147 Hemodynamic Imaging in Brain Metastases: ASL vs. Hypercapnic BOLD INTRODUCTION Advances in imaging techniques have made MRI a powerful tool for investigating not only brain function but also brain physiology and auto-regulatory status. One such method, that now sees routine clinical application is Arterial Spin Labeling (ASL). ASL is non-invasive, and can provide diagnostically relevant, quantitative parameters related to hypo- or hyper-perfusion.1–3 Multi post label delay (multiPLD) methods can even be used to infer the presence of collateral cerebral blood flow (CBF) pathways through their ability to estimate arterial arrival time (AAT) or characterize artserial transit artifacts (ATA). Together these ASL metrics can provide valuable physiological information in healthy subjects and can also identify diseaserelated auto-regulatory changes in patient populations. A major cerebral auto-regulatory mechanism responsible for maintaining adequate CBF is cerebrovascular reactivity (CVR). CVR is reflective of smooth-muscle cell mediated blood flow control, and represents a major compensatory mechanism in diseases that compromise cerebral hemodynamics.4–6 The CVR response can be assessed and spatially mapped using Blood oxygenation level-dependent (BOLD) MRI in combination with controlled hypercapnic stimuli. This technique is distinct from resting-state and/or task-based BOLD MRI, where either spontaneous or evoked neuronal signals modulate the BOLD signal change, providing information related to brain function. CVR measurements can be interpreted as regional indicators of healthy or disease-impaired vasculature.7 Impairments often manifest as negative signal responses, where a vasodilatory stimulus can cause paradoxical decrease in CBF (known as vascular steal) to an area with exhausted dilatory reserve, due to a reduction in vascular resistance in neighboring, non-exhausted regions.8 Finally, analysis of dynamic CVR characteristics can provide information on temporal aspects of the CVR response that are encompassed in the hemodynamic response lag. 9–11 Changes in perfusion characteristics and cerebrovascular function have been found in multiple different patient populations, including patients with brain tumors.12–14 Growth of intracranial masses, like primary brain tumors or brain metastases, can cause local disruptions of the hemodynamic environment. Metastatic cells have to proceed through a range of developmental steps in order to form macrometastases; (1) cells arrest in the small microvessels, (2) cells extravasate to enter the brain tissue, (3) cells perpetuate into a strict perivascular position, and (4) vascularization is secured through either co-optive or angiogenic growth depending on the tumor type.15 By vascular co-option, angiogenesis and dilation of blood vessels associated 6
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