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Epilepsy
 

Epilepsy

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    Epilepsy Epilepsy Presentation Transcript

    • Seizure & Epilepsy Prof. Nabil Khalil
    • Definitions
    • Seizure   A sudden wave of synchronous electrical activity in brain that usually affects how a person feels or acts for a short time Some seizures can hardly be noticed, while others are totally disabling
    • Epilepsy     A condition that affects central nervous system (CNS) had at least 2 seizures not caused by some known medical condition like alcohol withdrawal or extremely low blood sugar not indicate anything about the cause of the seizures, what type they are, or how severe they are
    • Momentary loss of consciousness  Fit  Faint  Fake(False)
    • Transient loss of consciousness History and Physical Light-headedness Sweating Prolonged standing Precipitants eg.micturition Chest pain Palpitation Slow heart rate Low blood pressure Déjà vu Jamais vu Aphasia Olfactory aura Epigastric sensation Tongue biting Post event delirium Focal neurodeficit Witness account Pallor Sweating Slow pulse Low BP Syncope Syncope Seizure Aphasia Delirium Myoclonus Head turn or convulsion Automatism after pallor, Posturing sweating Convulsion and Postictal collapse delirium Convulsive syncope Seizure
    • Character Syncope Epileptic seizure usually upright any Time daytime day or nighttime Color pallor normal or cyanotic Aura dizziness, visual blurring possible specific aura common uncommon Duration brief brief or prolonged Incontinence rare more common Position Autonomic
    • Character Syncope Epileptic seizure occasionally brief tonic seizure or clonic jerks variable Automatism none absence,CPS Disorientation, posictal rare can occur with GTC,CPS Motor activity
    • Nonepileptic causes for spells  Physiologic        Tremor Vasovagal syncope Cardiac arrhythmias Migraine Medication adverse effects Transient ischemic attacks Autonomic dysfunction
    • Nonepileptic causes for spells  Psychologic        Anxiety Panic attacks Mood disorder Personality disorder Psychosis Somatiform illness Psychogenic seizures
    • Phase of seizures  Preictal phase or aura or warning  Ictal phase : simple or complex partial or generalized tonic-clonic seizure  Postictal phase or recovery period : last from seconds to minutes to hours
    • Precipitants of seizure  Sleep and lack of sleep  Drugs and alcohol  Intercurrent illness : infection, fever electrolyte imbalance  Menstruation  Stress and worry  Other precipitants-reflex epilepsy
    • Classification of seizure  Partial (focal, localized) seizures  Generalized seizures (convulsive or non- convulsive)  Unclassified epileptic seizures
    • Partial (focal, localized)seizures 1. Simple partial seizures (preserved consciousness) 2. Complex partial seizures (impaired consciousness) 3. Partial seizures evolving to secondarily generalized seizures
    • 1. Simple partial seizures (preserved consciousness) With - motor signs - somatosensory or special sensory systems - autonomic symptoms or signs - psychic symptoms
    • 2. Complex partial seizures (impaired consciousness) - Simple partial onset followed by impairment of conscious - With impairment of consciousness at onset
    • 3. Partial seizures evolving to secondarily generalized seizures - Simple partial seizures evolving to generalized seizures - Complex partial seizures evolving to generalized seizures - Simple partial seizures evolving to complex partial seizures evolving to generalized seizures
    • Generalized seizures (convulsive or nonconvulsive) - Absence seizures Typical absences Atypical absences - Myoclonic seizures - Clonic seizures - Tonic seizures - Tonic-clonic seizures - Atonic seizures (astatic seizures)
    • Unclassified epileptic seizures - Neonatal seizures - Recurrent status epilepticus - Rare or ‘isolated’ seizures
    • Epileptic seizure Seizure description and EEG Seizure type (s) All clinical a laboratory d neuroimagi Etiology
    • Seizure Idiopathic Generalized epilepsy likely Features of focal epilepsy Epilepsy or PNES Provoked seizures EEG EEG MRI/CT brain Video EEG Treat cause +/- AED PNES=psychogenic non-epileptic seizures AED=antiepileptic drug
    • Laboratory investigation CBC FBS, BUN, Creatinine Electrolyte , Liver function test , Ca+2 Mg+2 Electro-encephalography (EEG) Video EEG Neuroimaging : CT Scan, MRI, MR Spect, PET Special investigation : ammonia, lactate, pyruvate etc.
    • Electroencephalogram
    • What value is the EEG?  Add weight to the clinical diagnosis  Aid classification of epilepsy  Detection of the structural brain lesion.
