Brian R. Chambers
University of Melbourne
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Featured researches published by Brian R. Chambers.
Stroke | 2003
Tracey Baird; Mark W. Parsons; Thanh G. Phan; Kenneth Butcher; Patricia Desmond; Brian M. Tress; Peter G. Colman; Brian R. Chambers; Stephen M. Davis
BACKGROUND AND PURPOSE Hyperglycemia at the time of ischemic stroke is associated with increased mortality and morbidity. Animal studies suggest that infarct expansion may be responsible. The influence of persisting hyperglycemia after stroke has not previously been examined. We measured the blood glucose profile after acute ischemic stroke and correlated it with infarct volume changes using T2- and diffusion-weighted MRI. METHODS We recruited 25 subjects within 24 hours of ischemic stroke symptoms. Continuous glucose monitoring was performed with a glucose monitoring device (CGMS), and 4-hour capillary glucose levels (BGL) were measured for 72 hours after admission. MRI and clinical assessments were performed at acute (median, 15 hours), subacute (median, 5 days), and outcome (median, 85 days) time points. RESULTS Mean CGMS glucose and mean BGL glucose correlated with infarct volume change between acute and subacute diffusion-weighted MRI (r>or=0.60, P<0.01), acute and outcome MRI (r=0.56, P=0.01), outcome National Institutes of Health Stroke Scale (NIHSS; r>or=0.53, P<0.02), and outcome modified Rankin Scale (mRS; r>or=0.53, P=0.02). Acute and final infarct volume change and outcome NIHSS and mRS were significantly higher in patients with mean CGMS or mean BGL glucose >or=7 mmol/L. Multiple regression analysis indicated that both mean CGMS and BGL glucose levels >or=7 mmol/L were independently associated with increased final infarct volume change. CONCLUSIONS Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with worse functional outcome. There is an urgent need to study normalization of blood glucose after stroke.
The New England Journal of Medicine | 1986
Brian R. Chambers; John W. Norris
Five hundred asymptomatic patients with cervical bruits were followed prospectively by clinical and Doppler examination for up to four years (mean, 23.2 months) to identify the variables predicting outcome. Thirty-six patients had strokes or transient ischemic attacks, 51 had cardiac ischemic events, and 45 died. At one year the incidence of cerebral ischemic events (transient ischemic attacks and strokes) was 6 percent, that of cardiac ischemic events was 7 percent, and that of death was 4 percent. The overall incidence of stroke at one year was 1.7 percent (1 percent in patients without previous transient ischemic attacks), but the incidence was 5.5 percent in patients with severe carotid-artery stenosis (greater than 75 percent). Cerebral ischemic events were most frequent in patients with severe carotid-artery stenosis (P less than 0.0001), progressing carotid-artery stenosis (P less than 0.0005), or heart disease (P less than 0.0005) and in men (P less than 0.025). The degree of carotid-artery stenosis on initial presentation was a powerful predictor of neurologic sequelae. Patients with asymptomatic cervical bruits have a higher risk of a cardiac ischemic event than of a stroke. Although the risk of cerebral ischemic events is highest in patients with severe carotid-artery stenosis, in most instances even these patients do not have strokes without some warning.
Neurology | 1987
Brian R. Chambers; John W. Norris; Bette L. Shurvell; Vladimir Hachinski
We evaluated factors affecting mortality and quality of life in 1,013 patients with acute stroke followed for 2 to 8 years. In cerebral infarction, the major determinants for short-term mortality were impaired consciousness, leg weakness, and increasing age. The major determinants for long-term mortality were low level of activity at hospital discharge, advanced age, male sex, heart disease, and hypertension.
Cerebrovascular Diseases | 2005
Malcolm R. Macleod; Stephen M. Davis; Peter Mitchell; Richard P. Gerraty; Gregory J Fitt; Graeme J. Hankey; Edward G. Stewart-Wynne; D. Rosen; John J. McNeil; Christopher F. Bladin; Brian R. Chambers; Geoffrey K. Herkes; Dennis Young; Geoffrey A. Donnan
Background: Patients with ischaemic stroke due to occlusion of the basilar or vertebral arteries may develop a rapid deterioration in neurological status leading to coma and often to death. While intra-arterial thrombolysis may be used in this context, no randomised controlled data exist to support its safety or efficacy. Methods: Randomised controlled trial of intra-arterial urokinase within 24 h of symptom onset in patients with stroke and angiographic evidence of posterior circulation vascular occlusion. Results: Sixteen patients were randomised, and there was some imbalance between groups, with more severe strokes occurring in the treatment arm. A good outcome was observed in 4 of 8 patients who received intra-arterial urokinase compared with 1 of 8 patients in the control group. Conclusions: These results support the need for a large-scale study to establish the efficacy of intra-arterial thrombolysis for acute basilar artery occlusion.
