Added Value of Arterial Spin Labeling in Detecting Posterior Reversible Encephalopathy Syndrome as a Stroke Mimic on Baseline Neuroimaging: A Single Center Experience

Abstract

Differentiating stroke from stroke mimics is a diagnostic challenge in every day practice. Posterior Reversible Encephalopathy Syndrome (PRES) is an important stroke mimic with nonspecific symptomatology, making prompt and accurate diagnosis challenging. Baseline neuroimaging plays a pivotal role in detection and differentiation of stroke from many common mimics and is thus critical in guiding appropriate management. In particular, MR perfusion (MRP) imaging modalities provide added value through detection and quantification of multiple physiological parameters. Arterial Spin Labeling (ASL) is a non-contrast, noninvasive MRP technique increasingly used in clinical practice; however, there is limited description of ASL in PRES in the existing literature. In this single center retrospective pilot study, we investigate the added value of ASL in detecting PRES in the largest series to date. We hope this study can serve as the basis for larger scale investigations exploring the utility of ASL in detecting stroke mimics such as PRES for accurate and efficient management of such patients.

Keywords: MR perfusion; PRES; arterial spin labeling; perfusion imaging; stroke imaging; stroke mimic.

Figure 1

Case 1: A 45-year-old male brought in by ambulance after being found down with seizure activity in the setting of positive urine toxicology screen for cocaine and methamphetamines as well as severe hypertension of 235/101. Past medical history notable HIV on HAART, chronic Hepatitis C, ESRD on HD, and remote right frontal hemorrhage. MRI brain at initial presentation demonstrates abnormal FLAIR hyperintensity (A,B) in the subcortical white matter of the right greater than left occipital lobes with corresponding mixed ASL signal hyperintensity and hypointensity in these regions (G,H). No DWI (C,D) or SWI (F) signal abnormality aside from remote right frontal hemorrhage. No focal arterial high-grade stenosis or occlusion on MR angiography (E). Case 2: A 68-year-old female presenting with seizure activity in setting of past medical history notable for CKD, DM, HTN, HLD, CHF, and COPD. MRI brain at initial presentation demonstrates abnormal FLAIR hyperintensity (I) in the bilateral thalami, bilateral posterior limbs of the internal capsules, bilateral external capsules, and left putamen with more subtle signal hyperintensity in the subcortical white matter of the left occipital lobe. Corresponding ASL signal hyperintensity (L) in the left greater than right occipital lobes. No associated DWI (J) or SWI (K) signal abnormality in these regions, although the patient was noted to have a punctate acute infarct in the right temporo-occipital region (not shown). No focal arterial high-grade stenosis or occlusion on MR angiography (M).

Figure 2

Case 3: A 53-year-old male presenting with seizure activity and past medical history notable for EtOH cirrhosis status post recent liver transplant on tacrolimus complicated by post-operative AKI on intermittent HD. MRI brain at initial presentation demonstrates abnormal FLAIR hyperintensity (A) in the left thalamus, posterior limb of the left internal capsule, and cortex/subcortical white matter of the left frontal and bilateral occipital lobes. DWI (B) and ADC (C) demonstrate predominantly T2 shine through in the left thalamus/internal capsule. ASL (D) demonstrates increased signal in the corresponding territories (solid white arrows) with notable severe border-zone hypoperfusion in the bilateral watershed territories (gray dashed arrows). No focal arterial high-grade stenosis or occlusion on MR angiography (E). Case 4: A 21-year-old male presenting with seizure activity in setting of hypertension of 177/113 with past medical history notable for thrombocytopenia, oliguric renal failure on intermittent HD secondary to atypical hemolytic uremic syndrome, hemophagocytic lymphohistiocytosis on etoposide/steroids, and prior history of PRES. MRI brain demonstrates abnormal FLAIR hyperintensity (F) in the cortex and subcortical white matter of the bilateral frontal lobes and bilateral parieto-occipital regions with slight asymmetric signal hyperintensity in the right caudate nucleus. ASL (I) demonstrates increased signal in the corresponding bilateral frontal, parietal, and occipital regions. No DWI/ADC (G) or SWI (H) signal abnormality. No focal arterial high-grade stenosis or occlusion on MR angiography (J).

Figure 3

Case 5: A 64-year-old female presenting with uncontrolled hypertension of 205/93 and past medical history notable for sickle cell anemia. MRI brain at initial presentation demonstrates abnormal FLAIR hyperintensity (A) in the subcortical white matter of the bilateral parieto-occipital regions with corresponding regions of ASL signal hyperintensity (D). No DWI (B) or SWI (C) signal abnormality. No focal arterial high-grade stenosis or occlusion on MR angiography (E). Case 6: A 61-year-old male presenting with acute unresponsiveness in setting of prolonged hospital course due to COVID-19 pneumonia/ARDS with refractory hypoxemia and hypercarbia complicated by cardiac arrest, gastrointestinal bleeding, hypotension on pressors, and eventual bilateral lung transplant on tacrolimus. MRI brain demonstrates ASL signal hyperintensity (I) in the bilateral occipital lobes with asymmetrically increased signal in the right thalamus. Findings correspond to subtle FLAIR hyperintensity (F) with mild vascular congestion on post-contrast imaging (G). No DWI (H) signal abnormality. No focal arterial high-grade stenosis or occlusion on MR angiography (J).