HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Correspondence to:

ARTICLES: V. Bouilleret, F. Semah, F. Chassoux, M. Mantzaridez, A. Biraben, R. Trebossen, and M. -J. Ribeiro Basal ganglia involvement in temporal lobe epilepsy: A functional and morphologic study Neurology 2008; 70: 177-184 [Abstract] [Full text] [PDF]

Correspondence: Submit a response to this article

Correspondence published:

Basal ganglia involvement in temporal lobe epilepsy: A functional and morphologic study

David S. Goldstein   (8 April 2008)

Reply from the authors

Franck Semah, Viviane Bouilleret and Maria-Joao Ribeiro   (8 April 2008)

Basal ganglia involvement in temporal lobe epilepsy: A functional and morphologic study 8 April 2008
David S. Goldstein, Clinical Neurocardiology Section, CNP, DIR, NINDS, NIH 10 Center Drive MSC-1620, Bethesda, MD 20892-1620 Send Correspondence to journal: Re: Basal ganglia involvement in temporal lobe epilepsy: A functional and morphologic study goldsteind{at}ninds.nih.gov David S. Goldstein	I read the report by Bouilleret et al. with interest [1] and request clarification on a few issues. The first concerns the involvement of the substantia nigra. From the results of the SPM2 analyses depicted in Figure 1, it appears from the position of the cross-hairs in the [18F]fluorodo-L-DOPA scan that the region distinguishing the patients is in the dorsal medial midbrain, perhaps corresponding to the peri-aqueductal gray region, whereas the substantia nigra is in the ventral midbrain and off the midline. Can the authors provide a more convincing image depicting decreased [18F]fluorodo-L-DOPA-derived radioactivity in the substantia nigra of the patients? The second is about the mechanism of decreased [18F]fluorodo-L-DOPA-derived radioactivity in the basal ganglia. In 1988, we found that cortical foci of patients with intractable temporal lobe epilepsy have increased tissue concentrations of DOPA and dopamine, compared to uninvolved cortex in the same patients. [2] These findings would suggest increased synthesis and storage of catecholamines in the affected regions. Would the authors be willing to offer a pathophysiologic mechanism leading to increased cortical catecholamine storage at the level of the seizure focus and apparently decreased storage at the level of the basal ganglia? References 1. Bouilleret V, Semah F, Chassoux F et al.Basal ganglia involvement in temporal lobe epilepsy: A functional and morphologic study. Neurology 2008;70:177-184. 2. Goldstein DS, Nadi NS, Stull R, Wyler AR, Porter RJ. Levels of catechols in epileptogenic and non-epileptogenic regions of the human brain. J Neurochem 1988;50:225-229. Disclosure: The author reports no disclosures.
Reply from the authors 8 April 2008
Franck Semah, Service Hospitalier Frédéric Joliot, I2BM/DSV 4, Place du General Leclerc, 91401 Orsay Cedex, France, Viviane Bouilleret and Maria-Joao Ribeiro Send Correspondence to journal: Re: Reply from the authors maria-joao.ribeiro{at}cea.fr Franck Semah, et al.	The dopaminergic changes in patients with severe epilepsy are under-evaluated and unclear. In our study, the localization of the abnormal decrease of [18F]fluoro-L-DOPA uptake corresponded to the striatum and to the substantia nigra (SN) according to the Talairach coordinates. Previous studies, mainly conducted in Parkinson disease (PD), have demonstrated that [18F]fluoro-L-DOPA uptake can be detected using PET in the striatum and in the SN. [6] SN is one of the major structures of basal ganglia circuitry where activity is modulated by the cortex through direct and indirect trans-subthalamic and striatal pathways. Several studies have shown that pharmacological inhibition of SN could suppress seizures in various models of epilepsy [7]. In our study, we assessed in vivo using PET and [18F]fluoro-L-DOPA, the dopaminergic involvement in patients with temporal lobe epilepsy. In the study by Goldstein et al., the concentration of cathecols was measured in epileptogenic and non-epileptogenic regions in vitro by liquid chromatography with electrochemical detection and this could not be performed using [18F]fluoro-L-DOPA PET. The PET scanner probably doesn't allow the detection of small differences in regions with a low level of dopamine neurons such as the cortex. Experimental and clinical reports have suggested that the basal ganglia system is involved in the propagation or in the control of epileptic seizures [8,9]. These studies suggested that dysfunctioning of dopaminergic neurotransmission could be associated with enduring discharges. Several experimental studies have shown that ictal activity is associated with an increased metabolism of dopamine. Electroshock-induced tonic-clonic seizures in rats increased striatal accumulation of dopamine metabolites. [10] Using [18F]fluoro-L-DOPA PET, it is not possible to determine whether the dopamine deficit observed in epileptic patients is due to cell loss or reduced storage. However, the bilateral changes in the caudate and in the putamen that are equally affected suggest that the loss of dopaminergic neurons is not the main pathophysiological mechanism. In PD, the deficit is asymmetric and more severe in the putamen than in the caudate. Furthermore, in our study, the absence of gray matter volume reduction assessed by MRI in the striatum confirmed that neuronal loss is not the main pathophysiological mechanism of the [18F]fluoro-L-DOPA uptake decrease. Finally, as dopamine has been considered to take part in the seizure control system, our results suggest that recurrent seizures could induce an increase in the turnover in dopamine, resulting in a secondary depletion either in striatum and SN. References 6. Ribeiro MJ, Vidailhet M, Loc'h C, et al. Dopaminergic function and dopamine transporter binding assessed with positron emission tomography in Parkinson disease. Arch Neurol. 2002;59:580-586. 7. Deransart C, Le-Pham BT, Hirsch E, Marescaux C, Depaulis A. Inhibition of the substantia nigra suppresses absences and clonic seizures in audiogenic rats, but not tonic seizures: evidence for seizure specificity of the nigral control. Neuroscience. 2001;105:203-211. 8. Deransart C, Riban V, Lê B, Marescaux C, Depaulis A. Dopamine in the striatum modulates seizures in a genetic model of absence epilepsy in the rat. Neuroscience. 2000;100:335-344. 9. Depaulis A, Moshé SL. The basal ganglia and the epilepsies: translating experimental concepts to new therapies. Epileptic disorders. 2002;4(suppl 3):S7-S93. 10. Starr MS, The role of dopamine in epilepsy. Synapse 1996;22:159-194. Disclosure: The authors report no disclosures.