Dexamethasone and Enhancing Solitary Cerebral Mass Lesions: Alterations in Perfusion and Blood-tumor Barrier Kinetics Shown by Magnetic Resonance Imaging

Iain D. Wilkinson(Sheffield Teaching Hospitals NHS Foundation Trust), David A. Jellineck(Sheffield Teaching Hospitals NHS Foundation Trust), David T. Levy(Sheffield Teaching Hospitals NHS Foundation Trust), Frederik L. Giesel(German Cancer Research Center), C.A.J. Romanowski(Sheffield Teaching Hospitals NHS Foundation Trust), B. Miller(Sheffield Teaching Hospitals NHS Foundation Trust), Paul D. Griffiths(University of Sheffield)
Neurosurgery
March 30, 2006
Cited by 41

Abstract

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.


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