scholarly journals Comparison of cerebrovascular reactivity tests: a pilot human study

2019 ◽  
Vol 8 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Michael Bodo ◽  
Richard Mahon ◽  
Alex Razumovsky ◽  
Efim Kouperberg ◽  
Michael Crimmins ◽  
...  

Abstract In neurosurgery intensive care units, cerebrovascular reactivity tests for neuromonitoring are used to evaluate the status of cerebral blood flow autoregulation; lack of autoregulation indicates a poor patient outcome. The goal of neuromonitoring is to prevent secondary injuries following a primary central nervous system injury, when the brain is vulnerable to further compromise due to hypoxia, ischemia and disturbances in cerebral blood flow and intracranial pressure. Ideally, neuromonitoring would be noninvasive and continuous. This study compares cerebrovascular reactivity monitored by rheoencephalography, a noninvasive continuous monitoring modality, to cerebrovascular reactivity measured by currently used neuromonitoring modalities: transcranial Doppler, near infrared spectroscopy and laser Doppler flowmetry. Fourteen healthy volunteer subjects were measured. The tests used for comparison of cerebrovascular reactivity were breath-holding, hyperventilation, CO2 inhalation, the Valsalva maneuver, and the Trendelenburg and reverse Trendelenburg positions. Data for all modalities measured were recorded by computers and processed off line. All measured modalities reflected cerebrovascular reactivity with variabilities. Breath-holding, CO2 inhalation, and the Valsalva maneuver caused CO2 increase and consequent brain vasodilatation; hyperventilation caused CO2 decrease and brain vasoconstriction. The Trendelenburg and reverse Trendelenburg positions caused extracranial blood volume changes, which masked intracranial cerebrovascular reactivity. The hyperventilation test proved ineffective for measuring cerebrovascular reactivity with rheoencephalography due to respiratory artifacts. Some discrepancies among the


Pain Medicine ◽  
2020 ◽  
Vol 21 (11) ◽  
pp. 3012-3017
Author(s):  
Igor Petrušić ◽  
Ana Podgorac ◽  
Aleksandra Radojičić ◽  
Jasna Zidverc-Trajković

Abstract Background Previous studies suggest that increased cerebrovascular reactivity might be a feature of patients who have migraine with aura (MwA). The correlation between the clinical presentation of migraine with aura and transcranial Doppler parameters remains unclear. Objective The main aim of this study was to explore cerebral blood flow, vascular resistance, and cerebrovascular reactivity in women MwA. Also, the relationships between hemodynamic conditions and aura characteristics are examined. Design Cross-sectional study. Setting Headache Center, Neurology Clinic, Clinical Center of Serbia. Subjects Fifty-four women MwA and 49 healthy controls (HCs). Methods Transcranial Doppler sonography examination was used to determine blood flow mean velocity (MV) and pulsatility index (PI), as well as breath-holding index (BHI), in 15 arterial segments comprising the circle of Willis. Results A total of 54 women MwA and 49 HCs were studied. The PIs of all segments of the left and right middle cerebral arteries and the left and right anterior cerebral arteries were significantly higher in MwA with regards to HCs. Also, both the left and right BHIs were significantly higher in MwA than HCs. In addition, MVs of the right vertebral artery and the first segment of the basilar artery were significantly lower in MwA than HCs. Longer duration of migraine aura showed a weak negative correlation with the PI of the left posterior cerebral artery. Conclusions Our findings suggest increased vessel pulsatility, abnormal cerebrovascular reactivity, and decreased cerebral blood flow velocity in several arterial segments of the Willis circle in women MwA.



2019 ◽  
Author(s):  
Suk Tak Chan ◽  
Karleyton C. Evans ◽  
Tian Yue Song ◽  
Juliett Selb ◽  
Andre van der Kouwe ◽  
...  

AbstractHypercapnia during breath holding is believed to be the dominant driver behind the modulation of cerebral blood flow (CBF). Here we showed that the cerebrovascular responses to brief breath hold epochs were coupled not only with increased partial pressure of carbon dioxide (PCO2), but also with a decrease in partial pressure of oxygen (PO2). We used transcranial Doppler ultrasound to evaluate the CBF changes during breath holding by measuring the cerebral blood flow velocity (CBFv) in the middle cerebral arteries, a pair of cerebral arteries that supply most parts of the brain. The regional CBF changes during breath hold epochs were mapped with blood oxygenation level dependent (BOLD) signal changes as surrogate of CBF changes using functional magnetic resonance imaging (fMRI) technique. Given the interdependence of the dynamic changes between PCO2 and PO2, we found that the breath-by-breath O2-CO2 exchange ratio (bER), namely the ratio of changes in PO2 (ΔPO2) to changes in PCO2 (ΔPCO2) between end inspiration and end expiration, was superior to either ΔPO2 or ΔPCO2 alone in coupling with the changes of CBFv and BOLD signals under breath hold challenge. The regional cerebrovascular reactivity (CVR) results derived by regressing BOLD signal changes on bER under breath hold challenge resembled those derived by regressing BOLD signal changes on end-tidal partial pressure of CO2 (PETCO2) under exogenous CO2 challenge. Our findings provide a novel insight on the potential of using bER to better quantify CVR changes under breath hold challenge, although the physiological mechanisms of cerebrovascular changes underlying breath hold and exogenous CO2 challenges are potentially different.



