Dissociation of cerebral blood flow, glucose metabolism, and electrical activity in pediatric brain death

1993 ◽  
Vol 79 (5) ◽  
pp. 752-755 ◽  
Author(s):  
Michael D. Medlock ◽  
William C. Hanigan ◽  
Robert P. Cruse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Brain Death ◽  
Electrical Activity ◽  
Closed Head Injury ◽  
Content Type ◽  
Positron Emission ◽  
Mononuclear Cell Infiltrates ◽  
Fine Print

✓ A 2-month-old infant demonstrated clinical brain death 48 hours after suffering a closed head injury accompanied by cardiac arrest. Two nuclear cerebral blood flow (CBF) studies demonstrated normal perfusion. On the 11th day following injury, cerebral electrical activity ceased and a normal glucose metabolic gradient between gray and white matter was documented on positron emission tomography. Autopsy revealed widespread necrosis with mononuclear cell infiltrates throughout all cerebral cortical layers. Nine children have previously been described with clinical brain death, electrocerebral silence, and evidence of CBF by radionuclide scan. The dissociation between cerebral electrical activity and blood flow may be explained by an increase in cranial volume allowed by the expansile neonatal skull, preventing both intracranial hypertension and a reduction in perfusion pressure. The persistence of glucose metabolism may be associated with the presence of inflammatory microglial cells in the ischemic cortex. The authors conclude that persistence of CBF and glucose metabolism in brain-dead children may not indicate neuronal survival. If repeated neurological examinations with or without electroencephalography support the diagnosis of brain death, the presence of CBF and glucose metabolism should not alter this conclusion.

Improvement in cerebral blood flow and metabolism following subarachnoid hemorrhage in response to prophylactic administration of the hydroxyl radical scavenger, AVS, (±)-N,N′-propylenedinicotinamide: a positron emission tomography study in rats

2000 ◽  
Vol 92 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Seiji Yamamoto ◽  
Weiyu Teng ◽  
Shigeru Nishizawa ◽  
Takeharu Kakiuchi ◽  
Hideo Tsukada
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Emission Tomography ◽  
Radical Scavenger ◽  
Content Type ◽  
Prophylactic Administration ◽  
Positron Emission ◽  
Hydroxyl Radical Scavenger ◽  
Fine Print

Object. The hydroxyl radical scavenger (±)-N,N′-propylenedinicotinamide (AVS) has been shown to ameliorate the occurrence of vasospasm following experimental subarachnoid hemorrhage (SAH) and to reduce the incidence of delayed ischemic neurological deficits (DINDs) in patients with SAH. The authors investigated whether prophylactic administration of AVS could improve cerebral blood flow (CBF) and cerebral glucose utilization (CGU) following SAH in rats.Methods. Anesthetized rats were subjected to intracisternal injection of blood (SAH group) or saline (control group). Either AVS (1 mg/kg/min) or saline (vehicle group) was continuously injected into the rat femoral vein. Forty-eight hours later, positron emission tomography scanning was used with the tracers 15O-H2O and 18F-2-fluoro-d-glucose to analyze quantitatively CBF and CGU, respectively, in the frontoparietal and occipital regions (12 regions of interest/group).In SAH rats receiving only vehicle, CBF decreased significantly (p < 0.05, Tukey's test) and CGU tended to decrease, compared with values obtained in control (non-SAH) rats receiving vehicle. In rats that were subjected to SAH, administration of AVS significantly (p < 0.05, Tukey's test) improved CBF and CGU in both the frontoparietal and occipital regions compared with administration of vehicle alone.Conclusions. Prophylactic administration of AVS improves CBF and CGU in the rat brain subjected to SAH, and can be a good pharmacological treatment for the prevention of DINDs following SAH.

Cerebral blood flow and metabolism in severely head-injured children

1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cerebral Blood Volume ◽  
Closed Head Injury ◽  
Volume Index ◽  
Content Type ◽  
Gcs Score ◽  
Fine Print

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.

