Progression of Structural Damage after Status Epiepticus in Rat: A 6-Months Video-EEG and MRI Follow-Up Study.
Abstract number :
I.04
Submission category :
Year :
2001
Submission ID :
312
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
A. Pitkänen, MD, PhD, Epilepsy Research Laboratory, A.I.Virtanen Institute, Kuopio, Finland; J. Nairismägi, MD, NMR Research Group, A.I.Virtanen Institute, Kuopio, Finland; J. Nissinen, MSc, Epilepsy Research Laboratory, A.I.Virtanen Institute, Kuopio, Fi
RATIONALE: A critical question regarding the use of neuroprotectants to alleviate damage caused by status epilepticus (SE) is: how long does the damage continue to progress? This was investigated in rats by using multiparametric MRI combined with video-EEG monitoring.
METHODS: Bipolar stimulating electrode was implanted into the left amygdala of adult Sparague-Dawley rats (n=16). SE was induced by a 20-30 min stimulation (100 ms train of 1 ms, 60 Hz, 400 [mu]A, every 0.5 sec). Stimulation electrode was removed and seizure activity was recorded with video-EEG monitoring via cortical platinum electrodes. MRI was performed using a scanner operating at 4.7 T (a bird-cage-type volume-coil, coronal 1 mm slice -2.8 mm from bregma, matrix 128*256, FOV 35 mm). Diffusion (Dav, TR=1.5 s, TE=55 ms, b-values: 0, 470, 856 s/mm2) and T2 (TE=20-60 ms, TR=1.5 s, 4 averages) images were sequentially acquired. T1rho was quantified at the same time points (variable length 10-90 ms, adiabatic spin-lock pulses followed by a fast spin echo imaging sequence, TR=2.5 s, echo spacing =10 ms, 16 echoes/excitation, 4 averages). Regions analyzed included the amygdala, piriform cortex, hippocampus, and thalamus.
RESULTS: At 2 days, T2 was prolonged in the amygdala (ipsi/contra, 62/64%), pirifom cortex (70/69%), and hippocampus (27/4%) as well as in the thalamus (45%). At 9, 23 and 50 days, T2 remained elevated but tended to decrease in the ipsilateral amygdala (to 17/6% at 50 days), (to 14/6%) hippocampus, and the thalamus (to 12%). Changes in T1rho parallelled the changes in T2 even though the abnormalities were more pronounced and remained elevated by 18-34% even at day 50 in all areas except the thalamus. At 2 days, Dav in the amygdala and the piriform cortex did not differ from controls, whereas it was increased in the hippocampus (27/20%) and thalamus (14%). At later time points, Dav became elevated in all areas and remained abnormal even at 50 days (24/14% amygdala, 29/31% piriform cortex, 32/28% hippocampus, 12% thalamus). MRI parameters during the first 23 days did not predict the severity of epilepsy at later time points.
CONCLUSIONS: SE causes structural alterations which continue for longer than 1 month. Relaxation times elevate rapidly after SE, decrease thereafter, but remain abnormal for weeks. Structural abnormalities detected as an increased diffusion, however, become more evident over the weeks. Our data suggest that time window of opportunity for neuroprotectants after SE is weeks rather than days or hours.
Support: Academy of Finland, Vaajasalo Foundation, Sigrid Juselius Foundation