EPILEPSY AND SYNCOPE. Ivo Bekavac, MD, PhD

Transcription

1 EPILEPSY AND SYNCOPE Ivo Bekavac, MD, PhD

2 SEIZURE Sudden change in behavior that is the consequence of brain dysfunction. Epileptic seizures result from electrical hypersynchronization of neuronal networks in the cerebral cortex. Epilepsy recurrent epileptic seizures due to genetically determines or acquired brain disorder % of the population Provoked seizures due to metabolic disturbance, drug or alcohol withdrawal, acute neurologic disorders such as stroke or encephalitis Nonepileptic seizures sudden changes in behavior that resemble epileptic seizures but are not associated with the typical neurophysiological changes that characterize epileptic seizures.

3 Syncope Loss of consciousness due to hypoperfusion/absent perfusion to the cerebral hemispheres or brainstem (hypotension, cardiac dysrhythmia, VBI)

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8 Cerebrovascular Syncope Vertebrobasilar insufficiency (VBI) Migraine (basilar migraine) Takayasu disease Carotid sinus syncope

9 Etiology of Seizures Less than 50% have an identifiable cause Post-traumatic seizures (head trauma) Brain tumors Stroke Intracranial infection Cerebral degeneration Congenital brain malformations Inborn errors of metabolism

10 Classification Simple partial Complex partial Generalized tonic-clonic Less common varieties oabsence omyoclonic o Psychogenic

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12 Acute symptomatic seizures

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16 Clinical features History Prior seizures (including febrile seizures) Seizures precipitants or triggers (photic) Seizure symptoms and signs (aura, CPS, GTC) Postictal state (postictal paresis, confusion, suppressed alertness) Other aspects of the patient history (past medical history, medications, family history) Physical and neurologic examination

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26 Diagnostic studies Laboratory screening Causative metabolic abnormalities Prolactin (low sensitivity) Other seizure biomarkers (CPK, cortisol, WBC, LDH, PCO2, NH3, NSE) Electrocardiogram Lumbar puncture Electroencephalography Neuroimaging

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39 ANTIEPILEPTIC DRUG THERAPY When to start AED therapy Choosing an AED Combination therapy Side effects of therapy Specific adverse reactions Generic substitution Alcohol intake Nonadherence with AED therapy

40 Drug-resistant epilepsy Surgical treatment Temporal lobectomy Extratemporal cortical resection Hemispherectomy Corpus callosotomy Ketogenic diet Vagus nerve stimulation therapy

41 Special populations Women of childbearing age 1. Effect of AED on the fetus 2. Folic acid supplementation (4mg/day for VPA/CBZ 1-3 months prior to conception, mg/day other AED) 3. Contraception 4. Fertility Post-stroke seizures (when to treat?) Older patients

42 Complications of epilepsy Mortality Personal injury MVA (driving restrictions) Psychosocial issues Depression and psychiatric disease Cognitive impairment Medical comorbidities

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47 STATUS EPILEPTICUS

48 Introduction A single unremitting seizure with a duration longer than 5-10 minutes, or frequent clinical seizures without an interictal return to the baseline clinical state

49 Epidemiology 100, ,000 episodes of SE/year in the USA Refractory SE (ongoing seizures after 1 st and 2 nd line AED):30-43% Encephalitis Subtherapeutic level = nonrefractory Nonconvulsive >GTC SE = refractory

50 Etiology predisposing factors AED noncompliance or discontinuation Withdrawal syndromes (EtOH, barbiturates, baclofen, benzodiapines-alprazolam) Acute structural injury (tumor, stroke, TBI, SAH, cerebral anoxia/hypoxia, infection Remote or longstanding structural injury (prior head injury, CP, prior NSG, AVM) Metabolic abnormalities (hypoglycemia, hepatic encephalopathy, uremia, pyridoxine deficiency, hyponatremia, hyperglycemia, hypocalcemia, hypomagnesemia) Use or overdose drugs that lower the seizure threshold (theophylline, imipenem, penicillin G, metronidazole, isoniazid, tricyclics, bupropion, Li, clozapine, flumazenil, cyclosporine, lidocaine, bupivacaine) NORSE (new onset refractory SE), unclear etiology, high mortality

