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Biomedical subjects

William J Powers

Publications and source records attributed to William J Powers.

15 recordsLinked to original sources
PubMed2006

National Institute of Neurological Disorders and Stroke-Canadian Stroke Network vascular cognitive impairment harmonization standards.

BACKGROUND AND PURPOSE: One in 3 individuals will experience a stroke, dementia or both. Moreover, twice as many individuals will have cognitive impairment short of dementia as either stroke or dementia. The commonly used stroke scales do not measure cognition, while dementia criteria focus on the late stages of cognitive impairment, and are heavily biased toward the diagnosis of Alzheimer disease. No commonly agreed standards exist for identifying and describing individuals with cognitive impairment, particularly in the early stages, and especially with cognitive impairment related to vascular factors, or vascular cognitive impairment. METHODS: The National Institute for Neurological Disorders and Stroke (NINDS) and the Canadian Stroke Network (CSN) convened researchers in clinical diagnosis, epidemiology, neuropsychology, brain imaging, neuropathology, experimental models, biomarkers, genetics, and clinical trials to recommend minimum, common, clinical and research standards for the description and study of vascular cognitive impairment. RESULTS: The results of these discussions are reported herein. CONCLUSIONS: The development of common standards represents a first step in a process of use, validation and refinement. Using the same standards will help identify individuals in the early stages of cognitive impairment, will make studies comparable, and by integrating knowledge, will accelerate the pace of progress.

Brain↗
PubMed2005

Indications for cerebral revascularization for patients with atherosclerotic carotid occlusion.

Patients with complete carotid occlusion and recent ischemic symptoms are at high risk for subsequent stroke, particularly those with evidence of severe hemodynamic impairment due to poor collateral flow. Treatment options for these patients include direct extracranial to intracranial arterial bypass, or interventions aimed at improving collateral sources of flow such as endarterectomy or angioplasty and stenting of the ipsilateral external carotid artery, the contralateral carotid artery, or the vertebral arteries. The evidence supporting the use of these procedures for patients with complete occlusion of the carotid artery will be the focus of this article. The use of physiologic imaging to select subgroups of patients at high risk due to hemodynamic factors will also be discussed.

Journal Article↗
PubMed2005

Effect of normal saline bolus on cerebral blood flow in regions with low baseline flow in patients with vasospasm following subarachnoid hemorrhage.

OBJECT: Arterial vasospasm is the most common cause of delayed ischemic neurological deficits (DINDs) and one of the major causes of disability following subarachnoid hemorrhage (SAH). Current management of vasospasm involves intravascular volume expansion and hemodynamic augmentation with the goal of increasing cerebral blood flow (CBF). The purpose of this study was to examine the effects of volume expansion on regional (r)CBF in patients with DIND following SAH. METHODS: The authors measured quantitative rCBF on positron emission tomography (PET) scans in six patients with aneurysmal SAH who had developed clinical signs of vasospasm. All patients were kept in a euvolemic state prior to the onset of vasospasm. At the onset of vasospasm, global and rCBF were measured before and after the administration of a normal saline bolus of 15 ml/kg administered over 1 hour. Two patients then received saline infusions of 5 ml/kg x hr over the following 2 to 3 hours and underwent hourly serial CBF measurements. Global and rCBF data were calculated in each patient. The mean rCBF in areas with low flow at baseline (< or = 25 ml/[100 g x min]) increased from 19.1 +/- 3.0 to 29.9 +/- 9.7 ml/(100 g x min) (p = 0.02) with volume expansion. This change was sustained over the following 2 to 3 hours. Pulmonary capillary wedge pressure, mean arterial blood pressure, cardiac output, and central venous pressure did not change significantly during this intervention. CONCLUSIONS: In euvolemic patients with vasospasm, intravascular volume expansion with a normal saline bolus raised CBF in regions of the brain most vulnerable to ischemia.

Adult↗
PubMed2004

Primary angiitis of the central nervous system at conventional angiography.

PURPOSE: To retrospectively determine the sensitivity and specificity of cerebral angiography for the diagnosis of primary angiitis of the central nervous system (CNS). MATERIALS AND METHODS: Institutional review board approval was obtained, and informed consent was not required. Thirty-eight patients (13 men, 25 women; mean age, 55 years) had undergone cerebral angiography followed by cortical and leptomeningeal biopsy for possible primary angiitis of the CNS during an 8-year period. Angiography reports were reviewed by investigators blinded to the results of biopsy. Angiographic findings were categorized as typical for vasculitis, normal, or other. Sensitivity and specificity of cerebral angiography for the diagnosis of primary angiitis of the CNS were calculated. RESULTS: Fourteen patients had typical angiographic findings of vasculitis. None had primary angiitis of the CNS at brain biopsy (60% specificity). Specific pathologic diagnoses other than primary angiitis of the CNS were made in six patients. Findings of brain biopsy in the remaining eight patients were nondiagnostic. Repeat angiograms were obtained in three of the eight patients. One patient demonstrated interval improvement in multiple focal intracranial arterial stenoses and two demonstrated worsening. Primary angiitis of the CNS was found at biopsy in two of the remaining 24 patients (0% sensitivity). One of the two patients had slow filling of a single distal cortical artery, and the other patient had multiple regions of abnormally prolonged capillary blush. CONCLUSION: In this series, patients suspected of having primary angiitis of the CNS on the basis of clinical and angiographic findings did not have primary angiitis of the CNS at biopsy. Typical angiographic findings of primary angiitis of the CNS are often associated with other specific pathologic diagnoses, which emphasizes the importance of brain biopsy.

