Hostname: page-component-cd9895bd7-dk4vv Total loading time: 0 Render date: 2024-12-25T16:55:19.979Z Has data issue: false hasContentIssue false
  • English
  • Français

Neuropathologic Studies of 'Epileptogenic' Tissue

Published online by Cambridge University Press:  02 December 2014

Harry V. Vinters
Harry V. Vinters*
Affiliation:
David Geffen School of Medicine at UCLA, Section of Neuropathology, Ronald Reagan-UCLA Medical Center, Los Angeles, California, USA
*
David Geffen School of Medicine at UCLA, Section of Neuropathology, Ronald Reagan-UCLA Medical Center, 650 Charles Young Drive South, CHS room 18-170, Los Angeles, California, 90095-1732, USA. Email: [email protected]
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

This mini-review will summarize some of the major contributions of Neuropathology to understanding the structural basis of several forms of intractable epilepsy. Because of space limitations, only selected morphologically defined brain abnormalities will be considered and illustrated. By definition, the types of specimen encountered by Neuropathologists are those resected to treat intractable seizure disorders. One can therefore infer that the 'lesions' encountered in some way caused or at least contributed to the epilepsy, though the leap from observed neuropathologic abnormalities to 'seizuregenesis' is not always straightforward—indeed often is very tortuous and obscure. Nevertheless, a Neuropathologist working with a team of neurologists, neurosurgeons, electrophysiologists, neuropsychologists, and others, can contribute to a richer understanding of why seizures are triggered within human brain tissue, and therefore how they may be more effectively treated.

Résumé

RÉSUMÉ

Cette mini-revue constitue un sommaire de certaines des contributions majeures de la neuropathologie à la compréhension des éléments structuraux de base de plusieurs types d'épilepsies pharmacorésistantes. Nous avons choisi de traiter et d'illustrer certaines anomalies cérébrales définies au point de vue morphologique, étant donné les contraintes d'espace. Par définition, les spécimens qu'examinent les neuropathologistes sont ceux qui ont été prélevés au cours du traitement chirurgical de l'épilepsie pharmacorésistante. On peut donc déduire que les « lésions » observées ont causé en quelque sorte ou ont pour le moins contribué à l'épilepsie, bien que le lien entre les anomalies neuropathologiques observées et la genèse des crises ne soit pas toujours direct mais souvent plutôt confus et obscur. Néanmoins, un neuropathologiste qui travaille avec une équipe de neurologues, de neurochirurgiens, d'électrophysiologistes, de neuropsychologues, ainsi qu'avec d'autres spécialistes, peut contribuer à une meilleure compréhension de la raison pour laquelle les crises sont déclenchées dans le tissu du cerveau humain et donc aux moyens par lesquels elles pourraient être traitées plus efficacement.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 39 , Issue S6 , November 2012 , pp. S20 - S24
Copyright
Copyright © The Canadian Journal of Neurological 2012

