Altered pain and thermal sensation in subjects with isolated parietal and insular cortical lesions.

Altered pain and thermal sensation in subjects with isolated parietal and insular cortical lesions.
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DOI:
10.1016/j.ejpain.2009.10.002
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发表时间:
2010-05
期刊:
European journal of pain (London, England)
影响因子:
--
通讯作者:
Lenz FA
Lenz FA
中科院分区:
其他
文献类型:
--
作者:
Veldhuijzen DS;Greenspan JD;Kim JH;Lenz FA

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皮层损伤后感觉功能的研究通常包括多个皮层、白质和丘脑结构的损伤。我们现在验证这样的假设,即解剖学上局限于特定的岛叶和顶叶结构及其下皮层白质的病变与不同类型的感觉丧失有关。通过定量感觉测试(QST)测量感觉损失,并相对于正常值进行统计评估。所有7名患有岛岛和/或顶叶病变的受试者均表现为热感觉减退,尽管病变的病因不同。寒热痛觉减退仅发生在最广泛的顶叶和岛叶病变的受试者中,这种病变发生在子宫内。冷异常性痛在临床上和阈值上发生在两个孤立的岛叶后/岛叶后皮层缺血性病变的受试者中,以及在两个很少或没有岛叶受累的顶叶皮层病变的受试者中。中枢性疼痛发生在两个临床异常性疼痛的受试者中,继发于孤立的岛叶后皮层/岛叶后皮层病变,而前叶和后顶叶皮层不受影响。这些结果表明,非疼痛性冷热感觉是由顶叶和岛叶皮质结构共同介导的,因此该系统中任何部位的病变都可能降低敏感性。相比之下,热痛更强烈,需要这些相同结构的更大的皮质损伤才能产生痛觉减退。此外,冷异常性痛可能是由局限性病变引起的,这些病变也会产生热感觉减退,但并非所有这些病变都是如此。
Studies of sensory function following cortical lesions have often included lesions which multiple cortical, white matter, and thalamic structures. We now test the hypothesis that lesions anatomically constrained to particular insular and parietal structures and their subjacent white matter are associated with different patterns of sensory loss. Sensory loss was measured by quantitative sensory testing (QST), and evaluated statistically with respect to normal values. All seven subjects with insular and/or parietal lesions demonstrated thermal hypoesthesia, although the etiology of the lesions was heterogeneous. Cold and heat hypoalgesia were only found in the subject with the most extensive parietal and insular lesion, which occurred in utero. Cold allodynia occurred clinically and by thresholds in two subjects with isolated ischemic lesions of the posterior insular/ retroinsular cortex, and by thresholds in two subjects with a lesion of parietal cortex with little or no insular involvement. Central pain occurred in the two subjects with clinical allodynia secondary to isolated lesions of the posterior insular/retroinsular cortex, which spared the anterior and posterior parietal cortex. These results suggest that nonpainful cold and heat sensations are jointly mediated by parietal and insular cortical structures so that lesions anywhere in this system may diminish sensitivity. In contrast, thermal pain is more robust requiring larger cortical lesions of these same structures to produce hypoalgesia. In addition, cold allodynia can result from restricted lesions that also produce thermal hypoesthesia, but not from all such lesions.
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