Epilepsy in Patients With a Brain Tumour

Focal Epilepsy Requires Focused Treatment

Marjolein de Groot; Jaap C. Reijneveld; Eleonora Aronica; Jan J. Heimans


Brain. 2012;135(4):1002-1016. 

In This Article

Abstract and Introduction


Brain tumours frequently cause epileptic seizures. Medical antiepileptic treatment is often met with limited success. Pharmacoresistance, drug interactions and adverse events are common problems during treatment with antiepileptic drugs. The unpredictability of epileptic seizures and the treatment-related problems deeply affect the quality of life of patients with a brain tumour. In this review, we focus on both clinical and basic aspects of possible mechanisms in epileptogenesis in patients with a brain tumour. We provide an overview of the factors that are involved in epileptogenesis, starting focally at the tumour and the peritumoral tissue and eventually extending to alterations in functional connectivity throughout the brain. We correlate this knowledge to the known mechanisms of antiepileptic drugs. We conclude that the underlying mechanisms of epileptogenesis in patients with a brain tumour are poorly understood. The currently available antiepileptic drugs have little to no influence on the known epileptogenic mechanisms that could contribute to the poor efficacy. Better understanding of focal changes that are involved in epileptogenesis may provide new tools for optimal treatment of both the seizures and the underlying tumour. In our opinion, therapy for every patient with a brain tumour suffering from epilepsy should first and foremost aim at eliminating the tumour as well as the epileptic focus through resection combined with postoperative treatment, and only if this strategy does not result in adequate seizure control should medical antiepileptic treatment be intensified. If this strategy, however, results in sustained seizure freedom, tapering of antiepileptic drugs should be considered in the long term.


Brain tumours may arise from brain tissue (primary brain tumours, e.g. astrocytic, oligodendroglial and glioneuronal tumours) or from malignancies elsewhere in the body, e.g. lung cancer and melanoma (secondary brain tumours). Seizures are a frequent symptom in patients with a brain tumour. The incidence varies between 30 and 100% and depends on the tumour type, with slow-growing tumours being the most epileptogenic (van Breemen et al., 2007). The impact of epilepsy on the total disease burden is high and additionally, both epilepsy and the use of antiepileptic drugs predispose to deterioration of cognitive function (Klein et al., 2003), already a major problem in patients with a brain tumour (Douw et al., 2009; Hilverda et al., 2010).

The specific events that occur in a lesion and lead to seizures are unknown. Many studies have assessed the efficacy of antiepileptic drugs, but relatively few have investigated the mechanisms that underlie epileptogenesis. Altogether, little progress has been made in recent years and many patients with a brain tumour with epilepsy suffer from ongoing seizures due to pharmacoresistance. In a large cohort study, complete seizure control was achieved in only 20 of 158 (12.6%) patients with a brain tumour (Hildebrand et al., 2005). In 15–58% of cases of low-grade glioma, the epilepsy appears to be intractable (Duffau et al., 2002).

Understanding the mechanisms that underlie epileptogenesis in brain tumours is essential to identify new treatment targets and to develop effective treatment. In this review we will comment on the current state regarding the treatment of both epilepsy and tumour, and review the current knowledge on underlying mechanisms of epileptogenesis in patients with a brain tumour. Further, we provide suggestions for optimal treatment and future research.


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