Infarction of 'non-core-non-penumbral' tissue after stroke: multivariate modelling of clinical impact

被引:42
作者
Alawneh, Josef A. [1 ]
Jones, Peter Simon [1 ]
Mikkelsen, Irene Klaerke [2 ]
Cho, Tae-Hee [3 ]
Siemonsen, Susanne [4 ]
Mouridsen, Kim [2 ]
Ribe, Lars [2 ]
Morris, Rhiannon S. [1 ]
Hjort, Niels [2 ]
Antoun, Nagui [5 ]
Gillard, Jonathan H. [5 ]
Fiehler, Jens [4 ]
Nighoghossian, Norbert [3 ]
Warburton, Elizabeth A. [6 ]
Ostergaard, Leif [2 ]
Baron, Jean-Claude [1 ,7 ]
机构
[1] Univ Cambridge, Addenbrookes Hosp, Neurol Unit, Dept Clin Neurosci,Stroke Res Grp, Cambridge CB2 2QQ, England
[2] Aarhus Univ Hosp, Ctr Functionally Integrat Neurosci, DK-8000 Aarhus, Denmark
[3] CREATIS CRMN, Hop Neurol Pierre Wertheimer, Hosp Civils Lyon, F-69777 Lyon, France
[4] Univ Med Ctr Hamburg Eppendorf, Dept Neuroradiol, D-20246 Hamburg, Germany
[5] Univ Cambridge, Dept Radiol, Cambridge CB2 2QQ, England
[6] Addenbrookes Hosp, Stroke Unit, Cambridge CB2 2QQ, England
[7] Univ Paris 05, INSERM, UMR894, F-75014 Paris, France
基金
英国医学研究理事会;
关键词
stroke; perfusion imaging; penumbra; clinical recovery; cerebral ischaemia; EARLY NEUROLOGICAL DETERIORATION; PERFUSION COMPUTED-TOMOGRAPHY; ACUTE ISCHEMIC-STROKE; VIABILITY THRESHOLDS; CEREBRAL INFARCTION; THROMBOLYSIS; EVOLUTION; DIFFUSION; VOLUME; SCALE;
D O I
10.1093/brain/awr100
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
There is considerable intersubject variability in early neurological course after anterior circulation stroke, yet the pathophysiology underlying this variability is not fully understood. Here, we hypothesize that, although not predicted by current pathophysiological models, infarction of 'non-core-non-penumbral' (i.e. clinically silent) brain tissue may nevertheless occur, and negatively influence clinical course over and above the established positive impact of penumbral salvage. In order to test this hypothesis, non-core-non-penumbral tissue was identified in two independent prospectively recruited cohorts, using computed tomography perfusion, and magnetic resonance perfusion- and diffusion-weighted imaging, respectively. Follow-up structural magnetic resonance imaging was obtained about 1 month later in all patients to map the final infarct. The volumes of both the acutely silent but eventually infarcted tissue, and the eventually non-infarcted penumbra, were determined by performing voxel-wise analysis of the acute and follow-up image sets, using previously validated perfusion thresholds. Early neurological course was expressed as change in National Institutes of Health Stroke Scale scores between the acute and 1-month assessments, relative to the acute score. The relationship between the acutely silent but eventually infarcted tissue volume and early neurological course was tested using a multivariate regression model that included the volume of non-infarcted penumbra. Thirty-four and 58 patients were recruited in the computed tomography perfusion and magnetic resonance perfusion cohorts, respectively (mean onset-to-imaging time: 136 and 156 min; 27 and 42 patients received intravenous thrombolysis, respectively). Infarction of acutely silent tissue was identified in most patients in both cohorts. Although its volume (median 0.2 and 2 ml, respectively) was much smaller than that of salvaged penumbra (59.3 and 93 ml, respectively), it was substantial in similar to 10% of patients. As expected, salvaged penumbra strongly positively influenced early neurological course. Even after correcting for the latter effect in the multivariate model, infarction of acutely silent tissue independently negatively influenced early neurological course in both cohorts (P = 0.018 and 0.031, respectively). This is the first systematic study to document infarction of acutely silent tissue after anterior circulation stroke, and to show that it affects a sizeable fraction of patients and has the predicted negative impact on clinical course. These findings were replicated in two independent cohorts, regardless of the perfusion imaging modality used. Preventing infarction of the tissue not initially at risk should have direct clinical benefit.
引用
收藏
页码:1765 / 1776
页数:12
相关论文
共 42 条
[1]   Hemodynamic Factors and Perfusion Abnormalities in Early Neurological Deterioration [J].
Alawneh, Josef A. ;
Moustafa, Ramez Reda ;
Baron, Jean-Claude .
STROKE, 2009, 40 (06) :E443-E450
[2]   THRESHOLDS IN CEREBRAL-ISCHEMIA - THE ISCHEMIC PENUMBRA [J].
ASTRUP, J ;
SIESJO, BK ;
SYMON, L .
STROKE, 1981, 12 (06) :723-725
[3]   Clinical correlations of diffusion and perfusion lesion volumes in acute ischemic stroke [J].
Baird, AE ;
Lövblad, KO ;
Dashe, JF ;
Connor, A ;
Burzynski, C ;
Schlaug, G ;
Straroselskaya, I ;
Edelman, RR ;
Warach, S .
CEREBROVASCULAR DISEASES, 2000, 10 (06) :441-448
[4]   CLASSIFICATION AND NATURAL-HISTORY OF CLINICALLY IDENTIFIABLE SUBTYPES OF CEREBRAL INFARCTION [J].
BAMFORD, J ;
SANDERCOCK, P ;
DENNIS, M ;
BURN, J ;
WARLOW, C .
LANCET, 1991, 337 (8756) :1521-1526
[5]   Differential Pathophysiological Mechanisms of Stroke Evolution between New Lesions and Lesion Growth: Perfusion-Weighted Imaging Study [J].
Bang, Oh Young ;
Kim, Gyeong Moon ;
Chung, Chin Sang ;
Kim, Suk Jae ;
Kim, Keon Ha ;
Jeon, Pyoung ;
Saver, Jeffrey L. ;
Liebeskind, David S. ;
Lee, Kwang Ho .
CEREBROVASCULAR DISEASES, 2010, 29 (04) :328-335
[6]  
Beaulieu C, 1999, ANN NEUROL, V46, P568, DOI 10.1002/1531-8249(199910)46:4<568::AID-ANA4>3.0.CO
[7]  
2-R
[8]   Hemorrhagic transformation of ischemic brain tissue -: Asymptomatic or symptomatic? [J].
Berger, C ;
Fiorelli, M ;
Steiner, T ;
Schäbitz, WR ;
Bozzao, L ;
Bluhmki, E ;
Hacke, W ;
von Kummer, R .
STROKE, 2001, 32 (06) :1330-1335
[9]   PROGRESSION OF STROKE AFTER ARRIVAL AT HOSPITAL [J].
BRITTON, M ;
RODEN, A .
STROKE, 1985, 16 (04) :629-632
[10]   Neuroimaging, the ischaemic penumbra, and selection of patients for acute stroke therapy [J].
Donnan, GA ;
Davis, SM .
LANCET NEUROLOGY, 2002, 1 (07) :417-425