As observed in corpus callosum O4 + OLs during homeostasis (Fig
the two conditions share common pathogenic mechanisms and influence each other Excessive glutamate release and activation of glutamate receptors promotes glioma growth, cell death and epileptic activity GABAergic signalling is antiproliferative, whereas chloride accumulation is required for mitosis and migration of tumour cells, and is responsible for epileptogenic depolarizing GABAergic activity in neurons The molecular target of rapamycin (mTOR) signalling pathway and epigenetic abnormalities are also involved in epileptogenesis and tumour growth As a result of the shared pathogenic mechanisms, antiepileptic drugs can have antitumour effects, and antitumour therapy can control seizures Single drug therapies targeting the shared mechanisms are now being assessed for combined seizure and tumour control, and have the advantage of lower risks of adverse effects and drug interactions Abstract Epilepsy often develops in patients with glioma, and the two conditions share common pathogenic mechanisms
It all comes down to bioavailability
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doi:10.1002/nbm.2772, PMID: 22281935 Puri BK, Agour M, Gunatilake KD, Fernando KA, Gurusinghe AI, Treasaden IH (2009) An in vivo proton neurospectroscopy study of cerebral oxidative stress in myalgic encephalomyelitis (chronic fatigue syndrome)
