Robson Holly, Specht Karsten, Beaumont Helen, Parkes Laura M, Sage Karen, Lambon Ralph Matthew A, Zahn Roland
Department of Psychology and Clinical Language Sciences, University of Reading, UK.
Department of Biological and Medical Psychology, University of Bergen, Norway; Department of Clinical Engineering, Haukeland University Hospital, Bergen, Norway.
Cortex. 2017 Jul;92:249-260. doi: 10.1016/j.cortex.2016.11.002. Epub 2016 Nov 10.
Behavioural impairment post-stroke is a consequence of structural damage and altered functional network dynamics. Hypoperfusion of intact neural tissue is frequently observed in acute stroke, indicating reduced functional capacity of regions outside the lesion. However, cerebral blood flow (CBF) is rarely investigated in chronic stroke. This study investigated CBF in individuals with chronic Wernicke's aphasia (WA) and examined the relationship between lesion, CBF and neuropsychological impairment. Arterial spin labelling CBF imaging and structural MRIs were collected in 12 individuals with chronic WA and 13 age-matched control participants. Joint independent component analysis (jICA) investigated the relationship between structural lesion and hypoperfusion. Partial correlations explored the relationship between lesion, hypoperfusion and language measures. Joint ICA revealed significant differences between the control and WA groups reflecting a large area of structural lesion in the left posterior hemisphere and an associated area of hypoperfusion extending into grey matter surrounding the lesion. Small regions of remote cortical hypoperfusion were observed, ipsilateral and contralateral to the lesion. Significant correlations were observed between the neuropsychological measures (naming, repetition, reading and semantic association) and the jICA component of interest in the WA group. Additional ROI analyses found a relationship between perfusion surrounding the core lesion and the same neuropsychological measures. This study found that core language impairments in chronic WA are associated with a combination of structural lesion and abnormal perfusion in non-lesioned tissue. This indicates that post-stroke impairments are due to a wider disruption of neural function than observable on structural T1w MRI.
中风后的行为障碍是结构损伤和功能网络动态改变的结果。急性中风时经常观察到完整神经组织的灌注不足，这表明病变区域以外的区域功能能力下降。然而，慢性中风中脑血流量（CBF）很少被研究。本研究调查了慢性韦尼克失语症（WA）患者的CBF，并检查了病变、CBF与神经心理损伤之间的关系。对12名慢性WA患者和13名年龄匹配的对照参与者进行了动脉自旋标记CBF成像和结构MRI检查。联合独立成分分析（jICA）研究了结构病变与灌注不足之间的关系。偏相关分析探讨了病变、灌注不足与语言测量之间的关系。联合ICA显示，对照组和WA组之间存在显著差异，反映出左后半球有大面积的结构病变，以及一个相关的灌注不足区域延伸至病变周围的灰质。在病变同侧和对侧观察到了远处皮质灌注不足的小区域。在WA组中，神经心理测量（命名、复述、阅读和语义联想）与感兴趣的jICA成分之间存在显著相关性。额外的ROI分析发现，核心病变周围的灌注与相同的神经心理测量之间存在关系。本研究发现，慢性WA的核心语言障碍与结构病变和非病变组织中异常灌注的组合有关。这表明中风后的损伤是由于神经功能的更广泛破坏，而不仅仅是在结构T1w MRI上可观察到的。
