Can dementia cause seizures and how common is it

Yes, dementia can cause seizures, and the connection is more common than most families expect. Research published in Neurology estimates that people with...

Yes, dementia can cause seizures, and the connection is more common than most families expect. Research published in Neurology estimates that people with Alzheimer’s disease face a six to ten times greater risk of developing seizures compared to the general population of the same age. The risk climbs as the disease progresses, with some studies suggesting that up to 22 percent of individuals with Alzheimer’s will experience at least one seizure during the course of their illness. For families already managing the daily weight of cognitive decline, a sudden seizure can be terrifying and disorienting — a 74-year-old woman with moderate Alzheimer’s, for instance, might be sitting quietly at breakfast when her body stiffens and she loses consciousness for ninety seconds, leaving her spouse scrambling to understand what just happened. The relationship between dementia and seizures runs deeper than coincidence.

Neurodegeneration damages the brain’s electrical networks, and as neurons die or malfunction, they can fire in chaotic bursts that produce seizures. This is not limited to Alzheimer’s — Lewy body dementia, frontotemporal dementia, and vascular dementia all carry elevated seizure risks, though the rates vary. What makes the situation particularly tricky is that many seizures in dementia patients are subtle, not the dramatic convulsions most people picture. They may appear as brief staring spells, unexplained confusion, or sudden behavioral changes that get mistakenly chalked up to the dementia itself. This article breaks down why dementia increases seizure risk, which types of dementia carry the highest risk, how to recognize seizures that don’t look like seizures, what treatment options exist and their real tradeoffs, and what families should discuss with their neurologist.

Table of Contents

Why Does Dementia Cause Seizures and How Common Is It Across Different Types?

The fundamental reason dementia leads to seizures is structural brain damage. In Alzheimer’s disease, the accumulation of amyloid plaques and tau tangles disrupts normal neuronal communication. Healthy neurons transmit electrical signals in organized patterns. When those neurons are damaged or surrounded by toxic protein deposits, they can misfire — sending erratic electrical discharges that spread across brain regions and trigger a seizure. Think of it like corroded wiring in an old house: the connections are still there, but the signals travel unpredictably. The prevalence varies significantly depending on the type of dementia. Alzheimer’s disease, the most studied, shows seizure rates between 10 and 22 percent over the disease’s full course.

Early-onset Alzheimer’s, which strikes before age 65, carries an even higher seizure risk — some research from the Mayo Clinic puts it closer to 30 percent in familial cases linked to specific genetic mutations like presenilin-1. Dementia with Lewy bodies shows seizure rates around 8 to 15 percent. Vascular dementia, caused by small strokes or chronic blood vessel damage, also elevates risk because each area of dead brain tissue can become a seizure focus. Frontotemporal dementia generally carries a lower seizure risk than Alzheimer’s, though it is still above the baseline for the general elderly population. One complicating factor is that seizure risk is not evenly distributed across the timeline of the disease. A person in the earliest stages of Alzheimer’s has a relatively modest increase in risk. By the severe and late stages, when extensive brain tissue has been lost, the risk spikes. This is why seizures often appear as a late-stage complication, though they can occasionally be among the first noticeable symptoms — sometimes even before a dementia diagnosis has been made.

Why Does Dementia Cause Seizures and How Common Is It Across Different Types?

Recognizing Seizures in Dementia Patients When Symptoms Overlap

One of the biggest challenges with seizures in dementia is that they frequently go unrecognized. The dramatic tonic-clonic seizure — full-body convulsions, loss of consciousness, falling to the ground — accounts for only a fraction of seizure activity in this population. Far more common are focal seizures and subclinical seizures that produce symptoms easily mistaken for dementia progression. A person might stare blankly for thirty seconds, smack their lips, pick at their clothing, or become suddenly and inexplicably confused for an hour. Caregivers and even clinicians often attribute these episodes to the dementia rather than investigating whether seizure activity is involved. A 2020 study in JAMA Neurology used continuous EEG monitoring on Alzheimer’s patients and found that subclinical epileptiform activity — abnormal electrical discharges that don’t produce obvious seizures — was present in over 40 percent of participants. This matters because that silent electrical chaos may actively accelerate cognitive decline.

