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Cerebral Autoregulation in the Microvasculature Measured with Near-Infrared Spectroscopy

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Cerebral Autoregulation in the Microvasculature Measured with Near-Infrared Spectroscopy Journal of Cerebral Blood Flow & Metabolism (2015) 35, 959–966 © 2015 ISCBFM All rights reserved 0271-678X/15 $32.00 www.jcbfm.com ORIGINAL ARTICLE Cerebral autoregulation in the microvasculature measured with near-infrared spectroscopy Jana M Kainerstorfer, Angelo Sassaroli, Kristen T Tgavalekos and Sergio Fantini Cerebral autoregulation (CA) is the mechanism that allows the brain to maintain a stable blood flow despite changes in blood pressure. Dynamic CA can be quantified based on continuous measurements of systemic mean arterial pressure (MAP) and global cerebral blood flow. Here, we show that dynamic CA can be quantified also from local measurements that are sensitive to the microvasculature. We used near-infrared spectroscopy (NIRS) to measure temporal changes in oxy- and deoxy-hemoglobin concentrations in the prefrontal cortex of 11 human subjects. A novel hemodynamic model translates those changes into changes of cerebral blood volume and blood flow. The interplay between them is described by transfer function analysis, specifically by a high-pass filter whose cutoff frequency describes the autoregulation efficiency. We have used pneumatic thigh cuffs to induce MAP perturbation by a fast release during rest and during hyperventilation, which is known to enhance autoregulation. Based on our model, we found that the autoregulation cutoff frequency increased during hyperventilation in comparison to normal breathing in 10 out of 11 subjects, indicating a greater autoregulation efficiency. We have shown that autoregulation can reliably be measured noninvasively in the microvasculature, opening up the possibility of localized CA monitoring with NIRS. Journal of Cerebral Blood Flow & Metabolism (2015) 35, 959–966; doi:10.1038/jcbfm.2015.5; published online 11 February 2015 Keywords: brain imaging; cerebral blood flow measurement; cerebral hemodynamics; near-infrared spectroscopy; optical imaging INTRODUCTION questioned the validity of the autoregulation curve introduced Cerebral autoregulation is the mechanism that maintains cerebral by Lassen by showing that the slope of CBF as a function of MAP is blood supply, hence cerebral blood flow (CBF), approximately dependent on whether MAP increases or decreases, invalidating constant despite changes in mean arterial blood pressure (MAP) the plateau of the autoregulation curve. In general, the accuracy of or, more precisely, despite changes in cerebral perfusion pressure measuring autoregulation based on two points, on the auto- (CPP; defined as the difference between MAP and intracranial regulation curve is questionable, with the measurements being pressure). This mechanism is valid for a certain range of CPP, several minutes apart from each other, since CBF depends on a namely 50 to 150 mm Hg.1–3 Within that range, changes in CPP number of factors, such as partial pressure of carbon dioxide (pCO2), cerebral metabolism, and hematocrit, which all can lead to vasomotor adjustments in cerebrovascular resistance (CVR) 3,7 1 change while MAP reaches a new steady state, whereas the thus allowing CBF to remain relatively constant. Lassen con- change in MAP alone is what drives autoregulation. structed, based on measurements reported in the literature, a so- The second category of autoregulation assessment is based on called autoregulation curve, which shows a CBF plateau in the measuring dynamic changes of CBF in response to dynamic aforementioned CPP range, essentially showing that CBF remains changes in MAP, hence this is referred to as dynamic cerebral constant. Assessing the boundaries of this plateau and whether autoregulation. Regardless of the exact measurement setup, the the autoregulation mechanism is intact or impaired is critical, underlying idea is that after a step change in MAP, CBF will first since impaired autoregulation can lead to cerebral ischemia or react to such MAP change and will then return to its original value brain damage because of abnormal perfusion. Therefore, deter- within a finite amount of time, where this amount of time is a mining the effectiveness of cerebral autoregulation is relevant for measure of autoregulation efficiency. The faster CBF returns to its a variety of patient populations. baseline value, the better is the autoregulation mechanism. This In general, the assessment of autoregulation can be classified delayed CBF adaptation was first observed in animals.8 Aaslid into two categories. The first category considers only steady-state et al9 introduced a thigh cuff–based method of inducing fast MAP or static relationships between CBF and MAP, without taking time changes, which is the most frequently used method to induce