Near Infrared Light Scattering Changes Following Acute Brain Injury

Abstract

Acute brain injury (ABI) is associated with changes in near infrared light absorption reflecting haemodynamic and metabolic status via changes in cerebral oxygenation (haemoglobin oxygenation and cytochrome-c-oxidase oxidation). Light scattering has not been comprehensively investigated following ABI and may be an important confounding factor in the assessment of chromophore concentration changes, and/or a novel non-invasive optical marker of brain tissue morphology, cytostructure, hence metabolic status. The aim of this study is to characterize light scattering following adult ABI. Time resolved spectroscopy was performed as a component of multimodal neuromonitoring in critically ill brain injured patients. The scattering coefficient (μ's), absorption coefficient and cerebral haemoglobin oxygen saturation (SO2) were derived by fitting the time resolved data. Cerebral infarction was subsequently defined on routine clinical imaging. In total, 21 patients with ABI were studied. Ten patients suffered a unilateral frontal infarction, and mean μ' s was lower over infarcted compared to non-infarcted cortex (injured 6.9/cm, non-injured 8.2/cm p=0.002). SO2 did not differ significantly between the two sides (injured 69.3%, non-injured 69.0% p=0.7). Cerebral infarction is associated with changes in μ' s which might be a novel marker of cerebral injury and will interfere with quantification of haemoglobin/cytochrome c oxidase concentration. Although further work combining optical and physiological analysis is required to elucidate the significance of these results, μ' s may be uniquely placed as a non-invasive biomarker of cerebral energy failure as well as gross tissue changes.

Keywords: Brain injury; Cerebral ischaemia; Near infrared spectroscopy; Scattering.

Fig. 17.1

Mean μ′_s (834 nm) and SO2 for each day post intensive care admission in cerebral hemispheres demonstrating infarction versus no infarction. The lower scattering in infarcted cerebral hemisphere is evident, whereas there is no appreciable pattern with SO₂

Fig. 17.2

Two-layer model simulation of the effect of cerebral μ′_s on TPSF data at source detector separations of 2 and 4 cm. It can be seen that the TPSF has much greater sensitivity to μ′_s changes in the deep layer at 4 cm source detector separation than 2 cm. A two-layer semi-infinite slab geometry was used in this simulation, layer 1 (1 cm depth, μ_a 0.1/cm and μ′_s 10/cm), layer 2 (5 cm depth, μ_a 0.1/cm and μ′_s 6/cm or 10/cm) using a model from Liemert et al. [8]