Early neurological deterioration after thrombolysis: Clinical and imaging predictors

Simonsen, Claus Z; Schmitz, Marie Louise; Madsen, Mads; Mikkelsen, Irene Klærke; Chandra, Ronil V.; Leslie‐Mazwi, Thabele M; Andersen, Grethe

doi:10.1177/1747493016650454

Cited by 75 publications

(80 citation statements)

References 22 publications

(31 reference statements)

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“…In our study, the rate of END was 14.6%, which is similar to previous results (6–38%) [18-22], although the definition of END differed between studies. Here we have chosen the cutoff of at least 2 points deterioration at the 72-h NIHSS as proposed by Siegler et al [9] that seems to be more adapted in our patients with severe strokes at admission to avoid a “ceiling effect” and to take into account END related to malignant edema.…”

Section: Discussionsupporting

confidence: 81%

“…Here we have chosen the cutoff of at least 2 points deterioration at the 72-h NIHSS as proposed by Siegler et al [9] that seems to be more adapted in our patients with severe strokes at admission to avoid a “ceiling effect” and to take into account END related to malignant edema. This event was strongly associated with poor functional outcome as reported in previous studies [19, 22-24]. …”

Section: Discussionsupporting

confidence: 60%

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Impact of Brain Atrophy on Early Neurological Deterioration and Outcome in Severe Ischemic Stroke Treated by Intravenous Thrombolysis

et al. 2018

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Background: Brain atrophy has shown a protective effect on the risk of early neurological deterioration (END) related to malignant edema in patients with hemispheric infarction but could be deleterious on the outcome. Aims: We aimed to assess whether brain atrophy has an impact on the risk of END and on the outcome in severe ischemic strokes after intravenous (IV) thrombolysis. Methods: From a prospective thrombolysis registry, 137 patients who had a National Institutes of Health Stroke Scale (NIHSS) ≥15, MRI at admission, and IV thrombolysis were included. Relative cerebral volume was calculated. END was defined as a ≥2-points deterioration 72-h NIHSS and a good outcome as a modified Rankin Scale (mRS) ≤2 at 3 months. A multiple logistic regression analysis with a stepwise backward procedure was performed. Results: END and a good outcome were observed, respectively, in 20 (14.6%) and 48 (37.5%) patients. In univariate analysis, predictors of END included age (p = 0.049), diabetes (p = 0.041), and parenchymal hemorrhage (p = 0.039). In multivariate analysis, age (p = 0.018) was significantly associated with END. Brain atrophy was not associated with END even in subgroup analysis according to the baseline infarct size. In univariate analysis, age (p = 0.003), prestroke mRS (p = 0.002), hypertension (p = 0.006), baseline NIHSS (p = 0.002), END (p = 0.002), proximal occlusion (p = 0.006), and recanalization at 24 h (p < 0.001) were associated with a good outcome. Only baseline NIHSS (p = 0.006) was associated with a good outcome after adjustment. Conclusions: We did not find any impact of brain atrophy on the risk of END and the outcome at 3 months in severe ischemic strokes after IV thrombolysis.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 60%

Impact of Brain Atrophy on Early Neurological Deterioration and Outcome in Severe Ischemic Stroke Treated by Intravenous Thrombolysis

et al. 2018

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“…1,2 Although END may have straightforward causes, such as symptomatic intracerebral hemorrhage, malignant edema, and early recurrent stroke, no clear mechanism is found in ≈2/3 of END cases, to be referred to as unexplained END below. [1][2][3] We previously reported that unexplained END is associated with higher blood glucose, no previous use of antiplatelets, larger diffusion-perfusion mismatch, persistent proximal occlusion, and diffusion-weighted imaging lesion growth beyond the initial ischemic penumbra. 2,4 This led us to suggest that unexplained END is linked to secondary hemodynamic compromise in the context of persistent occlusion, with potential mechanisms including in situ thrombus extension and new embolic events in the same arterial territory.…”

mentioning

confidence: 99%

Is Unexplained Early Neurological Deterioration After Intravenous Thrombolysis Associated With Thrombus Extension?

