Brain tumor-related epilepsy …

Jessica W Templer MD

Neuro-Oncology

Updated 07.06.2025
Released 06.24.2022
Expires For CME 07.06.2028

Brain tumor-related epilepsy

Author: Jessica W Templer MD

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Editor: Rimas V Lukas MD

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Brain tumor-related epilepsy

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Introduction

Overview

Seizures can be associated with nearly all brain tumors that have a cortical predilection. Although the incidence varies depending on several factors, including tumor grade, type, and location, seizures have a significant impact on patients’ quality of life regardless of the etiology. In some cases, seizures not only contribute to morbidity and mortality but can also serve as a reminder of their cancer diagnosis.

As our knowledge of tumor markers advances, we are gaining deeper insights into the interplay between neurons, tumor cells, and the immunologic microenvironment that leads to tumoral epilepsy. This article provides a summary of the current literature on the epidemiology, pathophysiology, medical and surgical management, and prognosis in this patient population.

Key points

	• Risk of tumoral epilepsy is greatest with lower grade tumors compared to higher grade tumors.
	• Neuronal hyperexcitability and tumor infiltration are intimately linked through several known mechanisms. The direct impact of treating seizures on tumor behavior in the clinical setting remains unknown.
	• Expanding knowledge of tumor genetics is revealing links to epilepsy risk (eg, IDH, BRAF v600E), paving the way for identifying at risk patients and targeted treatments for both oncology and seizure management.

Historical note and terminology

By virtue of the conspicuous symptoms associated with seizures, such as convulsions and impairment of consciousness, epilepsy has been depicted in ancient texts and meticulously documented in medical texts since the time of the Babylonians (46). The first known report of tumor-related epilepsy was documented by Hughlings Jackson in 1882 (60). The case report described a man with seizure onset at the age of 28, with variable semiology, including focal dystonic seizures and aphasic seizures that intermittently progressed to convulsions. A glial tumor in the left hemisphere was discovered at autopsy.

In time, the brain tumors most commonly associated with epilepsy included glioneuronal tumors, ie, ganglioglioma (1926) and dysembryoplastic neuroepithelial tumors (1988) (55).

As a group, these low-grade tumors were the first tumors to be included in the category of “long-term epilepsy-associated tumors” (LEATs) when the term was first defined by Luyken in 2003 (40). Since then, the term LEAT has also evolved to encompass papillary glioneuronal tumors, angiocentric gliomas, isomorphic diffuse gliomas, multinodular and vacuolating neuronal tumors, and polymorphous low-grade neuroepithelial tumors (55). Although the tumors included in the category have been established, the current understanding of LEATs as an entity is evolving with access to molecular genetic testing and DNA methylation profiling. In the most recent WHO classification, molecular markers are incorporated in tumor classification (39).

Over the last decade, genetic markers, including IDH mutations, BRAF v600E mutations, PIK3CA, FGFR1, NF1, and PTPN11, have been identified as key factors in tumor-related epilepsy (01; 38). Whereas IDH 1/2 mutations contribute to glioma-related epilepsy, BRAF v600E, PIK3CA, and PTPN11 are associated with LEAT.

Although our understanding of the pathogenesis of tumor-related epilepsy continues to evolve, shared mechanisms between oncogenesis and epileptogenesis suggest that these two entities are intimately related. A bi-directional relationship between glioma progression and neuronal hyperexcitability has been identified (64). Although there is an unquestionable need for seizure control for clinical purposes, the potential benefit for oncologic reasons remains to be understood.

The ultimate goal is to identify actionable therapeutic targets through a better understanding of the pathogenesis of tumor-related epilepsy. Highlights of discoveries in the pathogenesis of tumor-related epilepsy in addition to new treatment strategies, including IDH inhibitors in the case of low-grade glioma, are further discussed.

The terms “tumor-related epilepsy,” “brain tumor–related epilepsy,” and “tumoral epilepsy” are often used interchangeably to describe any patient at risk of seizures if they are without antiseizure medications in the context of a brain tumor. Seizures may occur at any point during the course of a patient’s disease, including prior to resection, in the context of ongoing radiation or chemotherapeutic treatment, or after completion of standard-of-care management. As such, epilepsy management in patients with tumor-related epilepsy must be re-evaluated on an ongoing basis to assess whether adjustments in their medication are warranted.

