The frontotemporal dementia evidence guide
Frontotemporal dementia is a group of brain diseases that usually affect behavior, personality, language, or movement before memory becomes the main problem. These changes can make a brief seizure-related interruption in speech, response, behavior, or movement difficult to recognize.
This guide explains how often seizures have been reported, how events can appear, why the different forms of the disease matter, and what researchers still need to learn about electrical activity without obvious outward signs.
Start here
A Finnish study found more diagnosed epilepsy beginning ten years before frontotemporal dementia was diagnosed and continuing afterward. This is a pattern across a group. A seizure in one person does not predict that the person will develop frontotemporal dementia. [1]
The disease may already affect conversation, initiative, social behavior, or movement. A seizure may briefly interrupt awareness, speech, behavior, or movement in a way that starts suddenly and repeats in a similar form. [2]
Studies of diagnosed seizures do not show how much unnoticed electrical activity occurs. Most people in a recent FTD study did not have an EEG, leaving a major gap in what researchers can say. [2]
How often seizures are reported
Studies report different percentages because they count different events, groups, and periods of time. One counted diagnosed epilepsy near the FTD diagnosis. Another counted several types of recorded seizures in a specialty clinic. A third reviewed seizures across the full course of disease.
A 2025 Finnish study included 245 people with FTD, 2,416 similar people without FTD, and 1,326 people with Alzheimer's disease. At the time of the FTD diagnosis, 6.5% had diagnosed epilepsy, compared with 1.8% of the matched controls. The study counted registered epilepsy diagnoses rather than every possible event or single seizure. [1]
Hashmi and colleagues reported seizures in 24 of 317 people with FTD. The group included people with established epilepsy, a single seizure without an immediate cause, and one seizure related to a recent stroke. The 7.6% figure therefore covers more than diagnosed epilepsy alone. [2]
A German study found seizures in 6 of 53 people whose frontotemporal brain disease was confirmed after death. The records covered the period from first symptoms to death. This small, selected group does not represent everyone living with FTD. [4]
In the Finnish study, epilepsy was already more common among people who would later receive an FTD diagnosis. Five years after diagnosis, prevalence reached 11.2% among those still alive. This was not an EEG screening study and does not quantify silent seizures. [1]
| Time relative to FTD diagnosis | FTD group | Matched controls |
|---|---|---|
| 10 years before | 3.3% | 0.8% |
| 5 years before | 4.9% | 1.3% |
| Year of diagnosis | 6.5% | 1.8% |
| 5 years after, among survivors | 11.2% | 2.2% |
These are cross-sectional prevalence estimates at specified times, not the probability that an individual will develop epilepsy over the next five years. The 95% confidence interval for FTD prevalence was 4.0% to 10.4% at diagnosis and 7.2% to 16.9% five years later. The later denominator includes only survivors.
The study used two Finnish regions and specialist-validated dementia diagnoses. Epilepsy classification relied on diagnostic codes rather than systematic EEG or detailed event review. Single seizures without an epilepsy diagnosis were excluded. Although the study also included Alzheimer's disease, the FTD versus Alzheimer's difference was not statistically significant at the year of diagnosis. The results do not establish a universal ranking between dementia types. [1]
Beagle's 2017 study estimated a 3.0% chance of a seizure over time in 348 people across a broader FTD group. It counted new seizures without an immediate cause and included several related movement and language conditions. Its definitions and follow-up differed from the newer studies. [3]
A specialty clinic, an epilepsy register, and a brain bank capture different parts of the clinical picture. Their percentages cannot be averaged into one headline range. Together, they support a meaningful association while leaving the exact frequency uncertain.
How seizures can appear
In Hashmi's 2025 study, 12 of the 24 people with seizures had focal seizures, meaning the seizures began in one area or network of the brain. Ten of those 12 had changes in awareness. Reports included lack of response, staring, repeated movements, and brief periods of not knowing where they were. These examples come from a small clinical group. [2]
The person stops an activity, stares, or does not respond in the way they normally would. An observer may notice a distinct beginning and ending. Apathy, distraction, or reduced engagement can also affect responsiveness, so the sequence and context matter.
