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Neuronal Damage after Ischemic Injury in the Middle Cerebral Arterial Territory: Deep Watershed versus Territorial Infarction at MR Perfusion and Spectroscopic Imaging¹

¹ From the Department of Electrical Engineering, National Taiwan University, Taipei, R.O.C. (Y.J.L., H.W.C., I.J.H.); Department of Radiology, Tri-Service General Hospital and National Defense Medical Center, Number 325, Section 2, Cheng-Kung Rd, Neihu 114, Taipei, Taiwan, R.O.C. (Y.J.L., C.Y.C., H.W.C., C.S.L., S.C.C.); and Institute of Statistics Science, Academia Sinica, Taipei, Taiwan, R.O.C. (M.L.). Received May 31, 2002; revision requested July 29; final revision received April 11, 2003; accepted May 14. Supported in part by National Science Council grants NSC-89–2320-B-016–056-M08 and NSC-90–2213-E-002–003. Address correspondence to C.Y.C. (e-mail: sandy0928@seed.net.tw).

View larger version (24K): [in a new window]   Figure 1. Plot illustrates mean ratios of lesion-to-tissue rCBV at MR imaging performed at six defined stages of stroke, from hyperacute (<6 hours) to late chronic (30-31 days). TI lesions showed a progressively increasing pattern of rCBV from hypoperfusion at hyperacute to hyperperfusion at early chronic stage. WI lesions showed persistent postischemic hyperperfusions throughout the six stages. Stages at which the mean difference between TI and WI reached statistical significance (P < .01) are shown (*).

View larger version (25K): [in a new window]   Figure 2. Plot illustrates mean relative NAA values at six defined stages of TI and WI, from hyperacute (<6 hours) to late chronic (30-31 days). Patients with TI showed complete loss of relative NAA within 4 days after ictus. Patients with WI showed higher relative NAA (0.8 at acute stage and about 0.6 at the four subsequent stages), implying neuron survival. Stages at which the mean difference between TI and WI reached statistical significance (P < .01) are shown (*).

View larger version (23K): [in a new window]   Figure 3. Plot illustrates mean relative lactate values at six defined stages of TI and WI, from hyperacute (<6 hours) to late chronic (30-31 days). Patients with TI exhibited high levels of lactate at hyperacute (1.44 ± 0.69) and acute (2.21 ± 1.27) stages. Patients with WI showed relatively stable relative lactate values between about 0.4 and 0.6. Stages at which the mean difference between TI and WI reached statistical significance (P < .01) are shown (*).

View larger version (97K): [in a new window]   Figure 4. Time course of TI of the right middle cerebral artery, as demonstrated on ADC maps (top row), rCBV maps (middle row), and proton MR spectra (bottom row) at 2 (first image from left), 7 (second image from left), 14 (third image from left), and 30 (fourth image from left) days after stroke symptom onset in a 51-year-old male patient. Rectangles on the ADC maps indicate the voxels included for spectral analysis, and white borders show the region of interest for rCBV analysis. Pseudonormalization of ADC commenced at about 2 weeks after ictus, before which the evolution of postischemic reperfusion can be clearly depicted on the rCBV maps. Both loss of relative NAA and significant presence of relative lactate at acute stage are seen in the spectra.

View larger version (90K): [in a new window]   Figure 5. Time course of WI of the right middle cerebral artery, as depicted on ADC maps (top row), rCBV maps (middle row), and proton MR spectra (bottom row) at 2 (first image from left), 7 (second image from left), 14 (third image from left), and 30 (fourth image from left) days after stroke symptom onset in a 57-year-old female patient. Rectangles on the ADC maps indicate the voxels included for spectral analysis, and white borders show the region of interest for rCBV analysis. ADC evolution is much less significant. Persistently increased rCBV is seen. Relative NAA decreased only partially (compared with normal tissue, spectra not shown), with relative lactate level varying from 0.9 (acute) to 0.3 (late chronic).

View larger version (25K): [in a new window]   Figure 6. Proposed model for pathophysiologic time course of human ischemic stroke. Thicker arrows indicate more significant and faster changes. WI likely results from a preexisting reduction in cerebral perfusion pressure that induces cerebral autoregulation with rCBV increase. Possible elevated oxygen extraction fraction further protects the neurons from experiencing energy deficiency. These factors lead to a generally slower stroke progression. On the other hand, TI causes an abrupt cerebral ischemia, without a chance to develop sufficient collateral arteries during the critical period. As a result, complete loss of living neurons occurs early, and subsequent alterations in rCBV are deemed ineffective. Lac = lactate, rOEF = relative oxygen extraction fraction.