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DOI: 10.1055/s-0032-1301572
Decreased Dopamine D2/D3-Receptor Binding in the Temporal Lobe and the Bilateral Basal Ganglia in patients with Temporal Lobe Epilepsy
Dopamine is an endogenous neuromodulator in cortical circuits and basal ganglia. In animal models, it is known to affect seizure threshold and might have a neuroprotective role in temporal lobe epilepsy (TLE).1 In animal models of TLE activation of D1- has a pro- and of D2-receptors (D2R) an anticonvulsant effect.
To quantify D2/D3 receptor binding we studied 26 patients with TLE and 18 controls by PET using the high affinity dopamine D2/D3 receptor ligand 18F-Fallypride ([18F]FP) suitable for imaging extrastriatal binding. TLE was defined by interictal and ictal video-EEG, MRI and 18F-Fluorodesoxyglucose-PET. A voxel based analysis with statistical parametric mapping (SPM8) was performed. Anatomical regions of interest (ROIs) were drawn on patient and control MRIs coregistered with [18F]FP-PET.
Compared to the control group, [18F]FP binding potential (BPND) was significantly reduced on ROI analysis in the affected temporal lobe with accentuation of the temporal pole (p<0.001) but even more widespread in the superior, inferior, the anterior part of the medial temporal gyrus (p<0.01), and the bilateral putamen (p<0.01). Voxel based group analysis confirmed these results. Comparisons between the effected and the unaffected side showed an even more pronounced reduction of D2R availability in the affected temporal lobe [(temporal pole (p<0.001; –32%); inferior, medial and superior gyrus (p<0,001; ~–20%)].
The areas of reduced D2R availability correspond to “the irritative zone” surrounding and the basal ganglia, which are suspected to be involved in a control circuit for epileptic seizures.2 These results indicate that D2/D3 receptors might play a specific role in the pathophysiology of mesial TLE. The results are in line with evidence from animal studies suggesting a neuroprotective role of dopamine through the inhibitory control of glutamate neurotransmission and excitotoxicity in epilepsy.
Literatur: 1. Bozzi Y, Vallone D, Borrelli E. Neuroprotective role of dopamine against hippocampal cell death. J Neurosci, 2000;20: 8643-9. 2. Deransart, C. and A. Depaulis (2002). The control of seizures by the basal ganglia? A review of experimental data. Epileptic Disord 4 Suppl 3: S61-72.