J Clin Neurol.  2017 Apr;13(2):129-137. 10.3988/jcn.2017.13.2.129.

Role of Perfusion-Weighted Imaging in a Diffusion-Weighted-Imaging-Negative Transient Ischemic Attack

• Lee SH
• Nah HW
• Kim BJ
• Ahn SH
• Kim JS
• Kang DW
• Kwon SU

• KMID: 2376013
• DOI: http://doi.org/10.3988/jcn.2017.13.2.129

Abstract

BACKGROUND AND PURPOSE
The absence of acute ischemic lesions in diffusion-weighted imaging (DWI) in transient ischemic attack (TIA) patients makes it difficult to diagnose the true vascular etiologies. Among patients with DWI-negative TIA, we investigated whether the presence of a perfusion-weighted imaging (PWI) abnormality implied a true vascular event by identifying new acute ischemic lesions in follow-up magnetic resonance imaging (MRI) in areas corresponding to the initial PWI abnormality.
METHODS
The included patients underwent DWI and PWI within 72 hours of TIA and also follow-up DWI at 3 days after the initial MRI. These patients had visited the emergency room between July 2009 and May 2015. Patients who demonstrated initial DWI lesions were excluded. The initial PWI abnormalities in the corresponding vascular territory were visually classified into three patterns: no abnormality, focal abnormality, and territorial abnormality.
RESULTS
No DWI lesions were evident in initial MRI in 345 of the 443 TIA patients. Follow-up DWI was applied to 87 of these 345 DWI-negative TIA patients. Initial PWI abnormalities were significantly associated with follow-up DWI abnormalities: 8 of 43 patients with no PWI abnormalities (18.6%) had new ischemic lesions, whereas 13 of 16 patients with focal perfusion abnormalities (81.2%) had new ischemic lesions in the areas of initial PWI abnormalities [odds ratio (OR)=15.1, 95% confidence interval (CI)=3.6-62.9], and 14 of 28 patients with territorial perfusion abnormalities (50%) had new lesions (OR=3.7, 95% CI=1.2-11.5).
CONCLUSIONS
PWI is useful in defining whether or not the transient neurological symptoms in DWI-negative TIA are true vascular events, and will help to improve the understanding of the pathomechanism of TIA.

Keyword

perfusion-weighted imaging; transient ischemic attacks; focal perfusion abnormality

MeSH Terms

Emergency Service, Hospital
Follow-Up Studies
Humans
Ischemic Attack, Transient*
Magnetic Resonance Imaging
Perfusion

Figure

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  Fig. 1 Representative cases from the transient ischemic attack cohort. A: Normal perfusion: initial diffusion-weighted imaging (DWI), perfusion-weighted imaging (PWI), magnetic resonance angiography (MRA), and follow-up DWI showing no significant lesions. B: Focal perfusion abnormality: PWI showing a prolonged time to peak (TTP) involving the focal middle cerebral artery (MCA) territory (arrow) without vascular abnormality in MRA; a follow-up DWI showed new ischemic lesions (arrow) in the area corresponding to the initial PWI abnormality. C: Territorial perfusion abnormality: PWI showing prolonged TTP involving the entire MCA territory (arrow) with occlusion of the left MCA (arrow); new ischemic lesions appeared in follow-up DWI (arrow) in the area corresponding to the initial PWI abnormality. D: Perfusion abnormality: PWI showing prolonged TTP involving the entire MCA territory (arrow) with severe stenosis in the right MCA (arrow); however, follow-up DWI did not reveal new ischemic lesions in the area corresponding to the initial PWI abnormality.

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  Fig. 2 Flowchart of patients in the prospective cohort and the retrospective validation cohort. DWI: diffusion-weighted imaging, MRI: magnetic resonance imaging, TIA: transient ischemic attack.

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  Fig. 3 (A) No-reflow phenomenon and (B) effects of chronic hypoperfusion due to major-artery flow restrictions. A-I: Normal blood flows into microvessels from major vessels.22 A-II: Obstruction of a cerebral artery restricts the blood flow and oxygen supply to the brain.2223 A-III: The no-reflow phenomenon. Progression of ischemic injury results in compression of the microvascular lumen by both intrinsic vascular pathology and extrinsic forces, and the eventual collapse of the microvascular lumen, which may contribute to focal ischemia.24 B-I: Collateral arteries can contribute to the maintenance of a nonischemic state due to collateral perfusion circulation. B-II: Systemic hypotension leads to severe hypoperfusion, which induces the clinically symptomatic stage. B-III: Irreversible residual ischemic lesions fall into the infarct despite perfusion restoration. Adapted from Greif et al. Nature 2014;508:50-51.22 Adapted from Hall et al. Nature 2014;508:55-60.23 Adapted from Garcia et al. J Neuropathol Exp Neurol 1974;33:408-421, with permission of Oxford University Press.24

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