Clinical manifestations

Presentation and course

	• Seizures are a common presentation for patients with brain tumors. The prevalence of seizures is closely linked to the tumor type.
	• In general, seizures are more frequently seen in patients with low-grade tumors (ie, dysembryoplastic neuroepithelial tumors) compared to high-grade tumors (ie, IDH-wildtype glioblastoma).
	• The presence of an isocitrate dehydrogenase (IDH) mutation is associated with a higher risk of seizures in gliomas.
	• Long-term epilepsy-associated tumors (LEATs) have the highest likelihood of seizure freedom after gross total resection among all brain tumors.
	• The extent of resection is significantly related to the likelihood of seizure freedom after resection of a low-grade glioma.

The prevalence of seizures associated with brain tumors is variable and is most significantly associated with the tumor grade; however, advances in molecular genetic classifications suggest that tumor genetics play a significant role in the risk for seizures.

Of all tumor types, epilepsy is seen in 30% or more of patients with brain tumors (58). Low-grade tumors (eg, neuroepithelial tumors) are more epileptogenic, with seizures seen in up to 100% of patients with dysembryoplastic neuroepithelial tumors and in 80% to 90% of patients with gangliogliomas (58). IDH-mutated subtypes of WHO grade 2 or 3 gliomas are associated with seizures more often than IDH wild-type (wt) gliomas, with seizures seen in 50% to 80%. However, the increased frequency of seizures has not been seen in patients with IDH-mutated grade 4 astrocytomas compared to glioblastoma IDHwt (68; 20). In addition, patients with IDH-mutated low-grade tumors are more likely to develop pharmacoresistant seizures compared to those with IDHwt tumors (16). Seizures are seen in 29% to 49% of patients with grade 4 gliomas (independent of IDH mutation status) (58).

Preoperative seizures are reported in 29% to 60% of patients with meningiomas with risk factors, including male sex, absence of headache, and peritumoral edema (58; 27). After meningioma resection, approximately 70% of those with preoperative epilepsy become seizure free. New postoperative seizures have been reported in 0% to 42.9% (27; 35).

With respect to brain metastases, seizures are seen in approximately 20% to 35% of patients (58). Of all patients with systemic cancer, approximately 20% develop brain metastases, with lung, breast, and melanoma being the most common (27; 28; 51). Risk factors associated with brain metastases and seizures may include younger age, parietal location, and recurrent tumor, although these require further validation (51).

Prognosis and complications

Long-term epilepsy-associated tumors (LEATs). It is uncommon for LEATs (WHO grade 1) to undergo malignant transformation, but it has been reported. Prognosis from an oncologic standpoint is excellent, although these lesions are highly epileptogenic. Approximately 80% to 100% of patients have seizures, and they are often medically refractory (28).

Low-grade gliomas. Diffuse astrocytomas and oligodendrogliomas will inevitably undergo malignant transformation to a high-grade glioma (WHO grade 3 or 4). As such, when the tumor is still within the low-grade classification (WHO grade 2), treatment goals include delaying time to malignant transformation as well as seizure control, in addition to improving progression-free survival and overall survival. Patients with seizures in the context of low-grade gliomas have better prognosis compared to those without a history of seizures. The largest observational study of 1509 patients with low-grade gliomas found that approximately 90% had a history of seizures, and those with seizures at diagnosis had increased malignant, progression-free, and overall survival compared to those without a history of seizures (48). These findings may be influenced by the IDH mutational status of the tumors. IDH-mutated tumors harbor a higher risk of seizures but also a better prognosis. IDH mutational status was not routinely evaluated in all patients at the time of the aforementioned study.

In terms of the prognosis of tumor-related epilepsy, seizure control is significantly related to the extent of resection for patients with low-grade gliomas (26; 67). Approximately 70% of patients who undergo gross total resection (of FLAIR abnormality on MRI) are seizure free (Engel class I), whereas approximately 30% continue to have seizures (Engel class II to IV) (12; 26). One group has proposed that the threshold for the extent of resection is 80% as seizure freedom (for a limited timeframe) is often attained in this population when at least 80% of total tumor volume resection is achieved (67). However, it is estimated that no more than 45% of patients are eligible for gross total resection as low-grade gliomas tend to grow close to or within eloquent regions of the brain (52). Seizure control (Engel class I) has been reported in 43% to 47% of patients with subtotal resection and 8% of patients with biopsy alone (12; 26). Therefore, the goal of resection is to maximize reduction of tumor burden for both oncologic as well as seizure purposes. Studies of seizure frequency in gliomas are limited by the utilization of patient-reported outcomes of seizure frequency and by the typical lack of lifelong follow-up, which can be of decades’ duration in patients with low-grade gliomas.

