Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients

2000 ◽  
Vol 93 (2) ◽  
pp. 183-193 ◽  
Author(s):  
Anthony Marmarou ◽  
Panos P. Fatouros ◽  
Pal Barzó ◽  
Gennarina Portella ◽  
Masaaki Yoshihara ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Tissue ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Brain Swelling ◽  
Tissue Water ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling.Methods. Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (± standard deviation) percentage of swelling due to water was 9.37 ± 8.7%, whereas that due to blood was −0.8 ± 1.32%.Conclusions. The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

Cerebrovascular carbon dioxide reactivity assessed by intracranial pressure dynamics in severely head injured patients

1995 ◽  
Vol 82 (3) ◽  
pp. 386-393 ◽  
Author(s):  
Masaaki Yoshihara ◽  
Kuniaki Bandoh ◽  
Anthony Marmarou
Keyword(s):  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Blood Volume ◽  
Volume Change ◽  
Volume Index ◽  
Content Type ◽  
Coma Scale ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI × Δlog(ICP)/ΔPCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.

Effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure

1987 ◽  
Vol 66 (4) ◽  
pp. 548-554 ◽  
Author(s):  
Seigo Nagao ◽  
Tsukasa Nishiura ◽  
Hideyuki Kuyama ◽  
Masakazu Suga ◽  
Takenobu Murota
Keyword(s):  
Intracranial Pressure ◽  
Reticular Formation ◽  
Cerebral Blood Volume ◽  
Systemic Arterial Pressure ◽  
Brain Swelling ◽  
Dorsomedial Nucleus ◽  
Medullary Reticular Formation ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

✓ The authors report the results of a study to evaluate the effect of stimulation of the medullary reticular formation on cerebral vasomotor tonus and intracranial pressure (ICP) after the hypothalamic dorsomedial nucleus and midbrain reticular formation were destroyed. Systemic arterial pressure (BP), ICP, and local cerebral blood volume (CBV) were continuously recorded in 32 cats. To assess the changes in the cerebral vasomotor tonus, the vasomotor index defined by the increase in ICP per unit change in BP was calculated. In 29 of the 32 animals, BP, ICP, and CBV increased simultaneously immediately after stimulation. The increase in ICP was not secondary to the increase in BP, because the vasomotor index during stimulation was significantly higher than the vasomotor index after administration of angiotensin II. The vasomotor index was high during stimulation of the area around the nucleus reticularis parvocellularis. In animals with the spinal cord transected at the C-2 vertebral level, ICP increased without a change in BP. These findings indicate that the areas stimulated in the medullary reticular formation play an important role in decreasing cerebral vasomotor tonus. This effect was not influenced by bilateral superior cervical ganglionectomy, indicating that there is an intrinsic neural pathway that regulates cerebral vasomotor tonus directly. In three animals, marked biphasic or progressive increases in ICP up to 100 mm Hg were evoked by stimulation. The reduction of cerebral vasomotor tonus and concomitant vasopressor response induced by stimulation of the medullary reticular formation may be one of the causes of acute brain swelling.

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.

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients

1987 ◽  
Vol 66 (6) ◽  
pp. 883-890 ◽  
Author(s):  
Anthony Marmarou ◽  
Angelo L. Maset ◽  
John D. Ward ◽  
Sung Choi ◽  
Danny Brooks ◽  
...  
Keyword(s):  
Severe Head Injury ◽  
Ventricular Catheter ◽  
Outflow Resistance ◽  
Content Type ◽  
Relative Contribution ◽  
Temporal Course ◽  
Head Injured ◽  
Predominant Factor ◽  
Injured Patients ◽  
Fine Print

✓ The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.

Role of hydrodynamic processes in the pathogenesis of peritumoral brain edema in meningiomas

2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  
Keyword(s):  
Contrast Agent ◽  
Brain Edema ◽  
Brain Tissue ◽  
Magnetic Resonance Images ◽  
Content Type ◽  
Extracellular Contrast Agent ◽  
Peritumoral Brain Edema ◽  
Hydrodynamic Processes ◽  
Fine Print

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

1994 ◽  
Vol 80 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Michael G. O'Sullivan ◽  
Patrick F. Statham ◽  
Patricia A. Jones ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ct Scan ◽  
Intracranial Hypertension ◽  
Mass Lesion ◽  
Midline Shift ◽  
Pressure Monitoring ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP ≥ 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP ≥ 30 mm Hg) and duration. Reduced CPP (≤ 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

High-risk mild head injury

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon
Keyword(s):  
Head Injury ◽  
High Risk ◽  
Mild Head Injury ◽  
Radiographic Findings ◽  
Content Type ◽  
Head Injured ◽  
Definition Of ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.

Acute brain edema in fatal head injury: analysis by dynamic CT scanning

1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa
Keyword(s):  
Head Injury ◽  
Brain Edema ◽  
Subdural Hematoma ◽  
Ct Scans ◽  
Acute Subdural Hematoma ◽  
Dynamic Ct ◽  
Content Type ◽  
Injured Patients ◽  
Fine Print ◽  
Diffuse Brain

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.

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