CENTRAL PAIN AND THALAMIC HYPERACTIVITY - A SINGLE PHOTON-EMISSION COMPUTERIZED TOMOGRAPHIC STUDY
CENTRAL PAIN AND THALAMIC HYPERACTIVITY - A SINGLE PHOTON-EMISSION COMPUTERIZED TOMOGRAPHIC STUDY
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DOI：
10.1016/0304-3959(91)90224-l
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发表时间：
1991-12-01
期刊：
影响因子：
7.4
通讯作者：
DEGOS, JD
中科院分区：
文献类型：
--
作者：
CESARO, P;MANN, MW;DEGOS, JD
5例中枢性卒中后疼痛（CPSP）患者接受根据以下范例进行研究：在静脉注射IMP后20 min，对每位患者进行单光子发射计算机断层扫描（SPECT），使用[I-123] N-异丙基-碘苯丙胺（IMP）;在此期间，刺激患者以再现其自发性疼痛。 在这5名患者中，2名患者在中风后出现CPSP伴痛觉过敏（CT扫描显示，1名患者的病变累及丘脑-皮质通路，另1名患者累及丘脑）; 2名患者在大脑中动脉区域中风后出现CPSP，但没有痛觉过敏;最后1名患者在手腕骨折后出现痛性肌营养不良。 在两例有痛觉亢进的病例中，SPECT显示对应于丘脑区域的中央区域的对侧相对亢进。 在其他三名患者中未观察到这一点。 在两名痛觉亢进患者中，刺激对侧无痛臂进行第二次SPECT扫描，未显示丘脑区域有任何活动过度。 这些结果表明，丘脑神经元活动过度可能是某些神经过敏综合征的特征，并与我们以前在大鼠中获得的结果一致，丘脑内侧神经元抑制的丧失可能是某些脑卒中综合征后神经过敏的主要特征。
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 [I-123]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.