Regions Of Abnormal Perfusion Research Articles

Plain Computed Tomography With Spectral Imaging Findings of Early Cerebral Ischemia.

To investigate the findings of plain spectral computed tomography (CT) with multiparameter of early cerebral ischemia. Thirty-three patients with suspected early cerebral ischemia who received a one-stop CT examination (plain scan with spectral CT imaging mode, CTP and CTA) of the brain were enrolled in this study. No clear lesion was observed in any patient on the plain CT. However, the CTA displayed evidence of vascular stenosis and the CTP displayed a corresponding low perfusion area consistent with early cerebral ischemia. Regions of interest were placed in the abnormal perfusion regions and the contralateral symmetric regions on plain CT. Then, the CT value of the monochromatic images (70 kV), the slope of the spectral HU curve, blood (iodine), iodine (water), and water (iodine) concentrations were measured. A paired t-test was performed for data comparison. The receiver operating characteristic curve was used to evaluate diagnostic performance. The CT values of the ischemic regions at 70 keV, the spectral HU curve, water, and blood values of the ischemic measurements were slightly lower than those of the contralateral symmetric regions (P < .05). Monochromatic images at 70 keV had the highest area under the curve value, and the sensitivity and specificity were 90.0% and 63.0%, respectively. The difference of monochromatic CT values, spectral HU curve, and basic material concentrations between the early cerebral ischemia region and the contralateral symmetric region on spectral CT imaging may provide a reference with the diagnosis of early cerebral ischemia.

Superficial Temporal Artery to Middle Cerebral Artery Bypass in Acute Ischemic Stroke and Stroke in Progress

Surgical reperfusion may be beneficial in patients with acute ischemic stroke who are ineligible for thrombolysis. To evaluate the outcome of superficial temporal artery to middle cerebral artery (STA-MCA) bypass in acute stroke and stroke in progress. The clinical and radiological data of 9 patients treated by STA-MCA bypass requiring urgent reperfusion but ineligible for intra-arterial thrombolysis (IAT) were reviewed. Pooled analysis was performed of published literature concerning STA-MCA bypass in acute stroke (21 cases in 2 articles). Of the 9 patients enrolled, symptom aggravation occurred during medical treatment in 4 patients and after IAT in 2. Three patients were ineligible for IAT despite being within 8 hours of symptom onset. Bypass significantly improved National Institutes of Health Stroke Scale scores (preoperatively, 12.4±4.88; 3 days postoperatively, 8.6±6.39, P=.046; discharge, 5.4±5.15, P=.008; 3 mo postoperatively 3.7±4.82, P=.008) without significant infarction growth by diffusion weighted imaging (preoperatively, 15.0±8.87 mL; 7 days postoperatively, 15.2±8.28 mL; P=.110). Abnormal perfusion regions (mean transit time>145% of contralateral side value) were reduced in all cases (2.63±0.93 mL). Good outcomes (modified Rankin scale≤2) were achieved by 6 patients. Pooled analysis with our patients showed a significant neurological improvement (P<.001) and a good outcome in 25 (83.3%) patients without hemorrhage or complication. STA-MCA bypass may be beneficial to patients with acute stroke or stroke in progress who are ineligible for IAT. Furthermore, it appears safe when the infarction is small. These findings indicate that STA-MCA bypass could be considered as a treatment option in selected patients with acute stroke or stroke in progress.

SPECT Imaging for Brain Improvement Quantification in a Patient With Cerebrotendinous Xanthomatosis

Cerebrotendinous xanthomatosis is a rare recessive autosomal disease caused by mutations of the sterol 27-hydroxylase gene (CYP27), which leads to reduced synthesis of bile acids, particularly chenodeoxycholic acid (Cali et al, J Biol Chem. 1991;266:7779-7783; Gallus et al, Neurol Sci. 2006;27:143-149). The disease is characterized by progressive neurologic dysfunction due to accumulation of cholestanol in neurologic tissues (Moghadasian et al, Arch Neurol. 2002;59:527-529; Selva-O'Callaghan et al, Rheumatology. 2007;46:1212-1213). Long-term treatment with chenodeoxycholic acid can arrest or even reverse progression of the disease (Pierre et al, J Inherit Metab Dis. In press).Brain SPECT with 740 MBq of Tc-99m ethyl cysteinate dimmer, using a double-head gamma camera (Siemens E.cam) with high-resolution, low-energy parallel collimators was performed in our patient at onset and 2 years after starting chenodeoxycholic acid treatment. SPECT acquisitions were performed using a 360-degree orbit, 1 image/30 seg/3 degree, and 128 × 128 matrix. Reconstruction was by means of filtered back-projection, Butterworth 5/0.25, without attenuation correction. Pre- and post-SPECT dicom images were reoriented into Talairach space using NeuroGam (Segami Corporation). To visually identify abnormal perfusion regions, volume render brain image was computed, where abnormal perfusion regions were found by comparing with age-matched normal database, and Brodmann areas (BA) were quantified. Pre- versus post-treatment changes were computed by means of relative percentage between counts. Post-treatment SPECT showed better perfusion than pretreatment SPECT with an increase between 5% and 10% in frontal cortex (BA 9, BA 24, BA 32, BA 46, BA 47), parietal cortex (BA 5, BA 31), and temporal cortex (BA 20, BA 22, BA 28, BA 36, BA 37, BA 38), and with an increase of more than 10% in frontal cortex (BA 45) and parietal cortex (BA 23). This case illustrates the benefit of bile acid therapy for halting and even reversing neurologic retardation in this condition.

