Your browser doesn't support javascript.
loading
Implications and limitations of magnetic resonance perfusion imaging with 1.5-Tesla pulsed arterial spin labeling in detecting ictal hyperperfusion during non-convulsive status epileptics.
Goto, Katsuhiro; Shimogawa, Takafumi; Mukae, Nobutaka; Shono, Tadahisa; Fujiki, Fujio; Tanaka, Atsuo; Sakata, Ayumi; Shigeto, Hiroshi; Yoshimoto, Koji; Morioka, Takato.
Affiliation
  • Goto K; Department of Neurosurgery, Harasanshin Hospital.
  • Shimogawa T; Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University.
  • Mukae N; Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University.
  • Shono T; Department of Neurosurgery, Harasanshin Hospital.
  • Fujiki F; Departments of Neurology, Harasanshin Hospital.
  • Tanaka A; Radiology, Harasanshin Hospital.
  • Sakata A; Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Hospital.
  • Shigeto H; Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
  • Yoshimoto K; Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University.
  • Morioka T; Department of Neurosurgery, Harasanshin Hospital.
Surg Neurol Int ; 13: 147, 2022.
Article in En | MEDLINE | ID: mdl-35509552
ABSTRACT

Background:

Recent our reports showed that 3-T pseudocontinuous arterial spin labeling (3-T pCASL) magnetic resonance perfusion imaging with dual post labeling delay (PLD) of 1.5 and 2.5 s clearly demonstrated the hemodynamics of ictal hyperperfusion associated with non-convulsive status epilepticus (NCSE). We aimed to examine the utility of 1.5-T pulsed arterial spin labeling (1.5-T PASL), which is more widely available for daily clinical use, for detecting ictal hyperperfusion.

Methods:

We retrospectively analyzed the findings of 1.5-T PASL with dual PLD of 1.5 s and 2.0 s in six patients and compared the findings with ictal electroencephalographic (EEG) findings.

Results:

In patients 1 and 2, we observed the repeated occurrence of ictal discharges (RID) on EEG. In patient 1, with PLDs of 1.5 s and 2.0 s, ictal ASL hyperperfusion was observed at the site that matched the RID localization. In patient 2, the RID amplitude was extremely low, with no ictal ASL hyperperfusion. In patient 3 with lateralized periodic discharges (LPD), we observed ictal ASL hyperperfusion at the site of maximal LPD amplitude, which was apparent at a PLD of 2.0 s but not 1.5 sec. Among three patients with rhythmic delta activity (RDA) of frequencies <2.5 Hz (Patients 4-6), we observed obvious and slight increases in ASL signals in patients 4 and 5 with NCSE, respectively. However, there was no apparent change in ASL signals in patient 6 with possible NCSE.

Conclusion:

The detection of ictal hyperperfusion on 1.5-T PASL might depend on the electrophysiological intensity of the epileptic ictus, which seemed to be more prominent on 1.5-T PASL than on 3-T pCASL. The 1.5-T PASL with dual PLDs showed the hemodynamics of ictal hyperperfusion in patients with RID and LPD. However, it may not be visualized in patients with extremely low amplitude RID or RDA (frequencies <2.5 Hz).
Key words