Rare pitfall in the magnetic resonance imaging of status epilepticus

Abstract

Brain MRI in Status Epilepticus (SE) is often helpful in diagnosis, lateralization and localization of the seizure focus. MRI changes in SE include predominantly ipsilateral diffusion weighted imaging (DWI) changes in the hippocampus and pulvinar or similar changes involving basal ganglia, thalamus, cerebellum, brain stem and external capsule (Chatzikonstantinou et al., 2011 [1]). These changes are thought to be due to transient vasogenic and cytotoxic edema due to either transient damage or breakdown of blood brain barrier, proportional to the frequency and duration of the epileptic activity (Amato et al., 2001 [2]). Such changes may also be reflected on T2- weighted and T2-Fluid-Attenuated Inversion Recovery (FLAIR) sequences of MRI. Herein, we present a case of a transient FLAIR cerebrospinal fluid (CSF) hyperintensity on the second MRI brain in a patient with focal status epilepticus. This imaging finding led to diagnostic confusion and was initially thought to represent subarachnoid hemorrhage. However, lumbar puncture, brain computed tomography (CT), and a follow-up brain MRI ruled out that possibility and other CSF pathologies. We concluded that the transient FLAIR changes in the second brain MRI were related to a rare imaging pitfall caused by Gadolinium enhancement of CSF on the FLAIR sequence, popularly referred to as hyperintense acute reperfusion marker (HARM).

Keywords: FLAIR; HARM; MRI pitfall; Status Epilepticus; Subarachnoid space.

Fig. 1

A–C: Axial images from brain MRI with three different sequences (DWI, FLAIR and GRE, respectively) at the time of presentation showing no abnormalities. D-F: Axial MRI images (in above sequence): Subarachnoid hyperintensity on FLAIR sequence (E) over the left parietal and frontal convexity with no corresponding changes on DWI (D) or GRE (F). G-I: Axial MRI images (in above sequence), showing complete resolution of the subarachnoid FLAIR hyperintensity (H) along the left parietal and frontal convexity with no abnormalities on DWI (G) or GRE (I).

Fig. 2

This composite picture shows the onset (left), organization (middle), and termination (right) of electrographic seizure. The seizure started in the left central region as 12–15 Hz rhythmic activity (underlined by blue bar). This was followed by organization, with spread into left temporal chain as 3 Hz semirhythmic activity, and appearance of 5–7 Hz sharp waves admixed with faster activity in left central region (middle panel). This is associated with dense EMG artifact on right side. Finally, the seizure terminated as 2–3 Hz polymorphic activity admixed with fast activity in the central region, over left hemisphere. Time base = 30 mm/s, Display sensitivity = 7 μV/div, Low frequency filter = 1 Hz and High frequency filter = 50 Hz. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Fig. 3

A–B: Coronal and axial FLAIR images, respectively, showing subarachnoid hyperintensity over the left parietal and frontal convexity. C: Axial T1 post-contrast image shows absence of any pathological enhancement. D: Axial brain CT image shows no evidence of subarachnoid blood.