Rationale and Objectives
Magnetic resonance (MR) imaging (MRI) provides information that can be used to estimate the symptom onset in patients with wake-up stroke (WUS). Time-resolved MR angiography (MRA) is the fastest available MR sequence technique for vessel assessment, and the different phases acquired can provide information about cerebral perfusion. The aim of this study was to evaluate the diagnostic performance of time-resolved MRA both for the assessment of vessel morphology and for the feasibility of perfusion.
Materials and Methods
Nineteen patients with WUS were included. Image quality and vessel pathologies were evaluated and correlated to time-of-flight–MRA ( n = 14), computed tomography–angiography ( n = 4), sonography ( n = 12), and conventional angiography ( n = 6). The temporal delay of signal enhancement in all pixels of the time-resolved MRA measurement after contrast injection was evaluated and compared to dynamic susceptibility contrast-enhanced (DSC) perfusion imaging ( n = 13).
Results
Time-resolved MRA resulted in the diagnosis of large vessel disease in 14 of 19 patients, involving the internal carotids ( n = 4), the vertebral arteries ( n = 3), and the circle of Willis ( n = 10). All severe vascular pathologies which influence patients’ acute stroke therapy were obtained by time-resolved MRA. Overestimation of stenoses in two of 14 patients resulted in sensitivity and specificity of 100% and 71%, respectively. Time-to-peak (TTP) estimations were hampered by movement artifacts in four patients (31%). Compared to DSC, the area of TTP delay was comparable in size and localization without relevant overestimation or underestimation.
Conclusions
Time-resolved MRA is a valuable technique in patients with WUS with high sensitivity and high negative predictive value. Cerebral perfusion estimation can be performed in selected cases for therapy decision but can be hampered by patient movement.
Noncontrast brain computed tomography (CT) is considered the first line of imaging in patients with suspected acute stroke because of its broad availability and acquisition speed. Because intravenous tissue plasminogen activator (tPA) is the most important therapy for acute ischemic stroke, any contraindications—notably intracranial hemorrhage—have to be ruled out as fast as possible before starting thrombolytic therapy. Noncontrast CT is often combined with CT-angiography (CTA) and CT-perfusion (CTP) imaging to evaluate the underlying stroke cause. Recent technological advances have contributed to more widespread use of new neuroimaging modalities and strategies such as diffusion-weighted (DWI) magnetic resonance (MR) imaging (MRI), cerebral perfusion imaging, and MR angiography. Although DWI is only available in MRI, perfusion imaging and angiography are available in both CT and MRI, which can be beneficial to patient evaluation and management in special cases. MRI is more sensitive than CT for the detection of early infarction, small infarcts, and those in the brain stem and posterior fossa .
In some instances, MRI may be the first imaging test performed, for example, in patients with unknown symptom onset, such as patients with wake-up stroke (WUS). Patients with WUS have often been excluded from thrombolysis because of the unknown time of symptom onset. However, stroke severity is similar in both patient groups, and it has been reported that patients with WUS may benefit from thrombolysis . In WUS, comprehensive stroke evaluation is more important as tPA is still under evaluation in this setting.
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Materials and methods
Patient Population
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Imaging Protocol
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Time-resolved MRA
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Imaging Parameters of the Additionally Acquired MRI Sequences
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Evaluation of Time-resolved MRA
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DSC Time-to-peak Analysis
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Feasibility of an Ultrafast MR Protocol
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Statistical Analysis
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Results
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Table 1
Patients’ Characteristics
Patient No. Age, years Sex Clinical Symptoms Stroke Classification MRI Findings FLAIR–DWI Vascular Findings MR Perfusion Analysis Acute Stroke Therapy Clinical Outcome 1 84 F Dysarthria, hemiparesis (left side), hemineglect PACI, TOAST 2 MCA infarction Occlusion MCA PWI/DWI mismatch Mechanical thrombectomy Clinical improvement 2 52 F Dysarthria, hemiparesis (right side) LACI, TOAST 3 Small infarction MCA No stenosis or occlusion No mismatch Conservative Minimal clinical improvement 3 80 M Aphasia, hemiparesis (right side) PACI, TOAST 2 MCA infarction, no mismatch Occlusion MCA (M2; right side) No mismatch Conservative Minimal clinical improvement 4 82 M Facial nerve paresis, somnolent LACI, TOAST 2 Small thalamic infarction, no mismatch Stenosis ICA Not performed Conservative Clinical improvement 5 84 M Hemiparesis (left side) PACI, TOAST 2 Small MCA infarction, no mismatch MCA stenosis (M1; right side) PWI/DWI mismatch MCA stenting Clinical improvement 6 60 M Hemiparesis (left side) LACI, TOAST 3 Small MCA infarction, no mismatch Stenosis MCA (M2) No mismatch Conservative Stable 7 59 M Aphasia, hemiplegia (right side) TACI, TOAST 2 MCA infarction, with FLAIR DWI mismatch Occlusion ICA and MCA PWI/DWI mismatch Stenting