Imaging Oral Presentation

FC03.04 - Investigating the temporal relationship between inflammation and fdNIRS-measured hypoxia in an MS population  

Speakers
  • Q. Shafqat
Authors
  • Q. Shafqat
  • D. Adingupu
  • T. Evans
  • S. Jarvis
  • L. Brown
  • L. Metz
  • J. Dunn
Presentation Number
FC03.04
Presentation Topic
Imaging
Lecture Time
13:36 - 13:48

Abstract

Background

Previously, we used frequency domain near-infrared spectroscopy (fdNIRS), a non-invasive imaging modality, to show that brain hypoxia exists in a subset of MS patients. Currently, there is limited knowledge on the effects of hypoxia in MS. However, some studies suggest that hypoxia may exacerbate inflammation of the central nervous system (CNS). It is important to elucidate the time-course of hypoxia in relation to inflammation to further understand its role in MS.

Objectives

The aim of the present study was to use fdNIRS to determine if hypoxia in MS resolves quickly or if it is a chronic condition.

Methods

We used fdNIRS to quantify cortical microvasculature hemoglobin saturation (StO2) in 55 controls and 85 MS patients. StO2 values that were 2 standard deviations (SD) below the control mean were defined as hypoxic (<55.7%). Arterial oxygen saturation (SaO2) was measured using a pulse oximeter to confirm that reduced StO2 was not systemic in origin. To determine whether the temporal pattern of StO2 relates to changes in acute CNS inflammation, we recruited a subset of MS patients (hypoxic: n=12; normoxic: n=7) for a longitudinal study. We measured StO2 once a week for 4 consecutive weeks, and then once a month for 5 subsequent months. Due to COVID-19-related lab closures, we were only able to obtain StO2 data for the first 8 weeks for 13 of these patients (hypoxic: n=8; normoxic: n=5).

Results

StO2 in MS patients was significantly lower compared to controls (57.6±7.6% vs. 62.3±3.6%, respectively, p=0.002), with no differences in SaO2. For the longitudinal study, we found that StO2 values for normoxic and hypoxic MS groups did not change significantly over the course of 8 weeks (F (9, 36.9) =1.44, p=0.255).

Conclusions

To our knowledge, we are the first group to use fdNIRS to identify a subset of MS patients who experience persistent brain hypoxia. As hypoxia in MS patients persists beyond 4 weeks, we argue that it can present as a chronic condition. This indicates that, in these patients, physiological responses such as angiogenesis have not occurred or are not sufficient to result in resolution of hypoxia. With such chronic hypoxia we would predict that in these patients, some symptoms may be a result of this chronic hypoxia. Also, we argue that such chronic hypoxia could exacerbate and further stimulate a pathological immune response (a hypoxia inflammation cycle).

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