Chapter 58: Epilepsy
1. Chapter Overview
Epilepsy is not exclusively a disease of the young. In fact, incidence rates exhibit a bimodal distribution, with the highest peak occurring in older adults (aged 65 and above). However, because the clinical manifestations of seizures in the elderly are notoriously subtle and often masked by multimorbidity, geriatric epilepsy is frequently underdiagnosed, misdiagnosed, or diagnosed late.
2. Secondary Etiology
Unlike idiopathic or genetic epilepsies prevalent in youth, new-onset epilepsy in older adults is overwhelmingly secondary to acquired structural brain insults (symptomatic epilepsy):
Cerebrovascular Disease: The leading cause of geriatric epilepsy (accounting for up to 50% of cases with a known etiology). The risk of developing an epileptogenic focus is remarkably high following an ischemic or hemorrhagic stroke.
Neurodegenerative Diseases: Particularly in the later stages of Alzheimer's disease, patients are highly susceptible to unprovoked seizures.
Other Causes: Brain tumors, metabolic disturbances (e.g., severe hyponatremia, hypoglycemia), head trauma, and CNS infections. However, up to one-third of cases remain cryptogenic (of unknown cause despite modern investigation).
3. Atypical Clinical Presentation
Seizure Semiology: Older adults rarely present with classic generalized tonic-clonic seizures ("grand mal"). The vast majority experience focal onset impaired awareness seizures (formerly complex partial seizures). These manifest subtly as sudden staring spells, unresponsiveness, purposeless automatisms (e.g., lip-smacking, picking at clothes), or transient memory lapses.
The Postictal State: This is a critical hallmark in the elderly. While younger patients may recover within hours, an older adult's postictal confusion, profound lethargy, or focal weakness (Todd's paresis) can persist for days or even up to a week. This prolonged state is routinely misdiagnosed as delirium, an acute stroke, or a sudden worsening of dementia.
4. Diagnostic and Differential Challenges
Differential Diagnosis: Clinicians must meticulously distinguish epilepsy from syncope (especially cardiogenic syncope with myoclonic jerks, frequently mistaken for a convulsion), Transient Ischemic Attacks (TIAs), delirium, and Transient Global Amnesia (TGA).
Investigations: Routine Electroencephalograms (EEGs) have lower sensitivity in older adults; a normal EEG does not rule out epilepsy. High-resolution MRI is indispensable for identifying underlying structural lesions (e.g., silent infarcts or tumors).
5. Principles of Pharmacotherapy and the Polypharmacy Dilemma
Threshold for Treatment: Because the recurrence risk is exceedingly high and even a single generalized seizure can result in devastating falls, fractures, or cardiopulmonary compromise in a frail body, Antiseizure Medications (ASMs) are typically initiated after the first unprovoked seizure in older adults.
Initiation and Titration: The cardinal rule is "Start low, go slow." The aging brain is exquisitely sensitive to neurocognitive side effects; rapid titration easily provokes cognitive slowing, dizziness, and ataxia (leading to catastrophic falls).
Drug Selection and Interactions: Given ubiquitous polypharmacy, traditional enzyme-inducing ASMs (like phenytoin and carbamazepine) must be actively avoided. They severely disrupt the metabolism of vital cardiovascular and anticoagulant medications. Moreover, carbamazepine and oxcarbazepine carry a high risk of inducing severe hyponatremia. Newer-generation ASMs (e.g., levetiracetam, lamotrigine) are the preferred first-line agents due to their favorable pharmacokinetic profiles and lack of significant drug-drug interactions.
—Brocklehurst’s Textbook of Geriatric Medicine and Gerontology