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Epilepsy management
- 1. Approach and ManagementOutline of Epilepsy Presented by Dr. Ashish Chowdhury MD, Phase- B Resident Department of Neurology, BSMMU
- 2. Core components Approach History Physical examination Investigations Management outline Non pharmacological Pharmacological Surgical Others
- 3. History History regarding seizure Whether the episode in question is a seizure History is the key From a witness Type and duration of bodily movements When and where Level of alertness and responsiveness during and immediately after the episode Skin color and breathing Tongue biting and Incontinence Postictal period If a witness is not available, then a telephone call to observers may give more information than does sophisticated laboratory testing
- 4. History History regarding seizure From patient Recollection of event of the immediately preceding episode Previous H/O seizure
- 5. History History regarding seizuretypes Generalized or focal If generalized Convulsive or Non convulsive If focal Consciousness impaired or not
- 6. History History regarding subjectivepsychic state Aura – stereotypic perceptual disturbances experienced by patient preceding seizure Illusions Hallucinations Visual, Auditory, Olfactory, Somatosensory, Gustatory, Vertiginous, Visceral-autonomic Depersonalization states Affective experiences Each of these subjective psychic states may constitute the entire seizure or some combination may occur and immediately precedes a period of altered awareness
- 7. History History regarding Autmatism More or less coordinated motor activity Occurring when cognition is impaired For which the subject is usually (not always) amnesic afterward may consist of an inappropriate continuation of preictal motor activity Signifies focal temporal lobe or limbic seizure lip-smacking, chewing or swallowing movements salivation, fumbling of the hands or shuffling of the feet Patients may walk around in a daze or act inappropriately (undressing in public, speaking incoherently, etc.)
- 8. History Predisposing factor Historyof febrile seizures Family history of seizures Genetic disorder Epileptogenic factors Prior head trauma Stroke Tumor CNS infection In children – Birth history, Developmental history
- 9. History Precipitating factors Sleepdeprivation Missed doses of anti-epileptic drugs in treated patients Systemic diseases Electrolyte or metabolic derangements Acute infection Drugs that lower the seizure threshold Alcohol or illicit drug use
- 10. Drugs causing orlowering threshold of seizure
- 11. Physical examination General examination Pulse (rate/rhythm), BP (/ , postural), temp Signs of trauma/ scar mark, tongue- bite Facial haemangioma, neurofibromatosis, adenoma sebaceum
- 12. Physical examination Neurological examination Eliciting signs of cerebral hemispheric disease Careful assessment of mental status (including memory, language function, and abstract thinking) may suggest lesions in the anterior frontal, parietal, or temporal lobes Testing of visual fields will help screen for lesions in the optic pathways and occipital lobes Screening tests of motor function such as pronator drift, deep tendon reflexes, gait, and coordination may suggest lesions in motor (frontal) cortex Cortical sensory testing (e.g., double simultaneous stimulation) may detect lesions in the parietal cortex.
- 13. Differentials Syncope Pseudoseizure Panic attack Cardiac arrhythmias TIA Migraine Hypoglycemia Episodic confusion Cataplexy Narcolepsy
- 14. Differentials Epileptic Seizure Pseudoseizure Onset Sudden Anywhere Any time even at Sleep Gradual In front of attendance Not at sleep Sex Any W : M = 3 : 1 Consciousness Altered in GTCS Retained Tongue bite Dribbling of Saliva from angle of mouth Common (At lateral border) Common Uncommon (At tip) Uncommon Urinary and Bowel incontinence May present Uncommon Pelvic Thrusting Rare Common Asynchronous Thrashing limbs Rare Common Rolling over bed Uncommon Common Cyanosis Common Rare Injury Common Rare Duration Sec. to Min ( <5min) Min to Hours Resistance to eye opening & limb movement Unusual Common Hand falling on face Common Unusual Pupil Dilated Normal H/O Sexual exploitation/deprivation Unusual Usual Induced by suggestion Rare Often Post-ictal symptoms Usual Absent EEG Abnormal Normal Serum Prolactin High Normal
- 15.
