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Brain Tumor and Seizures: Pathophysiology and Its Implications for Treatment Revisited
Author(s) -
Schaller Bernhard,
Rüegg Stephan J.
Publication year - 2003
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.2003.05203.x
Subject(s) - pathophysiology , epilepsy , neuroscience , brain tumor , medicine , glutamate receptor , receptor , bioinformatics , pathology , biology
Summary: Seizures affect ∼50% of patients with primary and metastatic brain tumors. Partial seizures have the highest incidence, followed by secondarily generalized, depending on histologic subtype, location, and tumor extent. The underlying pathophysiologic mechanisms of tumor‐associated seizures are poorly understood and include theories of altered peritumoral amino acids, regional metabolism, pH, neuronal or glial enzyme and protein expression, as well as immunologic activity. An involvement of changed distribution and function of N ‐methyl‐ d ‐aspartate subclass of glutamate receptors also has been suggested. The often unpredictable responses to seizures after surgical tumor removal add substantial evidence that multiple factors are involved. The therapy of tumor‐related seizures is far from perfect. Several factors contribute to these treatment difficulties, such as tumor growth and drug interactions; however, one of the main reasons for poor seizure control may result from the insufficient or even absent influence of the currently available antiepileptic drugs (AEDs) on most of the pathophysiologic mechanisms of tumor‐related seizures. Studies are needed to elucidate more clearly the pathophysiologic mechanisms of tumor‐related seizures and to identify and develop the optimal AEDs.