High-grade gliomas. The largest series to date examining features of tumor-related epilepsy in patients with malignant gliomas (WHO grade 3 and 4) evaluated 648 patients (505 with glioblastoma, 143 with astrocytoma WHO grade 3); 24% of the patients presented with seizures, and a total of 77% were seizure-free 12 months after surgery (11). Most importantly, seizure recurrence in patients who had postoperative seizure control was significantly associated with tumor recurrence. This study did not incorporate the contemporary molecular markers (eg, IDH mutational status). A systematic review of post-treatment epilepsy (ie, surgery, radiation, or both) reported a prevalence of approximately 25% among patients with WHO grade 3 or 4 gliomas (30).

Meningiomas. Prior observational studies have reported a linear growth rate of 2 to 4 mm per year for asymptomatic meningiomas; however, some meningiomas have a nonlinear growth rate, and some do not grow over time (09). Surveillance imaging is key to understanding the behavior of a patient’s meningioma. The true growth rate of symptomatic meningiomas is unknown as the majority of symptomatic lesions are treated with resection. Grade 2 and 3 meningiomas have a high risk of recurrence after gross total resection: 50% for grade 2 and 90% for grade 3 tumors at 5 years (09).

When seizures occur in the context of a meningioma, patients often undergo surgical resection. Approximately 90% of patients remain seizure free if they did not have seizures prior to resection, whereas only 60% of patients with seizures prior to resection are seizure free (14).

Brain metastases. Risk factors for postoperative seizures after resection of metastatic lesions include younger age, recurrent tumor, supratentorial location, and incomplete resection (51; 66). Interestingly, peritumoral edema and extent of resection are not associated with postoperative seizures (51). In a study of patients who were seizure-free prior to resection with a single supratentorial metastatic lesion, 30% of the patients who had a biopsy or subtotal resection developed seizures after surgery; 5% of the patients who underwent a gross total resection of the metastatic lesion developed seizures (66).

Seizures may be secondary to causes beyond the tumor itself, including radionecrosis after radiotherapy, cavernomas secondary to whole-brain radiotherapy, opportunistic CNS infections, or drugs that lower the seizure threshold (eg, bupropion, cisplatin) (58).

Biological basis

	• Seizures do not often arise from the tumor itself. They arise from the peritumoral tissue and, rarely, from distant locations outside of the peritumoral region.
	• The epileptogenicity of the peritumoral tissue is likely due to multiple factors, including but not limited to a hyperexcitable environment, mechanical disruption, and cortical damage.
	• The peritumoral environment is hyperexcitable, and this is due, in part, to an imbalance of excessive glutamate and reduced inhibitory GABA transmission. The relationship between this imbalance and the tumor genetic mutations identified in brain tumors is still being explored.
	• Additional hypotheses for causes of tumor-related epilepsy include free radical formation, alterations in neuronal function and connectivity, and alterations in expression of specific genes and proteins.
	• Tumor-related epilepsy is often refractory to the currently available antiseizure medications. This is thought to be due, in part, to the presence of multidrug resistance proteins.

Etiology and pathogenesis

Seizures often do not arise from the tumor itself. The epileptogenic cortex often lies in the peritumoral region and, in some cases, may be located beyond the peritumoral region (44; 50). Furthermore, it is clear that the cause of tumor-related epilepsy is multifactorial as no single tumor entity or features are unequivocally associated with seizures.

There are multiple theories explaining tumor-related epilepsy, although epileptogenicity likely arises at the intersection of these theories. These hypotheses are centered around the microcellular environment and structural causes. Mechanical compression, the inflammatory microenvironment, increased excitation and decreased inhibition at the neurotransmitter level, and structural damage from the balance of vascularization and oxygen demand likely all play a role (19).

The morphological changes that are present in peritumoral tissue also likely play a role in epileptogenicity. These changes can include aberrant neuronal migration, enhanced intracellular communication through gap junction channels, imbalance between local inhibitory and excitatory mechanisms (including glutamate concentrations), morphological alterations of synaptic vessels, and inflammatory processes (59).

Long-term epilepsy-associated tumors (LEATs). Over the last several years, certain genetic markers have been seen among specific WHO grade 1 tumors, including mutations in BRAF V600E (gangliogliomas), FGFR1 mutations (DNTs), and MYB (angiocentric glioma, isomorphic diffuse glioma, and papillary glioneuronal tumors) (19). The relationship between these mutations and epileptogenicity is still being understood. In the case of LEATs, two primary hypotheses have been proposed to explain tumoral epilepsy: one is the “tumorocentric approach” in which epileptogenicity is a consequence of the tumor itself, and the other is an “epileptocentric approach” in which the peritumoral cortical region is infiltrated by the tumor, resulting in neurotransmitter imbalance leading to tumoral epilepsy (19).

