Arterial spin labeling perfusion MRI applications in drug-resistant epilepsy and epileptic emergency

Abstract

Epilepsy affects all age groups and is one of the most common and disabling neurological disorders worldwide. Drug-resistant epilepsy (DRE), status epilepticus (SE), and sudden unexpected death in epilepsy (SUDEP), which are associated with considerable healthcare costs and mortality, have always been difficult to address and become the focus of clinical research. The rapid identification of seizure onset and accurate localization of epileptic foci are crucial for the treatment and prognosis of people with DRE, SE, or near-SUDEP. However, most of the conventional neuroimaging techniques for assessing cerebral blood flow of people with epilepsy are restricted by time consumption, limited resolution, and ionizing radiation. Arterial spin labeling (ASL) is a newly powerful non-contrast magnetic resonance imaging technique that enables the quantitative evaluation of brain perfusion, characterized by its unique advantages of reproducibility and easy accessibility. Recent studies have demonstrated the potential advantages of ASL for the diagnosis and evaluation of epilepsy. Therefore, in this review, we discussed the complementary value of ASL in evaluating and characterizing the basic substrates underlying refractory epilepsy and epileptic emergencies.

Keywords: Arterial spin labeling; Cerebral blood flow; Drug-resistant epilepsy; Epileptic emergency; SUDEP; Status epilepticus.

Fig. 1

Principles of ASL. A "labeled" image and a "control" image are respectively acquired when the blood-water magnetization is inverted or not. The subtraction of these two images yields a perfusion-weighted image. Permission was granted by Hernandez-Garcia et al. (© Elsevier [14]) to reuse this figure

Fig. 2

Examples of different patterns of postictal hypoperfusion seen on subtracted ASL. a Right mesial temporal sclerosis (arrow) on MRI and a "lobar" pattern of hypoperfusion on postictal ASL; the presumed seizure onset zone (SOZ) was in the right mesial temporal lobe. b Left temporal hypometabolism (arrow) on interictal PET image and a "regional" pattern of hypoperfusion on postictal ASL; the presumed SOZ was in the left temporal lobe. c No lesions on MRI and independent, bilateral mesial temporal SOZs based on intracranial VEEG monitoring, and a left "hemispheric" pattern of hypoperfusion on postictal ASL from a left mesial temporal seizure. Permission was granted by Gaxiola-Valdez et al. (© Oxford University Press [22]) to reuse this figure

Fig. 3

Examples of brain MRI sequences and EEGs of four representative patients with SE. a Brain MRI: (1) The left frontal, temporal cortices and left thalamus hyperperfusion on ASL; subtle increased perfusion in the left thalamus and lateral temporal lobe on dynamic susceptibility contrast (DSC); the left thalamus and insula changes on fluid-attenuated inversion recovery (FLAIR) and DWI. (2) Definite left frontal and temporal lobes hyperperfusion on ASL and DSC; no changes on FLAIR; subtle restrictions in the left thalamus and insula on DWI. (3) Definite left hippocampus hyperperfusion on ASL; no signal changes on DSC, FLAIR, or DWI. (4) Subtle hyperperfusion in the bilateral frontal cortices on ASL; subtle T2 hyperintensity in the left frontal cortex. b EEG: (1) Left frontotemporal periodic discharges. (2) Left frontotemporal periodic discharges. (3) Left temporal rhythmic delta activity with evolution indicating an electrographic seizure. (4) Right frontal theta rhythm evolving to beta activity, indicating an electrographic seizure. Permission was granted by Kim et al. (© Springer Nature [38]) to reuse this figure

Fig. 4

Thalamic and cerebral cortical hyperperfusion on ASL in patient with separate two NCSE episodes. a, b Episode 16; c, d Episode 17. a EEG showing apparent spatiotemporal evolution from the left frontal to left temporo-parietal regions. b ASLshowing left hemispheric cortical hyperperfusion (white arrows) without thalamic hyperperfusion. c EEG showing bilateral 1 Hz periodic discharges with right hemispheric predominance. d ASL showing bilateral thalamic hyperperfusion (yellow arrowheads) and left fronto-temporal cortical hyperperfusion (white arrows). Permission was granted by Ohtomo et al. (© Oxford University Press [43]) to reuse this figure

Fig. 5

Examples of different patterns of postictal hypoperfusion in brainstem respiratory centers. a Image from a patient with monthly focal to bilateral tonic-clonic seizures (FBTCS). Subtraction cerebral blood flow (CBF) map (baseline-postictal) showed hypoperfusion > Δ15 CBF units in the right ventral medulla (yellow arrow) across 3 axial slices. b Image from a patient with infrequent FBTCS (< 1 per year). Subtraction CBF map (baseline-postictal) showed no significant hypoperfusion in any of the brainstem respiratory center regions of interest. Permission was granted by Liu et al. (© Wolters Kluwer Health [45]) to reuse this figure