Adult↗
PubMed2004

Activation of human medial prefrontal cortex during autonomic responses to hypoglycemia.

Studies in humans implicate the medial prefrontal cortex (MPFC) in complex cognitive and emotional states. We measured regional cerebral blood flow (CBF) four times each during euglycemia (5.2 +/- 0.2 mmol/liter) and hypoglycemia (3.0 +/- 0.3 mmol/liter) in nine normal human volunteers. Autonomic responses during hypoglycemia were manifested by increases in neurogenic symptoms, heart rate, and plasma levels of epinephrine, norepinephrine, and pancreatic polypeptide. Typical symptoms of hypoglycemia were mild, and none reflected evidence of cognitive or emotional stress. Quantitative CBF fell 6-8% in the cerebrum, brainstem, and cerebellum. Analysis of regional CBF differences identified neuronal activation during hypoglycemia in bilateral MPFC (areas 24 and 32) and bilateral thalamus. These results provide evidence that the MPFC participates in the autonomic responses to simple physiological stimuli in humans.

Adolescent↗
PubMed2003

Prognosis of patients with suspected primary CNS angiitis and negative brain biopsy.

The authors retrospectively analyzed 25 patients who had a nondiagnostic brain biopsy for clinically suspected primary CNS angiitis to determine the effect of immunosuppressive therapy on 1-year outcome. Good outcome was seen in 6 of 10 treated patients and in 8 of 15 untreated patients (p= 0.93). These findings do not indicate that the addition of immunosuppressive therapy significantly enhances outcome of patients with clinically suspected primary angiitis of the CNS and a nondiagnostic brain biopsy.

Adult↗
PubMed2003

The Carotid Occlusion Surgery Study.

The St. Louis Carotid Occlusion Study demonstrated that ipsilateral increased O2 extraction fraction (OEF) (Stage II hemodynamic failure) measured by positron emission tomography (PET) is a powerful independent risk factor for subsequent stroke in patients with symptomatic complete carotid artery (CA) occlusion. The ipsilateral ischemic stroke rate at 2 years has been shown to be 5.3% in 42 patients with normal OEF and 26.5% in 39 patients with increased OEF (p = 0.004). In patients in whom hemispheric symptoms developed within 120 days, the 2-year ipsilateral stroke rates were 12% in 27 patients with normal OEF and 50% in 18 patients with increased OEF. Previous PET studies have demonstrated that anastomosis of the superficial temporal artery (STA) to a middle cerebral artery (MCA) cortical branch can restore OEF to normal. The authors discuss the undertaking of a study that will test the hypothesis that STA-MCA anastomosis, when combined with the best medical therapy, can reduce ipsilateral ischemic stroke by 40% at 2 years in patients with symptomatic internal CA occlusion and Stage II hemodynamic failure occurring within 120 days after surgery. Only patients with increased OEF distal to a symptomatic occluded CA will be randomized to surgery or medical treatment. The primary endpoint will be all strokes and death occurring between randomization and the 30-day postoperative cut off (with an equivalent period in the nonsurgical group), as well as subsequent ipsilateral ischemic stroke developing within 2 years. It is estimated that 186 patients will be required in each group. Assuming that 40% of PET scans will demonstrate increased OEF, this will require enrolling 930 clinically eligible individuals.

Anticoagulants↗
PubMed2003

The use of positron emission tomography in cerebrovascular disease.

