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To the Editors:

We have read with great interest the article entitled Cavernoma-related epilepsy: Review and recommendations for management—Report of the Surgical Task Force of the ILAE Commission on Therapeutic Strategies, by Rosenow et al. [1]

The authors presented an interesting review of the strategies that could be adopted in case of cavernoma-related epilepsy (CRE), which is still a controversial issue.

We agree with the authors about the necessity to remove, whenever possible and without causing deficits, the surrounding cortical gliotic tissue, usually stained by hemosiderin.

Regarding CRE patients with dual and triple pathology, we also agree that these patients will not be rendered seizure free by the removal of a single lesion, but we think that in the majority of cases a noninvasive presurgical study (i.e., video–electroencephalography [EEG] monitoring) might be sufficient to define the epileptogenic zone. Furthermore, detection of the associated pathology, namely focal cortical dysplasia type IIIc, with magnetic resonance imaging (MRI) continues to be a challenge,[2] and identification is more often a result of histopathologic examination.

In cases of cavernoma associated with pharmacoresistant epilepsy or with a long history of epilepsy, the suspicion of a coexistent pathology hidden at MRI might arise, as in the case of glioneuronal tumors[3] or multiple cavernomas.[4] Therefore, we believe that a presurgical noninvasive neurophysiologic study (video-EEG monitoring) could be useful.

The association of cavernoma with hippocampal sclerosis or other lesions not detected by MRI but potentially epileptogenic, such as subtle forms of malformation of cortical development, emphasizes the importance of an extensive noninvasive presurgical study (video-EEG monitoring), which might suggest a possible correlation between the lesion and the identification of the epileptogenic zone. Consequently, the surgical strategy follows a tailored procedure apt to remove both the structural lesion and the epileptogenic area. However, during surgery in eloquent areas, the possible functional significance of pericavernous cerebral tissue, the preservation of which represents one of the main factors leading to the surgical procedure, should be borne in mind.

In addition, it is important to recommend a strict neuropathologic protocol that can highlight any associated pathology such as subtle forms of cortical dysplasias. Therefore, in case of focal epilepsy associated with only one cavernoma, as for patients with multiple cavernomas,[4] we consider it unnecessary and dangerous to recommend “invasive evaluations” associated with major risks. Such considerations are particularly relevant in this field where other associated vascular malformations, such as venous angiomas, or other developmental venous anomalies and microvascular abnormalities, might be present.[5]

Disclosure

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  2. Disclosure
  3. References

None of the authors has any conflict of interest to disclose. We confirm that we have read the Journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines.

References

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  2. Disclosure
  3. References
  • 1
    Rosenow F, Alonso-Vanegas MA, Baumgartner C, et al. Cavernoma-related epilepsy: Review and recommendations for management-Report of the Surgical Task Force of the ILAE Commission on Therapeutic Strategies. Epilepsia 2013;54:20252035.
  • 2
    Kim DW, Kim S, Park SH, et al. Comparison of MRI features and surgical outcome among the subtypes of focal cortical dysplasia. Seizure 2012;21:789794.
  • 3
    Giulioni M, Marucci G, Martinoni M, et al. Seizure outcome in surgically treated drug-resistant mesial temporal lobe epilepsy based on the recent histopathological classifications. J Neurosurg 2013;119:3747.
  • 4
    Rocamora R, Mader I, Zentner J, et al. Epilepsy surgery in patients with multiple cerebral cavernous malformations. Seizure 2009;18:241245.
  • 5
    Abla A, Wait SD, Uschold T, et al. Developmental venous anomaly, cavernous malformation, and capillary telangiectasia: spectrum of a single disease. Acta Neurochir (Wien) 2008;150:487489; discussion 489.