Cerebral Hypoperfusion In Patients Research Articles

Hypoperfusion and Ischemia in Cerebral Amyloid Angiopathy Documented by 99mTc-ECD Brain Perfusion SPECT

Cerebral amyloid angiopathy (CAA) is known to be an important cause of spontaneous cortical-subcortical intracranial hemorrhage in normotensive older persons. CAA can also manifest as leukoencephalopathy, brain atrophy, and ischemia secondary to hypoperfusion. Our goal was to verify cerebral hypoperfusion in patients with CAA using (99m)Tc-ethylcysteinate dimer ((99m)Tc-ECD) brain perfusion SPECT. A total of 11 patients (5 men and 6 women; age range, 58-78 y; mean age +/- SD, 70.0 +/- 7.0 y) with clinically and radiologically established probable CAA who underwent (99m)Tc-ECD SPECT were included. (99m)Tc-ECD SPECT scans were also obtained from 13 age-matched healthy control subjects (7 men and 6 women; age range, 60-79 y; mean age +/- SD, 66.7 +/- 6.4 y) for comparison. The relative regional cerebral blood flow values obtained for patients and controls were compared using software. Compared with controls, patients with probable CAA showed hypoperfusion in the inferior parietal lobule of both parietal lobes (Brodmann area [BA] 40), middle temporal gyrus of the left temporal lobe (BA 39), postcentral gyrus of the right parietal lobe, superior temporal gyrus of the right temporal lobe (BA 22), superior temporal gyrus of the right frontal lobe (BA 10), inferior temporal gyrus of the left temporal lobe (BA 20), and both caudate bodies (P < 0.0001, t = 4.65). Patients with probable CAA had significantly decreased cerebral perfusion and may be at risk for leukoencephalopathy, atrophy, and ischemia.

Perfusion differences on SPECT and PWI in patients with acute ischemic stroke

The purposes of the present study were to compare the flow defect volumes on perfusion-weighted magnetic resonance imaging (PWI) and (99m)Tc-labeled ethylcysteinate dimer ((99m)Tc-ECD) single photon emission computed tomography (SPECT) at acute and subacute stages of ischemic stroke and to analyze the relationship between the detected flow defects on the two methods and neurological status and clinical outcomes. Perfusion defects on PWI and SPECT were measured within 48 h and on day 8 of the onset of stroke from 22 patients with their first-ever acute supratentorial ischemic stroke. The primary neurological status was evaluated prior to the imaging. Clinical outcome was assessed at 3 months after the onset of the stroke. The volumes of cerebral blood flow (CBF) defects did not differ between SPECT and PWI within the 48-h examinations. However, the volume of CBF defect was significantly larger on SPECT than on PWI on day 8 (p = 0.03). Within the 48-h examinations, the CBF defect volumes on SPECT and PWI were comparably related to the neurological status. On day 8, the CBF defect volume on SPECT showed higher correlation to the neurological status and more precisely predicted the clinical outcomes at 3 months than PWI. (99m)TC-ECD-SPECT and PWI both have ability to detect cerebral hypoperfusion in patients with ischemic stroke but with some differences. The value of SPECT is more accurate in terms of the delayed outcome, such as prognosis and rehabilitation planning.

Cerebral Oxygenation Monitoring for Detecting Critical Cerebral Hypoperfusion in Patients with Multiple System Atrophy during the Head-up Tilt Test

Near infrared spectroscopy (NIRS) is a non-invasive optical technique to monitor cerebral tissue oxygen saturation (ScO(2)). The purpose of this study was to reveal the usefulness of ScO(2) monitoring in evaluating cerebral circulation in patients with autonomic failure. Nineteen patients with multiple system atrophy (MSA), who had autonomic failure, and 10 age-matched normal control subjects participated. In addition to blood pressure monitoring, ScO(2) was recorded by a near-infrared spectroscopy instrument during head-up tilt (HUT) test. HUT tests induced postural symptoms in 9 MSA patients (presyncopal group), but not in 10 MSA patients (non-presyncopal group) or in any of the controls. ScO(2), which decreased slightly in the controls and MSA patients, did not differ significantly between the MSA and control groups. With regard to MSA subgroups, the ScO(2) reduction in the presyncopal group (-3.1+/-1.7%) was significantly larger than in the non-presyncopal group (-0.9+/-0.5%, P<0.005) and controls (-1.1+/-1.0%, P<0.05). The systolic blood pressure decreases during HUT in the non-presyncopal (-35.2+/-16.1 mmHg, P<0.01) and presyncopal (-54.3+/-27.5 mmHg, P<0.0005) groups were significantly greater than that in the control group (4.0+/-10.7 mmHg), but the difference between presyncopal and non-presyncopal groups was not significant. In our study, ScO(2) reduction seemed to be associated with presyncopal symptoms. ScO(2) monitoring may be useful to detect cerebral hypoperfusion in MSA patients with autonomic failure.

Blood Pressure Reduction for Vascular Risk

The importance of lowering blood pressure (BP) in hypertensive subjects is well-known and recent studies suggest that lowering of BP in patients who may already be in the normotensive range further reduces the risk of vascular events, particularly stroke. Epidemiological data have also shown that lower BP and antihypertensive treatment may be associated with cognitive impairment once cerebrovascular disease is established. However, the relationship between hypertension and cerebrovascular disease is more complex than suggested by epidemiological or intervention studies. Cerebral imaging studies have shown that cerebral blood flow (CBF) is reduced in areas of small-vessel disease (SVD) and the degree of hypoperfusion correlates with disease severity. Furthermore, impaired neuropsychological performance has been found to correlate with cerebral hypoperfusion in patients with established SVD. These findings raise questions surrounding the desirability of lowering of BP beyond a certain level in such patients. It is conceivable that indiscriminate BP reduction may compromise cerebral perfusion and function in these patients, increasing the risk of cognitive decline and cerebrovascular disease progression. Randomized clinical trials addressing the relationship between antihypertensive treatment and vascular cognitive impairment are lacking. Further studies are therefore needed to assess the cognitive consequences of BP reduction in people with established cerebrovascular disease. This will help to direct appropriate protective strategies and treatments in a vulnerable group of people, many of whom have hypertension and cerebrovascular disease at the same time.

