Seizures are often associated with childhood, but the highest rate of new-onset epilepsy occurs in adults aged 60 and older. This late-onset presentation differs fundamentally from childhood cases, which are frequently linked to genetic factors or developmental issues. In older individuals, new seizures are overwhelmingly a symptom of acquired brain pathology, reflecting cumulative damage from age-related diseases. The causes are diverse, ranging from structural injuries and vascular disease to systemic metabolic problems, requiring a thorough investigation for diagnosis and treatment.
Cerebrovascular Events
Cerebrovascular disease, particularly stroke, is the most common cause of new-onset seizures in the older population, accounting for 30% to 50% of cases. Seizures may occur acutely (within the first week) or as a delayed consequence, leading to Post-Stroke Epilepsy (PSE). Acute seizures are often triggered by immediate changes like tissue swelling, ischemia, or electrolyte imbalances in the brain.
The enduring risk comes from the delayed development of PSE, which can manifest months or years after the initial event. Both ischemic (clot-related) and hemorrhagic strokes can create a lesion that becomes a seizure focus. As the brain heals, the damaged area is replaced by glial scar tissue, which disrupts normal neural circuitry and lowers the seizure threshold of surrounding neurons. Strokes that involve the cerebral cortex carry a significantly higher risk of seizure development than those located deep within the brain structure.
Hemorrhagic strokes are associated with a greater long-term risk of developing PSE compared to ischemic strokes. This difference is due to the greater local tissue disruption and the presence of blood products, which are highly irritating to neurons. Predicting which stroke survivors will develop chronic epilepsy is complex, but the location and size of the affected area are major determining factors.
Structural Changes from Tumors and Prior Injury
Seizures can be the first sign of a structural mass or fixed damage from an earlier trauma. Brain tumors, both primary and metastatic, account for 10% to 30% of late-onset epilepsy cases. The tumor mass irritates surrounding brain tissue, and the associated swelling (edema) and chemical changes destabilize the electrical activity of nearby neurons.
Slower-growing, lower-grade primary tumors, such as gliomas and meningiomas, are often more likely to cause seizures than highly aggressive tumors. This tendency occurs because the slower growth allows time for the brain to integrate the tumor into its electrical network, creating a chronic seizure focus. Metastatic tumors, commonly originating from cancers in the lung, breast, or skin, also pose a significant seizure risk, particularly in the frontal or temporal lobes.
Traumatic Brain Injury (TBI) can leave behind scar tissue that acts as a focus for seizure activity many years later. Older adults are at increased risk for falls, which can result in subdural hematomas or concussions that cause fixed structural damage. This old scar tissue can become epileptogenic, generating abnormal electrical discharges that manifest as seizures.
Medication Side Effects and Metabolic Imbalances
Seizures can frequently be traced to systemic or drug-related factors that temporarily lower the brain’s seizure threshold. Polypharmacy (the use of multiple medications) is a common scenario that increases the chance of drug interactions or side effects that trigger seizures. Specific drug classes known to increase seizure risk include certain antidepressants, antipsychotic medications, and high-dose antibiotics.
The abrupt discontinuation of some medications, particularly benzodiazepines or alcohol, can also provoke withdrawal-related seizures. The brain’s chemistry is suddenly deprived of an inhibitory influence, leading to neuronal hyperexcitability. This type of acute symptomatic seizure may resolve once the underlying cause is corrected and does not lead to a diagnosis of chronic epilepsy.
Metabolic disturbances represent another cause of acute seizures in this age group. Conditions that compromise the body’s internal balance, such as severe electrolyte abnormalities, can impair brain function. Examples include:
- Hyponatremia (low sodium)
- Hypoglycemia (low blood sugar)
- Complications from advanced liver failure
- Complications from kidney failure
These imbalances interfere with the normal electrical signaling of neurons, making them susceptible to uncontrolled firing.
The Influence of Neurodegenerative Conditions
Neurodegenerative disorders, which involve the progressive loss of nerve cells, represent a growing cause of late-onset seizures. Conditions like Alzheimer’s disease and Vascular Dementia are associated with a five- to tenfold increased risk of developing epilepsy. This relationship is complex and often bidirectional.
In Alzheimer’s disease, the accumulation of abnormal proteins and resulting cell death disrupt the brain’s inhibitory circuits. The loss of inhibitory neurons leads to a state where brain cells are more easily excited, increasing the susceptibility to seizures.
Parkinson’s disease is another neurodegenerative condition linked to an increased incidence of seizures. The loss of inhibitory control contributes to this heightened risk. While these conditions may not be the most common cause compared to stroke, they provide a significant context for seizure development in individuals already experiencing cognitive decline.