Noninvasive Detection of Cerebral Hypoperfusion and Reversible Ischemia from Reductions in the Magnetic Resonance Imaging Relaxation Time, T₂

Abstract

The hypothesis was tested that hypoperfused brain regions, such as the ischemic penumbra, are detectable by reductions in absolute transverse relaxation time constant (T2) using magnetic resonance imaging (MRI). To accomplish this, temporal evolution of T2 was measured in several models of hypoperfusion and focal cerebral ischemia in the rat at 9.4 T. Occurrence of acute ischemia was determined through the absolute diffusion constant D(av) = 1/3 TraceD, while perfusion was assessed by dynamic contrast imaging. Three types of regions at risk of infarction could be distinguished: (1) areas with reduced T2 (4% to 15%, all figures relative to contralateral hemisphere) and normal D(av), corresponding to hypoperfusion without ischemia; (2) areas with both reduced T2 (4% to 12%) and D(av) (22% to 49%), corresponding to early hypoperfusion with ischemia; (3) areas with increased T2 (2% to 9%) and reduced D(av) (28% to 45%), corresponding to irreversible ischemia. In the first two groups, perfusion-deficient regions detected by bolus tracking were similar to those with initially reduced T2. In the third group, bolus tracking showed barely detectable arrival of the tracer in the region where D(av) was reduced. We conclude that T2 reduction in acute ischemia can unambiguously identify regions at risk and potentially discriminate between reversible and irreversible hypoperfusion and ischemia.

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

“…Previous studies showed within the ADC lesion, qT 1 and qT 2 (5,6) change in opposite (5,6). Recent data point to two-phase response of qT 1 upon ischaemia onset; in complete forebrain ischaemia the fast response levels by two minutes (20) whereas in the core, the rapid increase lasts up to 25 minutes post MCAo (16).…”

“…Within regions of decreased ADC in rat focal ischaemia, quantitative T 2 relaxation times (qT 2 ) also decrease due to metabolic changes (6,16) and cytotoxic oedema (17). The decrease is followed by a quasi-linear increase over time (2,4) caused by altered hydrodynamics and tissue degradation (17,18).…”

Estimation of the Onset Time of Cerebral Ischemia Using T 1ρ and T 2 MRI in Rats

“…12 However, during the early minutes of ischemia, single Hahn echo T 2 MRI shows T 2 shortening observed both at 4.7 T and 9.4 T due to the negative blood oxygenation level-dependent effect. 18,31 Shortening of T 2 has also been reported acutely in patients imaged at 1.5 T. 32 The presence of such T 2 shortening results in a situation in which there is a time point when T 2 in the stroke tissue shows no difference to contralateral nonischemic tissue. In our data set, the ⌬T 2 zero crossover time greatly varies between striatum and cortex.…”

Cerebral Diffusion and T2: MRI Predictors of Acute Mountain Sickness during Sustained High-Altitude Hypoxia

“…In ischemia, the earliest T 2 effect is a decrease in the relaxation time. Grohn et al, 10,11 showed that this is because of a negative blood oxygenation level-dependent effect directly related to decreased perfusion (without significant increase in CMRO 2 ), and suggested that in this context, reduced T 2 might indicate a period of ischemia in which tissue injury is fully reversible. In the current studies, perfusion was increased during sustained hypoxia, 12 and the arterial and venous compartments contain increased deoxyhemoglobin, so blood oxygenation level-dependent changes will add to the observed reduction in T 2,index .…”