A familiar phrase or task suddenly stops. Speech arrest and behavioral arrest are possible focal seizure features discussed in the FTD literature. Compare the episode with the person's usual language ability and usual pauses, rather than with how they communicated before dementia. [1]
Some focal events involve automatic movements or a sensory change. FTD can itself produce repetitive actions, and a person with language impairment may struggle to describe an internal sensation. Repetition alone does not make a behavior epileptic. [2]
Convulsive seizures also occurred in the clinical cohort. Some focal seizures progressed to bilateral convulsions. Record what happened before the shaking as well as the event itself and the person's recovery; the most visible part may not be the beginning. [2]
Example of a useful event description
“Usually answers yes or no despite difficulty finding words. During breakfast, stopped chewing and did not respond to their name for about a minute. Then began responding again. The same sequence happened twice this week.”
This note records how the event differed from the person's usual language difficulty, how long it lasted, and whether the same sequence happened again. Those details can help a clinician decide what requires further evaluation.
Describe the event before deciding its cause. A sudden beginning, a similar sequence each time, and a recognizable recovery make an episode worth reporting to the care team. A clinician still needs the wider medical history and, when appropriate, testing.
How the forms of FTD differ
Some forms of FTD mainly change behavior. Others mainly affect language or movement. These outward patterns do not always reveal the brain changes causing them, which is important when comparing seizure studies. [5]
| Form of FTD | What may already be usual | Which details help |
|---|---|---|
| Behavioral variant FTD bvFTD | Apathy, disinhibition, loss of empathy, repetitive behavior, and changes in eating. | Was there a discrete interruption in awareness or response, distinct from the ongoing behavioral pattern? What happened immediately before and afterward? |
| Semantic variant primary progressive aphasia svPPA | Progressive difficulty understanding words and recognizing their meaning. | Was the person unable to understand the question, or did their response abruptly change from what is usual for them? Could they respond in a familiar nonverbal way? |
| Nonfluent/agrammatic primary progressive aphasia nfvPPA | Effortful speech, speech-planning difficulties, or impaired grammar. | Was there a new, time-limited interruption beyond the usual speech difficulty? Did awareness, movement, or recovery also change? |
| FTD with motor features or overlapping syndromes | Weakness, stiffness, movement difficulty, or jerks may complicate an account of an event. | Did a new episode differ from the established movement problem? Were there changes in responsiveness, falls, or recovery that another observer could describe? |
Clinical descriptions: [5]. Motor-spectrum cohort context: [2] [3].
Hashmi's study recorded seizures in behavioral, semantic, and nonfluent forms. Behavioral variant FTD was the largest group in the study, but the researchers found no clear difference in seizure frequency among the forms. [2]
An earlier study recorded no seizures in its semantic-variant group, while the newer study recorded seven. A small result from one study should not be turned into a rule that one form is unaffected. [2] [3]
Fainting, acute illness, metabolic disturbance, medication effects, and sleep-related events may require a different explanation and response. Prior head injury or stroke also matters. An FTD diagnosis does not establish the cause of a new seizure or a new episode. [2] [7]
Logopenic primary progressive aphasia is often associated with Alzheimer's pathology. A language-led dementia should not automatically be assigned FTD-specific seizure estimates. [5]
What EEG studies have found
An EEG records the brain's electrical activity. It may show a seizure, a brief seizure-related discharge between seizures, or more general changes in brain function. Each finding means something different.
