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In the present work a novel model to simulate mass effect caused by brain tumors is described. The progression of the tumor is modeled by means of a deterministic reaction- diffusion equation, which is discretized on a highresolution voxel grid. This model does not inherently account for the mass effect of the tumor. Therefore, the computed tumor cell density is linked to a parametric deformation model.

In this article, we propose a framework for modeling glioma growth and the subsequent mechanical impact on the surrounding brain tissue (mass-effect) in a medical imaging context. Glioma growth is modeled via nonlinear reaction-advection-diffusion, with a two-way coupling with the underlying tissue elastic deformation. Tumor bulk and infiltration and subsequent mass-effects are not regarded separately, but captured by the model itself in the course of its evolution. Our formulation is fully Eulerian and naturally allows for updating the tumor diffusion coefficient following structural displacements caused by tumor growth/infiltration. We show that model parameters can be estimated via optimization based on imaging data, using efficient solution algorithms on regular grids. We test the model and the automatic optimization framework on real brain tumor data sets, achieving significant improvement in landmark prediction compared to a simplified purely mechanical approach.

Motivated by the need for methods to aid the deformable registration of brain tumor images, we present a three-dimensional (3D) mechanical model for simulating large non-linear deformations induced by tumors to the surrounding encephalic tissues. The model is initialized with 3D radiological images and is implemented using the finite element (FE) method. To simulate the widely varying behavior of brain tumors, the model is controlled by a number of parameters that are related to variables such as the bulk tumor location, size, mass-effect, and peri-tumor edema extent. Model predictions are compared to real brain tumor-induced deformations observed in serial-time MRI scans of a human subject and 3 canines with surgically transplanted gliomas. Results indicate that the model can reproduce the real deformations with an accuracy that is similar to that of manual placement of landmark points to which the model is compared.

MRI and CT of 32 children with pathologically proven supratentorial “intra-axial” tumours were retrospectively reviewed. Twelve histological types were included. The location of tumours is helpful for diagnosis. Cysts, calcification, and haemorrhage were found in 69%, 44% and 22%, respectively. Perifocal haemosiderin deposits were typical of cavernous angioma. An unenhanced CT high density was characteristic in some tumours, especially germinoma. Strong mass effect with marked perifocal oedema was suggestive of a malignant tumour. Although final diagnosis requires pathological study, these findings give some information for initial planning of treatment.

To determine when and how the size and characteristics of intracranial aneurysms change following endovascular treatment, MRI was employed to follow up five patients for 2 or 3 years after interventional procedures. In parent artery occlusion group, the size of the aneurysm reduced to approximately 30% of the intial volume between 4 months and 1 year following the treatment, when hyperintense area in the aneurysm on T1-weighted images changed to the isointense area. There were only slight decreases in volume after 1 year. In the intra-aneurysmal occlusion group, the volume reduction and signal intensity changes were less than those of parent artery occlusion on postembolisation MRI. Parent artery occlusion tends to decrease the aneurysmal volume faster than intra-aneurysmal occlusion and may be better treatment for the patients with mass effect due to the aneurysm.

Brain edema is a major complication of several types of intracranial pathology such as ischemia, tumor and hemorrhage. Since the deleterious influence of brain edema is related primarily to a mass effect, basic knowledge of the mechanical properties of brain tissue is necessary in order to understand the process of edema-mediated tissue injury such as cerebral herniation and demyelination. In the present investigation, we measured regional differences in the tissue compliance of edematous as well as normal brain tissue in cats subjected to cryogenic injury. We observed that an increase in regional tissue compliance was closely associated with an increase in the tissue water content.

MR angiography (MRA) was performed in 25 patients with primary intracranial tumours in association with a standard brain spin-echo technique, in order to assess its technical feasibility and its clinical usefulness. MRA findings were compared with those of angiography (digital subtraction or conventional). The results indicate that MRA can accurately depict the mass effect of cerebral neoplasms on major cerebral vessels with a good correlation with angiography; however MRA is still insufficient for precise evaluation of the vascular supply and neovascularisation of tumours.

Management of elevated intracranial pressure is a common problem in neurosurgical patients presenting with a mass effect due to tumors, hemorrhage, or hydrocephalus. There are cases where intracranial hypertension persists despite conventional therapy. There are also circumstances where rapid control of the ICP is needed without the delay of onset required by some of the presently available agents. Most of the presently acutely used agents (i.e. mannitol, hyperventilation) act through their effect on reducing cerebral blood volume.

Although the appearance of ischaemic cerebral infarcts in computed tomographic (CT) scans is often characteristic (ref 1–6), atypical appearances may cause diagnostic errors. Awareness of these potential pitfalls is neccessary for accurate interpretation.

Patients with hypertensive intracerebral hemorrhage (HIH) are thought to deteriorate neurologically during the 2nd week after onset, even after the initial treatment has been successful and neurologic recovery has been noted earlier. Correspondingly, several authors have revealed that the mass effect shown on the CT scan is most prominent at 10–15 days after the onset of HIH [9, 13, 19]. The low-density area encircling the hematoma, which appears late and causes augmentation of the mass effect, has been thought to be the vasogenic type of brain edema [1, 8].

Fifty-nine consecutive patients with extradural hematoma — admitted from Dec. 1st. 1977 to Nov. 30th 1981 — had a CT-scan performed prior to surgery. The GCS was recorded at the time of CT-scanning, and the “best GCS” recorded for the time period from the injury to the CT-scanning.

Intracranial hypertension is a well-recognized complication in the perioperative management of patients with malignant supratentorial brain tumors of every cell-type, and this always is a serious concern with regard to optimal anesthetic care (Bedford et al. 1982). The compromised intracranial compliance caused by these tumors could be based on at least two possible mechanisms. One possibility is that the tumor causes an expanding mass lesion that gradually exhausts the pressure-volume reserves of the cranial compartment such that a relatively small increase in cerebral blood volume within normal brain can produce a large increase in ICP. An alternative possibility is that impaired cerebrovascular reactivity in the tumor mass might result in large increases in cerebral blood flow and consequent intracranial hypertension whenever arterial blood pressure or CO2 tension increases. To our knowledge the relative role of these two possible mechanisms for intracranial hypertension have not been studied in a systematic fashion, although both are often invoked whenever ICP problems are discussed in managing malignant supratentorial tumors.