Search Results

You are looking at 31 - 40 of 255 items for :

  • "cerebrovascular reactivity" x
  • Refine by Access: all x
Clear All
Restricted access

Oxidative metabolic activity of cerebral cortex after fluid-percussion head injury in the cat

Robert B. Duckrow, Joseph C. LaManna, Myron Rosenthal, Joseph E. Levasseur, and John L. Patterson Jr.

✓ To assess the metabolic and vascular effects of head trauma, fluid-percussion pressure waves were transmitted to the brains of anesthetized, paralyzed, and artificially ventilated cats. Changes in the redox state of cytochrome a,a 3, and relative local blood volume were measured in situ by dual-wavelength reflection spectrophotometry of the cortical surface viewed through an acrylic cranial window implanted within the closed skull. Initial fluid-percussion impacts of 0.5 to 2.8 atm peak pressure produced consistent transient oxidation of cytochrome a,a 3, and increases of cortical blood volume. These changes occurred despite the presence of transient posttraumatic hypotension in some cases. Also, impact-induced alterations of vascular tone occurred, independent of the presence or absence of transient hypertension in the posttraumatic period. These data demonstrate that hypoxia does not play a role in the immediate posttraumatic period in cerebral cortex, and are consistent with the idea that after injury there is increased cortical energy conservation. These data also support the concept that head trauma alters the relationship of metabolism and cerebral circulation in the period immediately after injury.

Restricted access

Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes

J. Paul Muizelaar, Enoch P. Wei, Hermes A. Kontos, and Donald P. Becker

✓ There is no proof that osmotic agents such as mannitol lower intracranial pressure (ICP) by decreasing brain water content. An alternative mechanism might be a reduction in cerebral blood volume through vasoconstriction. Mannitol, by decreasing blood viscosity, would tend to enhance cerebral blood flow (CBF), but the cerebral vessels would constrict to keep CBF relatively constant, analogous to pressure autoregulation. The cranial window technique was used in this study to measure the pial arteriolar diameter in cats, together with blood viscosity and ICP changes after an intravenous bolus of 1 gm/kg of mannitol. Blood viscosity decreased immediately; the greatest decrease (23%) occurred at 10 minutes, and at 75 minutes there was a “rebound” increase of 10%. Vessel diameters decreased concomitantly, the largest decrease being 12% at 10 minutes, which is exactly the same as the 12% decrease in diameter associated with pronounced hyperventilation (PaCO2 30 to 19 mm Hg) in the same vessels; at 75 minutes vessel diameter increased by 12%. With hyperventilation, ICP was decreased by 26%; 10 minutes after mannitol was given, ICP decreased by 28%, and at 75 minutes it showed a rebound increase of 40%. The correlation between blood viscosity and vessel diameter and between vessel diameter and ICP was very high. An alternative explanation is offered for the effect of mannitol on ICP, the time course of ICP changes, the “rebound effect,” and the absence of influence on CBF, all with one mechanism.

Restricted access

Effect of pentobarbital on the reactivity of isolated human cerebral arteries

Jesús Marín, Ramiro D. Lobato, Mercedes L. Rico, Mercedes Salaices, and Julio Benitez

the arteriolar level would trigger a vasoconstriction of this particular sector (the Bayliss effect), thereby decreasing total CBV. Whatever the mechanism, further in vivo studies are needed to elucidate how barbiturates modify cerebrovascular dynamics in order to achieve a reduction of intracranial volume. The present experiments indicate that high doses of barbiturates used in iatrogenic coma (between 10 −4 M and 10 −3 M or even greater) decrease cerebrovascular reactivity. This evidence is indirectly supported by the observation that these agents not only

Free access

Occipital artery to middle cerebral artery bypass in pediatric moyamoya disease: rescue therapy after failed revascularization

Akikazu Nakamura, Akitsugu Kawashima, Hugo Andrade-Barazarte, Takayuki Funatsu, Juha Hernesniemi, and Takakazu Kawamata

, additional revascularization procedure, symptoms (presence or recurrence), pre- and postoperative cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) changes, PCA stenosis and progression, PCA-related and nonrelated symptoms, and latest follow-up. We evaluated anatomical features regarding PCA stenosis, progression, CBF, and CVR in the 10 hemispheres. FIG. 1. Flow diagram demonstrating the inclusion and exclusion criteria. Radiological Evaluation The patients underwent preoperative MRI, MR angiography (MRA), digital subtraction angiography (DSA), and iodine-123

