Ruyi Zhang1, Hea Ree Park2, Hosung Kim3, Gele Qin1, Eun Yeon Joo4, and Lirong Yan3
1Department of Electric Engineering, University of Southern California, Los Angeles, CA, United States, 2Inje University College of Medicine, GoyangSouth, Korea, Republic of, 3Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States, 4Sungkyunkwan University School of Medicine, Seoul, Korea, Republic of
Synopsis
In
this study, we comprehensively studied the regional hemodynamic measures
including CBF, cerebral blood volume (CBV), and time-related hemodynamic
parameters in OSA patients using Gadolinium contrast agent (Gd)-base dynamic
susceptibility contrast MRI.
INTRODUCTION
Obstructive sleep apnea (OSA), which is
known as the most frequent type of Sleep-Disorders, is characterized by
repetitive episodes of the upper airway’s obstructions during sleep.1
OSA leads to hypoxia and sleep fragmentation, 2 which eventually
harms the brain. The hypoxia-induced hemodynamic changes, which may be
associated with degenerative processes, impaired systemic or cerebral vascular
regulation, may further induce the region structural and functional deficits in
the brain. Previous perfusion imaging studies have mainly focused on studying
cerebral blood flow (CBF) alterations in OSA population (refs). In this study,
we comprehensively studied the regional hemodynamic measures including CBF,
cerebral blood volume (CBV), and time-related hemodynamic parameters in OSA
patients using Gadolinium contrast agent (Gd)-base dynamic susceptibility
contrast MRI.METHODS
Participants and MRI protocol:
25
patients with OSA (all male, mean age 4510,
range=23-65, mean BMI 26.93.2,
range=21.9-39.3) and 25 healthy volunteers (4 females,
mean age 389 years,
range=28-57, mean BMI 23.61.9,
range=17.8-26.4) participated in this study after providing written informed
consent. MRI images were acquired using a Philips 3.0-T
MRI scanner (Intera Achieva 3T) with an eight-channel sensitivity-encoding head
coil. High-spatial-resolution axial T2*-weighted echo planar images were
acquired using the following sequence parameters: TR=1,720 ms, TE=35 ms,
FOV=240×240 mm, matrix=256×256, slices=50, slice thickness=5.0 mm, gap=1.5 mm,
number of dynamic scans=50, and temporal resolution=1.8 s. Brain
structural images were acquired using T1-weighted coronal spoiled gradient recalled
(SPGR) MRI (TR=10 ms, TE=4.6 ms, matrix=480×480,
slices= 360, slice thickness=0.5 mm).
Image processing:
Multi-parametric perfusion maps including
CBF, CBV, mean transit time (MTT), and time to peak (TTP) from DSC images by
deconvolution of the image series with arterial input function, according to
the general kinetic model. As DSC only provided semi-quantitative CBF, the CBF
map was normalized by the mean intensity for each subject. All the parametric
perfusion maps were normalized to the NMI space and then smoothed with a kernel
size of 8x8x8mm3. A two-sample t-test was employed to compared the
voxel-based difference between OSA and normal groups while age and BMI were included as covariance. RESULTS
Figure 1 shows the regions with
significant reduction of CBF in OSA patients compared to normal subjects.
Significant CBF reduction is found in right secondary visual cortex regions,
right ventral anterior cingulate cortex and right dorsal posterior cingulate
cortex. Figure 2 shows obvious CBV difference occurring in right anterior
prefrontal cortex, right associative visual cortex and right fusiform gyrus. As
for MTT, in Figure 3, the main changes are shown in left and right Visuo-Motor Coordination
and left temporopolar area. In figure 4, at last, the variation in TTP is in right
premotor cortex and supplementary motor cortex and both right and left retrosubicular
area. CONCLUSION
Increasing evidence suggests that OSA causes
deficits of cerebral function in multiple brain regions, which could be
associated with regional hemodynamic changes. Multiple hemodynamic parameter
can be derived from DSC perfusion imaging, which could provide a comprehensive
evaluation of local hemodynamic changes in OSA. Acknowledgements
No acknowledgement found.References
1.
Berry, Richard B et al. “Rules for
scoring respiratory events in sleep: update of the 2007 AASM Manual for the
Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea
Definitions Task Force of the American Academy of Sleep Medicine.” Journal of
clinical sleep medicine : JCSM : official publication of the American Academy
of Sleep Medicine vol. 8,5 597-619. 15 Oct. 2012, doi:10.5664/jcsm.2172
2.
Foldvary-Schaefer, N. R., &
Waters, T. E. (2017). Sleep-Disordered Breathing: CONTINUUM: Lifelong Learning
in Neurology, 23(4), 1093‑1116.
3.
Bucks, RS; Olaithe, M; Eastwood, P
(2012). "Neurocognitive Function in Obstructuve Sleep Apnea: A
Meta-Review". Respirology. 18 (1): 61–70.
4.
Olaithe, M; Bucks, RS; Hillman, DR;
Eastwood, PR (2017). "Cognitive Deficits in Obstructive Sleep Apnea:
Insights from a Meta-Review and Comparison with Deficits Observed in COPD,
Insomnia and Sleep Deprivation". Sleep Medicine Reviews. 38: 39–49.
5.
Schwab, Richard J.; Kim, Christopher;
Bagchi, Sheila; Keenan, Brendan T.; Comyn, François-Louis; Wang, Stephen;
Tapia, Ignacio E.; Huang, Shirley; Traylor, Joel; Torigian, Drew A.; Bradford,
Ruth M.; Marcus, Carole L. (2015). "Understanding the Anatomic Basis for
Obstructive Sleep Apnea Syndrome in Adolescents". American Journal of
Respiratory and Critical Care Medicine. 191 (11): 1295–1309.
6.
Frank Gaillard; et al. "Dynamic
susceptibility contrast (DSC) MR perfusion". Radiopaedia. Retrieved
2017-10-14.
7.
Ding, S. L.; Van Hoesen, G. W.;
Cassell, M. D.; Poremba, A. (2009). "Parcellation of human temporal polar
cortex: A combined analysis of multiple cytoarchitectonic, chemoarchitectonic,
and pathological markers". The Journal of Comparative Neurology. 514 (6):
595–623.