Peritumoral epilepsy: Relating form and function for surgical success

Abstract

Seizures are a prominent symptom in patients with both primary and secondary brain tumors. Medical management of seizure control in this patient group is problematic as the mechanisms linking tumorigenesis and epileptogenesis are poorly understood. It is possible that several mechanisms contribute to tumor-associated epileptic zone formation. In this review, we discuss key candidates that may be implicated in peritumoral epileptogenesis and, in so doing, hope to highlight areas for future research. Furthermore, we summarize the current role of antiepileptic medications in this type of epilepsy and examine the changes in surgical practice which may lead to improved seizure rates after tumor surgery. Lastly, we speculate on possible future preoperative and intraoperative considerations for improving seizure control after tumor resection.This article is part of a Special Issue entitled “NEWroscience 2013”.

Metastatic breast cancer cells induce altered microglial morphology and electrical excitability in vivo

“…Primary and metastatic brain tumours can have a range of neurological consequences such as headaches, mild cognitive impairment, and epileptic seizures [12]. This aspect of the disease burden in the brain has a significant impact on quality of life and is difficult to treat as the mechanistic basis is poorly understood [10][11][12]. Several mechanisms have been proposed to explain the presentation of tumour-associated epilepsy, including disrupted glutamate homeostasis, altered ion channel expression, altered network activity, and inflammation [52][53][54][55].…”

“…The installation of a cranial imaging window was based on procedures described previously [39]. Mice (8)(9)(10)(11)(12)(13)(14)(15)(16)(17) weeks old; n = 23) were anaesthetised using isoflurane and the head was stabilised in a stereotaxic frame (Kopf Instruments). Cerebral oedema was treated perioperatively with dexamethasone (2 μg/g body weight; intramuscular injection).…”

“…Furthermore, patients with metastatic brain tumours present with neurological symptoms including cognitive impairment and epileptic seizures [8,9], and this can have a significant impact on quality of life. However, the pathophysiological mechanisms underlying the cause of neurocognitive impairment and tumour-associated epilepsy are poorly understood [10][11][12]. Thus, there is an urgent need to better understand the mechanisms regulating seeding and expansion of brain metastases and their neurological sequelae in order to develop new effective therapies.…”

Plasticity in Single Axon Glutamatergic Connection to GABAergic Interneurons Regulates Complex Events in the Human Neocortex

“…In addition, evidence in animal models suggests the involvement of group I mGluR-mediated plasticity in neocortical learning processes, and perturbation of the mGluR-dependent plasticity has been reported with mental decline [43]. Therefore, the human-specific microcircuit features may also be substrates for pathological processes resulting in cognitive decline and other neurological and neuropsychiatric dysfunctions that we as a species are vulnerable to [57–61]. …”

Metastatic breast cancer cells induce altered microglial morphology and electrical excitabilityin vivo

“…Furthermore, patients with metastatic brain tumours present with neurological symptoms including cognitive impairment and epileptic seizures (8,9), and this can have a significant impact on quality of life. However, the pathophysiological mechanisms underlying the cause of neurocognitive impairment and tumour-associated epilepsy are poorly understood (10)(11)(12).…”