References

1. Engel, J. Current concepts—surgery for seizures. N Engl J Med. 1996;334:647–52.CrossRefGoogle Scholar
2. Mathieson, G. Pathologic aspects of epilepsy with special reference to the surgical pathology of focal cerebral seizures. Adv Neurol. 1975;8:107–38.Google Scholar
3. Blumcke, I, Spreafico, R. Cause matters: A neuropathological challenge to human epilepsies. Brain Pathol. 2012;22:347–9.CrossRefGoogle ScholarPubMed
4. Mischel, PS, Nguyen, LP, Vinters, HV. Cerebral cortical dysplasia associated with pediatric epilepsy. Review of neuropathologic features and proposal for a grading system. J Neuropathol Exp Neurol. 1995;54:137–53.CrossRefGoogle ScholarPubMed
5. Sofroniew, MV, Vinters, HV. Astrocytes: Biology and pathology. Acta Neuropathol. 119:7–35.CrossRefGoogle Scholar
6. Wirenfeldt, M, Babcock, AA, Vinters, HV. Microglia—insights into immune system structure, function, and reactivity in the central nervous system. Histol Histopathol. 2011; 26:519–30.Google ScholarPubMed
7. Crino, PB, Miyata, H, Vinters, HV. Neurodevelopmental disorders as a cause of seizures: neuropathologic, genetic, and mechanistic considerations. Brain Pathol. 2002;212–33.CrossRefGoogle ScholarPubMed
8. Blumcke, I, Thom, M, Aronica, E, Armstrong, DD, Vinters, HV, et al. The clinicopathologic spectrum of focal cortical dysplasias: A consensus classification proposed by an ad hoc Task Force of the ILAE Diagnostic Methods Commission.Google Scholar
9. Rasmussen, T, Olszewski, J, Lloyd-Smith, D. Focal seizures due to chronic localized encephalitis. Neurology. 1958; 8:435–45.CrossRefGoogle ScholarPubMed
10. Vinters, HV, Wang, R, Wiley, CA. Herpesviruses in chronic encephalitis associated with intractable childhood epilepsy. Hum Pathol. 1993;24:871–9.CrossRefGoogle ScholarPubMed
11. Farrell, MA, Droogan, O, Secor, DL, Poukens, V, Quinn, B, Vinters, HV. Chronic encephalitis associated with epilepsy: Immunohistochemical and ultrastructural studies. Acta Neuropathol. 1995;89:313–21.CrossRefGoogle ScholarPubMed
12. Cepeda, C, Hurst, RS, Flores-Hernandez, J, Hernandez-Echeagaray, E, et al. Morphological and electrophysiological characterization of abnormal cell types in pediatric cortical dysplasia. J Neurosci Res. 2003;72:472–86.CrossRefGoogle ScholarPubMed
13. Cepeda, C, Andre, VM, Yamazaki, I, Hauptman, JS, et al. Comparative study of cellular and synaptic abnormalities in brain tissue samples from pediatric tuberous sclerosis complex and cortical dysplasia type II. Epilepsia. 2010; 51 (suppl. 3):160–165.Google Scholar
14. Farrell, MA, DeRosa, MJ, Curran, JG, Secor, DL, et al. Neuropathologic findings in cortical resections (including hemispherectomies) performed for the treatment of intractable childhood epilepsy. Acta Neuropathol. 1992;83:246–59.CrossRefGoogle ScholarPubMed
15. Vinters, HV, Fisher, RS, Cornford, ME, Mah, V, et al. Morphological substrates of infantile spasms: Studies based on surgically resected cerebral tissue. Child’s Nerv Sys. 1992; 8:8–17.CrossRefGoogle ScholarPubMed
16. Aronica, E, Becker, AJ, Spreafico, R. Malformations of cortical development. Brain Pathol. 2012; 22:380–401.CrossRefGoogle ScholarPubMed
17. Taylor, DC, Falconer, MA, Bruton, CJ, Corsellis, JA. Focal dysplasia of cerebral cortex in epilepsy. J Neurol Neurosurg Psychiatry. 1971;34:369–87.CrossRefGoogle ScholarPubMed
18. Salamon, N, Andres, M, Chute, DJ, Nguyen, ST, et al. Contralateral hemimicrencephaly and clinical-pathological correlations in children with hemimegalencephaly. Brain. 2006;129 (Pt. 2):352–65.CrossRefGoogle ScholarPubMed
19. Cook, SW, Nguyen, ST, Hu, B, Yudovin, S, et al. Cerebral hemispherectomy in pediatric patients with epilepsy: comparison of three techniques by pathological substrate in 115 patients. J Neurosurg. 2004;100 (Suppl):125/141.Google ScholarPubMed
20. Palmini, A, Najm, I, Avanzini, G, Babb, T, et al. Terminology and classification of the cortical dysplasias. Neurology. 2004;62(6 Suppl 3):S2–8.CrossRefGoogle ScholarPubMed
21. Hadjivassiliou, G, Martinian, L, Squier, W, Blumcke, I, Aronica, E, Sisodiya, SM, et al. The application of cortical layer markers in the evaluation of cortical dysplasia in epilepsy. Acta Neuropathol. 2010; 120:517–28.CrossRefGoogle ScholarPubMed
22. Cepeda, C, Andre, VM, Levine, MS, Salamon, N, Miyata, H, Vinters, HV, et al. Epileptogenesis in pediatric cortical dysplasia: the dysmature cerebral developmental hypothesis. Epilepsy Behav. 2006;9:219–35.CrossRefGoogle ScholarPubMed
23. Miyata, H, Chiang, AC, Vinters, HV. Insulin signaling pathways in cortical dysplasia and TSC-tubers: tissue microarray analysis. Ann Neurol. 2004;56:510–19.CrossRefGoogle ScholarPubMed
24. Goto, J, Talos, DM, Klein, P, Qin, W, Chekaluk, YI, et al. Regulable neural progenitor-specific Tsc1 loss yields giant cells with organellar dysfunction in a model of tuberous sclerosis complex. Proc Natl Acad Sci USA. 108:E1070–9.Google Scholar
25. Wirenfeldt, M, Clare, R, Tung, S, Bottini, A, Mathern, GW, Vinters, HV. Increased activation of Iba1+ microglia in pediatric epilepsy patients with Rasmussen’s encephalitis compared with cortical dysplasia and tuberous sclerosis complex. Neurobiol Dis. 2009; 34:432–40.CrossRefGoogle ScholarPubMed
26. Wagner, AS, Yin, NS, Tung, S, Mathern, GW, Vinters, HV. Intimal thickening of meningeal arteries after serial corticectomies for Rasmussen encephalitis. Hum Pathol. 2012; 43:1308–13.CrossRefGoogle ScholarPubMed
27. Thom, M, Blumcke, I, Aronica, E. Long-term epilepsy-associated tumors. Brain Pathol. 2012;22:350–79.CrossRefGoogle ScholarPubMed