Magnetic Resonance Imaging in Experimental Models of Brain Disorders

Abstract

Summary:This review gives an overview of the application of magnetic resonance imaging (MRI) in experimental models of brain disorders. MRI is a noninvasive and versatile imaging modality that allows longitudinal and three-dimensional assessment of tissue morphology, metabolism, physiology, and function. MRI can be sensitized to proton density, T 1 , T 2 , susceptibility contrast, magnetization transfer, diffusion, perfusion, and flow. The combination of different MRI approaches (e.g., diffusion-weighted MRI, perfusion MRI, functional MRI, cellspecific MRI, and molecular MRI) allows in vivo multiparametric assessment of the pathophysiology, recovery mechanisms, and treatment strategies in experimental models of stroke, brain tumors, multiple sclerosis, neurodegenerative diseases, traumatic brain injury, epilepsy, and other brain disorders. This report reviews established MRI methods as well as promising developments in MRI research that have advanced and continue to improve our understanding of neurologic diseases and that are believed to contribute to the development of recovery improving strategies.

Acute blood–brain barrier opening in experimentally induced focal cerebral ischemia is preferentially identified by quantitative magnetization transfer imaging

“…Vasogenic edema reportedly causes a small increase in T 1 (37). In accordance with this, ischemia and reperfusion barely affected T 1 values in the three regions.…”

“…The transverse relaxation rate correlates well with tissue water content, and its increase in cerebral ischemia is thought to reflect vasogenic (mostly interstitial) edema (37). Since the formation of such edema often follows BBB opening, an elevation in T 2 may well indicate the latter.…”

Bench to Bedside: The Quest for Quality in Experimental Stroke Research

“…Although traditionally experimental stroke research has focused on early mechanisms of damage, only recently a surprising capacity of the central nervous system (CNS) for regeneration and plasticity has been identified, raising the hopes of developing therapeutic approaches based on these findings (Chen et al, 2002;Lindvall and Kokaia, 2004;Savitz et al, 2004Savitz et al, , 2002Roitberg, 2004;Chopp and Li, 2002). Further progress in the field has come from a recent tremendous expansion of the methodological portfolio of experimental stroke research, ranging from genome-wide transcriptional and protein expression screens (Carmichael, 2003;Hubner et al, 2005), to the targeted deletion or overexpression of candidate genes (Liang et al, 2004), to sophisticated highresolution in vivo imaging (Dijkhuizen and Nicolay, 2003).…”

Temporal profile of T2-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

“…Lesion Type-Dependent Relaxation Time Changes T 1 and T 2 relaxation times are sensitive to an increase in free, extracellular water, such as in vasogenic edema, but might also be influenced by other factors after ischemia, such as bound water pools or the BOLD effect (Dijkhuizen and Nicolay, 2003;Horikawa et al, 1986). Increases of MR relaxation times have been shown to correlate to loss of 2,3,5-triphenyltetrazolium chloride (TTC) stain, which matches loss of metabolic cell viability in vasogenic edema, even before neuropathological signs of cell damage (Bose et al, 1988).…”