Gliomas. Glioma-related epilepsy is due to complex dynamic relationships between neurons, glia, and microglia that we are only beginning to understand.

Malignant glial cells and neurons have a bidirectional relationship that is now recognized as driving not only hyperexcitability leading to seizures but also tumor progression. Glial cells become embedded within the neuronal circuitry via presynaptic neurons and postsynaptic glioma cells. A positive feedback loop and continued synapses are formed, and the hyperactive state is maintained (36).

Similar to LEATs, genetic mutations also play a role in tumor-related epilepsy. A primary example is that of IDH-mutant tumors carrying a significantly higher risk of tumor-related epilepsy. Although the wild-type forms of isocitrate dehydrogenase (IDH) 1 and 2 oxidize isocitrate into alpha-ketoglutarate when the enzyme is mutated, alpha-ketoglutarate is reduced to D-2-hydroxyglutarate (D2HG). It was previously thought that the structural similarity between D2HG and glutamate increases neuronal excitability (13); however, this has fallen out of favor as it does not appear that D2HG activates NMDA or AMPA receptors via competitive inhibition (45; 18). Interestingly, even when exogenous D2HG is applied to 3D human cortical spheroids (including both cortical neurons and glial cells), spheroid firing increases even in the absence of glioma cells. When IDHmut glioma cells or IDHwt glioma cells are added and infiltrate the cortical spheroids, those with IDHmut glioma cells demonstrate increased neuronal firing rates, whereas the IDHwt glioma cell firing rates remain stable over time (18).

Neurotransmitter imbalance creates a hyperexcitable microenvironment. Glutamate, in its true state, likely plays a role in the increased risk of seizures with brain tumors. Glutamate, the primary excitatory neurotransmitter in the brain, is increased due to upregulation of glutamine, glutamine synthetase protein, and glutamine synthetase enzyme activity in glioblastoma (50). Furthermore, gliomas release neurotoxic levels of glutamate, which has been associated with the high expression of system xc^-, an antiporter that is responsible for extracellular glutamate release in exchange for cysteine uptake (08; 56). Although the tumor itself is releasing glutamate, peritumoral astrocytes are less able to remove glutamate; at the same time, microglia may release glutamate in response to glioma cell signaling (08). The presence of glutamate not only causes excitability but also contributes to cell death, allowing tumor growth (56).

Although glutamate plays a role in NMDA receptor activation, reduced inhibitory GABAergic transmission is also a factor in glioma-related epilepsy. In the case of gliomas, this is likely by downregulation of KCC2, a potassium chloride co-transporter (08). KCC2 functions to maintain a chloride gradient across neurons, thereby regulating GABA (gamma-aminobutyric-acid) function. In mouse models of gliomas, KCC2 expression is downregulated in the peritumoral tissue (as well as nontumoral epileptic cortex), which leads to increased intracellular chloride and thereby inhibits GABA activity, resulting in a lower seizure threshold (56).

Meningiomas. Similar to gliomas and WHO grade 1 tumors, epileptogenicity is driven by morphologic, biochemical, and metabolic causes. An imbalance between increased excitability and decreased inhibition exists due to increased excitatory synapses and loss of inhibitory synapses within the perilesional cortex (21). Although the underlying pathophysiological mechanism of tumor-related epilepsy with meningiomas has yet to be determined, it is likely multifactorial.

Epidemiology

	• Seizures are seen in approximately 30% to 100% of patients with brain tumors, depending on the tumor type.
	• Seizures are the presenting symptom for 20% to 40% of patients with brain tumors.
	• Low-grade tumors are more likely to be associated with seizures.

Of all tumors, brain tumors make up approximately 1% to 2% of tumors in adults (41). Among all patients with brain tumors, seizures are seen in approximately 30% to 100%, depending on the tumor type (28). Combining all tumor types, seizures are the onset symptom in 20% to 40% of patients with brain tumors. Of all patients with epilepsy, brain tumors are the cause of seizures in 6% to 10% of patients (41).

Low-grade lesions are more epileptogenic than high grade, although genetic features play a role. Patients who present with seizures are at a higher risk for continued seizures throughout their disease course, regardless of tumor type, antiseizure medication, and treatment. Brain tumors that are supratentorial, cortically based, and located in the frontotemporal regions are more commonly associated with seizures (58).

Long-term epilepsy-associated tumors (LEATs). Seizures are common in LEATs and occur in almost 100% of dysembryoplastic neuroepithelial tumors and in 80% to 90% of gangliogliomas. The mean age of onset for dysembryoplastic neuroepithelial tumors is 15 years of age and for gangliogliomas is 16 to 19 years of age, although they can be first identified at later ages as well. The average age for undergoing tumor resection for a WHO grade 1 tumor is 30 years of age (28).