- 16. Differentials Cardiac arrhythmias Completeheart block (adams- strokes syndrome ), prolonged arrest or critical reduction in heart rate may lead to loss of consciousness- tonic/clonic jerks, cyanosis # Do ECG urgently, if necessary 24 hours ECG monitoring. Severe hypoglycemia Intermittent behavior change or GTCS may occur along with palpitation & sweating (↑catecholamine) estimate blood Sugar urgently.
- 17. Differentials Migraine Classical migrainewith visual or somatosensory aura & basilar migraine Occipital lobe seizures may be followed by a migraine-like headache . The aura in migraine typically lasts 5 to 60 minutes , epileptic auras are usually less than 30 seconds Visual aura in migraine is most commonly a fortification spectrum or scintillating scotoma, whereas colored circles are the most common aura in occipital lobe seizures Basilar migraine starts with brainstem manifestations
- 18. Management Patient education Treatment of underlying conditions Avoidance of precipitating factors Antiepileptic medications or surgery Addressing a variety of psychological and social issues
- 20. Education of Patient& relatives Common disorder Causes and nature of disease 1st aid management of seizure Patient can perform normal work & Social life Avoid Activities / Places increase risk of seizure Occupation Medications Compliance Regular Follow up
- 21. Management Treatment of underlyingconditions Correction of abnormal serum electrolytes or glucose Avoidance of drugs causing seizure Treatment of structural CNS lesion such as a brain tumor, vascular malformation, or brain abscess
- 22. Management Avoidance of precipitatingfactors Optimize sleep quality Modification of drinking habit Avoidance of stimuli for ‘Reflex epilepsy’ Stress relaxation – Physical exercise, meditation, counselling
- 23. Management Pharmacological therapy Whento Initiate Antiepileptic Drug Therapy Selection of Antiepileptic Drugs Initiation and monitoring of drug therapy When to discontinue therapy
- 24. Management Pharmacological therapy When toInitiate Antiepileptic Drug Therapy Antiepileptic drug therapy should be started in any patient with recurrent seizures of unknown etiology or a known cause that cannot be reversed Single seizure with Structural CNS lesion – Tumour, trauma, infection Abnormal neurologic examination Seizures presenting as status epilepticus Postictal Todd’s paralysis Strong family history of seizures Abnormal EEG
- 25. Management Pharmacological therapy Selectionof Antiepileptic Drugs Seizure type Epilepsy syndrome Efficacy Cost Pharmacokinetic profile Adverse effects Patient’s related medical condition
- 26. Antiepileptic drugs A. Classical •Phenytoin • Phenobarbital • Carbamazepine • Valproate • Ethosuximide • Primidone B. Newer • Lamotrigine • Levetiracetam • Oxcarbazepine • Topiramate • Gabapentin • Felbamate • Tiagabine • Vigabatrine • Zonisamide • Rufinamide
- 27. Antiepileptic drugs…….. 1. sodiumchannel blocker: • Valproate • Phenytoin • Phenobarbital • Carbamazepine • Oxcarbazepine • Gabapentin • Lamotrigine • Topiramate 2. Calcium channel blocker: • Ethosuximde • Zonisamide • Phenobarbital
- 28. Antiepileptic drugs……. 3. Drugsthat potentiate GABA • Phenobarbital • Diazepam • Clonazepam • Lorazepam • Valproate • Gabapentin • Vigabatrin • Tiagabine
- 29. Common strategies ofaction of AEDs • Modification of ion conductancs • Increase inhibitory (GABA nergic)transmission • Decrease excitatory( glutamtergic) activity • Inhibit repetitive excitatory neuronal firing
- 30. AEDs…… DRUGS ADULT CHILD mg/kg S/E Valproicacid 1000-3000 30-60 Ataxia,tremor,sedation,weight gain,thrombocytopenia,transient alopecia,hyperammonemia Carbamazepine 600-1200 20-30 SJS;ataxia,dizziness,diplopia,aplastic anemia;leukopenia,hepatotoxicity,hypon atremia Levetiracetam 500-3000 20-60 Sedation,fatigue,ataxia,mood change,anemia,leukopenia Oxcarbazepine 900-2400 10-40 Like CBZ
- 31. AEDs….. Phenytoin 300- 400 4-7 Ataxia,dizziness,diplopia,confusion,gum hypertrophy,lymphadenopathy,hirsutism ,osteomalacia,facialcoarsening,rash Phenobarbital 90-200 3-5 Ataxia,dizziness,sedation,confusion,depression,decrea se libido,rash Lamotrigine 300- 500 0.5 Ataxia,dizziness,diplopia,sedation,headache skin rash,SJS Clonzepum 2-10 0.01- 0.2 sedation, dizziness, cognitive impairment ACTH 40-60 U/d HTN
