Near-infrared oximetry of the brain

Abstract

Near-infrared (IR) light easily penetrates biological tissue, and the information offered by in vivo spectroscopy of cerebral oxygenation is detailed and comes with a high temporal resolution. Near-IR light spectroscopy (NIRS) reflects cerebral oxygenation during arterial hypotension, hypoxic hypoxaemia and hypo- and hypercapnia.

As determined by dual-wavelength NIRS, the cerebral O₂ saturation integrates the arterial O₂ content and the cerebral perfusion, and as established for skeletal muscle, NIRS obtains information on tissue oxygenation and metabolism beyond that obtained by venous blood sampling.

Caveats of cerebral NIRS include insufficient light shielding, optode displacement and a sample volume including muscle or the frontal sinus mucous membrane. The relative influence from the extracranial tissue is minimized by optode separation and correction for an extracranial sample volume, or both.

The natural pigment melatonin and also water are of little influence to spectroscopic analysis of cerebral oxygenation, whereas bilirubin systematically lowers ScO₂ and attenuates the detection of changes in cerebral oxygenation.

By NIRS, reduction of cytochrome oxidase is demonstrated during hypoxic hypoxaemia and head-up tilt-induced arterial hypotension, but the changes are small. In the clinical setting, NIRS offers useful information in patients with both systemic and local cerebral circulatory impairment, for example, during cranial trauma, surgery on the cerebral arteries, orthostasis and acute heart failure.

Whereas mapping of the brain circulation is needed for jugular venous sampling to reflect either global or local oxygenation, the determination of cerebral oxygenation by NIRS has the advantage of localized monitoring of the cerebral cortex.

Introduction

In the near-infrared (IR) band, light penetrates biological tissue quite easily and transcranial spectroscopy quantifies concentration changes of cerebral compounds if only their absorption spectra are known. Water comprises the larger portion of biological tissue, and a spectroscopic `window' opens because the extinction of light by water is lower at wavelengths from ∼700 to ∼1000 nm than at other wavelengths. The O<sub>2</sub> carrying pigments, haemoglobin and cytochrome c oxidase (aa<sub>3</sub>), have well-defined absorption spectra that are influenced by O<sub>2</sub> binding. It is analysis of the attenuation spectra of such pigments (spectroscopy) or the determination of the absorption of light at selected wavelengths (spectrophotometry), that is used to follow oxygenation in vivo. With a temporal resolution of half a second, near-infrared spectroscopy (NIRS) reflects cerebral changes in oxygenated (HbO<sub>2</sub>) and deoxygenated haemoglobin (Hb), oxidated cytochrome c (CytO<sub>2</sub>) and oxygen saturation (ScO<sub>2</sub>) on a `bedside' basis.

The principle of tissue spectroscopy for O₂ is well-known, and `pulse oximetry' of the arterial O₂ saturation (SaO₂) is based on the ear oximeters of Millikan (1942). In what is now a classic paper, Jöbsis (1977) described brain spectroscopy with near-IR wavelengths in the cat, and since then the annual number of published papers on NIRS has increased dramatically. Near-IR techniques include continuous intensity spectroscopy, time resolved spectroscopy and intensity modulated spectroscopy [for a review see Delpy and Cope (1997)]. In vivo spectroscopy may be applied for any chromophore with a distinct absorbance peak(s) in the near-IR part of the spectrum, for example, nitrosyl haemoglobin (Cooper et al., 1996), glucose (Zeller et al., 1989; Muller et al., 1997), or, as used for determination of CBF, indocyanine green (Roberts et al., 1993). However, NIRS is used foremost to determine the oxygenation of haemoglobin and cytochrome oxidase.

Considering tissue haemoglobin oxygenation, similar—though not identical—information is obtained with determination of the O₂ content of the venous outflow from the brain (Jacobsen and Enevoldsen, 1989), magnetic resonance imaging (Ogawa et al., 1990) or invasively with oxygen electrodes (Clark, 1981) or microdialysis (Zauner et al., 1997). Intracellular hypoxia may be assessed by NIRS since the terminal enzyme of the mitochondrial respiratory O₂ metabolism chain, cytochrome oxidase, has an absorbance peak from 780 to 870 nm that disappears with reduction (Chance, 1994a). The NIRS also offers the possibility of determining cerebral blood flow (CBF), conventionally assessed by nitrous oxide wash out (Kety and Schmidt, 1945), ¹³³xenon clearance (Lassen, 1964; Obrist et al., 1967), positron emission tomography (Frackowiak et al., 1980), or indirectly by transcranial Doppler determined cerebral artery blood velocity [V_mean; Aaslid et al. (1982)]. The NIRS provides digital information on oxygenation in the sample volume, that is, regional cerebral oxygenation, and research into NIRS has focused on the exact determination of tissue oxygenation [for a review see Delpy and Cope (1997)]. The NIRS technique is developed to provide non-invasive in vivo optical imaging of the brain. Some brain mapping of O₂ metabolism is made possible by changing the probe position systematically, and Benaron and Stevenson (1993)have developed an image of a rat using near-IR light.

Clinical research has focused on neonates partly because their cranium and brain may be transilluminated. In pre-term babies, NIRS offers information on cerebral haemoglobin content, blood volume and flow [for a review see Wyatt et al. (1989); Wyatt (1994)]. Within safety margins for light intensities, photons penetrate 7 or 8 cm of tissue (Delpy et al., 1988; Harris et al., 1994a) and reflectance spectroscopy must be applied for the head of a child or an adult.

This paper reviews studies of cerebral NIRS as applied to adult humans in health and disease. The NIRS theory is summarized; spectroscopic studies of muscle are discussed for comparison; and studies of infants and animals are included only to the extent they elucidate NIRS of the adult brain. The brain has a limited capacity to sustain anoxia, and the implied aim of this review is to establish the level of cerebral deoxygenation that is associated with clinical symptoms.