Regional cerebral hypoperfusion in patients with celiac disease

Background Neurological and psychiatric disorders occur in approximately 10% of patients with celiac disease. Although some of these alterations respond to a gluten-free diet, the etiology of these abnormalities is uncertain. Because of a case report that cerebral hypoperfusion in a celiac patient resolved after a gluten-free diet, we studied brain perfusion changes in untreated celiac patients, treated celiac patients, and healthy controls. Methods A total of 15 untreated celiac patients without conditions affecting brain perfusion were enrolled; none had neurological or psychiatric disorders other than anxiety or depression. We also studied 15 celiac patients who were on a gluten-free diet for almost 1 year, and 24 healthy volunteers of similar sex and age. All subjects underwent cerebral single photon emission computed tomography examination. Results Of the 15 untreated celiac patients, 11 (73%) had at least one hypoperfused brain region, compared with only 1 (7%) of the 15 celiac patients on a gluten-free diet and none of the controls ( P = 0.01). Cerebral perfusion was significantly lower ( P <0.05) in untreated celiac patients, compared with healthy controls, in 7 of 26 brain regions. No significant differences in cerebral perfusion were found between celiac patients on a gluten-free diet and healthy controls. Conclusion There is evidence of regional cerebral blood flow alteration in untreated celiac patients.

Flujo sanguíneo en la hemorragia cerebral. ¿Hay hipoperfusión asociada? Un estudio con doppler transcraneal

To evaluate, using transcranial Doppler, changes in parameters in patients with cerebral hematoma, as compared with controls, for detection of possible regional hypoperfusion. We studied 24 patients with cerebral hematomas and 15 healthy volunteers. The volume of the hematoma and the hypodense area was determined by computerized axial tomography of the skull at the time of admission. The average speed and index of pulsation of the anterior, middle and posterior cerebral arteries were measured in both hemispheres using transcranial Doppler within the first 100 hours. The differences between the averages were analysed using the ANOVA test and the correlations with Pearson's coefficient of correlation. The average speeds, except in the anterior cerebral artery, were lower in both hemispheres in the patients than in the controls (p < 0.001). There were interhemispherical differences in the average speeds in the patients (p = 0.06). The indices of pulsatility were greater in both hemispheres in the patients than in the controls (p < 0.001). These differences were independent of age, sex and arterial blood pressure. The average speed in the ipsilateral middle cerebral artery showed excellent correlation with the size of the hypodense area (r = -0.92) and the hematoma (r = -0.89). The indices of pulsatility showed little correlation with the size of the lesion. There was moderate correlation between transcranial Doppler and clinical scales. Transcranial Doppler detects cerebral hypoperfusion in patients with hematoma. The excellent correlation of the average speed in the middle cerebral artery with the size of the lesion and the low correlation of the indices of pulsatility, which did not show interhemispherical asymmetry, suggest that the mechanisms of hipoperfusion are different from the intracranial hypertension.

Compensatory mechanisms for chronic cerebral hypoperfusion in patients with carotid occlusion.

The purpose of this experiment was to assess long-term cerebral hemodynamic and metabolic changes in patients with increased oxygen extraction fraction (OEF) in the hemisphere distal to an occluded carotid artery who remain free of stroke. Methods--Ten patients with increased OEF and no interval stroke underwent repeated positron emission tomography examinations 12 to 59 months after the initial examination. Quantitative regional measurements of cerebral blood flow, cerebral blood volume, cerebral rate of oxygen metabolism (CMRO2), and OEF were obtained. Regional measurements of the cerebral rate of glucose metabolism (CMRGlc) were made on follow-up in 5 patients. Statistical significance (P<0.05) was measured with t tests and linear regression analysis. The ipsilateral/contralateral OEF ratio declined from a mean of 1.16 to 1.08 (P=0.022). Greater reductions were seen with longer duration of follow-up (P=0.023, r=0.707). The cerebral blood flow ratio improved from 0.81 to 0.85 (P=0.021). No change in cerebral blood volume or CMRO2 was observed. CMRGlc was reduced in the ipsilateral hemisphere (P=0.001 compared with normal), but the CMRO2/CMRGlc ratio was normal. Increased OEF improves in patients with carotid occlusion and no interval stroke. This improvement in OEF is due to an improvement in collateral blood flow.

Abnormal Cerebral Blood Flow Associated with Antiphospholipid Antibody Syndrome —Four Case Reports—

Patients with antiphospholipid antibody syndrome manifesting as neurological symptoms (one patient with twice repeated cerebral ischemic symptoms in the left parietal and frontal lobes, and the other patient with cerebral infarction of the right temporal lobe) and non-neurological symptoms (one patient with occlusion of the superior mesenteric artery and the other patient with thrombophlebitis) underwent cerebral blood flow (CBF) studies using xenon-enhanced computed tomography. The patients with neurological symptoms had decreased CBF at the affected sites. The patients with non-neurological symptoms had decreased CBF in the left parietal and temporal lobes and/or corona radiata. Subtle preclinical thrombosis may cause chronic cerebral hypoperfusion in patients with antiphospholipid antibody syndrome.