to the imbalance between the proconvulsant estrogen and anticonvulsant progestogen DIFFERENTIAL DIAGNOSIS Condition mimicking Seizures: True Seizure Vs Pseudoseizure Features & Lab findings True Seizure Pseudoseizure 1. Pseudoseizure Resemble known seizure types Yes No 2. Syncope Tongue bite Yes No 3. Some sleep disorders Duration Short Long 4. Hypoperfusion in brain Post-Ictal Phenomena Present Absent 5. Cardiac Arrhythmia Injury Yes No 6. Emotional Outburst Occurs during sleep Yes No 7. Dissociative fugue Can be precipitated by suggestion No Yes 8. Drop Attacks EEG during attack Abnormal No Change 9. Migraine EEG after attack No Change 10. Hypoglycaemia Slowing pattern Serum prolactin (after attack) Raised No change Anti Epileptic drug usage Suppress seizures No Change (may worsen) EPILEPTIC SEIZURE VERSUS SYNCOPE Syncope Tonic-clonic seizure Position Upright Any Facial colour Paleness Cyanosis Onset Gradual; introduced by dizziness, blurring of vision Sudden; can start by ‘aura’ (simplex partial seizure) Twitchings Rarely (‘convulsive syncope’) Always Enuresis Rarely Often Tongue bite No Often Duration 10-20 seconds Few minutes Postictal confusion No Yes Perspiration Pronounced Not typical DIAGNOSIS OF EPILEPSY Thorough History taking : From patients From reliable valid informants From observer (who observed seizures) Physical Examination: Specially neurological system Higher Psychic function Laboratory Investigation: S. Electrolytes, S. Prolactin, Blood sugar, CBC, TFT, LFT, RFT, CSF study Imaging: EEG, Video EEG telemetry, CT Scan of Brain, MRI of Brain, MRS, PET, SPECT. Polysomnography MANAGEMENT OF EPILEPSY Medical treatment: Immediate care of seizures Move persons away from danger Recovery position (semi prone) Ensure clear airway Do not insert anything into mouth Urgent medical attention- (patent airway, O2 , Should not be left alone after recovery Consider about regular AED Surgical treatment: Indicated when seizures shown to be intractable to medical treatment. Removal of epileptic focus (eg:mesial temporal sclerosis) Anterior Temporal Lobectomy Corpus callostomy Subpial transection Vagus Nerve stimulation Ketogenic diet anticonvulsant, investigate cause) GUIDELINES FOR ANTICONVULSANT THERAPY Start with one first line drugs Start with low dose: Gradually increase to effective dose or until side effects. Check compliance If first drug fails due to side effects or continue seizures, start second line drugs whilst gradually withdrawing first. Try Three AED singly before using combinations Beware about drug interactions Do not use more than two drugs in combination at any one time If above fails consider occult structural or metabolic lesion and whether seizures are truly epileptic. CHOICE OF ANTI EPILEPTIC DRUGS Epilepsy Type Partial and /or Secondary GTCS First-Line Second-Line Third-Line Carbamazepine Lamotrigine Oxcarbazepine Topiramate S. Valporate(in children) S. Valporate Tiagabine Gabapentin Clobazum Phynytoin Phenobarbital Vigabatrin Acetazolamide Primary GTCS S. Valporate Lamotrigine Topiramate Carbamazepine Phynytoin Gabapentin Phenobarbital Tiagabine Acetazolamide Absence S. Valporate Lamotrigine Ethosuximide Clonazepum Acetazolamide Myoclonic S. Valporate Clonazepum Piracetam Lamotrigine Phenobarbital PHARMACOLOGY OF AEDS II. Steady state Phenytoin Phenobarbital Binding to plasma proteins 7-20 days 10-30 Primidon 2-5 Valproate 2-5 Carbamazepine 3-5 Ethosuximid 7-12 Clobazam 4-5 Lamotrigine 3-10 Topiramate 3-6 Gabapentin 2-5 Vigabatrin 2-5 