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Imaging the Effects of Oxygen Saturation Changes in Voluntary Apnea and Hyperventilation on Susceptibility-Weighted Imaging - AJNR News Digest
May 2015
Brain

Imaging the Effects of Oxygen Saturation Changes in Voluntary Apnea and Hyperventilation on Susceptibility-Weighted Imaging

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Yulin Ge

Over the last decade, susceptibility weighted imaging (SWI) has grown tremendously as a new clinical face in routine brain MRI in addition to T1- and T2-weighted imaging. It is particularly useful in detecting small intracranial hemorrhages and venous anomalies due to its increased sensitivity to higher susceptibility materials such as iron and deoxyhemoglobin 1.  Although SWI is often used for high-resolution MRI venograms, the wealth of information underlying its superior venous contrast is often overlooked. Just like the blood oxygen level-dependent (BOLD) technique, venous visibility on SWI is dependent upon the venous blood oxygenation level.  Compared to BOLD, SWI provides much higher spatial resolution and venous definition. It also has the distinct advantage of enabling the exploration of cerebrovascular reactivity (CVR), which is characterized by hemodynamic responses such as the changes in the caliber of cerebral arteries and cerebral blood flow (CBF) in response to various neuronal-induced or external vasoactive stimuli.  The external hemodynamic modulators including voluntary respiratory challenges are of clinical interest for evaluation of cerebral vasomotor responses or CVR, which may be impaired in many neurologic diseases such as stroke, Alzheimer disease and multiple sclerosis.

Our study in the American Journal of Neuroradiology 2 was to assess cerebral venous blood oxygenation changes during simple voluntary breath-holding (apnea) and hyperventilation by use of SWI at 3T.  We found that changes in venous visibility caused by short respiratory challenges can be directly visualized on SWI venogram and such findings highlight the sensitivity of SWI to venous oxygenation changes that are associated with cerebral hemodynamics changes during short breath-holding and hyperventilation. Our data indicate that venous oxygenation level is higher during voluntary breath-holding (due to increased blood CO2 and increased blood flow and oxygen delivery) and lower during hyperventilation (due to lower blood CO2 and subsequent vasoconstrictive effects). As a result, venous vasculature visibility on SWI venograms is enhanced for hyperventilation and diminished for apnea. In daily clinical practice, SWI venogram is therefore not only a static-state technique in detecting venous architecture abnormalities, it also has dynamic properties and may afford a quick method to assess underlying blood flow modulation and oxygen metabolic pathophysiology in various disease states 3.

We are currently working to improve quantitative measures of venous oxygenation quantification4,5 and to develop noninvasive imaging biomarkers for cerebral oxygen metabolism. In addition, we have developed a MR compatible gas delivery system for MRI mapping of cerebrovascular reactivity6 with well-controlled CO2 mixture and end-tidal CO2 monitoring. This will reduce patient discomfort from breath-holding and hypercapnia and increase quantitative capacity.  The imaging protocol includes the assessment of CVR using SWI, BOLD or arterial spin labeling during mild hypercapnia (ie, fixed 5% CO2, 21% O2, and 74% N2) and room air breathing. Such a system has the potential to be used in broad clinical applications and in better understanding brain vascular pathophysiology.7

References

  1. Haacke EM, Mittal S, Wu Z, et al. Susceptibility-weighted imaging: technical aspects and clinical applications, part 1AJNR Am J Neuroradiol 2009;30:19–30, 10.3174/ajnr.A1400
  2. Chang K, Barnes S, Haacke EM, et al. Imaging the effects of oxygen saturation changes in voluntary apnea and hyperventilation on susceptibility weighted imaging. AJNR Am J Neuroradiol 2014;35:1091–95, 10.3174/ajnr.A3818
  3. Ge Y, Zohrabian VM, Osa EO, et al. Diminished visibility of cerebral venous vasculature in multiple sclerosis by susceptibility-weighted imaging at 3.0 Tesla. J Magn Reson Imaging 2009;29:1190–94, 10.1002/jmri.21758
  4. Lu H, Ge Y. Quantitative evaluation of oxygenation in venous vessels using T2-relaxation-under-spin-tagging MRI. Magn Reson Med 2008;60:357–63, 10.1002/mrm.21627
  5. Xu F, Ge Y, Lu H. Noninvasive quantification of whole-brain cerebral metabolic rate of oxygen (CMRO2) by MRI. Magn Reson Med 2009;62:141–48, 10.1002/mrm.21994
  6. Lu H, Liu P, Yezhuvath U, et al. MRI mapping of cerebrovascular reactivity via gas inhalation challenges. J Vis Exp 2014;94:e52306, 10.3791/52306.
  7. Marshall O, Ge Y, Lu H, et al. Impaired cerebral vascular reactivity in multiple sclerosis. JAMA Neurol 2014;71:1275–81, 10.1001/jamaneurol.2014.1668

 

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