51 Complications and outcome Mortality- 20% (1 st episode of SE) 69-81% after anoxia Etiology, older age, medical comorbidity, > initial APACHE-II score) Metabolic stress, rhabdomyolysis, lactic acidosis Aspiration pneumonitis Neurogenic pulmonary edema Cardiac injury Neuronal death (after min)

52 Diagnosis Neurologic examination Electroencephalogram Single photon emission computed tomography MRI

53 Neurologic examination Nonconvulsive SE Level of consciousness Observation for automatic movements or myoclonus Asymmetric features on examination Motor responses

54 Electroencephalogram Extremely valuable tool Continuous seizure activity

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59 Single photon emission computed tomography Increased perfusion during status May persist for weeks after SE

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62 Magnetic resonance imaging The best tool to reveal the structural lesions that may trigger SE Abnormalities during SE (cell edema)- may persist for days-weeks

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64 Benzodiazepines Diazepam mg/kg, IV effect in seconds, t max/2 in in CSF in 3 min, lasts <20 min. Stops seizure in 50-80%, 50% recurrence if no 2 nd agent introduced. Rectal gel. Lorazepam 0.1 mg/kg IV effect in two minutes. Midazolam 0.2 mg/kg bolus, continuous infusion mcg/kg min

65 Phenytoin 50 mg/min, total 20 mg/kg Risk of hypotension and cardiac arrhythmias Fosphenytoin Pro-drug of phenytoin Up to 150 mg/min, IV/IM Intensify seizures caused by cocaine, other local anesthetics

66 Barbiturates Phenobarbital- 20 mg/kg infused at a rate mg/min (t/2 100 h) Pentobarbital loading dose of 10 mg/kg, up to 100 mg/min, continuous infusion 1-4 mg/kg/h)

67 Propofol Hypotension, respiratory depression, metabolic acidosis, cardiac dysfunction

68 Valproic acid Slow infusion, up to 20 mg/min Safe up to 10 mg/kg/min

69 Newer AED Topiramate Levetiracetam Lacosamide

70 Assessment and support Rapid neurologic examination Rapid general evaluation IV catheter placement Electrolytes, ABG, cardiac

71 Initial pharmacologic therapy for patients in an ER or hospital setting Lorazepam (0.02 to 0.03 mg/kg) cumulative dose of 0.1 mg/kg, max 2 mg/min) Diazepam (0.1 mg/kg IV) Midazolam (0.05 mg/kg IV) If no IV access midazolam 10 mg IM (>40 kg), 5 mg (13-40 kg) Phenytoin (but not fosphenytoin) and any of benzodiazepines are incompatible (precipitation) if infused through the same IV line. Phenytoin (20 mg/kg) mg/min (100 PE/min for fosphenytoin) 30 min

72 Treatment of refractory seizures SE refractory to 1 st line of AED NICU management Another 10 mg/kg phenytoin Phenobarbital Pentobarbital Midazolam Propofol

73 Hemodynamically stable patients High dose barbiturates Phenobarbital 20 mg/kg, max 100 mg/min Pentobarbital 100 mg/kg EEG monitoring, clinical & subclinical seizures, burst suppression If seizures terminated with pentobarbital 1-4 mg/kg/hr X 24 hrs, then tape off over following 24 hrs Vasopressor support (phenylephrine or dopamine)

74 Patients at high risk for respiratory failure Propofol (severe COPD, severe debilitation, cancer) to minimize the duration of sedation. Start 1-2 mg/kg/hr, titrated over next min up to mg/kg/h, <18-48 hours If not successful midazolam or barbiturates

75 Malignant SE 20% of refractory SE

76 Out-of-hospital/prehospital treatment Safe and effective

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