Pronounced (>90%) binding phenytoin valproate Moderate (30-80%) binding carbamazepine clobazam lamotrigine No or minimal (<20%) binding gabapentin vigabatrin topiramate ethosuximid When do we start antiepileptic medication (AED)? Which AED to choose? When and how do we switch AEDs? When is polytherapy needed? When can AEDs be discontinued? Pregnancy Driver’s licence MEDICAL TREATMENT OF EPILEPSY More than one non-provoked, well-documented seizure AEDs are usually not started after the first seizure (needs individual assessment) WHEN DO WE START TREATMENT? Preventive treatment is not justified MECHANISM OF ACTION OF AEDS Inhibition of voltage gated Na, Ca channels Na: phenytoin, carbamazepine, oxcarbazepine, lamotrigine, topiramate, felbamate, zonisamide Ca: ethosuximid, valproate? lamotrigine, topiramate, zonisamide Potentiaton of GABA mediated inhibition phenobarbital, benzodiazepins, vigabatrin, tiagabine, topiramate, valproate, gabapentin, felbamate Decrease of glutamate mediated felbamate, topiramate excitation EFFICACY OF AEDS All seizure types: absence, myoclonic, generalised tonicclonic seizures, partial seizures valproate, lamotrigine, topiramate clobazam, clonazepam phenobarbital, primidon felbamate levatiracetam, zonisamide Partial seizures, generalised tonic-clonic seizures carbamazepine, oxcarbazepine gabapentin, vigabatrin, tiagabine phenytoin Absence ethosuximid PHARMACOLOGY OF AEDS I. Hepatic metabolism valproate, carbamazepine, oxcarbazepine, lamotrigine, topiramate, clobazam, clonazepam, phenobarbital, primidon, phenytoin, ethosuximid, felbamate, tiagabin No metabolism gabapentin, vigabatrin (topiramate, levatiracetam) Hepatic enzyme induction carbamazepine, phenytoin, phenobarbital, primidon (oxcarbazepine) Hepatic enzyme inhibition valproate, felbamate Inadequate dose → dose escalation Lack of compliance → measure blood AED levels False diagnosis: the patient doesn’t have epilepsy ‘Pseudoseizures’ → precise description of seizure, EEG / video monitoring Inadequate selection of AED True inefficacy of AED → AED switch Other AED on monotherapy AED combination POSSIBLE CAUSES OF AED INEFFICACY Partial epilepsies Juvenile myoclonic epilepsy First AED in monotherapy: 43% Second AED in monotherapy: 7% Other monotherapies: 2% First AED (valproate) in monotherapy: 85% AED combination: 5% Total in remission: 57% THERAPEUTIC SUCCESSREMISSION RATES Altogether 65-70% of patients with epilepsy respond well to AED treatment. Teratogenic In normal population: 2-3% In women on AEDs: 4-9% Teratogenic risk risk is increased High AED dose Fluctuating plasma levels Polytherapy Occurrence of spina bifida in the family Folic acid deficiency EPILEPSY AND PREGNANCY Before conception: Attain the best possible seizure control with the lowest possible AED dose, preferably in monotherapy Folic acid profilaction 4 mg/day During pregnancy: During first trimester supplement folic acid 4 mg/nap Change medication only if seizure control worsens Screening of fetal malformations (ultrasound on week 16 and 20, AFP) In case of enzyme inductor AEDs, give vitamin K in the third trimester EPILEPSY AND PREGNANCY: WHAT TO DO? Breast feeding is not contraindicated with women on AEDs. Sleep deprivation can provoke seizures. EPILEPSY AND BREAST FEEDING Driving is prohibited for one year after a seizure with loss of consciousness Driving 2-3 is permitted: years of seizure free interval with patients on AEDs 2-3 years of seizure free interval after withdrawal of AEDs EPILEPSY AND DRIVING AED: