Reply: On the Role of Medial Pulvinar Thalamic (PuM) Nucleus in Temporal Lobe Epilepsy
1 INSERM, U 751, Laboratoire de Neurophysiologie et Neuropsychologie, Marseille, France, 2 Université de la Méditerranée, Faculté de Médecine, Marseille, France, 3CHU Timone, Service de Neurophysiologie Clinique, Marseille, France, 4Laboratoire Traitement du Signal et de L'Image, INSERM U642, Université de Rennes 1, France and 5CHU Timone, Service de Neurochirrugie Fonctionnelle et Stéréotaxique, Marseille, France
Correspondence to: Fabrice Bartolomei. Service de Neurophysiologie Clinique CHU Timone-264 Rue st Pierre. 13005-Marseille, France. E-mail: fbartolo{at}medecine.univ-mrs.fr
Sir, We thank Prof. Mauguiere for his comments concerning our article recently published in Brain (Guye et al., 2006
).
Our article follows previous works from our group studying the interdependencies between signals from several regions of the brain during partial seizures (Bartolomei et al., 1999; 2002; 2004; Wendling et al., 2003). The main objective of these works was to anatomically and functionally define the networks that generate seizures and/or are involved in seizure propagation.
Patients included in this study mainly presented with anteromesial temporal lobe epilepsy (10) and three had lateral temporal lobe epilepsy (TLE).
We described a gradual synchronization between the temporal lobe and the thalamus (mainly PuM) that was particularly marked in mesial TLE seizures. In addition some patients had early synchronization of thalamic and temporal lobe signals.
One of the main findings of our study was to correlate the degree of thalamocortical synchrony and ictal loss of consciousness, a finding confirming previous hypotheses about the mechanisms of consciousness alteration in TLE (Blumenfeld et al., 2004).
In the following we will discuss four points/concerns raised by F. Mauguière
- (i) He suggests that some of our results might be biased by the fact that we studied only four regions explored by SEEG.
We disagree with this opinion, because in the present article, as in our previous publications, we first visually studied all the brain regions explored in each patient before applying a method of quantification of interdependencies.
This is of course the first step in analysing data from any SEEG exploration in order to make a decision about surgery in a given patient. The SEEG diagram provided in the article shows only the electrode positions for regions studied by signal analysis. However, the mean number of electrodes implanted in these patients was eight (corresponding to a total of 80 to 120 contacts), exploring the temporal lobe and when necessary extratemporal cortices. Examples of complete SEEG diagrams can be found in previous articles from our group.
Finally, given the large number of possible interactions [N sites allow (N2–N)/2 different correlations values] we restricted our quantification to four regions involved in seizure generation or propagation, but only after careful visual analysis.
- (ii) Mauguière discussed the results obtained in patients with lateral TLEs (LTLE). He mentioned that in the Rosenberg et al. study (Rosenberg et al., 2006), ‘LVFA (low voltage fast activity), which is the hallmark of cortical seizure onset, was significantly more frequently observed in PuM for seizures with lateral temporal onset than for those with mesial temporal onset’.
Two of our three patients with lateral TLE had seizures restricted to the first temporal gyrus during a large part of their seizures and presented no loss of consciousness. Other parts of the temporal neocortex or the temporo–parieto–occiptal junction region were spared. Delayed propagation to the PuM was found without low-voltage discharge.
A low degree of thalamocortical correlation was found in these two cases. In the third case, a larger part of the lateral neocortex, including the second temporal gyrus and the parietal cortex, rapidly involved the PuM in the form of a tonic discharge. This case is illustrated in Figure 4 of our article (last seizure).
We think that there are no real discrepancies between our data and those published by Rosemberg et al. Any apparent differences are probably due to differences in the population studied. Indeed the so-called lateral-TLE cases included in the Lyon study actually involved a large territory of not only lateral temporal cortex but also extra temporal cortices (see for example Figure 5 in the article of Rosenberg et al. (2006), which corresponds to an occipito-temporal seizure). These features are therefore not characteristic of ‘pure’ lateral temporal lobe seizures.
In addition, we can note that in this kind of seizure, with rapid onset, LVFD are observed in large remote regions and probably reflect a widespread diffusion of the seizure not only to the thalamus but also to large cortical areas. Therefore in this situation, it is difficult to prove a specific role for the thalamus in seizure spread.
We agree with Prof. Mauguière that seizures restricted to the first temporal gyrus interact less with the PuM than seizures involving associative cortex of the temporal and extratemporal regions.
- (iii) Mauguière mentioned later that ‘Ictal thalamo-cortical synchrony is likely to be common, if not constant, between the cortical seizure area and the thalamic nuclei with which this area is connected’.
The study of Rosenberg et al. (2006) is purely descriptive. The only way to demonstrate that two signals are in relationship is to quantify the interdependencies using signal processing methods estimating ‘synchrony’ or degree of correlation. The fact that two regions are involved by an ictal discharge does not imply that the two signals are related. This point is illustrated in our article, since in the majority of patients we observed higher correlations between neocortex and thalamus than between mesial structures and neocortex. In addition, decorrelation may be demonstrated, particularly between two structures generating low-voltage rapid discharges (Wendling et al., 2003).
- (iv) F. Mauguière finally concludes that ‘it is premature to consider ictal thalamo-cortical synchrony as a clinically relevant indicator for epilepsy surgery prognosis’.
Here again we disagree with him. Indeed, the estimation of the extent of an epileptogenic network appears to us a crucial way to understand why a surgical resection may fail.
We do think that the quantification of an epileptogenic network by the way of studying interdependencies between signals is a potential tool to study the mechanisms of epilepsy surgery failures. In the present study, we found that an early correlation between the temporal lobe and the thalamus is associated with a poorer surgical outcome. Late synchrony in contrast is not related to surgical prognosis. These results may be viewed as an indicator of the extent of the epileptogenic network to structures remote from the temporal lobe and a potential explanation for the failure of anterior temporal lobectomy.
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