PERFUSION MRI CHANGES DURING STATUS EPILEPTICUS IN THE RAT PILOCARPINE MODEL
Abstract number :
3.115
Submission category :
1. Translational Research
Year :
2009
Submission ID :
10209
Source :
www.aesnet.org
Presentation date :
12/4/2009 12:00:00 AM
Published date :
Aug 26, 2009, 08:12 AM
Authors :
M. Choy, M. Lythgoe, J. Wells, E. Proctor, D. Thomas, D. Gadian and Rod Scott
Rationale: There is a known relationship between convulsive status epilepticus (SE) and hippocampal injury, although the precise causes of hippocampal vulnerability remain uncertain, potential mechanisms include excitotoxicity and ischaemia. It is hypothesised that during the early phase of seizures, CBF increases in the cortex to meet energy demand, but it remains uncertain whether these compensatory mechanisms occur in the hippocampus. Therefore we used perfusion MRI to investigate CBF changes following pilocarpine-induced SE in the fentanyl/medetomidine anaesthetised rat. Methods: Thirteen adult Sprague-Dawley rats were anaesthetised with fentanyl/medetomidine, and placed on a specially modified animal holder to reduce the effects of seizures-associated motion. Arterial spin labelling perfusion imaging was performed contiguously for up to 3 hours. Methylscopolamine i.p. (1mg/kg) was given to reduce mortality. Either pilocarpine (375mg/kg) (n=7) for induction of SE or saline (n=6) was administered. Diazepam (10mg/kg) was administered i.p. 90 min after the onset of SE. Results: We have demonstrated that there are time-dependent differences between the regional CBF responses in the cortex and the hippocampus during pilocarpine-induced SE. More specifically, while increases in cortical CBF were observed during the early stages of SE, only a limited CBF change was seen in the hippocampus. The subsequent lack of difference between the two regions during the later stages of SE may reflect the hypothesised local failure of the vascular system due to persistent seizure activity. Conclusions: These data support the hypothesis that during SE a relative ischaemia may contribute to the selective vulnerability in the hippocampus.
Translational Research