The incidence of new-onset seizures increases significantly in older adults (aged 65 and above), resulting in the highest rate of developing epilepsy. This is largely attributed to age-related changes and acquired disorders affecting the brain’s structure and function. Unlike younger populations, new-onset seizures in the elderly are a consequence of underlying acquired brain pathology. Identifying the specific cause is paramount because it directly influences medical management and treatment strategy.
Atypical Presentation of Seizures in Older Adults
Seizures in older adults often present subtly, leading to misdiagnosis or delayed recognition. The classic generalized tonic-clonic seizure, involving full-body convulsions, is less common. Instead, focal-onset impaired-awareness seizures are seen more frequently, often reflecting new, localized brain lesions.
These subtle events might manifest as a momentary blank stare, brief confusion, or repetitive, automatic movements (automatisms), such as lip-smacking or fumbling with clothes. Such episodes are easily mistaken for dementia, transient ischemic attacks (TIAs), or simple syncope. The period of postictal confusion tends to be more prominent and prolonged, sometimes lasting for hours or days.
Cerebrovascular Disease
Cerebrovascular disease is the single most common identified cause of new-onset seizures and epilepsy in the elderly, accounting for an estimated 30% to 50% of all cases. Both ischemic strokes (blocked blood flow) and hemorrhagic strokes (bleeding) can form gliotic scar tissue in the brain. This scar tissue disrupts normal electrical activity, creating a focus of abnormal excitability that can trigger a seizure.
Seizures may occur acutely, within the first week of a stroke, or develop later, leading to post-stroke epilepsy. The latency period between the initial stroke and recurrent seizures can span months to years. Hemorrhagic strokes, which irritate brain tissue, and strokes affecting the cortex carry a higher risk of subsequent seizures compared to deeper strokes.
Chronic cerebral ischemia, often related to small vessel disease, is also a significant contributor. These small, cumulative injuries may not cause an obvious stroke but can progressively lower the seizure threshold. Silent cerebral infarcts seen on imaging often explain the origin of the seizures. Furthermore, an individual who develops new-onset epilepsy late in life has a two to three-fold increased risk for a subsequent stroke.
Structural and Degenerative Changes
Structural changes not primarily vascular in origin are another major category contributing to new-onset seizures. Brain tumors, including primary and metastatic lesions, are implicated in approximately 10% to 30% of new cases. The tumor’s mass effect and surrounding inflammation can irritate adjacent brain tissue, leading to seizure activity.
Neurodegenerative diseases, particularly Alzheimer’s disease and other forms of dementia, also increase seizure susceptibility. Underlying pathology, such as the accumulation of amyloid plaques and neurofibrillary tangles, can alter neuronal excitability and damage brain circuits. The risk often correlates with the severity and duration of dementia; up to 20% of people with Alzheimer’s disease may develop epilepsy.
The long-term effects of past traumatic brain injury (TBI) can surface as seizures decades later. Even minor injuries sustained earlier in life can lead to the slow development of scar tissue or chronic subdural hematomas (blood collections) that become epileptogenic over time. A remote history of head trauma remains a persistent risk factor for developing late-onset epilepsy.
Systemic and Medication-Related Factors
Causes originating outside the brain often involve systemic conditions that disrupt the chemical balance required for normal brain function. Metabolic derangements are common, and acute symptomatic seizures can be provoked by conditions like hyponatremia (low sodium levels) and hypoglycemia (low blood sugar). Severe organ dysfunction, such as kidney failure (uremia) or advanced liver disease, allows toxins to build up, interfering with brain chemistry and lowering the seizure threshold.
Acute systemic infections, like sepsis, or central nervous system infections, such as meningitis or encephalitis, can trigger seizures by causing inflammation or fever. These infectious and metabolic causes are considered acute symptomatic seizures and may not lead to long-term epilepsy once the underlying condition is corrected.
Medication management is complex due to polypharmacy (the use of multiple medications). Many common prescription drugs, including certain antibiotics, psychotropic medications, and pain relievers, can lower the seizure threshold. Age-related changes in liver and kidney function affect drug metabolism and clearance, increasing the risk of dose toxicity and drug-drug interactions. Abrupt withdrawal from substances like alcohol or sedative medications can also induce acute symptomatic seizures.
When the Cause Remains Undetermined
Despite a thorough diagnostic workup, including high-quality brain imaging (MRI), electroencephalography (EEG), and extensive laboratory blood work, a definitive cause for new-onset epilepsy remains elusive in a notable percentage of elderly patients. This is often referred to as “epilepsy of unknown cause” or “cryptogenic epilepsy.” Estimates suggest that up to 50% of late-onset cases may fall into this category.
The diagnostic process systematically rules out structural, vascular, and metabolic causes. Even when the cause is not identified, clinicians often suspect occult cerebrovascular disease or subtle degenerative changes not clearly visible on standard scans. Although the etiology is unknown, the diagnosis of epilepsy still necessitates appropriate treatment to control seizures and prevent complications.