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丘脑的微血管灌注异常在有痛和无痛性糖尿病多发性神经病中的表现：1 型糖尿病疼痛发病机制的一个线索。

Microvascular perfusion abnormalities of the Thalamus in painful but not painless diabetic polyneuropathy: a clue to the pathogenesis of pain in type 1 diabetes.

机构信息

Diabetes Research Department, Royal Hallamshire Hospital, Sheffield, UK.

出版信息

Diabetes Care. 2011 Mar;34(3):718-20. doi: 10.2337/dc10-1550. Epub 2011 Jan 31.

DOI:10.2337/dc10-1550
PMID:21282344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3041213/
Abstract

OBJECTIVE

The pathogenesis of painful diabetic neuropathy (DN) remains undetermined, with both central and peripheral mechanisms implicated. This study investigates whether thalamic perfusion abnormalities occur in painful DN.

RESEARCH DESIGN AND METHODS

Eighteen subjects with type 1 diabetes (no DN = 6, painful DN = 5, painless DN = 7) and six healthy volunteers (HV) were recruited. Microvascular perfusion characteristics (relative cerebral blood volume [rCBV], flow [rCBF], and transit time [tt(FM)]) of the thalamus and caudate nucleus were assessed using magnetic resonance perfusion imaging. The caudate nucleus was chosen to serve as an in vivo control region.

RESULTS

Subjects with painful DN had significantly greater thalamic rCBV (means [SD]; painful DN, 228.7 [19.5]; no DN, 202.3 [25.8]; painless DN, 216.5 [65.5]; HV, 181.9 [51.7]; P = 0.04) and the longest tt(FM)(s) (painful DN, 38.4 [3.6]; no DN, 35.3 [13.2]; painless DN, 35.9 [13.7]; HV, 33.7 [14.9]; P = 0.07). There was no significant difference in markers of caudate nucleus perfusion.

CONCLUSIONS

Painful DN is associated with increased thalamic vascularity. This may provide an important clue to the pathogenesis of pain in DN.

摘要

目的

痛性糖尿病周围神经病变（DN）的发病机制尚不清楚，涉及中枢和外周机制。本研究旨在探讨痛性 DN 是否存在丘脑灌注异常。

研究设计和方法

招募了 18 名 1 型糖尿病患者（无 DN=6 例，痛性 DN=5 例，无痛性 DN=7 例）和 6 名健康志愿者（HV）。采用磁共振灌注成像评估丘脑和尾状核的微血管灌注特征（相对脑血容量[rCBV]、血流[rCBF]和转运时间[tt（FM）]）。尾状核被选为体内对照区域。

结果

痛性 DN 患者的丘脑 rCBV（均值[标准差]；痛性 DN，228.7[19.5]；无 DN，202.3[25.8]；无痛性 DN，216.5[65.5]；HV，181.9[51.7]；P=0.04）和最长 tt（FM）（s）（痛性 DN，38.4[3.6]；无 DN，35.3[13.2]；无痛性 DN，35.9[13.7]；HV，33.7[14.9]；P=0.07）均显著升高。尾状核灌注标志物无显著差异。

结论

痛性 DN 与丘脑血管增多有关。这可能为 DN 疼痛的发病机制提供了重要线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b77/3041213/e39e0329dc02/718fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b77/3041213/e39e0329dc02/718fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b77/3041213/e39e0329dc02/718fig1.jpg

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