The Application Study Of FMRI In Abnormal Metabolism Of Brain In Diabetes Mellitus

Objective To explore the application value of MRS in brain injury of diabetic ketoacidosis; To explore the application value of inspection acetone body(β-hydroxy butyrate and acetone/acetocaetate) MRS in diabetic ketoacidosis; To explore the application value of ratios of NAA/Cr and Cho/Cr during DKA and improve after recovery in brain injury; To explore the influence of acetone body on cerebral edema formation during DKA.Methods 17 patients with DKA underwent cerebral MRI, DWI and 1H-MRS during DKA treatment (0-12 hours after initiating therapy) and after recovery from the episode (72 hours or more after the initiation of therapy): 0 within 4 hours of the start of treatment for DKA; five, at 4-8 hours; and twelve, at 8-12 hours. MRI, DWI and MRS was repeated after their recovery from the DKA episode at >72 hours after the start of treatment. ADC was measured in the right basal ganglia and semioval center three times respectively, aquired the average ADC. We compared the average ADC during DKA and after recovery. We measured peak heights of NAA, Cr, and Cho, Lac,β-OHB and AcAc in the right basal ganglia, the occipital gray matter and periaqueductal gray matter respectively. NAA/Cr and Cho/Cr were compared during the acute illness and recovery periods in three regions. NAA/Cr was also compared during the acute illness in three regions each other.Results 15 patients with mild DKA, 2 patients with midrange DKA, 0 patients with s- evere DKA. Cerebral edema is not found on T2FLAIR and DWI of all patients on two MRS. ADC is measured in right basal ganglia and semioval center respectively, there were no signi- ficant difference in ADC in two regions (right basal ganglia t=-0.94, P>0.05; semioval center t=0.77, P>0.05).β-OHB was detected in 1 patient (5.9%) within 4-8 hours, and no within 8- 12hours. AcAc was not detected in all patients within12 hours. Lactate was in three of 17 pat- ients during DKA, 2 within 4-8 hours of treatment, 1 within 8-12 hours of treatment. Lactate was not detected after recovery in more 72 hours. In the basal ganglia, the ratio of NAA/Cr w- as significantly lower during DKA treatment compared with that after recovery (t=-7.01, P< 0.05). There was a trend toward lower NAA/Cr ratios during DKA treatment in the occipital gray matter and the periaqueductal gray matter (the occipital gray matter t=-2.88, P<0.05; the periaqueductal gray matter t=-2.41, P<0.05). There were significant changes in NAA/Cr ratio- s during the acute DKA in three regions each other (F=8.40, P<0.01). In contrast, there were no significant changes in Cho/Cr ratios in any region (the basal ganglia t=1.03, P>0.05; the occipital gray matter t=-0.12, P>0.05; the periaqueductal gray matter t=0.86, P>0.05).Conclusion 1. In patients with DKA,β-OHB accumulates in the brain during DKA, and it can be detected on MRS. 2. Care should be taken in interpreting MRS results in patients with DKA to avoid erroneously attributingβ-OHB peaks to lactate. 3. NAA/Cr ratios are decreased in children during DKA and improve after recovery. This finding suggests that during DKA neuronal function or viability or both are compromised and improve after treatment and recovery. MRS can be used to evaluate neuronal injury of patients with DKA.