Seizures and Epilepsy

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Table 3-13. CHAPTER 3 Seizures and Epilepsy ■ 37 Drug–Drug Interactions: Effects on Serum Concentration of Adding a Second Antiepileptic Drug to First Antiepileptic Drug Original Drug Added Drug Effects of Added Drug on Serum Concentration of Original Drug Carbamazepine Clonazepam No change Phenobarbital Decrease Phenytoin Decrease Primidone Decrease Clonazepam Phenobarbital Decrease Phenytoin Decrease Valproate No change Ethosuximide Carbamazepine Decrease Methylphenobarbital Increase Phenobarbital No change Phenytoin No change Primidone No change Valproate Increase or no change Phenobarbital Carbamazepine No change Clonazepam Data conflicting Methsuximide Increase Phenytoin Increase Valproate Increase Phenytoin Carbamazepine Increase or decrease Clonazepam Data conflicting Ethosuximide No change Methsuximide Increase Phenobarbital Decrease, increase, or no change Primidone No change Valproate Decrease Primidone Carbamazepine Increased concentration of derived phenobarbital Clonazepam No change Ethosuximide No change Phenytoin Increased concentration of derived phenobarbital Valproate Increase Valproate Carbamazepine Decrease, increase, or no change Clonazepam No change Ethosuximide No change Phenobarbital Decrease Phenytoin Decrease Primidone Decrease From Geyer J, Keating J, Potts D, Carney P, eds. Neurology for the Boards. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2006. Multifocal clonic seizures involve several body parts, often in a migrating pattern. Generalized clonic seizures are rarely observed in newborn because of the incomplete myelination of the brain. 58–61 Tonic. Focal tonic seizures result in sustained posturing of a limb, the trunk, or the neck. These seizures are usually accompanied by EEG changes. Generalized tonic seizures exhibit tonic extension of all limbs (mimicking decorticate posturing) or tonic flexion of upper limbs and tonic extension of lower limbs (mimicking decerebrate posturing). There are no EEG changes in 85% of cases. 58–61 Myoclonic. Focal myoclonic seizures usually involve flexor muscles of an upper extremity. Often, there are no EEG changes. Conversely, generalized myoclonic seizures exhibit bilateral jerks of both upper and lower limbs, and may resemble infantile spasms. These generalized seizures are more likely to have EEG changes. 58–61
38 ■ Section 2: Common Pediatric Neurologic Problems Syndromes Benign familial neonatal seizures Benign familial neonatal seizures occur as a genetic disorder with an autosomal dominant inheritance pattern associated with chromosome 20q. The seizures typically start on day of life 2 or 3. The neonate may have as many as 10 to 20 seizures per day. The syndrome is usually self-limited and benign, but approximately 10% of cases progress to an antiepileptic drug-requiring seizure disorder. Neurological development is normal. 58–61 Fifth-day fits Fifth-day fits usually begin on day of life 4 to 6. The seizures are typically multifocal clonic seizures and are frequently associated with apnea. The seizures usually last for less than 24 hours. Fifth-day fits progress to status epilepticus in 80% of cases. 58–61 Benign neonatal sleep myoclonus Benign neonatal sleep myoclonus begins during the first week of life. The seizures are usually bilateral myoclonic jerks that last for several minutes and occur only during NREM sleep. The EEG is normal or slow. The seizures worsen with the administration of benzodiazepines. The seizures usually resolve within 2 months and neurological outcome is normal. 58–61 Benign myoclonus of early infancy Benign myoclonus of early infancy has an onset at age 3 to 9 months but it can be much earlier. The seizures resemble infantile spasms but the EEG is normal. The seizures usually occur while the patient is awake. The seizures disorder may continue for 1 to 2 years but neurological outcome is normal. 58–61 Treatment The clinician should first search for underlying etiologies producing the seizures and treat (hypoglycemia, hypocalcemia, sepsis). If the clinician cannot find a readily identifiable and treatable etiology, the frontline agent of choice for treating seizures is phenobarbital (see Table 3-14 for dosing suggestions). 62 Phenobarbital as a single agent will stop seizure activity in 42% of patients. When the seizure does not respond to a single agent, phenytoin is added with an increase in efficacy to 65%. Currently, fosphenytoin, the salt ester of phenytoin, is preferred in the neonate because it is an aqueous solution that is soluble in glucose-containing solutions, can be administered more quickly than phenytoin, and will not cause “purple glove syndrome.” 62 Purple glove syndrome is necrosis or injury of the soft tissue that can occur with intravenous infusion of the highly alkaline phenytoin. The drug of choice for neonates in status is lorazepam. This agent has several properties that make it ideal—a long half-life and a small volume of distribution, which prolongs its retention at high levels in the brain. REFERENCES Table 3-14. Neonatal AED Dosing Suggestions Phenobarbital—20 mg/kg load over 10 to 15 min. If necessary add more phenobarbital in 5-mg/kg boluses Fosphenytoin—20 mg/kg at 1 mg/kg/min Ativan—0.1 mg/kg From Rennie J, Boylan G. Treatment of neonatal seizures. Arch Dis Child Fetal Neonatal 2007;92:F148–F150. 1. Hauser WA, Beghi E. First seizure definitions and worldwide incidence and mortality. Epilepsia. 2008; 49(suppl 1): 8-12. 2. Teasell R, Bayona N, Lippert C, Villamere J, Hellings C. Post-traumatic seizure disorder following acquired brain injury. Brain Inj. 2007;21:201-214. 3. Statler KD. Pediatric posttraumatic seizures: epidemiology, putative mechanisms of epileptogenesis and promising investigational progress. Dev Neurosci. 2006;28: 354-363. 4. Agrawal A, Timothy J, Pandit L, Manju M. Post-traumatic epilepsy: an overview. Clin Neurol Neurosurg. 2006; 108:433-439. 5. Weber YG, Lerche H. Genetic mechanisms in idiopathic epilepsies. Dev Med Child Neurol. 2008;50:648-654. 6. Leventer RJ, Guerrini R, Dobyns WB. Malformations of cortical development and epilepsy. Dialogues Clin Neurosci. 2008;10:47-62. 7. Steinlein OK. Genetics and epilepsy. Dialogues Clin Neurosci. 2008;10:29-38. 8. Griffith JF, Ch’ien LT. Herpes simplex virus encephalitis. Diagnostic and treatment considerations. Med Clin North Am. 1983;67:991-1008. 9. Geyer J, Keating J, Potts D, Carney P, eds. Neurology for the Boards. 3rd ed. Philadelphia: Lippincott Williams & Wilkins;2006. 10. Riviello JJ. Classification of seizures and epilepsy. Curr Neurol Neurosci Rep. 2003;3:325-331. 11. Durón RM, Medina MT, Martínez-Juárez IE, et al. Seizures of idiopathic generalized epilepsies. Epilepsia. 2005;46:34-47. 12. Gardiner M. Genetics of idiopathic generalized epilepsies. Epilepsia. 2005;46(suppl 9):15-20. 13. Jallon P, Latour P. Epidemiology of idiopathic generalized epilepsies. Epilepsia. 2005;46(suppl 9):10-14.
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