Stroke | 1984
Brian R. Chambers; John W. Norris
Asymptomatic cervical bruits with their implication of underlying carotid artery disease, carry an established but low risk of stroke. In spite of the rising numbers of patients subjected to carotid endarterectomy for this condition, there is little evidence that the benefits outweigh the risks. Outcome data from community studies and the current prospective Toronto study of patients with asymptomatic neck bruits indicate that the annual stroke rate is 1-2%, and the annual cardiac death rate is 2-4%. Published data of the results of carotid surgery suggest that surgical risks outweigh any possible benefits, unless a subgroup with spontaneous stroke risk of at least 5% can be identified. Stroke Vol 15, No 6, 1984
Stroke | 2005
Anne L. Abbott; Brian R. Chambers; Jacinda L. Stork; Christopher Levi; Christopher F. Bladin; Geoffrey A. Donnan
Background and Purpose— We tested the hypothesis that transcranial Doppler embolic signal (ES) detection identifies an increased risk of ipsilateral carotid stroke or transient ischemic attack (TIA) in subjects with asymptomatic severe carotid stenosis. Methods— Subjects with duplex-determined 60% to 99% carotid stenosis, without other apparent cerebroembolic sources, underwent 6-monthly neurological assessment and 60-minute ES monitoring. ES positivity was defined as ≥1 ES detected in ≥1 study, ES negativity as no ES in any study, and consistent ES negativity as no ES in any study where ≥6 studies were performed. Rates of ipsilateral carotid stroke/TIA were calculated using Kaplan–Meier analysis and correlated with ES status using odds ratios (ORs) and Cox proportional hazards regression analysis. Results— A total of 202 subjects (138 male; mean age 74 years; mean follow-up 34 months) were recruited. The average annual rate of ipsilateral carotid stroke/TIA was 3.1%. A total of 231 arteries were monitored at least once (mean 4.3 studies/artery). Six of 60 (10.0%) ES-positive arteries had an ipsilateral carotid stroke/TIA compared with 12 of 171 (7.0%) ES-negative arteries (OR, 1.47; 95% CI, 0.43, 4.48; P=0.624) and 2 of 41 (4.9%) consistently ES-negative arteries (OR, 2.17; 95% CI, 0.36, 22.90; P=0.59). Differences in survival free of ipsilateral carotid stroke/TIA according to ES status were not statistically significant. Conclusions— Although there were more ipsilateral carotid cerebrovascular events among ES-positive arteries, this was not statistically significant. Less labor-intensive techniques are required to make further study and clinical application practical.
Journal of Clinical Neuroscience | 2002
Tracey Baird; Mark W. Parsons; P. Alan Barber; Ken S. Butcher; Patricia Desmond; Brian M. Tress; Peter G. Colman; George Jerums; Brian R. Chambers; Stephen M. Davis
Diabetes mellitus is a complex metabolic syndrome with significant effects on the systemic and cerebral vasculature. The incidence and severity of ischaemic stroke are increased by the presence of diabetes, and outcome from stroke is poorer. More than one third of patients admitted with acute stroke are hyperglycaemic at presentation. Reasons for the altered prognosis in diabetes associated stroke are multifactorial. A direct influence of hyperglycaemia at the time of ischaemia is likely to be important. The use of novel methods to delineate stroke topography and pathophysiology such as MR spectroscopy, diffusion and perfusion weighted MRI appear helpful in delineating the effects of hyperglycaemia on stroke pathophysiology. Randomised clinical trials to determine optimal management for patients with hyperglycaemia following stroke are ongoing. Such trials will determine if aggressive control of acute hyperglycaemia following stroke has similar benefits to that observed following acute myocardial infarction. Clinicians responsible for stroke patients should be aware of the importance of adequate glycaemic control in both primary and secondary prevention of stroke.