Low-grade gliomas. Seizures are seen in 65% to 90% of patients with low-grade gliomas. A systematic review and meta-analysis identified predictors of postoperative seizure control in patients undergoing surgical resection of low-grade gliomas (53). Improved seizure outcome was seen in patients 45 years of age or older and with gross total resection compared to subtotal resection. Seizures with an onset 1 or more years prior to surgery as well as focal seizures (compared to generalized convulsions) were associated with poorer seizure control.

High-grade gliomas. Seizures are seen in 25% to 60% of patients with high-grade gliomas. Tumor location is a significant risk factor for seizures in patients with high-grade gliomas, specifically, superficial cortical areas or tumors in the temporal lobe, frontal lobe, or insula (22). In a voxel-based study of patients with no history of seizures in glioblastoma multiforme, tumor presence in the superior frontal, inferior occipital, and inferoposterior temporal lobes was associated with an increased risk of seizures after surgery (10). In addition, patients with multifocal disease have a higher risk of seizures compared to those with a singular tumor (24). This may merely represent a greater amount of cortex affected by the tumor.

Prevention

	• Based on the current AAN recommendations, there is no recommendation for the use of prophylaxis medications to prevent seizures in patients with brain tumors who have not already experienced seizures. However, this statement was made in 2000 and has not been re-evaluated using newer antiseizure medications.
	• Perioperative antiseizure medications are commonly used for prophylaxis with surgery for brain tumors, although the data are conflicting.

In 2000, the Quality Standards Subcommittee of the American Academy of Neurology (AAN) performed a meta-analysis of four randomized clinical trials and eight observational studies and reported that there appears to be no benefit for the prophylactic use of antiseizure medications in patients with brain tumors (32). None of the included trials showed a statistically significant difference in seizure incidence versus seizure freedom between patients with and without antiseizure medication prophylaxis. However, the meta-analysis included studies evaluating the use of phenytoin, carbamazepine, phenobarbital, and valproic acid. This meta-analysis did not review the outcome with newer antiseizure medications (ie, levetiracetam, lacosamide).

Since the 2000 AAN guidelines were published in 2021, the Society for Neuro-Oncology (SNO) and European Association of Neuro-Oncology (EANO) updated their recommended practice parameter for the use of antiseizure medications in patients with brain tumors (65). Based on an updated meta-analysis using studies examining newer, nonenzyme-inducing agents (ie, levetiracetam), the same recommendation was made. Providers should not prescribe antiseizure medication prophylaxis to seizure-naive patients with brain tumors.

The use of prophylactic antiseizure medications around the time of tumor resection is common, although the data regarding the benefit of using antiseizure medications perioperatively in patients without a history of seizures are conflicting. The aforementioned SNO/EANO practice parameter also indicated that based on their analysis, there is insufficient evidence (level C) to recommend that antiseizure medications be used in the perioperative period (65).

Diagnostic workup

	• The steps included in a diagnostic evaluation depend on the treatment goals.
	• The first step should always be to verify the concordance between a patient’s epilepsy and the brain tumor.
	• For low-grade lesions, diagnostic workup is often driven by the patient’s epilepsy, whereas oncologic goals drive the decision making for high-grade lesions.

The diagnostic evaluation for patients with tumor-related epilepsy significantly depends on the tumor type and treatment goals. In all cases with lesional epilepsy, the first question that should be addressed is whether a histological diagnosis is necessary. If a tissue diagnosis is needed, the surgery should be optimized with a surgical approach that will render the patient seizure free.

Further neurophysiologic studies should be considered if there are elements that are discordant when obtaining seizure history, including an EEG, ambulatory EEG, or possibly an epilepsy monitoring unit (EMU) admission. Similar neurophysiologic studies should be considered in pharmacoresistant epilepsy in the context of a lesion as epilepsy surgery may be warranted.

Low-grade lesions. Clinical decision making in cases of low-grade lesions is often guided by the patient’s epilepsy. In cases of pharmacoresistant epilepsy, additional neurophysiologic studies as well as imaging studies can help guide resection and increase the likelihood of seizure freedom. More specifically, patients may undergo an EEG and an EMU admission with continuous scalp video-EEG recording to confirm that seizure semiology, neurophysiologic data, and imaging are concordant. In guiding epilepsy surgery, a PET, SPECT, and MEG may be considered. Furthermore, a comprehensive neuropsychological evaluation may have value. Invasive EEG may be warranted in patients whose data are discordant or for whom suspected focal cortical dysplasia is associated with the lesion. Importantly, this testing should not significantly delay the timing of surgery as prolonged duration of seizures has been associated with poorer seizure outcome after surgery (40; 53).

