TY - JOUR
T1 - Glioma-associated epilepsy
T2 - Toward mechanism-based treatment
AU - Snijders, Tom J.
AU - Berendsen, Sharon
AU - Seute, Tatjana
AU - Robe, Pierre A.
PY - 2017/3/1
Y1 - 2017/3/1
N2 - Epilepsy is common in glioma patients, and glioma-related epilepsy has a strong impact on patients' quality of life. Glioma-related epilepsy has a unfavorable clinical course when compared to other types of symptomatic epilepsy, with low rates of seizure freedom, common relapses of seizures after seizure-free periods, and a severe outcome in case of intractable seizures (status epilepticus). Translational research is starting to elucidate the specific pathophysiological mechanisms in this disease: the molecular-biological characteristics of the tumor result in metabolic changes in the glioma and the peritumoral region. These changes lead to abnormal neuronal and non-neuronal signaling changes in the tumor's surroundings and in the brain's global functional network ("connectome"). Anti-neoplastic treatments often cause amelioration of epilepsy, possibly by reverting the pathophysiological pro-epileptogenic processes in the tumor. Further research should focus on these pathophysiological mechanisms and on the possibilities for new mechanism-based anti-epileptic treatments. Clinical trials for gliomas should incorporated epilepsy as an outcome measure.
AB - Epilepsy is common in glioma patients, and glioma-related epilepsy has a strong impact on patients' quality of life. Glioma-related epilepsy has a unfavorable clinical course when compared to other types of symptomatic epilepsy, with low rates of seizure freedom, common relapses of seizures after seizure-free periods, and a severe outcome in case of intractable seizures (status epilepticus). Translational research is starting to elucidate the specific pathophysiological mechanisms in this disease: the molecular-biological characteristics of the tumor result in metabolic changes in the glioma and the peritumoral region. These changes lead to abnormal neuronal and non-neuronal signaling changes in the tumor's surroundings and in the brain's global functional network ("connectome"). Anti-neoplastic treatments often cause amelioration of epilepsy, possibly by reverting the pathophysiological pro-epileptogenic processes in the tumor. Further research should focus on these pathophysiological mechanisms and on the possibilities for new mechanism-based anti-epileptic treatments. Clinical trials for gliomas should incorporated epilepsy as an outcome measure.
KW - Epilepsy
KW - Glioblastoma
KW - Glioma
KW - Pathophysiology
UR - http://www.scopus.com/inward/record.url?scp=85016771211&partnerID=8YFLogxK
U2 - 10.21037/tcr.2017.03.03
DO - 10.21037/tcr.2017.03.03
M3 - Article
AN - SCOPUS:85016771211
SN - 2218-676X
VL - 6
SP - S337-S341
JO - Translational Cancer Research
JF - Translational Cancer Research
ER -