Brain Tumour-Related Epilepsy

When a brain tumour and seizures become part of the same neurological problem

A brain tumour can affect much more than the space it occupies on an MRI scan. Some tumours alter the electrical behaviour of nearby brain tissue and the wider networks connected to it. When epileptic seizures occur in association with a brain tumour, clinicians often use the term brain tumour-related epilepsy, or BTRE.

This can occur with primary tumours that begin in the brain and with secondary tumours — metastases — that have spread to the brain from cancer elsewhere in the body. Seizure risk varies considerably according to tumour type, molecular biology, location, growth pattern and the surrounding brain tissue. Reviews commonly report seizures in a substantial proportion of people with brain tumours, with particularly high rates in some slower-growing, cortically based tumours.

That variation matters. A tumour does not have to be highly malignant to be highly epileptogenic, and a tumour that causes seizures is not automatically aggressive.

Why can a tumour cause seizures?

A tumour-related seizure is not simply the result of a lump physically “pressing on the brain”.

The tissue around a tumour may undergo complex biological changes. Research has implicated altered glutamate signalling, reduced inhibitory GABA activity, inflammation, blood-brain barrier disruption, changes in extracellular ions and wider network reorganisation. In some IDH-mutant gliomas, the metabolite D-2-hydroxyglutarate has also been investigated as part of the link between tumour biology and neuronal hyperexcitability.

This helps explain why epileptic activity may arise from brain tissue around a tumour rather than simply from the visible centre of the lesion.

It also reinforces an important principle: the abnormality seen on an MRI and the network generating seizures are related questions, but they are not necessarily identical.

Tumour type matters

Seizure risk is particularly high in some slow-growing, cortically based tumours, including tumours sometimes grouped as low-grade epilepsy-associated tumours. Examples include dysembryoplastic neuroepithelial tumours (DNETs) and gangliogliomas.

These may first become apparent because of recurrent seizures. Some people may live with epilepsy for years before the underlying lesion is identified or treated. When seizures have been occurring for a long time, the epileptic network can involve tissue beyond the visible tumour.

Diffuse gliomas can also be strongly associated with epilepsy. Seizures are common in lower-grade gliomas and may sometimes be the first manifestation of the disease. Higher-grade gliomas can also produce seizures, but their clinical course and biological behaviour are different.

Brain metastases, meningiomas and numerous other intracranial tumours can also be associated with seizures. There is therefore no single form of “brain tumour epilepsy”.

Location matters — but location alone is not enough

Tumours involving or irritating cerebral cortex are generally more likely to produce seizures than lesions in areas that are less directly involved in cortical electrical networks.

Frontal, temporal, parietal and occipital tumours may therefore produce very different seizure manifestations. A temporal tumour might be associated with altered awareness, déjà vu, unusual smells, fear or automatisms. A tumour affecting motor networks might produce focal jerking or tonic posturing. Occipital involvement can produce visual seizure symptoms.

But symptoms cannot identify tumour pathology on their own.

Seizure semiology tells clinicians something about the network being activated. Imaging tells them about structure. EEG provides physiological evidence. Histopathology and molecular testing determine what the tumour actually is. Those pieces have to be interpreted together.

A seizure can be the first sign

For some people, a first seizure is what leads to the brain scan that discovers a tumour.

That does not mean that every first seizure indicates a brain tumour. There are many more common explanations for seizures, and many people with epilepsy have no tumour.

However, structural brain imaging is an important part of investigating appropriate first seizures and newly diagnosed focal epilepsy because clinicians need to identify potentially important structural causes. NICE recommends standard structural MRI as the initial diagnostic imaging test for suspected glioma, unless MRI is contraindicated, and referral to a specialist multidisciplinary team at first radiological diagnosis.

One seizure may change treatment

In many epilepsy settings, the distinction between a single unprovoked seizure and established epilepsy is important. Brain tumour-related seizures are a particular clinical situation because the underlying structural lesion can confer a substantial risk of further seizures.

Contemporary neuro-oncology practice generally supports starting antiseizure treatment after a verified tumour-associated seizure rather than waiting for repeated events.

The exact diagnosis still matters. Not every transient neurological event in somebody with a tumour is necessarily epileptic. Tumours can also cause weakness, language disturbance, headache, altered cognition, vascular complications and other neurological events that may enter the differential diagnosis.

What about people who have never had a seizure?

This is an important distinction.

Giving an antiseizure medication simply because somebody has a newly diagnosed brain tumour does not routinely prevent a first seizure sufficiently to justify prophylactic treatment. The Society for Neuro-Oncology and European Association of Neuro-Oncology guideline recommends that people with newly diagnosed brain tumours who have never had a seizure should not routinely receive antiseizure medication solely to reduce the risk of a first seizure.

This is very different from treating somebody who has already experienced a tumour-associated seizure. Avoiding unnecessary prophylaxis also reduces exposure to adverse effects and drug interactions.

Choosing an antiseizure medication

There is no universal antiseizure medication that is right for every person with a brain tumour.

The choice has to take into account seizure type, age, other medical conditions, cognitive and psychiatric effects, pregnancy considerations where relevant, kidney and liver function, other medication, chemotherapy or targeted treatment, and potential drug interactions.

Modern neuro-oncology practice often favours antiseizure medicines with fewer hepatic enzyme interactions over older strongly enzyme-inducing drugs because cancer treatment can already involve complex pharmacology. Levetiracetam is frequently used, but frequency of use does not mean it is automatically the best choice for every individual. Behavioural or psychiatric adverse effects can be important for some people, and other medicines may therefore be preferable according to individual circumstances.