- 33. Adverse Effects ofAEDs: Common Typically dose-related: Dizziness , Fatigue , Ataxia, Diplopia all AEDs Irritability levetiracetam Word-finding difficulty topiramate Weight loss/anorexia topiramate, zonisamide, felbamate Weight gain valproate (also associated with polycystic ovarian syndrome ) carbamazepine, gabapentin, pregabalin C-Slide 33American Epilepsy Society 2010
- 34. Adverse Effects ofAEDs: Serious Typically Idiosyncratic: Rash –SJS,TEN Carbamazepine ,Phenytoin, lamotrigine, zonisamide, Renal stones Topiramate, zonisamide Anhydrosis, heat stroke Topiramate Acute closed-angle glaucoma Topiramate C-Slide 34American Epilepsy Society 2010
- 35. Adverse Effects ofAEDs: Serious Typically Idiosyncratic: Aplastic anemia felbamate, zonisamide, valproate, carbamazepine Hepatic Failure valproate, felbamate, lamotrigine, phenobarbital Peripheral vision loss vigabatrin Hyponatremia carbamazepine, oxcarbazepine C-Slide 35American Epilepsy Society 2010
- 36. Antiepileptic Drug Interactions AEDs that may induce metabolism of other drugs: Carbamazepine (auto induction), phenytoin, phenobarbital, primidone AEDs that inhibit metabolism of other drugs: valproate, felbamate AEDs that are highly protein bound: valproate, phenytoin, tiagabine, carbamazepine, oxcarbazepine topiramate is moderately protein bound Other drugs may alter metabolism or protein binding of AED (especially antibiotics, chemotherapeutic agents & antidepressants)
- 37. Management Pharmacological therapy Selectionof Antiepileptic Drugs
- 38. Epilepsy syndromes Childhood absenceValproate, ethosuximide, levetiracetam Juvenile myoclonic Valproate, levetiracetam GTCS on awakenig Valproate, levetiracetam Infantile spasm/west syndrome ACTH, Vigabatrine, valproate, clonazepam. Lennox- Gastaut syndrome Valproate, topiramate, lamotrigine,clonazepam, felbamate, rufinamide Benine epilepsy with centrotemporal spikes Valproate, carbamazepine, oxcarbazepine,lamotrigine,levetiracetam Reflex epilepsy Clonazepam, valproate, carbamazepine, and phenytoin (as well as many of the new antiepileptic drugs)
- 39. Management Pharmacological therapy Initiationand monitoring of drug therapy Start with one first-line drug Start at a low dose; gradually increase dose until effective control of seizures is achieved or side-effects develop (drug levels may be helpful) Optimize compliance (use minimum number of doses per day) If first drug fails (seizures continue or side-effects develop), start second first-line drug, followed if possible by gradual withdrawal of first If second drug fails (seizures continue or side-effects develop), start second-line drug in combination with preferred first-line drug at maximum tolerated dose (beware interactions)
- 40. Management Pharmacological therapy Initiationand monitoring of drug therapy If this combination fails (seizures continue or side-effects develop), replace second-line drug with alternative second-line drug If this combination fails, check compliance and reconsider diagnosis (Are events seizures? Occult lesion? Treatment compliance/alcohol/drugs confounding response?) Consider alternative, non-drug treatments (e.g. epilepsy surgery, vagal nerve stimulation) Use minimum number of drugs in combination at any one time
- 41. Management Pharmacological therapy Initiation andmonitoring of drug therapy Monitoring of side effect profile Therapeutic level
- 42. Management Pharmacological therapy Whento discontinue therapy About 50–60% of patients who have their seizures completely controlled with antiepileptic drugs can eventually discontinue therapy Patients with following profile have greatest chance of remaining seizure free after drug withdrawal Complete medical control of seizures for 1–5 years Single seizure type, with generalized seizures having a better prognosis than focal seizures Normal neurologic examination, including intelligence No family history of epilepsy Normal EEG.
