Pierre Cesaro, Mann Michael W, Moretti Jean Luc, Defer Gilles, Roualdès Brigitte, Nguyen Jean Paul, Degos Jean Denis
Département de Neurosciences Médicales, C.H.U. Henri Mondor, 94000 Creteil France Service de Médecine Nucléaire, CHU Avicenne, 93000 Bobigny France.
Pain. 1991 Dec;47(3):329-336. doi: 10.1016/0304-3959(91)90224-L.
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.
