Seizures may be the first or sometimes the only manifestation of patients with glioma in clinics. The aim of operation is to eliminate epilepsy far beyond mere resection of tumor mass. The underlyling mechanisms of glioma-associated epileptogenesis are poorly understood. Recently the theory of amino-acid like neurotransmitters in chemical synapse is gradually accepted. However, the molecular mechanisms remain to be further investigated on how glutamate release is regulated and how synaptic homeostasis in peripheral neurons is kept or disturbed. So detailed studies are needed to clarify specific molecular target and provide proper evidence for optimal antiepileptic drugs in glioma-associated epileptoge-nesis.
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