Brain Advance Access originally published online on June 8, 2007
Brain 2007 130(8):e77; doi:10.1093/brain/awm119
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Complexities in the association of human blood–brain barrier disruption with seizures: importance of patient population and method of disruption
Functional Neuroimaging Laboratory, Department of Psychiatry; Comprehensive Epilepsy Center, Department of Neurology, Weill Cornell Medical College, USA
Correspondence to: Tracy Butler, Box 140, 1300 York Avenue New York, NY 10021, USA E-mail: tab2006{at}med.cornell.edu
In "Blood–brain barrier leakage may lead to progression of temporal lobe epilepsy" (van Vliet et al., 2007
), the authors found that osmotic opening of the blood–brain barrier (BBB) resulted in transient or permanent increased seizure frequency in chronically epileptic rats. They relate these results to findings in humans that osmotic BBB opening using mannitol induces seizures in patients with brain tumours. However, the evidence that mannitol causes seizures in humans is based primarily on studies of patients with brain tumours who do not have epilepsy (Marchi et al., 2007). An alternate human parallel might be patients with chronic epilepsy subjected to mechanical BBB opening. Transient mechanical BBB disruption follows most neurosurgical procedures, and is commonly visualized on MRI or CT as parenchymal, meningeal and/or other patterns of contrast enhancement lasting hours to weeks (Knauth et al., 1999). Mechanical BBB disruption occurs when patients with chronic, intractable epilepsy undergo neurosurgical implantation of electrodes to localize their seizure onsets in preparation for subsequent resective epilepsy surgery. In this situation, increased seizure frequency is not typically noted (such an increase would actually be clinically helpful, since it would allow seizures to be recorded and the epileptogenic zone identified more rapidly). Instead, there is anecdotal evidence that implantation of intracranial electrodes may decrease seizure frequency, rarely resulting in permanent cessation of seizures (Katariwala et al., 2001; Butler et al., 2003). This suggests that the effect of BBB disruption on seizure frequency depends importantly on other factors. One relevant factor may be increased neuronal exposure to antiepileptic medication when mechanical BBB disruption circumvents pathological, epilepsy-related upregulation of BBB-based drug transporter mechanisms (Dombrowski et al., 2001). Other relevant factors may include unintended disruption of epileptogenic networks during electrode implantation, and/or use of perioperative corticosteroids. Additional work in animal models could clarify these important issues.
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Butler T, Bazil C, Goodman R, Hirsch L, Leary L, Karceski S, et al. Therapeutic implantation of intracranial electrodes. [Abstract]. Epilepsia (2003) 44 s9:332.
Dombrowski SM, Desai SY, Marroni M, Cucullo L, Goodrich K, Bingaman W, et al. Overexpression of multiple drug resistance genes in endothelial cells from patients with refractory epilepsy. Epilepsia (2001) 42:1501–6.[CrossRef][Web of Science][Medline]
Katariwala NM, Bakay RA, Pennell PB, Olson LD, Henry TR, Epstein CM. Remission of intractable partial epilepsy following implantation of intracranial electrodes. Neurology (2001) 57:1505–7.
Knauth M, Aras N, Wirtz CR, Dorfler A, Engelhorn T, Sartor K. Surgically induced intracranial contrast enhancement: potential source of diagnostic error in intraoperative MR imaging. Am J Neuroradiol (1999) 20:1547–53.
Marchi N, Angelov L, Masaryk T, Fazio V, Granata T, Hernandez N, et al. Seizure-promoting effect of blood-brain barrier disruption. Epilepsia (2007) 48:732–42.[CrossRef][Web of Science][Medline]
van Vliet EA, da Costa Araujo S, Redeker S, van Schaik R, Aronica E, Gorter JA. Blood-brain barrier leakage may lead to progression of temporal lobe epilepsy. Brain (2007) 130:521–34.
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