Changes in cerebral blood flow during PaCO2 variations in patients with severe closed head injury: comparison between the Fick and transcranial Doppler methods

1998 ◽  
Vol 88 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
Aram Ter Minassian ◽  
Eliane Melon ◽  
Caroline Leguerinel ◽  
Carlo Alberto Lodi ◽  
Françis Bonnet ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Transcranial Doppler ◽  
Closed Head Injury ◽  
High Group ◽  
Content Type ◽  
Closed Head ◽  
Fine Print ◽  
Group 1

Object. The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. Methods. The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, “high” and “low,” with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (Δ)AVDO2 and ΔMCAv was not different from identity in the low group (1/ΔAVDO2 = 1.08 × ΔMCAv − 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/ΔAVDO2 = 1.46 × ΔMCAv − 0.4, r = 0.83, p < 0.001). Conclusions. In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.

Pulsatile cerebral echo in diagnosis of brain death

1978 ◽  
Vol 48 (6) ◽  
pp. 866-875 ◽  
Author(s):  
Sumio Uematsu ◽  
Thomas D. Smith ◽  
A. Earl Walker
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Death ◽  
Simple Method ◽  
Cerebral Angiogram ◽  
Content Type ◽  
Cerebral Pathology ◽  
Conclusive Diagnosis ◽  
Electroencephalogram Eeg ◽  
Fine Print

✓ Conclusive diagnosis of brain death can be made by the demonstration of prolonged cessation of cerebral blood flow. This report describes a simple method to determine the presence or absence of the blood flow in the brain by recording the pulsatile midline echo on one channel of the electroencephalogram (EEG) or on any four-channel monitoring system in the intensive care unit. A firm transducer holder has been developed to eliminate artifacts caused by transducer motion. The pulsations of the midline echo are assumed to be the result of displacement of the midline structures by the arterial injection of each cardiac systole. Thus, the absence of these midline pulsatile echoes correlates with the absence of cerebral blood flow and, if the absence persists over 30 minutes in the presence of normal blood pressure, then the result is brain death. Twenty-eight cases of clinical brain death with electrocerebral silence of EEG and 18 obtunded patients with various types of cerebral pathology were examined by the echo-pulsation technique. Twenty-six of the 28 cases showed no pulsation of the midline echo. The validity of the technique was documented in four cases by four-vessel cerebral angiogram.

Influence of early posttraumatic hypothermia therapy on cerebral blood flow and glucose metabolism after fluid-percussion brain injury

1999 ◽  
Vol 90 (3) ◽  
pp. 510-519 ◽  
Author(s):  
Weizhao Zhao ◽  
Ofelia F. Alonso ◽  
Judith Y. Loor ◽  
Raul Busto ◽  
Myron D. Ginsberg
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Glucose Utilization ◽  
Linear Regression Analysis ◽  
Data Sets ◽  
Imaging Data ◽  
Content Type ◽  
Fluid Percussion ◽  
Fine Print

Object. Using autoradiographic image averaging, the authors recently described prominent foci of marked glucose metabolism-greater-than-blood-flow uncoupling in the acutely traumatized rat brain. Because hypothermia is known to ameliorate injury in this and other injury models, the authors designed the present study to assess the effects of posttraumatic therapeutic hypothermia on the local cerebral metabolic rate of glucose (LCMRglu) and local cerebral blood flow (LCBF) following moderate parasagittal fluid-percussion head injury (FPI) in rats.Methods. Either cranial hypothermia (30°C) or normothermia (37°C) was induced for 3 hours in matched groups of rats immediately after FPI; LCMRglu and LCBF were assessed 3 hours after concluding these temperature manipulations.In rats subjected to FPI, regardless of whether normothermia or hypothermia ensued, LCBF was reduced relative to the sham-injury groups. In addition, when FPI was followed by hypothermia (FPI—30°C group), the subsequent LCBF was significantly lower (35–38% on average) than in FPI—37°C rats. Statistical mapping of LCBF difference imaging data revealed confluent cortical and subcortical zones of significantly reduced LCBF (largely ipsilateral to the prior injury) in FPI—30°C rats relative to the FPI—37°C group. Local glucose utilization was reduced in both hemispheres of FPI—37°C rats relative to the sham-injury group and was lower in the right (traumatized) hemisphere than in the left. However, LCMRglu values were largely unaffected by temperature manipulation in either the FPI or sham-injury groups. The LCMRglu/LCBF ratio was nearly doubled in FPI—30°C rats relative to the FPI—37°C group, in a diffuse and bihemispheric fashion. Linear regression analysis comparing LCMRglu and LCBF revealed that the FPI—37°C and FPI—30°C data sets were completely nonoverlapping, whereas the two sham-injury data sets were intermixed.Conclusions. Despite its proven neuroprotective efficacy, early posttraumatic hypothermia (30°C for 3 hours) nonetheless induces a moderate decline in cerebral perfusion without the (anticipated) improvement in cerebral glucose utilization, so that a state of mild metabolism-greater-than-blood-flow dissociation is perpetuated.