INDICATIONS AND DOSAGE AED Seizure type Dose Doses Therapeutic range per day range (mg/day) (μmol/L) 250-2000 2-3 30-50 Carbamazepine Partial,Secondary GTCS, Sodium Valporate Primary & Secondary GTCS, Absence, Myoclonus 400-2500 1-2 NA Phenytoin Partial, Secondary GTCS 150-350 1 40-80 Lamotrigine Lorazepum Clonazepum 25-500 4 i.v. 1-8 1-2 -2-4 NA NA NA Ethosuximide Partial, secondary GTCS Status Epilepticus Partial (adjunctive), Myoclonus Childhood Abssence 500-1500 2 200-700 Topiramate Partial, secondary GTCS 200-600 1-2 NA Phenobarbital Partial, secondary GTCS 60-100 1 50-150 AED: SIDE EFFECTS AED Side Effects Neurological Sodium Valporate Carbamazepine Phenobarbital Topiramate Phenytoin Ataxia, Nystagmus, Diplopia, Tremor Ataxia, Nystagmus, Diplopia Ataxia, Nystagmus, Diplopia Neuropathy Ataxia Ataxia, Nystagmus, Diplopia, Tremor, Dystonia, Asterixis Neuropathy Cognitive & behavioral Drowsiness Drowsiness Drowsiness Drowsiness Dermatological Rashes, Alopecia Rashes, SJS, Rashes Confusion Drowsiness ---- Hematological Blood dyscrasias Megalobastic Anaemia, Osteomalacia ---- Blood dyscrasias Osteomalacia Endocrine Hepatology & Kidney Pancreatitis Liver damage Blood Dyscrasias, Thrombo-cytopenia ------- ------- ---Nephro-lithiasis ---Liver damage Others Nausea, Weight Gain Hyponatremia Foliate deficiency, Depression (adults), Excitement (Children), SLE SLE Facial Dysmorphism Foliate deficiency Drug Interactions Other AEDs, Antimalarials Other AEDs, OCP, Antimalarials, Corticosteroids Other AEDs, CCB,OCP, Digoxin, Antidepressant, Antimalarials Nausea, depression, Taste alteration, Weight loss Other AEDs, OCP Rashes, Hirsutism, Gum Hypertrophy, Other AEDs, OCP, Anti Arrythmic, Antimalarials, Corticosteroids Thyroxine WITHDRAWAL OF AED After complete control of seizures for 2-4 years, withdrawal of Anti Epileptic drugs may be considered. But in case of special professional group (car driver, machine man etc) withdraw the AED after keen follow-up. AED should be tapered during the stopping of medications. Slow reduction by increments over at least 6 months. If the patient is taking two AEDs one drug should be slowly withdrawn before the second is tapered. PROGNOSIS Generalized seizures are more readily controlled than partial seizures. Childhood onset epilepsy (particularly classical absence seizures) carries the best prognosis for successful drug withdrawal. The presence of a structural lesion makes complete control of epilepsy less likely. Epilepsy outcome: After 20 years 50% seizure-free, without drugs, for last 5 years 20% seizure-free, continue to take medication, for last 5 years 30% seizures continue in spite of adequate dose of AEDs. Refractory epilepsy: When seizure control is not achieved with the first two appropriate and well tolerated AED schedules taken PSYCHIATRIC COMORBIDITIES IN EPILEPSY Mood variation: Nearly 1 in 3 patients of epilepsy report significant concern about their mood. Depression: Upto 55% prevalent in patients with epilepsy. Suicide rate: In depressed patients with epilepsy is 5 times higher than that in the general population and 25 times higher in patients with complex partial seizures of temporal lobe origin. Anxiety : Upto 50% prevalent in patients with epilepsy. Psychosis: Incidence of Psychosis 3.3% in patients with idiopathic generalized epilepsy, 14% in Temporal lobe epilepsy. In the concern of severity; Psychosis occurs in 0.6-0.7% patients with epilepsy in community and 19-27% of epilepsy patients who require hospitalization.