Characterization of Experimental Ischemic Brain Edema Utilizing Proton Nuclear Magnetic Resonance Imaging

Abstract

Summary:Correlations between Tl and T2 relaxation times and water and electrolyte content in the normal and ischemic rat and gerbil brains were studied by means of both nuclear magnetic resonance (NMR) spectroscopic and imaging methods. In the spectroscopic experiment on excised rat brains, Tl was linearly dependent on tissue water content and T2 was prolonged in edematous tissue to a greater extent than expected by an increase in water content, showing that T2 possesses a greater sensi tivity for edema identification and localization. Changes in Na + and K + content of the tissue mattered little in the prolongation of relaxation times. Serial NMR imaging of gerbil brains insulted with permanent hemispheric isch- Proton nuclear magnetic resonance (NMR)imaging enables sensitive detection of cerebral ischemia within several hours after the onset of dis ease (Buonanno et aI. , 1983; Mano et aI. , 1983; Spetzler et aI. , 1983). T1 (spin-lattice) and T2 (spin-spin) relaxation times are prolonged in isch emic tissue, and the degree of damage and extent of injury can be pictorialized by NMR imaging. Pro longation of relaxation times is considered to be a result of the development of brain edema (Go and Edzes, 1975; Naruse et aI. , 1982). However, the contrast of the NMR image is arbitrarily controlled by the pulse sequence used. As a consequence, the Abbreviations used: IR, inversion recovery; NMR, nuclear magnetic resonance; PO, proton density; SE, spin echo; SR, sat uration recovery; TE, time to echo; n, time of inversion; TR , time of repetition. 212emia offered early lesion detection in TJ-and especially T2-weighted images (detection as soon as 30 min after insult). The progressive nature of lesions was also imaged. Calculated TJ and T2 relaxation times in regions of interest correlated excellently with tissue water con tent (r = 0.892 and 0.744 for T 1 and T2, respectively). As a result, detection of cerebral ischemia utilizing NMR imaging was strongly dependent on a change in tissue water content. The different nature of Tl and T2 relax ation times was also observed.

Dynamic changes of ADC, perfusion, and NMR relaxation parameters in transient focal ischemia of rat brain

“…These authors also showed that T 1, remained elevated or increased in tissue destined to undergo neuronal damage, whereas it normalized in areas in which such injury did not develop during the first day after ischemia. The postischemic increase in T 2 was more pronounced than that of T 1 , and was also inversely correlated with ADC recovery, fully in line with the long-known relationship between irreversible ischemic injury and breakdown of the bloodbrain barrier (35,36). Increased barrier permeability promotes the formation of vasogenic edema, leading to an increase of net tissue water content.…”

“…Ischemic T 1 alterations have been described (33) and can be attributed, at least in part, to a decline in blood flow and/or the above-described magnetization transfer effects (34). The increase in T 2 is ascribed to edema formation, which is most pronounced in irreversibly damaged tissue (35)(36)(37)(38). During the 90-min vascular occlusion, this is mainly cytotoxic edema, because blood-brain barrier breakdown (a criterium of vasogenic edema) is observed only after much longer intervals (35,36).…”

“…The increase in T 2 is ascribed to edema formation, which is most pronounced in irreversibly damaged tissue (35)(36)(37)(38). During the 90-min vascular occlusion, this is mainly cytotoxic edema, because blood-brain barrier breakdown (a criterium of vasogenic edema) is observed only after much longer intervals (35,36). The main characteristic of cytotoxic edema is the fluid shift from the extracellular into the intracellular compartment, reflected by the steep decline in ADC (1,4,5).…”

Nifedipine treatment reduces brain damage after transient focal ischemia, possibly through its antioxidative effects

“…In particular, the T2 change is shown to be larger than the T1 change. 32,33 In fact, our data showed parallel changes in ischemic lesion volume and water content (Figure 3). …”

Stroke onset time estimation from multispectral quantitative magnetic resonance imaging in a rat model of focal permanent cerebral ischemia

“…qT 1 increases gradually over time from stroke onset within regions of decreased diffusion (16,9). Pathophysiological mechanisms thought to underlie this qT 1 increase are similar to qT 2 , including altered water dynamics and content in ischaemic tissue (14,19) qT 1 is additionally sensitive to changes in cerebral blood flow and volume (16,20), temperature (21), pH (22) and tissue oxygen tension (16 Five male Wistar rats (300 -400 g, Animal Resource Facility, University of Eastern Finland, Kuopio, Finland) underwent permanent middle cerebral artery occlusion (MCAo) (24). All rats were anesthetized with isoflurane through a facemask (maintained at 1.5 -2.4%) for the duration of the operation and MRI.…”