Quantitative MR analysis of glucocorticoid effects on peritumoral edema associated with intracranial meningiomas and metastases.

OBJECTIVE: The purpose of our study was to quantify peritumoral brain edema (PTE) in vivo using NMR relaxation time imaging, as the longitudinal relaxation time T1 is proportional to tissue water content, and to use the method for monitoring the effects of glucocorticoids (GCCs) on PTE in brain tumor patients as a function of time.
MATERIALS AND METHODS: Relaxation time imaging (T1 maps) was done on a 1.5 T MR scanner on 23 brain tumor patients [13 cerebral metastases (METs), 10 intracranial meningiomas (MMs), and 9 benign and 1 anaplastic MM] before, and 1, 3, and 7 days after initiation of GCC treatment (dexamethasone 0.26-0.64 mg/kg bw). In addition, 7 patients were studied for 14-63 days of treatment. Imaging analysis included mean T1 of the edema area as a function of time, and an image histogram evaluation technique, which measures 50% of the edema area, where T1 is highest (corresponding to the highest water content of the area), termed the "super-edema." Using a conversion equation, mean T1 in the edema area was recalculated into a percent of tissue water content.
RESULTS: After 7 days of GCC treatment total edema area was reduced by 10.3% in the MET patients. The average reduction in mean T1 was 4.6% after 24 h of treatment and 13.5% after 7 days. Expressed in terms of percent tissue water content, the average edema resorption rate in the MET patients was 0.4 +/- 0.1% H2O/day (p < 0.02). Super-edema area was reduced by 64% after 7 days (p < 0.0001). None of the benign MMs responded to GCC treatment, either in edema size or in mean T1, unlike the anaplastic type, in which there was a response comparable to that in the MET patients. The effect of GCCs in up to 63 days of treatment is demonstrated. It is shown that after 40-63 days of GCC treatment, PTE water content is close to the upper normal range for white matter.
CONCLUSION: PTE is heterogeneous in terms of the spatial distribution of T1 and, thereby, water content. GCCs reduce T1 in PTE around cerebral metastases significantly after a few days of treatment, possibly through a mechanism that reduces edema production below the level of edema resorption. PTE surrounding benign MM was not affected by GCC treatment, contrary to one anaplastic MM, which leads to the speculation that malignant tumors may produce substances that are affected by GCCs and are prerequisites for a GCC effect. Significant reductions in the highest T1 area (super-edema area) were observed after 24 h of treatment. The anti-edema effect of GCC may last at least 63 days. A lower dose-dependent threshold for the effect seems to exist. The possible mechanisms of actions of the GCCs on PTE are discussed.