Seners

Hurford

Tisserand

et al. 2017

Stroke

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Given our underlying hypothesis that thrombus extension underlies unexplained END, only patients with both arterial occlusion on admission and persistent occlusion on 24 hours imaging, in whom Background and Purpose-Early neurological deterioration (END) after anterior circulation stroke is strongly associated with poor outcome. Apart from straightforward causes, such as intracerebral hemorrhage and malignant edema, the mechanism of END occurring after intravenous thrombolysis remains unclear in most instances. We tested the hypothesis that unexplained END is associated with thrombus extension. Methods-From our database of consecutively thrombolysed patients, we identified anterior circulation stroke patients who had both admission and 24-hour T2* magnetic resonance imaging, visible occlusion on admission magnetic resonance angiography and no recanalization on 24-hour magnetic resonance angiography. END was defined as ≥4 National Institutes of Health Stroke Scale-point deterioration on 24-hour clinical assessment and unexplained END as END without clear cause. The incidence of susceptibility vessel sign extension on T2* imaging, defined as any new occurrence or extension of susceptibility vessel sign from admission to 24-hour follow-up magnetic resonance, was compared between patients with unexplained END and those without END. Results-Of 120 eligible patients for the present study, 22 experienced unexplained END. Susceptibility vessel sign extension was present in 41 (34%) patients and was significantly more frequent in the unexplained END than in the no-END group (59% versus 29%, respectively; adjusted odds ratio=3.96; 95% confidence interval, 1.25-12.53; P=0.02). Conclusions-In this study, unexplained END occurring after thrombolysis was independently associated with susceptibility vessel sign extension, suggesting in situ thrombus extension or re-embolization. These findings strengthen the need to further investigate early post-thrombolysis administration of antithrombotics to reduce the risk of this ominous clinical event.

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“…[8,9] The frequency of neurological deterioration in this singlecenter study was 15.4%, which was higher than that of a retrospective study which assessed deteriorations within the first two days [10] and lower than those of two prospective studies (35% and 37%, respectively). [11,12] The studies for early neurological deterioration in non- thrombolyzed patients were found to have frequencies between 13 to 37% [13][14][15][16][17] Our patients with neurological progression had worse NIHSS scores on discharge, compared to non-progressive patients (8 vs 3.7), while the NIHSS scores were not different on admission between these two groups.…”

Section: Discussionmentioning

confidence: 50%

Progression in acute ischemic stroke: Is widespread atherosclerotic background a risk factor?

Sumer

Özön

2017

Turk J Phys Med Rehab

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Objectives:In this study, we aimed to investigate the causes and conditions related with progression and outcome of progressive acute ischemic stroke. Patients and methods:In this prospective study, a total of 78 acute ischemic stroke patients (32 males, 46 females; mean age 70±12.8 years; range 34 to 95 years) were included between February 2006 and October 2010. The patients were classified into two groups as those with and without progression according to the National Institute of Health Stroke Scale (NIHSS). Risk factors for ischemic stroke, stroke subtypes, and radiological investigations and prognosis were compared between the progressive and non-progressive patients.Results: Neurological deterioration occurred in 12 patients (15%). Progressive acute ischemic stroke patients had carotid stenosis compared to non-progressive patients (50% vs 19%), and ischemic cardiac disease (33% vs 6%) more common in the patients with progression. Mortality during hospital stay and long term-outcomes were similar between the groups. Conclusion:Our study results suggest that widespread atherosclerotic diseases may induce neurological progression.

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Early neurological deterioration after thrombolysis: Clinical and imaging predictors

Cited by 75 publications

References 22 publications

Impact of Brain Atrophy on Early Neurological Deterioration and Outcome in Severe Ischemic Stroke Treated by Intravenous Thrombolysis

Impact of Brain Atrophy on Early Neurological Deterioration and Outcome in Severe Ischemic Stroke Treated by Intravenous Thrombolysis

Is Unexplained Early Neurological Deterioration After Intravenous Thrombolysis Associated With Thrombus Extension?

Progression in acute ischemic stroke: Is widespread atherosclerotic background a risk factor?

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