Dexamethasone and enhancing solitary cerebral mass lesions: alterations in perfusion and blood-tumor barrier kinetics shown by magnetic resonance imaging.

Objective: Glucocorticoid analogues are often administered to patients with intracranial space-occupying lesions. Clinical response can be dramatic, but the neurophysiological response is not well documented. This study sought to investigate the blood-lesion barrier, blood-brain barrier, and cerebral perfusion characteristics of patients who have undergone such therapy using magnetic resonance imaging.

Methods: Seventeen patients with intracranial mass-enhancing lesions underwent magnetic resonance imaging before and after 3 days of high-dose dexamethasone therapy. Assessments of blood-lesion barrier and blood-brain barrier integrity were based on a dynamic T1-weighted exogenous contrast technique that yielded the normalized maximal change in contrast uptake (T1-uptake). Perfusion was assessed using a dynamic T2*-weighted exogenous contrast technique to yield relative regional cerebral blood volume and first-moment mean transit time. Comparisons were made in T1-uptake, regional cerebral blood volume, and first-moment mean transit time of both enhancing lesion and contralateral normal-appearing white matter (CNAWM) obtained before and after dexamethasone.

Results: Significant reduction in T1-uptake was observed (19% decrease, P < 0.005) within enhancing pathological tissue, whereas no significant alteration was detected in CNAWM. Regional cerebral blood volume was significantly reduced in both enhancing tissue (28% decrease, P < 0.005) and in CNAWM (20% decrease, P < 0.001). Bolus first-moment mean transit time significantly increased (2.0 s prolongation, P < 0.05) in CNAWM, whereas there was no significant change (1.4 s prolongation, P > 0.05) within enhancing tissue.

Conclusion: Glucocorticoid-analogue therapy not only affects the permeability of the blood-lesion barrier and lesion blood volume but also affects blood flow within normal-appearing contralateral parenchyma. There is a need for controls in steroid therapy in magnetic resonance imaging studies, which involve assessments of cerebrovascular function.