Acute stroke magnetic resonance imaging: current status and future perspective

Abstract

Cerebral stroke is one of the most frequent causes of permanent disability or death in the western world and a major burden in healthcare system. The major portion is caused by acute ischemia due to cerebral artery occlusion by a clot. The minority of strokes is related to intracerebral hemorrhage or other sources. To limit the permanent disability in ischemic stroke patients resulting from irreversible infarction of ischemic brain tissue, major efforts were made in the last decade. To extend the time window for thrombolysis, which is the only approved therapy, several imaging parameters in computed tomography and magnetic resonance imaging (MRI) have been investigated. However, the current guidelines neglect the fact that the portion of potentially salvageable ischemic tissue (penumbra) is not dependent on the time window but the individual collateral blood flow. Within the last years, the differentiation of infarct core and penumbra with MRI using diffusion-weighted images (DWI) and perfusion imaging (PI) with parameter maps was established. Current trials transform these technical advances to a redefined patient selection based on physiological parameters determined by MRI. This review article presents the current status of MRI for acute stroke imaging. A special focus is the ischemic stroke. In dependence on the pathophysiology of cerebral ischemia, the basic principle and diagnostic value of different MRI sequences are illustrated. MRI techniques for imaging of the main differential diagnoses of ischemic stroke are mentioned. Moreover, perspectives of MRI for imaging-based acute stroke treatment as well as monitoring of restorative stroke therapy from recent trials are discussed.

Fig. 1

Fluid-attenuated inversion recovery (FLAIR; a) image and gradient recalled echo (T2*; b)-weighted image of an intracerebral hemorrhage in the left thalamus. The typical hypointense appearance of the hemorrhage on the T2*-weighted image is caused by the susceptibility effect of the paramagnetic deoxyhemoglobin

Fig. 2

Diffusion-weighted image (DWI; a) in a patient with right basal ganglia infarction. The reduction of Brownian molecular motion in the extracellular space of the infarcted tissue due to cytotoxic edema is displayed as hyperintense signal (arrow). The apparent diffusion coefficient (ADC; b) image shows a hypointense signal (arrow) of the infarcted tissue due to a consecutive reduction of free water diffusion

Fig. 3

Perfusion imaging (PI) in the same patient of Fig. 2 with right middle cerebral artery infarction. Color-coded parameter images of the cerebral blood flow (CBF; a), cerebral blood volume (CBV; b), mean transit time (MTT; c), and time to peak (TTP; d)

Fig. 4

Perfusion/diffusion mismatch in a patient with left middle cerebral artery occlusion. Note the small area of infarct core (arrow) in the diffusion-weighted image (DWI; a) in comparison with the large area of perfusion abnormality (arrows) in mean transit time (MTT; b) resulting in positive mismatch with a large penumbra

Fig. 5

Magnetic resonance angiography (MRA; a) in the same patient of Fig. 4 with left distal middle cerebral artery occlusion. Digital subtraction angiography (DSA; b) revealed the identical site of occlusion. After intra-arterial thrombolysis, complete recanalization of the middle cerebral artery was achieved (c)

Fig. 6

Cerebral venous sinus thrombosis of the right transverse sinus and confluens of sinus on venous contrast-enhanced magnetic resonance angiography (CE-MRA; a; arrows) and contrast-enhanced T1-weighted image (b; arrow). Susceptibility-weighted images demonstrate the consecutive venous collaterals with enlarged cortical veins (c, d)

Fig. 7

Patient with right internal carotid artery dissection of the transcranial portion. The fat saturated T1 (T1-FS)-weighted images in transverse (a) and coronal (b) orientation show the hyperintense signal of the intramural methemoglobin (arrow). The contrast-enhanced magnetic resonance angiography (CE-MRA; c) shows marked narrowing of the intravascular lumen (arrow) at the site of dissection

Fig. 8

Scheme of brain involvement in acute stroke. A core of irreversibly infarcted tissue (red zone) is surrounded from a peripheral region of ischemic but potentially salvageable tissue in the early phase of acute ischemic stroke, referred to as penumbra (orange zone). Without early recanalization, the infarct core gradually expands to include the penumbra (red arrows)