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(Epilepsy & Behavior 2008;12:501)

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  • Abnormal ↑ propensity to develop excess electrical discharges (e.g., abnormal balance between excitation & inhibition)
  • Seizure may be immediate response to pathological oscillatory networks (Epilepsia 2003;44:44)
    • Networks in brain generate oscillations that are dependent & critical elements of formation of seizure; inhibitory neuronal communications regulate synaptic transmission; intrinsic neuronal communications regulate ability of neuron to maintain burst firing
    • As brain transitions from normal to abnormal, there may be greater spread & neuronal recruitment after combination of events: enhanced connectivity, enhanced excitatory transmission, failure of inhibitory actions, changes in the intrinsic neuronal properties (Lancet 2006;367:1087)
    • Generalized epilepsies: seizure activity appears to begin on both hemispheres of the brain; many generalized epilepsies genetically determined with mutations in voltage-gated K+, Cl, & Na+ channels, & ligand-gated acetylcholine & GABAA receptors; includes absence, atonic, clonic, myoclonic, tonic, tonic-clonic, infantile spasms
    • Partial epilepsies: begin focally in 1 hemisphere & can secondarily generalize (i.e., spread to other hemisphere); sometimes due to focal pathological alteration (e.g., tumor)
      • Simple partial seizures (SPS) (e.g., awareness or consciousness is not impaired): exhibit behavior depending on lobe of origin; motor signs, somatosensory, autonomic symptoms, psychiatric, & visual symptoms
      • Complex partial seizures (CPS) (e.g., awareness or consciousness is impaired): can start with simple partial seizure that evolves into altered awareness; may begin with altered awareness, blank stare, or confusion (in patients >65yo, may be only evidence of seizure activity)
    • Seizures can be classified as either “unknown” or epilepsy syndromes (e.g., juvenile myoclonic epilepsy); can also be classified as idiopathic, symptomatic, or unknown/undetermined
    • Status epilepticus: prolonged epileptic activity that may be life threatening

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  • Treatment goals: “no seizures & no side effects” → improve QOL by balancing seizure control with side effects; eliminate seizures → ultimate goal, attainment should not be reached at expense of ↑ SE & ↓ QOL; treat common comorbidities such as depression, anxiety, sleep disorders, pain syndromes, & HA/migraine
    • If breakthrough seizure, always “round up the usual suspects” → assess nonadherence to seizure drug therapy, including NPO status for medical procedures; ask patient about sleep deprivation (e.g., a change in sleep pattern), ↑ emotional stress, new physical stress (e.g., flu & other illness); look for drugs that ↓ seizure threshold or alter metabolism of existing antiepileptic drugs (AEDs)
    • Drugs-drug classes reported to precipitate seizures: amphetamines, antidepressants (TCAs), antihistamines, antipsychotics, baclofen (abruptly withdrawn), β-lactams, bupropion, cephalosporins, cocaine, cyclosporine, dalfampridine, estrogen, imipenem, iodinated contrast dyes, isoniazid, lithium, local/general anesthetics, meperidine, methotrexate, methylphenidate, penicillins, pyrimethamine, quinolones, sympathomimetics, tacrolimus, theophylline, tramadol

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Principles of Epilepsy Management

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(N Engl J Med 2004;359:166)

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  • Confirm diagnosis of epilepsy → choose drug therapy based on seizure type, comorbidities, side effect profile, age of the patient, teratogenicity, drug interactions, cost, & tolerability
  • Begin with monotherapy: if seizure free → assess side effect profile & QOL; if intolerable side effects → ↓ dose & reassess seizure control; if seizure control not adequate ...

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