Even with rapid development of other neuroimaging modalities such as MR imaging and CT, PET is the only technique that provides accurate, quantitative measurements of regional hemodynamics and metabolism in human subjects. Through the use of these combined measurements, we have greatly expanded our knowledge of the pathophysiology of cerebrovascular disease of different types. It has been possible to document the compensatory responses of the brain to reductions in perfusion pressure and to directly relate these responses to prognosis. PET measurements of OEF identify a subgroup of patients who have carotid occlusion and who are at increased risk for recurrent stroke who cannot be identified by any other clinical or arteriographic means. These measurements of OEF are being used to identify high-risk patients for inclusion in a clinical trial to assess the efficacy of surgical revascularization in reducing the subsequence of ipsilateral ischemic stroke. In acute ischemic stroke, attempts have been made to define the "ischemic penumbra" and to predict tissue viability and clinical outcome, although the reliability of PET markers of ischemia in distinguishing viable from irreversibly damaged tissue needs to be confirmed with independent data sets. Much work has been devoted to the investigation of the metabolic effects of infarcts and hemorrhages on remote areas of the brain; the clinical importance of such findings appears to be minimal. Early studies of recovery from stroke suggested functional reorganization of the brain, but further investigations with more rigorous experimental design need to be performed. Given the case of performing such studies with functional MR imaging, it is likely that this technology will supplant PET for this specific indication. The importance of ischemia as a secondary mechanism of brain injury has been addressed in ICH and SAH. PET demonstrated that hematomas exert a primary depression of metabolism rather than inducing ischemia in the surrounding tissue. It also documented the integrity of autoregulation and provided clinically useful information regarding the safety of blood pressure reduction after ICH. Studies in SAH have differentiated the primary effects of the hemorrhage on cerebral hemodynamics and metabolism from those of vasospasm. PET studies are time-consuming, expensive, and require extensive facilities and technical support. In the field of cerebrovascular disease, PET has served as a specialized research tool at a few centers to help elucidate the pathophysiology of stroke. Up until now, however, PET scans in individual patients have not been demonstrated to be necessary for making patient care decisions. Whether the role of PET expands to impact the management of individual patients will depend on the results of investigations like the Carotid Occlusion Surgery Study that directly assess the ability of PET to influence patient outcome.

Acute Disease↗
PubMed2003

Measurement of cerebral blood flow in chronic carotid occlusive disease: comparison of dynamic susceptibility contrast perfusion MR imaging with positron emission tomography.

BACKGROUND AND PURPOSE: Our purpose was to evaluate the accuracy of cerebral blood flow (CBF) measurements obtained by using dynamic susceptibility contrast-enhanced MR imaging, including the influence of arterial input function (AIF) selection, compared with those obtained by using [(15)O]-H(2)O positron emission tomography (PET) for patients with chronic carotid occlusion. METHODS: MR images and PET scans were obtained of seven patients with unilateral carotid occlusion and were co-registered for region of interest analysis. PET CBF maps were generated by using the autoradiographic method. MR imaging CBF maps were calculated by deconvolution of the susceptibility time curve with a proximal middle cerebral artery AIF and were converted to absolute flow rates either by assuming a constant contralateral white matter CBF value of 22 mL/100 mL/min or by using individually determined PET white matter CBF values. RESULTS: Although CBF values measured by PET and MR imaging were positively correlated for every patient, the slopes and y intercepts of the regression lines varied widely among patients. The correlation was better when individual white matter CBF values measured by PET were used to scale the white matter CBF values measured by MR imaging (r = 0.84, P <.0001) than when constant contralateral CBF values were assumed (r = 0.54, P <.0001). The choice of AIF ipsilateral or contralateral to the occluded carotid artery made no statistically significant difference (P >.05) to the correlation coefficient, slope, or y intercept of the MR imaging versus PET CBF regressions for six of the seven patients. CONCLUSION: Although linearly correlated with CBF values measured by PET, dynamic susceptibility contrast-enhanced MR imaging was not accurate for measuring absolute CBF values. AIF selection relative to the side of carotid occlusion did not significantly affect calculated MR imaging CBF values for six of the seven patients.

Aged↗
PubMed2002

Variability of cerebral blood volume and oxygen extraction: stages of cerebral haemodynamic impairment revisited.