2008 ◽  
Vol 28 (7) ◽  
pp. 1369-1376 ◽  
Author(s):  
Inna Sukhotinsky ◽  
Ergin Dilekoz ◽  
Michael A Moskowitz ◽  
Cenk Ayata

Cortical spreading depression (CSD) evokes a large cerebral blood flow (CBF) increase in normal rat brain. In contrast, in focal ischemic penumbra, CSD-like periinfarct depolarizations (PID) are mainly associated with hypoperfusion. Because PIDs electrophysiologically closely resemble CSD, we tested whether conditions present in ischemic penumbra, such as tissue hypoxia or reduced perfusion pressure, transform the CSD-induced CBF response in nonischemic rat cortex. Cerebral blood flow changes were recorded using laser Doppler flowmetry in rats subjected to hypoxia, hypotension, or both. Under normoxic normotensive conditions, CSD caused a characteristic transient CBF increase (74 ± 7%) occasionally preceded by a small hypoperfusion (−4 ± 2%). Both hypoxia ( pO2 45 ± 3 mm Hg) and hypotension (blood pressure 42 ± 2 mm Hg) independently augmented this initial hypoperfusion (−14 ± 2% normoxic hypotension; −16 ± 6% hypoxic normotension; −21 ± 5% hypoxic hypotension) and diminished the magnitude of hyperemia (44 ± 10% normoxic hypotension; 43 ± 9% hypoxic normotension; 27 ± 6% hypoxic hypotension). Hypotension and, to a much lesser extent, hypoxia increased the duration of hypoperfusion and the DC shift, whereas CSD amplitude remained unchanged. These results suggest that hypoxia and/or hypotension unmask a vasoconstrictive response during CSD in the rat such that, under nonphysiologic conditions (i.e., mimicking ischemic penumbra), the hyperemic response to CSD becomes attenuated resembling the blood flow response during PIDs.



2006 ◽  
Vol 100 (3) ◽  
pp. 850-857 ◽  
Author(s):  
Kenneth M. Tichauer ◽  
Derek W. Brown ◽  
Jennifer Hadway ◽  
Ting-Yim Lee ◽  
Keith St. Lawrence

Impaired oxidative metabolism following hypoxia-ischemia (HI) is believed to be an early indicator of delayed brain injury. The cerebral metabolic rate of oxygen (CMRO2) can be measured by combining near-infrared spectroscopy (NIRS) measurements of cerebral blood flow (CBF) and cerebral deoxy-hemoglobin concentration. The ability of NIRS to measure changes in CMRO2 following HI was investigated in newborn piglets. Nine piglets were subjected to 30 min of HI by occluding both carotid arteries and reducing the fraction of inspired oxygen to 8%. An additional nine piglets served as sham-operated controls. Measurements of CBF, oxygen extraction fraction (OEF), and CMRO2 were obtained at baseline and at 6 h after the HI insult. Of the three parameters, only CMRO2 showed a persistent and significant change after HI. Five minutes after reoxygenation, there was a 28 ± 12% (mean ± SE) decrease in CMRO2, a 72 ± 50% increase in CBF, and a 56 ± 19% decrease in OEF compared with baseline ( P < 0.05). By 30 min postinsult and for the remainder of the study, there were no significant differences in CBF and OEF between control and insult groups, whereas CMRO2 remained depressed throughout the 6-h postinsult period. This study demonstrates that NIRS can measure decreases in CMRO2 caused by HI. The results highlight the potential for NIRS to be used in the neonatal intensive care unit to detect delayed brain damage.



2001 ◽  
Vol 1 ◽  
pp. 168-180 ◽  
Author(s):  
Lars Edvinsson ◽  
Peter J. Goadsby ◽  
Rolf Uddman

Amylin and adrenomedullin are two peptides structurally related to calcitonin gene-related peptide (CGRP). We studied the occurrence of amylin in trigeminal ganglia and cerebral blood vessels of the cat with immunocytochemistry and evaluated the role of amylin and adrenomedullin in the cerebral circulation by in vitro and in vivo pharmacology. Immunocytochemistry revealed that numerous nerve cell bodies in the trigeminal ganglion contained CGRP immunoreactivity (-ir); some of these also expressed amylin-ir but none adrenomedullin-ir. There were numerous nerve fibres surrounding cerebral blood vessels that contained CGRP-ir. Occasional fibres contained amylin-ir while we observed no adrenomedullin-ir in the vessel walls. With RT-PCR and Real-Time�PCR we revealed the presence of mRNA for calcitonin receptor-like receptor (CLRL) and receptor-activity-modifying proteins (RAMPs) in cat cerebral arteries. In vitro studies revealed that amylin, adrenomedullin, and CGRP relaxed ring segments of the cat middle cerebral artery. CGRP and amylin caused concentration-dependent relaxations at low concentrations of PGF2a-precontracted segment (with or without endothelium) whereas only at high concentration did adrenomedullin cause relaxation. CGRP8-37 blocked the CGRP and amylin induced relaxations in a parallel fashion. In vivo studies of amylin, adrenomedullin, and CGRP showed a brisk reproducible increase in local cerebral blood flow as examined using laser Doppler flowmetry applied to the cerebral cortex of the a-chloralose�anesthetized cat. The responses to amylin and CGRP were blocked by CGRP8-37. The studies suggest that there is a functional sub-set of amylin-containing trigeminal neurons which probably act via CGRP receptors.





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