courses of changes in MAP and CBF into account. This can be rapid MAP perturbations. For this, pneumatic cuffs are placed achieved by infusion of drugs, which do not have an effect on the ’ fl – around the subjects thighs and are in ated 20 to 40 mm Hg cerebral vasculature or metabolism but change MAP.4 6 Measure- above systolic pressure for at least 2 minutes. The release of the ments of CBF are performed during baseline as well as during the thigh-cuff pressure results in MAP dropping by ~ 10 to 20 mm Hg. altered MAP state. This yields two values of CBF and their Since Aaslid et al have shown that MAP and CBF return to baseline difference in relation to the MAP change is indicative of within ~ 15 seconds after thigh-cuff release, changes in cerebral autoregulation. A recent review on static autoregulation7 metabolism and hematocrit can be neglected over this time Department of Biomedical Engineering, Tufts University, Medford, Massachusetts, USA. Correspondence: Dr JM Kainerstorfer, Department of Biomedical Engineering, Tufts University, 4 Colby Street, Medford, MA 02155, USA. E-mail: [email protected] This research was supported by the National Institutes of Health (Grant no. R01-CA154774) and by the National Science Foundation (Award no. IIS-1065154). Received 16 September 2014; revised 17 December 2014; accepted 6 January 2015; published online 11 February 2015 Microvascular autoregulation with NIRS JM Kainerstorfer et al 960 scale.3,9 Furthermore, the method is quick and can therefore be and CBF. Based on literature, it is known that the autoregulation repeated multiple times on the same subject for monitoring mechanism can be described as a high-pass filter for which MAP is applications. However, since the time window in which the an input and CBF in an output.11,17 We adopt this idea of autoregulation mechanism can be studied is ~ 15 seconds, only a describing dynamic autoregulation with a high pass filter, but we limited number of measurement techniques exist, which can use local microvascular CBV (measured by T(t) and hypothesized capture these fast transients in CBF. Transcranial Doppler (TCD) is to be directly linked to the local arterial blood pressure) as input, such an imaging technique with a sufficient temporal resolution; it and local microvascular blood flow (measured by NIRS and our measures CBF velocity (CBFV) in the middle cerebral artery (MCA). hemodynamic model) as output. The cutoff frequency of the high- Under the assumption that the diameter of the MCA does not pass filter, which is inversely related to the CBF recovery time change, CBFV can be taken to be a reliable representation of discussed above, quantifies the effectiveness of autoregulation.23 9,24,25 global CBF. Together with continuous blood pressure measure- Changes in PaCO2 have been shown to influence CA. The ments, the dynamics of MAP changes and CBF changes can be mechanism is hypothesized to be linked with the effect of PaCO2 assessed with an adequate temporal resolution for dynamic (CA) on cerebrovascular reactivity (enhancement during hypocapnia assessment. and suppression during hypercapnia),9 which in turn is associated Such measurements of dynamic changes in CBF in response to with the vascular dilation during hypercapnia and vascular sudden changes in MAP, where the time of CBF recovery is constriction during hypocapnia.24 Hypocapnia reduces CBF, while indicative of autoregulation, have already been used in numerous also reducing the response time of CBF after a step change in 10 disease models, where it has been found that cerebral MAP.2,9 This reduced response time is an indicator of improved autoregulation is altered or impaired in patients with a variety of CA. Since hypocapnia can be induced by performing 11 12 conditions such as autonomic failure, diabetes, Parkinson’s hyperventilation,9 we have measured healthy volunteers during 13 14 disease, and stroke. normal breathing and hyperventilation to induce a predictable Using the CBF recovery time, different methods exist to assess change (increase during hyperventilation) in cerebral autoregula- fi and quantify autoregulation. One such method de nes autoregula- tion. We show that local NIRS measurements, which are mostly tion by the rate of regulation, which is given by the temporal slope sensitive to the cerebral microvasculature, together with hemo- of CVR recovery, where CVR = CPP/CBF, after the sudden perturba- 9,15 dynamic perturbations induced by a fast thigh-cuff release, can tion in the thigh-cuff release method. A steeper slope of CVR as a measure these different levels of autoregulation effectiveness in function of time indicates a better autoregulation mechanism. the cerebral microvasculature. Another method to quantify autoregulation from the CBF recovery after the cuff release is based on an autoregulation index, which is introduced in a second-order differential equation
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