    • EEG minute interictal EEG –useful when clinical suspicion of epilepsy  Timing is important  30   Within 24 hr of generalized convulsion: 50% have abnormal EEG First 48 hr: 21-34% have epileptiform activity  Sleep EEG or sleep-deprived EEG might increase diagnostic yield
    • Normal EEG
    • Primary generalized epilepsy—ictal EEG
    • Primary generalized epilepsyinterictal EEG
    • Burst of generalized spike and wave discharges—typical absence seizure
    • EEG monitoring
    • Video Monitoring  Helpful in determining nature of seizure disorder (epilepsy, convulsive syncope, or psychogenic seizures)
    • Indication for neuroimaging in patients with seizures  Partial seizure  Late onset unprovoked seizure (age > 25)  Unexplained neurological signs  Focal slow waves EEG  poor control or new symptoms / signs
    • Neuroimaging  In the absence of trauma: CT and MRI brain for patients presenting with suspected first unprovoked seizure or with a focal neurological deficit.  MRI is preferable for looking for neuronal migrational disorders, major malformations, vascular anomalies, tumors
    • The causes of epilepsy  Genetic factor  Congenital abnormalities  Trauma and the effect of craniotomy  CNS infection  Cerebrovascular disease  Cerebral tumors  Alzheimer’s disease and other degenerative disease  Others
    • Neurocysticercosis
    • Cerebral infarction
    • Intracerebral hemorrhage
    • Brain tumor or metastasis
    • Lt mesial temporal sclerosis
    • Cortical dysplasia
    • 52 year old woman with intractable seizure PET scan
    • PET using F-18 FDG-- Decreased FDG uptake in both temporal lobes, right worse then left but otherwise relatively symmetric
    • What to do?  Generalized seizure  Loosening the patient’s clothing  Lower the patient gently to the floor, turn them onto their side and cushion head  Nothing is put into the mouth  Remove any items that could cause injury
    • What to do? ---Generalized seizure    When the seizure is over, allow the patient to rest or sleep If they are able to return to their feet, help them home Obtain medical help if they continue to experience breathing problems once the seizure is over, or if the seizure lasts a long time(over 10 mins), or when another attack quickly follows the first
    • What to do?  Partial    seizures Stay with the patients throughout the seizure Protect them from any dangerous object Taking care not to restrain them in anyway
    • First aids
    • Treatment
    • Treatment ------------------------------
    • Choose a drug : considering the following factors  The seizure type and prognosis  Age  The possibility of pregnancy  Toxicity  Drug interaction
    • RISK OF RECURRENT SEIZURE  The recurrence risk follow a first unprovoked seizure  50  Over 10  twice as likely to have another seizure if you have a recurrence occur within 3 months within 2 years of initial seizures known brain injury or brain abnormality
    • RISK OF RECURRENT SEIZURE (cont)  If you do have two seizures, there's about 80% chance that you'll have more
    • Factors predictive of a high rate of seizure recurrence after the first unprovoked seizure  Abnormal neurologic status by NE or imaging  EEG abnormalities (especially epileptiform)  Partial seizures
    • Counseling before treatment 1. Aims of treatment 2. Prognosis and duration of the expected treatment 3. Importance of compliance 4. Side effects
    • Starting antiepileptic treatment Prospective risks Usual clinical Factors that may modify of epilepsy practice usual practice Single seizure No treatment Progressive cerebral disorder Clearly epileptic EEG 2 or more seizure widely separated precipitating, (eg, drugs, alcohol,reflex stimuli) Monotherapy Seizures in time (> 1 year) Identified factors
    • Antiepileptic Drug Development More Antiepileptic drugs 20 Levetiracetam Tiagabine 15 Topiramate Felbamate Zonisamide 10 Ethosuximide Phenobarbital Bromide Phenytoin Oxcarbazepine Fosphenytoin Gabapentin Lamotrigine Vigabatrin Sodium Valproate 5 Pregabalin Carbamazepine Benzodiazepines Primidone 0 1840 1860 1880 1900 1920 1940 Calendar year 1960 1980 2000
    • First-line choice of AEDs according to seizure type Seizure type First line Absence (typical and atypical) Myoclonic VPA, LTG Tonic-clonic Atonic Simple and complex partial, with or without secondary generalization Unclassifiable VPA VPA, CBZ, PHT, PB VPA CBZ, PHT, PB,OXC,LTG,TPM, GBP VPA
    • Advantages of Monotherapy  Better seizure control  Reduced side effects  Absence of drug interactions  Reduced teratogenic effects  Better compliance  Reduced cost of medication  Improved quality of life
    • Expected outcomes of AED therapy Monotherapy Well controlled 65% Unsatisfactorily controlled 35% Well Add-on therapy controlled 10% Multiple drug therapy Unsatisfactorily controlled 25% Well controlled 5% Unsatisfactorily controlled 20%
    • Managing newly diagnosed epilepsy Newly diagnosed epilepsy 47% First drug Seizure free 13% Second drug Seizure free Refractory Rational duotherapy Surgical assessment
    • Adverse effect of AED  Dose related  Idiosyncratic / allergic  Chronic toxicity  Teratogenicity