Free access

Occipital artery to middle cerebral artery bypass in pediatric moyamoya disease: rescue therapy after failed revascularization

Akikazu Nakamura, Akitsugu Kawashima, Hugo Andrade-Barazarte, Takayuki Funatsu, Juha Hernesniemi, and Takakazu Kawamata

revascularization procedure, additional revascularization procedure, symptoms (presence or recurrence), pre- and postoperative cerebral blood flow (CBF) and cerebrovascular reactivity (CVR) changes, PCA stenosis and progression, PCA-related and nonrelated symptoms, and latest follow-up. We evaluated anatomical features regarding PCA stenosis, progression, CBF, and CVR in the 10 hemispheres. FIG. 1. Flow diagram demonstrating the inclusion and exclusion criteria. Radiological Evaluation The patients underwent preoperative MRI, MR angiography (MRA), digital

Restricted access

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

Masaaki Yoshihara, Kuniaki Bandoh, and Anthony Marmarou

✓ 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.

Restricted access

Cerebral oxygenation, vascular reactivity, and neurochemistry following decompressive craniectomy for severe traumatic brain injury

Chi Long Ho, Chee Meng Wang, Kah Keow Lee, Ivan Ng, and Beng Ti Ang

techniques are increasingly used in the modern NICU and have been incorporated into protocol-driven treatment regimens. 6 In addition to physiological monitoring, derived indices provide clinicians with useful information to guide targeted therapy in the neurointensive care setting. The PRx is one such index that takes advantage of the relationship between MABP and ICP by quantifying cerebrovascular reactivity and providing an approximation to the cerebrovascular autoregulatory reserve. 3 , 17 Whereas targeted protocol therapies have been shown to improve outcome, the

Restricted access

Encephaloduroarteriosynangiosis for cerebral proliferative angiopathy with cerebral ischemia

Case report

Kenichi Kono and Tomoaki Terada

around the precentral region ( Fig. 5 ). A technetium-99m–labeled ethyl cysteinate dimer ( 99m Tc-ECD) SPECT study demonstrated hypoperfusion and severely impaired cerebrovascular reactivity both without and with an acetazolamide challenge test over the affected hemisphere ( Fig. 6 left). These imaging studies showed that cerebral ischemia caused the patient's neurological deficits. Although the patient kept working, the neurological deficits caused him inconvenience in his daily life. F ig . 4. Axial FLAIR MRI studies obtained in 2013 show no infarcts

Free access

The profile of cognitive impairment and hemodynamic compromise in moyamoya: a single-center prospective cohort study

Annick Kronenburg, Pieter T. Deckers, Esther van den Berg, Monique M. van Schooneveld, Evert-Jan Vonken, Albert van der Zwan, Bart N. M. van Berckel, Maqsood Yaqub, Willem Otte, Catharina J. M. Klijn, and Kees P. J. Braun

cognitive impairment. 3 The exact profile of cognitive disturbances in MMV remains to be established, particularly in the Western world. 3 – 8 The [ 15 O]H 2 O-PET technique is used to determine the need for revascularization surgery and to optimize surgical strategy. This technique enables the assessment of regional cerebral blood flow and cerebrovascular reactivity (CVR) after acetazolamide challenge. 1 , 5 To what extent cognitive function is related to hemodynamic compromise remains unclear. Several studies have suggested that frontal hypoperfusion, white matter

Full access

Artifact removal from neurophysiological signals: impact on intracranial and arterial pressure monitoring in traumatic brain injury

Seung-Bo Lee, Hakseung Kim, Young-Tak Kim, Frederick A. Zeiler, Peter Smielewski, Marek Czosnyka, and Dong-Joo Kim

. Criteria for Clinical Events The proportions of 4 major clinical events (systemic hypotension, intracranial hypertension, cerebral hypoperfusion, and impaired cerebrovascular reactivity) were identified from the ABP and ICP signals. A systolic blood pressure < 90 mm Hg was considered systemic hypotension, mean ICP > 20 mm Hg and > 22 mm Hg were considered intracranial hypertension, CPP < 60 mm Hg was considered cerebral hypoperfusion, and PRx > 0.3 was considered impaired cerebrovascular reactivity. 1 , 4 , 6 Furthermore, the prevalence of events that call for immediate