The researchers found that patients with this hidden seizure activity declined faster on cognitive tests over the following year than those without it. In practical terms, this means that some of the “bad days” a dementia patient experiences — sudden worsening of confusion, inability to speak clearly, unusual agitation followed by deep sleep — might actually be seizure events or their aftereffects. However, if a person with dementia has a single unusual episode of confusion or staring, that alone does not confirm seizures. Urinary tract infections, medication side effects, dehydration, sleep deprivation, and even constipation can all cause sudden changes in behavior and cognition in people with dementia. The critical distinction is pattern: repeated, stereotyped episodes that look similar each time and resolve in a similar way point more strongly toward seizure activity. Families who suspect seizures should keep a detailed log of episodes, including time of day, duration, what the person was doing beforehand, and how long it took them to return to baseline. That log becomes invaluable when talking to a neurologist.

Estimated Seizure Prevalence by Dementia TypeEarly-Onset Alzheimer’s28%Late-Onset Alzheimer’s15%Lewy Body Dementia12%Vascular Dementia10%Frontotemporal Dementia5%Source: Aggregated from Neurology, JAMA Neurology, and Epilepsia journal studies (2018-2024)

The Role of EEG Monitoring and Why Standard Tests Often Miss Seizures

Electroencephalography, or EEG, is the primary tool for detecting seizure activity, but getting useful results from dementia patients presents real obstacles. A routine EEG lasts about 20 to 30 minutes and records the brain’s electrical activity through electrodes placed on the scalp. The problem is that many seizures in dementia patients are infrequent and brief. A person might have a seizure once every few days or once a week. The odds of capturing that event in a half-hour window are slim. Studies have shown that a single routine EEG misses epileptiform activity in up to 50 percent of cases where it is ultimately confirmed. Extended EEG monitoring — either through ambulatory EEG worn at home for 24 to 72 hours, or through inpatient video-EEG monitoring — dramatically improves detection rates. A case from a memory clinic at the University of California, San Francisco illustrates the point: a 68-year-old man with diagnosed Alzheimer’s was experiencing what his family described as “episodes” of sudden confusion and word-finding difficulty lasting five to ten minutes, occurring several times a week.

Two routine EEGs came back normal. An ambulatory 72-hour EEG captured multiple focal seizures originating from the left temporal lobe. Once treated with a low dose of levetiracetam, his episodes stopped and his family reported that his overall cognition seemed modestly but noticeably better. The practical barrier is access. Extended EEG monitoring is not available everywhere, particularly in rural areas, and it can be uncomfortable for dementia patients who may not understand why electrodes are glued to their scalp. Some patients pull off the equipment. Neurologists sometimes make a clinical judgment to trial antiseizure medication based on a strong history alone, without EEG confirmation, especially when repeated stereotyped episodes are well documented by caregivers. This is a reasonable approach in many cases, though it means monitoring for medication side effects becomes especially important.

The Role of EEG Monitoring and Why Standard Tests Often Miss Seizures

Treatment Options for Seizures in Dementia and Their Real Tradeoffs

Treating seizures in people with dementia requires balancing seizure control against the cognitive side effects that many antiseizure medications carry. This is not a straightforward calculus. The older generation of antiepileptic drugs — phenytoin, carbamazepine, valproic acid — are effective seizure suppressors but carry significant cognitive penalties. Phenytoin in particular can worsen confusion, impair coordination, and cause dizziness, all of which compound the existing challenges of dementia. Valproic acid has been associated with accelerated brain atrophy in some studies, making it a poor choice for a population already losing brain volume. Newer medications are generally preferred. Levetiracetam has become the most commonly prescribed antiseizure drug for dementia patients because it has relatively few drug interactions and a milder cognitive side-effect profile.

