Caroline D Rae1, Haider Naqvi2, Andrew Vakulin2,3, Angela D'Rozario2, Michael Green1, Hannah Openshaw2, Keith Wong2,4, Jong-Won Kim5, Delwyn J Bartlett6, Doug McEvoy7, and Ronald R Grunstein6
1The University of New South Wales, Randwick, Australia, 2NHMRC Centers of Research Excellence, CIRUS and NeuroSleep, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia, 33. Adelaide Institute for Sleep Health: A Flinders Centre of Research Excellence, School of Medicine, Flinders University, Adelaide, Australia, 4Sydney Medical School, The University of Sydney, Sydney, Australia, 5School of Physics, The University of Sydney, Sydney, Australia, 6NeuroSleep and Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia, 7Adelaide Institute for Sleep Health: A Flinders Centre of Research Excellence, School of Medicine, Flinders University, Adelaide, Australia
Synopsis
Here,
we investigated the potential for MRS/MRI markers to differentiate between
phenotypes of obstructive sleep apnea patients who are vulnerable, versus
resistant to vigilance failure, an indicator of driving impairment and accident
risk. Vulnerable patients (N = 15) and resistant patients (N = 30) were
differentiated on the basis of left orbito-frontal glutamate and aspartate and
also anterior cingulate glutathione levels. There was a trend towards lower
orbitofrontal creatine levels in vulnerable OSA subjects, but no group
differences in brain volumes.Introduction
Obstructive
sleep apnoea (OSA) is associated with driving impairment and accident risk [1]. However,
not all patients are impaired and identifying individuals at risk is clinically
challenging [2,3]. To help address this problem we used magnetic resonance
spectroscopy (MRS) and imaging to examine brain metabolite levels and
whole/regional brain volumes towards identifying potential markers to differentiate
between phenotypes of OSA patients who are vulnerable vs resistant to vigilance
failure.
Methods
Fifty-eight
OSA patients underwent overnight polysomnography (PSG) followed by a 28h extended
wakefulness challenge during which driving simulator and psychomotor vigilance
(PVT) were examined. 1-2 weeks prior to the extended wakefulness experiment, 45
of the 58 patients had a successful MRS/MRI scan. Based on a combination of median
split data from driving simulator crash and PVT lapse occurring following
extended wakefulness, patients were defined as vulnerable (n=15) or resistant
(n=30) to vigilance failure (Fig. 1). Baseline anthropometric, PSG variables, and brain
bioenergetics (MRS) in the left-orbitofrontal cortex (LOFC), anterior cingulate
cortex (ACC) and hippocampus (Hipp), as well as total grey, white matter and
hippocampal volumes were compared between the vulnerable and resistant patient groups.
Differences between groups were assessed using unpaired t-tests and
Mann-Whitney U tests.
Results
Compared
to resistant patients, vulnerable OSA patients exhibited greater sleepiness,
more severe OSA and hypoxemia (all p <0.05, Table 1). Furthermore, vulnerable OSA
group showed lower levels of ACC glutathione levels (2.0±1.1 vs 3.0±1.9,
p=0.029), LOFC glutamate levels (10.9±3.3 vs 13.4±4.3, p=0.034) and LOFC
Aspartate levels (18.3±1.7 vs 23.4±1.5, p=0.029). There was also a trend
towards lower LOFC creatine level in the vulnerable patients (9.2±0.6 vs 10.7±0.3),
but this did not reach statistical significance (p=0.052). There were no
significant brain volume difference between the groups (Table 2).
Conclusions
Baseline
PSG and MR spectroscopy may provide useful markers of vulnerability to vigilance
failure and driving impairment in OSA patients. Further work is necessary using
functional imaging, diffusion and fibre tracking to establish brain regions
responsible for vigilance control and failure in clinical OSA populations.
Acknowledgements
This
work has been funded by the National Health and Medical Research Council of
Australia (NHMRC).References
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