Only 13 of the 24 people in Hashmi's seizure group had EEG results. Three were reported as normal, seven had non-epileptiform abnormalities, two had epileptiform discharges, and one had a seizure recorded. The paper does not establish that the recorded seizure lacked clinical signs. [2]
Among 62 tested people without a clinical seizure history, the authors reported epileptiform discharges in two. Neither had events concerning for seizures. These are direct FTD observations of discharges without recognized clinical events, not two proven silent seizures. Testing was selective, not systematic population screening. [2]
The missing evidence is clear. These data cannot tell us how often seizures without outward signs occur in FTD, how reliably EEG detects them, or whether brief discharges affect language, behavior, or the course of dementia. Better studies are needed to answer those questions.
Limits of EEG detection
A normal EEG can leave epilepsy unresolved. The result depends on when and how long the brain was recorded, which areas the electrodes could detect, and what happened during the recording. [7]
A short EEG samples a limited period. Longer recordings may include ordinary activities and sleep, providing more time to capture activity that comes and goes. The report should say whether the person's familiar event occurred during the EEG.
Activity beginning in a small or deep brain area may not produce a clear signal at the scalp. In a two-person Alzheimer's study, electrodes near a deep memory area recorded seizures in one person that did not appear on scalp EEG. This finding explains a possible scalp-recording limit, but it does not measure how often FTD activity is missed. [8]
Movement, muscle activity, electrode problems, and harmless electrical patterns can complicate interpretation. Longer recordings also create more data to review. A computer may help identify possible signals, but the result still needs clinical review and testing in FTD. [10]
Recording time and signal visibility are separate limits. A longer EEG can add useful information because it provides more time to capture intermittent activity. It cannot guarantee that activity beginning deep in the brain will appear clearly at the scalp. FTD studies have not measured how often routine or longer EEG misses seizures without outward signs.
NICE guidance advises against using EEG to rule out epilepsy. It describes additional recording options when uncertainty persists and emphasizes the history, eyewitness accounts, and video when available. These are general epilepsy principles, not a recommendation to screen everyone with FTD or to use invasive electrodes routinely. [7]
Why recognition matters
A seizure disorder can affect how an event is investigated, treated, and followed. In FTD, care also needs to account for communication, behavior, daily function, and the work placed on families and care teams.
In the 2025 specialist-clinic cohort, 21 of the 24 people with seizures were reported as controlled on antiseizure medication at follow-up; the other three had no further episodes without medication. That is an encouraging clinical observation, not a guaranteed response rate or a comparison of treatments. [2]
Some medicines used for epilepsy are also prescribed for pain, anxiety, or behavioral symptoms. Both recent FTD studies found use beyond patients with diagnosed seizures. A prescription is not proof of epilepsy, and changes in alertness or behavior need to be considered alongside why each medicine was prescribed. [1] [2]
A speech-language professional may notice a pause in communication. A family member may notice a repeated sequence at home. A residential care worker may see the recovery. Seagull's practical emphasis is on sharing specific observations so that a brief event is not reduced to a vague label such as “behavioral deterioration.”
The reviewed FTD studies do not establish that treating seizures or isolated discharges slows dementia. The Finnish study found no significant mortality difference after adjusting for age at diagnosis. Associations reported in Alzheimer's disease should not be presented as proven FTD outcomes. [1] [2]
New detection technology
Researchers are studying ways to record for much longer periods and find signals that may be difficult to see during standard EEG review. The studies below involved people with epilepsy, not people with FTD.
Tested in epilepsy | Not yet tested in FTD
The prospective UMPIRE study implanted a bilateral subscalp EEG system in 26 adults with epilepsy. It investigated safety and recording performance over longer-term use. During simultaneous comparison recordings, all 25 seizures seen on scalp EEG in eight participants were also identified by the subscalp system. This is concordance with scalp recordings, not proof of detection of scalp-invisible seizures. [9]
Why Seagull is watching: prolonged recording could help investigate events that are infrequent or poorly recalled. For FTD, tolerability, consent, caregiver workload, electrode coverage, missed events, and clinical benefit would need dedicated evaluation. Under the scalp does not mean inside the brain. This early, manufacturer-supported epilepsy study does not establish an FTD indication.
