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Brainstem lesions and epilepsy

To the Editors: We read with great interest the article by Yagyu and his group entitled ‘‘Direct correlation between the facial nerve nucleus and hemifacial seizures associated with a gangliocytoma of the floor of the fourth ventricle: A case report’’ that was published in Epilepsia (Yagyu et al., 2011). In this report, they describe a case of hemifacial spasms caused by a dysplastic neuronal lesion of the floor of the fourth ventricle. The authors stated that this has also been reported elsewhere (Delalande et al., 2001). We have recently reported that brainstem lesions may be responsible for the presence of seizures in patients with multiple sclerosis (Papathanasiou et al., 2010). Together with the often relapsing–remitting forms of multiple sclerosis (MS) or in parallel with progressive forms of MS, epileptic seizures are sometimes observed. The occurrence of these seizures is no longer considered to be coincidental, but to be associated in most cases with the disease process of MS (Spatt et al., 2001). Many publications have sought to determine the potential mechanisms of epilepsy in patients with MS, using either magnetic resonance imaging (MRI) or electroencephalography (EEG). However, all of these studies focused their attention on finding lesions in the cerebral cortex and completely overlooked the brainstem (Thompson et al., 1993; Moreau et al., 1998; Sokić et al., 2001; Calabrese et al., 2008). Using evoked potentials, we had found in this large retrospective study that brainstem auditory and upper limb somatosensory evoked potentials were preferentially involved in MS patients with epilepsy, suggesting brainstem involvement. Studies performed over the last 30–50 years have shown that brainstem involvement in epilepsy in the majority of cases is related to generalized seizures (Faingold, 1987). However, there are some studies that show that it is possible to have focal epilepsy with brainstem lesions. An upper brainstem lesion has been reported to result in focal motor seizures repeatedly induced by alerting stimuli (Hirsch et al., 2008), and a focal epilepticus has been reported as a result of pontine activation due to hamartoma of the floor of the fourth ventricle (Pontes-Neto et al., 2006) similar to the Yagyu study. It may therefore be worthwhile, based on our study and studies by Yagyu and Delande, for these studies to reanalyze their data with special emphasis on the brainstem, with the possibility of finding a correlation between this brain area and epilepsy in MS. Future studies in relation to mechanisms of epilepsy, both in isolation and as a comorbid condition, should also include the brainstem in their evaluation.