Medication selection should be coordinated with the neurological and oncological treatment plan rather than considered separately from it.

Treating the tumour can treat the epilepsy

Brain tumour-related epilepsy is unusual because seizure treatment and treatment of the underlying cause can overlap directly.

Surgical removal of an epileptogenic tumour may substantially improve seizure control, particularly in appropriate low-grade and epilepsy-associated tumours.

But epilepsy surgery in this setting is not simply a matter of “remove what appears on MRI”. Surgeons may have to balance oncological tumour resection, seizure control and preservation of language, movement, memory, vision and other functions. Depending on location, this can involve functional imaging, neuropsychological assessment, intraoperative monitoring, awake surgery or other forms of functional mapping.

NICE recommends that surgical expertise for suspected low-grade glioma should include access to appropriate specialist techniques such as awake craniotomy, neurophysiological monitoring, neuroradiological support and image guidance where indicated.

The safest maximum tumour removal and the best epilepsy operation are therefore related goals, but they are not always exactly the same operation.

Radiotherapy and chemotherapy can also affect seizures

Effective tumour treatment may reduce seizure frequency by controlling the disease responsible for the epileptic network. For some gliomas, seizure control can therefore improve following oncological treatment as well as surgery.

The reverse can also occur. Treatment-related inflammation, oedema, surgery, tumour progression or other changes in the brain may alter seizure frequency.

That is why a change in seizures should not automatically be interpreted as “the epilepsy medication has stopped working”. The tumour, its treatment, medication adherence, metabolic factors and other neurological changes may all need consideration.

Can worsening seizures indicate tumour progression?

Sometimes — but not always.

A new seizure pattern, increasing frequency or breakthrough seizures in somebody who had previously been stable can prompt clinicians to reassess the tumour and surrounding brain.

However, seizures fluctuate for many reasons. Sleep deprivation, illness, medication changes, missed doses, treatment effects and other physiological stresses can all alter seizure control.

A breakthrough seizure therefore cannot, by itself, prove tumour progression. Clinical assessment and appropriate imaging are needed.

MRI and EEG answer different questions

MRI and neuroimaging are central to defining the tumour and structural changes around it. EEG records electrical activity. Neither replaces the other.

An EEG may show epileptiform activity, focal slowing or other abnormalities, but a normal routine EEG does not exclude tumour-related epilepsy.

Likewise, the presence of an MRI lesion does not automatically prove that every unusual event experienced by the person is an epileptic seizure. This is particularly important when somebody has a complicated neurological illness in which more than one type of event may occur.

Longer EEG monitoring or video-EEG may sometimes be needed when the nature of recurrent events remains uncertain. See also MRI Lesion Does Not Always Mean Seizure Cause.

Seizures after surgery

A person can continue to experience seizures after successful tumour surgery.

Several explanations are possible. The surrounding cortex may already have developed an established epileptic network. Residual tumour may remain because complete resection was unsafe. Postoperative tissue changes can affect cortical excitability. In other situations, seizures may gradually improve following surgery.

For this reason, antiseizure medication is not necessarily stopped immediately simply because the visible tumour has been removed. Withdrawal decisions require individual neurological and neuro-oncological assessment. Evidence around the optimal duration of antiseizure therapy and withdrawal in tumour-related epilepsy remains less certain than many other aspects of management.

Tumour recurrence and seizure recurrence are not the same thing

A returning seizure does not prove a tumour has returned. Likewise, radiological progression does not guarantee that seizures will worsen.

Tumour behaviour and epileptic-network behaviour overlap, but they are not interchangeable biomarkers.

That distinction is particularly important for people living through repeated MRI surveillance. A single seizure should not be used independently to draw conclusions about scan results that have not yet been obtained.

Cognition, mood and quality of life

The burden of brain tumour-related epilepsy is not confined to seizure counts.

People may simultaneously experience the neurological effects of the tumour, treatment-related fatigue, cognitive changes, medication adverse effects, uncertainty about recurrence, loss of driving eligibility, changes in employment and fear of further seizures.

Recent reviews emphasise neuropsychological, behavioural and quality-of-life effects as significant parts of the condition rather than peripheral concerns.

A medication that stops seizures but creates intolerable cognitive or behavioural effects may therefore still require reassessment. Seizure control is important, but so is the life of the person experiencing them.

Brain tumour-related epilepsy is multidisciplinary

The most effective care often sits between specialties.

Neuro-oncology addresses the tumour. Epileptology addresses seizure classification, seizure control and the epileptic network. Neurosurgery considers tissue diagnosis, tumour resection and sometimes seizure-producing tissue. Neuroradiology interprets structural and treatment-related changes. Neuropathology and molecular diagnostics identify what the tumour biologically is. Neuropsychology can help assess cognition, functional risks and changes over time.

The condition cannot always be divided neatly into “cancer treatment” on one side and “epilepsy treatment” on the other.

The key distinction

A brain tumour is a structural cause that can produce epilepsy, but the tumour and the epilepsy are not interchangeable.

A visible lesion does not tell clinicians everything about the seizure network. A seizure does not reveal the tumour’s grade. Breakthrough seizures do not automatically prove progression. A normal EEG does not exclude tumour-related epilepsy. And somebody who has never had a seizure should not automatically be placed on antiseizure medication simply because a tumour exists.

Brain tumour-related epilepsy is best understood as the interaction between tumour biology, surrounding brain tissue and electrical brain networks.

Sources and further reading

Evidence checked: September 2026.

This page is for general education and does not replace individual medical advice from a neurology, neuro-oncology or neurosurgical team.