However, it is not without drawbacks — irritability, agitation, and mood changes are well-documented side effects, and in a person already prone to behavioral symptoms from dementia, this can be a real problem. Lamotrigine is another option with a favorable cognitive profile, but it requires slow titration over weeks to avoid a dangerous skin reaction, and its seizure control takes time to establish. Lacosamide is increasingly used and generally well tolerated, though evidence in the dementia population specifically is still limited. The tradeoff that families and clinicians face is this: untreated seizures may accelerate cognitive decline, but the medications used to treat them can also worsen cognition and quality of life. The usual approach is to start with the lowest effective dose of a well-tolerated medication, monitor closely, and adjust. For many patients, particularly those with frequent or clearly identifiable seizures, the benefit of treatment outweighs the risks. For a patient with a single questionable seizure and advanced dementia where comfort is the primary goal, the calculation may be different. There is no universal right answer, and honest conversations between families and neurologists about goals of care are essential.

When Seizures Accelerate Cognitive Decline and Why Timing Matters

There is growing evidence that seizures do not simply coexist with dementia — they may actively make it worse. Research from Baylor College of Medicine published in 2021 demonstrated that Alzheimer’s patients who developed epilepsy showed faster rates of cognitive and functional decline compared to matched patients without seizures. The mechanism appears to involve a vicious cycle: neurodegeneration causes abnormal electrical activity, and that abnormal electrical activity in turn damages additional neurons and disrupts memory consolidation, feeding back into faster degeneration. This has significant implications for treatment timing. If seizures are identified and treated early, there may be an opportunity to slow the overall trajectory of cognitive decline — not just manage the seizures themselves.

Some researchers, including a group at Massachusetts General Hospital, are exploring whether treating subclinical epileptiform activity in Alzheimer’s patients who have never had an obvious seizure could slow disease progression. Clinical trials are underway, and preliminary results have been cautiously encouraging. The warning here is against both overreaction and underreaction. Not every person with dementia needs an EEG or antiseizure medication. But when a pattern of sudden, repeated cognitive fluctuations emerges — especially episodes that seem out of proportion to the patient’s usual baseline — it warrants investigation rather than dismissal. The cost of missing treatable seizures is not just the seizures themselves but the potential acceleration of the very disease families are fighting against.

When Seizures Accelerate Cognitive Decline and Why Timing Matters

Seizure Safety Planning for Dementia Caregivers

Caregivers managing both dementia and seizure risk need a practical safety plan. This starts with the physical environment: removing sharp-edged furniture from areas where the person spends the most time, ensuring the bed is low to the ground or has padded rails, and avoiding unsupervised bathing. During a seizure, the old advice about putting something in the person’s mouth is not just wrong — it is dangerous.

The correct response is to ease the person to the floor if they are standing, turn them on their side, protect their head, and time the seizure. Any seizure lasting longer than five minutes, or any seizure followed immediately by a second one without the person regaining awareness, is a medical emergency requiring a 911 call. For a caregiver like a daughter looking after her father with moderate Alzheimer’s and a new seizure diagnosis, the practical reality means keeping rescue medication such as midazolam nasal spray prescribed and accessible, programming emergency numbers into speed dial, and informing any other caregivers or adult day program staff about the seizure history and response protocol. It also means understanding that after a seizure, the person will likely be deeply confused and exhausted for hours — this postictal period can look like a major worsening of the dementia, but it is temporary and expected.

Emerging Research on the Dementia-Epilepsy Connection

The scientific understanding of the relationship between dementia and seizures is evolving rapidly. One of the most promising areas of research involves the concept that epileptic activity may actually be one of the earliest detectable signs of Alzheimer’s disease — potentially appearing years before memory symptoms. Studies using magnetoencephalography, a more sensitive form of brain wave recording, have detected abnormal neural oscillations in people with genetic risk factors for Alzheimer’s who are still cognitively normal. If validated, this could eventually lead to seizure-related biomarkers for early Alzheimer’s detection.