- 43. Management Pharmacological therapy When todiscontinue therapy It seems reasonable to attempt withdrawal of therapy after 2 years in a patient who meets all of the criteria Patient should be educated about risk of recurrence and potential benefit It is preferable to reduce the dose of the drug gradually over 2–3 months
- 44. Management Surgical therapy 20–30%of patients with epilepsy continue to have seizures despite efforts to find an effective combination of antiepileptic drugs Surgery can be very effective in this scenario Potentially curative Temporal lobectomy Extra temporal resection Hemispherectomy Palliative Partial resection of epileptogenic region Disconnection procedure to prevent seizure spread Corpus callosotomy Multiple subpial transections
- 45. Management Surgical therapy Complicationsof surgery are <5% 70% of patients treated with temporal lobectomy will become seizure free, and another 15–25% will have at least a 90% reduction in seizure frequency
- 46. Management Other therapy Vagusnerve stimulation Ketogenic diet Alternative diet
- 47. Management Other therapy Vagus nervestimulation Intermittent programmed electrical stimulation of left vagus nerve Clinical trials show that 35% of patients have a 50% reduction in seizure frequency and 20% experience a 75% reduction after 18 months of therapy FDA approved for refractory partial onset seizures and refractory depression
- 48. Management Other therapy Ketogenicdiet Main experience with children, with multiple seizure types Low carbohydrate, adequate protein, high fat 50% with a >50% seizure reduction, 30% with >90% reduction Side effects include kidney stones, weight loss, acidosis, dyslipidemia
- 49. Management Other therapy Alternative diet Modified Atkins diet • 10 g/day carbohydrates to start, fats encouraged • No protein, calorie, fluid restriction Low-glycemic index treatment • 40-60 g/day low-glycemic carbohydrates • Portions generally controlled
- 50. Upcoming modalities Stereotacticradiosurgery Laser thermoablation Deep brain stimulation (DBS)
- 51. • Status epilepticusrefers to continuous seizures or repetitive, discrete seizures with impaired consciousness in the interictal period. • The duration of seizure activity 15–30 min Harrison’s Neurology in Clinical Medicine,2nd ed.
- 52. Classification of SE TheTreiman classification is as follows: • Generalized convulsive status epilepticus • Subtle status epilepticus • Nonconvulsive status epilepticus (eg, absence, complex partial) • Simple partial status epilepticus
- 53. Management of convulsivestatus epilepticus
- 54. Initial • Ensure airwayis patent; give oxygen to prevent cerebral hypoxia • Check pulse, blood pressure and respiratory rate • Secure intravenous access • Send blood for: Glucose, urea electrolytes, calcium magnesium, liver function anti-epileptic drug levels Full blood count and clotting screen Storing a sample for future analysis (e.g. drug misuse)
- 55. • If seizurescontinue for > 5 mins: give diazepam 10 mg IV (or rectally) or lorazepam 4 mg IV; repeat once only after 15 mins • • Correct any metabolic trigger, e.g. hypoglycaemia Davidson’s Principle and Practice of Medicine;23rd ed.