ICA, mechanical thrombectomy, i.a. thrombolysis Clinical improvement 8 89 F Hemiparesis (right side), dysarthria PACI, TOAST 5 Mismatch, infarction without FLAIR hyperintensity No stenosis No mismatch i.v. thrombolysis Clinical improvement 9 86 M Dysarthria, hemianopsia, hemiparesis LACI, TOAST 3 Small infarction, no mismatch No stenosis No mismatch Conservative Stable 10 74 F Paresis (hand) LACI, TOAST 3 Small infarction, no mismatch No stenosis Not performed Conservative Clinical improvement 11 75 F Hypoesthesia LACI, TOAST 4 Small infarction, no mismatch MCA stenosis (M1; left side) Not performed Conservative Stable 12 58 F Somnolent, aphasia LACI, TOAST 4 Bleeding due to cerebral venous sinus thrombosis Cerebral venous sinus thrombosis Not performed Mechanical thrombectomy Clinical improvement 13 79 F Hemiplegia, aphasia TACI, TOAST 2 Infarction MCA, mismatch Occlusion ICA, MCA supplied via ACOM PWI/DWI mismatch i.v. thrombolysis Stable 14 37 M Vertigo, nystagmus, emesis PACI, TOAST 2 Small infarction middle cerebellar peduncle (right side), no mismatch Stenosis vertebral artery No mismatch Conservative Complete remission 15 84 F Hemiparesis and aphasia TACI, TOAST 1 Infarction without increase compared to FLAIR Occlusion MCA (M2) PWI/DWI mismatch i.v. thrombolysis Stable 16 62 M Hemiparesis, hemineglect, dysarthria TACI, TOAST 1 No mismatch Occlusion ICA and MCA (right side) No mismatch No lysis, decompressive craniectomy Stable 17 67 M Hemiparesis PACI, TOAST 2 MCA infarction, mismatch Occlusion MCA PWI/DWI mismatch Mechanical thrombectomy Clinical improvement 18 57 F Nystagmus, lateropulsion POCI, TOAST 5 PICA infarction, no mismatch No stenosis No mismatch Conservative Stable 19 77 F Hemiparesis, headache, somnolent PACI, TOAST 1 No mismatch, FLAIR-DWI, intraventricular hemorrhage Occlusion MCA Not performed Conservative Stable
ACOM, anterior communicating artery; DWI, diffusion-weighted imaging; F, female; FLAIR, fluid attenuated inversion recovery; i.a., intra-arterial; ICA, internal carotid artery; i.v., intravenous; LACI, lacunar infarct; M, male; MCA, medial cerebral artery; MR, magnetic resonance; MRI, magnetic resonance imaging; PACI, partial anterior circulation infarct; POCI posterior circulation infarct; PWI, perfusion-weighted imaging; TACI, total anterior circulation infarct; TOAST, Trial of Org 10172 in Acute Stroke Treatment.
Stroke classification: total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI), and posterior circulation infarct (POCI).
TOAST classification: 1) thrombosis or embolism due to atherosclerosis of a large artery, 2) embolism of cardiac origin, 3) occlusion of a small blood vessel, 4) other determined cause, and 5) undetermined cause.
Table 2
Results Time-resolved MRA
Vessel Findings Time-resolved MRA Image Quality Patient No. Result Time-resolved MRA Available Standard Sequence Result of Time-resolved MRA Compared to Standard No significant stenoses 3.15 ± 0.7 Pat. 2 Hypoplasia V4 (left side) TOF, DSA Hypoplasia V4 (left side) Pat. 9 Hypoplasia V4 (right side) TOF Hypoplasia V4 (right side) Pat. 10 Hypoplasia V4 (right side) Sonography Hypoplasia V4 (right side) Pat. 14 No stenoses TOF No stenoses Pat. 18 No stenoses TOF No stenoses ICA 3.18 ± 0.8 Pat. 4 Stenosis >70% Ultrasound Stenosis >70% Pat. 7 Occlusion DSA Stenosis >70% Pat. 13 Occlusion Sonography Occlusion Pat. 16 Occlusion Sonography Occlusion MCA 3.0 ± 0.8 Pat. 6 Stenosis >70% TOF Stenosis >70% Pat. 11 Stenosis >70% TOF, DSA Stenosis >70% Pat. 1 Occlusion TOF, DSA Occlusion Pat. 3 Occlusion TOF, DSA Occlusion Pat. 5 Occlusion TOF, DSA Stenosis >70% Pat. 7 Occlusion TOF, DSA Occlusion Pat. 15 Occlusion TOF Occlusion Pat. 16 Occlusion TOF Occlusion Pat. 17 Occlusion CTA, DSA Occlusion Pat. 19 Occlusion CTA, DSA Occlusion VA 3.08 ± 0.8 Pat. 6 Stenosis >70% TOF Stenosis >70% Pat. 14 Stenosis >70% Sonography Stenosis >70% BA 3.1 ± 0.7 — Dural venous sinus 3.4 ± 0.5 Pat. 12 Occlusion DSA Occlusion
BA, basilar artery; CTA, computed tomography–angiography; DSA, digital subtraction angiography; ICA, internal carotid artery; MCA, medial cerebral artery; MRA, magnetic resonance angiography; Pat., patient; TOF, time-of-flight; VA, vertebral artery.
The table shows the results of time-resolved MRA regarding the main vessels for therapy decision: internal carotid arteries, medial cerebral arteries, vertebral arteries, and the basilar artery.
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Clinical Therapy Decision
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Table 3
Feasibility of an Ultrafast MR Protocol
Recommended therapy Proposed Treatment Based on Clinical Symptoms and Ultrafast MRI Proposed Treatment Regarding All Sequences Conservative management 11 11 Intravenous thrombolysis 3 3 Interventional therapy 5 5
DWI, diffusion-weighted imaging; FLAIR, fluid attenuated inversion recovery; MR, magnetic resonance; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging.
The table shows the recommended therapy based on clinical symptoms and the ultrafast MRI on the left side (FLAIR, DWI, and time-resolved MRA) as well as the proposed therapy when all available sequences were considered.
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Discussion
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Evaluation of Intracranial and Extracranial Vessel Pathologies
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Perfusion Analysis
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Feasibility of an Ultrafast MR Protocol
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Conclusions
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