Perfusion Imaging in Pusher Syndrome to Investigate the Neural Substrates Involved in Controlling Upright Body Position

Brain damage may induce a dysfunction of upright body position termed “pusher syndrome”. Patients with such disorder suffer from an alteration of their sense of body verticality. They experience their body as oriented upright when actually tilted nearly 20 degrees to the ipsilesional side. Pusher syndrome typically is associated with posterior thalamic stroke; less frequently with extra-thalamic lesions. This argued for a fundamental role of these structures in our control of upright body posture. Here we investigated whether such patients may show additional functional or metabolic abnormalities outside the areas of brain lesion. We investigated 19 stroke patients with thalamic or with extra-thalamic lesions showing versus not showing misperception of body orientation. We measured fluid-attenuated inversion-recovery (FLAIR) imaging, diffusion-weighted imaging (DWI), and perfusion-weighted imaging (PWI). This allowed us to determine the structural damage as well as to identify the malperfused but structural intact tissue. Pusher patients with thalamic lesions did not show dysfunctional brain areas in addition to the ones found to be structurally damaged. In the pusher patients with extra-thalamic lesions, the thalamus was neither structurally damaged nor malperfused. Rather, these patients showed small regions of abnormal perfusion in the structurally intact inferior frontal gyrus, middle temporal gyrus, inferior parietal lobule, and parietal white matter. The results indicate that these extra-thalamic brain areas contribute to the network controlling upright body posture. The data also suggest that damage of the neural tissue in the posterior thalamus itself rather than additional malperfusion in distant cortical areas is associated with pusher syndrome. Hence, it seems as if the normal functioning of both extra-thalamic as well as posterior thalamic structures is integral to perceiving gravity and controlling upright body orientation in humans.

Is It Ethical to Have a Placebo Arm in Reperfusion Trials in the 3- to 6-Hour Time Window?

Geoffrey A. Donnan MD, FRACP Stephen M. Davis MD, FRACP Section Editors To date, no treatment has been proven to improve outcome when started >3 hours after the onset of acute ischemic stroke. Randomized placebo-controlled trials of new potential treatments are needed to: (1) determine if the treatment is effective; (2) determine if the treatment is effective in most patients or only in selected patients; and (3) determine, if only some patients benefit, the best way to select those whose benefit would outweighs risk. Intravenously administered tissue plasminogen activator has not been proven effective in randomized trials beyond 3 hours.1,2 However, pooled data from these and the NINDS trial and secondary analyses certainly suggest benefit up to 4.5 to 5.0 hours.3,4 Appropriately, whether tissue plasminogen activator is effective in the 3- to 6-hour time window is presently being tested in several ongoing placebo controlled studies. The International Stroke Trial-3 trial and ECASS III will determine if the drug is effective in such patients. The DEFUSE study suggests that only patients selected by finding regions of abnormal perfusion substantially larger than areas of irreversible damage on …

Analysis of Metabolic Indices in Regions of Abnormal Perfusion in Patients with High-Grade Glioma