- 56. Cont. If seizures continueafter 30 mins • IV infusion (with cardiac monitoring) with one of: Phenytoin: 15 mg/kg at 50 mg/min Fosphenytoin: 15 mg/kg at 100 mg/min Phenobarbital: 10 mg/kg at 100 mg/min • Cardiac monitor and pulse oximetry Monitor neurological condition, Blood pressure, Respiration Check Blood Gases
- 57. If seizures stillcontinue after 30–60 mins • Transfer to intensive care • Start treatment for refractory status with intubation, ventilation and general anaesthesia using propofol or thiopental EEG monitor
- 58. Once status controlled •Commence longer-term anticonvulsant medication with one of: • Sodium valproate 10 mg/kg IV over 3–5 mins, then 800–2000 mg/day • Phenytoin: give loading dose (if not already used as above) of 15 mg/kg, infuse at < 50 mg/min, then 300 mg/day • Carbamazepine 400 mg by nasogastric tube, then 400–1200 mg/day • Investigate cause • Mortality-20-30%
- 59. AEDs in specialsituations Contraception • Some AEDs induce hepatic enzymes that metabolise synthetic hormones, increasing the risk of contraceptive failure. • This is most marked with carbamazepine, phenytoin and barbiturates, • Clinically significant effects can be seen with lamotrigine and topiramate. • If the AED cannot be changed-High dose OCP • Sodium valproate and levetiracetam have no interaction with hormonal contraception.
- 60. Epilepsy & pregnancy 1.Preconceptioncounselling: regarding • seizure frequency, risk of fetal malformations,low IQ of baby • Seizure requency during pregnancy will remain unchanged in ~50% of women, increase in 30%, and decrease in 20%. • The overall incidence of fetal abnormalities in children born to mothers with epilepsy is 5–6%, compared to 2–3% in healthy women • Control seizure with drugs with lowest incidence of fetal malformation like CBZ, Lamotrigine. • The risk with Sodium valproate is higher. For some women, however, the type and frequency of their seizures may allow or them to safely wean o antiepileptic drugs prior to conception • Start folic acid 5mg/d for 2 months before conception
- 61. Condt… 2. During pregnancy: •It is currently recommended that pregnant women be maintained on effective drug therapy. • When possible, it seems prudent to have the patient on monotherapy at the lowest effective dose, especially during the 1st trimester. • Continue folic acid • Regular follow up :seizure control, serum antiepileptic drug level, screening for fetal anomalies • Give oral vit-k 20 mg daily to mother during the last month of Pg. At least last 2 wks or I/V vit-k 4 hr before birth.
- 62. Contd…. 3. After birth:Give vit-k injection 1mg I/M to infant 4. Breast feeding: • safe for the baby during breast-feeding in that only small amounts are excreted in lactated milk. • For example, carbamazepine in human milk is found to be 40 percent of the mother 's serum concentration which results in a neonatal blood level that is below the conventionally detectable amount. Phenytoin is excreted at15 percent of maternal serum concentration, and valproate, being highly protein bound, is virtually absent in breast milk. No adverse effects have been attributed to these small amounts of drug.(Adams 343)
- 63. Depression in Epilepsy Antiepilepticdrugs such as phenobarbital, vigabatrin, topiramate, tiagabine, levetiracetam,and clobazam can induce depressive symptoms in patients with epilepsy Carbamazepine, valproate, lamotrigine and pregabalin drugs are associated with mood stabilizing properties, so discontinuation may precipitate depression Suicide rate 5 times higher than that of general population SSRIs and SNRIs may reduce seizures and depressive symptoms Drug of choice-escitalopram and citalopram followed by sertraline. 63 American Epilepsy Society 2010
- 64. Post-stroke seizures • Strokeis the most common cause of seizures and epilepsy in population studies of adults over the age of 35years. • Seizures occurred within 24 hours of the stroke in 43 percent of patients • Late-onset seizures • Stroke severity and cortical location associated with seizures • Low frequency of recurrent seizures after stroke, and an absence of absolute predictors of poststroke epilepsy, the decision of when to treat patients for a poststroke seizure is difficult. • Most physicians empirically treat patients • Drugs of choice- Carbamazepine, Phenytoin, New AEDs
