## 1 Introduction
The currently recommended ASL technique is denoted as single post labeling delay (PLD) pseudo-continuous ASL (PCASL) imaging in which blood flowing through the labeling plane in the neck is inverted (label) for one image, and for the second, the net magnetization is not altered (control), followed by a waiting period known as the PLD to allow for the blood to reach the tissue and undergo perfusion. Another advantage of PCASL compared to other methods is its robustness over a range of blood flow velocities, which might be altered in patients, and also the low demand on the hardware of the scanners, which allows its use on most clinical devices [11]. After acquiring these two images, subtraction of the data shows qualitative brain perfusion. Due to the low signal difference between the label and control, the acquisition is repeated multiple times, keeping the parameters constant to acquire a high signal-to-noise ratio for the final images. ASL mainly allows for the visualization of gray matter perfusion. However, in tissues with perfusion alterations, such as tumors, these can be visualized using ASL irrespective of the originating tissue. Previous work already showed that it is possible to differentiate between HGGs and LGGs, which has already been presented in the literature [13; 14; 15]. ASL additionally has been used for discrimination between glioma recurrence and radiation damage [16], the grading of gliomas [17; 18; 19], and distinguishing between tumors and metastasis [20]. While these studies show the potential of ASL, they mainly address either differences with other tissues or correlate the findings with other methods. The inclusion of other biomarkers, such as MGMT, etc., however, has not yet been systematically analyzed by means of histogram analysis. Additionally, the surrounding edema has not yet been investigated by means of perfusion imaging. Cerebral edema is caused by a variety of factors and is not only limited to the presence of a tumor. However, in general, any tumor (or metastasis) in the brain results in tumor-surrounding edema. This occurs due to transcapillary filtration forces that are greater than the absorptive forces in the tissue. Thus, fluids transude into the tissue (i.e., the interstitial space) slowly. In the healthy brain, this inflow is normally counterbalanced by lymphatic flow, which then carries proteins and water back into the bloodstream. Tumors, however, lack this lymphatic system, and this physiological drainage system is not in place in and around the tumor. Other factors include a higher permeability of the tumor capillaries (compared to capillaries in healthy tissues), (temporary) occlusion of tumor capillaries by fast growth and subsequent compression, overproduction of collagen or polysaccharides and their accumulation, disaggregation of the matrix of the tumor cells, increased diffusion inside the cells, and cell death [4]. Because of these factors, the healthy osmotic gradient of the intra- and extracellular space cannot be maintained and thus leads to cell swelling, i.e., edema. The presence and amount of these factors vary between tumor entities, grades, and mutation. Having such changes in the cells translates to a reduced (or loss of) function in the brain tissue, which can be easily spotted using imaging modalities. Tumor edema can already be seen in T1-weighted images, which are generally not sensitive to free fluid, but are even more pronounced in T2/FLAIR images and especially DWI. These methods allow for a clear delineation of edema compared to not only the tumor but also the surrounding healthy tissue. Since the accumulation of fluid in multiple cells (the edema) can have a strong effect on tissue blood flow, additional considerations have to be made. As edema disturbs the equilibrium of the volume inside the constrained volume of the skull, such an increase needs to be compensated by secondary effects, e.g., reduction of the flow of other fluids, such as blood or cerebrospinal fluid.