The presence or degree of haemodynamic impairment due to occlusive cerebrovascular disease is often inferred from measurements of cerebral blood flow (CBF), cerebral blood volume (CBV), oxygen extraction fraction (OEF) and the cerebral rate for oxygen metabolism (CMRO2). However, the relationship of these variables, in particular CBV, to regional cerebral haemodynamics is not clearly established in humans with subacute or chronic disease. In the present study, we investigated the relationship of CBV to OEF, CBF and CMRO2, and to subsequent stroke risk in patients with unilateral carotid artery occlusion, in order to define better the associated haemodynamic and metabolic changes. We reviewed data from 81 patients with symptomatic carotid occlusion enrolled in a prospective study of haemodynamic factors and stroke risk. Measurements of CBV, CBF, OEF and CMRO2 were made on entry using PET. Patients were divided into groups by hemispheric ratios and absolute ipsilateral values of OEF and CBV, based on comparison with normal controls. Haemodynamic and metabolic values, risk factors and stroke risk were compared between groups. Based on hemispheric ratios, 45 patients had increased ipsilateral OEF; CBV was increased in 19 of these 45 patients. No differences in CBF, CMRO2 or clinical risk factors were found between these 19 patients and the remaining 26 patients with increased OEF and normal or reduced CBV. Thirteen ipsilateral strokes occurred during follow-up, and 10 of the 13 occurred in the 19 patients with increased OEF and CBV (log rank P < 0.0001). Thirty-two of the 68 patients with complete quantitative PET data had increased OEF by absolute ipsilateral values. CBV was increased in 20 of the 32 patients. No differences in CBF, CMRO2 or clinical risk factors were found between these 20 patients and the remaining 12 patients with increased OEF and normal CBV. Seven of the nine ipsilateral strokes that occurred in the 68 patients occurred in those 20 patients with increased OEF and increased CBV (log rank P = 0.003). The higher risk of ischaemic stroke in patients with increased OEF and CBV suggests that their degree of haemodynamic compromise is more severe than those with increased OEF and normal CBV. In patients with chronic carotid occlusion and increased OEF, increased CBV may indicate pronounced vasodilation due to exhausted autoregulatory vasodilation. The physiological explanation for the measurement of normal CBV in patients with increased OEF is less certain and may reflect preserved autoregulatory capacity.

Adult↗
PubMed2002

Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury.

OBJECT: Recently, concern has been raised that hyperventilation following severe traumatic brain injury (TBI) could lead to cerebral ischemia. In acute ischemic stroke, in which the baseline metabolic rate is normal, reduction in cerebral blood flow (CBF) below a threshold of 18 to 20 ml/100 g/min is associated with energy failure. In severe TBI, however, the metabolic rate of cerebral oxygen (CMRO2) is low. The authors previously reported that moderate hyperventilation lowered global hemispheric CBF to 25 ml/100 g/min but did not alter CMRO2. In the present study they sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/ min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2). METHODS: Two groups of patients were studied. The moderate hyperventilation group (nine patients) underwent hyperventilation to PaCO2 of 30 +/- 2 mm Hg early after TBI, regardless of intracranial pressure (ICP). The severe hyperventilation group (four patients) underwent hyperventilation to PaCO2 of 25 +/- 2 mm Hg 1 to 5 days postinjury while ICP was elevated (20-30 mm Hg). The ICP, mean arterial blood pressure, and jugular venous O2 content were monitored, and cerebral perfusion pressure was maintained at 70 mm Hg or higher by using vasopressors when needed. All data are given as the mean +/- standard deviation unless specified otherwise. The moderate hyperventilation group was studied 11.2 +/- 1.6 hours (range 8-14 hours) postinjury, the admission Glasgow Coma Scale (GCS) score was 5.6 +/- 1.8, the mean age was 27 +/- 9 years, and eight of the nine patients were men. In the severe hyperventilation group, the admission GCS score was 4.3 +/- 1.5, the mean age was 31 +/- 6 years, and all patients were men. Positron emission tomography measurements of regional CBF, cerebral blood volume, CMRO2, and oxygen extraction fraction (OEF) were obtained before and during hyperventilation. In all 13 patients an automated search routine was used to identify 2.1-cm spherical nonoverlapping regions with CBF values below thresholds of 20, 15, and 10 ml/ 100 g/min during hyperventilation, and the change in CMRO2 in those regions was determined. In the regions in which CBF was less than 20 ml/100 g/min during hyperventilation, it fell from 26 +/- 6.2 to 13.7 +/- 1 ml/ 100 g/min (p < 0.0001), OEF rose from 0.31 to 0.59 (p < 0.0001), and CMRO2 was unchanged (1.12 +/- 0.29 compared with 1.14 +/- 0.03 ml/100 g/min; p = 0.8). In the regions in which CBF was less than 15 ml/100 g/min during hyperventilation, it fell from 23.3 +/- 6.6 to 11.1 +/- 1.2 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.63 (p < 0.0001), and CMRO2 was unchanged (0.98 +/- 0.19 compared with 0.97 +/- 0.23 ml/100 g/min; p = 0.92). In the regions in which CBF was less than 10 ml/100 g/min during hyperventilation, it fell from 18.2 +/- 4.5 to 8.1 +/- 0 ml/100 g/min (p < 0.0001), OEF rose from 0.3 to 0.71 (p < 0.0001), and CMRO2 was unchanged (0.78 +/- 0.26 compared with 0.84 +/- 0.32 ml/100 g/min; p = 0.64). CONCLUSIONS: After severe TBI, brief hyperventilation produced large reductions in CBF but not energy failure, even in regions in which CBF fell below the threshold for energy failure defined in acute ischemia. Oxygen metabolism was preserved due to the low baseline metabolic rate and compensatory increases in OEF; thus, these reductions in CBF are unlikely to cause further brain injury.

Adolescent↗