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是什么导致了小的深部梗死的临床误诊?

What causes false clinical prediction of small deep infarcts?

作者信息

Lodder J, Bamford J, Kappelle J, Boiten J

机构信息

Department of Neurology, University Hospital Maastricht, The Netherlands.

出版信息

Stroke. 1994 Jan;25(1):86-91. doi: 10.1161/01.str.25.1.86.

DOI:10.1161/01.str.25.1.86
PMID:8266388
Abstract

BACKGROUND AND PURPOSE

Our goal was to identify factors that play a role in false clinical diagnosis of small deep infarcts.

METHODS

In 350 prospectively registered patients with a first supratentorial ischemic stroke, we clinically differentiated between lacunar and nonlacunar syndromes. Using computed tomography (CT), we distinguished small deep and territorial infarcts and also recorded leukoaraiosis and asymptomatic infarcts. Degree of initial handicap, potential source of cardioembolic stroke, and hypertension were also noted.

RESULTS

One hundred forty-seven patients had a lacunar and 203 a nonlacunar syndrome. Forty-two (12%) had a lesion visualized by CT that was compatible with a recent infarct but was considered inappropriate for the clinical syndrome: nineteen had a nonlacunar syndrome but a small deep infarct, and 23 had a lacunar syndrome but a territorial infarct. Patients with a nonlacunar syndrome but a small deep infarct were more severely disabled (a modified Rankin scale rating of 5) (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.25 to 14.88) and had a cardioembolic source (OR, 4.07; 95% CI, 1.04 to 15.95), leukoaraiosis (OR, 3.79; 95% CI, 1.32 to 10.05), or asymptomatic infarcts visualized by CT (OR, 4.13; 95% CI, 1.45 to 11.71) compared with 124 patients with a correctly diagnosed small deep infarct. Twelve of 19 patients with a nonlacunar syndrome but a small deep infarct had a lesion in the left hemisphere, and 9 of these 12 had "aphasia." Patients with a lacunar syndrome but a territorial infarct more often had a cardioembolic source (OR, 4.02; 95% CI, 1.15 to 14.03) and a pure motor syndrome (OR, 4.52; 95% CI, 1.55 to 13.18) than those with lacunar syndrome but a small deep infarct, although 21 (91%) were in the right hemisphere. Of the first 103 patients with lacunar stroke diagnosed by two of the study neurologists, 5 had an inappropriate lesion compared with 14 of the later 40 diagnosed by colleagues without a specific interest in cerebrovascular diseases (OR, 0.09; 95% CI, 0.03 to 0.26).

CONCLUSIONS

(1) Diagnosis of lacunar syndromes should not be influenced by deficit severity or the presence of a potential cardiac source of embolism. (2) Speech disorders should carefully be classified. (3) Routine tests of nondominant higher functions may be inadequate. (4) Doctors interested in cerebrovascular neurology have a lower failure rate in differentiating small deep infarcts from territorial infarcts than those less well-trained or interested in neurology. (5) Among the lacunar syndromes, pure motor syndrome may be the least specific predictor of a small deep infarct.

摘要

背景与目的

我们的目标是确定在小的深部梗死灶临床误诊中起作用的因素。

方法

在350例前瞻性登记的首次幕上缺血性卒中患者中,我们在临床上区分腔隙性和非腔隙性综合征。使用计算机断层扫描(CT),我们区分小的深部梗死灶和区域梗死灶,并记录脑白质疏松和无症状梗死灶。还记录了初始残疾程度、心源性栓塞性卒中的潜在来源以及高血压情况。

结果

147例患者为腔隙性综合征,203例为非腔隙性综合征。42例(12%)患者的CT显示有与近期梗死灶相符的病变,但被认为与临床综合征不符:19例为非腔隙性综合征但有小的深部梗死灶,23例为腔隙性综合征但有区域梗死灶。与124例诊断正确的小的深部梗死灶患者相比,非腔隙性综合征但有小的深部梗死灶的患者残疾程度更严重(改良Rankin量表评分为5分)(比值比[OR],4.31;95%置信区间[CI],1.25至14.88),且有心源性栓塞来源(OR,4.07;95%CI,1.04至15.95)、脑白质疏松(OR,3.79;95%CI,1.32至10.05)或CT显示的无症状梗死灶(OR,4.13;95%CI,1.45至11.71)。19例非腔隙性综合征但有小的深部梗死灶的患者中有12例病变位于左半球,这12例中有9例出现“失语”。与腔隙性综合征但有小的深部梗死灶的患者相比,腔隙性综合征但有区域梗死灶的患者更常有心源性栓塞来源(OR,4.02;95%CI,1.15至14.03)和纯运动综合征(OR,4.52;95%CI,1.55至13.18),尽管21例(91%)位于右半球。在由两位研究神经科医生诊断的前103例腔隙性卒中患者中,有5例病变不符,而在后来由对脑血管疾病无特殊兴趣的同事诊断的40例患者中有14例病变不符(OR,0.09;95%CI,0.03至0.26)。

结论

(1)腔隙性综合征的诊断不应受残疾严重程度或潜在心脏栓塞源的影响。(2)言语障碍应仔细分类。(3)对非优势半球高级功能的常规检查可能不够充分。(4)对脑血管神经病学感兴趣的医生在区分小的深部梗死灶和区域梗死灶方面的误诊率低于训练不足或对神经病学兴趣较低的医生。(5)在腔隙性综合征中,纯运动综合征可能是小的深部梗死灶最不具特异性的预测指标。

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