Tested in temporal lobe epilepsy | Not yet tested in FTD
Researchers trained a deep-learning system using simultaneous scalp and near-hippocampal recordings, then evaluated it in separate datasets. It identified signatures of hippocampal epileptiform activity that conventional visual review could miss. Participants had temporal lobe epilepsy or were controls; the study was not an FTD trial. [10]
Why Seagull is watching: the advance is in extracting a difficult signal, not merely automating visible spike counting. FTD studies would need to establish false-positive rates, performance across clinical presentations, and whether detected activity explains symptoms or changes care. Detecting a discharge signature is not the same as diagnosing a silent seizure.
Research insights
FTD varies in both its symptoms and the brain changes causing them. New findings are most useful when the people studied, the limits, and the connection with earlier work are clear.
Genetics | Muroni et al., 2022
In a sample of 84 people with FTD, 7.1% had epilepsy. The study found no clear difference based on whether a person carried the C9orf72 gene change. The results did not support epilepsy as a characteristic feature of that change. [6]
Seagull's perspective: Genetic case reports can reveal important possibilities without providing reliable risk estimates. Neither this small study nor the larger clinical studies establish a gene-based seizure prediction tool.
Brain imaging | Hashmi et al., 2026
A 2026 analysis examined MRI and PET scans from the same clinic group reported in 2025, using a broader seizure definition. Only seven people with seizures had PET scans, and six showed reduced activity in the temporal lobe. The differences between groups were not statistically clear. [11]
Seagull's perspective: Imaging may help researchers study shared areas of vulnerability. This small study did not validate a scan that can identify “seizure-prone FTD.” Its 10% seizure figure comes from a group that overlaps with the earlier 7.6% study, so it is not an independent confirmation.
Brain changes confirmed after death | Vöglein et al., 2022
Among 53 people whose frontotemporal brain disease was confirmed after death, seizures were recorded less often in the 39 with TDP-43 changes than in the 14 without them. Both groups and the seizure counts were small. The group without TDP-43 included several different types of brain change. [4]
Seagull's perspective: Future studies should separate the symptoms a person experiences from the brain changes causing them. This finding helps define that question, but it cannot predict seizure risk from a behavioral or language form of FTD.
What research needs to answer next
Studies support an association between FTD and seizures. The next step is to learn who is most affected, what current testing misses, and whether better detection improves daily life.
Larger studies that follow people over time should compare the behavioral, language, and movement forms of FTD. They should separate epilepsy that began earlier from new seizures and record brain changes, past brain injury, medications, and disease stage.
FTD studies should count visible seizures, seizures recorded without outward signs, and brief discharges separately. They also need to report sleep, electrode placement, recording length, and how the EEG was interpreted.
Studies should connect electrical findings to language, behavior, attention, sleep, everyday function, and caregiver experience. Association with an EEG finding is not enough to show that it caused a symptom or accelerated decline.
Trials are needed to determine whether identifying and treating otherwise unrecognized activity benefits people with FTD. They must measure adverse effects and care burden as well as seizure counts, and distinguish treatment of established epilepsy from treatment of isolated discharges.
FTD research supports taking seizures seriously. Researchers know far less about the frequency and effects of electrical activity without outward signs. Technology studies in epilepsy suggest directions for future FTD research. A clinician still needs to interpret an event description, examination, and any test results together.
Sources and evidence notes
Seagull checked the main clinical estimates against the full papers in its reference collection. The evidence was reviewed on 3 September 2026. This is an educational review rather than a clinical guideline or complete systematic review.
The guide prioritizes research from the past ten years. Each note explains what the study examined and how directly it applies to FTD. Group studies, brain-tissue studies, clinical guidance, and technology research answer different questions. Seagull's perspective is labeled separately.
Kilpeläinen A, et al. (2025). Prevalence of Epilepsy in Frontotemporal Dementia and Timing of Dementia Diagnosis. JAMA Neurology, 82, 715–721.
