BACKGROUND AND PURPOSE: Diffusion-weighted MR imaging (DWI) has emerged as tool for noninvasive and early detection of neuronal alterations. The aim of this study was to investigate the evolution of acute phase changes in different brain regions during experimental status epilepticus (SE) using DWI correlated with SE-induced neuronal cell loss. METHODS: DWI was performed in 20 rats before (baseline) and 3, 5, 10, 15, 20, 30, 45, 60, 90, and 120 minutes after onset of pilocarpine-induced SE. Apparent diffusion coefficients (ADCs) were calculated for the parietal cortex, temporal cortex, pyriform cortex, hippocampus, amygdala, and thalamus and compared with baseline. Neuronal cell loss was quantified at different time points after SE using cresyl-violet-staining. RESULTS: ADC-mapping demonstrated a significant transient increase in ADC (to 116 +/- 4% of baseline) in the very acute phase, starting 3 minutes after SE onset, lasting for 10 minutes, followed by a significant gradual decline in ADC in all animals. Compared with surviving animals (76 +/- 7%), decline in ADC was significantly lower for the animals who died within 2 hours for all regions of interest (63 +/- 6.5%, 0.45 +/- 0.03 x 10(-3) mm(2)/s) except the thalamus (P < .01, analysis of variance). There was good correlation between neuronal cell loss in specific brain regions 2 weeks after SE and maximal decrease in ADC (r > 0.76). CONCLUSION: Serial ultrafast DWI is a sensitive noninvasive technique for early detection and monitoring of seizure-induced neuronal alterations. Using ADC-mapping differentiation of regional severity of neuronal damage may be possible because there is good correlation between the maximal decrease in ADC in the acute phase of SE and late neuronal cell loss.
BACKGROUND AND PURPOSE: Diffusion-weighted MR imaging (DWI) has emerged as tool for noninvasive and early detection of neuronal alterations. The aim of this study was to investigate the evolution of acute phase changes in different brain regions during experimental status epilepticus (SE) using DWI correlated with SE-induced neuronal cell loss. METHODS: DWI was performed in 20 rats before (baseline) and 3, 5, 10, 15, 20, 30, 45, 60, 90, and 120 minutes after onset of pilocarpine-induced SE. Apparent diffusion coefficients (ADCs) were calculated for the parietal cortex, temporal cortex, pyriform cortex, hippocampus, amygdala, and thalamus and compared with baseline. Neuronal cell loss was quantified at different time points after SE using cresyl-violet-staining. RESULTS: ADC-mapping demonstrated a significant transient increase in ADC (to 116 +/- 4% of baseline) in the very acute phase, starting 3 minutes after SE onset, lasting for 10 minutes, followed by a significant gradual decline in ADC in all animals. Compared with surviving animals (76 +/- 7%), decline in ADC was significantly lower for the animals who died within 2 hours for all regions of interest (63 +/- 6.5%, 0.45 +/- 0.03 x 10(-3) mm(2)/s) except the thalamus (P < .01, analysis of variance). There was good correlation between neuronal cell loss in specific brain regions 2 weeks after SE and maximal decrease in ADC (r > 0.76). CONCLUSION: Serial ultrafast DWI is a sensitive noninvasive technique for early detection and monitoring of seizure-induced neuronal alterations. Using ADC-mapping differentiation of regional severity of neuronal damage may be possible because there is good correlation between the maximal decrease in ADC in the acute phase of SE and late neuronal cell loss.
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