Relation of cerebral blood flow to neurological status and outcome in head-injured patients

1979 ◽  
Vol 51 (3) ◽  
pp. 292-300 ◽  
Author(s):  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Hiromu Segawa ◽  
Carol A. Dolinskas ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vegetative State ◽  
Persistent Vegetative State ◽  
Low Oxygen ◽  
Content Type ◽  
Head Injured ◽  
Luxury Perfusion ◽  
Injured Patients ◽  
Fine Print

✓ Noninvasive studies of regional cerebral blood flow (CBF) were performed on 36 head-injured patients in varying degrees of coma, using the intravenous xenon-133 method. Serial examinations, averaging four per patient, were begun during the acute phase of illness and continued until death or recovery of normal consciousness. Comparison of the initial and final studies revealed that CBF declined to very low levels in all nine patients who died, and remained subnormal in a patient with persistent vegetative state. In contrast, 25 of 26 patients who recovered consciousness showed increases in blood flow. Because of the presence of both reduced and elevated blood flows on the initial study, CBF was not predictive of outcome. Absolute or relative hyperemia, observed in nine acute cases, was associated with either diffuse cerebral swelling (observed on computerized tomography) or recovery from systemic shock. Cerebral metabolic studies in hyperemic patients yielded a very low oxygen uptake and arteriovenous oxygen difference, indicating that the high blood flow was a true “luxury perfusion.” When instances of presumed luxury perfusion were excluded, CBF was positively correlated with level of consciousness, assessed on a four-point coma scale.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury

2002 ◽  
Vol 97 (5) ◽  
pp. 1045-1053 ◽  
Author(s):  
Matthias Oertel ◽  
Daniel F. Kelly ◽  
Jae Hong Lee ◽  
David L. McArthur ◽  
Thomas C. Glenn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Induced Hypertension ◽  
Metabolic Suppression ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

2001 ◽  
Vol 94 (3) ◽  
pp. 403-411 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
Janet M. Vargo ◽  
Carla A. Erickson ◽  
Richard L. Sutton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Hyperbaric Oxygenation ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Brain Injured ◽  
Csf Lactate ◽  
Injured Patients ◽  
Fine Print

Object. Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm. Methods. Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber. Conclusions. The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.

Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia

1991 ◽  
Vol 75 (5) ◽  
pp. 685-693 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar ◽  
Sung C. Choi ◽  
Pauline G. Newlon ◽  
Harold F. Young
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Neurological Status ◽  
Content Type ◽  
Head Injured ◽  
Adult Head ◽  
Injured Patients

✓ Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 ± 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p < 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF ≤ 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.

Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow

1992 ◽  
Vol 77 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar ◽  
Kuniaki Bandoh ◽  
Anthony Marmarou
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Tissue Stiffness ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of induced alterations in blood pressure on ICP and brain stiffness as indicated by the pressure-volume index (PVI) was studied during 58 tests of autoregulation of cerebral blood flow in 47 comatose head-injured patients. In patients with intact autoregulation mechanisms, lowering the blood pressure caused a steep increase in ICP (from 20 ± 3 to 30 ± 2 mm Hg, mean ± standard error of the mean), while raising blood pressure did not change the ICP. When autoregulation was defective, ICP varied directly with blood pressure. Accordingly, with intact autoregulation, a weak positive correlation between PVI and cerebral perfusion pressure was found; however, with defective autoregulation, the PVI was inversely related to cerebral perfusion pressure. The various blood pressure manipulations did not significantly alter the cerebral metabolic rate of oxygen, irrespective of the status of autoregulation. It is concluded that the changes in ICP can be explained by changes in cerebral blood volume due to cerebral vasoconstriction or dilatation, while the changes in PVI can be largely attributed to alterations in transmural pressure, which may or may not be attenuated by cerebral arteriolar vasoconstriction, depending on the autoregulatory status. The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high. On the other hand, induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should only be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.

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.

Cerebral blood flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions

1988 ◽  
Vol 68 (3) ◽  
pp. 424-431 ◽  
Author(s):  
Carl-Henrik Nordström ◽  
Kenneth Messeter ◽  
Göran Sundbärg ◽  
Wilhelm Schalén ◽  
Mats Werner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Lesions ◽  
Barbiturate Coma ◽  
Content Type ◽  
Cerebral Metabolic Rate ◽  
Head Injured ◽  
Barbiturate Therapy ◽  
Injured Patients ◽  
Cerebral Vasoreactivity

✓ Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (ΔCBF/ΔPaCO2 ≥ 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (ΔCBF/ΔPaCO2 < 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

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.

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