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Review
. 2022 Sep 5;4(1):45.
doi: 10.1186/s42466-022-00205-9.

Brain tumor related epilepsy: pathophysiological approaches and rational management of antiseizure medication

Sabine Seidel  1 , Tim Wehner  2 , Dorothea Miller  3 , Jörg Wellmer  2 , Uwe Schlegel  2 , Wenke Grönheit  2
Affiliations
Review

Brain tumor related epilepsy: pathophysiological approaches and rational management of antiseizure medication

Sabine Seidel et al. Neurol Res Pract. .

Abstract

Background: Brain tumor related epilepsy (BTRE) is a common complication of cerebral tumors and its incidence is highly dependent on the type of tumor, ranging from 10-15% in brain metastases to > 80% in low grade gliomas. Clinical management is challenging and has to take into account aspects beyond the treatment of non-tumoral epilepsy.

Main body: Increasing knowledge about the pathophysiology of BTRE, particularly on glutamatergic mechanisms of oncogenesis and epileptogenesis, might influence management of anti-tumor and BTRE treatment in the future. The first seizure implies the diagnosis of epilepsy in patients with brain tumors. Due to the lack of prospective randomized trials in BTRE, general recommendations for focal epilepsies currently apply concerning the initiation of antiseizure medication (ASM). Non-enzyme inducing ASM is preferable. Prospective trials are needed to evaluate, if AMPA inhibitors like perampanel possess anti-tumor effects. ASM withdrawal has to be weighed very carefully against the risk of seizure recurrence, but can be achievable in selected patients. Permission to drive is possible for some patients with BTRE under well-defined conditions, but requires thorough neurological, radiological, ophthalmological and neuropsychological examination.

Conclusion: An evolving knowledge on pathophysiology of BTRE might influence future therapy. Randomized trials on ASM in BTRE with reliable endpoints are needed. Management of withdrawal of ASMs and permission to drive demands thorough diagnostic as well as neurooncological and epileptological expertise.

Keywords: Antiseizure medication; Brain metastasis; Brain tumor related epilepsy; Glioma.

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Conflict of interest statement

T.W. has received of honoraria or consultation fees Eisai, UCB, GW, Angelini, Precisis and is a stock shareholder of Amgen. J.W. has received speaker fees from UCB, Eisai, Bial, GW pharmaceuticals, and Desitin. U.S. received speaker’s honoraria from Medac, GSK and Novartis. W.G. has received speaker´s honoraria, travel or accommodation payment fees from UCB, Eisei, Bial and Desitin. The other authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Overview of mechanisms driving brain tumor related epilepsy (simplified)
Fig. 2
Fig. 2
Brain tumor in the left middle frontal gyrus with cortical and subcortical T2/FLAIR hyperintense signal (A, B) and partial Gadolinium enhancement (C) in a 24-year-old male patient. A Axial T2, B coronal FLAIR, C coronal T1 with Gadolinium, D intraoperative situs with superimposed results from extraoperative subdural electrode recording and direct cortical stimulation, E intraoperative situs following resection of the tumor and adjacent epileptogenic area (histology: angiocentric glioma WHO grade 1). Figure modifed from Wehner et al. [85]
See this image and copyright information in PMC

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