GRAY MATTERS lamic structural abnormalities are derived from T1weighted magnetic resonance imaging (MRI) scans only and details on brain connectivity are still lacking and deserve more attention with larger samples.
Thalamotemporal impairment in benign temporal lobe epilepsy: Same hypotheses? To the Editors: We read with great interest the study by Keller et al.1 showing that there is an abnormal thalamic area connected to the temporal lobe and related to the extent of mesial temporal lobe damage in patients with temporal lobe epilepsy (TLE). Furthermore, the sample studied by Keller was of TLE patients with frequent seizures, a long history of epilepsy, and unilateral hippocampal pathology.1 Our group provides strong evidence about the existence of a common, often unrecognized clinical entity called benign TLE, which is characterized by seizure onset in adulthood, frequent familial history, rare simple partial seizures, and radiologic evidence of hippocampal sclerosis (Hs) in almost 40%, which was previously considered synonymous with drug-resistant epilepsy.2,3 Moreover, using voxel-based morphometry and cortical thickness we have confirmed mesial temporal lobe, parietal lobe, and thalamic abnormalities that were remarkably comparable to what is observed in patients with refractory TLE regardless of the presence of Hs.4,5 Of interest, our observations in benign TLE are consistent with the brain regions reported by Keller et al.1 This finding further enlarges the thalamocortical network being observed, even in patients with very mild epilepsy. Likewise to what many authors found in patients with refractory TLE,6,7 Keller interpreted their data giving several possible hypotheses such as the progressive thalamic damage due to seizure propagation from the connected epileptogenic temporal lobe; the intrinsic mesiotemporal excitotoxicity; and the degree of thalamic damage that is related to duration of epilepsy due to chronicity of TLE. Furthermore, all patients studied by Keller et al. had evidence of Hs and it is very well known that Hs may drive gray matter atrophy and voxel-based analysis consequently. On the other hand, all our patients with benign TLE2–5 had a very mild epileptic disorder with almost no seizures at long-term follow-up, had no significant correlation between either the duration of the epilepsy or the age at onset and extent of brain damage, thus it is reasonable to hypothesize that the thalamus might be primarily caught up in the epileptogenic network underlying TLE. Moreover and very exciting, we found the same pattern of thalamic damage in patients with benign TLE, without radiologic evidence of Hs and normal hippocampal volumetry.4,5 All these data1,4–7 support that the thalamus is centrally involved in the epileptogenic network of TLE, as also suggested by postsurgical studies reporting that the prognosis could be related to the extension of the epileptogenic network to the subcortical thalamic structure in TLE.8 Obviously as Keller et al. highlighted,1 all evidence of thaEpilepsia, 55(6):941–947, 2014
DISCLOSURE None of the authors has any conflicts 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.
Angelo Labate1,2 [email protected] Laura Mumoli1 Antonio Gambardella1,2 1 Institute of Neurology, University “Magna Græcia,” Catanzaro, Italy; and 2 Institute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Viale Europa, Germaneto (CZ), Italy REFERENCES 1. Keller SS, O’Muircheartaigh J, Traynor C, et al. Thalamotemporal impairment in temporal lobe epilepsy: A combined MRI analysis of structure, integrity, and connectivity. Epilepsia 2014;55:306–315. 2. Labate A, Gambardella A, Andermann E, et al. Benign mesial temporal lobe epilepsy. Nat Rev Neurol 2011;7:237–240. 3. Labate A, Ventura P, Gambardella A, et al. MRI evidence of mesial temporal sclerosis in sporadic “benign” temporal lobe epilepsy. Neurology 2006;66:562–565. 4. Labate A, Cerasa A, Gambardella A, et al. Hippocampal and thalamic atrophy in mild temporal lobe epilepsy: a VBM study. Neurology 2008;71:1094–1101. 5. Labate A, Cerasa A, Aguglia U, et al. Voxel-based morphometry of sporadic epileptic patients with mesiotemporal sclerosis. Epilepsia 2010;51:506–510. 6. Mueller SG, Laxer KD, Barakos J, et al. Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis. Epilepsia 2010;51:1436–1445. 7. Bonilha L, Edwards JC, Kinsman SL, et al. Extrahippocampal gray matter loss and hippocampal deafferentation in patients with temporal lobe epilepsy. Epilepsia 2010;51:519–528. 8. Guye M, Regis J, Tamura M, et al. The role of corticothalamic coupling in human temporal lobe epilepsy. Brain 2006;129:1917– 1928.
ANNOUNCEMENTS 31st International Epilepsy Congress 6–10 September, 2015; Istanbul.
