Studies of Tissue PO2 in Normal and Pathological Human Brain Cortex

Meixensberger, Jürgen; Dings, J.; Kuhnigk, Herbert; Roosen, K.

doi:10.1007/978-3-7091-9302-0_10

Cited by 79 publications

(69 citation statements)

References 21 publications

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“…The increase in brain tissue O 2 tension with hyperoxia appears to be much greater in pathological than in normal brain tissue. 30,35,46 Other studies have suggested that CBF at the site of the PO 2 probe might explain these observations. 20 There are significant changes in ARI in response to hyperoxia throughout the first few days after injury.…”

Section: Hyperoxiamentioning

confidence: 71%

Cerebral pressure autoregulation in traumatic brain injury

Rangel-Castilla

Gasco

Nauta

et al. 2008

FOC

183

104

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An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregulation is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperventilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.

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Section: Hyperoxiamentioning

confidence: 71%

Cerebral pressure autoregulation in traumatic brain injury

Rangel-Castilla

Gasco

Nauta

et al. 2008

FOC

183

104

View full text Add to dashboard Cite

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“…Small regions of ischemia imbedded within areas of normal or hyperemic flow may be missed applying global measurement methods using jugular bulb catheters. On the other hand, brain tissue oxygen tension pressure (PbtO 2 ) monitoring is suitable to detect focal changes in cerebral oxygenation pattern [45]. The technique, nevertheless, using intraparenchymatous brain catheters is an invasive method with a very small measurement volume of a few cubic millimeters, giving accurate results only if the probe is inserted directly into the area of interest.…”

Section: Discussionmentioning

confidence: 99%

Near-infrared spectroscopy extended with indocyanine green dye dilution for cerebral blood flow measurement: Median values in healthy volunteers

Mudra

Muroi

Niederer

et al. 2008

Opto-Electronics Review

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The cerebral blood flow (CBF) is an important vital parameter in neurointensive care. Currently, there is no non-invasive method for its measurement that can easily be applied at the bedside. A new tool to determine CBF is based on near-infrared spectroscopy (NIRS) applied together with indocyanine green (ICG) dye dilution. From a bilateral measurement on selected regions on the head of infrared (IR) absorption at various wavelengths during the dilution maneuver, the vascular perfusion characteristics of the two brain hemispheres can be determined in terms of mean transit time (mtt) of ICG, cerebral blood volume (CBV) and CBF.So far, on nine healthy volunteers, NIRS ICG dye dilution bihemispheric measurements were performed, which yielded to mtt given as median (range) of 9.3 s (5.1–16.3 s), CBV of 3.5 ml/100 g (1.7–4.1 ml/100 g), and CBF of 18.2 ml/(100 g×min) [11.1–48.6 ml/(100 g×min)]. Additionally, the blood flow index (BFI) was calculated with BFI= 13.8 mg/(100 g×s) [6.6–15.2 mg/(100 g×s)]. The Spearman rank correlation coefficient between CBF and BFI was RS = 0.76. However, as the Bland & Altman plot between CBFNIRS and the CBFBFI documents, the limits of agreement are rather wide (21.9±6.7). Under physiological conditions in healthy volunteers, no differences could be detected between the hemispheres.

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“…11,13,16,[25][26][27][28][29][30] However, the pathophysiological mechanisms after diffuse brain damage and SAH cannot be compared with the spaceoccupying edema after large focal ischemia, which might affect the value of the monitoring in these patients. 31 So far, no other studies of multimodal monitoring have been conducted in patients with large hemispheric infarction.…”

Section: Discussionmentioning

confidence: 99%