Mazya Michael V, Cooray Charith, Lees Kennedy R, Toni Danilo, Ford Gary A, Bar Michal, Frol Senta, Moreira Tiago, Sekaran Lakshmanan, Švigelj Viktor, Wahlgren Nils, Ahmed Niaz
1Department of Neurology, Karolinska University Hospital, Solna, Sweden.
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Eur Stroke J. 2018 Mar;3(1):29-38. doi: 10.1177/2396987317746003. Epub 2017 Nov 29.
Beyond intravenous thrombolysis, evidence is lacking on acute treatment of minor stroke caused by large artery occlusion. To identify candidates for additional endovascular therapy, we aimed to determine the frequency of non-haemorrhagic early neurological deterioration in patients with intravenous thrombolysis-treated minor stroke caused by occlusion of large proximal and distal cerebral arteries. Secondary aims were to establish risk factors for non-haemorrhagic early neurological deterioration and report three-month outcomes in patients with and without non-haemorrhagic early neurological deterioration.
We analysed data from the SITS International Stroke Thrombolysis Register on 2553 patients with intravenous thrombolysis-treated minor stroke (NIH Stroke Scale scores 0-5) and available arterial occlusion data. Non-haemorrhagic early neurological deterioration was defined as an increase in NIH Stroke Scale score ≥4 at 24 h, without parenchymal hematoma on follow-up imaging within 22-36 h.
The highest frequency of non-haemorrhagic early neurological deterioration was seen in 30% of patients with terminal internal carotid artery or tandem occlusions (internal carotid artery + middle cerebral artery) (adjusted odds ratio: 10.3 (95% CI 4.3-24.9), p < 0.001) and 17% in extracranial carotid occlusions (adjusted odds ratio 4.3 (2.5-7.7), p < 0.001) versus 3.1% in those with no occlusion. Proximal middle cerebral artery-M1 occlusions had non-haemorrhagic early neurological deterioration in 9% (adjusted odds ratio 2.1 (0.97-4.4), p = 0.06). Among patients with any occlusion and non-haemorrhagic early neurological deterioration, 77% were dead or dependent at three months.
Patients with minor stroke caused by internal carotid artery occlusion, with or without tandem middle cerebral artery involvement, are at high risk of disabling deterioration, despite intravenous thrombolysis treatment. Acute vessel imaging contributes usefully even in minor stroke to identify and consider endovascular treatment, or intensive monitoring at a comprehensive stroke centre, for patients at high risk of neurological deterioration.
除静脉溶栓外,大动脉闭塞所致轻度卒中的急性治疗缺乏相关证据。为了确定额外血管内治疗的候选者,我们旨在确定接受静脉溶栓治疗的大脑近端和远端动脉闭塞所致轻度卒中患者非出血性早期神经功能恶化的频率。次要目的是确定非出血性早期神经功能恶化的危险因素,并报告有和无非出血性早期神经功能恶化患者的三个月结局。
我们分析了来自SITS国际卒中溶栓登记处的2553例接受静脉溶栓治疗的轻度卒中患者(美国国立卫生研究院卒中量表评分0 - 5分)的数据以及可用的动脉闭塞数据。非出血性早期神经功能恶化定义为24小时时美国国立卫生研究院卒中量表评分增加≥4分,且在22 - 36小时内的随访影像上无实质血肿。
在30%的颈内动脉末端或串联闭塞(颈内动脉 + 大脑中动脉)患者中观察到非出血性早期神经功能恶化的最高频率(调整比值比:10.3(95%可信区间4.3 - 24.9),p < 0.001),在颅外颈动脉闭塞患者中为17%(调整比值比4.3(2.5 - 7.7),p < 0.001),而无闭塞患者为3.1%。大脑中动脉M1段近端闭塞患者中非出血性早期神经功能恶化为9%(调整比值比2.1(0.97 - 4.4),p = 0.06)。在有任何闭塞且发生非出血性早期神经功能恶化的患者中,77%在三个月时死亡或依赖他人。
颈内动脉闭塞所致轻度卒中患者,无论是否累及大脑中动脉串联病变,尽管接受了静脉溶栓治疗,仍有发生致残性恶化的高风险。即使在轻度卒中中,急性血管成像也有助于识别并考虑对有神经功能恶化高风险的患者进行血管内治疗或在综合卒中中心进行强化监测。