J Clin Neurol.  2009 Sep;5(3):107-119. 10.3988/jcn.2009.5.3.107.

Multimodal MRI for Ischemic Stroke: From Acute Therapy to Preventive Strategies

• Bang OY

• KMID: 2045416
• DOI: http://doi.org/10.3988/jcn.2009.5.3.107

Abstract

BACKGROUND AND PURPOSE
Conventional therapies for ischemic stroke include thrombolytic therapy, prevention of inappropriate coagulation and thrombosis, and surgery to repair vascular abnormalities. Over 10 years have passed since the US Food and Drug Administration approved intravenous tissue plasminogen activator for use in acute stroke patients, but most major clinical trials have failed during the last 2 decades, including large clinical trials for secondary prevention and neuroprotection. These results suggest the presence of heterogeneity among stroke patients. Neuroimaging techniques now allow changes to be observed in patients from the acute to the recovery phase. The role of MRI in stroke evaluation and treatment is discussed herein. MAIN CONTENTS: Three MRI strategies are discussed with relevant examples. First, the following MRI strategies for acute ischemic stroke are presented: diffusion-perfusion mismatch, deoxygenation (oxygen extraction and cerebral metabolic rate of oxygen), and blood-brain barrier permeability derangement in selected patients for recanalization therapy. Second, multimodal MRI for identifying stroke mechanisms and the specific causes of stroke (i.e., patent foramen ovale, infective endocarditis, and nonbacterial thrombotic endocarditis) are presented, followed by MRI strategies for prevention of recurrent stroke: plaque images and flow dynamics for carotid intervention. EXPECTATIONS: The studies reviewed herein suggest that using MRI to improve the understanding of individual pathophysiologies will further promote the development of rational stroke therapies tailored to the specifics of each case.

Keyword

atherosclerosis; stroke; perfusion; personalized treatment; MRI

MeSH Terms

Atherosclerosis
Blood-Brain Barrier
Endocarditis
Foramen Ovale, Patent
Humans
Neuroimaging
Perfusion
Permeability
Population Characteristics
Secondary Prevention
Stroke
Thrombolytic Therapy
Thrombosis
Tissue Plasminogen Activator
United States Food and Drug Administration
Tissue Plasminogen Activator

Figure

• 

  Fig. 1 Pretreatment DWI and PWI findings and final DWI findings of three patients with the target mismatch pattern (a PWI lesion that was ≥10 mL and ≥120% of the DWI lesion). A: Patients showing a favorable clinical response and no infarct growth after complete recanalization. B: Patients with good collaterals, showing minimal or no marked infarct growth after recanalization. C: Infarct growth was observed in patients with poor recanalization, despite recanalization. Figure modified from Bang et al.29 DWI: diffusion-weighted imaging, PWI: perfusion-weighted imaging, TTP: time to peak.

• 

  Fig. 2 DWI performed 4 h after symptom onset, disclosing multiple acute cortical and basal ganglia infarcts. A more extensive perfusion abnormality with mismatch was noted throughout the right middle cerebral artery (MCA) bed. However, CBV sustained the ischemic regions, and hypointense leptomeningeal and periventricular vessels were observed on GRE imaging. Recanalization with intra-arterial thrombolysis at 6 h resulted in complete reperfusion. No new lesions developed, as observed on the 90th day FLAIR imaging. Figure modified from Bang et al.103 DWI: diffusion-weighted imaging, CBV: cerebral blood volume, GRE: gradient-echo, FLAIR: fluid-attenuated inversion recovery.

• 

  Fig. 3 DWI (A) and PWI (B) findings of a patient who exhibited the no-match pattern (a PWI volume <120% of the DWI lesion volume). The lesion was located on a relatively silent brain area. (C) Relationship between the number of patients with mismatch and the odds of a favorable clinical response following early reperfusion, and the mismatch ratio (the volume ratio of Tmax ≥2 s over the DWI lesion).49 DWI: diffusion-weighted imaging, PWI: perfusion-weighted imaging.

• 

  Fig. 4 A case showing the malignant profile on baseline MRI (a DWI lesion ≥100 mL and/or a PWI lesion of Tmax delay ≥8 s and ≥100 mL). A: DWI performed 1 h after symptom onset, disclosing small acute cortical and basal ganglia infarcts. B: A more extensive perfusion abnormality with severe delay (Tmax ≥8 s, >100 mL) was noted throughout the right MCA distribution. C: Pretreatment permeability slope image showing breakdown of the BBB. The white line delineates the slope of increasing Gd concentration after bolus passage and expected decreasing concentration during later times. The green line represents the slope of increasing Gd concentration during later times in patients with a dysfunctional BBB. Figure modified from Bang et al.62 D: The patient showed clinical worsening with hemorrhagic transformation during follow-up. DWI: diffusion-weighted imaging, PWI: perfusion-weighted imaging, BBB: blood-brain barrier, MCA: middle cerebral artery, Gd: gadolinium.

• 

  Fig. 5 A case of multiple small infarcts within multiple vascular territories, suggesting cardioembolism or other causes. A transesophageal echocardiogram revealed mobile thrombi on the heart valve. A nodular lesion was found on chest examination, and the final diagnosis was established as nonbacterial thrombotic endocarditis caused by non-small-cell lung cancer. A: DWI, ADC, and T2-weighted images showing cerebral infarcts of varying ages, which suggest very active early recurrence over time and portends a high risk of further ischemic events.73 The patient was treated with anticoagulation. B: Signal intensities of different MRI parameters vary differently after the onset of ischemic stroke. DWI: diffusion-weighted imaging, ADC: apparent diffusion coefficient.

• 

  Fig. 6 Three cases with small, deep infarcts. A: Small, deep infarcts suggesting lacunar stroke, but MRA revealed MCA atherosclerosis, suggesting the presence of mural thrombi occluding the orifices of the lenticulostriate arteries. B: A relatively large, deep infarct but normal parent arteries, suggesting common trunk occlusion. High-resolution MRA (7.0 T) showing an example of four lenticulostriate arteries branching from a single trunk of the left MCA. Figure modified from Cho et al.83 C: A patient with previous lacunar stroke who developed pseudobulbar palsy during aggressive antiplatelet and anticoagulation therapy. DWI was negative, but GRE imaging showed multiple microbleeds in the bilateral basal ganglia and thalamus, and periventricular leukoariosis. MCA: middle cerebral artery, MRA: magnetic resonance angiography, DWI: diffusion-weighted imaging, GRE: gradient-echo.

• 

  Fig. 7 A case with carotid atherosclerosis. A: CT angiogram showing a stenotic lesion at the carotid bifurcation, as a result of an atherosclerotic plaque (low-density area) with surrounding foci of calcification. B: T1-weighted image obtained 7 and 14 min after administration of 0.2 mmol Gd/kg of Gd-diethylenetriamine penta-acetic acid (Gd-DTPA) in a human carotid artery (at 1.5 T). Following injection of Gd-DTPA, the necrotic lipid core and fibrous cap are clearly identified relative to the precontrast images. Figure from Briley-Saebo et al.86 C: MRI measurement of the wall shear stress vectors in normal subjects. The shape and location of wall surfaces that are subject to low wall shear stress differ from subject to subject. Figure modified from Zhao et al.100,102 Gd: gadolinium.

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