MR spectroscopic imaging (MRSI) and dynamic susceptibility-contrast MR imaging (DSC-MR imaging) are functional in vivo techniques for assessing tumor metabolism and vasculature characteristics. Because tumor hypoxia is influenced by tortuous, degraded, swollen, and angiogenic tumor vasculature, regions of abnormal perfusion parameters should coexist with changes in lactate and creatine metabolite levels. DSC-MR imaging and lactate-edited MRSI were performed on 38 treatment-naive patients with high-grade gliomas (17 grade III, 21 grade IV) before surgical diagnosis. Regions of abnormal perfusion were determined from peak height and percent recovery maps for each voxel within the spectroscopic imaging volume. Choline, creatine, and lactate levels within voxels experiencing only abnormal peak height (aPH), only abnormal recovery (aRec), and both abnormal peak height and recovery (aPH+aRec) were determined and compared to the surrounding T2 hyperintensity (T2h) and normal-appearing white matter. There were decreasing trends in volume from aPH to aRec to aPH+aRec regions for both grade III and grade IV gliomas. Grade IV gliomas exhibited significantly elevated choline in all abnormal perfusion regions, with reduced creatine and increased lactate in the aRec region relative to the surrounding T2h. Grade III gliomas showed trends toward increased creatine within the aPH region and reduced levels within the aRec region. Depressed creatine and elevated lactate levels confirmed the lack of oxygenation within regions of compromised vascular integrity. Identification of regions with leaky or dense vasculature and metabolic markers of hypoxia and cellular proliferation could be useful in determining the more aggressive part of the tumor for targeting, monitoring, and assessing effects of treatment.

Parametric mapping of the hepatic perfusion index with gadolinium-enhanced volumetric MRI

The purpose of this study was to adapt the hepatic perfusion index (HPI) methodology previously developed for MRI to derive 3D parametric maps of HPI, and to investigate apparent differences in HPI maps between a group of colorectal cancer patients and controls. To achieve this, a new and simpler approach to HPI calculation which does not require measurements from the aorta or portal vein is introduced, and assessed with large liver regions of interest (ROIs) in patients and controls. Several example HPI maps showing localized variation are then presented. The subject group consisted of 12 patients with known colorectal metastases, and 13 control subjects referred for routine contrast-enhanced spine imaging with no history of neoplastic disease. HPI was evaluated from serial T1 volume acquisitions acquired over the course of a Gd-DTPA bolus injection. Regions of abnormal perfusion were visible on the HPI maps derived for the patient group, manifested as areas of locally increased HPI extending around the visible margins of known metastases evident on the conventional contrast-enhanced images. This method for MR voxel-based parametric mapping of HPI has the potential to demonstrate regional variations in perfusion at the segmental and subsegmental level.

Comparison of MRI Perfusion Imaging and Single Photon Emission Computed Tomography in Chronic Stroke

There have been few direct comparisons between MR perfusion-weighted imaging (PWI) and established perfusion imaging techniques, and none in chronic stroke. We therefore studied 17 chronic hemispheric infarction patients (mean, 90 days) and compared hypoperfusion volumes determined from PWI maps of relative cerebral blood flow (rCBF) and volume (rCBV), and mean transit time (rMTT) with those measured with ⁹⁹Tc-HMPAO single photon emission computed tomography (SPECT). Comparisons were also made between infarct size (T₂-WI) and clinical scales. Correlations were found between lesion location and volume in all three PWI hemodynamic parameter maps with clinical state and lesions on SPECT and T₂-WI. In 3 patients, rCBF and rCBV lesions extended well beyond the borders of moderate-sized infarctions. We conclude that in chronic stroke, PWI can delineate regions of abnormal perfusion that reflect the degree of functional impairment and structural damage. The finding of peri-infarct hypoperfusion suggests that PWI may have the potential to provide a rapid and non-invasive template against which interventional strategies aimed at promoting functional recovery may be investigated.

Temporal correlation analysis of penumbral dynamics in focal cerebral ischemia.

A novel temporal correlation technique was used to map the first-pass transit of iodinated contrast agents through the brain. Transit profiles after bolus injections were measured with dynamic computed tomography (CT) scanning (1 image/s over 50 s). A rabbit model of focal cerebral ischemia (n = 6) was used, and dynamic CT scans were performed at 30, 60, 90, and 120 min postocclusion. Within the ischemic core, no bolus transit was detectable, demonstrating that complete ischemia was present after arterial occlusion. In the periphery of the ischemic distribution, transit dynamics showed smaller peaks, broadened profiles, and overall delay in bolus transit. A cross-correlation method was used to generate maps of delays in ischemic transit profiles compared with normal transit profiles from the contralateral hemisphere. These maps showed that penumbral regions surrounding the ischemic core had significantly delayed bolus transit profiles. Enlargement of the ischemic core over time (from 30 to 120 min postocclusion) was primarily accomplished by the progressive deterioration of the penumbral regions. These results suggest that (a) temporal correlation methods can define regions of abnormal perfusion in focal cerebral ischemia, (b) peripheral regions of focal cerebral ischemia are characterized by delays in bolus transit profiles, and (c) these regions of bolus transit delay deteriorate over time and thus represent a hemodynamic penumbra.