Another active research front involves repurposing antiseizure medications as disease-modifying treatments for Alzheimer’s. Levetiracetam, at low doses, has shown potential in animal models and small human trials to reduce abnormal network hyperexcitability and improve memory function in people with mild cognitive impairment. Larger trials are ongoing. While it is far too early to call any antiseizure drug an Alzheimer’s treatment, the blurring of boundaries between epilepsy research and dementia research is producing genuine insights that neither field would have reached alone. For families dealing with both conditions today, the most actionable takeaway is that seizures in dementia are not just a secondary nuisance — they are a meaningful clinical target that deserves attention and treatment.

Conclusion

Dementia and seizures are more closely linked than most people realize, with Alzheimer’s patients facing up to ten times the seizure risk of their peers. The challenge is that seizures in this population are often subtle — brief staring spells, unexplained confusion, sudden behavioral shifts — and easily mistaken for normal disease progression. Recognizing the possibility of seizures, documenting suspicious episodes carefully, and pursuing appropriate neurological evaluation can make a real difference in a patient’s quality of life and potentially slow cognitive decline.

Treatment requires navigating genuine tradeoffs between seizure control and medication side effects, and the right approach depends on the individual’s disease stage, seizure frequency, and care goals. Families should feel empowered to raise the question of seizures with their loved one’s medical team, especially when they observe repeated, patterned episodes of sudden worsening. This is a treatable problem, and addressing it is one of the concrete ways caregivers can advocate for better outcomes even in the face of a progressive disease.

Frequently Asked Questions

Can a seizure be the first sign of dementia?

Yes, though it is uncommon. In some cases, particularly with early-onset Alzheimer’s linked to genetic mutations, a new-onset seizure in a middle-aged or older adult with no prior seizure history can precede noticeable memory problems. Any unexplained new seizure in someone over 50 warrants a thorough neurological workup that includes cognitive screening.

Are seizures in dementia patients life-threatening?

Most individual seizures are not life-threatening, but they carry risks including falls, aspiration, and injury. Status epilepticus — a seizure lasting more than five minutes or repeated seizures without recovery between them — is a medical emergency that can be fatal without prompt treatment. The cumulative effect of repeated seizures may also worsen overall brain function.

Should every dementia patient be screened for seizures with an EEG?

Current guidelines do not recommend routine EEG screening for all dementia patients. However, an EEG should be considered when there are unexplained fluctuations in cognition, episodes of staring or unresponsiveness, unexplained falls, or sudden behavioral changes that follow a repetitive pattern. The threshold for testing should be low given how frequently seizures go undetected in this population.

Will treating seizures improve my loved one’s memory?

Treating seizures may stabilize cognition and slow the rate of decline, but it will not reverse damage already caused by the underlying dementia. Some families report modest improvements in alertness and day-to-day function after seizure treatment begins, particularly if the seizures were frequent. The primary goal is preventing further harm rather than restoring lost function.

Can dementia medications like donepezil cause seizures?

Cholinesterase inhibitors such as donepezil, rivastigmine, and galantamine can lower the seizure threshold in some patients, though this is relatively rare. The benefits of these medications for cognition generally outweigh the small added seizure risk. If a patient on cholinesterase inhibitors develops new seizures, the neurologist will weigh whether to continue, adjust, or discontinue the medication on a case-by-case basis.

What is the difference between a seizure and a TIA in someone with dementia?

Transient ischemic attacks and seizures can look similar — both may cause sudden confusion, speech difficulty, or weakness that resolves. Key differences include that TIAs tend to produce focal neurological deficits like one-sided weakness or slurred speech, while seizures more often involve altered awareness, repetitive movements, or staring. However, distinguishing between them often requires medical evaluation including imaging and sometimes EEG, and both warrant prompt medical attention.


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