High-grade lesions. These patients will often immediately go to surgery on discovery of the lesion. Immediate diagnostic work-up for epilepsy purposes is often unwarranted, although intraoperative ECoG could be considered. There are conflicting data regarding the value of ECoG in high-grade gliomas, although ECoG has not been prospectively studied in this patient population.

Meningiomas. Patients often undergo meningioma resection when the meningioma is symptomatic (eg, seizures, functional deficits, headaches). No prospective studies have looked at the value of EEG in patients with meningiomas undergoing evaluation or surgery. Although the sample size was small, one study evaluated the role of ECoG in patients with preoperative seizures undergoing meningioma resection and found that epileptiform discharge frequency pre-resection and post-resection did not correlate with postoperative epilepsy (29).

Management

	• The most commonly used antiseizure medication is levetiracetam due to its tolerability, lack of interactions with concurrent medications, and dosing regimen. However, mood side effects are common, and patients should be screened.
	• The role of surgery depends on the tumor type. In general, seizure frequency often improves with resection; however, ECoG may be considered.
	• When appropriate, chemotherapy and radiation may improve seizure frequency, particularly in infiltrating gliomas.
	• Antiseizure medication regimens should be routinely reassessed, both for the need to continue in light of ongoing oncologic treatments as well as tolerability.

Medical management

Treatment decisions in patients with tumor-related epilepsy, regardless of the type of tumor, are often driven by the goals of achieving seizure control and seizure freedom; improvement of quality of life; and improvement of survival (47).

In 2023, the Society for Neuro-oncology (SNO) published guidelines for the management of tumor-related epilepsy. Although there is no universally recommended first-choice antiseizure medication, understanding potential drug–drug interactions and adverse side effects are key to clinical decision making. Unfortunately, randomized controlled trials comparing antiseizure medications in this population are rare.

The most commonly used medication in patients with tumor-related epilepsy is levetiracetam as it does not have significant drug interactions, can be given as a loading dose, is safe in pregnancy overall, and is generally well-tolerated. However, mood side effects can be common and are more commonly seen in patients with frontal lobe tumors (03).

When levetiracetam is not tolerated or effective, lacosamide or lamotrigine are often the next agents of choice. One prospective study comparing lacosamide to levetiracetam in patients with tumor-related epilepsy found improved efficacy without mood side effects or impact on quality of life (42). Lamotrigine is similarly well-tolerated, but it takes time to increase the dose to a therapeutic dose. Therefore, it is not appropriate as an initial agent (without a concurrent medication). Benefits include safety during pregnancy and potential mood benefits. However, due to its slow titration schedule and its associated risk of severe cutaneous side effects (ie, Stevens-Johnson syndrome), it is often an impractical choice for this patient population. This is further complicated by the risk of cutaneous side effects from many CNS tumor treatments.

Zonisamide, clobazam, brivaracetam, or perampanel are additional medications to consider, keeping in mind potential side effects for the individual patient (eg, avoid zonisamide in patients with prior nephrolithiasis or clobazam in patients planning pregnancy).

In this population, it is important to re-evaluate the antiseizure medication(s) being used when a patient is on concurrent chemotherapy, immunomodulation, tyrosine-kinase inhibitors, or steroids (62).

Targeted treatment

RAS-RAF-MAPK pathway. Frequently, an alteration in the RAS-RAF-MAPK signaling pathway (eg, BRAF, FGFR, MYB/MYB1 genes) is observed among LEATs, likely contributing to the epileptogenic potential of these low-grade lesions.

BRAF inhibitors. Given the preponderance of the BRAF v600E mutation in pediatric low-grade gliomas (seen in 25% of dysembryoplastic neuroepithelial tumors, 50% of gangliogliomas, and 75% of pleomorphic xanthoastrocytomas), BRAF inhibitors have been investigated as monotherapy or in combination with the downstream MEK inhibitor (17). In a phase 2 trial, treatment with dabrafenib (a BRAF inhibitor) in conjunction with a MEK inhibitor (trametinib) showed longer progression-free survival and a greater response rate compared to standard chemotherapy (07). Unfortunately, seizure response rate was not assessed as part of this trial, although a single case report documented seizure response with the use of dabrafenib for ganglioglioma (49).