- 65. In case ofICH & SAH For ICH, seizure activity can cause further neuronal injury & coma For cerebellar Hmg & subcortical Hmg- No AED For other cases phenytoin for 1 month can be given If seizure occurs 2 wks after the event then long time prophyaxis Long time prophylaxis of AED is not recommended for SAH without seizure but should be if risk factors
- 66. Sudden Unexplained Deathin Epilepsy: SUDEP Definition: “sudden, unexpected, witnessed or unwitnessed, nontraumatic and non-drowning death in a patient with epilepsy where the postmortem examination does not reveal a toxicologic or anatomic cause of death, with or without evidence of a seizure and excluding documented status epilepticus.” C-Slide 66American Epilepsy Society 2010
- 67. Sudden Unexplained Deathin Epilepsy: SUDEP • Respiratory dysfunction may be an important contributing factor in SUDEP. • Suggests that positioning or stimulation of respiration may be important in the prevention of SUDEP. C-Slide 67American Epilepsy Society 2010
- 68. Recommendations for SUDEPprevention Optimize seizure control as promptly as possible • Re-evaluate epilepsy diagnosis and treatment as soon as 2 AEDs have failed, or when GTC szs are frequent despite initial AED treatment • Consider epilepsy surgery at that point • Maximize compliance with AEDs Use the least number of AEDs needed to control seizures • Add AED with the aim of replacing the current AED in a timely fashion (But not at the expense of worsening of seizure control) Educate patients and families C-Slide 68American Epilepsy Society 2010
- 69. First Aid Tonic-ClonicSeizure After seizure ends, turn person on side with face turned toward ground to keep airway clear, protect from nearby hazards Transfer to hospital needed for: • Multiple seizures or status epilepticus • Person is pregnant, injured, diabetic • New onset seizures DO NOT put any object in mouth or restrain C-Slide 69American Epilepsy Society 2010
- 73. Prognosis: Epilepsy: outcome after20 years 50% are seizure-free, without drugs, for the previous 5 yrs 20% are seizure-free for the previous 5 yrs but continue to take medication 30% continue to have seizures inspite of anti-epileptic therapy C-Slide 73
Editor's Notes
- #37 Antiepileptic drugs (AEDs) that are highly bound to serum proteins (e.g., phenytoin, valproate, and tiagabine) may be displaced from binding sites by other highly protein bound drugs (e.g., aspirin, warfarin, phenothiazines). In these cases, the serum concentration may not accurately reflect the unbound proportion of drug. Unbound (free) serum concentrations can be helpful in patients taking these drugs with other highly protein bound drugs, or in patients with significant renal disease or hypoalbuminemia. Most AEDs are metabolized by hepatic enzymes, and may either induce or inhibit hepatic metabolism of other drugs. The exceptions are gabapentin and levetiracetam which have no measurable hepatic metabolism. Induction of hepatic enzymes by AEDs such as carbamazepine, phenytoin and phenobarbital may cause increased metabolism and decreased serum concentrations of many other drugs, such as steroid hormones (i.e., oral contraceptives) or warfarin. Felbamate and valproate are metabolic inhibitors and can increase serum concentrations of other hepatically metabolized drugs. Conversely, other drugs (e.g., erythromycin or fluoxetine, potent inhibitors) may inhibit the metabolism of AEDs. It is sometimes difficult to predict what type of interaction will occur when two AEDs or an AED and another drug are used together.
- #65 Seizures occurred within 24 hours of the stroke in 43 percent of patients. related to local ion shifts and release of high levels of excitotoxic neurotransmitters in the area of ischemic injury. In contrast, an underlying permanent lesion that leads to persistent changes in neuronal excitability appears to be responsible for late-onset seizures after stroke