Authors
Hyun Yong Koh, Steven Tobochnik
Published in
Current opinion in neurology. Oct 20, 2026. Epub Oct 20, 2026.
Abstract
Discoveries relating to the cancer neuroscience of gliomas have reframed brain tumor-related epilepsy (BTRE) as the product of reciprocal interactions at the neural-tumor interface. This framework provides the rationale for targeted strategies to optimize both seizure control and brain tumor survival outcomes.
Feedforward dynamics involving hyperexcitability and cellular proliferation in glioma-infiltrated cortex drive synaptic remodeling of neural circuits that correlate with shorter survival. Seizure assessment metrics demonstrate that worsening seizure control may precede or align with progressive disease. In this context, early evidence indicates a potential role for targeted tumor-directed therapy in addition to antiseizure medications (ASMs) for optimizing seizure control. Noncontrolled studies evaluating ASM tapering strategies in BTRE suggest that tumor stability is more important for seizure control than the duration of seizure freedom.
BTRE involves dynamic and fluctuating seizure risk driven by tumor biology, tumor-directed therapy, and treatment response. Hyperexcitability at the cellular level and clinical seizure activity are increasingly understood as a reflection of tumor biology and a potentially modifiable target to improve outcomes. The addition of seizure assessments as secondary endpoints in brain tumor clinical trials may lead to a refined individualized and disease-specific approach to ASM management.
PMID:
42895304
Bibliographic data and abstract were imported from PubMed on 19 Oct 2026.
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