Chapter 36: Seizure Disorders – Antiepileptic Drug Therapy

The pathophysiology is rooted in abnormal neuronal conduction, where a large group of nerve cells fire synchronously due to an imbalance between excitatory neurotransmitters (like glutamate) and inhibitory neurotransmitters (like GABA). Seizures are classified using the International League Against Epilepsy (ILAE) system into three major groups: focal onset, generalized onset (e.g., tonic-clonic, absence), and unknown onset. Diagnostic criteria rely on patient history, physical examination, EEG, and neuroimaging (CT/MRI). The primary goal of treatment is complete seizure control, ideally achieved through monotherapy, while minimizing adverse drug effects. The chapter extensively details various Antiepileptic Drugs (AEDs), outlining their mechanisms of action, dosages, contraindications, and significant adverse effects—ranging from older agents like phenytoin (known for nonlinear kinetics and cardiac risk with rapid IV use) and carbamazepine (requiring HLA-B*1502 screening in Asian patients due to SJS/TEN risk) to broad-spectrum drugs like valproic acid (carrying black box warnings for hepatotoxicity, pancreatitis, and teratogenicity). Newer agents such as levetiracetam, lamotrigine, topiramate, and lacosamide are also reviewed, highlighting their distinct pharmacokinetics and interactions. Special emphasis is placed on the critical management of Status Epilepticus (SE), a medical emergency requiring immediate abortive therapy, typically starting with intravenous benzodiazepines like lorazepam, followed by non-benzodiazepine AEDs. Considerations for special populations, including pediatrics (Lennox-Gastaut syndrome, febrile seizures), geriatrics (due to altered drug clearance and protein binding), and women of childbearing age (pregnancy risk categories and contraceptive interactions), are also addressed, alongside the increasing importance of pharmacogenetics in AED selection.