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Gilles Defer

Publications and source records attributed to Gilles Defer.

3 recordsLinked to original sources

Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue.

We compared the striatal uptake of [(18)F]fluorodopa with [(76)Br]-FE-CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [(18)F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [(18)F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [(18)F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation.

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Central pain and thalamic hyperactivity: a single photon emission computerized tomographic study.

Five patients with central post-stroke pain (CPSP) accepted to be studied according to the following paradigm: a single photon emission computerized tomography (SPECT) using [123I]N-isopropyl-iodoamphetamine (IMP) was made in each patient 20 min following i.v. injection of IMP; during this time, the patients were stimulated in order to reproduce their spontaneous pain. Of the five patients, two had CPSP with hyperpathia following a stroke (with a lesion on CT scan involving the thalamo-cortical pathway in one and involving the thalamus in the other); two had CPSP following a stroke in the middle cerebral artery area, without hyperpathia; and the last patient suffered pain from algodystrophia following a fracture of the wrist. In the two cases with hyperpathia, SPECT demonstrated a contralateral relative hyperactivity in a central region corresponding to the thalamic area. This was not observed in the three other patients. In the two patients with hyperpathia, a second SPECT scan with stimulation of the contralateral pain-free arm did not demonstrate any hyperactivity in the thalamic area. These results suggest that a thalamic neuronal hyperactivity may characterize some hyperpathic syndromes and, in accordance with our previous results obtained in the rat, that the loss of inhibition on medial thalamic neurons may be a main feature of hyperpathia following certain cerebral stroke syndromes.

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