Upcoming Regional Congresses 11th European Congress on Epileptology 29 June to 3 July, 2014; Stockholm, Sweden. http:// www.epilepsystockholm2014.org/
944
Thalamotemporal impairment in benign temporal lobe epilepsy: Same hypotheses? To the Editors: We read with great interest the study by Keller et al.1 showing that there is an abnormal thalamic area connected to the temporal lobe and related to the extent of mesial temporal lobe damage in patients with temporal lobe epilepsy (TLE). Furthermore, the sample studied by Keller was of TLE patients with frequent seizures, a long history of epilepsy, and unilateral hippocampal pathology.1 Our group provides strong evidence about the existence of a common, often unrecognized clinical entity called benign TLE, which is characterized by seizure onset in adulthood, frequent familial history, rare simple partial seizures, and radiologic evidence of hippocampal sclerosis (Hs) in almost 40%, which was previously considered synonymous with drug-resistant epilepsy.2,3 Moreover, using voxel-based morphometry and cortical thickness we have confirmed mesial temporal lobe, parietal lobe, and thalamic abnormalities that were remarkably comparable to what is observed in patients with refractory TLE regardless of the presence of Hs.4,5 Of interest, our observations in benign TLE are consistent with the brain regions reported by Keller et al.1 This finding further enlarges the thalamocortical network being observed, even in patients with very mild epilepsy. Likewise to what many authors found in patients with refractory TLE,6,7 Keller interpreted their data giving several possible hypotheses such as the progressive thalamic damage due to seizure propagation from the connected epileptogenic temporal lobe; the intrinsic mesiotemporal excitotoxicity; and the degree of thalamic damage that is related to duration of epilepsy due to chronicity of TLE. Furthermore, all patients studied by Keller et al. had evidence of Hs and it is very well known that Hs may drive gray matter atrophy and voxel-based analysis consequently. On the other hand, all our patients with benign TLE2–5 had a very mild epileptic disorder with almost no seizures at long-term follow-up, had no significant correlation between either the duration of the epilepsy or the age at onset and extent of brain damage, thus it is reasonable to hypothesize that the thalamus might be primarily caught up in the epileptogenic network underlying TLE. Moreover and very exciting, we found the same pattern of thalamic damage in patients with benign TLE, without radiologic evidence of Hs and normal hippocampal volumetry.4,5 All these data1,4–7 support that the thalamus is centrally involved in the epileptogenic network of TLE, as also suggested by postsurgical studies reporting that the prognosis could be related to the extension of the epileptogenic network to the subcortical thalamic structure in TLE.8 Obviously as Keller et al. highlighted,1 all evidence of thaEpilepsia, 55(6):941–947, 2014
DISCLOSURE None of the authors has any conflicts 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.
Angelo Labate1,2 [email protected] Laura Mumoli1 Antonio Gambardella1,2 1 Institute of Neurology, University “Magna Græcia,” Catanzaro, Italy; and 2 Institute of Molecular Bioimaging and Physiology of the National Research Council (IBFM-CNR), Viale Europa, Germaneto (CZ), Italy REFERENCES 1. Keller SS, O’Muircheartaigh J, Traynor C, et al. Thalamotemporal impairment in temporal lobe epilepsy: A combined MRI analysis of structure, integrity, and connectivity. Epilepsia 2014;55:306–315. 2. Labate A, Gambardella A, Andermann E, et al. Benign mesial temporal lobe epilepsy. Nat Rev Neurol 2011;7:237–240. 3. Labate A, Ventura P, Gambardella A, et al. MRI evidence of mesial temporal sclerosis in sporadic “benign” temporal lobe epilepsy. Neurology 2006;66:562–565. 4. Labate A, Cerasa A, Gambardella A, et al. Hippocampal and thalamic atrophy in mild temporal lobe epilepsy: a VBM study. Neurology 2008;71:1094–1101. 5. Labate A, Cerasa A, Aguglia U, et al. Voxel-based morphometry of sporadic epileptic patients with mesiotemporal sclerosis. Epilepsia 2010;51:506–510. 6. Mueller SG, Laxer KD, Barakos J, et al. Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis. Epilepsia 2010;51:1436–1445. 7. Bonilha L, Edwards JC, Kinsman SL, et al. Extrahippocampal gray matter loss and hippocampal deafferentation in patients with temporal lobe epilepsy. Epilepsia 2010;51:519–528. 8. Guye M, Regis J, Tamura M, et al. The role of corticothalamic coupling in human temporal lobe epilepsy. Brain 2006;129:1917– 1928.
ANNOUNCEMENTS 31st International Epilepsy Congress 6–10 September, 2015; Istanbul.
Upcoming Regional Congresses 11th European Congress on Epileptology 29 June to 3 July, 2014; Stockholm, Sweden. http:// www.epilepsystockholm2014.org/
944
