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We read with interest the paper by Dr Alsaadi and colleagues on “potentially misleading extratemporal lobe lesions” in patients with symptoms of temporal lobe epilepsy.1 Most of their successfully operated patients with extratemporal lesions also had hippocampal atrophy on the operated side, which has positive prognostic value for mesiotemporal surgery in temporal lobe epilepsy, even in the presence of extratemporal lesions.2 Their material provides excellent evidence that not all lesions in an epileptic brain are epileptogenic, and in some cases epilepsy may originate from morphologically intact mesio-temporal structures in a lesioned brain. However, this situation is only one of the possible scenarios of the very complicated relations between mesiotemporal epilepsy and extratemporal lesions.
Another possibility is that mesiotemporal epilepsy is induced by secondary epileptogenesis from an extratemporal lesion. This possibility has not been clearly proven but there are reports of patients with mesiotemporal lobe epilepsy and potentially epileptogenic extratemporal lesions such as hypothalamic hamartomas, midline lesions, and retrosplenial lesions3 behaving like temporal lobe epilepsy. The poor surgical outcome when resection involves only the mesiotemporal structures and the good outcome when the extratemporal lesion is also resected may be explained on the basis of secondary mesiotemporal epileptogenesis from extratemporal sources.
A third possibility is that the temporal lobe acts as a symptomatogenic area for seizures spreading to it from an extratemporal source. In such cases resection of the temporal lobe may result in an Engel Ib outcome: auras persist but seizures stop.
The big question is how we can know whether the extratemporal lesion is epileptogenic or not—in other words, what is the chance of being successful when operating only on the temporal region, or only on the extratemporal lesion, or on both?
At present only clinical experience can help us in this regard. “Encephalomalacic lesions,” which form a majority of the authors’ extratemporal lesions, are not as epileptogenic as—for instance—the well known periventricular or diffuse nodular heterotopias. The latter types of extratemporal lesion are reported as being present in patients who did not become seizure-free after resection of the mesiotemporal structures.4,5 In agreement with Alsaadi et al and other workers,6 we do not consider arachnoid cysts to be epileptogenic unless they overlie a pathological cortex. Our impression is that post-traumatic lesions have an intermediate position, and the high epileptogenic potential of tumours is well known.
On the basis of similiar studies it would be helpful to make an epileptogenicity list of different brain lesions. In combination with an optimal preoperative examination schedule, this could help in preoperative decision making.
We appreciate the comments from Dr Szucs and colleagues. As not all of our patients became completely free from seizures after temporal lobe surgery, we cannot exclude secondary epileptogenesis or propagation through temporal structures in a minority of cases. Nevertheless, we expect that our outcomes would have been much worse if these mechanisms were responsible for temporal lobe epilepsy (TLE) or “apparent TLE” in most of our patients.
We agree that the suspected pathology of the extratemporal lesion is critical in determining the presurgical evaluation and the surgical plan. Many of our patients had aetiologies such as trauma that are commonly associated with multifocal brain pathology. We certainly suggest that suspicion for TLE be higher in these patients than in patients with extratemporal gliomas.
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