Direct FTD evidence, retrospective case-control study. 245 FTD participants, matched controls, and an Alzheimer's comparison group. Register-based epilepsy outcomes; not systematic EEG screening. Later estimates concern survivors.
Hashmi SA, et al. (2025). Co-morbid seizures in frontotemporal dementia: What do they tell us? Epilepsy Research, 218, 107640.
Direct FTD evidence, retrospective specialist-clinic cohort. 24 of 317 in the primary seizure analysis. Includes one acute stroke-related seizure alongside epilepsy and single unprovoked events. Small seizure group and selective EEG testing limit generalization.
Beagle AJ, et al. (2017). Relative Incidence of Seizures and Myoclonus in Alzheimer's Disease, Dementia with Lewy Bodies, and Frontotemporal Dementia. Journal of Alzheimer's Disease, 60, 211–223.
FTD-spectrum evidence, retrospective memory-center study. 348 in the FTD group, including PSP and corticobasal syndromes. The 3.0% result is a cumulative probability estimate, not a raw prevalence. Retained for its important cross-subtype comparison and relationship to newer studies.
Vöglein J, et al. (2022). Seizure prevalence in neurodegenerative diseases: a study of autopsy proven cases. European Journal of Neurology, 29, 12–18.
Pathology-confirmed evidence, retrospective brain-bank study. FTLD subgroup of 53 within 454 cases. Records cover the symptomatic course; seizure details, provoked status, and treatment were insufficiently characterized. FTLD is not interchangeable with every clinical FTD cohort.
de Souza LC, et al. (2022). Diagnosis of frontotemporal dementia: recommendations of the Scientific Department of Cognitive Neurology and Aging of the Brazilian Academy of Neurology. Dementia & Neuropsychologia, 16, 40–52.
Clinical diagnostic guidance. Supports descriptions of FTD presentations and language-variant distinctions, not seizure-frequency estimates.
Muroni A, et al. (2022). Does epilepsy contribute to the clinical phenotype of C9orf72 mutation in fronto-temporal dementia? Epilepsy & Behavior, 133, 108783.
Direct FTD evidence, small clinical genetic comparison. 84 participants. No significant epilepsy difference by C9orf72 status; does not establish equivalence or exclude smaller effects.
National Institute for Health and Care Excellence. Epilepsies in children, young people and adults (NG217): diagnosis and assessment. Accessed 3 September 2026.
General epilepsy guidance. Supports the role and limits of EEG and the importance of clinical assessment. Not an FTD-specific screening protocol.
Lam AD, et al. (2017). Silent hippocampal seizures and spikes identified by foramen ovale electrodes in Alzheimer's disease. Nature Medicine, 23, 678–680.
Alzheimer's case evidence, not FTD. Two participants with near-hippocampal recordings. Demonstrates scalp-invisible activity in selected cases; does not estimate FTD prevalence or justify routine invasive monitoring.
Halliday AJ, et al. (2025). The UMPIRE study: A first-in-human multicenter trial of bilateral subscalp monitoring for epileptic seizure detection. Epilepsia, 66, 3426–3439.
Prospective device research in epilepsy, not FTD. 26 implanted participants; manufacturer-supported with disclosed industry relationships.
Abou Jaoude M, et al. (2022). Noninvasive Detection of Hippocampal Epileptiform Activity on Scalp Electroencephalogram. JAMA Neurology, 79, 614–622.
Diagnostic algorithm research in temporal lobe epilepsy, not FTD. Independent validation datasets; no demonstrated FTD clinical benefit.
Hashmi SA, et al. (2026). Co-morbid seizures in frontotemporal dementia: MRI and PET correlations. Epilepsy & Behavior Reports, 34, 100863.
Direct FTD evidence, exploratory imaging analysis. Overlaps the 2025 clinic cohort and uses a broader seizure group. Small PET sample; imaging differences were not statistically significant.