IDH inhibitors. Although we continue to develop our understanding of the specific mechanisms by which D2HG promotes a hyperexcitable environment, data suggest that reducing the amount of D2HG via IDH mutant inhibitors may decrease seizure frequency. In working with the cortical spheroids previously mentioned when the IDHmut cortical spheroids were treated with IDHmut inhibitors (ie, AGI5198 and AG881), the neuronal firing rate significantly decreased (18). Although preclinical studies have shown promise, these findings have yet to be consistently demonstrated in clinical trials. The INDIGO trial (phase 3 clinical study evaluating vorasidenib, an IDH inhibitor in IDH-mutated gliomas) excluded patients with uncontrolled seizures (43). Preliminary data demonstrate that in patients with seizures the use of vorasidenib appears to decrease their frequency.

Surgical management

The role of surgery is most significantly related to tumor type.

Long-term epilepsy-associated tumors (LEATs). Given that LEATs are extremely unlikely to undergo malignant transformation, the surgical goal is often to treat the patient’s epilepsy. The largest study of 1493 pathologically confirmed LEATs from the European Epilepsy Brain Bank reported that 75.9% of the patients were free from disabling seizures 5 years after surgery (37).

The published seizure freedom rate among patients with LEATs ranges from 62% to 100% (17). Although seizure freedom is common, approximately up to 30% of patients do not become seizure free after surgery (05). It may be that our prior classification scheme of ganglioglioma versus dysembryoplastic neuroepithelial tumor, etc, was limited, and a better understanding of the tumor genotype using current technologies can allow for improved prognostication. Whole exome sequencing of patients with gangliogliomas has revealed that a complex genotype (ie, gains in other genes of the MAP kinase pathway, such as FGFR4, KRAS) was less likely to have seizure control after surgery (05).

Low-grade gliomas. Given that low-grade gliomas often present as expansile tumors on imaging, histological diagnosis is commonly warranted. If the distinction between low-grade glioma and focal cortical dysplasia is not clear, surveillance imaging (ie, repeat imaging with tumor volumetrics every 3 months) is required. The patient should undergo surgery if any change in volume is noted. Gross total resection portends the greatest likelihood for seizure freedom, with 80% of patients becoming seizure free for some interval after gross total resection (23).

High-grade lesions. Tumor resection is essential in the treatment of high-grade lesions. In grade 3 and 4 gliomas, approximately 77% of patients are transiently seizure free after the initial tumor resection (11; 63). The utility of intraoperative ECoG remains unclear in this patient population.

Meningiomas. The decision to proceed with resection for meningiomas is often related to whether the patient is symptomatic from the lesion (ie, neurologic deficits, seizures). Patients with asymptomatic meningiomas may undergo routine surveillance imaging to monitor growth rate but may not pursue surgery, especially when a gross total resection is not feasible given neuroanatomic limitations. Approximately 30% of patients with supratentorial meningiomas have preoperative seizures, with one in three patients continuing to have seizures after resection. Approximately 10% of patients without preoperative seizures have focal epilepsy after resection (25). After resection, patients with preoperative seizures, in-hospital seizures, and medical or surgical complications are at a higher risk for postoperative epilepsy (14). Interestingly, patients with seizures prior to surgery are less likely to have seizures after resection if preoperative peritumoral edema is present (02).

Metastatic lesions. Treatment options for brain metastases include medication, surgery, stereotactic radiosurgery, and whole-brain radiation therapy. There have been no trials comparing seizure outcomes for all of the various treatment options; however, one study evaluated seizure outcomes for radiation therapy and found no difference between whole-brain radiation therapy plus stereotactic radiosurgery versus whole-brain radiation therapy alone or stereotactic radiosurgery alone (31).

Concurrent oncologic treatment

IDH inhibitor use in low-grade gliomas. In August 2024, the FDA approved the use of vorasidenib for patients with WHO grade 2 IDH astrocytoma or oligodendroglioma following surgery. Treatment guidelines for this population were updated in April 2025. The timing to initiate vorasidenib continues to be explored, although current guidelines recommend offering vorasidenib to patients in whom, after one or more surgeries, additional treatment (ie, radiation or chemotherapy) can be deferred (04). As noted earlier, this agent appears to decrease seizure frequency in patients who are reporting seizures.

Chemotherapy for low-grade gliomas. There are growing data to support the use of temozolomide to reduce the frequency of seizures (54; 15). The use of upfront temozolomide in low-grade gliomas has been associated with more than 50% seizure reduction in 51% to 59% of patients and seizure freedom in 13% to 55% (63). Often, temozolomide is used upfront in high-grade gliomas, although it may be offered for low-grade gliomas (potentially along with radiation) when radiographic or symptomatic progression is seen. PCV (ie, procarbazine, lomustine, and vincristine) may also be considered as an alternative in these cases (04). Minimal data with seizures as an endpoint are currently available, although clinically, ongoing treatment with chemotherapy is often associated with improvement in seizure frequency.