    • Older AEDs Drugs Side effects CBZ Tegretol Diplopia, headache, dizziness, N/V, rash, mild leukopenia, mild hyponatremia PHT Ataxia,nystagmus, dysarthria, somnolence,gingival hyperplasia, hirsutism, acne, facial coarsening, folate, deficiency, osteopenia, peripheral neuropathy, cerebellar atropy VPA Dose-related tremor, weight gain,loss of hair, menstrual irregularities, PCOS, stupor and encephalopathy(rare), hepatotoxicity PB Somnilleta Sedation and behavioral problem(depression, agitation, hyperactivity) CZP clonezipzm revotril Sedation, ataxia, behavioral changes(depression)
    • AED interactions  CBZ : autoinduction, VPA, PHT, -PB  PHT : CBZ, VPA, PB  PB : CBZ, VPA, PHT  VPA : CBZ, PB, PHT
    • AEDs      Drug interaction with AED and other drugs: via effect on hepatic CYP450 enzyme system PB, primidone, PHT, CBZ induce CYP enz. : Accelerate breakdown of many prescribed lipid-soluble drugs metabolized by the same system: OCP, cytotoxic, antiarrythmic, warfarin VPA is a weak CYP enz. Inhibitor: Slow clearance of other AEDs such as PHT, LTG. Newer AEDs : less likely to interfere with hepatic metabolism. GBP, LEV,PGB,VGB do not undergo hepatic metabolism
    • Newer AEDs  Adjunctive  Some treatment of refractory epilepsy of these AEDs: LTG, GBP, OXC, TPM have also demonstrated efficacy as monotherapy
    • Effects of phenytoin levels Level (mg/ml) Effect 0-10 Subtherapeutic 10-20 Therapeutic 20-30 30-40 Mild toxicity; nystagmus, mild ataxia Moderate toxicity ; ataxia prominent > 40 Severe toxicity; ataxia, conscious ness, encephalopathy
    • Potential Causes of Treatment Resistant Epilepsy  Diagnostic    Non-epileptic events Wrong diagnosis of seizure types epileptic syndrome Missing of underlying causes lesions  Patient’s   errors: errors: Non-compliance Inappropriate life style, inappropriate metabolism
    • Potential Causes of Treatment Resistant Epilepsy  Treatment     Wrong choice of drugs Less optimal doses of drugs Inadequate dosing schedules Antiepileptic drug toxicity  Disease   errors: itself: Treatment resistant epilepsy metabolic disorder
    • Stopping antiepileptic treatment Absolute requirement  - years free of all seizures
    • Factors in favour  Childhood epilepsy Primary generalized epilepsy  Absence of cerebral disorder  Short duration of epilepsy  Normal EEG 
    • Adverse prognostic factors  Symptomatic etiology, identifiable brain pathology  Partial-onset seizures or Atonic seizures  Late-onset or first-year epilepsy  Specific epilepsy syndrome (particularly JME)  Abnormal EEGs  Multiple seizure types in the same patient  Additional mental or motor handicap  Long duration or severe epilepsy prior to treatment  Poor initial response to treatment
    • Features common to the surgically privileged seizure disorders       Presence of a well-circumscribed structural lesion on the MRI (lesional epilepsy) Presence of well-localized interictal epileptiform discharged on the EEG Clinical features of habitual seizures indicating focal onset Absence of discordance between above feature Focus localized by above features is surgically accessible and involves little or no eloquent cortex Absence of other potentially epileptogenic abnormalities
    • Status epilepticus A condition in which epileptic activity persists for 30 minutes or more
    • Common etiologies for status epilepticus in children and adolescents   Idiopathic Acute symptomatic     Remote symptomatic     Past stroke CNS infection Cerebral palsy Progressive encephalopathy    Electrolyte disturbance Encephalitis Head trauma Tuberous sclerosis Other neurodegeneration Febrile
    • Status epilepticus management
    • Epilepsy and pregnancy Seizure control Obstetric complication  Neonatal outcome  
    • Neonatal outcome  Risk of seizure (3 times > normal population)  developmental  congenital outcome anomalies 4-8% (2-3 times > normal population)
    • The most common malformation  Congenital  orofacial  neural heart disease cleft tube defect  intestinal atresia  urogenital defects Neural tube defect
    • Fetal antiepileptic drug syndrome (minor anomalies)  Facial dysmorphism  Distal digital hypoplasia  Developmental delay  Mental deficiency
    • Factors affecting neonatal outcome  AED  genetics  folic acid  socioeconomic  maternal health
    • Recommendations for managing Women With Epilepsy Before Conception  Educate  Review the family regarding risks classification of epilepsy  Determine most appropriate medicine for seizure control
    •  Determine need for continued medication - may discontinue if seizure-free for 2 or more years - do not discontinue medication if epilepsy syndrome suggests continued need for treatment  Reduce medicines to monotherapy, lowest dose possible  Start folic acid 1 mg/day  Eliminate other risk factors – smoking, drugs, alcohol
    • After conception  Do not change antiepileptic medication  Refer for prenatal care  Prescribe vitamins, including folic acid  Check ‘free’ drug levels every trimester and change doses as needed  Evaluate for neural tube defects at 12 to 16 weeks (ultrasound, alpha-fetoprotein, amniocentesis)
    •  Consider  Check vitamin K predelivery antiepileptic drug levels prior to delivery and increase doses if needed
    • After Delivery  Check levels  Examine infant
    • Thank you