Stroke | 1993
Christopher F. Bladin; Brian R. Chambers
Background and Purpose Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction. Methods Eighteen consecutive stroke patients with evidence of internal watershed infarction on computed tomography (CT) were studied. Results Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P<.001), cardiac disease (P<.01), and diabetes mellitus (P<.01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole. Conclusions Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.
Stroke | 2002
Amanda K. Gilligan; Romesh Markus; Stephen J. Read; Velandai K. Srikanth; Teruyuki Hirano; Gregory J Fitt; M. Arends; Brian R. Chambers; Stephen M. Davis; Geoffrey A. Donnan
Background and Purpose— Intracerebral hemorrhage is the most serious complication of thrombolytic therapy for stroke. We explored factors associated with this complication in the Australian Streptokinase Trial. Methods— The initial CT scans (≤4 hours after stroke) of 270 patients were reviewed retrospectively by an expert panel for early signs of ischemia and classified into the following 3 categories: no signs or ≤1/3 or >1/3 of the vascular territory. Hemorrhage on late CT scans was categorized as major or minor on the basis of location and mass effect. Stepwise, backward elimination, multivariate logistic regression analysis was used to identify risk factors for each hemorrhage category. Results— Major hemorrhage occurred in 21% of streptokinase (SK) and 4% of placebo patients. Predictors of major hemorrhage were SK treatment (odds ratio [OR], 6.40; 95% CI, 2.50 to 16.36) and elevated systolic blood pressure before therapy (OR, 1.03; 95% CI, 1.01 to 1.05). Baseline systolic blood pressure >165 mm Hg in SK-treated patients resulted in a >25% risk of major secondary hemorrhage. Early ischemic CT changes, either ≤1/3 or >1/3, were not associated with major hemorrhage (OR, 1.58; 95% CI, 0.65 to 3.83; and OR, 1.11; 95% CI, 0.45 to 2.76, respectively). Minor hemorrhage occurred in 30% of the SK and 26% of the placebo group. Predictors of minor hemorrhage were male sex, severe stroke, early CT changes, and SK treatment. Ninety-one percent of patients with major hemorrhage deteriorated clinically compared with 23% with minor hemorrhage. Conclusions— SK increased the risk of both minor and major hemorrhage. Major hemorrhage was also more likely in patients with elevated baseline systolic blood pressure. However, early CT changes did not predict major hemorrhage. Results from this study highlight the importance of baseline systolic blood pressure as a potential cause of hemorrhage in patients undergoing thrombolysis.
Stroke | 2003
Romesh Markus; David C. Reutens; Seiji Kazui; Stephen J. Read; Peter M. Wright; Brian R. Chambers; John Sachinidis; Henri Tochon-Danguy; Geoffrey A. Donnan
Background and Purpose— We sought to characterize the spatial and temporal evolution of human cerebral infarction. Using a novel method of quantitatively mapping the distribution of hypoxic viable tissue identified by 18F-fluoromisonidazole (18F-FMISO) PET relative to the final infarct, we determined its evolution and spatial topography in human stroke. Methods— Patients with acute middle cerebral artery territory stroke were imaged with 18F-FMISO PET (n=19; <6 hours, 4; 6 to 16 hours, 4; 16 to 24 hours, 5; 24 to 48 hours, 6). The hypoxic volume (HV) comprised voxels with significant (P <0.05; >1 mL) uptake on statistical parametric mapping compared with 15 age-matched controls. Central, peripheral, and external zones of the corresponding infarct on the anatomically coregistered delayed CT were defined according to voxel distance from the infarct center and subdivided into 24 regions by coronal, sagittal, and axial planes. Maps (“penumbragrams”) displaying the percentage of HV in each region were generated for each time epoch. Results— Higher HV was observed in the central region of the infarct in patients studied within 6 hours of onset (analysis of covariance [ANCOVA]; P <0.05) compared with those studied later, in whom the HV was mainly in the periphery or external to the infarct. HV was maximal in the superior, mesial, and posterior regions of the infarct (ANCOVA; P <0.05). Conclusions— These observations suggest that infarct expansion occurs at the expense of hypoxic tissue from the center to the periphery of the ischemic region in humans, similar to that seen in experimental animal models. These findings have important pathophysiological and therapeutic implications.