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急性孤立性双侧缺血性脑桥梗死的卒中恢复与病灶缩小:一例报告

Stroke recovery and lesion reduction following acute isolated bilateral ischaemic pontine infarction: a case report.

作者信息

Varsou Ourania, Stringer Michael S, Fernandes Catarina Dinis, Schwarzbauer Christian, MacLeod Mary Joan

机构信息

Aberdeen Biomedical Imaging Centre, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.

出版信息

BMC Res Notes. 2014 Oct 16;7:728. doi: 10.1186/1756-0500-7-728.

DOI:10.1186/1756-0500-7-728
PMID:25322939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4203895/
Abstract

BACKGROUND

Although pontine strokes account for a small percentage of all ischaemic events, they can be associated with significant initial disability. These lesions may be missed on computed tomography and therefore magnetic resonance imaging is generally preferred for the assessment of brainstem strokes. The aetiopathogenesis of isolated pontine infarcts, not due to a significant compromise (occlusion or dissection) in the vertebrobasilar territory, still remains to be fully characterised. These strokes present with different symptoms, depending on the lesion location and size, partly reflecting the anatomical variability of the vertebrobasilar vessels. Progressive neurological deterioration is relatively common and has been associated with the extension of such lesions. However, many patients with significant infarcts in the pons will do well in the future and initial diffusion-weighted imaging may not add useful prognostication to the clinical assessment. We discuss here a case where an initially progressive presentation was associated with a marked improvement in both clinical and radiological assessments at 42 days.

CASE PRESENTATION

A 49-year-old white British man presented with left-sided weakness, incoordination, unsteadiness, cerebellar ataxic dysarthria and dysphonia. A baseline magnetic resonance imaging scan with diffusion-weighted imaging, T1-weighted and T2-weighted sequences showed an acute bilateral pontine infarct. On a repeat scan at 42 days, there was a 57.5% decrease in the size of the lesion on the high-resolution three-dimensional T1-weighted image and a corresponding improvement in the symptoms and the clinical assessments of this patient. The reduction in infarct size was also comparable to the decrease calculated between the baseline diffusion-weighted and the follow-up fluid attenuated inversion recovery sequences.

CONCLUSION

This case report discusses the significant clinical improvement and corresponding lesion reduction in a patient that presented with worsening neurological symptoms and was diagnosed with acute bilateral ischaemic pontine infarction. Further studies, utilising structural and functional magnetic resonance imaging with follow-up scans, are needed to provide better insights into the underlying aetiopathology and recovery mechanisms of pontine stroke. These will help define the relationship between imaging parameters and outcome allowing for better prognosis along with the development of relevant rehabilitation programs for this group of patients.

摘要

背景

尽管脑桥卒中在所有缺血性事件中所占比例较小,但它们可能与严重的初始残疾相关。这些病变在计算机断层扫描中可能会被漏诊,因此磁共振成像通常更适合用于评估脑干卒中。孤立性脑桥梗死的病因发病机制,并非由于椎基底动脉区域的严重病变(闭塞或夹层),仍有待充分阐明。这些卒中根据病变位置和大小表现出不同症状,部分反映了椎基底动脉血管的解剖变异性。进行性神经功能恶化相对常见,且与此类病变的扩展有关。然而,许多脑桥有明显梗死的患者未来情况良好,初始弥散加权成像可能无法为临床评估增加有用的预后信息。我们在此讨论一例病例,该患者最初表现为进行性症状,在42天时临床和影像学评估均有显著改善。

病例介绍

一名49岁的英国白人男性出现左侧肢体无力、共济失调、不稳、小脑性共济失调性构音障碍和发音困难。基线磁共振成像扫描,包括弥散加权成像、T1加权和T2加权序列,显示急性双侧脑桥梗死。在42天的复查扫描中,高分辨率三维T1加权图像上病变大小减少了57.5%,该患者的症状及临床评估相应改善。梗死灶大小的减小也与基线弥散加权成像和随访液体衰减反转恢复序列之间计算出的减小程度相当。

结论

本病例报告讨论了一名出现神经症状恶化并被诊断为急性双侧缺血性脑桥梗死的患者,其临床显著改善及相应的病灶缩小情况。需要进一步利用结构和功能磁共振成像并进行随访扫描的研究,以更好地洞察脑桥卒中的潜在病因病理和恢复机制。这将有助于确定成像参数与预后之间的关系,从而实现更好的预后,并为这组患者制定相关的康复计划。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/a5b82e12d59e/13104_2014_3243_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/5f23e41e9a03/13104_2014_3243_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/792010dd7e6d/13104_2014_3243_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/88d855f7d201/13104_2014_3243_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/a5b82e12d59e/13104_2014_3243_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/5f23e41e9a03/13104_2014_3243_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/792010dd7e6d/13104_2014_3243_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/88d855f7d201/13104_2014_3243_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f95e/4203895/a5b82e12d59e/13104_2014_3243_Fig4_HTML.jpg

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