Dementia is a decline in mental ability marked by progressive neurodegeneration. Seizures are episodes of abnormal electrical activity in the brain. The risk of developing epilepsy is substantially elevated in individuals with dementia, particularly Alzheimer’s disease (AD) and vascular dementia, compared to the general elderly population. This connection reveals a complex interplay where the underlying brain changes of dementia create an environment for electrical overactivity.
The Underlying Neurological Vulnerability
The progressive destruction of brain tissue that defines dementia compromises the balance of electrical signaling. Neuronal damage and the loss of nerve cells disrupt established neural networks, leading to a state of hyperexcitability. This network instability causes neurons to fire uncontrollably, which lowers the seizure threshold. The brain’s system of inhibitory and excitatory signals becomes unbalanced, making the network prone to synchronous, abnormal electrical bursts.
In Alzheimer’s disease, the accumulation of abnormal proteins, specifically amyloid-beta (Aβ) plaques and neurofibrillary tangles composed of tau protein, plays a direct role in generating hyperexcitability. Aβ protein possesses epileptogenic properties, meaning it can actively promote the development of seizures, even in the early stages of the disease. The presence of these protein aggregates directly irritates neurons and alters synaptic communication, increasing the likelihood of electrical discharges.
Vascular dementia also significantly increases seizure risk, primarily due to the lasting effects of cerebrovascular events like stroke. Tissue damage from stroke or chronic reduced blood flow creates scars or lesions in the brain that act as focal points for the initiation of seizures. Conversely, in other dementias, such as Frontotemporal Dementia (FTD), the risk is less pronounced. The damage caused by neurodegeneration is compounded by chronic neuroinflammation, which further contributes to electrical irritability in the brain.
The risk of seizures tends to increase as dementia progresses and brain pathology accumulates, though seizures can occur early, particularly in genetic forms of AD. The onset of seizures is often associated with a faster rate of cognitive decline, suggesting that the electrical events themselves cause further damage. Active seizure activity may even promote the deposition of more amyloid plaques and tau tangles, creating a destructive cycle between the two conditions.
Identifying Atypical Seizure Manifestations
Seizures in older adults with dementia frequently present in subtle, non-convulsive ways that are easily mistaken for typical cognitive or behavioral symptoms. The most common presentations are often focal onset seizures, which begin in a specific region of the brain. These focal seizures may manifest as brief episodes of unresponsiveness, sudden staring spells, or temporary confusion that lasts only a few minutes.
Caregivers may observe subtle motor manifestations, known as automatisms, which are repetitive, involuntary movements. These automatisms can include:
- Lip-smacking.
- Chewing motions.
- Fumbling with clothes.
- Repetitive hand movements.
Such transient symptoms are difficult to distinguish from the day-to-day fluctuations in attention and behavior common in advanced dementia. Symptoms like brief memory lapses, sudden emotional shifts, or unexplained agitation can also be subtle indicators of underlying seizure activity.
A particularly serious and often overlooked presentation is Non-Convulsive Status Epilepticus (NCSE), which involves continuous or recurrent seizure activity without major physical convulsions. NCSE typically presents as a prolonged period of unexplained acute confusion, stupor, or fluctuating consciousness that can last for hours or even days. Since the patient is already cognitively impaired, this state may simply be attributed to a worsening of their dementia or delirium, delaying necessary diagnosis and treatment. Due to these atypical and subtle presentations, specialized testing is often required to confirm the presence of seizures.
Treatment Strategies and Prognosis
Confirming a seizure diagnosis often requires an Electroencephalogram (EEG) to record the brain’s electrical activity, though standard short-term EEGs may not always capture the subtle, deep-seated discharges. Neuroimaging, such as MRI or CT scans, is also routinely used to rule out other acute causes for the event, like a new stroke, tumor, or bleeding. Because seizures in dementia are associated with a high risk of recurrence, treatment with Antiepileptic Drugs (AEDs) is recommended after a confirmed first seizure.
Treating epilepsy in the context of dementia presents challenges due to the heightened sensitivity of the elderly brain and the presence of multiple other medications. Clinicians must select AEDs carefully because many of these drugs carry a risk of cognitive side effects, which can worsen existing dementia symptoms or increase the risk of falls. Medications that have a more favorable profile with fewer drug-drug interactions and less cognitive burden, such as certain newer AEDs, are preferred.
The approach to medication dosage is “start low and go slow,” beginning with a lower dose than used in younger patients and increasing it gradually. This cautious titration helps the patient’s body adjust and minimizes adverse effects. If the seizures are not managed, the prognosis for the underlying dementia worsens, as active seizures are linked to a more rapid decline in cognitive and functional status, as well as higher mortality rates. Effective seizure control is therefore an important component of managing the overall well-being and maintaining the quality of life for individuals living with dementia.