Relationship of early cerebral blood flow and metabolism to outcome in acute head injury

1990 ◽  
Vol 72 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Jurg L. Jaggi ◽  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Vegetative State ◽  
Closed Head Injury ◽  
Total Sample ◽  
Prognostic Indicators ◽  
Content Type ◽  
Blood Flows ◽  
Fine Print

✓ Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale. The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability. Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.

Early changes measured by magnetic resonance imaging in cerebral blood flow, blood volume, and blood-brain barrier permeability following dexamethasone treatment in patients with brain tumors

1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Tumors ◽  
Mr Imaging ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Clinical Effects ◽  
Content Type ◽  
Fine Print

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.

Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Vasospasm ◽  
Trigeminal Nerve ◽  
Nerve Endings ◽  
Noninvasive Method ◽  
Direct Stimulation ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.

Cerebral blood flow and vasoresponsivity within and around cerebral contusions

1996 ◽  
Vol 85 (5) ◽  
pp. 871-876 ◽  
Author(s):  
Mark R. McLaughlin ◽  
Donald W. Marion
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Repeated Measures ◽  
Closed Head Injury ◽  
Ct Scanning ◽  
Brain Parenchyma ◽  
Secondary Brain Injury ◽  
Content Type ◽  
Repeated Measures Analysis ◽  
Surrounding Parenchyma

✓ There is increasing evidence that regional ischemia plays a major role in secondary brain injury. Although the cortex underlying subdural hematomas seems particularly vulnerable to ischemia, little is known about the adequacy of cerebral blood flow (CBF) or the vasoresponsivity within the vascular bed of contusions. The authors used the xenon-enhanced computerized tomography (CT) CBF technique to define the CBF and vasoresponsivity of contusions, pericontusional parenchyma, and the remainder of the brain 24 to 48 hours after severe closed head injury in 10 patients: six patients with one contusion and four with two contusions, defined as mixed or high-density lesions on CT scanning. The CBF within the contusions (29.3 ± 16.4 ml/100 g/minute, mean ± standard deviation) was significantly lower than both that found in the adjacent 1-cm perimeter of normal-appearing tissue (42.5 ± 15.8 ml/100 g/minute) and the mean global CBF (52.5 ± 17.5 ml/100 g/minute) (p < 0.004, repeated-measures analysis of variance). A subset of seven patients (10 contusions) also underwent a second Xe-CT CBF study during mild hyperventilation (a PaCO of 24–32 mm Hg). In only two of these 10 contusions was vasoresponsivity less than 1% (range 0%–7.6%); in the rim of normal-appearing pericontusional tissue, it was 0.4% to 9.1%. The authors conclude that CBF within intracerebral contusions is highly variable and is often above 18 ml/100 g/minute, the reported threshold for irreversible ischemia. Intracontusional CBF is significantly reduced relative to surrounding brain parenchyma, and CO2 vasoresponsivity is usually present. In the contusion and the surrounding parenchyma, vasoresponsivity may be nearly three times normal, suggesting hypersensitivity to hyperventilation therapy. Given this possible hypersensitivity and relative hypoperfusion within and around cerebral contusions, these lesions are particularly vulnerable to secondary injury such as that which may be caused by hypotension or aggressive hyperventilation.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

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