Radiation therapy for low-grade gliomas. In a randomized European Organisation for Research and Treatment of Cancer trial evaluating the use of radiation therapy in low-grade gliomas, 75% of patients who had radiation therapy were rendered seizure-free during follow-up (63). Interestingly, patients with low-grade gliomas may have improvement in terms of seizures without noted improvement on imaging. Of note, radiation is associated with edema and necrosis in the acute setting, which may result in seizures. Typically, these seizures will respond to dexamethasone and antiseizure medications, although these medications may be weaned over time (33).

Glioblastoma. The data regarding the benefits of standard oncologic therapy, specifically on seizure control in patients with glioblastoma, are challenging to ascertain. The largest study to date, which evaluated seizure outcome in 648 patients with high-grade gliomas (both astrocytomas WHO grade 3 and glioblastoma combined), found that 87% (79 of 91) of patients with preoperative seizures were seizure-free at 6 months and 77% (51 of 66) were seizure-free at 12 months after surgery (11). Recurrence or worsening of seizures after patients have completed primary treatment is associated with progression of disease in approximately two-thirds of glioblastoma patients (63). An updated systematic review and meta-analysis reported a pooled prevalence of seizures after initial oncologic treatment as 25.5%, although heterogeneity among study variables was significant (30).

Special considerations

Pregnancy

Christopher Bonfield and Jonathan Engh provide a good overview of brain tumors and pregnancy (06). There are no specific guidelines for pregnant women with tumor-related epilepsy. Therefore, the recommendations are extrapolated from the literature on women with epilepsy and pregnancy. Ideally, an antiseizure medication regimen should be established prior to pregnancy (ie, determine goal antiseizure medication levels correlating to seizure freedom).

Experts agree that the benefit of preventing and treating seizures outweighs the risk of teratogenicity associated with antiseizure medications (61). However, the risk to the fetus should be minimized using medications associated with low risk of congenital malformations and impact on IQ. Lamotrigine and levetiracetam are associated with the lowest risk of congenital malformations (57). As such, these medications are often chosen for women of childbearing age with epilepsy. However, lamotrigine requires weeks to titrate to a therapeutic dose. Therefore, levetiracetam is often the first choice.

Most importantly, seizure medications should not be stopped if a patient discovers she is pregnant as a seizure may pose a major health risk to the mother and the fetus. Given that this patient population may have continued antiseizure medications in the postoperative setting and the postoperative risk of seizures remains unknown, it is optimal to continue the antiseizure medication during pregnancy.

Drug clearance increases during pregnancy for many of the commonly used antiseizure medications. If antiseizure medical levels decrease more than 35% of the baseline (nonpregnant level), there is a risk of seizure recurrence. Therefore, it is important to monitor drug levels during pregnancy. The frequency is typically determined by the degree of clearance changes (57).

Currently, folic acid is recommended by both the American Academy of Neurology and the Epilepsy Foundation for women of childbearing age who have epilepsy (34). The dosing is not entirely clear. Generally, 1 mg is recommended for women with epilepsy; however, those taking valproic acid should take 4 mg due to the higher risk of congenital malformations with valproic acid.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Jessica W Templer MD

Dr. Templer of Northwestern University has no relevant financial relationships to disclose.
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Editor

Rimas V Lukas MD

Dr. Lukas of Northwestern University Feinberg School of Medicine received honorariums from Jazz Therapeutics, Novocure, and Servier for speaking engagements, honorariums from Cardinal Health, Catalyx, Merck, and Novocure for advisory board membership, research support from BMS as principal investigator, and an honorarium from GT Medical Technologies for DSMB membership.
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Former Authors

Paula K Lee MD

Patient Profile

Age range of presentation: 0 months to 65+ years old
Sex preponderance: No sex preponderance
Heredity: No hereditary factors
Population groups selectively affected: No population group selectively affected
Occupation groups selectively affected: No occupation group selectively affected

ICD & OMIM codes

ICD-10: Epilepsy: G40

Localization-related (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures, not intractable, without status epilepticus: G40.209
ICD-11: Epilepsy due to tumours of the nervous system: 8A60.6

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Brain tumor-related epilepsy

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Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Medical management

Targeted treatment

Surgical management

Concurrent oncologic treatment

Special considerations

Pregnancy

References

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Patient Profile

ICD & OMIM codes

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