DWI is currently the only imaging method to investigate diffusion activities of water molecules in vivo; ADC reflects the diffusion speed of water molecules, and the fast diffusion of water molecules could be revealed with a larger ADC value with lower signals of DWI images. Therefore the changes of ADC value could reflect the water molecule diffusion status in post brain infarction periods [8, 10–12]. In superacute and acute brain infarction periods, the slowdown of water molecule diffusion could be explained by the cellular edema: following ischemia, the outflow of intracellular potassium ions and the inflow of calcium, sodium as well as water caused the swelling of the cells. The water molecules inside the cells were however bounded by cell membrane and organelles, and therefore diffuse much slower, causing the lower ADC values. Because of the relative balance in total amount of water in the acute phase after brain infarction, T2W1 often show no change even that the ADC value decreased, as found in 12 super acute cases in present manuscript - which suggested that the accuracy of using ADV value in diagnosis of brain infracted regions is 100% in our hand. This cannot be reach in routine MRI images. To normalize the ADC value and eliminate the individual differences, the present study measured the ADC value in the contralateral side to compute the rADC value [13, 14], which could be useful in comparative studies, even among individuals across countries.
In present study we showed that the average ADC and rADC value change with time period post-brain infarction, which is caused by pathophysiological changes following brain damages. In superacute and acute cases the rADC reached the lowest point, and began to increase in subacute cases, and appeared to be "normal" between 10-14 days after brain infarction happened. This could be explained by two possibilities: first, vessel-sourced edema caused injury to endothelial cells 5-6 hours after brain infarction, and exacerbated in subacute phase, leading to enhanced permeability of blood brain barrier, and increased movement of many molecules including water molecules in extracellular spaces; second, the cell membrane broken and released intracellular water molecules . In chronic phase the infracted brain tissues liquidize and were replaced by cerebrospinal fluid, which has a free movement of water molecules and the high ADC value when compared with brain tissues, leading to a rADC value more than 100%. Given the fact the ADC and rADC values vary during the post brain infarction period, we suggest that the combined analysis of ADC, rADC and routine MRI images could be important and useful in clinical diagnosis of the progression after brain infarction.
The other interesting point is the spatial distribution of ADC and rADC values within infracted region. In superacute and acute cases ADC values increase from the center to the side areas, suggesting that the decreases of ADC values could reflect the severity of the tissue damage. The surrounding regions of brain infarction area were considered to be plastic and could be re-perfused in proper conditions, or infracted if untreated . The gradient of ADC value thus provided a chance to diagnose the surrounding sensitive regions, to follow the efficacy of treatment and prediction of the recovery. In subacute phase the reversed gradient suggested the liquidation of infracted tissues from the center, and brought the increased ADC value. The "false normal" phenomena would appear in the late phase of subacute patients, and during this period the reperfusion could not save the brain tissue from necrosis. Moreover, this would point the possibility to use ADC values to predict the recovery into normal tissue or final degeneration after the intervention in patients with brain infraction .